Vascular stents

Current Problems in

Surgery ° Volume 36 Number 12 December1999

Vascular Stents Mark A. Mattos, MD

Mike G. Douglas, MD

Associate Professor of Surgery Section of Peripheral Vascular Surgery Department of Surgery Southern Illinois University School of Medicine Springfield, Illinois

Asheville Cardiovascular and Thoracic Surgeons, PA Asheville, North Carolina

Kim J. Hodgson, MD Professor and Chief Section of Peripheral Vascular Surgery Department of Surgery Southern Illinois University School of Medicine Springfield, Illinois

Scott N. Hurlbert, MD Colorado Springs Vascular, PC Colorado Springs, Colorado

John P. Henretta, MD Asheville Cardiovascular and Thoracic Surgeons, PA Asheville, North Carolina

Yaron Sternbach, MD

M. Ashraf Mansour, MD Assistant Professor of Surgery Division of Vascular Surgery Loyola University Chicago-Stritch School of Medicine Chicago, Illinois

Douglas B. Hood, MD Assistant Professor of Surgery Division of Vascular Surgery University of Southern California Medical Center Los Angeles, California

David S. Sumner, MD Professor Emeritus Section of Peripheral Vascular Surgery Department of Surgery Southern Illinois University School of Medicine Springfield, Illinois

Assistant Professor of Surgery Division of Vascular Surgery Strong Memorial Hospital/University of Rochester Rochester, New York

Mosby

Current Problems in

Surgery ° Volume 36 Number 12 December 1999

Vascular Stents Foreword In Brief Biographic Information Historical Perspective 5tent Designs Balloon-expandable Stents Self-expanding Stents Thermal-memory Expanding Stents Experimental Stents

Biologic Response Stent Types Balloon-expandable Stents Self-expanding Stents

Clinical Indications Deployment Techniques Palmaz Stent Deployment Wallstent Deployment

Results Arterial Stents Venous Stents

References

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Foreword Over this decade the specialty of vascular medicine has grown rapidly because of the contributions of vascular surgeons, cardiologists, radiologists, and basic scientists. Of particular importance for surgeons has been the development and application of endoluminal stents for patients with peripheral vascular disease. Recently, several centers have reported their experience with this new technology, and early clinical results have been most promising. In this issue of Current Problems in Surgely, Dr Mark Mattos from the Southern Illinois University School of Medicine and his colleagues have written an excellent monograph on "Vascular Stents." Their thorough review begins with an important historical perspective and then addresses stent design, biologic response, stent types, clinical indications, deployment techniques, and finally the results of the use of various prosthetic devices throughout the arterial and venous system. Their article is heavily referenced and particularly well illustrated. Dr Mattos and his colleagues have covered this broad field admirably. This monograph will serve as an excellent resource for medical students, house officers, and practicing clinicians who are interested in this rapidly developing field.

SamuelA. Wells, Jr, MD Editor-in-Chief

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In Brief The presumed need for safer, similarly effective, and less expensive alternatives to conventional "open" vascular surgical techniques has resulted in rapid advances in catheter-based technology and refinements in percutaneous interventional techniques. As a result, the number of published reports in the vascular surgery, radiology, and cardiology literature about endovascular procedures has increased exponentially since 1990. Percutaneous transluminal balloon angioplasty (PTA) is the most commonly performed endovascular procedure in the world today. However, the development and application of percutaneous endoluminal balloonexpandable and self-expanding metallic stents in the treatment of peripheral vascular disease represents the most important advance in the field of vascular surgery during the last 10 years. Our goal in writing this monograph is to detail the complete history and clinical impact of the endoluminal vascular stent, beginning with its initial conception and early development in the animal laboratory of Dr Charles T. Dotter 35 years ago to the present, at which time stents of various types and designs are being deployed in every available and accepting vascular bed. At the present time, the "ideal" stent does not exist. As a result, numerous stents, each with its own design characteristics, are available for implantation. Currently available stents are defined by their composition and method of expansion. Research laboratory investigations and clinical trials have focused on developing a stent that will possess those qualities believed necessary to provide superior short- and long-term patency rates while ensuring that complication rates are kept to a minimum. Specific stent characteristics are described to help the practicing clinician determine those desirable clinical characteristics and stent qualities, which will ensure optimal clinical success after implantation. Ultimately, the difference between success or failure after stent deployment will depend on the short- and long-term biologic response of the target vessel to the stent. It is critical that the modem clinician understands the dynamic interactions that occur at the cellular interface of the stent surface, vessel wall, and the blood itself. In this monograph, we summarize and catalog the sequence of cellular events that occur after endoluminal stent deployment. Furthermore, we provide an introduction to the problems of restenosis and stent-related infections after stent deployment. Presently a wide variety of stents are available for clinical implantation. Modem interventionists are constantly being bombarded by the product Curr Probl Surg, December 1999

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manufacturing industry with so-called new and improved stent designs and associated devices. These stents are being labeled and sold to the medical community as the ideal stent, each superior and more cost-effective than its competitor. A brief descriptive summary of currently available balloon-expandable, self-expanding, and thermal-memory-expanding stents is provided to give the clinician an introduction to the morass of stents now available for implantation into human subjects. Characteristics of stents that have received United States Food and Drug Administration approval for implantation in human iliac arteries are described in detail Despite extensive documentation in the vascular, radiology, and cardiology literature, the use of stents in the treatment of peripheral arterial and venous occlusive disease remains controversial and hotly debated among surgical interventionists and nonsurgical interventionists alike. Nonetheless, there are several clinical indications for which the use of stents after an inadequate balloon angioplasty is considered an acceptable alternative to a surgical bailout procedure. A comprehensive written and pictorial description detailing the use of stents for these specific clinical indications is presented in the text. The success of stent placement requires the performance of a routine sequence of maneuvers. Understanding and knowledge of and adherence to these technical steps will ensure the greatest chance for anatomic, hemodynamic, and clinical success after stent deployment. Nothing defeats the purpose of the use of stents more thoroughly than an iU-prepared interventionist with insufficient knowledge regarding the advantages and limitations of stent deployment. A description of the deployment techniques for the 2 stents approved by the United States Food and Drug Administration for use in human iliac arteries is summarized in this monograph. Endoluminal stents are being used with increased frequency for the treatment of peripheral vascular arterial occlusive disease. The original indications for stent deployment were typically for suboptimal results after PTA. However, the indications have continued to be expanded, and stents are now used to treat complete occlusions and as the primary treatment of peripheral atherosclerotic lesions. However, the long-term results after stent placement remain inconclusive because few randomized comparative clinical data are available to support the use of stents in any peripheral vascular bed. Drs Doug Hood, Ash Mansour, and Scott Hurlbert provide a thorough review and assessment of the available literature and provide an in-depth analysis of the short- and long-term value of stent placement in iliac, femoral-popliteal, and tibioperoneal arteries. 914

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The experience of stent placement in the aorta, renal, visceral, and brachiocephalic arteries is summarized in detail by Drs John Henretta, Yaron Sternbach, and myself. The authors provide a careful analysis and objective comparison of the reported results of stent deployment against PTA alone or traditional surgical treatment. The technique of stent deployment is described, and complication rates specific to the treated arterial bed are reported. Few areas in modern vascular surgery have attracted more attention and produced more controversy among and within the 3 major interventional societies than the deployment of stents in the treatment of extracranial carotid occlusive disease. I have sorted through the confusing and haphazardly collected data that are currently available regarding this explosive topic. The results are cataloged according to clinical indication and by the type of stent deployed. A thorough and objective analysis of all relevant data is provided to help the practicing clinician separate myth from reality regarding the present benefits, or lack thereof, in the use of endoluminal stents in this contentious area. The application of stents in the venous system has only recently gained favor with interventionists, and reports in the literature have increased steadily. Unfortunately, most of the published data in this area are retrospective and anecdotal, involve small numbers of patients, or provide inconsistent follow-up. Nonetheless, evaluation and analysis of the available data remain important, and the data are summarized in this monograph. Dr Scott Hurlbert provides a review of the published literature reporting on the use of stents in patients with hemodialysis access-related peripheral and central venous obstructions. Hemodialysis-access patency and function after stent placement are compared to the results after PTA alone or after surgical bypass. Furthermore; Dr Hurlbert describes the role of and current recommendations for stent placement in patients with effort vein thrombosis and iliofemoral venous thrombosis. Dr Mike Douglas summarizes the current indications and results of stent placement in the central venous systems of patients with malignant vena cava obstruction. Technical aspects and the specific requirements for successful stent placement are described, and stent-related complications are discussed. Finally, I would like to express my appreciation to my secretary, Maryl Berns, for her clerical support.

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Mark A. Mattos, MD, graduated from Weber . State College and from the University of Utah School of Medicine. He underwent his. general surgical training at the University of Iowa Hospitals and Clinics. He completed a 2-year vascular surgery fellowship at Southern Illinois University School of Medicine, under the supervision of David S. Sumner, MD. He received endovascular surgical training from Kim J. Hodgson, MD, during his vascular fellowship and first year as a full-time surgical faculty member in the Section of Peripheral Vascular Surgery at Southern Illinois University School of Medicine. He is currently Associate Professor of Surgery in the Section of Peripheral Vascular Surgery at Southern Illinois University School of Medicine. His clinical research interests have focused on the short- and long-term clinical outcomes after carotid endarterectomy, the use of the noninvasive laboratory in determining the natural history and clinical outcomes of arterial and venous disease. Presently he has a special focus and interest in the training and education of vascular surgeons in the vascular surgical subspecialty of endovascular therapy.

Kim J. Hodgson, MD, received his medical degree from the University of Pennsylvania and his general surgery training at Albany Medical Center. He completed a fellowship in peripheral vascular surgery at Southern Illinois University under the direction of David S. Sumner, MD. He then joined the faculty of Southern Illinois University where he developed an independent Endovascular Therapy Program within the Section of Peripheral Vascular Surgery. This unique program, the first of its kind established as an integral part of an accredited vascular surgery fellowship program, was designed to train vascular surgery fellows in the vascular subspecialty of diagnostic and therapeutic endovascutar therapy, provide opportunities to investigate emerging endovascular technologies, and provide comprehensive care to patients with vascular disease. He recently was promoted to Professor of Surgery at Southern Illinois University School of Medicine and succeeds David S. Sumner, MD, as Chief of the Section of Peripheral Vascular Surgery at Southern Illinois University School of Medicine. His current research interests relate to the training of vascular surgeons in endovascular diagnostic and therapeutic techniques, investigation of endoluminal grafting of aneurysmal and occlusive diseases, evaluation of endovascular stents for occlusive disease, and the efficacy of thrombolytic agents in the treatment of peripheral vascular disease.

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Scott N. Hurlbert, MD, received his undergraduate degree in chemical engineering and his medical degree from the University of Colorado. He completed his general surgical residency at the University of Colorado Health Sciences Center. He recently finished a 2-year fellowship in vascular surgery under the direction of David S. Sumner, MD, in the Section of Peripheral Vascular Surgery at Southern Illinois University School of Medicine. He currently is in the private practice of vascular surgery in Colorado Springs, Colorado, where he continues to perform endovascular surgery.

John P. Henretta, MD, obtained an undergraduate degree in chemistry from Wake Forest University and received a degree in medicine from the Medical College of Virginia. He completed his general surgical residency at East Carolina University Medical Center. He completed a 1-year endovascular surgery fellowship, followed by a 2-year fellowship in vascular surgery in the Section of Peripheral Vascular Surgery at Southern Illinois University School of Medicine. He presently is in the private practice of vascular surgery at Asheville Cardiovascular and Thoracic Surgeons, PA, in Asheville, North Carolina. His current clinical focus is on endovascular grafting for the treatment of abdominal aortic aneurysms.

Yaron Sternbach, MD, is a graduate of the University of Pennsylvania and the Faculty of Medicine at McGill University. He completed his training in general surgery at the Tufts-New England Medical Center. He recently completed an endovascular surgery fellowship in the Section of Peripheral Vascular Surgery at Southern Illinois University School of Medicine. He then served as the first clinical fellow in vascular surgery in the Division of Vascular Surgery at the Johns Hopkins Hospital. He currently is Assistant Professor of Surgery in the Division of Vascular Surgery at Strong Memorial Hospital/University of Rochester. His career plans include continued investigation in endovascular catheter-based therapies for vascular disease and the continuation of a surgical-based endovascular therapy program within the Division of Vascular Surgery.

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Michael G. Douglas, MD, graduated from Marshall University School of Medicine and completed his general surgical residency at the Mayo Clinic. He subsequently completed a fellowship in vascular surgery at Southern Illinois University School of Medicine. During his 2-year vascular surgery fellowship, he also received training in the subspecialty of endovascular surgery in the Section of Peripheral Vascular Surgery. Currently he is a practicing vascular surgeon for Asheville Cardiovascular and Thoracic Surgeons, PA, in Asheville, North Carolina. He remains active in several clinical research trials with an emphasis on new endovascular techniques for arterial occlusive and aortic aneurysmal disease.

M. Ashraf Mansour, MD, earned his medical degree and completed an internship in internal medicine at the University of Cairo. He then participated as a research fellow in hematology at Michigan State University. He completed a general surgical residency at the University of Colorado Health Sciences Center and served as Instructor of Surgery at the same institution. He then served 2 years in the United States Army at Ft Benning, Georgia. He completed a 2-year fellowship in vascular surgery at Southern Illinois University School of Medicine. His fellowship training included an extensive experience in percutaneous endovascular revascularization techniques. Since 1995 he has served as Assistant Professor of Surgery at the Loyola University Chicago-Stritch School of Medicine. His present research interests are in carotid artery disease and the study of plaque morphologic features with noninvasive modalities. His tong-term plans include the establishment of an endovascular therapy program within the Division of Vascular Surgery at Loyola University.

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Douglas B. Hood, MD, earned his medical degree from the University of Oklahoma and completed his general / surgery training at the Los Angeles County/University of Southern California Medical Center. He completed a 2-year fellowship in vascular surgery in the Section of Peripheral Vascular Surgery at Southern Illinois University School of Medicine. During his vascular fellowship, he received experience and training in endovascular surgical therapy, including diagnostic and therapeutic angiographic techniques. He currently is Assistant Professor of Surgery in the Division of Vascular Surgery at the University of Southern California School of Medicine in Los Angeles. His current clinical and research interests include establishing an endovascular surgery program within the Division of Vascular Surgery. / ~ L ~ L/ ~ / ~ / ~

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David S. Sumner, MD, is a graduate of The Johns Hopkins University School of Medicine. After 3 years on the house staff of The Johns Hopkins Hospital, he transferred to the University of Washington in Seattle, where he completed his general surgical residency and remained on the faculty as Clinical Investigator. From 1967 to 1970, he served as a Lieutenant Colonel with the United States Army at the Arctic Medical Research Laboratory in Fairbanks, Alaska. After his return to the University of Washington, he rose to the rank of Associate Professor and, in 1975, was appointed Professor of Surgery and Chief of the Section of Peripheral Vascular Surgery at Southern Illinois University School of Medicine. In 1984, he received the Distinguished Professor of Surgery Award at Southern Illinois University. He recently retired from active clinical practice and will serve as Professor Emeritus in the Section of Peripheral Vascular Surgery. His primary clinical and research interests include vascular hemodynamics and pathophysiologic investigation, evaluation of venous disease, and noninvasive vascular testing. / / f ~ ~

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Vascular Stents ~

dvances in catheter-based technology and refinements in percutaneous interventional vascular techniques have led to an exponential rise in the number of percutaneous endovascular procedures being used for the treatment of arterial and venous disease) ,2Percutaneous transluminal balloon angioplasty (PTA) remains the most commonly performed endovascular procedure today because it has become an acceptable form of treatment in numerous vascular beds. However, angioplasty has several drawbacks that limit its overall benefit, including elastic recoil, residual stenosis, intimal dissection associated with acute thrombosis, and early restenosis. These shortcomings have been shown to result in decreased shortand long-term patency rates. 3 Efforts to decrease the incidence of these angioplasty-related problems while maintaining and improving patency rates resulted in the development and application of percutaneous endoluminal balloon-expanding and self-expanding metallic endoskeletal devices known as "stents." The idea of providing endoluminal support to maintain the patency of a vessel after PTA is credited to the visionary thinking of Charles T. Dotter, MD, who initially proposed this concept 35 years ago. In 1964, he envisioned that his technique of graduated transluminal dilatation of totally occluded arteries might need further endoluminal support to maintain the patency of the arterial lumen: "Once a pathway has been created across an occluded segment, repeated dilatation or the temporary use of a Silastic endovascular (or in some cases paravascular) splint could maintain an adequate false lumen until the natural processes of fibrosis and re-intimalization had taken place.''4 However, it was not until 5 years later that he was able to put his visions to work in the animal research laboratory and publish the first manuscript on percutaneous stenting in 1969. 5 Dotter developed a method for the percutaneous transluminal placement of tubular devices into arterial beds (Fig 1). He placed these prosthetic tube grafts into normal femoral and popliteal arteries of 25 dogs. All of the tubular grafts became occluded as the result of thrombosis within 24 hours of implantation. Because of the initial discouraging results with these nonexpanding plastic tubular prostheses, the 6 final experiments were performed with tubular open-centered coilsprings with no. 5 stainless steel wire, 1 to 10 cm in length. Despite the fact that 4 of the 6 coilsprings developed thrombosis and occlusion within 24 hours, 2 coilsprings (1 cm in length) remained patent by serial angiography for more than 2 years 920

Curr Probl Surg, December 1999

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FIG 1, Artist's re-creation of original technique described by Dotter for percutaneous placement of an endoluminal tube graft stent through a guiding catheter. (Modified from Dotter CT. Transluminally-placed coilspring endarterial tube grafts: long-term patency in canine popliteal artery. Invest Radio11969;4:329-32.)

after implantation. Dotter concluded that an open-centered coilspring configuration may result in improved long-term patency rates. After this seminal article describing the technique of placing percutaneous transluminal stent devices, little interest or enthusiasm was generated in the interventional community for further development and use of intraluminal stents in the peripheral vascular system. This unfortunate delay in stent development occurred as a result of the wide acceptance of PTA in the treatment of various atherosclerotic vascular diseases after the preliminary pioneering work of Gruentzig in the early 1970s. 7 It was not until the limitations of balloon angioplasty in the treatment of coronary artery disease were identified did interest resurface for the use of percutaneous intraluminal stenting as a method to prevent abrupt vessel closures and decrease restenosis rates after P T A . 7 Fourteen years after Dotter's initial report on the use of a crude percutaneous intraluminal stent device, investigators began to develop and evaluate various stent designs, initially in the research laboratory and later during various clinical trials. Early investigations described the use of thermal-memory stents, and in 1983, 2 studies were published simultaneously describing the use of a thermally expandable stent coil comprised of the metal nitinol, an alloy comprised of nickel and tantalum.8,9This fabricated alloy exhibits propCurr Probl Surg, December 1999

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erties of thermal memory, which allows these devices to alter their shape from a linear configuration at lower room temperature to a coiled shape of predetermined diameter when placed in contact with warmer saline solution or blood. Dotter and colleagues8 provided a preliminary report describing the experimental technique for placement of the stem coil; Cragg and colleagues 9 reported their initial experience with nitinol-stent implantation into 4 canine aortas, describing angiographic patency up to 4 weeks. Cragg and colleagues l° followed up this report in 1984, with a second study evaluating thermal-memory stents, which assessed the presence, severity, and time course of stent restenosis after implantation in 9 canine aortas. Further innovations in stent design occurred in the mid-1980s and have continued into the 1990s because numerous investigators reported their experiences with the use of self-expanding and balloon-expandable stents. Many of these early prototypes had obvious design flaws and never progressed beyond use in animal laboratory studies.~t,~2 However, the limitations of these initial stent devices served as a starting point for the development of technically superior stents with improved delivery systems, ultimately leading to the introduction of the current generation of selfexpanding and balloon-expandable stents, t3-15 The first reported use of stent implantation in human peripheral (and coronary) arteries occurred in 1987 by Sigwart and colleagues, 16 who used the Medinvent (Medinvent SA, Lausanne, Switzerland) self-expanding mesh stent. Ten stents were placed in 6 patients (3 iliac and 4 femoral arteries) after the failure of balloon angioplasty. Patients received heparin, aspirin, and dipyridamole (Persantine) and underwent long-term treatment with acenocoumarol. Follow-up at 6 months revealed no evidence of angiographic restenosis, and all but 1 of the patients showed improvement in their clinical symptoms. Two years later in 1989, Gunther and colleagues 17 reported on the early results of a second-generation self-expanding stent, the Wallstent (Schneider Lnc, USA, Minneapolis, Minn). The preliminary results from this study, which were reported as a part of the European Wallstent Peripheral Artery Implant Study, indicated the technical feasibility of stent placement. Early stent patency rates were excellent and comparable to the reported results of clinically available balloon-expandable stent devices. Two years later in 1991, Gunther and colleagues TM reported on the first 100 cases involving implantation of the Wallstent in iliac arteries. Technical success in placement of the stent was achieved in 97% of the procedures, and the patency rates at 1-month and 3-month follow-up were 92% and 89%, respectively. Further analysis of the data from the European Wallstent study, involving larger numbers of cases with longer follow-up, .again noted continued excellent short- and long-term patency rates. 19 922

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The initial use of a balloon-expandable stent in human subjects was reported in 1988 by Palmaz and colleagues.2° Fifteen patients with symptomatic primary iliac artery stenoses underwent implantation of 3 mm x 30 mm Palmaz stents (Johnson and Johnson, Interventional Systems, Warren, NJ). No periprocedure occlusion or thrombosis occurred in any stent, and the early ankle-brachial index improved significantly from 0.68 to 0.96. Clinical improvement matched the angiographic patency and paralleled the hemodynamic improvement after stent implantation. This preliminary trial by Palmaz and colleagues was followed by a second study that reported on data from the first multicenter stent trial approved by the Food and Drug Administration (FDA) for the treatment of atherosclerotic iliac artery stenosis. 21 The results from this study indicated that implantation of the Palmaz stent in iliac arteries was safe and effective in both short- and long-term follow-up. These findings led to FDA approval for the use of the Palmaz stent in iliac arteries, resulting in the rapid and exponential increase in use of this stent (as well as numerous other stents) in the iliac arteries, and in other vascular beds not approved by the FDA. In summary, this brief overview on the historical conception and development of intraluminal stents has highlighted the rapid technologic advancements that have taken place since Dotter first reported on his crude intraluminal stent tube graft almost 30 years ago. Because research technology in stent design moves forward and interventional techniques continue to improve, the role of endovascular stents in the treatment of atherosclerotic vascular disease will adapt and change as well. Precisely what future clinical benefit these endoskeletal devices will provide in the acute and chronic treatment of atherosclerofic peripheral vascular disease remains to be determined.

Stent Designs To ensure optimal clinical success, endovascular stents should possess clinical characteristics that provide for percutaneous delivery, easy deployment, precise placement, elastic expansion, functional diversity, and biologic inertness and compatibility. Presently there is no "ideal" stent available that satisfactorily provides all of these design properties. Stent characteristics that are associated with easy rapid deployment include longitudinal flexibility, atraumatic percutaneous delivery, radiopacity, precise placement, symmetric apposition, and reliable expansion. Longitudinal fexibility coupled with percutaneous delivery minimizes unnecessary manipulation of a stent and helps to decrease potential insertion-related complications. Radiopacity of a stent provides the necessary visualization required for accurate placement of the stent at the target Curr Probl Surg, December 1999

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lesion. Reliable expansion produces symmetric apposition of the stent against the vessel wall, which maintains an adequate luminal diameter, prevents acute thrombosis and distal stent migration, and allows for complete endothelialization over the stent surface. Acceptable functional versatility in a stent is characterized by its ability to be deployed successfully in various arterial and venous vessels, having a high-constrained (compressed)-tounconstrained (expanded) expansion ratio, and possessing the capability to undergo incremental balloon dilatation. A high expansion ratio permits the use of a small-diameter delivery system to insert larger stents without an increased risk of trauma or other complications. Additionally, the presence of a small delivery system allows percutaneous placement of different stents from multiple access sites into the diseased lumens of either arteries or veins of various diameters. Controlled incremental stent expansion by balloon dilatation helps to decrease the risk of stent-to-vessel diameter mismatch and, in doing so, ensures that the apposition between the stent and vessel wall is maximized. High biocompatibility requires that the surface area of stents exhibit the dual function of being resistant to thrombus formarion and having the ability to minimize neointimal growth. Stable apposition of the stent to the vessel wall, a low metal-to-intima surface area ratio, and reduced stent wire thickness, all play a role in the reduction of excessive neointimal hyperplasia although enabling early endothelialization to occur on the stent surface after implantation. Rapid endothelialization associated with minimal neointimal development may provide the greatest opportunity for long-term stent patency.22 Several different stent designs and devices are presently undergoing evaluation in various clinical trials and research laboratory investigations. Current clinically available endovascular stents are constructed of metal, either stainless steel, tantalum, or nitinol, and are defined by their methods of expansion: balloon-expandable, self-expanding, or thermal-memory expanding.

Balloon-expandable Stents These stents are typically mounted on an angioplasty balloon in their constrained configuration, then compressed either manually or with a crimping tool to prevent dislodgment during insertion through the sheath and target vessel. On arriving at the target lesion, the balloon is inflated, and the stent is expanded to its intended unconstrained diameter (Fig 2). Some balloon-expandable stents come premounted on an angioplasty balloon so that the need for compression is eliminated. Most balloon-expandable stents exhibit excellent resistance to radial recoil (so-called "hoop 924

Curr Probl Surg, December 1999

FIG 2. Balloon-expandable Palmaz stent shown mounted on an angioplasty balloon in compressed (left) and expanded (right) configurations.

strength") and provide reliable expansion and stability; but because of their increased stiffness, longitudinal flexibility is sacrificed. Additionally, the diameter of balloon-expandable stents can be increased incrementally if necessary by reinflation with a larger angioplasty balloon. Curr Probl Surg, December 1999

925

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FIG .3. Self-expanding Wollstent depicted in constrained configuration within outer protective sheath (top) and in unconstrained, fully expanded configuration after withdrawal of the sheath (bottom).

Self-expanding stents Self-expanding stents do not require manual loading but are packaged preloaded in their constrained configuration within a delivery catheter-sheath system. After insertion through a percutaneous sheath and placement into the artery or vein, the overlying protective covering is withdrawn because the stent is held at the desired position within the vessel. Withdrawal of the protective covering allows the stent to become unconstrained and undergo selfexpansion to its predetermined diameter (Fig 3). Self-expanding stents offer the advantage of excellent longitudinal flexibility, which enables them to navigate tortuous or heavily diseased vessels easily. However, this increased flexibility, as compared with balloon-expandable stents, may be associated with a reduction in resistance to radial recoil. Self-expanding stents, unlike balloon-expandable stents, can only expand to their predetermined diameter.

Thermal-memory Expanding Stents Stents of this design are constructed of a nickel-titanium alloy known as "nitinol." Nitinol stents exhibit the shape-changing ability of "thermal memory" The unique memory capability of this metal allows stents to be deformed and compressed into a low-profile delivery system at room temperature. When this stent delivery system is inserted into the vessel and exposed to the higher body temperature, the nitinol stent "'remembers" its original shape and undergoes self-expansion to its unconstrained shape and diameter. Nitinol stent devices may be shaped as a coilspring wire or tubular prosthesis (Fig 4). Similar to self-expanding stents, nitinol stents can only expand to their predetermined shape and diameter. 926

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FIG 4. Vascucoil(left) coil-springwire and Symphony(Hght} tubular nitinotthermal-memoryexpanding stents.

Experimental Stents Several innovative stent designs have been studied experimentally, including stents composed of bioabsorbable materials (polyactic and polyglycolic acid), 23 stents of metallic design for temporary use in the acute clinical setting,24 and stents with prosthetic or biologically coated metal surfaces. 25 However, the clinical benefits of these experimental stent designs remain largely unknown and will require rigorous comparative evaluation before their role in the treatment of peripheral vascular disease is determined.

Biologic Response The ultimate goal of endovascular stent implantation is to create an environment between the metallic stent and blood vessel wall that allows for complete endothelialization of the stent surface and vessel wall. The preservation of the endothelium after stent implantation reduces the risk of acute thrombosis and allows for continued long-term vessel patency. The biologic response that ultimately determines whether re-endothelialization occurs after stent implantation depends on the interactions that occur at the interface between the stent, vessel wall, and blood components. These interactions are determined by various factors, which include Curr Probl Surg, December 1999

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FIG 5. A, Dilated human cadaver coronary artery with intimal and medial dissection and residual luminal stenosis. B, Dilated and stented human cadaver coronary artery with stent struts "tacking" up intima and medial tear (arrow). Note endothelial tissue mounds protruding between stent struts. (From Schatz RA. A view of vascular stents. Circulation 1989;79:445-57. By permission.)

the chemical composition, physical characteristics, and mechanical properties of the stent and the proliferative biologic resporise elicited by the vessel wall Palmaz and coUeagues 22,26 and others 27-3°have cataloged the sequence of events that occur after implantation of an intraluminal metallic stent in the arterial circulation. Typically, when a stent is properly deployed within the vessel, the metal struts are embedded into the wall that form depressions or indentations, and endothelial tissue mounds protrude between the latticework of the stent into the lumen (Fig 5). Immediately after stent deployment, the positive electrical charge of the stent attracts plasma proteins to its metallic surface, forming a randomly oriented layer of fibrinogen approximately 5 to 20 mm thick. This fibrinous layer then forms attachments with circulating platelets and fibrinous thrombus. Within 15 928

Curr Probl Surg, December 1999

minutes, irregular amorphous thrombotic clot forms over the depressions and embedded stent struts while the protruding tissue mounds remain uncovered by thrombus. By 24 hours, the thrombotic layer overlying the stent struts has undergone repeated remodeling and is eventually covered by a thin layer of fibrinogen strands oriented in the direction of the blood flow. At 1 week, the thrombus and fibrin overlying the embedded stent struts become covered with immature endothelial cells (neointima; Figs 6, A and 7, A). This re-endothelialization over the stent surface continues during the next several weeks as a result of multicentric endothelial growth from the adjacent tissue mounds. During the next few weeks, maturation of the endothelium continues, and smooth muscle cell proliferation occurs, as noted by the early invasion of myofibroblasts that are then replaced by proliferating fibroblasts. This proliferation occurs first in the area of the struts, then expands eccentrically, and fmally results in maximal neointimal thickness at 8 weeks after stent implantation (Figs 6, B-C and 7, B-C). At 32 weeks, the neointima has thinned and is then steadily replaced by collagen over the next several years (Figs 6, D and 7, D). Most currently available stents are composed of metal alloys, including tantalum, nitinol, and the medical grade 300-series stainless steels 304 and 316L. Other metals comprising the bulk of these stents include iron and chromium. These metals, by their nature, produce a foreign-body reaction after implantation, theoretically increasing the risk for thrombus formation on the stent surface. This thrombotic risk is dependent on the thin layer of metal oxide that forms on the stent surface and the influence it wields on the protein and cellular reactions that occur on the stent surface. This metal oxide layer is determined by the polishing process that occurs during stent production. The type of process chosen creates the final surface characteristics and helps to determine the thrombogenicity of the stent. An abrasive polishing process produces a crystalline-like stent surface that contains most of the metal elements comprising the stent oriented in a random fashion. The surface defects and granular roughness associated with a crystalline surface may induce flow turbulence and increase the risk of thrombus formation. Electropolishing, a finishing process used for stainless steels, removes most of the components from the stent surface, resulting in a uniform dominant metal oxide layer of chromium. This layer of chromium oxide produces a stable stent-tissue interface by avoiding excessive oxidation, thereby minimizing protein alterations and cellular reactions and decreasing the thrombogenicity of the stent. 31,32 The electrical charge of the stent surface has been suggested to have a role in the thrombogenic potential of the stent. Most metals and alloys Curt Probl Surg, December3.999

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FIG 6, Gross specimensof stented canine coronary artery. A, At 1 week, the stent is visible through thin translucentlayer of neointima. B, By 3 weeks, hemosiderindeposits become prominent.

used for endovascular stents have an electropositive charge in electrolyte solutions, in comparison with biologic tissues or the metal tantalum, which have an electronegative charge in solutions. The positive electrical charge of stents may serve as an attraction for electronegatively charged platelets, white blood cells, and other clotting factors, therefore theoretically increasing the risk of thrombus formation. However, the clinical importance of this electropositive charge in stents remains unclear, because this positive charge also attracts electronegative plasma proteins and fibrinogen, which may neutralize the surface charge of the stent and decrease its thrombogenicity. Tantalum, a metal used in the manufacture of various stents, has a net negative charge that is purported to decrease a 930

Curr Probt Surg, December 1999

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FIG 6 Cont'd. Gross specimens of stented canine coronary artery. C, At 8 weeks, the stent is now covered by thick neointimo. D, At 32 weeks, the intimo is seen clearly through a considerably thinned neointima. (From Penn IM, Levine SL, Schatz RA. Intravascular stents: the evolution from prototypes to clinical trials. In: Ahn SS, Moore WS, editors. Endovascular surgery. Philadelphia: WB Saunders Co; 1992. p 504-22. By permission.)

stent's thrombotic potential. However, the negative surface charge of a tantalum stent soon turns electropositive within hours of contact with air or electrolytic solutions and quickly assumes the characteristics and reactions inherent in other electropositive stents. Free surface energy or wetability is another surface property that influences how blood and its components will react in contact with a stent surface. This property is defined by the number of unsatisfied intermolecular bonds at the stent surface and determines whether a fluid droplet spreads over a solid surface. Critical surface tension is a measurement of this property and is calculated from the contact angle of a fluid droplet on the solid surface. A critical surface tension of 20 to 30 dynes/cm indicates the presence of a relatively thrombo-resistant surface. Most metals used in the manufacturing of endovascular stents have a critical surface tension greater than 30 dynes/cm and are therefore thrombogenic. Fortunately, the initial fibrinogen layer forming on the stent immediately after implantation has a critical surface tension somewhere in the thrombo-resistant range. 33 Curr Probl Surg, December 1999

931

L

FIG Z Photomicrograph of the gross specimen in Fig 6. A,. At I week, immature endothelial cells (arrows) line the early thrombus (T) and fibrin deposit after stent implantation. B, By 3 weeks, the thrombus has been replaced by myofibroblastic cells, with medial compression beneath the stent struL

Stent thrombogenicity may also be affected by the technique of stent deployment and the final location of the stent in relation to the vessel wall after implantation. Optimal deployment of a stent requires that the struts of the stent be embedded within the vessel wall, with a latticework of normal endothelium protruding between the depressed struts. Ideally, the stent struts can be embedded adequately if the final stent diameter is 10% 932

Curr Probl Surg, December 1999

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FIG 7 Cont'd. Photomicrograph of the gross specimen in Fig 6. ¢,, At 8 weeks, the greatest neointimal thicknessis found with fibroblast proliferation and medial thinning. D, At 32 weeks, mature endothelial cells (arrows) cover the thin sclerotic ground substance. L, Lumen; M, media; *, stent strut space. {From Penn IM, Levine St, Schatz RA. Intravascutar stents:the evolution from prototypes to clinical trials. In: Ahn SS, Moore WS, editors. Endovascular surgery. Philadelphia: WB Saunders Co; 1992. p 504-22. By permission.)

