Surgery of the aortic valve

Current Problems in

Surgery Volume 36

Number 6 June 1999

Surgery of the Aortic Valve Tirone E. David, MD Professor of Surgery and Head Division of Cardiovascular Surgery Toronto General Hospital University of Toronto Toronto, Ontario, Canada

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Current Problems in

Surgery Volume 36

Number 6 June 1999

Surgery of the Aortic Valve Foreword

425

In Brief

426

Biographical Information

430

Introduction

431

Functional Anatomy of the Aortic Valve

431

Pathologic Characteristicsof the Aortic Valve

436

Pathophysiologic Characteristicsof Aortic Stenosis

439

Pathophysiologic Characteristicsof Aortic Insufficiency

439

Diagnosis

442 442 442

Aortic Stenosis Aortic Insufficiency

Natural History Aortic Stenosis Aortic Insufficiency

Indications for Surgery Aortic Stenosis Aortic Insufficiency Aortic Root Aneurysm Prosthetic Valve Dysfunction

443 443 443 443 443 444 444 444

Surgical Options to Treat Aortic Valve Disease

445

Aortic Valve Repair

446 448

Selection of Patients for Aortic Valve Repair

Operative Techniquesfor Aortic Valve Repair Repair of Leaflet Prolapse Curr Probl Surg, June 1999

449 449 423

Repair of Incompetent Biscuspid Aortic Valve Remodeling of the Aortic Root for Dilatation of the Sinotubular Junction Remodeling of the Aortic Root and Correction of Dilated Aortic Annulus Reimplantation of the Aortic Valve Repair of the Aortic Valve in Aortic Dissections Subaortic Membranous Ventricular Septal Defect Rheumatic Aortic Insufficiency

Resultsof A o r t i c

Valve

Repair for Aortic Insufficiency

Aortic Valve Replacement Types of Heart Valves for Aortic Valve Replacement Hemodynamic Performance of Prosthetic Heart Valves

Operative Techniques Aortic Valve Replacement With Mechanical and Stented Bioprostheses Aortic Valve Replacement With Stentless Biologic Valves

Results of Aortic Valve Replacement

452 453 456 457 460 461 461 462 465 465 470 472 472 473 480 480 480 482

Operative Mortality Postoperative Complications Survival After Aortic Valve Replacement

Aortic Valve Endacarditis Surgery for Infective Endocarditis of the Aortic Valve Results of Surgery for Infective Endocarditis of the Aortic Valve

483 485 488

Reaperative Aortic Valve Surgery

489

References

491

424

Curr Probl Surg, June 1999

Foreword In this issue of Current Problems in Surgery Dr Tirone David writes about "Aortic Valve Surgery." He is Chief of Cardiovascular Surgery at the University of Toronto and a recognized authority in the field of heart surgery. He has a particular interest in afflictions of the aortic valve and related structures and has made significant contributions to our understanding of the operative management of patients with related disorders. His monograph is a highly clinical and thorough discourse on the topic and will be an excellent reference for surgical residents, fellows in cardiothoracic surgery, and practicing surgeons.

Samuel A. Wells, Jr, MD Editor-in-Chief

Curr Probl Surg, June 1999

425

In Brief Surgery of the aortic valve continues to evolve. Intraoperative transesophageal Doppler echocardiography and better methods of myocardial preservation have opened opportunities to develop new surgical approaches to treat aortic valve disease and to re-evaluate old ones. The morphologic characteristics and function of the aortic valve are interrelated to the aortic root and are best described as a single functional unit. The aortic root has 4 anatomic components: the aortic annulus, the leaflets, the aortic sinuses, and the sinotubular junction. The diameter of the aortic annulus is 15% to 20% larger than the diameter of the sinotubular junction. The lengths of the free margins of the leaflets are slightly larger than the diameter of the sinotubular junction. The most common cause of aortic stenosis (AS) in North America is degenerative calcification of the aortic valve and the second most common is congenital bicuspid aortic valve. The most common cause of aortic insufficiency (AI) is dilatation of the aortic root. Asymptomatic patients with AS or AI have a good prognosis. Once symptoms develop, however, the prognosis becomes poor. Operation should be considered to treat patients with symptomatic aortic valve disease. Operation should also be offered to patients with asymptomatic AS when the aortic valve area is less than 0.8 cm 2, the mean systolic gradient is greater than 50 mm Hg, or the flow velocity across the valve by echocardiography is more than 4 m/sec. Because of the deleterious effects of AI in the left ventricle, asymptomatic patients should undergo operation before irreversible myocardial changes develop. Patients with aortic root aneurysm should undergo operation when the diameter of the aortic root exceeds 60 mm, and even less in those with Marfan syndrome. Aortic valve repair is feasible in certain patients with AI. The mechanism of AI can often be determined by transesophageal echocardiography. Aortic valve repair is feasible in patients with AI caused by dilatation of the aortic root with normal leaflets, in those with bicuspid aortic valve with prolapse of one leaflet, and in patients with subaortic ventricular septal defect and prolapse of the right coronary leaflet. Prolapse of a single leaflet is corrected by either a triangular resection or plication of the central portion of the leaflet to shorten its free margin. Minor elongation of a leaflet can be corrected with a double layer of a 6-0 Gore-tex expanded polytetrafluoroethylene suture (W. L. Gore, Langstaff, Ariz) passed in and out in its free margin. If the aortic valve is bicuspid, the raphe should 426

Curr Probl Surg, June 1999

be excised and the diameter of the aortic annulus should be reduced by plicating the subcommissural triangles. Patients with AI resulting from dilatation of the aortic root can also have aortic valve repair. It is important to determine the mechanism of AI in these patients. The most common cause is dilatation of the sinotubular junction. The AI can be corrected easily by adjusting the diameter of the sinotubular junction with a tubular Dacron polyester graft. If the aortic sinuses are also dilated, they can be replaced with a properly tailored Dacron graft. In patients with Marfan syndrome the aortic annulus may also be dilated; a reduction annuloplasty is necessary during the remodeling of the aortic root. The results of aortic valve repair have been excellent. The operative mortality is low and recurrent AI is uncommon during the first decade after operation. There are numerous choices of heart valves for aortic valve replacement (AVR). It is difficult to decide which valve is best suited for an individual patient. Mechanical valves are thrombogenic and require lifelong anticoagulation with warfarin sodium. The risk of thrombosis of mechanical valves in the aortic position is approximately 0.2% per year. The risk of thromboembolic events (stroke and transient ischemic attacks) is approximately 2% per year. The risk of major hemorrhage with anticoagulation is also approximately 2% per year. Biologic aortic valves are less thrombogenic than mechanical valves and do not require anticoagulation. Thrombosis of a biologic valve in the aortic position is rare. Thromboembolism is uncommon: the risk is 1% to 2% per year with stented xenografts and less than 1% per year with pulmonary autografl, aortic valve homografts, and stentless xenografts. The major drawback of biologic valves is their limited durability. The pulmonary autograft conceivably could be a permanent aortic valve because it seldom suffers degenerative changes. For this reason it is ideally suited for young patients. Aortic valve homografts and glutaraldehyde-fixed xenograft valves suffer degenerative changes after implantation and will eventually fail. Their durability is highly dependent on the patient's age. They have similar durability in elderly patients, but the homograft may be more durable than porcine valves in the middle-aged patient. Stented xenograft and mechanical valves are obstructive, and mean systolic gradients of 15 to 25 mm Hg are common postoperatively. Small valves may leave unacceptably high transvalvular gradients that prevent complete regression of left ventricular hypertrophy after AVR. A patch enlargement of the aortic annulus is sometimes performed to implant a larger prosthetic valve to avoid high transvalvular gradients, but this procedure may increase the operative mortality rate. For this reason many surgeons have been reluctant to perform this procedure in elderly patients and argue that small prosCurt Probl Surg, June 5.999