to 15% greater than the adjacent vessel diameter. After adequate implantation, the protruding tissue mounds can begin the process of re-endothelialization over the thrombus-covered stent struts by multicentric growth. If the stent struts are not embedded properly in the vessel wall, protrusion Curr Probl Surg, December 1 9 9 9

933

of endothelial tissue mounds does not occur, and a continuous layer of thrombus forms over the entire stented surface. Multicentric endothelialization is blocked, and re-endothelialization must occur from the endpoints of the stent and is therefore much slower. There is much controversy regarding the biologic response to and the clinical relevance of radial compliance (rigidity) or longitudinal flexibility in preventing acute thrombosis and maintaining long-term vessel patency. Many investigators believe that longitudinal flexibility is a valuable characteristic for stent implantation because it allows placement of such stents in areas of vessel tortuosity and motion. However, it has been postulated that longitudinal motion of flexible stents may increase the severity of neointimal hyperplasia because of instability of the neointima, therefore negatively affecting the re-endothelialization of the stent and ultimately decreasing the long-term patency of these stents. 14The authors of these reports postulated that the decreased incidence of restenosis observed for rigid balloonexpandable Palmaz stents was, in part, related to the medial atrophy that occurred after stent implantation. Furthermore, these same authors stated that neointimal thickness should not exceed 100 ~tm 6 months after stent implantation.29 It was not until several years later that atrophy of the medial layer after Wallstent implantation was described by Vorwerk and colleagues.28 These authors demonstrated that the flexible self-expanding stents regularly induced layers of neointimal thickness similar to that reported for the inflexible Palmaz stent and concluded that medial atrophy was a persistent finding for both rigid and flexible stent designs. The incidence of restenosis or occlusion after percutaneous balloon angioplasty in the peripheral circulation has been reported between 20% and 50%, depending on the arterial bed treated, and is similar to the incidence observed in the coronary circulation.34,35Efforts to avoid luminal narrowing and the development of restenosis after angioplasty as the result of intimal hyperplasia led to the application of stents in both the peripheral and coronary circulations. Metallic stents are designed to serve as an internal scaffold to maintain the structure and intralluminal patency of the target vessel. Consequently, the deployment of stents has gained widespread use in peripheral arterial occlusive disease, despite a paucity of prospective data documenting their safety and efficacy. The ability of the stent to maintain or increase the internal diameter of the target vessel allows the interventionalist to use stents more aggressively and to offer an alternative treatment option for suboptimal results after other endovascular procedures. Stents clearly improve early anatomic results after failed or unsuccessful balloon angioplasty. Unfortunately, restenosis or occlusion after stent placement remains a significant problem, with reported long-term recurrent stenosis 934

Curr Probl Surg, December 3.999

rates up to 4 0 % . 36 The development of a progressive intimal hyperplastic response after stent implantation has been observed as the primary cause in the development of restenosis or occlusion within the stented arterial and venous segments (Fig 8). 37-39 Other investigators have shown that stent remodeling may contribute to the formation of restenosis. 38 Several investigators have suggested that restenosis occurring at the stent margins or central articulation is more frequently related to stent-induced neointimal hyperplasia compared with restenosis development within the stent itself, which may result from a combination of stent remodeling and the presence of intimal hyperplasia. Furthermore, Hoffman and colleagues37 suggested that the presence of a large plaque burden located at the junction between the stented and unstented vessel is the strongest periprocedural predictor for stent restenosis. The authors hypothesized that the presence of this plaque along with the development of neointimal hyperplasia at the stent margin was responsible for the appearance of restenosis in this area. They recommended that the margins of stents should only end in vessels with good lumen diameters and minimal plaque burden. Van Lankeren and colleagues38 reported a similar observation and recommended the use of a single long stent and the avoidance of articulated or multiple short stents for the treatment of occlusive dissection after angioplasty. Endoluminal stents maintain or increase the vessel lumen size and improve early anatomic results, but at the expense of excessive neointimal hyperplasia. Strategies directed at limiting this response have met with only partial success, and restenosis continues to complicate stenting procedures. Investigators have questioned whether the hyperplastic response was primarily determined by the amount of arterial expansion produced by stent deployment or whether the geometric design of the stent or the material on the stent surface in contact with the vessel wall also contributes. In a recent study, Rogers and Edelman34 noted that a 29% decrease in strut-strut intersections reduced vascular injury by 42%, neointimal hyperplasia by 38%, and thrombosis by 69%. They noted that coating the stainiess steel stent surface with an inert polymer eliminated the development of thrombosis but had no effect on vascular injury or neointimal hyperplasia. The authors concluded that geometric design and coating of the stent surface may be more important factors than the degree of poststent diameter in determining the extent of neointimal hyperplasia. Recent investigations have focused on the use of endovascular radiotherapy (brachytherapy) to avoid the intimal hyperplastic response and to limit the degree of restenosis.4°-45Irradiation affects neointimal proliferation by causing DNA damage and reproductive cell death, modulating the synthesis or release of specific growth factors responsible for cell proliferation, Curr Probl Surg, December 1999

935

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FIG 8. A, Wallstent visualized in the infrapopliteal position. Note that the Wollstent is fully expanded. B, Angiogram demonstratesthe presence of intimal hyperplasia within the Wallstent, resulting in restenosis at the margin and proximal portion of the stent.

and may induce apoptosis in some cell systems.44 Long-term histologic analysis of irradiated vessels showed diminished growth in the cellular population, a thinner, more compact cellular layer of the myofibroblasts, and qess myxoid degeneration compared with vessels that did not receive radiotherapy. These findings were believed to have occurred as a result of a reduced migration and mitosis rate of myofibroblastic cells after irradiation.43 Results of initial studies in both the peripheral and coronary arterial systems have been encouraging but involve small numbers of patients with 936

Curr Probl Surg, December 1999

limited follow-up data. Any perceived success of brachytherapy for reducing the incidence of restenosis after stent implantation must be balanced against its potential complications, including radiation-induced arteritis, peripheral artery stenosis, and secondary development of malignancy. When stents are placed in an environment where bacteria or other microorganisms are present, irreversible colonization can occur on the stent surface, and the normal process of events leading to tissue incorporation of the stent wilt be disrupted or prevented.26 This lack of complete endothelialization in the face of a bacterial presence has been postulated to be the result of greater adaptive mechanisms of bacteria for permanent attachment to a prosthetic surface in comparison with those.of competing host cells. 46 Little information is available in the literature regarding the incidence and related outcome of infected endovascular stents. To date there are 5 case reports of infection associated with the implantation of endovascular stents.47-49 In all 5 reports, Staphylococcus aureus was cultured. Histopathologic examination of the resected vessels revealed acute necrotizing infectious arteritis. Numerous bacterial colonies were observed to be attached to the intima and stent surface and remained free and floating within the intraluminal exudate, suggesting that the necrotizing infection occurred because of the bacteremia. Bacterial seeding through the needle puncture track with retrograde contamination after placement of the introducer sheath has been reported as a possible mechanism for a bloodborne stent infection. Others have suggested that the actual disruption and fracture of the arterial plaque after balloon angioplasty may serve as a source for bacterial seeding to this area, possibly increasing the risk of early stent infection after deployment and resulting in the loss of tissue incorporation of the stent. Consequently, prophylactic intravenous antibiotics are currently recommended before stent deployment to minimize bacterial contamination and to ensure adequate tissue incorporation.49

Stent Types. Many different endovascular stenting designs and devices are currently available for clinical use worldwide. Many of these stents are undergoing evaluation in ongoing clinical trials or are being studied experimentally in research laboratories. Other devices continue to be used clinically in vascular beds in which there is no scientific evidence supporting their safety or efficacy in the treatment of atherosclerotic and nonatherosclerotic peripheral vascular disease. Currently in the United States, only 2 stent devices are approved by the FDA for clinical use in the peripheral vascular system: the balloon-expandable Palmaz stent and the self-expanding WaUstent. Curr Probl Surg, December 1999

937

FIG 9. Three clinically available Palmaz stents in the compressed and dilated positions demonstrate rectangular slots in the constrained (compressed) position and diamond-shaped slots in the unconstrained (expanded) configuration. Note the articulated design of the middle stent, which permits bending of the stent to allow this rigid stent to readily pass across the aortic bifurcation or through tortuous vessels.

Balloon-expandable Stents Palmaz Stent. The Palmaz balloon-expandable stent (Johnson and Johnson Interventional Systems, Warren, NJ) is a 316L stainless steel tube with rows of staggered rectangular slots encompassing the entire surface area. This design allows for expansion to larger diameters on balloon expansion without sacrificing rigidity and radial, strength. The multiple rectangular slots, present when the stent is constrained, change their configuration to a diamond shape when the stent is dilated, allowing for full symmetric expansion (Fig 9). Minimal shortening of the stent occurs if it is properly sized before deployment. The stent wall thickness varies slightly but generally is in the 0.012-mm range. Although the stents provide superb resistance to radial recoil, their lack of flexibility (stiffness) makes it difficult for them to navigate through sharp bends and tortuous vessels or across the aortic bifurcation from a contralateral groin • approach. Invariably, deployment of these stents requires an ipsilateral antegrade or retrograde approach to the target lesion. These devices have been proved to have easy deliverability and deployment, reliable expansion, minimal migration, and good biocompatibility. Palmaz stent diameters and lengths range from between 1.0 to 3.0 cm and 4.0 to 12.0 cm, respectively. The stents do not need to be sized upwards, as is necessary for self-expanding stents, but rather their diameter can be increased to the 938

Curr Probl Surg, December 1999

desired size by incremental balloon dilation. The Palmaz stents are available in either an articulated or nonarticulated form and can be obtained either unmounted or premounted on an angioplasty balloon. In September 1991, the FDA approved the use of the Palmaz stent in the treatment of iliac artery occlusive disease. However, FDA approval, then and as it exists presently, was restricted to the use of a single Palmaz stent, the unmounted "P308" stent. This particular stent has an unconstrained diameter of 3.4 m m and length of 30 mm. It has the ability to undergo expansion to a minimal diameter of 8 m m up to a maximal expansion diameter of 12 mm. Each incremental increase in stent diameter is associated with an accompanying reduction in length (28.9 m m at an 8-mm diameter down to 26.2 m m at a 12-mm diameter). Extensive experience with these stents has shown that the non-FDA-approved "P294" and "P394" stents may be more versatile stents in the treatment of iliac occlusive disease simply because of their smaller 7F catheter delivery system. Gianturco-Roubin Stent. The Gianturco-Roubin stent (Cook Inc, Bloomington, Ind) is also named the "Bookbinder stent" because of its resemblance to the bindings on a book. It is comprised of a flexible stainless steel wire that is wrapped and compressed in a cylindric fashion with a reversing bend every 360 degrees (Fig 10).s° This particular design allows for a smaller constrained diameter, which permits the stent to be delivered without a protective sheath and to be deployed through a lowprofile 6F delivery system. However, it has a low expansion ratio that limits its use to smaller vessels. The Gianturco-Roubin stent currently has FDA approval for use in coronary arteries, but its design characteristics may make deployment of this stent in the distal peripheral arterial system desirable. Strecker Stent. The Strecker stent (Medi-tech Inc, Boston, Mass) is a knitted wire-mesh tubular stent design composed of a single tantalum wire filament 0.1 mrn in diameter. Tantalum metal has good radiopacity, is biologically inert, displays no ferromagnetic effects, and exhibits minimal shortening during expansion. This stent is chemically electropolished to create a negative charge on the stent surface charge. This negative charge is postulated to help repel platelets and reduce platelet adhesion from the stent surface. 51 The stent is constructed by a series of loosely connected interwoven loops, exhibiting flexibility, elasticity, and excellent compressibility in the radial and longitudinal directions. This stent has a high expansion ratio, and its diameter can be expanded to 6 times its unconstrained diameter ~ i g 11). 52 The diameter ranges of this stent are from 2 to 14 mm, with an achievable maximum length of 8 cm. The stent diameter is determined according to the number of loops per Curr Probl Surg, December 1999

939

FIG 10. Gianturco-Roubin "Bookbinder" stent. Stents are mounted on a balloon in its compressed (constrained) position and expanded on a balloon in an unconstrained configuration. Note the longitudinal flexibility of the stent. (From Roubin GS. Gianturco-Roubinstent. In: Kim D, Orron DE, editors. Peripheral vascular imaging and intervention. St Louis: Mosby Year-Book,Inc; 1992. p 532. [Courtesy of Cook, Inc, Bloomington, Ind.] By permission.)

stent circumference and the loop length of the metallic knit. The Strecker stent can be delivered with an 8F delivery system and does not require a protective sheath during placement. This stent has enjoyed widespread popularity in Europe, especially Germany, but is currently unavailable for clinical use in the United States.

Self-expanding Stents Wallstent. The self-expanding Wallstent endoprosthesis (Schneider USA, Inc, Minneapolis, Minn) is the second of 2 endovascular stent devices currently being used in the United States that have been approved by the FDA for clinical use in the iliac artery. Schneider USA, Inc, received FDA approval on May 28, 1996, for in~avascular use of its 6- to 10-mm diameter self-expanding Wallstents. The approved clinical indicag40

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FIG 11. Streckertantalum stent on balloon stentassembly.Note loosely connected interwoven loops permiffing flexibility and compressibility and high expansion ratio. (From Strecker EP, Hagen B, Liermann D, et al. Current status of the Strecker stent. Cardiol Clin 1994,12:674. By permission.)

dons for stent implantation were used after suboptimal results after PTA of c o m m o n and/or external iliac artery stenoses 10 cm or less in length. The Wallstent is constructed of 16 to 20 surgical-grade stainless steel illaments woven with a braiding angle of 124 degrees, creating a flexible tubular structure. The steel filament diameters are very thin, ranging from 0.075 to 0.17 mn'/, creating a thin-walled device. The crosspoints of the Wallstent filaments are thin, loose, and not bound together, providing for excellent longitudinal flexibility and reliable self-expansion, but poor radiopacity (Fig 12). These characteristics can be changed by altering the thickness and crisscrossed pattern of the unsoldered steel filaments. The Wallstent is resistant to 2-point radial compression. Unlike the Palmaz stent, which deforms if crushed, the Wallstent will retain its original shape. Wallstents are not the ideal stent for ostial lesions. The WaUstent maintains its maximal radial strength when both ends are embedded in the vessel wall. If 1 end of the stent is not anchored in tissue, as would be the case in the orifice of the c o m m o n iliac artery, the radial strength at the free end of the stent is decreased and may not fully support the vessel wall. The flexibility of the Wallstent enables it to be introduced through angulated vessels, tracked across the aortic bifurcation with ease, and deployed reliCurr Probl Surg, December 1999

941

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FIG 12, A, Wallstent with loose unbound steel filaments in a tubular configuration. II, Wallstent has longitudinal flexibility.

ably from a remote or contralateral (ie, common femoral artery) approach. Elongation of the WaUstent reduces the stent diameter, allowing its delivery on a relatively small 7F delivery catheter. The stent is available in various lengths and diameters, which permit long tortuous iliac artery lesions to be covered with a single stent. The stents will shorten by 20% to 30% of their constrained length during deployment, and on average a 0.5-mm change in 942

Curr Probl Surg, December 1999

vessel diameter yields a 10% to 15% change in stent length. The selected WaUstent diameter size should be greater by at least 1 mm or 10% of the vessel diameter to ensure tight apposition of the stent against the vessel wall and to avoid stent migration or embolization. Gianturco-Z Stent. The Gianturco-Z stent (Cook Inc) was designed originally for use in large-diameter vessels such as the vena cava, innominate vein, or aorta. It is a self-expanding stent constructed of a stainlesssteel wire bent in a zigzag Z-pattern to form a cylindric structure. 53 The larger devices are composed of 0.018- to 0.022-inch stainless steel wire and, because of the large caliber of the wire, are primarily used in vessels with diameters of 2 cm or greater. Smaller-sized stents, developed for deployment in vessels with diameters of 3 to 5 mm, were constructed with 0.008- to 0.010-inch wire (Fig !3). 54The larger stent has a high expansion ratio and exhibits the necessary expansile strength required for placement in stenotic large central vessels. The expansion force exhibited by this stent will vary according to the caliber of the wire, the size of the stent (diameter and length), and the number and angle of the bends. Deployment requires that this device is radially compressed into a Teflon delivery catheter (8F-12F), introduced to the target vessel, and then allowed to expand to its original diameter on retraction of the Teflon sheath. It is important to select a stent size that is approximately 10% to 20% larger than the intended vessel diameter to dilate the lumen adequately and prevent stent migration. Rabkin Nitinol Stent. The Rabkin stent (National Research Center of Surgery, Moscow, Russia) is a coiled nitinol wire with stent diameters and lengths ranging from 4 to 14 mm and 1.5 to 6.0 cm, respectively (Fig 14). Delivery of this stent is accomplished with a 7F delivery system.55The first stent implantation in humans with this device was performed in Russia in March 1984. Cragg Stent. The Cragg stent (MinTech, Paris, France) is a self-expanding tubular structure that is constructed from a monofilament of 0.27-mm diameter nitinol wire wound in a series of back-and-forth bends, resulting in a zig-zag configuration (Fig 15). 56 The nitinol wire is fixed with 7-0 polypropylene ligatures, which help to maintain its tubular shape and confine its expansion. This stent is reported to have good longitudinal flexibility and radial stiffness similar to the Wallstent. 57 Symphony Nitinol Stent. The Symphony stent (Boston Scientific Corp, Boston, Mass) is a self-expanding tubular prosthesis constructed of the metal alloy nitinol (Fig 16). The stent is provided prem0unted on an overthe-wire 7F delivery system within an overlying protective sheath, which acts to constrain and protect the stent during introduction into the vessel Curr Probl Surg, December 1999

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FIG 13. Photographs of Gianturco self-expanding stents (Z-stents).A, Large Gianturco stent with monofilament suture through end "eyes." (Courtesy of Cook, Inc, Bloomington, Ind,) B, Hand-made large Gianturco-Rosch self-expandable Z-stents. From left: double-body 15-ram diameter stent without barbs; 3body 18-mm diameter stent with barbs at its upper body; 4-body 18-mm diameter stent with barbs at its second lower body. (From RoschJ, Uchida BT, Hall LD, et al. Gianturco-Rosch expandable Z-stentsin the treatment of SVC syndrome. Cardiovasc Intervent Radial 1992;15:319-2Z [Courtesy of Cook, Inc, Bloomington, Ind.] By permission.) C, Small single self-expanding Z-stents for use in peripheral vessels. (From Charnsangavej C. Gianturco self-expanding stent. In: Kim D, arran DE, editors. Peripheral vascular imaging and intervention. St Louis:Mosby Year-Book, Inc; 1992. p 537-40. By permission.) 944

Curr Probl Surg, December 1999

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FIG 14. A, The Rabkinnitinol stentin i~ deployed (unconstrained)configuration.6, View of stentloaded over catheter before being stretched. (From RobkinJE, Rabkin nifinol stent. In: Kim D, Orron DE:,editors. Peripheral vascular imaging and intervention.St Louis:Mosby Year-Book,lnc; 1992. p 509-14. By permission.)

and before deployment. To ensure proper stent apposition against the vessel wall and to avoid stent migration, the stent must be oversized and placed in a vessel of smaller diameter than its unconstrained diameter. Currently in the United States, the Symphony stent is available for clinical use only as an FDA-approved investigationaI device for the treatment of patients with iliac artery stenosis after suboptimal balloon angioplasty. Vascucoil Stent. The Vascucoil stent (Medtronic Instent Inc, Eden Prairie, Minn) is a radiopaque, spring-shaped self-expanding stent comprised of a helically wound nitinol wire. The ends of the stent coil have tiny knobs that help to mount the stent device in a constrained configuration on the delivery catheter (7F-9F; Fig 17). The stent is reported to undergo rapid radial expansion, with an expansion ratio similar to or greater than other coiled self-expanding stents. Design advantages reportedly include increased radial strength, longitudinal flexibility, minimal Curr Probl Surg, December 1999

945

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FIG 15. These 2 Cragg stents are composed of nitinol wire bent into a zig-zag configuration and tied together with nonabsorbable ligatures to maintain tubular form. (From Cragg AH, De Jong SC, Barnhart WH, Landas SK, Smith TP. Nitinol intravascular stent: results or preclinical evaluation. Radiology 1993; 189:775-8. By permission.)

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FIG 16. The Symphony nitinol stent has a tubular design and relatively low metal-to-interstice ratio. (Courtesy of Boston Scientific Corp, Boston, Mass.) 94-6

Curr Probl Surg, December 1 9 9 9

FIG 1Z The Vascucoil stent is shown loaded on a catheter in its compressed (constrained) form and in its fully expanded (unconstrained) configuration. (Courtesy of Medtronic Instent Inc, Eden Prairie, Minn.)

intimal coverage, and the ability to be removed as a single straight wire. The Vascucoil stent is available in diameters from 4 to 8 mm. The stent has proved to be successful in earlier animal studies,58 and further investigation has been reported in a single-center clinical study in France. 59 Currently in the United States, the Vascucoil stent is undergoing evaluation in a multicenter clinical trial. Memotherm Stent. The Memotherm stent (C R Bard, Inc, Covington, Ga) is a tubular self-expanding nitinol stent with single-wall construction. There are no filament crossings, resulting in a smoother surface that, at least in theory, decreases the number of contact points for thrombus adherence. Other reported design advantages include longitudinal flexibility, radial strength, lack of foreshortening, and deployment through a low-profile 7F sheath (Fig 18). However, visibility has been reported to be poor, and its use may not be applicable in vessels with angles greater than 30 degrees. Curves of more than 30 degrees will cause the stent struts to protrude into the lumen of the lower aspect of the curve and produce a flow disturbance. In the United States, the Memotherm stent is indicated only for treatment of malignant biliary obstruction. However, results have been published that report its use in aortoiliac occlusive vascular disease in Britain, most recently by Raza and colleagues. 6°

Clinical Indications The vascular surgery literature documents numerous clinical situations in which placement of an endovascular stent after PTA is believed to be an acceptable therapeutic option as compared with PTA alone or open surgical revascularization. Reported indications for stentt implantation have included uncontrolled dissections, residual stenosis, acute occlusion, or Curr Probl Surg, December 1999

947

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FIG 18. The Memotherm stentis shown in its expanded (unconstrained) state. Note its tubular shape and longitudinal flexibility. (Courtesyof C R Bard Inc, Covington, Ga.)

elastic recoil after suboptimal angioplasty, the presence of intimal flaps, ulcerated plaque, recurrent stenosis, chronic occlusions, and in conjunction with PTA as a primary treatment option. Currently, the most common indication for the use of intraluminal stents has been to correct suboptimal results after PTA. In clinical practice, a PTA failure is defined by the presence of a 30% or greater diameter reducing residual stenosis on completion angiography or a systolic pressure gradient at rest of 5 m m or greater or 10 m m Hg or greater after injection of a vasodilator. The primary mechanism of action of PTA is known to be intimal plaque rupture or fracture, with or without localized dissection of the media. 61"65It has been postulated that the presence of an uncontrolled dissection after angioptasty may be the primary cause for early PTA failures. This type of dissection may become longer than the lesion itself, or it may produce a luminal obstruction or a residual stenosis, resulting in a significant reduction in blood flow. When a hemodynamically significant residual stenosis is left untreated .after balloon angioplasty, the appearance of fibromuscular hyperplasia at this area will narrow the lumen to an even 948

Curr Probl Surg, December 1999

greater degree, therefore increasing the risk for the development of recurrent stenosis and decreased long-term patency. Excessive uncontrolled dissection after angioplasty may expose a large area of subintimal collagen to the blood flow. The interaction between exposed subintimal collagen and the inherent clotting mechanisms of the blood increases the risk of acute thrombosis and acute vessel occlusion at the angioplasty site. Fig 19 illustrates a case in which excessive dissection developed after PTA of an external iliac artery. The completion angiogram demonstrated an unacceptable residual stenosis of greater than 30% as the result of the dissection. A Wallstent was then advanced over the aortic bifurcation from the contralateral femoral artery access site and positioned at the area of dissection. The Wallstent was deployed, and the dissection was tacked back against the vessel wall successfully, thereby correcting the residual stenosis and restoring the arterial lumen to its normal diameter. Some areas of vessel walls will have eccentric calcified plaque although the remaining area of the vessel wall does not have significant atherosclerotic disease. Balloon angioplasty of these vessels results in full expansion of the normal wall, whereas the diseased portion of wall does not expand to a similar degree. This may result in different intraluminal pressures being exerted on different areas of the vessel wall. The asymmetric expansion of the vessel theoretically produces inadequate intraluminal pressures, and insufficient fracturing of the plaque occurs, resulting in rapid recoil or spasm of the normal vessel wall once the balloon is deflated. This phenomenon is known as "elastic recoil." When elastic recoil is noted after balloon angioplasty, the primary stenosis appears unchanged or significant residual stenosis is noted to be present on completion angiography. The use of stenting to salvage this situation relies on the ability of the stent to provide an adequate intraluminal mechanical radial force strong enough to prevent elastic recoil, vasospasm, and residual stenosis (Fig 20). Stent deployment has also been recommended for use in the treatment of early recurrent stenosis after PTA (Fig 21). The development of recurrent stenosis depends on several variables, including the location of the stenosis, type of lesion, severity of stenosis, length of lesion, presence of residual stenosis after PTA, and presence of atherosclerotic risk factors. 66-7° The predominant cause associated with the development of recurrent stenosis is intimal or fibromuscular hyperplasia. Typically, hyperplasia develops during the first 6 to 12 months after primary PTA. Stent placement after PTA compared with angioplasty alone may be considered the treatment of choice for several anatomic lesions. Intimal flaps producing significant impairment of blood flow may be refractory to Curr Probl Surg, December 1999

949

A

B t FIG 19. This patient hod right lower extremity claudication. A, A diagnostic angiogmm identifies 2 significant stenoses in the right external iliac artery, li,'The 2 stenoses were dilated to 7 mm. Completion angiogram demonstrates a dissection producing a significant diameter reducing residual stenosisof greater than 30%. EIA, External iliac artery.

treatment with PTA alone. Apposition of the stent against the vessel wall ensures that the intimal flap is tacked sufficiently against the vessel wall, thereby maintaining a normal vessel lumen and satisfactory blood flow (Fig 22). Focal or extensive ulcerative stenoses producing either significant reductions in luminal diameter or serving as a source for distal emboli may be considered appropriate lesions for stent implantation, 950

Curr Probl Surg, December 1 9 9 9

FIG 19 Contd. C, Deployment of an 8~m diameter x 20-mm length Wallstent was then performed; the completion angiocjram demonstratesa widely patent vessellumen-withouta disseclion or residual stenosis.

thereby avoiding the risk of fracturing and dislodging plaque emboli to the lower extremities during balloon dilatation (Fig 23). Stentt placement may prove to be beneficial in the treatment of complete arterial occlusions. Numerous authors have recommended deployment of stents for these lesions, in response to the increased incidence of embolic complications, residual stenosis, and poor long-term patency that have been noted when PTA was performed alone (Fig 24). 67'70-77 Furthermore, if the presence of a stent can be shown to halt early intimal hyperplasia or late atherosclerotic disease progression at the angioplasty site, then the use of primary stenting (defined as the routine deployment of a stent regardless of the anatomic result after PTA) should be considered an acceptable alternative to angioplasty alone. Recent series have reported on the benefits of primary stent placement after angioplasty for various categories of atherosclerotic disease. 7°,78-83 However, whether or not primary deployment of stents can prevent the development of early recurrent stenosis and maintain long-term patency remains controversial. Many issues remain unresolved regarding its clinical efficacy and cost-effectiveness. Implementation of prospective randomized multicenter trials that compare primary PTA/stenting against FTA alone will be required to define the role of primary stenting in the treatment of occlusive atherosclerotic vascular disease. Curr Probl Surg, December 1999

951

A

B

FIG 20, This patient had a history of left lower extremity claudication. A, A pelvic angiogram demonstrates an eccentric plaque that is producing a significant stenosis in }he left distal common iliac artery (C/A) and proximal external iliac artery (EIA), B, Magnified view of the stenosis.

Deployment Techniques Successful placement and expansion of a balloon-expandable or selfexpanding stent in an artery requires several steps, which can be summarized as follows: obtaining percutaneous vascular access, placing a guidewire and introducer dilator/sheath assembly into the lumen of the artery, placing, a diagnostic catheter and performing diagnostic angiography, identifying the arterial lesion, measuring the arterial diameter and lesion length, selecting and preparing the angioplasty balloon, performing balloon angioplasty, completing an angiogram, acknowledging a suboptimal result after FFA, advancing a larger longer dilator/introducer sheath across the lesion, placing a balloon/stent assembly within the larger sheath at the site of failed FFA, 952

Curr Probl Surg, December 1999

C

/'\

D

•)

FIG 20 Cont'd. C, Stenosis was dilated to 6 mm. Completion angiogram demonstrates elastic recoil that results in a residual sten0sis of greater than 30%. D, A P294 Palmaz stent was deployed at the area of residual stenosis, and completion angiogram demonstrates a satisfactory anatomic result with minimal recoil and residual stenosis oF less than 20%.

withdrawing the sheath, repositioning of the stent at the lesion, deploying the stent, completing the angiogram, performing secondary balloon dilatation, removing the percutaneous sheath, and perfomaing hemostatic compression at the percutaneous puncture site.

Polmoz StentDeployment All patients are premedicated with 325 mg of acetylsalicylic acid before the procedure. Arterial access is achieved percutaneously through the ipsilateral common femoral artery with the Seldinger technique. Alternate Curr Probl Surg, December 1999

953

A

FIG 21. This patient had right lower extremity claudicalion. A, An initial angiogrom demonstrates a significant right common iliac artery stenosis. B, The stenosis was dilated to 8 ram, and no residual stenosis was noted. ¢, Within 3 months of the initial procedure, recurrent right lower extremity claudication developed. An angiogrom demonstrates early recurrent stenosis to the right common iliac artery at the site of the previous angioplasty. 954

Curr Probl Surg, December 1999

FIG 21 Cont'd. D and E, A 10-mm diameter x 20-mm length Watlstent was deployed primarily after repeat balloon angioplasly. Completion angiogram shows a widely potent right common lilac artery (CIA) without residual stenosis.

access sites, if the ipsilateral common femoral artery cannot be cannulated, include the contralateral common femoral, brachial, or axillary arteries. Once percutaneous access is achieved, a 0.035-inch guidewire is threaded through the needle into the arterial lumen (Fig 25); the needle is withdrawn; a dilator/sheath assembly is tracked over the wire into the lumen; and the dilator is withdrawn. The patient is then treated with heparin at a dose of 50 to 100 mg/kg to maintain an activated clotting time of 250 seconds or greater. A diagnostic angiogram is performed to locate the lesion, and the diameter of the adjacent artery and the length of the stenosis are then measured and recorded. An appropriately sized angioCurr Probl Surg, December 1999

955

~+~

A

l-

FIG 22. This patient had a history of right lower extremily ulceration despite a patent common femoral artery (CFA)-to-popliteal artery vein bypass graft. A, Selective angiogram demonstrates a significant flow-limiting intimal flap in the right external iliac artery (EIA) and a more proximal high-grade stenosis in the same artery. B, Magnified view of the intimal flap.

plasty balloon is selected, prepared, and tracked over the guidewire to the area of the stenosis (Fig 25). The balloon is inflated, and the result is assessed. If a residual stenosis of greater than 30% persists after PTA, the result is considered suboptimal, and stent placement is indicated (Fig 25). The balloon catheter is then withdrawn while guidewire access is maintained across the lesion at all times. A larger long dilator/introducer sheath (7F-10F) is introduced over the wire and advanced past the lesion (Fig 25). A stent of appropriate diameter and length is selected and mounted on the balloon catheter (or a premounted stent is selected). Care should be taken to ensure that the stent is mounted and crimped tightly between the 956

Curr Probl Surg, December 1999

FIG 22 Cont'd. ¢, An 8-mm diameter x 60-mm length Wallstent was deployed from the contralateral common femoral artery (CFA). Completion angiogram demonstratesthat the intimal flap has been tacked back successfully against the vessel wall and that the proximal stenosis has.been stented open without residual stenosis.The bypass graft remains patent, and the lateral circumflex artery has been preserved.

proximal and distal markers on the balloon catheter. We prefer to use a new balloon catheter for stent deployment if the original angioplasty balloon cannot be rewrapped sufficienOy small enough to permit safe mounting of the stent. A metal introducer (not shown), previously back-loaded over the distal end of the balloon/stent assembly, is then inserted through the hemostatic valve of the introducer sheath to prevent dislodgment of the stent as the balloon/stent assembly is tracked over the guidewire through the introducer sheath. Once the balloon/stent assembly has traversed the hemostatic valve, the metal introducer is withdrawn from the sheath to prevent excess bleeding. The baUoon/stent assembly is then advanced within the long protective introducer sheath under fluoroscopic guidance until the site of the failed t ~ A is reached (Fig 25). The introducer sheath is withdrawn, leaving the balloon/stent assembly uncovered. Contrast is injected to confirm the correct position of the stent at the residual stenosis. The balloon is inflated to its intended diameter. Once full stent deployment is observed, the balloon is deflated and removed, and completion angiography is performed to confirm satisfactory stent deployment (Fig 25).

WallstentDeployment All patients receive premedication with 325 mg of acetylsalicylic acid before stent implantation. Percutaneous arterial access is obtained with Curr Probl Surg, December 1999

957

B

FIG 23, This patient had left lower extremity claudication with focal ischemic changes to the toes that were thought to be the result of distal microembolization. A, An aorto-ilio-femoral angiogram demonstrates a significant long-segment stenosisof the left external iliac artery (EIA) with severe ulcerated plaque. CIA, Common iliac artery. B, Because the stenosis extended to the proximal left. common femoral artery, a hydrophilic guidewire was placed across the lesion from a contralateral approach.

the Seldinger technique. However, in contrast to the Palmaz stent, the flexibility of the Wallstent allows it to be deployed routinely from a contralateral common femoral artery approach. Most Wallstents require at least a 7F sheath for deployment. Stents over 12 mm in diameter require 10F or larger sheaths. The steps required for percutaneous access, placement of the guidewire, introduction of the dilator/sheath, systemic heparinization, performance of PTA, and the use of completion angiography to identify a suboptimal result after balloon angioplasty are exactly the same as described earlier for Palmaz stent placement (Fig 26). 958

Curr Probl Surg, December 1999

C

D

FIG 23 Cont'd. C, This was dilated to 5 mm with a 5-mm diameter x 4-cm length angioplasty balloon in an overlapping fashion, Completion angiogram shows persistentulceration and irregularity of the infima and the presence of a residual stenosis proximally. D, After deployment of an 8-mm diameter x 60-mm length Wallstent, completion angiogram demonstratesthat the ulcerated irregular intima has been excluded from the blood flow and that the residual stenosis has been eliminated.

Once it is determined that PTA was suboptimal and a residual stenosis is noted at the angioplasty site, a Wallstent is selected for implantation. The correct stent diameter should be 1 to 2 m m larger than the diameter of the target vessel. It is important to oversize the stent by at least 1 to 2 m m because the stent will not expand greater than its stated diameter, even with overdilation. The Wallstent is self-expanding and undergoes considerable shortening when it is deployed (Fig 27). Because of this marked shortening, the length of the selected stent is determined according to its final expanded diameter. The minimal stent length should be Curr Probl Surg, December 1999

959

FIG 24. This patient had a history of left lower extremily claudication. A, A diagnostic angiogram identifies a short occlusion of the above-knee popliteal artery.

longer than the lesion length so that adequate coverage is provided. The premounted Wallstent delivery system is flushed, loaded on a 0.035-inch guidewire through the introducer sheath, and advanced across the lesion (a long introducer sheath is not required). The stent is positioned so that the distal marker band is beyond the distal aspect of the lesion. The distal and proximal marker bands should be aligned with the entire lesion, because they approximate the final deployment position of the stent (Fig 26). The outer contracting membrane is retracted, and the stent is 960

Curr Probl Surg, December 1999

B

FIG 24 ConVd. B, A hydrophilic guidewire was passed through the occlusion; an ongioplasly balloon was tracked over the wire to the location of the occlusion, and the occlusion was dilated to 5 mm. Completion angiogram demonstrates a suboptimal result after PTA as noted by the presence of a significant residual stenosis. ¢, A P204 Palmaz stent was deployed successfully; completion angiogram demonstrates excellent blood flow in the area of the prior occlusion without residual stenosis. Curr Probl Surg, December 1999

961

A

B

C

D

FIG 25. Technique for percutaneous placement of a Palmaz stent. A, Percutaneousaccess is obtained, and a guidewire is passed across the lesion through an introducer sheath (not shown). B, An angioplasly balloon is tracked over thb guidewire to the site of the stenosis. C, The balloon is inflated, and PTA is performed. D, A larger, longer dilator/sheath assembly is advanced beyond the residual stenosis.

exposed and partially deployed. If the stent is deployed in an incorrect position, it cannot be pushed forward in its unconstrained form, and it must be recaptured to its constrained form (Fig 26). Attempts at pushing the stent forward may cause stent misalignment or vessel damage. The more recent Wallstent design, with the Unistep Plus (Schneider USA, Inc, Minneapolis, Minn) delivery system, permits recapturing of the stent even after 80% of the total length of the stent has been deployed. (In the original delivery system, if the stent was deployed in the wrong position it could not be recaptured but "wedge-locked" only; therefore the stent could only be pulled back distally.) Once the stent is completely recap-

962

Curr Probl Surg; December 1999

E

F

G

H

FIG 25 Cont'd. E, The balloon/stent assembly is passed within the sheath and positioned at the site of the residual stenosis. F, The sheath is retracted, leaving the stent unprotected. G, The balloon is dilated, and the stent is expanded into the plaque. H, The balloon is deflated and withdrawn. The Palmaz stent is completely expanded into the vessel walls, and the residual stenosishas disappeared.

tured through the outer contracting membrane, it can be advanced further beyond the lesion, brought back to the correct position, and redeployed at the proper location (Fig 26). If multiple stents are required, simple overlapping of the stents can be performed. After full deployment of the WaUstent, a completion angiogram is performed to ensure full stent expansion without residual stenosis (Fig 26). If the WaUstent does not expand completely, balloon dilatation can then be performed to ensure that the stent is firmly appositioned against the vessel walls.

Curr Probl Surg, December 1999

963

A

B

C

FIG 26. Technique for percutaneous placement of a Wallstent. A, B, and ¢, Steps are similar to those described before Patmaz stent placement (Fig 25). D, The Wallsteht is tracked over a guidewire and advanced beyond the stenosis.

Results

Arterial Stents lliac Artery Stents. The first report describing the implantation of a metallic stent in a human iliac artery was published in 1987.16 Since this seminal publication, there have been numerous studies that reported on the results of stents placed in the iliac m e d a l system. However, because of the widespread lack of adherence to uniform reporting standards as proposed initially by Rutherford and Beckers4 and later updated by Ahn and colleagues, 1 the direct comparison of reported results has been difficult. For example, many reports failed to include initial technical failures in the calculation of long-term success rates of the procedure, leading to overestimation of success when compared with the recommended method of cal964

Curr Probl Surg, December 1999

E

F

G

H

FIG 26 Cont'd. |, The stent is partially deployed but has shortened in an incorrect position, F, The stent must be recaptured before it can be advanced and repositioned properly. G, The Wallstent is partially deployed, this time in the correct position. H, Fully deployed Wallstent with complete expansion against the vesselwalls. Note that th~ residual stenosis is no longer present.

culating data based on an intent-to-treat basis. Other studies reported only primary success (or patency) rates, failing to include primary-assisted or secondary success, leading to underestimation of success after stent placement and making comparison with other studies that reported only cumulative patency rates clinically useless. Several studies reported success based on the treatment of iliac stenoses alone, whereas others included both iliac stenoses and occlusions, making direct comparisons confusing and clinically problematic. The criteria used to define success also vary. among reports, leading to further confusion. Depending on whether individual or combinations of clinical, hemodynamic, or anatomic criteria are used to determine success or patency, reported results might vary widely. Sullivan and colleagues82 illustrated this point well, reporting a 2-year sucCurr Probl Surg, December 1999

965

1

A

,'

FIG 27. A, Close-up view of the Wallstent in its constrained configuration.

cess rate of 84% when the thigh-brachial index was used to measure success versus 57% when the patient's clinical status was used. Therefore when attempting to compare the results of 2 or more studies, it is essential to identify the criteria used to define success or patency and to understand the statistical methods used to analyze and compare the reported data. Palmaz and colleagues,2°'85,86 Becker and colleagues,87 and Laborde and colleagues88 have reported the results of iliac stenting using the Palmaz stent in a large, prospective, multicenter trial. Included in the most recent report of this trial were 486 patients who underwent 587 procedures. 86The indications for stent placement in this study were an inadequate response to balloon angioplasty, defined as the presence of intimal dissection or elastic recoil producing a residual luminal stenosis of 30% or greater and/or a transstenotic mean pressure gradient of 5 m m Hg or more after injection of vasodilators 966

Curr Probl Surg, December 1999

\5~

..

-i • ";/

Q;

.

~ , 3 / \+

\+i \, \

z+

;;). /

B

C

FIG 27 Contd. B, Partially deployed Wallstent. Observe the marked shortening of the distal end of the stent as it self-expands to its unconstrained shape. Note that the distal marker band in the outer contracting membrane retracts back from the distal end of the catheter while the proximal marker band remains stationary. ¢, Waltstent fully expanded in its unconstrained configuration• Note that the proximal end of the stent has moved away from the proximal marker band during expansion.

distal to the treated segment; restenosis after previous iliac balloon angioplasty; and total iliac artery occlusion. In this study, 67.9% of patients underwent intervention for the treatment of claudication. Stents were placed in the common iliac artery in 66.5% of the patients, the external iliac artery in 19% of the patients, both the common and external iliac arteries in 13.1% of the patients, and the distal aorta in 1.4% of the patients. Immediate clinical success (defined as improvement of at least 1 clinical stage as defined in the ischemic ranking system used in the study) was obtained in 99.2% of patients. The average duration of follow-up was 13.3 _+ 11 months. Persistent clinical improvement was present in 90.9% of the patients at 12 months, 84.1% of the patients at 24 months, and 68.6% of the patients at 43 months. Curr Probl Surg, December 1 9 9 9

967

Follow-up angiography was performed in 201 patients at an average of 8.7 +_5.7 months. Angiographic patency was 91.9% at this interval. Initial technical failures were not reported in this study. Long-term results of the Palmaz stent determined by life-table methods were published by Henry and colleaguess9 in a report that included both iliac and femoral stenting procedures. Iliac lesions were present in 184 of the 310 patients. The indications for stenting were suboptimal results after PTA. Nine percent of the treated lesions were occlusions. Technical success was achieved in 309 of the 310 patients (99.7%). Follow-up arteriography was performed in 299 patients at 4 to 6 months after stent placement, and duplex scanning was performed at intervals thereafter. The mean length of follow-up was 35 months, Primary patency of the iliac stents was reported as 94% at 12 months, 91% at 24 months, 86% at 36 months, and 86% at 48 months. Secondary patency was 98% at 12 months, 96% at 24 months, 94% at 36 months, and 94% at 48 months. Cikfit and colleagues9° published their long-term results with iliac artery stenting using the Palmaz stent in 38 limbs. The indications for stenting were inadequate results with balloon angioplasty, restenosis after previous angioplasty, vessel occlusion, a lesion in an unfavorable location, and long or multiple lesions. Although the definition of patency was not specified and only one half of their patients underwent follow-up arteriography, the authors reported a primary patency rate of 87% at 12 months, 74% at 36 months, and 63% at 60 months. Ten limbs required repeat interventions, resulting in cumulative patency rates of 91% at 12 months, 91% at 36 months, and 86% at 60 months. Murphy and colleagues91 evaluated the long-term efficacy of iliac artery Palmaz stent placement in 83 patients (108 limbs) with limb ischemia. Immediate clinical success was 98.9%, and primary clinical success rates at 1 and 4 years of follow-up were 89% and 86.2%, respectively. Angiographic patency in 30 patients was noted to be 87.5% at latest follow-up. Interestingly, there was a large discrepancy between angiographic patency and segmental limb pressure measurements, in comparison with clinical success and angiographic patency, which correlated well with each other. The complication rate was 9.7% and the 30~ay procedural mortality rate was 1.2%. Tetteroo and colleagues 83 reported on Palmaz stents placed in the iliac arteries in a randomized study that compared primary stent placement versus primary angioplasty and selective stent placement. Palmaz stents were placed primarily in 143 patients. The initial hemodynamic success rate w a s 81%. Clinical success at 2 years was noted in 78% (29/37 patients). Anatomic patency as assessed by duplex examination was 71% at 2 years. The Wallstent has also been evaluated in a large, multicenter, prospective 968

Curr Probl Surg, December 1999

trial published by Martin and colleagues.92This study involved 225 patients, in whom 140 iliac stents and 90 femoral stents were placed (5 patients underwent both). The standard indications for stenting were used (acute angioplasty failure, restenosis after previous angioplasty, and complete occlusions). A patent superficial femoral artery or "well-developed deep collateral system" was required for placement of an iliac stent and inclusion in this protocol. Excluded from this study were patients with poor runoff distal to the stent. Seventy-seven percent of patients had claudication. Initial technical success was obtained in 97% of patients with iliac lesions, with initial clinical success occurring in 95%. The primary clinical patency, defined as the maintenance of the maximum postprocedure ankle- or thighbrachial index or maintenance of the postprocedure clinical grade, was 87% at 6 months, 81% at 12 months, and 71% at 24 months. Secondary patency was 91% at 12 months and 86% at 24 months. Angiography was performed in 66% of patients at a mean of 9.4 months after iliac stent placement. Angiographic patency at 6 months was 93%. Interestingly, 6 patients who were judged to have clinical failure had angiographically patent vessels. Vorwerk and colleagues 93 published a series of 109 patients with 118 iliac stenoses (9 bilateral lesions) who had Wallstents placed after suboptimal angioplasty. Three lesions involved the aortic bifurcation. No occlusions were included in this group. There were 115 patients with claudication (97%). The initial technical success of the procedure was 100%. With a combination of angiographic findings, ankle-ann indices, and clinical symptoms, the reported primary patency rate was 97% at 6 months, 95% at 12 months, 88% at 24 months, 86% at 36 months, 82% at 48 months, and 72% at 60 months. Secondary or assisted patency was 83% at 60 months. Long and colleagues94 reported a series of 49 patients with 52 iliac arteries treated with Wallstents. Angiographic follow-up was obtained in 47 patients (50 arteries) at a mean of 15 months. Angiographic primary patency was 85.3% at 12 months, 80.9% at 18 months, and 66.2% at 24 months. Murphy and colleagues 95 assessed the outcome of Wallstent placement to treat complex iliac artery stenoses or occlusions. Successful delivery of the stent was achieved in 91% of limbs. Primary patency rates were 78% at 1 year and 53% at 2 and 3 years. Secondary patency rates were better at 85% at 1 year and 82% at 32-month follow-up. Major complications occurred in 9% of patients. Long-term success and prognostic factors for Wallstent placement in 95 patients were evaluated by Sapoval and colleagues. 71 Primary and secondary patency rates were 80% and 90% at 1 year, respectively, and 61% and 86% at 4 years, respectively. Five factors were associated with longterm angiographic failure and are listed by the degree of hazard severity: Curt Probl Surg, Oeeember1.999

969

occlusion of the superficial femoral artery, absence of hypertension, stent diameter less than 8 mm, 2 or more stents implanted, and current tobacco consumption. The authors concluded that improved patency rates may be obtained after Wallstent placement by selecting patients according to the 5 prognostic factors listed earlier. Nawaz and colleagues 96 evaluated 144 patients (163 limbs) who underwent iliac artery stenting in an effort to determine the predictors of clinical outcome. The technical success rate was 95%. Primary and secondary clinical success rates were 90% and 92% at 1 year, respectively, and 84% and 87% at 3 years, respectively. Two factors were noted to have an adverse effect on outcome: residual pressure gradient (>10 mm Hg) and no treatment with aspirin. Ballard and colleagues97 performed a rigorous analysis of 72 patients who underwent placement of iliac stents in 98 limbs. Claudication was present in 53.1% of patients. The indication for stent placement was a poor angioplasty result in 26 arteries (26.5%). Stents were placed primarily in 72 arteries (73.5%). Stents were placed in 40 common iliac arteries and 19 external iliac arteries alone, and 19 stents were placed in both the common and external iliac arteries. Complete occlusions were present in 33 arteries (33.7%). Wallstents were used in 49 limbs, Palmaz stents were used in 42 limbs, and both stents were placed in combination in 7 limbs. The initial technical success rate (defined as a systolic pressure gradient less than 5 mm Hg across the treated lesion at the completion of the procedure) was 96.9% (95/98 arteries). Three additional procedures were complicated by acute occlusion because of extensive dissections. All were salvaged, by placement of an additional stent and were not counted as technical failures. Patency was determined arteriographically in 17 limbs (17.3%) or by indirect clinical criteria in the remaining 81 limbs (82.7%). The cumulative primary patency rate was 87.6% at 12 months, 61.9% at 18 months, and 55.3% at 24 months. The long-term results of the Strecker stent have been published in a series of 289 patients. 98 Two hundred forty-five of these patients (84.9%) had claudication. Complete vessel occlusion was present in 66 patients (22.8%). The indication for stent placement in the remaining patients was acute angioplasty failure in 223 patients (77.2%). The primary patency rate, based on ankle-brachial indices and clinical stage, was 85% at 36 months, 84% at 48 months, and 79% at 60 months. The Strecker stent was also evaluated in a series by Long and colleagues. 99 In that report, stents were placed in 64 limbs: 28 stents for vessel occlusion, 31 stents for arterial dissection, 3 stents after a poor angioplasty result, 1 stent for restenosis, and 1 stent for an eccentric, calcified lesion. Technical success was achieved in 98% of limbs. Angiographic 970

Curr Probl Surg, December 1999

follow-up was performed in 53 vessels (83%). The primary patency, determined either at angiography or by clinical means, was 84% at 12 months and 69% at 24 months. The secondary patency rate was 90% at 12 months and 81% at 24 months. The authors noted that initial dissection, stent region less than 60 mm, and total covering of the abnormal segment with the stent were significant predictors for good long-term results. There is little or no direct information comparing the long-term efficacy of various stents placed in the iliac artery. No randomized, prospective studies have been published that directly evaluate the success or patency rates between the different stent designs• In a report from Ballard and colleagues,97 no significant difference was noted in success rates after Palmaz stent implantation compared with the Wallstent. However, this was not a randomized series. Bosch and Hunink ~°° published a metaanalysis of the results of iliac artery stenting compared with balloon angioplasty alone that included more than 2000 patients• The results for Palmaz stents, Wallstents, and Strecker stents were combined. Immediate technical success was higher in the stent group (96%) than in the angioplasty group (91%). The immediate technical success rate for the treatment of complete iliac artery occlusions was equal (80%) for the 2 groups. The systemic complication rate (1%), local complication rate (9%-10%), and rate of major complications that required treatment (4%5%) were similar among groups. Excluding technical failures, the overall 4-year primary patency rate was 64% after angioplasty and 77% after stent placement. The risk of long-term failure was reduced by 39% after stent placement as compared with angioplasty. If technical failures were excluded, treatment of an occlusion versus a stenosis was not a significant variable affecting the long-term success. Four-year primary patency, with. technical failures included, was 64% for Strecker stents, 80% for Palmaz stents, and 70% for Wallstents, not a staustlcally significant difference. Whether or not a particular stent design provides greater clinical benefit and/or anatomic patency compared with other designs remains uncertain and can only be answered with a randomized, prospective trial. Table 1 summarizes the results after stent placement according to stent type. Several authors have attempted to identify factors that are associated with an improved likelihood of success after placement of iliac stents. 88,89'95,97,99J°H°3 Results of iliac stenting stratified according to clinical indication (claudication vs limb-threatening ischemia) have been conflicting. Laborde and colleagues88 demonstrated poorer results in patients with limb-threatening ischemia. Murphy and colleagues 1°2 demonstrated better results in those patients with a more severe preprocedure ischemic ranking. However, most authors have found no significant difference in •

Curr Probl Surg, December 1999

•

f

971

TABLE 1. Comparison of primary success or potency rates after iliac artery stenting by different stent types Pateney rates (%) Patients/limbs Study (flm't au/year) (n) 1-y 2-y 3-y 4-y 5-y Palmaz stent Patmaz/1992 Henry/1995 Cikfit/1995 Murphy/1995 Tetteroo/1995 Walls'tent Long/1991 Vorwerk/1995 Martin/1995 Murphy/1996 Sapoval/1996 Reyes/1997 Toogood/1998 Strecker stent Lierman/1992 Long/1995 Strecker/1996 Levi/1998 Memotherm stent Raza/1998

486/587 184/184

34/38 83/108 143/143 49/52 127/127 140/163 66/94 95/101 59/61 50/50

91c 94 87 89c 80c, 78h 85 87 81c 78 80 73

84c 91 74

86 74

69c 86 67

63

81

78

54

78c,85h, 71a 66 83 71c 53

53 61

88a

52/52 64/64 289/289 24/24

81a

22/22

96c

64

98* 69 85

84

79

au, Author;,c, clinical;h, hemodynamic;a, anatomic.

*Meanfollow-up,20 months.

results when the results were analyzed according to the patients' clinical data. Analysis according to the status of the runoff vessels (ie, superficial femoral artery) has also been inconsistent, although several authors have found that diseased or occluded runoff arteries were a strong predictor of failure. 88,97 In contrast to the results reported for balloon angioplasty alone, ~°4 no significant difference in long-term results has been demonstrated for placement of stents in the common iliac versus external iliac arteries. 89,95,1°3Lesion length 89,99,1°3and stent diameter89,1°1J°3 have been shown to affect the results inconsistently, as have diabetes 99,101,102 and smoking. 95,99,101,103 Overall, no factors have been identified that are consistently associated with either improved success or increased failure after iliac stenting. Because of the perceived poor results of balloon angioplasty for the treatment of complete iliac artery occlusions,~°4,1°5 primary stenting of these lesions has been advocated. 1°6-t°8In an early report, Ring and colleagues ~°5 noted a 50% technical failure rate because of the inability to advance a guidewire through the site of occlusion. In addition, a 40% rate of embolization was noted after balloon angioplasty of the lesions that were successful972

Curr Probl Surg, December 1999

ly traversed. C01apinto and colleagues75 noted a 22% failure rate of guidewire passage. However, of those lesions that were successfully dilated, a 4-year cumulative patency rate of 78% after angioplasty was reported. The embolization rate in that report was 3.1%. Johnston 1°4 reported an initial technical failure rate of 18.1% and, with technical failures excluded, success rates after angioplasty of occlusive lesions of 73.2% at 12 months, 64.7% at 24 months, and 58.8% at 36 months. More recent reports of iliac artery stenting for complete occlusions have documented an initial technical failure rate of 1.6% to 27%. 95'1°6-1°8 In a series of 127 patients with chronic iliac artery occlusions, Vorwerk and colleagues 72 noted successful wire passage in 103 patients (81%). That report also demonstrated a significant learning curve for successful wire passage, requiring fewer attempts in the last 53 patients than in the first 50 patients. The technical success of stent placement after achieving wire crossing was 98%. In 2 patients, re-entry into the aorta was subintimal after crossing a common iliac occlusion; stents were deployed but thrombosed within 24 hours because of proximal stent compression. Sapoval and colleagues71noted an embolization rate of 29% (5/17 patients) when balloon dilatation of the occlusive lesion was performed before stent placement. Conversely, a 4% embolization rate (1/26 patients) was noted when the stent was placed first, followed by balloon dilatation within the stent to achieve its full expansion. The stent acts to compress against the arterial wall the atherosclerotic plaque and thrombus that compose the occlusive material and to prevent dislodgment of this material. Primary stent placement without preliminary balloon dilatation is now considered the method of choice for the treatment of iliac occlusive lesions. Vorwerk and colleagues,7z reporting the results of primary stent placement. in iliac artery occlusions using the Wallstent, noted primary patency rates of 87% at 12 months, 81% at 36 months, and 54% at 60 months, excluding initial technical failures. Dyet and colleagues73 reported similar results using the WaUstent, with primary success in 85% of 72 patients at 12 months. Levi 1°9 reported an 81% patency rate at 15 months using Strecker stents to treat iliac artery occlusions. Although these results are slightly better than those noted by Colapinto and colleagues75 and Johnston 1°4 after angioplasty alone, a definitive trial has not been published that compares routine stenting of iliac occlusions with balloon angioplasty alone, with stenting reserved for the traditional indications of angioplasty failure. Blum and colleagues 1°8 reported a series of 47 patients who underwent angioplasty of iliac occlusive lesions, with stents placed only in those patients with residual narrowing by arteriography. Stents were initially placed in only 18 patients (38%), with an additional 2 patients receiving stents in the follow-up period. The cumulative Curr Probl

Surg, December 1999

973

TABLE2. Primarysuccessor patencyratesafter iliac artery stentingfor iliac artery occlusions

Patients/limbs Study (first au/year) (n) Vorwe¢/1995 Strecke~1996 Reyes/1997 Dyet/1997 Toogood/1998 Raza/1998 Le~/1998 Nawaz/1999 au,

127/127 66/66 59/61 72/72 50/50 22/22 24/24 98/98

1-y 87

85

Patency rates (%) 2-y 3-y 4-y 83 63 73 85 88a

81

78

85

85

88

84

~y

85

96c 81a 91

Author; c, clinical; h, hemodynamic;a, anatomic.

patency rate was excellent, at 87% over 53 months. Table 2 summarizes the results of stenting for iliac artery occlusions. Some authors have advocated routine "primary" stenting after PTA for all cases of iliac artery disease, regardless of the hemodynamic result achieved with balloon angioplasty a l o n e . 70,77,79,80 Theoretically, primary stenting is appealing. Compared with balloon angioplasty, placement of a stent produces a smoother endoluminal surface and results in blood flow that is more laminar. These factors, combined with the ability of the stent to exclude the subendothelial layers of the artery that are exposed after simple angioplasty, may lead to a lower incidence of restenosis from intimal hyperplasia. However, stents themselves also induce intimal hyperplasia, and the real question is whether the long-term results of iliac stenting are indeed superior to balloon angioplasty alone, with selective stenting to be reserved as a salvage procedure for the treatment of failures and acute complications. Sullivan and colleagues 82 reported their experience with primary stenting for 510 iliac artery lesions in 288 patients. Most of the patients (72.2%) had claudication. The initial technical failure rate was not reported, and the results were not ~abulated on an intent-to-treat basis. In those patients for whom stenting was successful, initial improvement in clinical status occurred in 74,6% of patients. Angiographic patency was 96% at 6 months, 81% at 12 months, and 73% at 24 months. These authors concluded that primary stenting can be performed safely and with reasonable patency rates, which seem to be improved compared with angioplasty alone. However, this study did not contain a control group who underwent angioplasty alone, and their conclusion cannot be considered definitive. Richter and colleagues7°,78,79have published in abstract form the results of a randomized, multicenter trial addressing the use of primary iliac stenting. The most recent report from this study included 247 patients. One hundred 974

Curr Probl Surg, December 1999

twenty-three patients were randomized to stent placement, with initial technical Success in 121 patients (98%). One hundred twenty-four patients were randomized to angioplasty alone, with technical success occurring in 113 patients (91%). The mean transstenotic gradient decreased from 29.4 to 1.4 mm Hg in the stent group and from 29.5 to 6.7 mm Hg in the angioplasty group. Initial clinical success was seen in 120 of 123 patients (98%) who received a stent and in 111 of 124 patients (90%) who underwent angioplasty alone. The cumulative 5-year angiographic patency rate was 93.6% in the stent group and 64.6% in the angioplasty group, with 5-year clinical success rates of 92.7% and 69.7%, respectively. These results suggest that primary stenting of iliac artery lesions may be more beneficial in terms of long-term patency and clinical success compared with the use of balloon angioplasty alone. However, because these data have not been published in a peer-reviewed manuscript form, the methods for accumulating the study data and the subsequent statistical analysis remain unknown. Accordingly, some degree of caution must be used when interpreting these results. Tetteroo and colleagues83 recently published the only peer-reviewed randomized trial to date that compares primary stent placement versus primary angioplasty followed by selective stent placement in patients with lifestyle-limiting intermittent claudication caused by iliac artery occlusive disease. Initial hemodynamic success was similar for both groups: 81% for patients undergoing primary stenting and 82% for those receiving primary angioplasty and selective stenting. Clinical success and cumulative patency rates were not significantly different between the 2 groups, at 78% versus 77% and 71% versus 70%, respectively. Complication rates were similar at 4% versus 7%. The authors concluded that because there were no significant differences in the technical results and clinical outcomes of the 2 treatment strategies, angioplasty followed by selective stent placement is the procedure of choice in this particular patient population because it is less expensive than primary placement of stents. Until primary iliac stenting is definitively proved to provide superior results over primary angioplasty alone, the added expense and risks of the implanted prosthesis probably do not justify the widespread adoption of a policy of routine iliac stenting. FemoropoplitealA~ery Stents. Atherosclerotic obstructive disease in the lower extremities occurs most commonly in the superficial femoral and popliteal arteries. Options for revascularization include bypass, endarterectomy, and endovascular techniques. Although many investigators demonstrated the feasibility and durability of PTA, a significant number of lesions remain inadequately treated with PTA alone, ll°-]z6 It is not uncommon to have acute dissection after the atherosclerotic plaque is cracked by the expanding balloon. Occasionally acute Curr Probl Surg, December 1999

97"5

TABLE 3. Analysis of primary and secondary patency, ra,tesafter femoropopliteal stenting Study (first au/year) Gunther/1989 Rousseau/1989 Zollikofer/1991 Do-Dai-Do/1992 Sapoval/1992 Uermann/1992 Strecker/1993 Bergeron/1995 Bray/1995 Henry/1995 Martin/1995 White/1995 Chatelard/1996 Gray/1997 Strecker/1997 Vroegindeweij/1997 Biamino/1997

Study design R R R P R R P, MC R P P P, MC R R P P RC R

Vessels i,f f,p i,f,p f,p f i,f,p i,f,p f f,p i,f,p i,f f,p f,p f f,p f,p f,p

Patients (#) 14 36 13 26 21 48 84 39 52 126 90 32 35 55 80 24 97

Female (%) 18 19 48 31 33 23 27 15 31 13 36 28 46 44 28 29 36

au, Author; R, retrospective; i, iliac; f, common and superficial femoral; W, Wallstent; p, popliteal; P, prospective; MC, multicenter; PZ, Palmaz stent; S, Strecker stent; NR, not reported; RC, randomized

controlled, *Two- to 12-months follow-up on iliac and femoropopliteal stents. 1"Twenty-monthsfollow-up. tAssisted primary patency. §Includes restenosis and reocclusion in the first 30 days.

occlusion ensues, and the only way to achieve vessel patency is by stent insertion. In a few lesions, particularly in the femoropopliteal segment, elastic recoil and residual stenosis are observed even after over-sizing the diameter of balloon used. Therefore stents were used initially for complicated angioplasties for bail-out maneuvers, for acute occlusions, and for significant residual stenosis after PTA (Table 3). 36'92"103'117"130 The long-term effects of stents, whether beneficial or detrimental, in the femoropopliteal segment are still not known because the studies with the longest follow-up do not exceed the 2- to 3-year mark. The primary patency rate for femoropopliteal stents ranges between 22% and 81% at 1 year (Table 3). Adjunctive measures with thrombolysis, atherectomy, or repeat balloon dilatation improve the 1-year secondary patency rates to between 43% and 96%. 36'92'117-130Balloon angioplasty and stent placement in the femoropopliteal segment is associated with an acute occlusion rate of 5% to 36%. 36'92'117"130Strecker and colleagues 1°3 found that reocclusion tends to occur in small-caliber vessels after anticoagulation is stopped. Bray and colleagues ~23noted a 10% rate of reocclusion and used thrombolysis for vessel recanalization. Do-dai-Do and colleagues 12° 976

Curr Probl Surg, December 1999

Stent type W W W W W S S PZ S PZ W W,S PZ W,PZ S PZ PZ, W

Acute thrombosis (%)

Restenosis rate (%)

7 23 36 19 19 NR 6 5 10 6 NR 6 NR 12§ 5 19 8

30 10 43 38 24 31 25 19 44 14 22 28 14 35 18 37 NR

l-y patency (%) Primary Secondary 79* 68 29 59 49 71¢ 80 81 79 81 61 75 80 22 76 63 57

89* 76 43 69 67 --89 82 96 84 89 83~ 46 NR 74 81

reported a 19% (5 patients) acute occlusion rate within the first I0 days after stent implantation; 2 patients were receiving anticoagulation, and 3 patients were not. All occlusions were successfully reopened with thrombolysis or catheter aspiration. Review of the available data suggests that the acute occlusion rate will depend on the type of lesion being addressed (eg, long vs short, occlusion vs stenosis) and whether intravenous and oral anticoagulation is being administered (Table 4). 131'132 Recurrent stenosis is another frequently reported complication after the use of stents and ranges between 20% and 40% over the first 2 years. 36,92,117-130 Although several investigators have demonstrated the presence of myointimal hyperplasia within the stent, others have found new lesions arising proximal to the stent. Zollikofer and colleagues 119 found 4 lesions of intimal hyperplasia, 2 lesions within and 2 lesions outside the stent. Sapoval and colleagues 121 found 5 lesions of intimal hyperplasia and treated them with repeat PTA. Strecker and colleagues 1°3 found that the restenosis rate was higher in patients with a recurrent stenosis, lesions in the mid or distal supertidal femoral artery, and long lesions requiring more than 1 stent. Bergeron and colleagues m22found a higher rate of restenosis in lesions in the distal and Curr Probl Surg, December 1999

97-7

TABLE 4. Lesioncharacteristics,methodsof anticoagulation,and follow-up in patientsundergoing femoropoplitealartery stenting

Complete Study (first au/year) occloMon (%)

Lesion length (cm)

Gunther/1989 Rousseau/1989 Zollikofer/1991 Do-Dai-Do/1992 Sapoval/1992 Uermann/1992 Strecker/1993 Bergeron/1995 Bray/1995 Henry/1995 Martin/1995 White/1995 Chatelard/1996 Gray/1997 Strecker/1997 Vroegindeweij/1997 Biamino/1998

1-20 1-30 3-23 4-15 1-17 0.2-48 1-15 1-30 1-20 1-15 1-10, >10 1-21 _<10 6-35 1-11 5 16t

71 30 80 100 82 60 10 57 61 33 35 47 29 89 59 17 NR

Antlcoagulation* Yes? Yes? Yes? Yes? Yes? Yes? No Yes~f Yes§ Yes¢ Yes? No Yes§ Yes~r Yes§ Yes? NR

Follow-up ABI IVDSA ABI anglo ABI anglo ABI duplex, TM ABI anglo ABI IVDSA ABI IVDSA ABI angio, angiescopy ABI duplex ABI duplex, IVDSA ABI anglo ABI duplex ABI duplex ABI duplex ABI ABI, duplex ABI

au, Author; ABI, ankle-brachialindex; IVDSA, intravenousdigital subtractionangiography;Anglo, angiography; Duplex, color-flowduplexscanning; TM, treadmill; NR, not reported, *Defined as use of intravenousheparinduringthe procedureand after the procedure for i to 5 days; some studies substituted low-molecularweightheparinfor intravenousheparin. l"Heparinand warfadn(Coumadin)for 3 to 6 months. ~Ticlopidine(Tictid)and aspirin. §Coumadinused selectively.

lower one third of the superficial femoral artery. In most reports, restenosis is not clearly separated from residual stenosis. 123 For an improved assessment of the vessel after angioplasty, Bergeron and colleagues 122 used angioscopy routinely with good results. All of their patients underwent the procedure in the operating room. Intravascular ultrasound may also help to select the lesions most likely to benefit from stents and also to detect the areas of residual or recurrent stenosis that will reqtiire more aggressive angioplasty.38,133,134,136 In one of the most carefully performed studies after PTA, Johnston and colleagues 67 found that, by stepwise regression, ihe variables influencing success rates were the indication (P = .012), the site (P = .005), the severity (P = .0003), and the runoff status (P = .0007). 8 Other studies have found that lesions with the following characteristics have the worst overall prognosis: long lesions, inadequate initial angioplasty, poor runoff, and stenosis or occlusion in diabetic patients. H°-H2A26,12sBecquemin and colleagues I l0 used a Cox proportional hazards model and found that the probability of success after PTA at 2 years was 80% for a stenosis of less than 2 cm and only 20% for an occlusion of larger than 2 cm. Similar observations were 978

Curr Probl Surg, December 1999

noted after placement of stents into femoropopliteal arteries. Bray and colleagues 123 observed that the 12-month patency rate was 95% for lesions shorter than 4 cm compared with 74% for those longer than 10 cm. Vessels that were initially treated for complete occlusion have a much lower patency than those with stenosis. Strecker and colleagues 128 observed a 73% 2year primary patency rate in vessels that received stents for stenosis compared with a 32% patency rate in those with occlusions. Sapoval and colleagues ~2x found that the diameter of the vessel influences the overall patency. Superficial femoral arteries of less than 5 mm in diameter had a lower patency rate than larger arteries. Henry and colleagues124had found that arteries with 7- to 8-mm diameters had a significantly higher 42-month patency rate compared with arteries 5 to 6 mm in diameter (P < .001). There is a significant discrepancy in the reported success rates for femoropopliteal stents. This wide-ranging variability deserves explanation. Despite the publication of reporting standards by the specialty societies, many authors have failed to adhere to these simple guidelines. 1,84,~36 Symptoms are often not clearly outlined, and most series include a wide variety of lesions that range from short stenosis to long occluded segments. Moreover, the status of the distal runoff is not specified clearly. The methods of anticoagulation during and after the procedure are not uniform (Table 4). The most important issue that prevents meaningful conclusions to be drawn from many studies is the type of follow-up. Many studies have clinical follow-up only or use periodic segmental arterial pressure measurement. Matsi and Manninen 136showed that clinical examinations alone can be misleading because there is a tendency to overestimate the actual vessel patency (82% vs 42%). Some investigators used intravenous digital subtraction angiography, which is known to be less sensitive than conventional arteriography. Only a few recent reports have routinely used colorflow duplex scanning to detect recurrent stenosis and occlusion (Table 4). The less-than-optimal overall results of femoropopliteal PTA contrast sharply with the generally good results obtained with iliac angioplasty. In a recent meta-analysis of several studies, Bosch and Hunink ~°° compared the results of stents in the iliac system with PTA alone. These investigators found that stent placement significantly improved the technical result (96% vs 91%; z test, P < .05) and reduced the risk of long-term failure by 39% compared with PTA alone. Different conclusions were reached by Vroegindeweij and colleagues 129 who randomized patients between stenthag after FrA versus PTA alone in the femoropopliteal arteries. The 1-year clinical and hemodynamic success rates were not significantly different: 74% with stent placement and 85% for FrA alone. Primary patency at 1 year, assessed by color-flow duplex ultrasound, was 62% for patients treatCurr Probl Surg, December 1999

979

ed with stents and 74% for patients undergoing PTA alone. The authors concluded that stent placement in the femoropopliteal arteries does not improve the clinical and hemodynamic outcome compared with PTA alone. Furthermore, the occlusion rate in patients treated with stents is higher. Complications after stent placement include puncture site bleeding or pseudoaneurysm, distal embolization, and stent deformation. Henry and colleagues TM reported a very low complication rate of 1%. Two hematomas and 1 pseudoaneurysm required operative repair. They also had 2 cases of distal emboli that required thromboaspiration. Strecker and colleagues~2sreported a 5% complication rate. They had 2 patients in whom arteriovenous fistulas (AVFs) developed after a popliteal puncture. Gray and colleagues127reported a 24.5% complication rate, including a 9% pseudoaneurysm rate and 3.6% with bleeding that required transfusion. They also had 4 deaths (7.2%) in the first 30 days. 36 Other authors reported a higher bleeding complication rate, in up to 12.2%. 92 The issue of stent placement in the common femoral artery and the popliteal segment behind the knee has been debated. In both those locations, hip and knee flexions cause considerable angulation of the artery and may predispose the patient to stent deformity and occlusion. Henry and colleagues TM had no untoward problems with 6"Palmaz stents in the common femoral and 1 Palmaz stent in the popliteal artery. Nevertheless, the presence of a stent in the common femoral artery may present a problem for the surgeon if the patient's condition requires subsequent operative intervention. Vascular control may be more difficult in the case of balloon-expanding devices because they are likely to be crushed by any vascular clamp and the arterial segment would need to be replaced. Behind the knee, because of the mobility of the popliteal artery, a self-expanding stent may be more suitable. Palmaz stents may be deformed in that location and cause acute occlusion. Zollikofer and colleagues H9 demonstrated arteriographically that bending the knee with a Wallstent did not cause a stenosis or occlusion. Intimal hyperplasia within the stent is the main cause for recurrent stenosis and occlusion after endovascular treatment (Fig 28). This has led many investigators to search for methods designed to control intimal hyperplasia.'Patients receive aspirin routinely, and many authors used oral anticoagulation for 3 to 6 months although long-term results have been inconsistent. Radiation therapy is one of the newest methods applied in an attempt to reduce myointimal hyperplasia. Although there are promising results in the coronary circulation, little information is available for femoropopliteal stents. Liermann and colleagues4° presented a preliminary experience with endovascular radiotherapy in '4 patients with a 2year follow-up and found no evidence of restenosis. 980

Curr Probl Surg, December 1999

FIG 28. Two-year follow-up angiogram demonstrates Wallstent in the right superficial femoral artery. Hemodynamically significant stenosis as a result of intimal hyperplasia is seen at the proximal aspect of stent

(arrow).