427

thetic valves have no adverse effect on the outcome of the operation. This may be true for elderly patients, but it is not the case for young ones. It may take more than a decade for the deleterious effects of left ventricular hypertrophy to become apparent. Stentless biologic valves are minimally obstructive to flow and the mean transvalvular gradients are consistently less than 10 iron Hg. They are ideal for the patient with a small aortic annulus. Aortic valve replacement with stented bioprostheses and mechanical valves is straightforward. The largest possible valve should be implanted in the aortic annulus to minimize the problem of prosthesis-patient mismatch. Patients with a dilated aortic root may require a composite replacement of the aortic valve and ascending aorta with a valved conduit. Aortic valve replacement with stentless biologic valves is a more difficult operation and the surgeon must have a good knowledge of the functional anatomy of the semilunar valves. The key concept to know is that the diameter of a semilunar valve annulus and the diameter of its sinotubular junction are a function of the size of its leaflets. Mismatch between the size of the leaflets in the donor valve and the size of the aortic root in the recipient causes AI and premature failure of the stentless biologic valve. The pulmonary autograft can be implanted in the subcoronary position if the sizes of the aortic and pulmonary roots are similar. Another method of implantation is the so-called root inclusion technique whereby the pulmonary root is implanted inside the recipient's aortic root. It can also be used for complete replacement of the aortic root. Attention must be paid to the diameters of the aortic annulus and the sinotubular junction when the pulmonary autograft is used for AVR. If the diameter of the aortic annulus is larger than the diameter of the pulmonary annulus by 3 mm or more, plication of the aortic annulus should be performed before the pulmonary autograft is implanted in the aortic root. The same should be performed for the sinotubular junction. An aortic valve homograft can also be implanted in the subcoronary position, or as a root inclusion or root replacement. As with the pulmonary autograft, mismatch in sizes should also be avoided because it may result in premature failure of the homograft. The Medtronic Freestyle valve (Medtronic, Minneapolis, Minn) is an intact porcine aortic root that can be implanted with use of the same techniques as used for the pulmonary autograft. The Toronto SPV bioprosthesis (St Jude Medical, St Paul, Minn) can be implanted only in the subcoronary position. The operative mortality for AVR ranges from 1% to 8%, depending on the patient's age, presence of infective endocarditis, functional class, ventricular function, coronary artery disease, and associated dis428

Curr Probl

Surg, June 1999

eases. In spite of improved methods of myocardial protection, low cardiac output syndrome occurs in approximately 10% of the patients. Intraoperative echocardiography is helpful in the management of this problem because it often determines its cause. Stroke occurs in approximately 2% of patients. Older age, coronary artery disease, infective endocarditis, and reoperative AVR are predictors of perioperative stroke. Complete heart block requiring a permanent pacemaker occurs in 3% to 5% of cases. Long-term survival after AVR is dependent on the patient's age at the time of operation, gender, left ventricular function, coronary artery disease, functional class before operation, and associated noncardiac diseases. The 10-year actuarial survival rate ranges from 43% to 84%, depending on these variables. Although a myriad of micro-organisms can cause infective endocarditis of the aortic valve, gram-positive cocci are responsible for the majority of cases. Staphylococcus aureus has become the most common offender; it can cause endocarditis in structurally normal aortic valves. Patients who have had AVR have a small but constant risk for development of prosthetic valve endocarditis. Echocardiography is an extremely valuable diagnostic tool in patients with aortic valve endocarditis. This technique can detect vegetations as small as 1 to 2 mm in size, but it is more reliable in native than in prosthetic valve endocarditis. Administration of appropriate antibiotics is the most important element in the treatment of infective endocarditis. Adjunctive operation is often necessary when the infection is caused by certain micro-organisms such as S aureus, in patients with large vegetations or aortic root abscess and in patients with prosthetic valve endocarditis. Aortic valve homografts are ideal for treating patients with aortic root abscess because they appear to be more resistant to reinfection than prosthetic valves are. The operative mortality rate for operation for native aortic valve endocarditis is approximately 5% to 10%, and for prosthetic valve endocarditis the operative mortality rate is at least twice as high. Patients who have had infective endocarditis once are more likely to have it again than those who have never had it. Aortic valve and aortic root reoperations are becoming increasingly more common as the number of patients with prosthetic valves increases. Bioprosthetic valve failure is the most common cause for reoperation. Infective endocarditis, paravalvular leakage with or without hemolysis, pannus, and prosthesis-patient mismatch are other reasons for reoperation. The risk for reoperative AVR is highly dependent on a patient's situation, such as the indication for surgery, timing, ventricular function, and associated cardiac and noncardiac diseases. Curr Probl Surg, June 1999

429

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Tirone E. David, M D, received his surgical training at the ? ~ State University of New York, Downstate Medical Center, at the Cleveland Clinic Hospital, and at the University of Toronto. He was appointed Assistant Professor of Surgery at the University of Toronto in 1978 and became Professor of Surgery in 1990. He is currently Chief of Cardiovascular Surgery at Toronto General Hospital. His principal research interests are heart valve disease and thoracic aortic aneurysms.