In summarizing the literature on endovascular stents in the femoropopliteal segment, there were 17 published reports inthe last 10 years. Except for the randomized controlled study by Vroegindeweij and colleagues, t29 most of the other reports were retrospective. The median 1-year patency rate was 71% (range, 22%-81%). The use of stents in the femoropopliteal segment shows that initial patency rates can be improved, but there is insufficient evidence that there will be any long-term benefit from their use in this location. TibioperonealArtery Stents. Although the placement of stents is widely used in the treatment of atherosclerotic iliac, femoral, and popliteal arterial disease, their use in patients with tibioperoneal arterial occlusive disease has been reported less frequently. The presence of a single focal stenosis with continuous distal flow to the foot would provide the optimal anatomic scenario for success after angioplasty or stenting. However, patients with lifestyle-limiting intermittent claudication rarely have focal distal arterial disease, and patients with severe limb-threatening ischemia typically have multilevel discontinuous atherosclerotic occlusive disease (ie, iliac, superficial femoral, and popliteal artery disease) and accordingly would not appear readily amenable to treatment by percutaneous methods. As such, traditional treatment of lesions located in the tibioperoneal arteries has been reserved for infrageniculate arterial bypass, with cumulative 5-year graft patency and limb salvage rates in some studies approaching 80% and 90%, respectively. 137'138 Curr Probl Surg, December 1999

981

However, as catheter-based technology has advanced and interventional techniques have improved, vascular interventionalists have redirected their attention towards the endovascular treatment of these more distal lesions. 59J39-152Nearly all of these reports describe the use of PTA alone. Only 2 studies have reported on the use of stenting for the treatment of tibioperoneal atherosclerotic occlusive disease. 59,147 Despite continued improvement in catheter and balloon design, reported results after angioplasty remain inconsistent. Technical success rates are variable and range from 60% to 100%. Success rates are equally as variable and are dependent on the method used to define patency (ie, clinical, hemodynamic, or anatomic). One-, 2-, and 3-year patency rates range from 53% to 89%, 32% to 83%, and 20% to 44%, respectively. 139-146,148q52Complications after angioplasty of tibioperoneal vessels occurred frequently, with major complications reported in 2% to 18% of patients. Restenosis at the angioplasty site was observed to develop early and often, with 3 reports describing incidences of 18%, 141 36%, 142 and 41%, ~5~respectively. The mortality rate has been reported to range from 0% to 3%. ~44 The use of stents in the treatment of tibioperoneal artery disease has been reported in only 2 studies. In 1993 Dorros and colleagues ~47provided the first case report involving the use of a stent in an infrapopliteal vessel. Stent deployment at the tibioperoneal trunk was performed as a salvage procedure to repair an intimal flap that developed after PTA. The intimal flap was treated successfully with stent placement, and the patient received warfarin (Coumadin). Unfortunately, 6 months later the patient experienced the development of recurrent symptoms of intermittent claudication after stopping his Coumadin therapy, and the stent was found to have occluded (along with 17 cm of the popliteal artery and 5 cm of tibioperoneal trunk and proximal peroneal artery). Thrombolysis and repeat balloon angioplasty were then performed to maintain secondary vessel patency to 12 months.~47Henry and colleagues59 reported on the use of a new self-expanding nitinol coilspring stent in 16 popliteal arteries and tibioperoneal trunks. These investigators reported a technical success of 100%, and 18-month primary and secondary patency rates of 87% and 100%, respectively. Based on these brief preliminary reports, specific clinical indications for the use of stents for the treatment of tibioperoneal disease cannot be determined. It is unlikely that isolated angioplasty or stent placement would result in sufficient distal perfusion to heal an ischemic ulcer or provide adequate long-term patency to be considered a clinically effective alternative to arterial bypass in this select group of patients. Furthermore, the complication rates after angioplasty are worrisome, and the high restenosis rates suggest that patients with claudication or limb ischemia will invariably experience 982

Curr Probl Surg, December 1999

the development of recurrent symptoms. Additionally, most of the studies that reported on the use of PTA are retrospective studies, involve selected patient populations, provide limited follow-up, and use different patency criteria and reporting standards to determine success after angioplasty. These shortcomings make it difficult, if not impossible, to compare the reported results after angioplasty, let alone the use of stents, against series reporting results of the current "gold standard" the infrageniculate arterial bypass. Therefore it remains unclear what role, if any, either of these procedures will have in the treatment of patients with atherosclerotic tibioperoneal artery disease. As such, the use of PTA for the treatment of tibioperoneal arterial occlusive disease should probably be limited to patients with ischemic rest pain or tissue loss and major contraindications to surgical procedures. Stents are recommended only for use as a bailout procedure to salvage complications after angioplasty. Aortic Stents. With the emergence of catheter-based therapies for vascular disease as a viable alternative to conventional operative procedures, relatively little attention has focused on intervention for occlusive disease within the aorta. Given the technical demands of aortic-level procedures, the profound metabolic response generated, and the potential for major morbidity, it would seem that patients who require aortic reconstruction stand to benefit greatly from recent advances in endovascular surgery. Severe occlusive disease of the abdominal aorta has been classified into several general patterns of atherosclerosis on the basis of the plaque distribution within the distal aorta, extension into the iliac vessels, and the presence of infrainguinal diseaseJ 53 Primary operative treatment has involved endarterectomy for discrete lesions, or aortofemoral bypasses, either in an end-to-end or end-to-side conformation, for more diffuse disease involving the iliac arteries. These operations have been generally successful, and the results have been durable. Nonetheless, with many patients with concomitant significant systemic illnesses, substantial morbidity may ensue after a general anesthetic, celiotomy, and, occasionally, a prolonged aortic crossclamp time. Intraoperative nerve damage may lead to impotence in up to one third of men undergoing such procedures. Pain management necessitates the use of parenteral narcotics and may result in intestinal ileus. When the perioperative course is free of complications, hospitalization of 5 to 7 days is not uncommon. Endoluminal techniques have been used in the treatment of aortic occlusive disease since 1980.154Although most of the early procedures were accomplished with PTA alone, reports have emerged that detail the use of either self-expanding or balloon-expandable stents in the aortic positionJ 55-~65 Sufficient long-term patency data regarding the use of primary stenting Curr Probl Surg, December 1999

983

instead of angioplasty alone have not been accumulated. Although in a recent review, Sniderman 163concluded that primary stenting is not warranted because of the clinical and angiographic success of PTA, one may postulate that, with further experience, particular lesion characteristics may be identified for which primary stenting may be indicated as in iliac disease. Beyond the treatment of atherosclerotic lesions of the aorta, stents have also been deployed in the treatment of aortic coarctation, 166"168Takayasu's arteritis, 167and for both chronic and acute aortic dissections. 168-171 Endovascular intervention may be undertaken in patients with either isolated stenoses of the abdominal aorta or those stenoses that appear in conjunction with iliac disease. As with other vascular lesions, treatment necessitates the ability to gain and maintain access across the lesions in question. Generally, a bilateral retrograde approach is then established through percutaneous cannulation of the common femoral vessels, and the patient undergoes anticoagulation with full-dose heparin. On the side planned for stent deployment, a larger sheath size may be required, depending on the diameter and type of available endoprosthesis. Currently, Wallstents up to 24 mm are available and must be deployed through sheath sizes up to 11F although similarly sized Palmaz stents may require introducers up to 13E The contralateral sheath should accommodate an appropriately selected balloon. If thrombus is present in the case of occlusion, preangioplasty thrombolysis may be used although intervention without thrombolysis at other sites has been successful. 172 Careful measurement of the aortic lumen is vital in selecting the appropriate balloon and stent. Image-based sizing is facilitated by calibration from a guidewire with radiopaque markings at known intervals. Alternatively, Diethrich ~73advocates routine interrogation of the aortic lumen by intravascular ultrasound (IVUS). IVUS provides accurate measurements of the luminal diameter and may be helpful in the evaluation of the outcome after angioplasty and stenfing. Generally, balloon angioplasty has been undertaken as the initial intervention. It may be accomplished with a single balloon when the lesion is proximal to the aortic bifurcation or the kissing balloon technique for lesions involving the bifurcation or in the event that a balloon of sufficient size is unavailable. Even if the single-balloon technique is used, luminal access in the contralateral iliac artery should be maintained with guidewire passage proximal to the lesion being treated. For cases in which the aortic stenosis lies in proximity to visceral branches of the aorta, care must be taken not to occlude them as a consequence of plaque fracture or progressive dissection. Difficulties one may anticipate in undertaking aortic procedures are 984

Curr Probl Surg, December "1999

similar to those identified with angioplasty and stenting at other sites. Thrombosis, peripheral embolism, and dissection are inherent risks. Misplacement of stents or migration may require surgical intervention if retrieval is not possible. At least one case of aortic rupture after angioplasty has been reported. 174 Most authors have reserved stent deployment for suboptimal results, which include inadequate dilatations with significant residual angiographic stenoses, residual pressure gradients, and dissections (Fig 29). The limited experience reported to date describes the use of both balloon-expandable devices and serf-expandable stents. Although the distal segment is generally affected, proximity to the visceral aortic branches demands careful measurements, attention to landmarks, and selective use of contrast infusion from an adjacent catheter to avoid inadvertent encroachment. Assessment of procedural success is by a combination of imaging moralities and pressure measurements. Completion angiography may be supplemented by IVUS to evaluate both the lumen and stent apposition to the aortic wall. Long-term follow-up is then performed with regular clinical evaluation, serial measurements of the ankle-brachial index, and selective use of duplex scanning. Early results remain encouraging although the long-term outcome has not yet been reported. In the experience reported by Diethrich and colleagues, 159 initial technical success was achieved in all 24 patients who underwent intraluminal stenting of the aorta, and 83% of patients experienced a rise in their ankle-brachial index of more than 0.15. Six patients with occlusions underwent thrombolysis, and 1 patient required plaque preangioplasty recanalization with pulsed holmium Yag laser. One third of the patients required more than 1 aortic stent. In a mean follow-up of 10 months, improvement of symptoms and the ankle-brachial index persisted in these patients. Complications were access-related hematomas in 3 patients and access-site thrombosis in 1 patient that necessitated operative intervention. Distal embolization in 2 patients who had undergone thrombolysis required surgical thrombectomy or thrombolysis as well. A smaller experience of 7 patients was reported by Long and colleagues 158on the use of both self-deploying and balloon-expandable stents. All procedures were technically successful, with 5 patients reporting improved exercise tolerance. Two patients required an additional intervention for restenosis within 2 weeks. In 3 patients, the inferior mesenteric artery had been covered by a stent, and 1 patient subsequently experienced the development of an ostial stenosis. In a recent series by Sheeran and colleagues, 161patients with midabdominal aortic stenoses were treated with stent placement after PTA (7 primarily, 3 selectively). Technical success was achieved in 100% of the patients; Curr Probl Surg, December 1999

985

B

FIG 29. A,, Diagnostic angiogram reveals 2 high-grade aortic stenoses. Note extensive proximal collateral circulation, 2 large patent lumbar arteries, and nonvisualization of the inferior mesenteric artery. B, Completion angiogram after PTA to the aortic lesions. Significant residual stenosis with dissection remains at proximal, and residual stenosisis present at distal stenosis.

during a mean follow-up of 1.6 years, clinical success was achieved in 8 of the 9 patients. The largest published series to date is a retrospective comparison of PTA and PTA with the Palmaz stent for the treatment of infrarenal abdominal aortic atherosclerotic stenoses. The records of 25 986

Curr Probl Surg, December 1999

C

FIG 29 Cont'd. ¢, Completion angiogram after placement of a Wallstent and PTA. Note that residual stenoses have resolved; collaterals have disappeared; lumbar arteries remain patent; and the inferior mesenteric artery is patent and now easily visualized.

patients from the Society for Cardiovascular and Interventional Radiology Transluminal Angioplasty and Revascularization Registry were analyzed.162 Thirteen patients were treated with I ~ A alone, and 12 patients were treated with thePalmaz stent. Technical success was achieved in 92% of patients treated with PTA alone and in 100% of those patients treated with the Palmaz stent. Short-term follow-up (mean, 14 months PTA alone; mean, 9 months PTA and stent) demonstrated equal clinical, hemodynamic, and anatomic efficacy between the 2 groups of patients who had an initially technically successful procedure. The authors suggested that PTA alone is the best initial treatment modality for this atherosclerotic lesion. Endovascular treatment of aortic dissection may be undertaken alone or in conjunction with proximal surgical repair. Fundamental to patient survival and a durable result is restoration of blood flow to the major aortic branch vessels. This may be accomplished by access to both the true and false lumens. A fenestration may be undertaken under IVUS or fluoroscopic guidance with subsequent balloon dilatation and deployment of either a balloon-expandable or self-deploying stent. Alternatively, the flow channel supplying any given branch vessel, whether a true or false lumen, may be kept patent with the aid of stent placement, thereby maintaining adequate perfusion of the vascular bed in question. In reporting the experience at Stanford in treating 22 patients with chronic or acute dissections, Curr Probl Surg, December 1999

987

Slonim and coUeagues 169describe technical success with revascularization in all patients. Two patients died in the perioperative period, and persistent relief of symptoms was achieved in the remaining patients over a mean follow-up of 13.7 months. It is becoming clear that endovascular procedures have gained a significant role in the treatment of aortic occlusive disease and constitute a legitimate option for a select group of patients. ~75Additional experience and long-term follow-up are necessary to better define future applications. Emergence of additional devices, including an array of covered stentgrafts, will ensure a dynamic future. Renal Artery Stents. Renovascular disease describes an anatomic condition that involves stenosis or occlusion of the renal artery. The diagnosis of renovascular disease does not necessarily imply symptoms. Associated symptoms include renovascular hypertension, congestive heart failure as the result of volume overload, and impairment of renal function. Surgical options for renovascular disease are multiple and depend on the anatomic constraints, patient condition, and surgeon performance. These include aortorenal bypass, endarterectomy, reimplantation, extra-anatomic reconstruction (ie, splenorenal or hepatorenal bypass), or, if branch vessels are involved, possible ex vivo reconstruction. With proper patient selection, this surgical approach has resulted in good short- and long-term patency and favorable clinical success. The addition of improved cardiac risk assessment, anesthetic technique and monitoring, and selective cardiac revascularization has helped to decrease the reported mortality rate to approximately 1% to 9%. 176~78Series that report surgical results for treatment of renovascular hypertension have shown cure rates of 55% to 76%, improvement rates of 14% to 39%, and failure rates of 1% to 11%. 176-181 The results of surgical treatment for atherosclerotic renal artery disease do not appear to be as good. Surgical revascularization in this setting has achieved cure rates of 15% to 58%, improvement rates"of 21% to 75%, and failure rates of 5% to 38%. The current gold standard for treatment of renovascular disease is surgical therapy, and benefits of alternative treatments must be compared against these surgical results. Renal artery angioplasty was first described by Gruntzig and colleagues ~82in 1978, and since then it has become a widely accepted form of therapy for renovascular disease. Balloon angioplasty has been performed successfully in the treatment of focal, nonostial, atherosclerotic renal artery stenoses and of fibromuscular dysplasia. Technical success rates (residual stenosis less than 30%) for PTA for nonostial atherosclerotic and fibromuscular dysplastic lesions are reported to be 90%. In favorable lesions, the long-term cumulative patency rate approaches 85%, 988

Curr Probl Surg, December 1999

and hypertension can be cured or improved in 80% to 90% of patients with fibromuscular dysplasia and in 30% to 75% of patients with atherosclerosis. 183-188Restenosis rates after PTA alone in these subgroups have been reported at 10% to 40% of patients. 186,189-t92With results nearly equivalent to those of surgical procedures, PTA is considered to be the treatment of choice for fibromuscular dysplasia and nonostial atherosclerotic lesions. As a result, stent placement is considered only as a rescue procedure for suboptimal PTA caused by elastic recoil and/or dissection. Unfortunately, the short- and long-term results of PTA for the treatment of ostial lesions have not occurred to a similar degree of success. Renal ostial lesions are comprised of bulky "spillover" atherosclerotic aortic plaque that encroaches on the origin of the renal artery. Therefore successful stretching of the vessel wall with cracking and remodeling of the surrounding plaque, which constitutes the classic mechanism of PTA, does not readily occur. Initial technical success rates for ostial lesions after PTA alone are lower, ranging between 25% and 70% and leading to subsquent high restenosis rates varying between 11% and 77% and to relatively poor clinical success rates of 0% to 40% in several s e r i e s . 186,192-194 For this reason PTA alone is considered inferior, and the primary placement of stents has been offered as a possible solution for improved results when ostial renal disease is treated (Fig 30). The choice of stent is largely operator dependent. The 2 most commonly used stents are the Palmaz stent and the WaUstent. There have been published reports that described the use of the Strecker stent and the Memotherm stent. 195'196 Both revealed reasonable success at initial placement, but no median or long-term follow-up is available, and currently the use of these stents in the renal position has been largely abandoned. There is a large body of experience in the use of the Palmaz stent for renovascular disease (Fig 31). This stent allows for precise placement, and the rigidity of this stent allows for maintained radial strength throughout its length, thereby proving advantageous for ostial lesions. 197This rigidity is a concern in the often tortuous and mobile renal artery. This concern has been resolved partly by the recognition that minimal stent length is best in the renal artery (preferably 10-15 mm). This provides for rapid, undisturbed arterial flow, considered by many to be an important factor in ensuring longterm vessel patency because it minimizes the poststent intimal hyperplastic response (Fig 32). An attempt to add flexibility to the Palmaz stem involved the addition of an articulated segment (Palmaz-Schatz stent). However, the added length and the design of this stem did not improve the results and perhaps even hurt medium-term and long-term patency and is no longer used routinely. 198-2°1The use of Wallstents gained early acceptance because they Curr Probl Surg, December 1999

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FIG 30. A 3-D reconstruction from a computed tomography scan of a left renal artery ostial stenosis. A, A view of the renal artery before stent placement. Note that the ostial lesion is comprised of renal artery plaque and "spillover" plaque from the aorta fsmall arrow).'Poststenotic dilatation of the renal artery is also present (large arrow). B, A view of the renal artery after stent placement. Aortic plaque has been fractured, and stenosis no longer is present after PTA and slenting (small arrow). Poststenoticdilatation is no longer seen (large arrow).

were more flexible, but misplacement was a significant problem. Without a precise proximal endpoint, anchoring the radial strength at the edges of the stent is significantly reduced in the treatment of an ostial stenosis. As it became evident that short stent length was more desirable, the importance of stent flexibility diminished. The early reports of renal artery stenting are plagued by short, inconsistent follow-up (median, 7 months; range, 2-60 months), unclear technical and clinical endpoints, and a lack of adequate statistical evaluation. Overall, the initial technical success rate approached 100%, with little or no difference noted between ostial and nonostial lesions. The use of stents for ostial 990

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FIG 31. An 87-year-old man with renal insufficiency and hypertension with a solitary left kidney with a high-grade ostial stenosis. A, Angiogram shows tortuous infrarenal aorta and left renal artery stenosis. LRA, Left renal artery. B, PTA and Patmaz stent placement was performed through a brachial artery approach because of infrarena{ tortuosity. Note the use of a guide catheter that allows for the evaluation of the procedure without loss of wire crossing. C, Final completion angiogram without wire shows no evidence of residual stenosis.Clinical follow-up indicated that the patient had stabilization of renal function and improvement of blood pressurecontrol. Curr Probl Surg, December 1999

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renal artery stenosis improves initial success rates from as low as 30% to nearly 100%. However, this improvement in initial patency did not always lead to long-term patency or prolonged clinical success. Restenosis was observed in 11% to 77% of arteries, and clinical success rates varied from 16% to 86%. 2°°'211 Recently, Hoffman and colleagues212reported on ostial renal artery stenosis treated by PTA alone. Immediate angiographic success was achieved in only 58% of patients, with improvement in 29% of patients and outright failure in 13% of patients. After PTA, hypertension was clinically "cured" in only 2% of patients, improved in 64% of patients, and considered a failure in 32% of patients. Less promising results were noted regarding the effect on renal function in this series. Renal function improved in 32% of patients but remained unchanged in 36% of patients and actually worsened in 30% of patients. Restenosis developed in 27% of cases at a mean follow-up of 11 months. By comparison, Tuttle and colleagues213 reported on their 5-year experience with the Palmaz stent in the treatment of ostial renal artery stenosis in 129 patients (98% of patients had hypertension; 57% of patients had renal dysfunction). Immediate technical success rates were 98% for patients undergoing stent replacement versus 11% for those patients undergoing PTA alone. The stent restenosis rate was 14% at 8.5 months. Control of hypertension improved in most patients, but the number of medications at 6 months was not significantly different from before stent placement. The renal function stabilized or improved in most patients. These outcomes were maintained over 24 months. The authors concluded that stent placement for ostial renal artery stenosis has a high success rate and low restenosis rate. Similar findings were recently reported by Henry and colleagues.2~4The authors evaluated the role of stenting in renal artery lesions (171 ostial, 73 nonostial) after the failure of PTA. The initial technical success rate was 99%. Five-year primary and secondary patency rates for ostial and nonostial lesions were 81% and 98% and 80% and 100%, respectively. No differences in patency were noted. Restenosis occurred in 11.4% of cases. Hypertension was reversed in 19% of cases, improved in 61% of cases, and remained unchanged in 20% of cases. Renal function was improved in 29% of cases, unchanged in 67% of cases, and worse in 4% of cases. The investigators concluded that renal artery stenting is safe and effective and may be an alternative to surgical procedures. They recommended stenting for all ostial lesions. Harden and colleagues215 monitored the renal function serially before and after stent insertion in 32 patients with renovascular renal failure. The immediate technical success rate was 100%, and the restenosis rate at 6 months was 12%. Renal function improved or stabilized in 22 of the 32 patients (69%). The effect of stent placement on the progression of renal failure was 992

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1999

B

i

¸

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FIG 32. A 56-year-old man with renovascular hypertension and a high-grade right renal artery ostial stenosis. A, Nonselective angiogram shows high-grade right renal artery ostial stenosis. B, Selective right renal ongiogram with a magnified view of the stenosis. Note the use of the renal guide catheter, which allows for angiographic evaluation without the loss of wire crossing and covered passage of the balloonmounted stent across the lesion. ¢, Completion angiogram shows satisfactory result after PTAand Palmaz stent placement to the right renal artery. The patient's hypertension was cured. Curr Probl Surg, December 1999

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analyzed by a comparison of the mean (SE) of the slopes of reciprocal serum creatinine values before and after stent placement. Progression of renal failure was significantly slowed after stenting, -4.34 (0.85) L ~tmol-I day-1 before stent placement versus -0.55 (1.0) L ~tmol-1 day-1 after stent placement (P < .01). A recent prospective randomized study by van de Ven and colleagues2~6 compared PTA alone versus PTA and stenting. Forty-two patients were assigned to receive PTA, and 43 patients were assigned to PTA and stenting. The primary success rate was significantly lower for PTA compared with PTA and stenting (57% vs 88%). The 6-month primary patency rate was inferior for PTA compared with PTA and stenting (29% vs 75%). Restenosis after successful primary procedure occurred in 48% of patients after PTA and in 14% of patients after PTA and stenting. Secondary rescue stenting was performed in 12 patients after failure of PTA alone. Evaluation based on intention to treat showed no difference in clinical results at 6 months for FTA (including secondary stenting) and primary PTA and stenting. A different conclusion regarding the benefits to renal artery stenting was reached by Fiala and colleagues}17 In this study, the authors reviewed the results of primary stenting of ostial renal artery stenosis. Twenty-one patients (25 arteries) with ostial renal artery stenosis and concomitant hypertension and renal insufficiency underwent renal artery PTA and primary stenting. The imme~ate technical success rate was 95%. Significant improvements in mean arterial blood pressure and decreases in serum creatinine levels were noted. However, 8 patients experienced the development of restenosis, and the cumulative restenosis rate was 65% at 24 months. The authors urged caution in the application of stenting for the treatment of ostial renal artery lesions. In summary, renal artery stenting appears to be a valuable adjunct to balloon angioplasty. It is rarely required for the percutaneous treatment of fibromuscular dysplasia. It is reserved primarily for failed angioplasty because of stenosis recoil or iatrogellic dissection for the treatment of main body atherosclerotic lesions of the renal artery. No clear benefit of primary stenting of these lesions has been shown; therefore this treatment should be limited to carefully constructed clinical trials. The use of stents in the percutaneous therapy of ostial lesions has drastically improved the initial success rate. There also appears to be an improvement in patency and restenosis rates although the follow-up is marred by inconsistency and only relatively short-interval evaluation. When renal artery stenting is performed the choice of stent is largely operator dependent. However, the placement precision and stent-end hoop strength would currently favor the Palmaz stent. Furthermore, flexibility issues and the 994

Curr Probl Surg, December 1999

issue of intimal hyperplasia favor short stentts limited to the length of the plaque with minimal overlap of uninvolved vessel intima. Fibromuscular dysplasia and focal main artery atherosclerotic disease of the renal artery may be treated effectively with balloon angioplasty with stenting reserved for angioplasty failures with comparable and acceptable results when compared with surgical procedures. Balloon angioplasty of ostial disease appears significantly inferior to the results of surgical procedures. Currently the clinical improvement rate after stenfing of ostial disease also appears inferior to those of surgical procedures. This may be due in part to a less aggressive attempt to show a causal relationship before intervention. A true prospective randomized trial between surgery and angioplasty/stenting would be necessary to clarify this issue but may be difficult to complete because of patients' unwillingness to randomize with a less invasive option available. Mesenteric Artery Stents. Chronic mesenteric arterial ischemia is an uncommon condition that occurs as the result of widespread atherosclerotic occlusive disease. Most investigators agree that most symptomatic patients will have hemodynamically significant stenoses in at least 2 of the 3 mesenteric vessels. The classic clinical presentation of chronic mesenteric ischemia is characterized by postprandial abdominal pain, progressive weight loss, and the eventual development of "food fear?' If left untreated, symptomatic patients will experience persistent nausea and vomiting and diarrhea and will eventually die of intestinal infarction or profound malnutrition as a consequence of long-term starvation. Surgical revascularization is considered the primary treatment modality in patients with chronic mesenteric ischemia with initial clinical success rates of up to 95% and long-term graft patency and clinical success rates approaching 80% to 90%. 218,219 However, despite these excellent results, earlier series reported higher morbidity and mortality rates after operation, leading to support for the use of PTA and stents as alternative treatment options in the management of selected patients with mesenteric ischemia. Mean technical success rates for mesenteric PTA have been reported at 88% (range, 79%-100%), with initial pain relief occurring in 85% (range, 60%-100%) of patients. The mean recurrence rate was 24%. Mortality rates were variable, ranging from 0% to 20% (mean, 2%), and morbidity rates were 0% to 16% (mean, 6%). The long-term clinical success rate varied from 76% (primary) to 93% (secondary). During a mean follow-up period of 12 to 39 months, primary and assisted-primary patency rates averaged 63% and 75%, respectively. Attempts to perform PTA for celiac stenosis as a result of median arcuate ligament compression have uniformly met with failure; therefore this is not recommended.219,22° Curr Probl Surg, December 1999

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The use of stents in patients with chronic mesenteric ischemia has been limited to the role of serving as a salvage procedure to correct suboptimal results or complications after PTA. 219,221-228Most of the reports in the literature have involved only a single patient and routinely describe the technical aspects of stent placement to treat residual stenosis, recoil, or dissection after angioplasty. Technical success by these authors was reported as 100% but usually required the performance of stent placement from an axiltary or high brachial artery approach. By using this antegrade approach as compared with a femoral approach, the sharp caudal angulation of the superior mesenteric artery is more easily accessed, thereby enabling greater directed force to the balloon and stent as they are passed across the stenosis. The Palmaz stent has been the stent of choice because of its rigidity, shorter lengths, and ability to undergo precise placement. Short-term clinical success as reported by these authors has been satisfactory, but the follow-up was short, ranging from 3 to 12 months. There is only a single report on a larger series of patients undergoing stent placement for the treatment of chronic mesenteric ischemia. Liermann and Streckera24 reported on the treatment of 12 patients with balloon-expandable Strecker stents after failed balloon angioplasty. Eleven of the 12 stents were placed through a brachial artery approach. The initial clinical success rate was reported to be 100%, but late restenosis associated with recurrent symptoms developed in 33% of the patients (4 patients). All 4 recurrences were treated successfully by repeat angioplasty. The long-term clinical success rate was 100% at a mean follow-up of 28 months. At the present time, open surgical revascularization remains the primary treatment option in patients with chronic mesenteric ischemia. Mesenteric PTA is an acceptable secondary therapeutic option when surgical therapy is contraindicated because of excessive comorbidities, the presence of a hostile abdomen, or both. The role for stents in the treatment of this entity should remain that of a salvage option for failures or complications after balloon angioplasty. Widespread application of stents in the treatment of chronic mesenteric ischemia is to be discouraged until the arrival of well-designed and carefully controlled clinical trials. Subclavian Artery Stents. Occlusion or stenosis of the proximal subclavian or innominate artery is caused most often by atherosclerotic disease. Because of this pathogenesis, there is a strong correlation with tobacco use. The average patient is 50 to 55 years of age, and there is a 2:1 prevalence of left-sided pathologic condition compared with the right side. 229 Many patients will show evidence of subclavian artery occlusive disease on the physical examination. Alternatively, the condition may be 996

Curr Probl Surg, December 1999

detected by duplex evaluation or arteriography with subclavian stenosis and associated steal. However, most of these patients will have no symptoms attributable to this anatomic defect. 23°,231A fairly well-defined group of symptoms are attributed to subclavian artery occlusive disease. The first and probably most common set of ~ymptoms includes those that are the result of vertebrobasilar ischemia because of retrograde flow in the ipsilateral vertebral artery. The second major symptom is ipsilateral upper extremity claudication. Patients with extra-anatomic axillary-to-femoral artery bypasses may have lower extremity claudication. Finally, with the advent of routine use of the internal mammary artery during coronary artery bypass grafting, proximal subclavian occlusive disease has been identified as a relatively rare cause of postsurgical angina and is labeled coronary-subclavian steal syndrome. 232,233 The first issue in performing endovascular therapy for occlusive subclavian artery disease is the approach. The access options are the groin or the ipsilateral brachial or axillary artery or a combination of both. A review of the literature describing balloon angioplasty and/or stenting of the subclavian or innominate artery does not indicate a significant improvement in the results with any of the mentioned approaches. With the concem about morbidity associated with brachial or axillary hematomas, the femoral route may be preferred to facilitate the larger sheaths required for stent deployment. TM The retrograde axillary or brachial approach may be preferred or even required to treat subclavian occlusions. This approach allows better catheter apposition to the occlusion to allow for improved wire manipulation in an attempt to cross occlusions. After obtaining access, and either before or after wire crossing of the lesion has been accomplished, the use of either an 8F guide catheter or a 7F long introducer catheter is recommended. This is important both for protected stent crossing of the target lesion if a Palmaz stent is chosen and for continued arteriographic evaluation during lesion manipulation without loss of balloon, stent, or wire position. Another technique to improve proper stent placement is deployment in the left anterior oblique projection. This incorporates the neutral opacity of aortic walls at its interface with aerated lung.TM Percutaneous balloon angioplasty of the subclavian or innominate arteries appears to be successful initially and fairly durable with low morbidity. A potential indication for primary stenting of an occlusive subclavian lesion is a plaque that is thought likely to embolize or in a situation in which embolization has already been attributed to the target lesion. Otherwise, stenting should probably be reserved for subclavian lesions that have failed balloon angioplasty. Failure is defined in this situation as more than 30% Curr Probl Surg, December 1999