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CurrProblSurg,June1999

Surgery of the Aortic Valve ~

urgery of the aortic valve continues to evolve. Intraoperative transesophageal Doppler echocardiography and better methods of myocardial preservation have opened opportunities to develop new approaches to treat patients with aortic valve disease and to re-evaluate old ones. This monograph is a review of aortic valve surgery as it was practiced in the last decade. Because I f'trmly believe that a sound knowledge of basic science is indispensable for surgeons, the fundamentals of anatomy and pathologic and pathophysiologic characteristics of the aortic valve are also included in this text.

Functional Anatomy of the Aortic Valve The morphologic characteristics and function of the aortic valve are interrelated to the aortic root and are best described as a single functional unit. The aortic root connects the left ventricle with the ascending aorta. The aortic root has 4 anatomic components: (1) aortoventricular junction or aortic annulus, (2) leaflets, (3) aortic sinuses or sinuses of Valsalva, and (4) sinotubular junction. The aortic annulus attaches the aortic root to the left ventricle. The aortic root is attached to the left ventricular myocardium in approximately 45% of its circumference and to fibrous structures (mitral valve and membranous septum) in the remaining 55%, as shown in Fig 1. The aortic annulus has a scalloped shape. Histologic examination of the aortic annulus reveals that the aortic root has a fibrous continuity with the anterior leaflet of the mitral valve and membranous septum, and it is attached to the muscular interventricular septum through fibrous strands as shown in Fig 2. The fibrous tissue that separates the aortic valve from the mitral valve is called the intervalvular fibrous body. An important structure immediately below the membranous septum is the bundle of His. The atrioventricular node lies in the floor of the right atrium between the tricuspid annulus and the coronary sinus orifice. This node gives origin to the bundle of His, which travels through the right fibrous trigone along the posterior edge of the membranous septum to the muscular interventricular septum. At this point the bundle of His divides into left and right bundle branches that extend subendocardially along both sides of the interventricular septum (Fig 1). The aortic leaflets are attached to the aortic root in a semilunar fashion (Fig 1). The segment of arterial wall of the aortic root delineated by a leaflet Curr Probl Surg, June 1999

431

FIG 1. Left ventricular ouffJowtract and aortic root. The aortic root is attached to ventricular muscle in approximately 45% of its circumference and to fibrous tissue in 55%. Left arrow, Lateral fibrous trigone below left coronary leaflet; right arrow, junction of membranous and muscular interventricular septum below right coronary leaflet. The bundle of His lies on the muscular interventricular septum immediately below the membranous septum.

proximally and by the sinotubular junction distally is called the aortic sinus or sinus of Valsalva. There are 3 aortic leaflets and 3 sinuses: the left, the right, and the noncoronary. The left main coronary artery arises from the left aortic sinus and the fight coronary artery arises from the right aortic sinus. The left main coronary artery orifice is closer to the aortic annulus than is the right coronary artery orifice. The triangular space underneath 2 leaflets is part of the left ventricle. The highest point of this triangle where 2 leaflets are attached is called the commissure; it is located immediately below the 432

Curr Probl Surg, June 1999

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FIG 2. Right, Photomicrograph of the aortoventricular junction along noncoronary aortic sinus. There is fibrous continuity be~een the aortic valve and mitral valve (intervalvular fibrous body). Left, Photomicrograph of the aortoventricular junction along the right coronary sinus and muscular venlricular septum. Connective tissue unites the aortic root to the ventricular septum. (From David TE. Aortic valve repair for management of aortic insufficiency. Adv Cardic Surg 1999. In press. Used by permission.) Curr Probl Surg, June 1999

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BASE FIG 3. Geometric relationships of the components of the aortic root. The length of the base of the aortic leaflet is approximately 1.5 times longer than the length of free margin (FM). The diameter of the aortic annulus (AA) is approximately 15% to 20% larger than the diameter of the sinotubular junction (STJ). The free margins of the leaflets extend from commissureto commissure,and the commissuresare immediately below the sinotubular junction. Therefore the diameter of the sinotubular junction cannot exceed the length of the free margin of the leaflets.

sinotubular junction. The 2 triangular spaces underneath the commissures of the noncoronary leaflet are fibrous structures, whereas the triangular space underneath the commissure between the right and left leaflets is mostly a muscular structure (myocardium). These triangles can be seen in Fig 1. The sinotubular junction represents the end of the aortic root. This is an important structure because the commissures of the leaflets are located immediately below it. Changes in the diameter of the sinotubular junction affect the motion and coaptation of the aortic leaflets. The geometry of the aortic root and its anatomic components vary somewhat from individual to individual, but the geometric relationships among the various components are fairly constant in any individual. Thus, the sizes of the aortic leaflets determine the diameters of the aortic annulus and the sinotubular junction, as well as the sizes of the sinuses of Valsalva. Each aortic leaflet has a crescent shape, and the length of its base is approximately 1.5 times longer than the length of its free margin. The lengths of the free margins vary from leaflet to leaflet in an individual; the noncoronary leaflet is often the largest of the 3, followed by the fight leaflet. The lengths of the free margins of the leaflets and the diameter of the aortic annulus are interrelated) Because the free margin of a leaflet extends from one commissure to another, the diameter of the aortic annulus cannot exceed the average lengths of the free margins of the leaflets (Fig 3). The diameter of the aortic annulus is 15% to 20% larger than the diameter of the sinotubular junction. 1 The anatomic relationships between the aortic root and surrounding structures are also important for cardiac surgeons. The fight aortic sinus 434

Curr Probl Surg, June 1999

FIG 4. Closure of the aortic valve is facilitated by eddies currents created by the aortic sinuses. The aortic sinuses ore also important to guarantee coronary artery perfusion during systole.

relates with the pulmonary root, right ventricular outflow tract, and body of the right ventricle. The subcommissural triangle between the right and noncoronary leaflets is in contact with the fight atrium. The proximal part of the noncoronary aortic sinus relates with the dome of the left atrium as well as with the right atrium. The left aortic sinus relates mostly with the dome of the left atrium. The aortic root is attached to contractile as well as fibrous components of the left ventricle. During systole the interventricular septum shortens and moves inward, and the anterior leaflet of the mitral valve is pushed away from the center of the left ventricular outflow tract. Therefore the area of the aortic root that is attached to the anterior leaflet of the mitral valve is exposed to greater tension than the area attached to the muscular interventricular septurn during systole. These dynamic changes in the geometry of the aortic annulus play a role in the function of the aortic valve. Although all 3 aortic leaflets open synchronously during systole, the noncoronary leaflet, its annulus, and commissures are exposed to greater stress (LaPlace's law). This may explain why the noncoronary aortic sinus and its annulus tend to dilate more than the other sinuses in patients with degenerative disease of the aortic root. The sinuses of Valsalva are important for maintaining coronary artery blood flow throughout the cardiac cycle as well as creating eddies currents to close the aortic leaflets during diastole (Fig 4). The aortic root is very elastic in young patients and expands considerably during systole Curr Probl Surg, June 1999

435

and shortens during diastole. However, the number of elastic fibers in the aortic root (as well as elsewhere in the aorta) decreases with age, and the aortic root becomes less compliant in older patients. It expands minimally during systole in elderly patients. In addition, the diameter of the sinotubular junction is increased in elderly patients and tends to become equal to the diameter of the aortic annulus.