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residual stenosis, flow-limiting subintimal dissection, pressure gradient across the lesion of more than 5 m m Hg, or arm pressure differential of more than 15 m m Hg systolic. 234 Ostial lesions along the aortic arch or the innominate artery in patients with right subclavian lesions, recurrent lesions, and recanalized occlusions may warrant a higher frequency of stenting because of the morphologic features. The balloon diameter chosen for PTA should either match or be slightly smaller than the diameter of the uninvolved adjacent subclavian artery with correction made for poststenotic dilatation. Most of the published reports that describe subclavian or innominate artery stenting have described the use of the Palmaz stent or the Wallstent. Palmaz stents appear to be the preferred stent in the reports because of the improved precision, of proximal and distal endpoint placement (Fig 33). This is especially true of more ostial lesions in which stent extrusion into the aortic arch could be detrimental and for lesions near the orifice of t h e vertebral artery in which ostial coverage could result in significant morbidity. Perceived disadvantages include the rigidity of the stent (for attempts to traverse tortuous access routes) and difficulties with placement at a curve in a vessel. Furthermore, this stent is more subject to deformation from external crushing or joint movement such as might occur often in the treatment of the distal subclavian or axillary artery. The Wallstent has been reported to have reasonable success in the treatment of subclavian lesions, but the number of reported cases is too low to compare adequately to the Palmaz stent or attest to its safety in this position. The clearest advantage of the Wallstent is its flexibility (Fig 34). It is relatively easy to negotiate a tortuous course to deployment, and it will conform to curved vessels. Finally, neither the Palmaz nor the Wallstent is approved for use in the subclavian or innominate arteries, and therefore the disease and the preference of the physician should direct their use. No clear advantage of anticoagulation after stenting has been demonstrated for stents in the subclavian or innominate position. However, with the significant concern of postprocedure thrombus formation and potential embolism, immediate heparinization for 12 to 24 hours and with at least chronic antiplatelet aspirin therapy is probably warranted. Surgical therapy provides excellent short- and long-term results, but is tainted with significant morbidity. Transthoracic surgical procedures are highly effective; but with a complication rate as high as 23% and with a mortality rate of nearly 8%, this is usually reserved for multivessel disease or with concomitant heart surgery. 235,236Extra-anatomic bypass affords a lower mortality rate, but morbidity remains significant, at between 8% and 15%. 23v,238The long-term success rate for carotid-subclavian bypass has been 998

Curr Probl Surg, December 1999

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B

FIG 33. A 49-year-old man with symptomatic left subclavian artery stenosis.A~ Angiogram shows focal stenosis in the proximal left subclavian artery. Pull-throughpressuresrevealed a 40-mm Hg gradient at rest. B, Completion angiogram shows successful treatment of the stenosis after PTA and the placement of a P294 Palmaz stent. The pressure gradient was no longer present, and the patient had complete resolution of symptoms.

reported as high as 87% at 5 years and 96% for transposition procedures. 238'239The results for PTA of the subclavian or innominate artery compare favorably. A compilation of the literature by Becker and colleagues, 3 which reviewed the treatment of 423 arteries, revealed a 92% initial success rate. The long-term success rate was estimated at 81%, with a 5% complication rate. Of these complications, fewer than 1% involved the central nervous system, the vast majority of these being temporary. Dorms and colleagues24° also reported a combined series of 201 lesions in 174 patients with an 84% Curr Probl Surg, December 1999

999

FIG 34. A 48-year-old man with symptomatic left subclavian artery stenosis.A, Angiogram shows proximal stenosis in left subclavian artery. Pressureto the left arm was 68"mm Hg lower than the pressure to the right arm. lit Completion angiogram at l-degree left anterior oblique projection shows mild residual stenosis of approximately 20% to 30% with minimal dissection.

immediate success rate and a 90% long-term clinical patency rate. Of these 201 lesions, only 18 were occlusions. A more directed evaluation of PTA for occlusions compiled by Duber and colleagues241 revealed only a 54% initial success rate. Most of these failures were the result of an inability to cross the occlusion with a guidewire. 241 Dorros and colleagues,24° in their own series, described a 100% immediate success rate in the treatment of 11 occluded lesions with a brachial approach without a clear breakdown of long-term patency rate. Distal embolization was noted in 3 of 11 patients (27%). Duber and colleagues241 had initial success in performing recanalization in 7 of 8 patients. The one immediate clinical failure was due to immediate reocclusion. However, 3 of 8 of the successful recanalizations had greater than 50% 1000

Curr Probl Surg, December 3.999

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FIG 34 Cont'd. ¢, Completion angiogram at 33-clegrees left anterior oblique proiection reveals a much greater hemodynamically significant residual stenosisand a more extensive hemodynamically significant dissection at the angioplasly site. D, Final completion angiogram after placement of a Wallstent. The residual stenosis and dissection have been corrected and are no longer present. Note that the internal mammary artery remains patent after placement of the Wallstent. The patient's symptoms resolved completely, and his arm pressuresbecame equal.

residual stenosis. Reobstruction occurred in 4 of these 8 patients at 8 to 16 months. Finally, 2 of these patients had embolic or thrombotic complication of the distal brachial artery. The results for subclavian or innominate artery stent treatment are similar to those for PTA alone. Initial technical success rates are excellent, ranging from 91% to 100%. 242-245 Early reports described the use of stents as a method to salvage suboptimal t ~ A r e s u l t s . 2 4 6 - 2 4 9 Kugelmess and colleagues 24s described one patient in whom a vertebrobasilar transient ischemic attack developed after PTA of a right subclavian artery stenosis with Curr Probl Surg, December 1999

1001

evidence of dissection-associated thrombus. Subsequent urokinase lysis followed by Palmaz stenting resulted in no residual defect and no further symptoms. This complication could perhaps have been avoided with primary stenting. Kumar and colleagues242 reported a series of primary stent placement in 27 consecutive patients with occlusive subclavian artery disease with a 100% initial success rate. The authors recommended primary stenting because it achieves better initial results than PTA alone, by preventing excessive intimal tears and abrupt vessel closure. In a large series by Sullivan and colleagues243 reporting on primary stenting of the subclavian, innominate, and common carotid arteries, initial technical success was achieved in 93.9% of subclavian arteries. Access was through the femoral artery in most of the cases, whereas a brachial artery approach was used in approximately one third of patients. The initial technical failures were due to the inability to cross to occlusions of the subclavian artery. Long-term patency was excellent, with 84% of the subclavian and innominate interventions being patent at 35 months. Unfortunately, the complication rate was relatively high, occurring in 17.8% of patients who underwent subclavian and innominate procedures. Complications were most common with the brachial artery approach and included access-site-related problems and embolization. Similar results were noted by Rodriguez-Lopez and colleagues, 244 who evaluated intermediate patency results after PTA with primary stenting of subclavian lesions of more than 70% stenosis. Primary stenting after PTA to the subclavian arteries was performed in 69 patients (70 arteries). The cumulative primary patency rate was 92% at 18 months, with a 7% asymptomatic restenosis rate identified by duplex scanning. The cumulative secondary patency rate increased to 96% at 18 months and continued to 90% at 30 months of follow-up. Henry and colleagues245reviewed the outcomes of 113 patients who underwent subclavian artery angioplasty with and without Palmaz stent placement over a 9-ye.ar period. Immediate technical success was achieved in 91% of patients. However, technical success occurred in only 47% of subclavian occlusions. During a mean followup of 4.3 __+2.9 years, primary and secondary patency for all patients based on an intent-to-treat basis at 8 years was 75% and 81%, respectively. In patients without initial stent placement, the rates were 69% and 76%; whereas in those undergoing stent placement, the rates were higher, at 87% and 94% at 2.5 years, but not significantly higher. The authors concluded that PTA alone or with stenting is safe and effective for treating subclavian artery occlusive disease. However, stents implanted for suboptimal F r A do not appear to improve the long-term patency significantly. In summary, lesions of the subclavian artery or innominate artery that are symptomatic warrant therapy. PTA has been demonstrated to have a high :1.002

Curr Probl Surg, December :1.999

initial success rate and low morbidity in the treatment of subclavian artery stenosis. These compare favorably with the results of surgical procedures. Although the long-term success rate is slightly lower than that for surgical procedures, repeat dilation after failure has shown reasonable success. 24s Furthermore, the concern of potential immediate embolism after balloon angioptasty and/or stent placement appears to be minimal. This may be explained in part by a well-recognized phenomenon of delayed reversal of vertebral artery flow after resolution of a proximal subclavian lesion. This has been reported as a delay of 20 seconds to several minutes.249This finding in conjunction with hyperemic flow to the reperfused arm may be protective against embolization to the vertebrobasilar circulation. This, however, does not afford protection to the right common carotid artery during treatment of innominate artery lesions, and therefore this clinical scenario requires careful consideration of options by the physician and patient. Stent therapy in conjunction with failed PTA appears to be a viable option with excellent initial success and low morbidity reported. Primary stenting has also been demonstrated to have good initial success and low morbidity. However, the long-term patency and safety have not been revealed; therefore this procedure cannot be advocated outside of special circumstances or as part of a well-constructed clinical trial. A prospective randomized study compari.ng t ~ A with or without stenting versus primary stenting could delineate this controversy. Currently balloon angioplasty is the procedure of choice for the treatment of symptomatic subclavian artery stenoses. Subsequent stenting for suboptimal results after PTA, restenosis, dissections, or ostial lesions appears safe with excellent early results. Primary stenting should probably be reserved for lesions with a high propensity for embolism or as part of a randomized trial. Results of PTA for subclavian artery occlusions are not as favorable, and these lesions are probably better served with surgical procedures. However, results after stent placement for occluded vessels appear promising although the study numbers are small. Further investigation regarding the benefit of stents for the treatment of subclavian artery occlusions is probably warranted. Carotid Artery Stents. Carotid endarterectomy (CEA), performed with a low pefioperative complication rate, remains the standard of care for the prevention of stroke in patients with severe atherosclerofic occlusive disease involving the internal carotid artery (ICA).25°-254It is the only form of cerebral revascularizafion for which there is definitive level I evidence of clinical effectiveness. The North American Symptomatic Carotid Endarterectomy Trial25°,251reported that CEA and the best medical therapy were superior to medical therapy alone in decreasing the incidence of any ipsilateral stroke in Curr Probl Surg, December 1999

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cases of symptomatic ICA stenosis of 50% to 69% and 70% to 99%. Among patients with stenosis of 50% to 69%, the 5-year rate of ipsilateral stroke was 22.2% among patients who were treated medically and 15.7% among those treated surgically (absolute risk reduction, 6.5%; relative risk reduction, 29%; P = .045). Among patients with severe stenosis of 70% to 99%, life-table estimates of the cumulative risk of any ipsilateral stroke at 2 years were 26% in the medical arm and 9% in the surgical arm (absolute risk reduction [_+ SE], 17% _ 3.5%; relative risk reduction, 65%; P < .001). Complementary findings were observed in the European Carotid Surgery Trial. 252,253 Results from the Asymptomatic Carotid Atherosclerotic Study demonstrated that CEA reduced the incidence of ipsilateral stroke and any periprocedural stroke or death in asymptomatic patients with stenosis of 60% to 99%. 254 After a median follow-up of 2.7 years, the aggregate risk over 5 years for ipsilateral stroke and any periprocedural stroke or death was estimated to be 5.1% for patients treated surgically and 11% for patients treated medically (aggregate risk reduction, 53%; 95% confidence interval, 22%-72%). The results from these trials serve as the guidelines for which any and all alternative forms of treatment must strive to achieve. Recent technologic advances in catheter-based therapy have generated great enthusiasm for the use of PTA alone and PTA with stenting as alternatives to CEA in the treatment of atherosclerotic carotid occlusive disease. Supporters for an interventional approach point out the theoretic benefits of PTA and stenting, including decreased neurologic and nonneurologic morbidity rates, shorter recovery periods, reduced costs, avoidance of a neck incision, fewer anesthetic risks, and presumably improved long-term patency rates. Numerous reports of PTA alone for the treatment of extracranial carotid occlusive disease have been published since 1983. 255,z56 Major stroke and complication rates from 0.5% to 10% have been reported, and early restenosis has occurred in up to 7% of patients. Although these results appear acceptable, no direct comparisons to CEA have been made, and the long-term efficacy of the procedure has not been established. As a result of these early experiences, investigators began evaluating PTA and stenting as an alternative treatment for carotid occlusive disease on the basis of the premise that routine stent deployment improves short- and long-term stroke rates and decreases complications. Unfortunately, most of the published experiences regarding carotid stenting are reported in the form of abstracts and anecdotal reports, with many coming from a single institutionZ~7-263; only one clinical series that compared carotid I ~ A and stenting versus CEA has undergone the scrutiny of a peer-reviewed, independent, externally adjudicated analysis. 264 ioo4

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A

B

FIG 35. A 45-year-old man who underwent right radical neck dissection followed by radiation experienced daily, acute transient ischemic attacks. A, Angiogram shows diffusely diseased internal and common carotid arteries. B, Completion angiogram shows satisfactory resolution of the long-diseased artery with a Palmaz P204 stentin the ICA overlapping with a 42 x 10-mmWallstent lhat extends down the common carotid artery. (From Dietrich EB, Ndiaye M, Reid DB. Stenting in the carotid artery: initial experience in 110 patients. J Endovasc Surg 1996;3:42-62. By permission.)

The indications for carotid stenting remain controversial and still much debated. Resolution of this issue will probably not occur until results from a randomized trial are completed, but until then several indications (albeit unsupported) seem to have been accepted by some investigators. These include the presence of severe ICA stenosis (>70%) in so-called "highrisk" patients, development of carotid restenosis, distal ICA lesions at the base of the skull that would require subluxation or dislocation of the mandible for surgical exposure, carotid stenosis after radical neck dissection, and postradiation carotid stenosis (Fig 35). A relatively small experience (approximately 650 procedures) in stenting of severe lesions of the ICA has been reported and published in a peer-reviewed context (Table 5). z57,z~9-268Technical success rates of 90% or greater have been reported,z57,265,266The periprocedural mortality rate was noted to be 0% to 1.8% in patients who underwent stenting. Periprocedural stroke rates after stent placement vary from 0% to 42%, most series reporting major stroke Curr Probl Surg, December 1999

1005

TABLE 5. Resultsafter PTAand stenfing of the ICA Study (first au/year) Diet~rich/1996 Roubin/1996* Yadav/1997* Jordan/1997* Criado/1997 Wholey/1997 Jordan/1998* Jordan/1998* Naylor/1998 Henry/1998 Mathur/1998*

Patients

No. of deaths (%)

No. of major strokes (%)

No. of miner strokes (%)

No. of transient isehemic attacks (%)

74 146 123 107 33 108 104 268 7 163 231

1 (1.4) 1 (0.7) 1 (0.9) 1 (0.9) 0 (0) 2 (1.8) 1 (0;9) 3 (1.1) 0 (0) 0 (0) 2 (0.7)

0 (0) 2 (1.4) 2 (1.6) 2 (1.9) 0 (0) 2 (1.8) 2 (1.8) 4 (1.5) 5 (42) 3 (1.7) 2 (0.7)

5 (6.8) 7 (4.8) 7 (5.7) 7 (6.6) 0 (0) 2 (1.8) 6 (5.9) 19 (7.1) 0 (0) 2 (1.1) 17 (6.2)

3 (4.0) NA NA NA 0 (0) 5 (4.4) NA 11 (4.1) 0 (0) 3 (1.7) NA

au, Author; NAo not available.

*Same institution.

rates between 0% to 2% and minor stroke rates between 0% to 6.8%. The overall stroke/mortality rate after carotid stenting ranged from 0% to 42%, but if the data from Naylor and colleagues264 are removed from the analysis, the stroke/mortality rates vary from 0% to 10%. Restenosis rates have remained fairly low, varying from 2% to 7%, although follow-up has been inconsistent and relatively short (usually < 1 year). Theron and colleagues269have reported a drop in their restenosis rates from 16% to 4% after stent deployment. Although these results would appear to be similar to the results after CEA in the randomized trials, the patient populations, clinical indications, severity of carotid disease, reporting of neurologic and nonneurologic complications, and methods of statistical analysis were not standardized and for the most part were profoundly different. As a consequence, there is significant difference of opinion regarding the efficacy of PTA and stenting of the carotid artery. The study reported by Naylor and colleagues264 represents a randomized trial that specifically compared PTA with stenting and CEA of the ICA. The trial was unique in that it was monitored by an independent data-monitoring committee. The trial was stopped short after randomization of only 23 patients because 5 of the 7 patients who underwent angioplasty and stenting experienced a stroke. All 10 CEAs proceeded without complication (P = .0034; only 17 patients received treatment before trial suspension). The trialists concluded that although carotid stenting has theoretic benefits over CEA, based on their experience, it cannot be used routinely in patients with symptomatic carotid disease who would otherwise undergo CEA. At the University of Alabama, a prospective observational study was performed to establish the safety and efficacy of carotid PTA with stenting. No fewer than 7 articles have been published that describe the results from that study. 257-263 1006

Curr Probl Surg, December 1999

Differences in opinion regarding the benefits of carotid stenting were noted among the primary authors, and the conclusions drawn from each article appeared to be dependent on the authors' respective medical or surgical specialities. Yadav and colleagues259reported a periprocedure combined stroke and mortality rate of 7.9%, an ipsilateral major stroke and death rate of 1.6%, and a 6-month restenosis rate of 4.9%. The primary author, a cardiologist, concluded that carotid PTA and stenting is feasible and can be performed with low restenosis and repeat intervention rates. Just 5 months later, Jordan and colleagues26° reported on the results from the same institution, comparing the results of 273 patients receiving either carotid PTA (n = 107 patients) or CEA (n = 166 patients) during a 14-month period. No differences in major stroke rates were noted between the 2 groups, but minor strokes occurred nearly 6 times more often after PTA and stenting compared with CEA (P < .001). Restenosis rates were also noted to be higher after PTA and stenting compared with CEA (4.5% vs 0.6%, respectively). The primary author, a vascular surgeon, concluded that PTA with stenting is not safer than CEA for the treatment of carotid artery stenosis, and longterm follow-up is needed to determine the ultimate durability of this new procedure. The different conclusions reached by these respective authors, ~vh0 evaluated the same study data, further underscore the need for a prospective randomized trial to help reach a decision regarding the benefits of carotid PTA and stenting. Further analysis of the study data from the University of Alabama helps to shed some light on the issues of cost, safety, and predicting complications after carotid PTA and stenting. Jordan and colleaguesTM reviewed the clinical results and hospital costs of patients who underwent carotid PTA and stenting and CEA. Total hospital charges per admission were higher for carotid stenting compared with CEA ($30,140 vs $21,670, respectively). The average postprocedure length of stay was similar for both groups, at 2.9 days (median, 2 days) for t ~ A and 3.1 days (median, 3 days) for CEA. The authors concluded that performance of carotid PTA and stenting could not be justified on the basis of reduced costs alone. The same authors then analyzed retrospectively whether carotid PTA and stenting (n = 268 patients) carried less anesthetic risk than CEA performed under regional anesthesia (n = 109 patients). Total stroke and mortality rates were 9.7% in patients who underwent carotid PTA and stenting and 0.9% in patients who underwent CEA with regional anesthesia (P = .0015). Cardiopulmonary events that required additional monitoring were higher after carotid PTA and stenting compared with CEA, at 32.8% versus 17.4% (P = .002), respectively. The authors stated that the proposed benefit of carotid PTA and stenting to avoid general anesthesia was not justified when compared with CEA perCurr Probl Surg, December 1999

1007

formed with local or regional anesthesia.262Mathur and colleagues263 analyzed the impact of various clinical, morphologic, and procedural determinants on the development of periprocedural strokes after primary carotid stenting in 231 patients (271 arteries). Multivariate analysis revealed that an age of more than 80 years (P = .006) and the presence of long or multiple stenoses (P = .006) were independent predictors of procedural strokes. Several investigators have suggested that carotid PTA and stenting may serve as a useful alternative to surgical procedures in the treatment of recurrent carotid stenosis. 25s,265'27°Unfortunately, there are few useful data to support this recommendation. Three series have reported data specific to the performance of carotid stenting for recurrent carotid stenosis. Diethrich and colleagues265 identified 18 patients who underwent PTA and placement of a Palmaz stent for recurrent stenosis. The periprocedure mortality rate was 5.6% (1 patient), and the stroke rate was 11.1% (2 patients) after stent placement. Two patients experienced transient ischemic attacks within 24 hours of the procedure. Better results were reported by Yadav and colleagues258 who treated 25 carotid arteries with PTA and stenting for recurrent carotid stenosis. One patient experienced a rrfinor stroke, for a periprocedural stroke rate of 4%. Eight patients returned for follow-up, and secondary recurrent stenosis did not occur. More recently Hobson and colleagues27° collected data on the endovascular treatment of patients with symptomatic and asymptomatic (80% or greater) recurrent carotid stenosis caused by myointimal hyperplasia. Carotid angioplasty and stenting was performed in 17 patients (9 women and 8 men). The technical success rate was 100%, and no strokes or deaths occurred during the 30-day periprocedural period. Secondary restenosis developed in 1 patient (6%) during a mean clinical follow-up of 11 months. Extensive use of PTA alone has also been avoided by many investigators because of the presumed potential for embolic stroke. Crawley and colleaguesTM reported on 28 patients who underwent transcranial Doppler evaluation of the middle cerebral artery during carotid PTA (n = 14 patients) or CEA (n -- 14 patients). These investigators reported that significantly more microembolic signals occurred during FleA than during CEA (mean number of microembolic signals during PTA, 202 _+ 119; during CEA 52 + 64; P = .001). However, the authors found no correlation between any of the measured parameters and the periprocedural stroke rate. Markus and colleagues172noted similar findings using the transcranial Doppler aft~.i: carotid PTA. During carotid angioplasty, multiple embolic signals were detected immediately after balloon inflation in 9 of 10 subjects. Eight of the 9 subjects remained asymptomatic whereas 1 experienced a minor ipsilateral cerebral ischemic event. The authors concluded 1008

Curr Probl Surg, December 1999

that embolization is common during carotid angioplasty but usually asymptomatic. Despite the fairly convincing results from these 2 studies, the current belief is that carotid stenting reduces the incidence of cerebral embolization; as a result, stents are deployed routinely regardless of the result after carotid PTA. Support for this concept comes from Bergeron and colleagues273 who treated 32 carotid arteries. Stents were placed in 13 arteries, and there were 7 complications, all occurring in patients who did not receive stents. However, not all authors agree that carotid stenting protects against cerebral embolization. McCleary and colleagues274 evaluated 9 patients with a contralateral carotid occlusion who underwent carotid angioplasty and stenting with near-infrared spectroscopy, continuous jugular venous oximetry, and transcranial Doppler ultrasonography to detect hemodynamic ischemia and embolic events. The authors recorded significant ischemia in 4 of 9 patients during crossing of the lesion and observed showers of emboli in all 9 patients during balloon inflation and stent deployment. They concluded that angioplasty and stenting in this high-risk group may not provide any advantage over conventional surgery in terms of hemodynamic ischemia and cerebral embolization. The choice of the appropriate stent for deployment in the carotid artery is open to debate. The stents most frequently used are the Palmaz stent and Wallstent. The Palmaz stent offers the advantage of precise deployment, rigidity, and excellent radial strength (Fig 36). However, although the radial force of the Palmaz stent is beneficial in maintaining luminal patency, it has not prevented stent deformation from occurring in several series 257,263,265,266The Wallstent has the advantage o.f being flexible, making deployment easier in tortuous arteries. It also appears to be able to cover the external carotid artery with little or no sequelae. Henry and colleagues 268noted that of 74 external carotid arteries covered by a Walistent only 1 of the arteries (1.3%) went on to experience the development of subsequent thrombosis. In summary, CEA remains the treatment of choice for atherosclerotic occlusive disease of the carotid artery. Carotid PTA and stenting, although being promoted as a satisfactory alternative to CEA, so far has been unable to live up to its potential. The proposed benefits of reduced morbidity and mortality rates, shorter recovery times, improved short- and long-term outcomes, decreased restenosis rates, and reduced costs have not yet been realized for any patient subgroups. Therefore the use of carotid PTA and stenting outside of a randomized trial employing an outside indePendent data-monitoring committee is not recommended in any clinical circumstance. The acceptance by the National Institutes of Health to fund a randomized clinical trial to compare CEA and carotid stenting, the Carotid Revascularization Curr Probl Surg, December 1999

1009

q 4 FIG 36. A, Diagnostic angiogram shows a stenosis at the carotid bifurcation. B, The initial stent, a Palmaz P204, was placed at the origin of the ICA. ¢, The external carotid artery was stented with a Palmaz P154 stent. D, A second P204 stent w a s deployed in the common carotid with a slight overlap into the ICA. {From Diethrich EB, Ndiaye M, Reid DB. Stenting in the carotid artery: initial experience in 110 patients. J Endovasc Surg 1996;3:42-62. By permission.)

Endarterectomy versus Stent Trial, 275 should help to answer some of the clinical questions posed by the use of carotid stenting. The primary outcomes for this trial include (1) any stroke, myocardial infarction, or death during the 30-day perioperative or periprocedural period; or (2) ipsilateral stroke after 1010

Curr Probl Surg, December 1999

i-

FIG 37. A 64-year-old man with mediastinal carcinoma and neck, face, and left arm swelling. A, Initial venogram reveals severe stenosis of the left innominate vein and moderate stenosis of the proximal right innominate vein and upper SVC. B, Immediate poststent venogram after placement of a 3-body stent into the left innominate vein. Note the good expansion of the previously stenotic veins, (From RoschJ, Uchida BT, Hall LD, et al. Gianturco-Rosch expandable Z-stents in the treatment of superior vena cava syndrome. Cardiovasc Intervent Radiol 1992;15:319-2Z By permission.)

30 days. Unfortunately, the sample size for the study is approximately 3000 symptomatic patients and is expected to take several years to complete. The trial is scheduled to start in the latter part of 1999. Interventionalists and noninterventionalists, alike, should be reminded that carotid PTA and stenting are not approved for use in the carotid artery, and utmost restraint is recommended regarding their use and deployment.

Venous Stents Vena Caval Stents. The most common application of stents in thevenous system has been for the treatment of vena caval syndrome. Obstructions of the superior vena cava (SVC) or inferior vena cava (IVC) are most commonly due to malignant neoplasms (Fig 37). Benign processes account for only 3% to 20% of vena caval o b s t r u c t i o n s . 276'277 Malignant disease typically results in obstruction by extrinsic compression on the soft, compliant vena cava or by direct tumor invasion of the caval wall, resulting in loss of elasticity or intmluminal tumor growth.TM Malignant tumors that cause vena caval syndrome are typically advanced, representing end-stage disease, and are associated with an average life expectancy of only 3 to 10 months.276,278-281 Benign obstructions are caused by a variety of processes, including mediCurr Probl Surg, December 1999

1011

FIG 38. A, IVC syndrome. A large metastatictumor in the left lobe of the liver caused displacement and almost complete obstruction of the IVC at the level of the diaphragm (arrow). Note collateral (C) pathways through the epidural venous system for blood flow to the heart and tumor (t) center.

asfinal and retroperitoneal fibrosis, which result in progressive constriction of the vena caval wall. Indwelling central venous catheters, trauma, and previous surgical procedures have also been reported to cause vena cava obstruction. Stenosis or occlusion of either the SVC or IVC can cause severe and equally incapacitating symptoms of venous congestion. Obstruction of the SVC may result in dyspnea, dysphagia, facial and upper limb edema, and severe headache with visual disturbances and alterations in the state of consciousness.282 Obstruction of the IVC can cause severe swelling of the abdomen and legs or hepatic venous congestion leading to Budd-Chiari syndrome (Fig 38). The severity of symptoms in both the SVC and IVC depends on the anatomic location of the obstruction, the degree of narrowing, and the speed with which it occurs. Malignant disease often progresses rapidly, and a small percentage of patients present with acute life-threatening SVC obstruction. 274,280,283 Benign processes often produce more 1012

Curr Probl Surg, December 1999

FIG 38 Cont'd. B, After 3 double Z-type stents (3 x 5 cm) were placed, flow is restored to the IVC, and collateral circulation is no longer visible. (From Oudkerk M, Heystraten MJ, Stoter G. Stenting in malignant vena caval obsiruction. Cancer 1993;71:141-6. By permission.)

gradual narrowing of the vena cava. The goal of therapy in most malignant and benign cases of vena caval syndrome is aimed at palliation of the venous obstructive symptoms. The first reported successful placement of an intravascular stent for the treatment of malignant SVC obstruction was in 1986. 284 During the next 10 years, there were 38 studies identified in the literature reporting on 324 patients treated with placement of intravascular stents for vena cava Curr Probl Surg, December 1999

1013

obstruction (Table 6). 284-32I Stents were placed for SVC obstruction in 244 patients and for IVC obstruction in 80 patients. Two hundred sixty-one patients had malignant caval obstruction, and 63 patients had benign caval obstruction. Three types of stents have been used for the treatment of vena caval obstruction: the Gianturco Z-type stent, the Wallstent, and the Palmaz stent. The largest reported experience has been with the Gianturco stent, which accounts for 63% of stents placed. Wallstents have been placed in 30% of cases (Fig 39), and Palmaz stents have been placed in 7% of cases. Each stent has its own theoretic advantages and disadvantages for use in venous obstructions. The Gianturco stent consists of a more open structure that may be less thrombogenic and is less apt to cause obstruction of side branches bridged by the stent. Wallstents and Palmaz stents are more tightly woven and therefore may be stronger and more resistive to tumor ingrowth; on the other hand, they could be potentially more thrombogenic because of a larger amount of exposed metal. Both the Gianturco and Wallstent devices are self-expanding and will apply continuous outward pressure on the venous walls, theoretically assisting in patency with continued stent expansion after deployment (Fig 40). Despite the structural differences of each stent, the overall results of each device do not differ significantly. Excellent results are reported for the treatment of vena cava obstruction with intravascular stent placement. The overall initial technical success rate for stent placement in patients with caval obstruction is 98%. Among the patients in whom stent placement was technically successful, total or partial initial relief of symptoms has been obtained in 95% of patients. Relief from symptoms persisted until death or the length of clinical follow-up in 90% of patients. Primary patency, primary-assisted patency, and secondary patency rates until the time of death or last clinical follow-up were 86%, 90%, and 94%, respectively, for the overa.ll group. When analyzed separately, the results for benign disease are slightly better than the results for malignant obstructions. Thrombolytic therapy is a valuable adjunct to stenting for benign and malignant obstructions, particularly in cases of acute vena caval thrombosis. Thrombolytic therapy has been required to open thrombotic occlusions before the placement of stents in approximately 30% of cases. Malignant Vena Cava Obstruction.--Intravascular stent placement is clearly the procedure of choice for patients with malignant caval obstruction whose condition has not responded to previous conventional treatment with radiotherapy or chemotherapy. Approximately 75% of patients with malignant vena cava obstruction received radiotherapy and/or 1014

Curr Probl Surg, December 1999

chemotherapy before treatment with intravascular stenting. 284-321There is now growing sup'port for primary treatment with stenting before, or instead of, conventional therapy for malignant vena caval obstruction. The main advantage of stenting is the prompt resolution of obstructive symptoms, usually within 24 to 72 hours. Radiotherapy is successful in relieving most symptoms associated with malignant SVC obstruction in up to 94% of cases. 322 Symptoms, however, may take up to 3 weeks to regress, 282.3~3and recurrent SVC obstruction occurs in 10% to 32% of c a s e s . 276"281'282 Radiotherapy has resulted in acute worsening of symptoms in some patients because of transient radiation-induced tumor swelling. Treatment of recurrent vena caval obstructions with further radiotherapy is limited because most patients receive maximum dosages with the initial treatment. Chemotherapy has been less effective but is used in the treatment of certain sensitive tumors. 276The addition of chemotherapy has not enhanced the effects of radiotherapy significantly, and caval obstruction has recurred in 30% of patients who were successfully treated with chemotherapy.TM The use of balloon angioplasty alone has largely been abandoned for the treatment of malignant caval obstructions because of the high rate of primary failure and recurrence. Angioplasty with balloon catheters can frequently expand the venous lumen, but occlusion usually recurs immediately after deflation of the balloons. 287 When performed immediately before stenting, balloon angioplasty is useful for assessing the toughness of the malignant stricture and providing exact localization of the stenosis. TM In addition, fight malignant strictures may require initial balloon dilatation before the placement of a stent. 285"288Surgical bypass of either an SVC or IVC obstruction is a major endeavor associated with high morbidity rates and is not suitable for most patients with advanced malignan.t disease and short life expectancy. Intravascular stenting has been successful in the treatment of both primary and recurrent malignant vena cava obstructions. The initial technical success rate for stent placement in patients with malignant vena cava obstruction was 98%. Of these technically successful cases, total or partial initial relief of symptoms was obtained in 95% of patients. The relief of symptoms persisted until death or the length of clinical follow-up in 89% of patients. Primary patency, primary-assisted patency, and secondary patency rates until the time of death or last clinical follow-up were 84%, 88%, and 93%, respectively, for patients with malignant obstruction. Significantly poorer results have been reported in patients with caval obstructions totally enveloped by malignant tumors. 3°9 Benign vena cava obstruction.---Conventional management of benign Curr Probl Surg, December 1999

1015

TABLE 6.