Pathologic Characteristicsof the Aortic Valve Anatomically normal tricuspid aortic valves may become calcified late in life and cause aortic stenosis (AS). This type of lesion is called dystrophic calcification, senile calcification, or degenerative calcification of the aortic valve. The range of histopathologic lesions includes calcification, condroid and osseous metaplasia, neorevascularization, inflammation, and lipids deposition. 2 The pathogenesis of degenerative calcification of the aortic valve is not well understood. Aging is certainly the most important epidemiologic factor} -7 Degenerative calcification is an active inflammatory process with some similarities (eg, lipid deposition, macrophage and T-cell infiltration, and basal membrane disruption) and some dissimilarities (presence of prominent calcification and small numbers of smooth muscle cells) to atherosclerosis. 4,6 Aging and high levels of lipoprotein (a) were found to be related to aortic valve sclerosis in a rural Japanese community.3 Degenerative calcification of the aortic valve is the most common cause of AS in elderly patients in North America. 7,8 Bicuspid aortic valve is common and probably occurs in 1% to 2% of the population. It usually functions satisfactorily and does not cause hemodynamic problems until late in life when it becomes calcified and stenotic. The calcified bicuspid aortic valve is the second most common cause of AS in elderly patients. 7-9 A bicuspid aortic valve can also cause aortic insufficiency (AI), particularly in young patients in whom the aortic root is frequently dilated, l° Most patients with bicuspid aortic valves have 3 aortic sinuses. The 2 leaflets are of different sizes and the larger one usually has a raphe instead of a commissure. This raphe extends from the midportion of the leaflet to the aortic annulus, and its insertion in the aortic root is often at a lower level than the other 2 commissures. A bicuspid aortic valve with 2 aortic sinuses and no raphe is uncommon. The left coronary artery is dominant in most patients with a bicuspid aortic valve. A unicusp aortic valve is less common than the bicuspid aortic valve and usually causes AS. It is characterized by the presence of only 1 commissure. Both unicusp and bicuspid aortic valves are congenital anomalies of the aortic root that are often associated with premature degenerative changes in the media of the wall of the aortic root and ascending aorta. These 436

Curr Probl Surg, June i 9 9 9

patients are at risk for the development of chronic degenerative aneurysms of the ascending aorta and type A aortic dissection, u The quadricusp aortic valve is a rare anomaly that can cause AI. Three cusps are usually of similar size and 1 is hypoplastic. A subaortic membranous ventricular septal defect can cause AI because of distortion of the aortic annulus and leaflet prolapse. Initially the leaflet prolapse is the result of distortion of the annulus alone, but with time its free margin may become elongated and aggravate the degree of prolapse with worsening of AI. Patients with congenital supravalvular AS frequently have dilated aortic sinuses, redundant aortic valve leaflets, and a very narrow sinotubular junction. 12 In some patients the leaflets may be thickened and have restricted motion. The coronary artery orifices may also become stenotic. Dilatation of the aortic root is the most common cause of AI in North America. 8,~3 Dilatation of the sinotubular junction is a common cause of AI. The aortic valve can be bicuspid or tricuspid in these patientsJ 3,14 In our experience older patients with ascending aortic aneurysms and AI frequently have a normal aortic annulus and normal or minimally diseased leaflets, and the AI is largely the result of dilatation of the sinotubular junction. ~4.~5In younger patients the aneurysms tend to be more proximal and involve the sinuses of Valsalva, aortic annulus (annuloaortic ectasia), and sinotubular junction. These pathologic features are encountered in patients with Marfan syndrome or its forma frusta. Aortic dissections involving the ascending aorta can cause AI because of preexisting dilatation of the aortic root or by detachment of 1 or more commissures of the aortic valve, resulting in prolapse of the leaflets. Rheumatic aortic valve disease is still common in certain parts of the developed worldJ 6 This disease causes fibrosis, thickening, and contraction of the aortic leaflets, often with commissural fusion. In later stages the leaflets can become calcified. Rheumatic fever can cause AS and AI. It is possible that some postinflammatory aortic valve lesions are not rheumatic in origin.~7 Bacterial and fungal infections of the aortic valve usually occur in patients with preexisting aortic valve disease (bicuspid aortic valve is the most common one) but can also occur in patients with a normal aortic valve. The infection destroys 1 or more leaflets, resulting in AI. Ankylosing spondylitis, Reiter's syndrome, osteogenesis imperfecta, rheumatoid arthritis, systemic lupus erythematosus, and idiopathic giant cell aortitis are connective tissue disorders that can be associated with AI. The anorexigenic drugs phenteramine and fenfluramine can also cause AI. An increasingly more common cause of aortic valve disease is malCurr Probl Surg, June 1999

437

TABLE 1. Surgical pathologic features of the aortic valve in 1773 patients Predominant lesion