Placement of intravascular stents for vena covo obstruction: 3 8 studies Technical success

No. of cases Author

Year

SVC

IVC

Chamsan-

1986

1M

--

113

--

Rosoh Putnam Furui

1987 1988 1990

Solomon Chatelain Rosch

1991 1991' 1992

Irving

1992

2M 2M --6M 1B 20M 2B 17M 1B 14M 1M 6M 2M 1M 17M 4M 1B -6B 18 18 20M 12M

--6M 3B -1B --2M 1B 8M -------1B ------3M --1B -23M --38 -lOB ---

gavej

Oudkerk Cassidy Kishi Eng Edwards Dyet Wat~kinson

1992 1992 1993 1993 1993 1993 1993

Berger Rosenblum Dodds Lindsay Gaines Crowe

1993 1993 1994 1994 1994 1995

Entwisle Stock Francis Hennequin

1995 1995 1995 1995

Furui Wilkinson Hemphil Simo Ge Kaul Rosent~al Oudkerk

1995 1995 •995 1995 1995 1996 1996 1996

1B 1M 14M 1B 14M 18 16M 6M 28 -1B -1B 30M

Shah Xu Althaus MacLellar~ Tobert Schranz Subtotals

1996 1996 1996 1996

13M --3B

-17B 1B 1B

1996

18 219M 258

-42M 38B

244

80

Totals

M, Malignant; B, benign;

1016

Type of stent

GZ, Gianturco-Z;

SVC

IVC

SVC

--

1/1

1/1

--

1/1

2/2 2/2 --6/6 1/1 20/20 2/2 17/17 1/1 14/14 1/1 6/6 2/2 1/1 17/17 4/4 1/1 -6/6 i/1 1/1 18/20 11/12

--6/6 3/3 -1/1 --2/2

GZ

1/1

GZ GZ GZ GZ1, P5 ~V GZ GZ GZ19, W3 GZ GZ GZ GZ W W P 5P, 1W P W GZ GZ9, P1, W1

0/1 W W W W GZ P4, W2 GZ GZ P W P GZ17, W13 GZ6, W6 GZ W P P 199GZ (63%) 95W (30%) 24P (7%)

Initial r e l i e f of symptoms

13/14 1/1 14/14

-3/3 --1/1

1/1

--

16/16 6/6 2/2 m 1/1 w 1/1 17/17, 13/13 12/13 w -3/3

23/23 --3/3 -10/10 ---

1/1

2/2 2/2 --6/6 i/i 20/20 2/2 17/17 1/1 14/8

1/1 8/8 -------1/1 ------

-17/17 1/i 1/1

IVC

616 3/3 I/I -2/2 1/1 8/8

i/1 6/6 2/2

11'1 17/17 4/4 1/i -

--

1/1

-

6/6 1/I 1/1 18/18 11/11

m

3/3

i/I

12/13 I/i 13/14

i/I 13/16 6/6 2/2 --

1/1 22/23

3/3

1/1 -1/1

10/10

13/17, 12/13 6/6, 6/6 --3/3

--17/17 I/I IIi

1/1 -M: 2 5 6 / 2 6 1 (98%) B: 6 2 / 6 3 (98%)

1/1 M: 2 4 2 / 2 5 6 (95%) B: 6 1 / 6 2 (98%)

3 1 8 / 3 2 4 (98%)

3 0 3 / 3 1 8 (95%)

W, Wallstent; P, Palmez. Curr Probl Surg, December 1999

Late relief of symptoms

Primary

Secondary patency

Assisted

patency

primary patency

SVC

IVC

SVC

IVC

1/1

--

1/1

--

SVC 1/1

1/1

--

1/1

--

1/1

2/2

2/2

---

2/2 2/2

---

2/2 2/2

IVC

SVC

IVC

--

1/1

--

--

1/1

--

--

2/2 2/2

--6/6 3/3

6 mo 1-2 mo 2-13 mo

--

~7-103 days 5-11 mo 1-12 mo

--

Follow-up 5 wk to 5 mo

--

6/6

--

5/6

--

6/6

--

--

3/3

--

3/3

--

3/3

--

6/6 1/1 20/20 2/2 17/17

--

4/6 1/1 19/20 2/2 17/17

~ 1/1 --2/2

5/6 1/1 19/20 2/2 17/17

--

1/1 --2/2

1/1 --2/2

6/6 1/1 20/20 2/2 17/17

1/1 --2/2

0/i

1/1

0/I

I/I

0/1

i/i

O/i

1/1

8/8

8/8 ----

11/14 1/1 6/6 2/2

8/8 ---

--

11/14 1/1 6/6 2/2

--

12/14 1/1 6/6 2/2

8/8 ----

1 wk to 9 mo 51 days 4-14 mo 3-6 mo

--

1/1

--

1/1

--

1/1

--

3

---

15/17 4/4

---

15/17 4/4

---

15/17 4/4

---

3 wk to 7 mo 7 wk to 9 mo

--

1/1

--

1/1

--

1/1

--

1/1

-6/6

1/1 --

-6/6

1/1 --

-6/6

1/1 --

--

1/1

--

1/1

--

1/1

--

--

0/1

--

0/1

--

1/1

--

--

13/18 6/11

---

14/18 11/11

--

--

--

15/18 11/11

---

3/3 --

1/1

3/3

12/13

10/13

--

3/3 --

1/1 13/13

3/3 --

1/1

--

1/1

--

--

1/1

--

13/14

i/i

13/14

1/1

1/1

13/14

1/1

1/i 11/16 4/6 2/2

--

--

--

1/1

--

21/23 ---

1/1 11/16 5/6 2/2

1/1 10/13 1/1 13/14 1/1

--

3/3

--

3/3

21/23 --3/3

11/16 6/6 2/2 --

21/23 --3/3

I/I

--

1/1

--

6/6 2/2 -1/1

--

1/1

--

--

9/10

--

10/10

--

10/10

--

1/1 17/17, 9/13 6/6,6/6

--

1/1

--

--

--

---

--

16/17

--

-17/17

--

1/1

--

--

1/1

--

1/1

3/3

1/1

3/3

-17/17 1/1 1/1

1/1 17/17, 9/13 6/6, 6/6 --

10/10 ---

--

13/17, 9/13 6/6,5/6

1/1 13/17, 9/13 6/6, 5 / 6 -3/3

1/1

3/3

1/1

i/I

--

1/1

--

11/14 1/1 5/6 2/2 1/1 15/17 4/4 1/1 -6/6 1/1 1/1 15/18 11/11

i/I

--

--

--

21/23 ---

11/16

-17/17

M: 2 2 8 / 2 5 6 (89%) B: 5 8 / 6 2 (93%)

M: 2 1 6 / 2 5 6 (84%) B: 5 8 / 6 2 (93%)

1/1 M: 2 2 5 / 2 5 6 (88%) B: 6 0 / 6 2 (97%)

1/1 M : 2 3 7 / 2 5 6 (93%) B: 6 1 / 6 2 (98%)

2 8 6 / 3 1 8 (90%)

2 7 4 / 3 1 8 (86%)

2 8 5 / 3 1 8 (90%)

2 9 8 / 3 1 8 (94%)

C u r r Probl S u r g , D e c e m b e r 1 9 9 9

3 days to 30 mos

mo

26 days 3.23 mo 5 mo 9 mo 1-59 wk 5-243 days

3 wk 2-272 days 6 mo 2 days to 14 mo 1-8 mo 2 9 4 2 9 days 6-18 mo 3-34 mo 6 mo 1-13 mo 10 days 1/2-34 mo 1-10 mo 2 0 2 6 mo 3 mo 3-12 mo No follow-up

1017

vena caval obstruction starts with elevation either of the lower extremities for involvement of the IVC or of the head and upper torso for involvement of the SVC, along with anticoagulation to limit propagation of thrombus while allowing time for the development of adequate collateral circulation. Despite these measures, many patients experience venous hypertensive symptoms. For patients who remain refractory to medical management, further treatment has traditionally depended on surgical bypass. The patency of surgical bypass grafts created to relieve vena cava obstruction in patients with nonneoplastic causes has been poor. Unsatisfactory surgical results have been reported despite the use of various techniques, as a result of compression and t h r o m b o s i s . 278'323'324 This is particularly true for prosthetic conduits. The best surgical results for SVC obstruction have been reported with spiral saphenous vein bypass conduits.325The high morbidity and poor patency rates associated with surgical bypass operations for caval obstruction make alternative interventions more attractive. Percutaneous balloon angioplasty has been performed for the treatment of benign obstructions Of the vena cava with s o m e success. 326-330 Success is somewhat limited by recoil secondary to fibrosis and scarring in the venous wall. 326-330 When performed for benign IVC obstructions, a 50% sustained patency rate at 2 years has been demonstrated. 3~8Poorer results have been reported after PTA of benign caval obstructions in patients with total occlusion, long-segment stenosis, suboptimal initial results, or prior restenosis. In these patients, primary stenting may be indicated.3~ The use of intravascular stents for the treatment of benign vena cava obstruction has been very successful. Overall, the initial technical success rate for stent placement was 98%. Of these teclanically successful cases, total or partial initial relief of symptoms was obtained in 98% of patients. The relief of symptoms persisted until death or the length of clinical follow-up in 93% of patients. The follow-up period in. most of the patients with stent placement for benign obstruction is less than 1 year, but patency has been documented beyond 36 months. Primary patency, primaryassisted patency, and secondary patency rates until the time of death or last clinical follow-up were 93%, 97%, and 98%, respectively, for patients with benign obstructions. There is insufficient long-term evidence to advocate primary stenting in all patients with benign vena cava obstructions. It is uncertain whether or not these stents will hold up to years of stress, without breakage or migration, in patients with normal life expectancy. Regardless, stenting is successful at least in the short term for benign disease, and stent failure will most likely not preclude palliation, if needed, by alternative surgical means. Complication rates in the literature vary from 0%, in many studies, to as 1018

Curr Probl Surg, December 1999

high as 3 6 % . 292 A total of 45 major complications related to stent placement were reported in the review of 318 patients who were treated for vena caval syndrome, representing an overall complication rate of 14%. Minor complications such as mild transient chest and back pain, benign arrhythmias, fever, cellulitis, and mild congestive heart failure were excluded from the calculation. Also excluded were complications related to anticoagtflation, because there is no consensus about the need for patients to undergo anticoagulation after stenting. Most major and all minor complications were well tolerated and easily treated. In fact, most major stentrelated complications could be prevented by various technical maneuvers such as improved assessment of venous luminal diameter and measurement of the extent of disease and more precise placement of the stent. New, improved stent designs may reduce the incidence of stent breakage. The most common major complication reported was stent thrombosis with vena cava occlusion. Most cases of stent thrombosis and vena cava reocclusion did result in recurrence of symptoms. Thrombolytic therapy can play an important role in salvaging secondary patency after stent thrombosis and occlusion, particularly for early stent thrombosis. Early thrombosis occurring within 30 days after stent placement was noted in 19 patients, 11 of whom (58%) underwent successful recanalization with thrombolytic therapy. Late thrombosis developed in 7 patients, only 2 of whom (29%) were successfuUy reopened with thrombolytic therapy. The use of poststent thrombolysis increased the overall late stent patency rate from 90% to 94%. There is considerable disagreement in the literature regarding the need to use anticoagulants after stent placement for vena cava obstruction. Some authors support indefinite anticoagulation29° or the use of anticoagulants for several months,297 whereas others report no benefit. 29~The main concem is the inherent thrombogenicity of the stainless steel stent. 331 Many authors support the use of anticoagulants until endothelialization of the stent occurs, which has been estimated to occur between 1 and 3 w e e k s . 332 Most studies recommend poststent anticoagulation in selected patients with increased risk for thrombus formation, such as those with caval thrombus before stenting or residual stenosis after stenting. The major stent-related complications included stent breakage in 6 patients and stent migration in 6 patients. None of these 12 complications resulted in recurrent symptoms, but most of the complications required a second procedure. Most cases of stent migration occurred because of an error in the estimation of the caval size resulting in too small a stent being placed, which subsequently became dislodged. There was 1 case reported in which the stent was positioned improperly, resulting in persistence of Curr Probl Surg, December 1999

1019

a

'

.....*~:iN .....

o

:.~

FIG 39. A 52-year-old man with malignant mesothelioma and right-sided pleural mass. A, Inferior veno cavagram demonstrated obstruction of upper IVC with numerous collateral veins. B, Completion inferior vena cavagram after insertion of a Wallstent (arrows). (From Entwisle KG, Watkinson AF, Hibbert J, Adam A. The use of the Wallstent endovascular prosthesis in the treatment of malignant inferior vena cava obstruction. Clin Radiol 1995;50:310-3. By permission.)

symptoms. Residual or recurrent stenosis adjacent to or within the stent was reported in 8 patients, 2 of whom were subsequently and successfully re-treated. Several patients were found to have restenoses of varying severity remote from the previously placed stent during poststent followup as the result of the progression of the disease. Fortunately, most of these remote stenofic areas resulted in mild or no recurrence of symptoms. 1020

Curr Probl Surg, December 1999

n

n FIG 40. A 68-year-old man with severe SVC syndrome because of bronchogenic carcinoma, A, Initial

venogram reveals occlusion of the SVC, thrombus in its main tributaries, and filling of collaterals. B, Follow-up venogram after local infusion of urokinase shows lysis of thrombi and severe stenosis of distal SVC. ¢, Completion venogram immediately after placement of a double-body stent with a skirt shows good expansion of the stent and excellent flow in the SVC. D, Superior vena cavagram 2 months after stent placement reveals further expansion of the stent and improved flow. (From RoschJ, Uchida BT, Hall LD, et al. Gianturco-Rosch expandable Z-stents in the treatment of superior vena cava syndrome. Cardiovasc Intervent Radiol 1992; 15:319-27. By permission.) Curr Probl Surg, December 1999

1021

Other major nonspecific complications were mainly due to the invasiveness of the procedure. These included 1 vein dissection and 1 retroperitoneal hemorrhage related to venous injury. Recurrent symptoms occurred in at least 4 patients without an identifiable reason. There are several technical details of stent placement that could prevent most stent-related complications. A stent of adequate length must be used so that it completely covers both the proximal and distal extents of the stenosis to prevent residual or recurrent stenosis adjacent to the stent. The stent diameter should exceed the transverse diameter of the patent portion of the cava near the obstructive lesion by 2 to 5 mm to help prevent stent migration. 3°9,331More precise estimation of the luminal diameter may be accomplished with balloon angioplasty before stenting. In the case of SVC obstruction, the stent should be placed far enough proximally to secure patency of at least 1 irmominate vein. In summary, intravascular stent placement is a safe, effective, and durable treatment for symptoms associated with vena cava Obstruction of either benign or malignant cause. Stenting offers more durable results compared with balloon angioplasty alone and less morbidity than surgical bypasses. Long-term assisted vena caval patency rates exceed 93% for patients with malignant disease and 98% for patients with benign disease. Long-term relief of symptoms is obtained in 89% of patients with malignant disease and in 93% of patients with benign disease. The complication rate of stent placement for vena cava obstruction is relatively low compared with other more traditional treatment modalities. Thrombolytic therapy is an important adjunct to therapy both before and after stenting for many patients with thrombotic caval obstructions. The need for anticoagulation after stenting a caval obstruction remains controversial. Stents have been shown to be particularly helpful in patients with malignant caval obstruction, especially for those whose condition has failed to respond to conventional therapy. Because the life exl~ectancy is limited in patients with malignant ven~t cava obstructions, stenting most often provides permanent relief of symptoms in these patients. Permanent relief of symptoms for benign caval obstructions has not yet been proved, but the results to this point are encouraging. Most patients who were reported in the literature had undergone intravascular stenting as a secondary procedure after failure of more traditional treatment modalities. Many authors today, however, support intravascular stenting as a primary therapy for both benign and malignant vena cava obstructions. When longer-term results are available, expanded treatment of vena cava obstructions with intravascular stenting will likely occur. 1022

Curr Probl Surg, December 1999

Upper Extremity Venous Stents Hemodialysis Access.--Preservation of hemodialysis vascular access is a major goal for physicians rendering care to patients with end-stage renal disease (ESRD). A well-functioning native AVF or prosthetic arteriovenous graft (AVG) is the lifeline for patients undergoing chronic maintenance hemodialysis.333 Cumulative 1-year patency rates in recent series for Brescia-Cimino AVFs vary from 71% to 88% compared with 67% to 93% for AVGs. TM Unfortunately, patients with AVGs will require 3 to 4 times as many secondary procedures to maintain equivalent cumulative patency rates reported for patients with A V F s . 335"336 The most common cause of fistula or graft failure is thrombosis related to decreased fistula blood flow. Primary causes of decreased flow include venous outflow stenosis and increased external postdialysis compression to the fistula. Less common causes include midgraft stenosis, central venous obstruction, hypotension, hypovolemia, hypercoagulable states, and mefial inflow stenosis. Diminished blood flow increases not only the risk of thrombosis but also decreases dialysis function by reducing extracorporeal blood flow. The failure of PTA alone to provide a durable solution for the treatment of this venous stenosis is perhaps related to the nature and location of these lesions. Venous outflow and graft-vein anastomotic stenoses typically are hyperplastic lesions composed of smooth muscle cells with extensive amounts of collagen, elastin, and flbroblasts, 337 During balloon dilation, instead of plaque fracture occurring as with atherosclerotic lesions, hyperplastic venous stenoses primarily undergo stretching and dissection, frequently resulting in immediate elastic recoil, collapse of the vessel, thrombosis, or residual stenosis.338 Central venous stenoses develop intimal hyperplasia as a result of increased blood flow and turbulence produced from the downstream AVF or AVG. Cen~al veins have the added problem that they may develop phlebosclerosis and perivenous fibrosis from repeated placement of temporary hemodialysis catheters, leading to excessive external compression. External compression may also develop as a result of repetitive venous trauma experienced at the thoracic outlet. The combined effect of intraluminal hyperplasia and external fibrosis observed in the central venous stenoses makes effective long-term treatment of these lesions problematic. Traditionally, the standard treatment for failing or thrombosed grafts has been surgical thrombectomy and/or revision. However, restenosis and secondary graft failure rates remain high after operation with 6-month and 1year primary patency rates reported to be 20% to 55% and 3% to 23%, respectively, depending on the type of procedure performed (Table 7). 339"343 Furthermore, surgical revision often requires the insertion of temporary percutaneous dialysis catheters, with loss of an additional access site or outCurr Probl Surg, December 1999

1023

flow vein. During the past 10 years, PTA has been used extensively to salvage failing or failed AVFs or AVGs. Numerous series have suggested that percutaneous therapy improves on the observed results after surgical revision, decreases overall costs, and provides a comparable minimally invasive alternative to surgery. 332'344-346However, reports that used life-table analysis indicate that patency rates and fistula function after percutaneous intervention are variable and describe results similar to those reported for surgical intervention. Patency rates after PTA range from 23% to 64% at 6 months and 7% to 44% at 1 year. 339.340,345-352The wide range in reported patency rates is likely due to the different types of lesions being treated. Beathard, 345 in a large study involving more than 500 balloon dilations of hemodialysis access stenoses, found that patency rates depended on the number of stenoses, the anatomic location, and the severity and the length of stenosis or occlusion. Patency with balloon angioplasty has been shown to improve with repeated dilations. Turmel-Rodrigues and colleagues348reported a 44% primary patency at 1 year that improved to 71% with repeated dilations. There were approximately 3.1 interventions per graft per year. The use of endovascular stents has been recommended as an alternative treatment to overcome the anatomic challenges presented by hemodialysisrelated venous stenoses. Stents have several perceived advantages over balloon dilation, which may lead to improved venous patency and overall fistula or graft function rates. Stents help to limit elastic recoil in compliant veins, reapproximate damaged and dissected intima to the vessel wall, and act as an internal mechanical support to counteract external fibrotic compression. However, reported 6-month and 1-year primary patency rates for endovascular stents do not appear significantly different from surgical procedure or angioplasty alone, at 12% to 73% and 0% to 68%, respectively. 338"349-355 Comparison of reported results for all 3 treatment modalities remains difficult to assess because most series included varied indications for stent placement, small numbers of patients and interventions, heterogeneous target vessels, multiple stent types and designs, short clinical follow-up, inconsistent data collection, and insufficient statistical analysis. Many of the early indications for endovascular stenting included salvage of suboptimal angioplasty results (Fig 41). Turmel-Rodrigues and colleagues348inserted Wallstents in 9 rapidly recurring stenoses after PTA. After stent placement, the ratio of additional procedures for restenoses decreased from 3.1 before stent placement to 0.44 per year per stenosis after stent placement. The mean time between 2 procedures increased from 3.6 months before stent placement to 15.2 months after stent placement. No life-table data were provided. Four years later, the same authors updated their series this time using life-table analysis to determine patency rates. Primary paten"1024

Curr Probl Surg, December "1999

TABLE 7. Life-tableanalysis of patency rates for AVFs and AVGs after the first intervention Primary p ~ e n c y (%)

Study InterventJon

(first author)

Year

Interventions(n)

6-me

1-y

2-y

Cumulative p a t e n c y (%) 6-mo

1-y

2-y

67 28

62 19

42 --

8a,

78

68

43 41 57

25 31 45

-24

93

71

62

/,

Surgery Brooks Dapunt Puckett Brotman Hurlbert*

1987 1987 1988 1994 1997

19 37 52 112 83

Brooks Dapunt Glanz Beathard TurmeI-Rodrigues Beathard Kanterman Quinn Hoffer

1987 1987 1987 1992 1993 1993 1995 1995 1997

244 37 141 536 70 30 54 47 20

Quinn Beathard Schoenfeld Gray Quinn Vorwerk Hoffer TurmeI-Rodrigues

1992 1993 1994 1995 1995 1995 1997 1997

25 30 25 56 50 65 17 52

55 20 30

20 3 23

-20

PTA

61 53 64 63 31 23

38 44 28 41 10 7

22 30 --

--

64 81

64 47

73 72 68 46 27 56 12 58 47

58 17 68 20 11 31 0 23 20

25

80

80

93 76 80 88

93 333 71 86

77

---

69 100

60 88

---

--

95

79

Stent

-w

14

42 --

N --

PTA, Percutaneoustransluminal angioplasty. *Unpublished data,

cy rates at 6 months and 1 year after stent placement for AVGs and AVFs were 58% and 23% and 47% and 20%, respectively. The mean interval for repeat procedures increased from 3.2 months before stenting to 6.9 months after stenting for AVGs and 2.9 months to 6.2 months for AVFs. The authors concluded that placement of stents is valuable for the treatment of failed dilations and will double the time interval between reinterventions for early restenosis (<6 months).355 Gray and colleagues353reported a primary patency rate of 46% at 6 months and 20% at 12 months with Wallstents placed in 56 venous stenoses (Fig 42). The secondary patency rate was 76% at 6 months but only 33% at 1 year. Most restenoses appeared within the stent. Similarly, Vorwerk and colleagues354placed WaUstents in 92 venous stenoses for either insufficient balloon angioplasty or primarily in central venous stenoses (Fig 43). Life-table analysis showed the primary patency rate at 6 Curr Probl Surg, December 1999

1025

FIG 41. A, Image of hemodialysis shunt after balloon dilation of a recurrent venous stenosis. B,, Stenosis has resolved after angioplasty and placement of 2 overlapping stents. ¢, Four months after insertion, the stents remain expanded, but hyperplastic intima narrows the lumen. (From Gunther RW, Vorwerk MD, Bohndorf K, et al. Venous stenoses in dialysis shunts: treatment with self-expanding metallic stents. Radiology 1989;170:401-5. By permission.)

months was 56%, which fell to 31% at 1 year. With repeat angioplasty, the secondary patency rate was improved to 88% at 6 months and 86% at I year. Because of the reasonable success reported after stent placement for salvage of PTA failures, several authors advocated primary stent deployment regardless of the outcome after PTA. The first report on primary stent placement for hemodialysis-related stenoses involved the use of a modified self-expandable Gianturco stent. 352Twenty-five stents were placed in 13 peripheral, 10 central, and 2 anastomotic access sites (21 stenoses, 4 occlusions). Primary patency rates at 6 months and 1 year were 73% and 58%, respectively, but dropped to 25% by the second year of follow-up. Shoenfeld and colleagues, 338who used both Wallstents and Palmaz stents to treat central venous obstructions in patients being treated with hemodialysis, reported a 68% primary patency rate that continued from 6 months to 17 months of follow-up. Unfortunately only 5 patients were 1026

Curr Probl Surg, December 1999

FIG 42. A,~. Digital subtraction angiogram demonstrates an area of high-grade innominate stenosis (arrow). II, A 10 x 42-mm Wallstent was deployed and dilated to 10 mm, and minimal residual stenosis can be seen (arrow). (From Gray RJ, Horton KM, Dolmatch BL, et al. Use of Wallstents for hemodialysis access-related venous stenoses and occlusions untreatabte with balloon angioplasty. Radiology

1995; 195:479-84. By permission.)

followed for more than 6 months, and the authors did not stratify their patency data for the type of stent deployed. Nonetheless, the authors concluded that stenting of central veins was practical, effective, and durable. Presently there are 3 published prospective randomized studies that compare F r A alone with PTA and stent placement. B e a t h a r d 349 prospectively randomized 58 graft-venous anastomotic stenoses to undergo PTA alone or PTA and stenting with a self-expanding Gianturco stent. The author found no difference in primary patency rates between the 2 groups and concluded that the Gianturco stent offered no advantage in the treatment of graft-vein anastomotic stenoses. An intermediate report by Quinn and coUeagues352 reported primary and secondary patency rates for peripheral and central venous sites. Six-month and 1-year primary stent patency rates for peripheral lesions were 27% and 11%, respectively. Primary patency rates for PTA alone over the same intervals were 31% and 10%, respectively. Six-month and 1-year primary stent patency rates for central lesions were 11% and 11%, respectively. The patency rates for PTA alone were just 23% and 12%, respectively. There was no significant difference in patency rates between the groups. On the basis of these results, the authors suggest that primary placement of Gianturco stents for peripheral venous stenoses offers no benefit compared with PTA alone and has a limited role in the management of these lesions. No comment was made regarding the use of stents for central venous stenoses because of the limited number of patients in the study. Finally, a more recent study by Hoffer and colleagues35Ireported dismal patency rates for both PTA alone and PTA with WaUstent. The I-year primary patency rate Curr Probl Surg, December 1999

1027

FIG 43. Central venous occlusion. &, Angiogram shows complete occlusion at the level of the right axi[lary vein (arrow). B, Balloon dilation performed to recanalize a small channel. ¢, Reconstruction of central venous outflow is completed by placing stents from the axillary to the brachiocephalic vein. (From Vorwerk D, Guenther RW, Mann H, et al. Venous stenosis and occlusion in hemodialysis shunts: follow-up results of stent placement in 65 patients. Radiology 1995; 195:140-6. By permission.)

was less than 10% for both groups, at 7% and 0%, respectively. Furthermore, the authors concluded that the extra costs associated with primary Wallstent placement for the treatment of peripheral venous stenoses were unwarranted and produced little clinical benefit. Other authors have tried to determine whether there are subgroups of venous stenoses that do remain patent longer with stent placement. Kovalik and colleagues356compared angioplasty versus angioplasty and Wallstent in central venous stenoses in patients being treated with hemodialysis (Fig 44). They found that patients with a greater than 50% recoil in the central vein after dilation had a recurrence twice as fast as if there was no recoil (2.9 months versus 7.6 months). The authors then stented patients with a greater than 50% recoil or restenosis without recoil and found that stenting increased the patency of the elastic vessels to 8.6 months to recurrence but had little effect on the patency of the veins without recoil. As in other studies, patency was improved with secondary interventions. In summary, the role of endovascular stents for the treatment of hemodialysis-related venous stenoses remains uncertain. Overall primary patency rates after PTA with stent placement are not significantly different from patency rates reported for PTA alone. Stent placement should be reserved for use in salvage situations after suboptimal PTA (ie, significant recoil or restenosis, occlusive dissection, vessel rupture).' Primary stent placement is not indicated for anastomotic or peripheral venous stenoses. Primary stent placement may be valuable for a specific subset of central venous stenoses or occlusions. The ultimate benefit of endovascular stents in the dialysis population may reside in the ability to increase the reintervention interval after deployment. A prospective randomized multicenter trial that compares the 3 treatment modalities is necessary to determine the exact role of stents in 1028

Curr Probl Surg, December 1999

hemodialysis-related access stenoses. Until then, controversy will continue regarding the treatment of choice for correction of these troublesome lesions. Effort Thrombosis.--Endovascular stents have been used for patients with residual axiUary or subclavian vein stenosis after PTA in patients with effort thrombosis, also known as Paget-von Schroetter syndrome, traumatic thrombosis, thoracic inlet syndrome, or venous thoracic outlet syndrome. The cause of the syndrome is usually extrinsic compression of the subclavian vein at the thoracic inlet that produces damage to the venous intima and results in a fibrous scar within the vein as it passes over the rib. 357 Thrombosis occurs in the presence of aberrant thoracic outlet musculature, primarily after vigorous use of the extremity. Treatment of this condition is by a staged multimodal approach. The best results have been obtained by thrombolysis of the thrombosed vein followed by surgical decompression of the thoracic outlet. 35s-36° Balloon angioplasty or stent placement after thrombolysis without thoracic outlet decompression usually results in a rapid rethrombosis and/or deformation of the stent. 359-363 Angioplasty and stenting have been used successfully to manage residual stenosis within the vein after the extrinsic compression has been removed (Fig 45). Stents have been recommended as an adjunct if a 50% or greater residual stenosis persists after balloon angioplasty. 363Wallstents and Giantttrco and Palmaz stents have been used in this setting. The selfexpandable stents have an advantage over the balloon-expandable stents in this application because they are much more resistant to 2-point compression. Any balloon-expandable stent that is subjected to 2-point compression will be deformed permanently. Bjarnason and colleagues364report the collapse of a Palmaz stent that was placed in the subclavian vein and subjected to just such compression. Self-expanding stents are much more resilient and will resume their previous shape after compression. Most of the reported stent experience for the treatment of effort thrombosis has come from 2 recent series involving 11 and 5 patients, respectively, 363'365 and 3 earlier case reports involving a total of 4 patients. 364,366,367 Meier and colleagues363reported on the use of the WaUstent after unsuccessful PTA in 11 patients with Paget-yon Schroetter syndrome. Stent placement was technically successful in all patients, and 8 of the 11 patients (72%) remained asymptomatic or exhibited minimal symptoms in late follow-up. However, 6 patients experienced some anatomic or clinical complication, including rethrombosis (n = 3 patients), stent fracture (n = 2 patients), or restenosis (n = 1 patient). Each complication was associated with the lack of first rib resection. In contrast to these results, Beygui and colleagues365reported successful stent placement in just 2 of 5 patients with subclavian vein thrombosis. The 3 failures in this series occurred in patients Curr Probl Surg, December 1999

1029

FIG 44. A, Pre-stentvenogram of central venous lesions. Subclavian vein stenosis (A) and stenosisat junction of the subclavian vein and the superior vena cava (B). B, Post-stentvenogram of central vein. Wallstent (arrow) placed across both areas of stenosiswith good blood flow and no residual stenosis. (From Kovalik EC, Newman GE, Suhocki P, Knelson M, Schwab SJ. Correction oF central venous stenoses:use of angloplash/and vascular WaUstents. Kidney International 1994;45:1177-81. By permission.)

with secondary venous thrombosis related to malignancy, field radiation therapy, or central venous catheterization. There is no evidence that stent placement decreases the risk of rethrombosis and maintains long-term venous patency. Further evaluation in the form of long-term prospective studies is necessary to determine whether stent placement can be advocated in patients with effort thrombosis.

Lower Extremity Venous Stents Iliofemoral-popliteal Stents.--Stents have been used for a wide variety of indications in the lower extremity venous system. The cause for most of 1030

Curr Probl Surg, December 1999

A

FIG 45. A, Initial venogram demonstrates thrombus within the right axillosubclavian vein and severe proximal stenosis (arrowhead~. B, Residual thrombus and residual stenosis after balloon angioplasly. C, Wallstent in subclavian vein. Thrombus and residual stenosis have resolved. (From Cohen GS, Braunstein L, Ball DS, Domeracki F. Effort thrombosis: effective h'eatment with vascular stent after unrelieved venous stenosis following a surgical release procedure. Cardiovasc Intervent Radial 1996;t9: 37-9. By permission.) Curr Probl Surg, December 1999

1031

these venous stenoses or occlusions is either extrinsic compression for malignancy or fibrosis or intrinsic narrowing from postoperative, congenital, or acquired webs. The larges~ series that has reported on the use of balloon angioplasty and stents in the lower extremity venous system is from Nazarian and colleagues368 (Fig 46). They report a series of 59 lesions from the IVC to the superficial femoral vein. WaUstents and Gianturco stents were primarily used in this study. Approximately one half of the stents were placed for compression of the vein by an extrinsic malignancy. Thrombolysis was initiated before angioplasty if the vein was thrombosed. The overall 1year patency rate was 50%. There was no significant difference between the type of stent used, stenosis versus occlusion, or left- versus right-sided iliac stents. Stents placed in the iliac veins only were shown to remain patent longer than stents deployed in both the iliac and femoral veins (64% vs 25%). The secondary patency rate was 81% overall.Again, there was no significant difference in patency between the type of stent used, stenosis versus occlusion, or left-sided versus right-sided iliac stents. The secondary patency rate was found to be better in stents placed for benign causes than for malignant causes (94% vs 64%). Other studies of lower extremity venous stenting are primarily case reports. Zollikofer and colleagues 369 reported on 5 patients who underwent angioplasty and stenting of lower extremity venous stenoses with Wallstents. These stents were placed in the common iliac, common femoral, and superficial femoral veins. One patient had venous compression as the result of malignancy, and the other patients had intrinsic stenoses from postoperative changes. All 5 stents were patent from 6 weeks to 58 months after implantation. There have also been reports of stents being used for iliac compression syndrome. Iliac compression syndrome is seen as thrombosis of the left common iliac vein. It is caused by compression of the .vein by the overlying right common iliac artery and the underlying pelvic brim (May-Thumer syndrome). Fibrous bands often form w~thin the vein at the site of compression. The patients are usually women in their third decade of life after an operation, pregnancy, or prolonged bedrest. 37° Berger and colleaguesTM report 1 patient with iliac compression syndrome who was treated with catheter-directed thrombolysis and a Palmaz stent. The vein was patent by duplex ultrasonography 6 months after placement. One series from Rilinger and colleagues372 described treating 3 patients with iliac compression syndrome with surgical thrombectomy and Palmaz stenting. These stents were patent, and the patients were asymptomatic at 3 to 10 months after implantation. Surgical therapy for this condition has been successful 75% to 85% 1032

Curr Probl Surg, December 1999

FIG 46. A, Right lilac venogram shows a tight focal stenosis of the distal external vein (straight white arrows) with diffuse, moderate stenosisof the proximal external common lilac vein (arrowheads). Collateral venous outflow is indicated (curved black arrow). B, Radiograph shows dilation of 2 overlapping 68 x lOmm Wallstents with a 10-mm x 4-cm balloon. ¢, Completion right Sac venogram shows no residual stenosis. Note that collateral vein is no longer seen {see A). (From Nazarian GK, Bjarnason H, Dietz CA, Bernadas CA, Hunter DW. lliofemoral venous stenoses:effectivenessof treatment with metallic endovascular stents. Radiology 1996;200:193-9. By permission.)

of the time. 373,374Whether endovascular techniques are superior to surgical procedures in this uncommon condition is unknown. Lower-extremity venous stenting has also been described for stenosis resulting from radiation therapy, 375retroperitoneal fibrosis, 376 and hemodialysis graft venous outflow stenosis. 377 Semba and Dake 378reported a series of 27 limbs with iliofemoral deep venous thrombosis that were treated with catheter-directed thrombolysis. Stents were used in 14 limbs for residual stenosis or residual thrombus. This study found an immediate technical and clinical success rate of 85%. There were no follow-up data. It is not yet proved that thrombolysis and stenting of residual stenosis in iliofemoral deep venous thrombosis are superior to conventional management. Mark A. Mattos, MD, wants to thank his current and former vascular surgery colleagues at Southern Illinois University School of Medicine for their efforts and determination in the completion of each of their respective sections in this monograph and his secretary, Maryl Berns, for her clerical support.