AS

No. of patients 795 Tricuspid calcific 378 (48%) Bicuspid aortic valve 280 (35%) Other congenital 11 (1.4%) Rheumatic 51 (6.4%) Annuloaortic ectasia 0 Aortic dissection 0 Prosthetic valve 27 (3.4%) Dilatation of sinotubular junction 0 Unknown 48 (6°/0)

AI 616 35 (5.6%) 97 (16°/0) 7 (1.1%) 86 (14%) 97 (16%) 89 (14%) 105 (17%) 79 (13%) 21 (3.4%)

Mixed lesion

362 117 72 6 98 3 0 41 0 25

(32%) (20°/0) (1.7%) (27%) (0.8%) (11%) (7%)

Total

1773 530 449 24 235 100 89 173 79 94

(30%) (25%) (1.3%) (13%)* (5.6°/0) (5%) (10°/0) (4.4%) (5.3%)

*One hundred sixty-five patients also had mitral valve surgery for rheumatic disease.

functioning prosthetic valves. Bioprosthetic aortic valves fail because of tissue degeneration. Mechanical heart valves may fail because of fibrous ingrowth, dehiscence, thrombosis, or infection. Structural failure of the currently used mechanical valves is rare. The pulmonary autograft, when used for aortic valve replacement (AVR), seldom suffers degenerative changes. Dysfunction of this valve is usually the result of technical errors or dilatation of the pulmonary root in the aortic position. Cryopreserved aortic valve homografts are viable at the time of operation, but from the first day of implantation there is progressive collagen hyalinization and loss of normal cellularity, including the endothelium and deep connective tissue cells, t8,19 Eventually the dead cells become calcified but the collagen remains intact longer. This process is accelerated in children and young adults and is slower in older patients. Aortic valve homografts frequently calcify after a few years in children. The degenerative changes in aortic homografts are probably immune mediated because the heart valves in transplanted hearts do not degenerate at the same rate as aortic valve homografts. 2° Glutaraldehyde-fixed porcine aortic valves and bovine pericardial valves also suffer degenerative changes. These changes are related to mechanical stress and calcification. Thus better designed stents that minimize mechanical stress on the leaflets have improved the durability of these valves. 21,2z Calcification is particularly troublesome in young patients. Antimineralization treatment of the glutaraldehyde-fixed tissues may retard or even prevent calcification and extend the durability of these valves in younger patients. Between 1993 and 1997, 1915 patients underwent surgery for aortic valve or aortic root disease at the Toronto General Hospital. There were 1252 (65%) men and 663 (35%) women whose mean age was 60 years 438

Curr Probl Surg, June 1999

(range 16 to 90 years). One third of these patients were older than 70 years. Concomitant coronary artery disease was present in 37% of the patients. The aortic valve leaflets were normal in 142 patients who had acute or chronic aneurysms of the aortic root or ascending aorta; in the remaining 1773 patients the aortic valve was stenotic or incompetent or had both lesions. Table 1 summarizes the pathologic features of the aortic valve in 1773 patients who had valve dysfunction.

Pathophysiologic Characteristics of Aortic Stenosis Acquired AS develops gradually during a prolonged period of time. The cardiac output is maintained for many years in spite of fairly high transvalvular gradients owing to parallel replication of sarcomeres and concentric left ventricular hypertrophy. As the left ventricle becomes more hypertrophic, it also becomes less compliant and the left ventricular enddiastolic pressure and left atrial pressure rise. The contraction of the left ventricle becomes increasingly more isometric and the peripheral pulse pressure decreases. Late in the course of the AS, the cardiac output, the stroke volume, and also the left ventricular-aortic pressure gradient decline, whereas the left atrial pressure rises and so do the pressures on the fight side of the heart. The left ventricular end-diastolic volume increases only late in the course of the disease. Fig 5 summarizes the pathophysiologic features of AS. 23 The degree of AS is considered to be severe when the aortic valve orifice is reduced to less than 0.5 cm2/m2 of body surface area or the peak systolic gradient is in excess of 50 mm Hg with normal cardiac output. Histologic examination of hypertrophic hearts discloses unusually large nuclei, loss of myofibrils, accumulation of mitochondria, large cytoplasmic areas devoid of contractile material, and proliferation of fibroblasts and collagen fibrils in the interstitial spaces. 24 Acute AS (such as sudden occlusion of an artificial heart valve) causes left ventricular dilatation, reduction of the stroke volume, and reduction of cardiac output. Depending on the degree of left ventricular outflow obstruction, shock develops and the patient dies if treatment is not instituted promptly.