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REFERENCES I. Aim SS, Rutherford RB, Becker GJ, et al. Reporting standards for lower extremity arterial endovaseular p r o c u r e s . J Vase Surg 1993;17:1103-7. 2. Ferguson JM, Stonebridge PA. Endovascular surgery. J R Coil Surg Edin 1996; 41:23-231. 3. Becker GJ,: Katzen BT, Dake MD. Noncoronary angioplasty. Radiology 1989; 170:921-40. 4. Dotter CT, Judkins MP~ Transluminal treatment of arteriosclerotic obstruction. Circulation 1964;30:654-70. 5. Dotter CT. Transluminally-placed coilspring endarterial tube grafts: long-term pateney in canine popliteal artery. InVest Radiol 1969;4:329-32. 6. Gruentzig A, Hopff M. Perkutane Rekanalization chromischer arteriler Verschloss miteineur neuen Dilatatiouscatheter: Modification der Dotter-Technik. Deutsch Med Wochenseriff 1974;99:2502-10. 7. Block PC, Fal|on JT, Elmer D. Experimental angioplasty: lessons from the laboratory. AJR Am J Roentgenol 1980;135!907-12. 8. Dotter CT, Busehann RW, MeKinney MK, Rosch J. Transluminal expandable nitinol coil stent grafting: preliminary report. Radiology 1983;147:259-60. 9. Cragg A, Lung G, Rysavy J, et al. Nonsurgical placement of arterial endoprostheses: a new techniqueusing nitinol wire. Radiology 1983;147:261-3. 10. Cragg A, Lung G, Rysavy J, et al. Percutaneous arterial grafting. Radiology 1984;150:45-9. 11. Maass D, Zollikofer CL, Largiader F, Senning A. Radiological follow-up of transluminally inserted vascular endoprostheses: an experimental study using expanding spirals. Radiology 1984;150:659-63. 12. Wright KC, Wallace S, Charnsangavej C, et al. Percutaneous endovascular stents: an experimental evaluation. Radiology 1985;156:69-72. 13. Palmaz JC, Windelar SA, Garcia F, et al. Atherosclerotic rabbit aortas: expandable intraluminal grafting. Radiology 1986;160:723-6. 14. Rousseau H, Puel J, Joffre F, et al. Self-expanding endovascular prosthesis: an experimental study. Radiology 1987;164:709-14. 15. Roubin GS, Robinson KA, King SB, et al. Early and late results of intracoronary arterial stenting after coronary angioplasty in dogs. Circulation 1987;76:891-7. 16. Sigwart U, Puel J, Mirkowitch V, et al. lntravascular stents to prevent occlusion and restenosis after transluminal angioplasty. N Engl J Med 1987;316:701-6. 17. Gunther RW, Vorwerk D, Bohndorf K, et al. Iliac and femoral artery stenoses and occlusions; treatment with intravascular stents. Radiology 1989;172:725-30. 18. Gunther RW, Vorwerk D, Antonucci F, et al. I~ac artery stenosis or obstruction after unsuccessful balloon angioplasty: treatment with a self-expanding stent. AJR Am J Roentgenol 1991;156:389-93. 19. Vorwerk D, Gunther RW. Stent placement in iliac arterial lesions: three years of clinical experience with the Wallstent. Cardiovasc Intervent Radiol 1992;15:285-90. 20. Palmaz JC, Richter G, Noeldge G, et al. Intraluminal stents in atherosclerotic iliac artery stenosis: preliminary report of a multicenter study. Radiology 1988;168: 727-31. 21. Palmaz JC, Sehatz RA, Richter G, et al. Intraluminal stenting of atherosclerotic iliac artery stenosis: preliminaryreport of a multicenter stud~, [abstract]. Circulation 1988;78(suppl):II-415. 1034

Curr Probl Surg, December 1999

22. Palmaz JC, Tio FO, Schatz RA, Alvarado R, Rees C, Garcia O. Early endothelialization of balloon-expandable stents: experimental observations. J Intervent Radiol 1988;3:119-24. 23. Slepian MJ, Schindler A. Polymeric endoluminal paving/sealing: a biodegradable alternative to intracoronary steming [abstract]. Circulation 1988;78(suppl):II409. 24. Ixie T, Furui S, Yamaguchi T, Makita K, Sawada S, Takenaka E. Relocatable Gianturco expandable metallic stents. Radiology 1991;178:575-8. 25. Dichek DA, Neville RF, Zweibel JA, Freeman SM, Leon MB, Anderson WF. Seeding of intravascular stents with genetically engineered endothelial cells. Circulation 1989;80:1347-53. 26. Palmaz JC. Intravascular stents: tissue-stent interactions and design considerations. AIR Am J Roentgenol 1993;160:613-8. 27. Schatz RA, Palmaz JC, Tio FO, et al. Balloon expandable intracoronary stents in the adult dog. Circulation 1987;76:450-7. 28. Vorwerk D, Redha F, Neuerburg J, Clerc C, Gunther RW. Neointima formation following arterial placement of self-expanding stents of different radial force: experimental results. Cardiovasc Intervent Radiol 1994;17:27-32. 29. Schatz RA. A view of vascular stents. Circulation 1989;79:445-57. 30. Penn IM, Levine SL, Schatz RA. Intravascular stents: the evolution from prototypes to clinical trials. In: Ahn SS, Moore WS, editors. Endovascular surgery. Philadelphia: WB Saunders Co; 1992. p 504-22. 31. Ratner BD, Johnston AB, Lenk TJ. Biomaterial surfaces. J Biomed Mater Res 1987;21:59-89. 32. DePalma VA, Baler RE, Ford JW, Gott VL, Furuse A..Investigation of three-surface properties of several metals and their relationship to blood compatibility. J Biomed Mater Res 1972;3:37-75. 33. Bair RE, Dutton RC. Initial events in interaction o f blood with a foreign surface. J Biomed Mater Res 1969;3:191-206. 34. Rogers C, Edelman ER. Endovascular stent design dictates experimental restenosis and thrombosis. Circulation 1995;91:2995-3001. 35. Glagov S. Intimal hyperplasia, vascular modeling, and the restenosis problem. Circulation 1994;89:2888-91. 36. Liermalm D, Strecker EP, Peters J. The Strecker stent: indications and results in iliac and femoropopliteal arteries. Cardiovasc Intervent Radiol 1992;15:298-305. 37. Hoffman R, Mintz GS, Kent KM, et al. Serial intravascular ultrasound predictors of restenosis at the margins of Palmaz-Schatz stents. Am J Cardiol 1997;79:951-3. 38. Van Lankeren W, Gussenhoven F.J, van Kints MJ, van tier Lugt A, van Sambeek MR. Stent remodeling contributes to femoropopliteal artery reatenosis: an intravascular ultrasound study. J Vase Surg 1997;25:753-6. 39. Sala, TA, Taylor B, Suggs WD, Hanson SR, Lumsden AB. Reaction to injury following balloon angioplasty and intravascular stent placementin the canine femoral artery. Am Surg 1994;60:353-7. 40. Liermann DD, Bottcher HD, Kollath J, etal. Prophylactic endovascular radiotherapy to prevent intimal hyl~rplasia after stent implantation in femoropopliteal arteries. Cardiovasc Intervent Radiol 1994; 17:12-6. 41. Bottcher HD, Schopohl B, Liermann D, Kollath J, Adamietz IA. Endovascular irradiation: a new method to avoid recurrent stenosis after stent implantation in periphCurr Probl Surg, December 1999

1035

42.

43.

44. 45. 46. 47. 48. 49. 50. 51.

52. 53. 54.

55. 56. 57. 58. 59. 60. 61.

1036

eral arteries: technique and preliminary results. Int J Radiat Oncol Biol Phys 1994;29:183-6. Schopohl B, Leirmann D, Pohlit LJ, et al. 192IR endovascular brachytherapy for avoidance of intimal hyperplasia after percutaneous transluminal angioplasty and stent implantation in peripheral vessels: 6 years of experience. Int J Radiat Oncol Biol Phys 1996;36:835-40. Liermann DD, Bauernsachs R, Schopohl B, Bottcher HD. Five year follow-up after brachytherapy for restenosis in peripheral arteries, Semin Interv Cardiol 1997; 2:133-7. Fortunato JE, Glagov S, Bassiouny HS. Irradiation for the treatment of intimal hyperplasia. Ann Vasc Surg 1998;12:495-502. Williams DO. Radiation vascular therapy: a novel approach to preventing restenosis. Am J Cardiol 1998;81:18E-20E. Gristina AG. Biomaterial centered infection: microbial adhesion versus tissue integration. Science 1987;237:1588-95. Chalmers N, Eadington DW, Gandanhamo D, GiUespie IN, Ruckley CV. Case report: infected false aneurysm at the site of an iliac stent. Br J Surg 1993;66:946-8. Guest SS, Kirsch CM, Baxter R, Sorooshian M, Young J. Infection of a subclavian venous stent in a hemodialysis patient. Am J Kidney Dis 1995;26:377-80. Latham JA, Irvine A. Infection of endovascular stents: an uncommon but important complication. Cardiovasc Surg 1999;7:179-82. Roubin GS. Gianturco-Roubin stent. In: Kim D, Orron DE, editors. Peripheral vascular imaging and intervention. St Louis: Mosby Year-Book, Inc; 1992. p 532-6. Sawyer PN, Stanczewski B, Srinivasan S, et al. Electron microscopy and physical chemistry of healing in prosthetic heart valves, skirts, and struts. J Thoracic Cardiovasc Surg 1974;67:25-43. Strecker EP, Hagen B, Liermann D, et al. Current status of the Strecker stent. Cardiol Clin 1994;12:674-87. Rosch J, Uchida BT, Hall LD, et al. Gianturco-Rosch expandable Z-stents in the treatment of superior vena cava syndrome. Cardiovasc Intervent Radiol 1992;15:319-27. Chamsangavej C. Gianturco self-expanding stent. In: Kim D, On-on DE, editors. Peripheral vascular imaging and intervention. St Louis: Mosby Year-Book, Inc; 1992. p 537-40. Rabkin JK. Rabkin nitinol stent, In: Kim D, Orron DE, edit9rs. Peripheral vascular imaging and intervention. St Louis: Mosby Year-Book, Inc; 1992. p 509-14. Cragg AH, De Jong SC, Barnhart WH, La.ndas SK, Smith TP. Nitinol intravascular stent: results of preclinical evalhation. Radiology 1993;189:775-8. Hausegger Ir,~, Cragg AH, Lammer J, et al. Uiac artery stent placement: clinical experience with a nitinol stent. Radiology 1994;190:199-202. Beyar R, Henry M, Shofti R, et al. Self-expandable nitinol stent for cardiovascular applications: canine and human experience. Cathet Cardiovasc Diagn 1994;32:162-70. Henry M, Amor M, Beyar R, et al. Clinical experience with a new nitinol selfexpanding stent in peripheral arteries. J Endovasc Surg 1996;3:369-79. Raza Z, Shaw JW, StonebridgePA, McCollum FT. Managementof iliac occlusionswith a new self-expandingendovascularstent. Eur J Vasc Endovasc Surg 1998;15:439-43. Holmes DR, Vliestra RE, Smith HC, et al. Restenosis after percutaneous transluminal coronary angioplasty (PTCA): a report from the PTCA Registry of the National Heart, Lung and Blood Institute [abstract]. Am J Cardiol 1984;53:77C. Curr Probl Surg, December 1999

62. Castaneda-Zuniga WR, Formanek A, Tadavarthy M, et al. The mechanism of balloon angioplasty. Radiology 1980;135:565-71. 63. Hoffman MA, Fallon JT, Greenfield AJ, Waltman AC, Athanasoulis CA, Block PC. Arterial pathology after percutaneous transluminal angioplasty. A JR Am J Roentgenol 1981;137:147-9. 64. Block PC, Myler RK, Stertzer S, Fallon JT. Morphology after transluminal angioplasty in human beings. N Engl J Med 1981;305:382-5. 65. Waller BE Pathology of transluminal balloon angioplasty used in the treatment of coronary heart disease. Hum Pathol 1987;18:476-84. 66. Spence RK, Freiman DB, Gatenby R, et al. Long-term results of transluminal angioplasty of the iliac and femoral arteries. Arch Surg 1981;I 16:1377-86. 67. Johnston KW, Rae M, Hogg-Johnston SA, et al. 5-year results of a prospective study of percutaneous translurninal angioplasty. Ann Surg 1987;206:403-13. 68. Capek P, McLean GK, Berkowitz HD. Femoropopliteal angioplasty: factors influencing long-term success. Circulation 1991 ;83(suppl):1-70-1-80. 69. Johnston KW. Femoral and popliteal arteries: reanalysis of results of balloon angioplasty. Radiology 1992;183:767-71. 70. Richter GM, Noeldge G, Roeren T, et al. First long-term results of a randomized multicenter trial: iliac balloon-expandable stent placement versus regular percutaneous transluminal angioplasty [abstract]. Radiology 1990;177:152. 71. Sapoval MR, Chatellier G, Long AL, et al. Self-expanding stents for the treatment of iliac artery obstructive lesions: long-term success and prognostic factors. AJR Am J Roentgenol 1996; 166:1173-9. 72. Vorwerk D, Guenther RW, Schurmann K, Wendt G, Peters I. Primary stent placement for chronic iliac artery occlusions: follow-up results in 103 patients. Radiology 1995;194:745-9. 73. Dyet JF, Gaines PA, Nicholson AA, et al. Treatment of chronic iliac artery occlusions by means of percutaneous endovascular stent placement. JVIR 1997;8: 349-53. 74. Reyes R, Maynar M, Lopera J, et al. Treatment of chronic iliac artery occlusions with guide wire recanalization and primary stent placement. JVIR 1997;8:1049-55. 75. Colapinto RF, Stronell RD, Johnston KW. Transluminal angioplasty of complete iliac obstructions. AJR Am J Roentgenol 1986;146:859-62. 76. Cambria RP, Faust G, Gusberg R, et al. Percutaneous angioplasty for peripheral arterial occlusive disease. Arch Surg 1987;122:238-87. 77. Toogood G J, Torrie EPH, Magee TR, Galland RB. Early experience with stenting for iliac occlusive disease. Eur J Vasc Endovasc Surg 198; 15:165-8. 78. Richter GM, Roeren T, Noeldge G, et al. Prospective randomized trial: iliac stenting versus PTA [abstract]. Angiology 1992;43:268. 79. Richter GM, Roeren T, Brado M, Noeldge G. Further update of the randomized trial: iliac stent placement versus PTA: morphology, clinical success rates, and failure analysis [abstract]. J Vasc Interv Radiol 1993;4:30-1. 80. Tetteroo E, Haaring C, van der Graaf Y, van Schaik JPJ, van Engelen AD, Mali WPTM. Intraarterial pressure gradients after randomized angioplasty or stenting of iliac artery lesions. Cardiovasc Intervent Radiol 1996;19:411-7. 81. Noeldge G, Richter GM, Roeren T, Brado M, Allenberg JR, Kauffmann GW. A randomised trial of iliac stenting versus PTA in iliac artery stenoses and occlusions: updated 6-year results [abstract]. J Endovasc Surg 1996;3:99-100. Curr Probl Surg, December 1999

1037

82. Sullivan TM, Childs MB, Bacharach JM, Gray BH, Piedmonte MR. Percutaneous transluminal angioplasty and primary stenting of the iliac arteries in 288 patients. J Vase Surg 1997;25:829-39. 83. Tetteroo E, van der GraafY, Bosch JL, et al (for the Dutch Iliac Stent Trial Study Group). Randomised comparison of primary stent placement versus primary angioplasty followed by selective stent placement in patients with iliac-artery occlusive disease. Lancet 1998;351:1153-9. 84. Rutherford RB, Becker GJ. Standards for evaluating and reporting the results of surgical and percutaneous therapy for peripheral arterial disease. J Vase Interv Radiol 1991;2:169-74. 85. Palmaz JC, Garcia OJ, Schatz RA, et al. Placement of balloon-expandable intraluminal stents in iliac arteries: first 171 procedures. Radiology 1990;174:969-75. 86. Palmaz JC, Laborde JC, Rivera FJ, Encarnacion CE, Lutz JD, Moss JG. Stenting of the iliac arteries with the Palmaz stent: experience from a multicenter trial. Cardiovase Intervent Radiol 1992; 15:291-7. 87. Becker GJ, Palmaz JC, Rees CR, et al. Angioplasty-induced dissections in human iliac arteries: management with Palmaz balloon-expandable intraluminal stents. Radiology 1990;176:31-8. 88. Laborde JC, Palmaz JC, Rivera FJ, Encarnacion CE, Picot MC, Dougherty SP. Influence of anatomic distribution of atherosclerosis on the outcome of revascularization with iliac stent placement. J Vasc Interv Radiol 1995;6:513-21. 89. Henry M, Amor M, Ethevenot G, et al. Palmaz stent placement in iliac and femoropopliteal arteries: primary and secondary patency in 310 patients with 2-4 year follow-up. Radiology 1995;197:167-74. 90. Cikrit DF, Gustafson PA, Dalsing MC, et al. Long-term follow-up of the Palmaz stent for iliac occlusive disease. Surgery 1995; 118:608-14. 91. Murphy TP, Khwaja AA, Webb MS. Aortoiliac stent placement in patients treated for intermittent claudication. J Vase Interv Radiol 1998;9:421-8. 92. Martin EC, Katzen BT, Benenati JF, et al. Multicenter trial of the Wallstent in the iliac and femoral arteries. J Vase Interv Radiol 1995;6:843-9. 93. VorwerkD, Gunther RW, Schurmann K, Wendt G. Aortic and iliac stenoses: followup results of stem placement after insufficient balloon angioplasty in 118 cases. Radiology 1996;198:45-8. 94. Long AL, Page PE, Raynaud AC, et al. Percutaneous itiac agery stent: angiographic long-term follow-up. Radiology 1991;180:771-8. 95. Murphy TP, Webb MS, Lambiase RE, et al. Percutaneous revascularization of complex iliac artery stenoses and occlusions with use of Wallstents: three-year experience. J Vase Interv Radiol 1996;7:21-7. 96. Nawaz S, Cleveland T, Gaines P, Beard J, Chan P. Aortoiliac stenting, determinants of clinical outcome. Eur J Vase Endovasc Surg 1999;17:351-9. 97. Ballard JL, Sparks SR, Taylor FC, et al. Complications of iliac artery stent deployment. J Vase Surg 1996;24:545-55. 98. Strecker EP, Boos IBL, Hagen B. Flexible tantalum stents for the treatment of iliac artery lesions: long-term patency, complications, and risk factors. Radiology 1996; 199:641-7. 99. Long AL, Sapoval MR, Beyssen BM, et al. Strecker stent implantation in iliac arteries: patency and predictive factors for long-term success. Radiology 1995;194:739-44.

1038

Curr Probl Surg, December 1999

100. Bosch JL, Hunink MGM. Meta-analysis of the results of percutaneous transluminal angioplasty and stent placement for aortoiliae occlusive disease. Radiology 1997;204:87-96. 101. Damaraju S, Cuasay L, Le D, Strickman N, Krajcer Z. Predictors of primary pateney failure in Wallstent self-expanding endovascular prostheses for iliofemoral occlusive disease. Tex Heart Inst J 1997;24:173-8. 102. Murphy KD, Encarnacion CE, LeVA, Palmaz JC. Iliac artery stent placement with the Palmaz stent: follow-up study. J Vase Interv Radiol 1995;6:321-9. 103. Strecker EP, Hagen B, Liermann D, Schneider B, Wolf HRD, Wambsganss J. Iliae and femoropopliteal vascular occlusive disease treated with flexible tantalum stents. Cardiovasc Intervent Radiol 1993; 16:158-64. 104. Johnston KW. Iliac arteries: reanalysis of results of balloon angioplasty. Radiology 1993;186:207-12. 105. Ring EJ, Freiman DB, McLean GK, Schwarz W. Percutaneous recanalization of common iliac artery occlusions: an unacceptable complication rate? AJR Am J Roentgenol 1982;139:5870. 106. Rees CR, Palmaz JC, Garcia O, et al. Angioplasty and stenting of completely occluded iliac arteries. Radiology 1989;172:953-9. 107. Yedlicka JW, Ferral H, Bjarnason H, Hunter DW, Castaneda-Zuniga WR, Amplatz K. Chronic iliac artery occlusions: primary reeanalization with endovascular stents. J Vase Interv Radiol 1994;5:843-7. 108. Blum U, Gabelmann A, Redecker M, et al. Percutaneous recanalization of iliae artery occlusions: results of a prospective study. Radiology 1993;189:536-40. 109. Levi N. Percutaneous recanalization of itiac artery occlusions with the Strecker stent. J Cardiovasc Surg 1998;39:287-9. 1 t0. Beequemin JP, Cavillon A, Haiduc E Surgical transluminal femoropopliteal angioplasty: multivariate analysis outcome. J Vasc Surg 1994;19:495-502. 111. Capek P, McLean GK, Berkowitz HD. Femoropopliteal angioplasty: factors influencing long-term success. Circulation 1991 ;83:I-70-80. 112. Hunink MGM, Donaldson MC, Meyerovitz MF, et al. Risks and benefits of femoropopliteal percutaneous balloon angioplasty. J Vase Surg 1993;17:183-94. 113. Jorgensen B, Tonnesen KH, Holstein P. Late hemodynamic failure following percutaneous transluminal angioplasty for long and multifocal femoropopliteal stenoses. Cardiovasc Intervent Radiol 1991; 14:290-2. 114. Krepel VM, van Andel GJ, van Erp WFM, Breslau PJ. Percutaneous angioplasty of the femoropopliteal artery: initial and long-term results. Radiology 1985;156:325-8. 115. Matsi PJ, Manninen HI, Vanninen RL, et al. Femoropopliteal angioplasty in patients with claudication. Radiology 1994;191:727-33. 116. Murray RR, Hewes RC, White RI, et al. Long-segment femoropopliteal stenoses: Is angioplasty a boon or bust? Radiology 1987; 162:473-6. 117. Gunther RW, Vorwerk D, Bohndorf K, et al. Iliac and femoral artery stenoses and occlusions: treatment with intravascular stents. Radiology 1989;172:725-30. 118. Rousseau HP, Raillat CR, Joffre FG, et al. Treatment of femoropopliteal stenoses by means of self-expandable endoprostheses: midterm results. Radiology 1989; 172:961-4. 119. Zollikofer CL, Antonucci E Pfyffer M, et al. Arterial stent placement with use of the Wallstent: midterm results of clinical experience. Radiology 1991; 179:449-56.

Curr Probl Surg, December 1999

1039

120. Do-dai-Do, Triller J, Walpoth BT, et al. A comparison study of self-expandable stents vs balloon angioplasty alone in femoropopliteal artery occlusions. Cardiovasc Intervent Radio! 1992;t5:306-12. 121. Sapoval MR, Long AL, Raynaud AC, et al. Femoropopliteal stent placement: longterm results. Radiology 1992; 184:833-9. 122. Bergeron P, Pinot JJ, Poyen V, et al. Long-term results with palmaz stent in the superficial femoral artery. J Endovasc Surg 1995 ;2:161-7. 123. Bray AE, Liu WG, Lewis WA, et al. Strecker stents in the femoropopliteal arteries: value of duplex ultrasonography in restenosis assessment. J Endovasc Surg 1995; 2:150-60. 124. Henry M, Amor M, Ethevenot G, et al. Palmaz stent placement in iliac and femoropopliteal arteries: primary and secondary patency in 310 patients with 2-4 year follow-up. Radiology 1995;197:167-74. 125. White GH, Liew SCC, Waugh RC, et al. Early outcome and intermediate follow-up of vascular stents in the femoral and popliteal arteries without long-term anticoagulation. J Vase Surg 1995;21:270-81. 126. Chatelard P, Guibourt C. Long-term results with a Palmaz stent in the femoropopliteal arteries. J Cardiovasc Surg 1996;37:67-72. 127. Gray BH, Sullivan TM, Childs MB, et al. High incidence of restenosis/reocclusion of stents in the percutaneous treatment of long-segment superficial femoral artery disease after suboptimal angioplasty. J Vasc Surg 1997;25:74-83. 128. Strecker EPK, Boos IBL, Gottmann D. Femoropopliteal artery stent placement: evaluation of long-term success. Radiology 1997;205:375-83. 129. Vroegindeweij D, Vos LD, Tielbeek AV, et al. Balloon angioplasty combined with primary stenting versus balloon angioplasty alone in femoropopliteal obstructions: a comparative randomized study. Cardiovasc Intervent Radiol 1997;20:420-5. 130. Biamino G, Scheinert D, Vogt A, et al. Carotid angioplasty: technique and early results [abstract]. J Endovasc Surg 1998;5:I-4. 131. Savader SJ, Venbrux AC, Mitchell SE, et al. Percutaneous transluminal atherectomy of the superficial femoral and popliteal arteries: long-term results in 48 patients. Cardiovasc Intervent Radiol 1994;17:312-8. 132. Gray BH, Olin JW. Limitations ofpercutaneous transluminal angioplasty with stenting for femoropopliteal arterial occlusive disease. Semin Vasc Surg 1997;10:8-16. 133. Gerritsen GP, Gussenhoven EJ, The SHK, et al. Intmvascular.ultrasonography before and after intervention: in vivo comparison with angiography. J Vasc Surg 1993; 18:31-40. 134. Vogt KC, Just S, Rasmussen JG, Schroeder TV. Prediction of outcome after femoropopliteal balloon angioplasty by intravascular ultrasound. Eur J Vasc Endovasc Surg 1997;13:563-8. 135. Rutherford RB, Flanigan DP, Gupta SK, et al. Suggested standards for reports dealing with lower extremity ischemia. J Vasc Surg 1986;4:80-94. 136. Matsi PJ, Manninen HI. Impact of different patency criteria on long-term results of femoropopliteal angioplasty: analysis of 106 patients with claudication. J Vasc Interv Radiol 1995;6:159-63. 137. Taylor LM, Edwards JM, Porter JM. Present status of reversed vein bypass grafting: five-year results of a modem series. J Vasc Surg 1990;11:193-206. 138. Donaldson MC, Mannick JA, Whittemore AD. Femoral-distal bypass with in situ greater saphenous vein: long-term results using the Mills valvulotome. Ann Surg 1991;213:457-66. 1040

Curr Probl Surg, December 1999

139. Schwarten DE, Cutliff WB. Arterial occlusive disease below the knee: treatment with percutaneous transluminal angioplasty performed with low-profile catheters and steerable guide wires. Radiology 1988;169:71-4. 140. Brown KT, Shoenberg NY, Moore ED, Saddekni S. Percutaneous lxansluminal angioplasty of infrapopliteaI vessels: preliminary results and technical considerations. Radiology 1988;169:75-8. 141. Horvath W, Oertl M, Haidinger D. Percutaneous transluminal angioplasty of crural arteries. Radiology 1990;177:565-9. 142. Dorros G, Lewin RF, Jamnadas P, Mathiak LM. Below-the-knee angioplasty: tibioperoneal vessels, the acute outcome. Cathet Cardiovasc Diagn 1990;19:170-8. 143. Schwarten DE. Clinical and anatomical considerations for nonoperative therapy in tibial disease and the results of angioplasty. Circulation 1991;83(suppl):I86-90. 144. Bull PG, Mendel H, Hold M, Schlegl A, Denck H. Distal popliteal and tibioperoneal transluminal angioplasty: long-term follow-up. J Vase Interv Radiol 1992; 3:45-53. 145. Saab MH, Smith DC, Aka PK, Brownlee RW, Killeen JD. Percutaneous transluminal angioplasty of tibial arteries for limb salvage. Cardiovasc Intervent Radiol 1992;15:211-6. 146. Brown KT, Moore ED, Getrajdman GI, Saddekni S. Infrapopliteal angioplasty: long-term follow-up. J Vasc Interv Radiol 1993;4:139-44. 147. Dorros G, Hall P, Prince C. Successful limb salvage after recanalization of an occluded infrapopliteal artery utilizing a balloon expandable (Palmaz-Schatz) stent. Cathet Cardiovasc Diagn 1993;28:83-8. 148. Sivananthan UM, Browne TF, Thorley PJ, Rees MR. Percutaneous transluminal angioplasty of the tibial arteries. Br J Surg 1994;81:1282-5, 149. Bolia A, Sayers RD, Thompson MM, Bell PRF. Subintimal and intraluminal recanalization of occluded crural arteries by percutaneous balloon angioplasty. Eur J Vasc Surg 1994;8:214-9. 150. Varty K, Bolia A, Naylor AR, Bell PRF, London NJM. Infrapopliteal percutaneous transluminal angioplasty: a safe and successful procedure. Eur J Vase Endovasc Surg 1995;9:341-5. 151. Treiman GS, Treiman RL, Ichikawa L, Van Allan R. Should percutaneous transluminal angioplasty be recommended for treatment of infrageniculate popliteal artery or tibioperoneal trunk stenosis? J Vasc Surg 1995;22.~457-65. 152. Dorros G, Jaff MR, Murphy KJ, Mathiak L. The acute outcome of tibioperoneal vessel angioplasty in 417 cases with claudication and critical limb ischemia. Cathet Cardiovase Diagn 1998;45:251-6. 153. Thompson RW, Anderson CB. Aortoiliac occlusive disease. In: Callow AD, Ernst CB, editors. Vascular surgery. Stamford (CT): Appleton and Lange; 1995. 154. Grollman JH, Del Vicario M, Mittal AK. Percutaneous transluminal abdominal aortic angioplasty. AJR 1980; 134:1053-4. 155. Vorwerk D, Gunther RW, Bohndorf K, Keulers P. Stent placement for failed angioplasty of aortic stenoses: report of two cases. Cardiovasc Intervent Radiol 1991; 14:316-9. 156. Lim MCL, Choo M, Tan HC. Stenting of stenosis of the abdominal aorta. Singapore Med J 1995;36:562-5. 157. Kang E. Balloon expandable intravascular stent in infrarenal aortic stenosis. Nebraska Medical Journal 1995;80:329-31. Curr Probl Surg, December 1999

1041

158. Long A, Gaux JC, Raynaud AC, et al. Infrarenal aortic stents: initial clinical experience and angiographie follow-up. Cardiovasc Intervent Radiol 1993;16:203-8. 159. Diethrich EB, Osvaldo S, Gustafson G, Heuser RR. Preliminary observations on the use of the Palmaz stent in the distal portion of the abdominal aorta. Am Heart J 1993;125:490-501. 160. E1 Ashmaoui A, Do DD, Triller J, et al. Angioplasty of the terminal aorta: followup of 20 patients treated by PTA or PTA with stents. Eur J Radiol 1991;13:113-7. 161. Sheer'an SR, Hallisey. MJ, Ferguson D. Percutaneous transluminal stent placement in the abdominal aorta. J Vase Interv Radiol 1997;8:55-60. 162. Westcott MA, Bonn J. Comparison of conventional angioplasty with the Palmaz stent in the treatment of abdominal aortic stenoses from the STAR registry. J Vase Interv Radiol 1998;9:225-3 I. 163. Sniderman KW. Noncoronary vascular stenting. Prog Cardiovasc Dis 1996;39:141-64. 164. Suarez de Lezo J, Pan M, Romero M. Tailored stent treatment for severe supravalvular aortic stenosis. Am Heart J 1995;129:1002-8. 165. Redington AN, Hayes AM, Ho SY. Transcatheter stent implantation to treat aortic coarctation in infancy. Br Heart J 1993;69:80-2. 166. Gambhir DS, Trehan V, Rastogi P. Self--expanding Wallstent deployment in an adult with coarctation of the aorta. Indian Heart J 1996;48:409-11. 167. Sawada S, Tanigawa N, Kobayashi M, et al. Treatment of Takayasu's aortitis with self-expanding metallic stents (Giantureo stents) in two patients. Cardiovasc Intervent Radiol 1994;17:102-5. 168. Slonim SM, Nyman U, Semba CP, et al. Aortic dissection: percutaneous management of ischemic complications with endovascular stents and balloon fenestration. J Vase Surg 1996;23:241-53. 169. Slonim SM, Nyman U, Semba CP, et al. True lumen obliteration in complicated aortic dissection: endovascular treatment. Radiology 1996;201:161-6. 170. Peterson AH, Williams DM, Rodriguez JL, Francis IR. Percutaneous treatment of a traumatic aortic dissection by balloon fenestration and stent placement. AIR Am J Roentgenol 1995; 164:1274-6. 171. Marty-Ane C-H, Alric P, Prudhomme M, et al. Intravascular stenting of traumatic abdominal aortic dissection. J Vase Surg 1993;23:156-61. 172. Ballard JL, Taylor FC, Sparks SR, Killeen JD. Stenting without thrombolysis for aortoiliac occlusive disease: experience in 14 high-risk patients. Ann Vase Surg 1995;9:453-8. 173. Diethrich EB. Endovascular treatment of abdominal aortic occlusive disease: the impact of stents and intravascular ultrasound imaging. Eur J Vase Surg 1993;7:228-36. 174. Berger T, Sorensen R, Konrad J. Aortic rupture: a complication of transluminal angioplasty. AIR Am J Roentgenol 1986;146:373-4. 175. Diethrich EB. Endovascular techniques for abdominal aortic occlusions, hat Angiol 1993;12:270-80. • 176. Benjamin ME, Dean RH. Techniques in renal artery reconstruction. Ann Vase Surg 1996;10:306-14. 177. Stanley JC. The evolution of surgery for renovaseular occlusive disease. Cardiovasc Surg 1994;2:195-202. 178. Stanley JC, Ernst CG. Renal artery occlusive disease and renovascular hypertension. In: Callow A, Ernst C, editors. Vascular surgery: theory~and practice. Stamford (CT): Appleton and Lange; 1995. p 653-76. 1042

Curr Probl Surg, December 1999

179. Dean RH. Surgical management of renovascular disorders. In: Rutherford R, editor. Vascular surgery. 4th ed. Philadelphia: WB Saunders; 1995. p 1371-455. 180. Dean RH. Operative management of mnovascular hypertension. In: Bergen JJ, Yao JST, editors. Surgery of the aorta and its body branches. New York: Grune and Stratton; 1979. p 377-90. 181. Dean RH, Hansen KL Renovascular hypertension. In: Moore W, editor. Vascular surgery: a comprehensive review. 5th ed. Philadelphia: WB Satmders; 1998. p 521-42. 182. Gruntzig A, Kuhlmann K, Vereter W. Treatment of renovascular hypertension with percutaneous transluminal dilatation of renal artery Stenosis. Lancet 1978;1:501-2. 183. Schwarten DE. Translurninal angioplasty of renal artery stenosis: 70 experiences. Am J Radiol 1980;35:969-74. 184. Tegtmeyer CJ, Elson J, Glass TA, et al. Percutaneous transluminal angioplasty: the treatment of choice of renovascular hypertension due to fibromuscular dysplasia. Radiology 1982;143:632-7. 185. Tegtmeyer CJ, Selby JB, Hartwell GD, Ayers C, Tegtmeyer V. Results and complications of angioplasty in fibromuscular disease. Circulation 1991;83(suppl): 155-61. 186. Sos TA, Picketing TG, Sniderman KW, et al. Percutaneous transluminal renal angioplasty in renovascular hypertension due to atherom or fibromuscular dysplasia. N Engl J Med 1983;309:274-9. 187. MiUan VG, McCauley J, Koppleman RI, et al. Percutaneous transluminal renal angioplasty in nonatherosclerotic renovascular hypertension: long-term results. Hypertension 1985;7:668-74. 188. Becker GJ, Katzen BT, Dake MD. Non-coronary angioplasty. Radiology 1989;170:921-40. 189. Pouin PF, Dame B, Citatellier G, et al. Restenosis after a first pereutaneous transluminal renal angioplasty. Hypertension 1993;21:89-96. 190. Tegtmeyer CJ, Kellum CD, Ayers C. Percutaneous transluminal angioplasty of the renal artery. Radiology 1984;153:77-84. 191. Schwarten DE. Percutaneous transluminal angioplasty of the renal arteries: intravenous digital subtraction angiography for follow-up. Radiology 1984;150:369-73. 192. Cicuto KP, McLean GK, Oleaga JA, Freiman DB, Grossman RA, Ring E3. Renal artery stenosis: anatomic classification for percutaneous transluminal angioplasty. AJR Am J Roentgenol 1981; 137:599-601. 193. Baart AL, Wilms G, Amery A, Vermylen J, Suy R. Percutaneous transhminal renal angioplasty: initial results and long-term follow-up in 202 patients. Cardiovasc Intervent Radiol 1990;13:22-8. 194. Klinge J, Mall WP, Puylaert C, Ceyshes G, Beching WB, Feldberg M. Percutaneous transluminal angioplasty: initial and long-term results. Radiology 1989;171:501-6. 195. Kuhn FB, Kutkuhn B, Torsello G, et al. Renal artery stenosis: preliminary results of treatment with Strecker stent. Radiology 1991;180:367-72. 196. Rabkin IH, Natzulishvili ZG, Rabkin DI, et al. Nitinol endoprosthetie reconstruction of renal arteries. Journal of Interventional Radiology 1991;6:87-91. 197. Dyet JF. Endovascular stents in the arterial system: current status. Clin Radiol 1997;52:83-108. 198. Baert AL. Renal artery stent placement. Radiology 1994;191:619-21. 199. Palmaz JC. Intravascular stenting: from basic research to clinical application. Cardiovasc Intervent Radiol 1992;15:279-84. Curr Probl Surg, December 1999

1043

200. Rees CR, Palmaz JC, Becher GJ, et al. Pahnaz stent in atherosclerotic stenoses involving the ostia of the renal arteries: preliminary report of a mul'dcenter study. Radiology 1991;181:507-14,. 201. Dorros G, Prince C, Mathiak L. Stenting of a renal artery stenosis achieves better relief of the obstructive lesion than balloon angioplasty. Cathet Cardiovasc Diagn 1993;29:191-8. 202. Dorros G, Ja.ff M, Jain A, Dufeh C, Mathiak L. Follow-up of primary PalmazSchotz stent placement for atherosclerotic renal artery stenosis. Am J Cardiol 1995;75:1051-5. 203. Hennequin LM, Joffre FG, Rousseau HP, et al. Renal artery stent placement: longterm results with the Wallstent endoprosthesis. Radiology 1994;191:713-9. 204. Raynand AC, Beyssen BM, Turmel-Rodrigues LE, et al. Renal artery stent placement: immediate and midterm technical and clinical results. J Vase Intervent Radiol 1994;5:849-58. 205. Van de Ven P, Bentler J, Kaatee R, et al. Transluminal vascular stent for ostial atherosclerotic renal artery stenosis. Lancet 1995;346:672-4. 206. MacLeod M, Taylor A, Baxter G, et al. Renal artery stenosis managed by Palmaz stent insertion: technical and clinical outcome. J Hypertens 1995;13:1791-5. 207. Henry M, Amor M, Henry I, et al. Stent placement in the renal artery: three years experience with the Palmaz stent. J Vase lntervent Radiol 1996;7:343-50. 208. Iannone L, Underwood P, Nath A, Tannenbaum M, Gheli M, Clevenger L. Effect of primary balloon expandable renal artery stents on long-term patency, renal function, and blood pressure in hypertensive and renal insufficient patients with renal artery stenosis. Catheter Cardiovasc Diagn 1996;37:243-50. 209. Runback J, Jacobs L Percutaneous renal artery stent placement for hypertension and azotemia: pilot study. Am J Kidney Dis 1996;28:214-9. 210. Blum U, Krumm B, Flugel P, et al. Treatment of ostial renal-artery stenoses with vascular endoprosthesis after unsuccessful balloon angioplasty. N Engl J Med 1997;336:459-65. 211. Boisclair C, Therasse E, Oliva V, et al. Treatment of renal angioplasty failure by percutaneous renal artery stenting with Palmaz stents: rnidterm technical and clinical results. AJR Am J Roentgenol 1997;168:245-51. 212. Hoffman O, Carreres T, Sapoval MR, et al. Ostial renal artery stenosis angioplasty: immediate and mid-term angiographic and clinical results. J Vase Intervent Radiol 1998;9:65-73. 213. Tattle KR, Chouinard RF, Webber JT, et al. Treatment of atherosclerotic ostial renal artery stenosis with the intravascular stent Am J Kidney Dis 1998;32:611-22. 214. Henry M, Amor M, Henry I, et al. Stents in the treatment of renal artery stenosis: long-term follow-up. J Endovasc Surg 1999;6:42-51. 215. Harden PN, MacLeod MJ, Rodger RS, et al. Effect of renal-artery stenting on progression of renovascular renal failure. Lancet 1997;349:1133-6. 216. Van de Ven PJ, Kaatee R, Beutler JJ, et al. Arterial stenting and balloon angioplasty in ostial atherosclerotic renovaseular disease: a randomized trial. Lancet 1999;353:282-6. 217. Fiala LA, Jackson MR, Gillespie DL, O'Donnell SD, Lukens M, Gorman P. Primary stenting of atherosclerotic renal artery ostial stenosis. Ann Vase Surg 1998; 12:128-33. 218. Taylor LM, Porter JM. Treatment of chronic visceral ischemia. In: Rutherford RB, editor. Vascular surgery. 4th ed. Philadelphia: WB Saunders; 1995. p 1301-1 I. 1044

Curr Probl Surg, December 1999

219. Nyman U, Ivancev K, Lindh M, Uher E Endovascu!ar treatment of chronic mesenteric ischemia: report of five cases. Cardiovasc Intervent Radiol 1998;21:305-13. 220. Allen RC, Martin GH, Rees CR, et al. Mesentedc angioplasty in the treatment of chronic mesenteric ischemia. J Vase Surg 1996;24:415-23. 221. Finch IJ. Use of Palmaz stent in ostial celiac artery stenosis. J Vase Interv Radiol 1992;3:633-7. 222. Ozdil E, Padkh KP, Krajcer Z, Angelini P. Stent placement in a patient with Takayasu's arteritis. Cathet Cardiovasc Diagn 1996;38:373-6. 223. Linblad B, Lindh M, Chuter T, Ivancev K. Superior mesentede artery occlusion treated with PTA and stent placement. Eur J Vase Endovasc Surg 1996;11:493-5. 224. Liermann D, Strecker EP. Tantalum stents in the treatment of stenotic and occlusive diseases of abdominal vessels. In: Liermann D, editor. Stents: state of the arts and future developments. Watertown (MA): Polyscience Publications (Boston Scientific); 1995. p 127-34. 225. Maleux G, Wilms G, Stockx L, Vancleemput J, Baert AL. Percutaneous recanalization and stent placement in chronic proximal superior mesenteric artery occlusion. Eur Radiol 1997;7:1228-30. 226. Busquet J. Intravascutar stenting in the superior mesenteric artery for chronic abdominal angina. J Endovasc Surg 1997;4:380-4. 227. Waybill PN, Enea NA. Use of a Palrnaz stent deployed in the superior mesenteric artery for chronic mesenteric ischemia. J Vase Interv Radiol 1997;8:1069-71. 228. Forauer AR, McLean GK. Primary stenting of the superior mesenteric artery for treatment of chronic mesenteric ischemia: a case report. Angiology 1999;50:63-7. 229. Herring M. The subclavian steal syndrome: a review. Am Surg 1997;43:220-8. 230. Bogey W, Demasi R, Tripp M, Vithalani R, Johnsrude I, Powell S. Percutaneous transluminal angioplasty for subclavian artery stenosis. Am Surg 1994;60:103-6. 231. Hennerici M, Klemm C, Rautenberg W. The subclavian steal phenomenon: a common vascular disorder with RAB neurologic deficits. Neurology 1988;38:669-73. 232. Georges N, Ferretti J. Percutaneous transluminal angioplasty of subclavian artery occlusion for treatment of coronary-subclavian steal. Am J Radiol 1993;161:399-400. 233. Perrault L, Carder M, Judon G, Lemarbre L, Hebert Y, Pelletier L. Transluminal angioplasty of the subclavian artery in patients with internal mammary grafts. Ann Thorac Surg 1993;56:927-30. 234. Sueoha B. Percutaneous transhiminal stent placement to treat subclavian steal syndrome. J Vase Intervent Radiol 1996;7:351-6. 235. Gerely Z, Andrus C, May A, et al. Surgical treatment of occlusive subclavian artery disease. Circulation 1981;64 (Suppl. 11): 228-230. 236. Beebe H, Sterh C, Johnson M, et al. Choices of operation for subclavian-vertebral arterial disease. Am J Surg 1980;139:616-23. 237. Abarahma A, Robinson P, Khon M. Porchiocephalic revascularization: a comparison between carotid-subclavian artery bypass and axilloaxiUary artery bypass. Surgery 1992;112:84-91. 238. Sandman W. Transposition procedures for proximal subclavian artery atherosclerosis causing cerebral steal syndrome. In: Ernst C, Stanley J, editors. Current therapy in vascular surgery. 9th ed. Philadelphia: Decher; 1991. p 122-5. 239. Farina C, Mingoli A, Schultz R, et al. Percutaneous transluminal angioplasty versus surgery for subclavian artery occlusive disease. Am J Surg 1989;158:511-4. 240. Dorros G, Lawin R, Jamnadas P, Mathiak L. Peripheral transluminal angioplasty of Curr Probl Surg, December 1999

1045

241.

242.

243.

244.

245. 246.

247.

248.

249.

250.

251. 252.

253.

254. 255. 256.

257.

1046

the subclavian and innominate arteries utilizing the brachial approach: acute outcome and follow-up. Cathet Cardiovasc Diagn 1990;19:7I-6. Duber C, Klaus J, Kopp H, Schmiedt W. Percutaneous transluminal angioplasty for occlusion of the subclavian artery: short and long-term results. Cardiovasc'Intervent Radio1 1992;15:205-10. Kumar K, Dorros G, Bates M, Palmer L, Mathiah L, Dugeh C. Primary stent deployment in occlusive subclavian artery disease. Cathet Cardiovasc Diagn 1995; 34:281-5. Sullivan TM, Gray BH, Bacharach JM, et al. Angioplasty and primary stenting of the subclavian, innominate, and common carotid arteries in 83 patients. J Vase Surg 1998;28:1059-65. Roddguez-Lopez JA, Werner A, Martinez R, Torruella I_J, Ray LI, Diethrich DB. Stenting for atherosclerotic occlusive disease of the subclavian artery. Ann Vasc Surg 1999;13:254-60. Henry M, Amor M, Henry I, Ethevenot G, Tzvetanov K, Chaff Z. Percutaneous transluminal angioplasty of the subclavian arteries. J Endovasc Surg 1999;6:33-41. Jaeger H, Mathias K, Kemphes U. Bilateral subclavian steal syndrome: treatment with percutaneous transluminal angioplasty and stent placement. Cardiovasc Intervent Radiol 1994;17:328-32. Mufti S, Young K, Schulthesis T. Restenosis following subclavian artery angioplasty for treatment of coronary subclavian steel syndrome: definitive treatment with Palmaz stent placement. Cathet Cardiovasc Diagn 1994;33:172-4. Kugelmess A, Kim D, Kuntz R, Carrozza J, Bulm D. Endoluminal stenting of a subclavian artery stenosis to treat ischemic in distribution of a patent left internal mammary graft. Cathet Cardiovasc Diagn 1994;33:175-7. Lyon R, Shonnerd K, McCarter D, Hammond S, Ferguson D, Rholl IC Supra-aortic arterial stenoses: management with Palmaz balloon-expandable intraluminal stents. J Vasc Intervent Radiol 1996;7:825-35. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with highgrade carotid stenosis. N Engl J Meal 1991;325:445-53. Barnett HIM, TaylorW, Eliasziw M, et al. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. N Engl J Med 1998;339:1415-25. European Carotid Surgery Trialists' Collaborative Group. MRC European carotid surgery trial: interim results for symptomatic patients with severe (70-99%) or mild (0-29%) carotid stenosis. Lancet 1991;337:.1235-43. European Carotid Surgery Trialists' Collaborative Group. Randomized trial of endarterectomy for recently symptomatic carotid stenosis: final results of the MRC European carotid surgery trial (ECST). Lancet 1998;351:1379-87. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA 1995;273:1421-8. Becker GJ. Current and future treatment of carotid bifurcation atherosclerofic disease: a perspective. J Vasc Intervent Radiol 1997;8:3-8. Gil-Peralta A, Mayol A, Gonzales Marcos JR, et al. Percutaneous transluminal angioplasty of the symptomatic atherosclerotic carotid arteries: results, complications, and follow-up. Stroke 1996;27:2271-3. Roubin GS, Yadav S, Iyer SS, Vitek J. Carotid stent-supported angioplasty: a neurovascular intervention to prevent stroke. Am J Cardiol 1996;78(suppl):8-12. Curr Probl Surg, December 1999

258. Yadav JS, Roubin GS, King P, Iyer S, Vitek J. Angioplasty and stenting for restenosis after carotid endarterectomy: initial experience. Stroke 1996;27:2075-9. 259. Yadav JS, Roubin GS, Iyer S, et al. Elective stenting of the extracranial carotid arteries. Circulation 1997;95:376-81. 260. Jordan WD, Schroeder PT, Fisher WS m, McDowell HA. A comparison of angioplasty with stenting versus endarterectomy for the treatment of carotid artery stenosis. Ann Vasc Surg 1997;11:2-8. 261. Jordan WD, Roye GD, Fisher WS m, Redden D, McDowell HA. A cost comparison of balloon angioplasty and stenting versus endarterectomy for the treatment of carotid artery stenosis. J Vasc Surg 1998;27:16-24. 262. Jordan WD, Voellinger DC, Fisher WS, Redden D, McDowell HA. A comparison of carotid angioplasty with stenting versus endarterectomy with regional anesthesia. J Vase Surg 1998;28:397-403. 263. Mathur AM, Roubin GS, Iyer SS, et al. Predictors of stroke complicating carotid artery stenting. Circulation 1998;97:1239-45. 264. Naylor AR, Bolia A, Abbott RJ, et al. Randomized study of carotid angioplasty and stenting versus carotid endartereetomy: a stopped trial. J Vase Stag 1998;28:326-34. 265. Diethrich EB, Ndiaye M, Reid DB. Stenting in the carotid artery: initial experience in 110 patients. J Endovasc Surg 1996;3:42-62. 266. Wholey MH, Wholey MH, Jarmolowski CR, Eles G, Levy D, Buecthel J. Endovascular stents for carotid artery occlusive disease. J Endovasc Surg 1997; 4:326-38. 267. Criado F J, Wellons E, Clark NS. Evolving indications for and early results of carotid artery stenting. Am J Surg 1997;174:111-4. 268. Henry M, Amor M, Masson I, et al. Angioplasty and stenting of the extracranial carotid arteries. J Endovasc Surg 1998;5:292-304. 269. Theron J, Payelle G, Coskun O, et al. Carotid artery stenoses: treatment with protected balloon angioplasty and stent placement. Radiology 1996;201:627-36. 270. Hobson RW, Goldstein JE, Jamil Z, et al. Carotid restenosis: operative and endovascular management. J Vase Surg 1999;29:228-38. 271. Crawley F, Clifton A, Buckenham T, Loosemore T, Taylor RS, Brown MM. Comparison of hemodynamic cerebral isehemia and microembolic signals detected during carotid endarterectomy and carotid angioplasty. Stroke 1997;28:2460-4. 272. Markus HS, Clifton A, Buckenham T, Brown MM. Carotid angioplasty: detection of embolie signals during and after the procedure. Stroke 1994;25:2403-6. 273. Bergeron P, Chambran P, Bianca S, et al. Endovaseular treatment of carotid arteries: failures and limitations. J Mal Vase 1996;21(suppl): 123-31. 274. McCleary A J, Nelson M, Dearden NM, Calvey TA, Gough MJ. Cerebral haemodynamics and embolization during carotid angioplasty in high-risk patients. Br J Surg 1998;85:771-4. 275. Hobson RW II, Brott T, Ferguson R, et al. CREST: carotid revaseularization endarterectomy versus stent trial. Cardiovascular Surgery 1997;5:457-8. 276. Perez J, Presant C, van Amburg A. Management of superior vena cava syndrome. Semin Oncol 1978;5:123-34. 277. Parish J, Marschke R, Dines D, Lee R. Etiologic considerations in superior vena cava syndrome. Mayo Olin Proe 1981;56:407-13. 278. Chen J, Bongard F, Klein S. A contemporary perspective on superior vena cava syndrome. Am J Surg 1990;160:207-11. Curr Probl Surg, December 1999

1047

279. Little A, Golomb H, Ferguson M, et al. Malignant superior vena cava obstruction reconsidered: the role of diagnostic surgical intervention. Ann Thorac Surg 1985; 40:285-8. 280. Armstrong B, Perez C, Simpson J, et al. Role of irradiation in the management of superior vena cava syndrome. Int J Radiat Oncol Biol Phys 1987; 13:531-9. 281. Spiro S, Shah S, Harper P, et al. Treatment of obstruction of the superior vena cava by combination chemotherapy with and without irradiation in small-cell carcinoma of the bronchus. Thorax 1983;38:501-5. 282. Jahangiri M, Taggart D, Goldstraw P. Role of mediastinoscopy in superior vena cava obstruction. Cancer 1993;71:3006-8. 283. Braunwald E, Isselbacher K, Petersdorf R. Harrison's principles of internal medicine. Vol 2. llth ed. Tokyo: Blakiston; 1988. p 1128. 284. Charnsangavej C, Carrasco C, Wallace S, et al. Stenosis of the vena cava: preliminary assessment of treatment with expandable metallic stents. Radiology 1986;161:295-8. 285. Rosch J, Bedell J, Putnam J, et al. Gianturco expandable wire stents in the treatment of superior vena cava syndrome recurring after maximum-tolerance radiation. Cancer 1987;60:1243-6. 286. Putnam J, Uchida B, Antonovic R, Rosch J. Superior vena cava syndrome associated with massive thrombosis: treatment with expandable wire stents. Radiology 1988; 167:727-8. 287. Furni S, Sawada S, Irie T, et al. Hepatic inferior vena cava obstruction: treatment of two types with Gianturco expandable metallic stents. Radiology 1990;176:665-70. 288. Solomon N, Wholey M, Jarmolowski C. Intravascular stents in the management of superior vena cava syndrome. Cathet Cardiovasc Diagn 1991;23:245-52. 289. Chatelain P, Meier B, Friedli B. Stenting of superior vena cava and inferior vena cava for symptomatic narrowing after repeated atrial surgery for D-transposition of the great vessels. Br Heart J 1991;66:466-8. 290. Rosch J, Uchida B, Hall L, et al. Gianturco-Rosch expandable Z-stents in the treatment of superior vena cava syndrome. Cardiovasc Intervent Radiol 1992; 15:319-27. 291. Irving J, Dondelinger R, Reidy J, et al. Gianturco self-expanding stents: clinical experience in the vena cava and large veins. Cardiovasc Intervent Radiol 1992; 15:328-33. 292. Oudkerk M, Heystraten F, Stoter G. Stenting in malignant vena caval obstruction. Cancer 1993;71:142-6. 293. Edwards R, Cassidy J, Taylor A. Case report: superior vena cava obstruction complicated by central venous thrombosis-treatment with thrombolysis and GianturcoZ stents. Clin Radiol 1992;45:278-80. 294. Kishi K, Sonomura T, Mitsuzane K, et al. Self-expandable metallic stent therapy for superior vena cava syndrome: clinical observations. Radiology 1993;189: 531-5. 295. Eng J, Sabanathan S. Management of superior vena cava obstruction with selfexpanding intraluminal stents. Scand J Thor Cardiovasc Surg 1993;27:53-5. 296. Edwards R, Jackson J. Case report: superior vena caval obstruction treated by thrombolysis, mechanical thrombectomy and metallic stents. Clin Radiol 1993;48:215-7. 297. Dyet J, Nicholson A, Cook A. The use of the Wallstent endovascular prosthesis in the treatment of malignant obstruction of the superior vena cava. Clin Radiol 1993;48:381-5. 1048

Curr Probl Surg, December 1999

298. Watkinson A, Hansell D. Expandable Wallstent for the treatment of obstruction of the superior vena cava. Thorax 1993;48:915-20. 299. Berger H, Hilbertz T, Zuhlke K, et al. Balloon dilatation and stent placement of suprahepatic caval anastomotic stenosis following liver transplantation. Cardiovasc Intervent Radiol 1993;16:384-7. 300. Rosenblum J, Leef J, Messersmith R, et al. Intravascular stents in the management of acute superior vena cava obstruction of benign etiology. Journal of Parenteral and Enteral Nutrition 1993;18:362-6. 301. Dodds G, Harrison J, O'Laughlin M, et al. Relief of superior vena cava syndrome due to fibrosing mediastinitis using the Palmaz stent. Chest 1994;106:315-8. 302. Lindsay H, Chermells P, Perrins E. Successful treatment by balloon venoplasty and stent insertion of obstruction of the superior vena cava by an endocardial pacemaker lead. Br Heart J 1994;71:363-5. 303. Gaines P, Bell A, Anderson P, et al. Superior vena caval obstruction managed by the Gianturco Z stent. Clin Radiol 1994;49:202-8. 304. Crowe M, Davies C, Gaines P. Percutaneous management of superior vena cava occlusions. Cardiovasc Intervent Radiol 1995;18:367-72. 305. Entwisle A, Watkinson H, Adam A. The use of the Wallstent endovascular prosthesis in the treatment of malignant inferior vena cava obstruction. Clin Radiol 1995; 50:310-3. 306. Stock K, Jacob A, Proske M, et al. Treatment of malignant obstruction of the superior vena cava with the self-expanding Wallstent. Thorax 1995;50:1151-6. 307. Francis C, Starkey I, Errington M, Gillespie I. Venous stenting as treatment for pacemaker-induced superior vena cava syndrome. Am Heart J 1995;129:836-7. 308. Hennequin L, Fade O, Fays J, et al. Superior vena cava stent placement: results with the Wallstent endoprosthesis. Radiology 1995;196:353-61. 309. Fumi S, Sawada S, Kuramoto K, et al. Gianturco stent placement in malignant caval obstruction: analysis of factors for predicting the outcome. Radiology 1995;195:147-52. 310. Wilkinson P, MacMahon J, Johnston L. Stenting and superior vena caval syndrome. Ir J Med Sci 1995;164:128-31. 311. Hemphill D, Sniderman K, Allard J. Management of total parenteral nutrition-related superior vena cava obstruction with expandable metal stents. Journal of Parenteral and Enteral Nutrition 1995;20:222-7. 312. Simo G, Echenagusia A, Camunez F, et al. Stenosis of the inferior vena cava after liver transplantation: treatment with Gianturco expandable metallic stents. Cardiovasc Intervent Radiol 1995; 18:212-6. 313. Ge S, Shiota T, Rice M, et al. Transesophageal ultrasound imaging during stent implantation to relieve superior vena cava-to-intra-atrial baffle obstruction after mustard repair of transposition of the great arteries. Circulation 1995;91:2679-80. 314. Kaul U, Agarwal R, Jain P, et al. Management of idiopathic obstruction of the hepatic and suprahepatic inferior vena cava with a self-expanding metallic stent. Cathet Cardiovasc Diagn 1996;39:2523-7. 315. Rosenthal E, Qureshi S, Tynan M, BucknaU C. Percutaneous pacemaker lead extraction and stent implantation for superior vena cava occlusion due to pacemaker leads. Am J Cardiol 1996;77:670-2. 316. Oudkerk M, Kuijpers T, Schmitz PI, et al. Self-expanding metal stents for palliative treatment of superior vena caval syndrome. Cardiovasc Intervent Radiol 1996; 19:146-51. Curr Probl Surg, December 1999

1049

317. Shah R, Sabanathan S, Lowe R, Mearns A. Stenting in malignant obstruction of superior vena cava. J Thorac Cardiovasc Surg 1996;112:335-40. 318. Xu K, He F, Zhang H, et al'. Budd-Chiari syndrome caused by obstruction of the hepatic inferior vena cava: immediate and 2-year treatment results of transluminal angioplasty and metallic stent placement. Cardiovasc Intervent Radiol 1996; 19:32-6. 319. Althaus S, Perkins J, Soltes G, Glickerman D. Use of a Wallstent in successful treatment of IVC obstruction following liver transplantation. Transplantation 1996;61:669-72. 320. MacLellan-Tobert S, Cetta F, Hagler D. Use of intravascular stents for superior vena caval obstruction after the Mustard operation. Mayo Clin Proc 1996;71:1071-6. 321. Schranz D, Michel-Behnke I, Schimd F, Oelert H. Gradual angioplasty and stent implantation to treat complete superior vena cava occlusion after mustard procedure. Cathet Cardiovasc Diagn 1996;38:87-90. 322. Gomes M, Hufnagel C. Superior vena cava obstruction. Ann Thoracic Surg 1975;20:344-51. 323. Davenport D, Ferree C, Blake D, Raben M. Radiation therapy in the treatment of superior vena cava obstruction. Cancer 1978;42:2600-3. 324. Scherck J, Kerstein M, Stansel H. The current status of vena caval replacement. Surgery 1974;76:209-33. 325. Doty D, Doty J, Jones K. Bypass of superior vena cava. J Thorac Cardiovasc Surg 1990;99:889-96. 326. Sherry C, Diamond N, Meyers T, et al. Successful treatment of superior vena cava syndrome by venous angioplasty. AIR Am J Roentgenol 1986; 147:834-5. 327. Ali N, Ewer N, Balakrishnam P, et al. Balloon angioplasty for superior vena cava obstruction. Ann Intern Med 1987;107:856-7. 328. Capek P, Cope C. Percutaneous treatment of superior vena cava syndrome. A JR Am J Roentgenol 1989; 152:183-4. 329. Walpole H, Lovett K, Chaung V, et al. Superior vena cava syndrome treated by percutaneous balloon angioplasty. Am Heart J 1988;115:1303-4. 330. Martin L, Henderson J, Millikan W, et al. Angioplasty'for long-term treatment of patients with Budd-Chiari syndrome. AIR Am J Roentgenot 1990;154:1007-10. 331. Schultz J, Lindenauer S, Penner J, et al. Determinants of thrombus formation on surfaces. ASAIO Trans 1980;26:279-83. 332. Schatz R, Palmaz J, Tio F, et al. Balloon-expandable intracoronary stents in the adult dog. Circulation 1987;76:450-7. 333. Woods JD, Turenne MN, Strawderman P,L, et al. Vascular access survival among incident hemodialysis patients'in the United States. Am J Kidney Dis 1997;30: 50-7. 334. Brothers TE, Morgan M, Robison JG, et al. Failure of dialysis access: Revise or replace? J Surg Res 1996;60:312-6. 335. Mayers JD, Markell MS, Cohen LS, Hong J, Lundin P, Friedman EA. Vascular access surgery for maintenance hemodialysis: variables in hospital stay. ASAIO J 1992;38:113-5. 336. Anderson RC, DeBord JR. Tertiary vascular access surgery for chronic hemodialysis. Semin Dial 1995;8:88-94. 337. Swedberg SH, Brown BG, Sigley R, et al. Intimal fibromuscular hyperplasia at the venous anastomosis of PTFE grafts in hemodialysis patients. Circulation 1989;80:1726-36. 1050

Curr Probl Surg, December 1999

338. Shoemfeld R, Hermans H, NovickA, et al. Stenting of proximal venous obstruction to maintain hemodialysis access. J Vasc Surg 1994;19:532-9. 339. Brooks JL, Sigley RD, May KJ, Mack RM. Transluminal angioplasty versus surgical repair of stenosis of hemodialysis grafts. Am J Surg 1987;153:530-1. 340. Dupunt O, Feurstein M, Rendl KH, Prenner K. Transluminal angioplasty versus conventional operation in the treatment of haemodialysis fistula stenosis: results from a 5 year study. BrJ Surg 1987;74:1004-5. 341. Puckett J, Lindsay S. Midgraft curettage as a routine adjunct to polytetrafluoroethylene hemodialysis access grafts. Am J Surg 1988;156:139-43. 342. Brotman DN, Pandos S, Faust GR, Doscher W, Cohen JR. Hemodialysis graft salvage. J Am Coll Surg 1994;178:431-4. 343. Hurlbert SN, Mattos MA, Henretta JP, et al. Natural history of polytetrafluoroethylene (PTFE) hemodialysis access grafts after the first thrombotic event. Presented at the Society for Clinical Vascular Surgery's 26th Annual Symposium on Vascular Surgery, March 1998, Coronado, Calif (submitted for publication). 344. Schwab SJ, Raymond JR, Saeed M, Newman GE, Dennis PA, Bollinger RR. Prevention of hemodialysis fistula thrombosis. Early detection of venous stenosis. Kidney Int 1989;36:707-11. 345. Beathaxd GA. Percutaneous transvenous angioplasty in the treatment of vascular access stenosis. Kidney Int 1992;42:1390-7. 346. Kant~rman RY, Vesely TM, Pilgram TK, Guy BW, Windus DW, Picus D. Dialysis access grafts: anatomic location of venous stents and results of angioplasty. Radiology 1995; 195:135-9. 347. Glanz S, Gordon DH, Butt KMH, Hong J, Lipkowitz GS. The role of percutaneous angioplasty in the management of chronic hemodialysis fistulas. Ann Surg 1987; 206:777-81. 348. Turmel-Rodrigues L, Pengloan J, Blanchier D, et al. Insufficient dialysis shunts: improved long-term patency rates with close hemodynamic monitoring, repeated percutaneous balloon angioplasty, and stent placement. Radiology 1993; 187:273-8. 349. Beathard GA. Gianmrco self-expanding stent in the treatment of stenosis in dialysis access grafts. Kidney Int 1993;43:872-7. 350. Quinn SE Schuman ES, Demlow TA, et al. Percutaneous transluminal angioplasty versus endovascular stent placement in the treatment of venous stenoses in patients undergoing hemodialysis: intermediate results. J Vasc Interv Radiol 1995; 6:851-5. 351. Hoffer EK, Sultan S, Herskowitz MM, Daniels ID, Sclafani SJA. Prospective randomized trial of a metallic intravascular stent in hemodialysis graft maintenance. J Vasc Interv Radiol 1997;8:965-73. 352. Quinn SF, Schuman ES, Hall L, et al. Venous stenoses in patients who undergo hemodialysis: treatment with self-expandable endovascular stents. Radiology 1992;183:499~504. 353. Gray RJ, Horton KM, Doltnatch BL, et al. Use of Wallstents for hemodialysis access-related venous stenosis and occlusions untreatable with balloon angioplasty. Radiology 1995;195:479-84. 354. Vorwerk D, Guenther RW, Mann H, et al. Venous stenosis and occlusion in hemodialysis shunts: follow-up results of stent placement in 65 patients. Radiology 1995;195:140-6; 355. Turmel-Rodrigues LA, Blanchard D, Pengloan J, et al. Wallstents and Craggstents Curr Probl Surg, December 1999

1051

356.

357. 358. 359.

360, 361. 362. 363.

364. 365. 366.

367.

368.

369.

370. 371. 372. 373. 374.

1052

in hemodialysis grafts and fistulas: results for selective indications. J Vase Interv Radiol 1997;8:975-82. Kovalik EC, Newman GE, Suhoeki P, Knelson M, Schwab SJ. Correction of central venous stenoses: use of angioplasty and vascular Wallstents. Kidney Int 1994; 45:1 I77-81. Hurlbert SN, Rutherford RB. Primary subelavian-axillary vein thrombosis. Ann Vase Surg 1995;9:217-23. Urschel HC, Razzuk MA. Improved management of the Paget-Schroetter syndrome secondary to thoracic outlet compression. Ann Thorac Surg 1991;52:1217-21. Thompson RW, Schneider PA, Nelkin NA, et al. Circumferential venolysis and paraclavicular thoracic outlet decompression for effort thrombosis of the subclavian vein. J Vase Surg 1992;16:723-32. Maelaeder HI. Evaluation of a new treatment strategy for Paget-Schroetter syndrome: spontaneous thrombosis of the axillary-subclavian vein. J Vasc Surg 1993;17:305-17. Glanz S, Gordon DH, Lipkowitz GS, Butt KMH, Hong J, Sclafani SJA. Axillary and subclavian vein stenosis: pereutaneous angioplasty. Radiology 1988;168:371-3. Malcynski J, O'DonneU TF, Mackey WC, Millan VA. Long-term results of treatment for axillary subclavian vein thrombosis. Can J Surg 1993;36:365-71. Meier GH, Pollak JS, Rosenblatt M, Dickey KW, Gusberg RJ. Initial experience with venous stents in exertional axillary-subclavian vein thrombosis. J Vase Surg 1996;24:974-83. Bjarnason H, Hunter DW, Crain MR, Ferral H, Miltz-Miller SE, Wegryn SA. Collapse of a Palmaz stent in the subclavian vein. Am J Radiol 1993; 160:1123-4. Beygui RE, Oleott C, Dalman RL. Subclavian vein thrombosis: outcome analysis based on etiology and modality of treatment. Ann Vase Surg 1997;11:247-55. Hall LD, Murray JD, Boswell GE. Venous stent placement as an adjunct to the staged, multimodal treatment of Paget-Schroetter syndrome. J Vasc Interv Radiol 1995;6:565-70. Cohen GS, Bratmstein L, Ball DS, Domeracki E Effort thrombosis: effective treatment with vascular stent after unrelieved venous stetlosis following a surgical release procedure. Cardiovasc Intervent Radiol 1996;19:37-9. Nazarian GK, Bjarnason H, Dietz CA, Bemadas CA, Hunter DW. Iliofemoral venous stenoses: effectiveness of treatment with metallic endovascular stents. Radiology 1996;200:193-9. Zollikofer CL, Antonucci F, Stuckmann G, Mattias P, Bruhlmann WF, Salomonowitz EK. Use of the Wallstent in the venous system including hemodialysis-related stenoses. Cardiovasc Intervent Radiol 1992;15:334-41. Cockett FB, Thomas/VII.The iliac compression syndrome. Br J Surg 1965;52:816-21. Berger A, Jaffe JW, York TN. Iliac compression syndrome treated with stent placement. J Vase Surg 1995;21:510-4. Rilinger N, Gorich J, Mickley V, et al. Endovascular stenting in patients with iliac compression syndrome. Invest Radiol 1996;31:729-33. Rigas A, Vamroyarmis A, Tsardakas E. Iiiac compression syndrome. J Cardiovasc Surg 1970;11:389-92. Taheri SA; Williams J, Powell S. Iliocaval compression syndrome. Am J Surg 1987;154:169-72.

Curr Probl Surg, December 1999

375. Elson JD, Becker GJ, Wholey MH, Ehrman KO. Vena caval and central venous stenoses: management with Palmaz balloon-expandable intraluminal stents. J Vasc Interv Radiol 1991;2:215-23. 376. Vorwerk D, Guenther RW, Wendt G, Neuerburg J, Schurmann K. Iliocaval stenosis and iliac venous thrombosis in retroperitoneal fibrosis: percutaneous treatment by use of hydrodynamic thrombectomy and stenting. Cardiovasc Intervent Radiol 1996; 19:40-2. 377. Sawada S, FugiwaraY, Koyama T, et al. Application of expandable metallic stent to the venous system. Acta Radiologica 1992;33:156-9. 378. Semba CP, Dake MD. Iliofemoral deep venous thrombosis: aggressive therapy with catheter-directed thrombolysis. Radiology 1994; 191:487-94.

Curr Probl Surg, December 1999

1053