Pathophysiologic Characteristics of Aortic Insufficiency With AI the left ventricle must eject the forward stroke volume plus the regurgitant volume into the systemic circulation, which is a high-pressure system. The low diastolic aortic pressure facilitates ventricular emptying during early systole. The hemodynamic consequences of AI are dependent on the intensity and the chronicity of the regurgitant volume into the Curr Probl Surg, June 1999

439

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FIG 5. Pathophysiologic features of aortic stenosis. Left ventricular (LV) outflow tract obstruction results in increased left ventricular systolic pressure, increased left ventricular ejection time (LVET), increased left ventricular diastolic pressure, and decreased aortic (Ao) pressure. Increased left ventricular systolic pressure with left ventricular volume overload will increase the left ventricular mass, which may lead to left ventricular dysfunction and failure. Increased left ventricular systolic pressure, left ventricular mass, and left ventricular ejection time will increase myocardial oxygen (02) consumption. Increased left ventricular ejection time will result in a decrease of the diastolic time (myocardial perfusion time). Increased left ventricular diastolic pressure and decreased aortic diastolic pressure will decrease the coronary perfusion pressure. Decreased diastolic time and coronary perfusion pressure will decrease the myocardial oxygen supply. Increased myocardial oxygen consumption and decreased myocardial oxygen supply will produce myocardial ischemia, which will further deteriorate the left ventricular function. 1", Increased; $, decreased. (From Boudoulas H, Gravanis MB. Valvular heart disease. In: Gravanis MB, editor. Cardiovascular disorders: pathogenesis and pathophysiology. St Louis: Mosby-Year Book; 1993. p 64-11Z Used by permission.)

left ventricle. Other important factors are the area of the regurgitant oririce, the diastolic pressure gradient between the aorta and the left ventricle, the left ventricular compliance, and the heart rate. Chronic AI results in a gradual increase in the left ventficular end-diastolic volume. Initially the left ventricular end-diastolic pressure remains normal. As the diameter of the left ventricle increases, left ventricular wail stress also increases and promotes replication of the sarcomeres in series with consequential eccentric left ventricular hypertrophy.25 Because of this eccentric hypertrophy, the left ventricular ejection fraction is well preserved in spite 440

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f i g 6. Pathophysiologic features of aortic insufficiency. Aortic regurgitation will result in increased left ventricular (LV) volume, increased stroke volume, increased aortic (AoJ systolic pressure, and decreased effective stroke volume. Increased left ventricular volume will result in increased left ventricular mass, which may lead to left ventricular dysfunction and failure. Increased left ventricular stroke volume will produce increased systolic pressure and prolongation of the left ventricular ejection time (LVET). Increased left ventricular systolic pressure will result in further increases in left ventricular mass. Increased left ventricular systolic pressure and ejection time will increase myocardial oxygen (02) consumption. Increased left ventricular ejection time will result in a decrease in the diastolic time. Decreased diastolic time (myocardial perfusion time), diastolic aortic pressure, and effective stroke volume will decrease myocardial oxygen supply. Increased myocardial oxygen consumption and decreased myocardial oxygen supply will produce myocardial ischemia, which will further deteriorate left ventricular function. LVEDP, Left ventricular end-diastolic pressure; $, increased; $, decreased. (From Boudoulas H, Gravanis MB. Valvular heart disease. In: Gravanis MB, editor. Cardiovascular disorders: pathogenesis and pathophysiology. St Louis: Mosby-Year Book; 1993. p 64-117. Used by permission.)

of a large left ventricular end-diastolic volume. Late in the course of chronic AI, the left ventricular end-diastolic volume and end-diastolic pressure increase and the ejection fraction decreases. Fig 6 summarizes the pathophysiologic features of AI. z3 In acute AI the normal left ventricle cannot accommodate the regurgitant diastolic volume and the left ventricular end-diastolic pressure rises rapidly above the left atrial pressure, leading to premature closure of the mitral valve. In cases of severe AI cardiovascular collapse is inevitable. Curr Probl Surg, June 1999

441

Diagnosis Aortic Stenosis. Patients with AS remain asymptomatic for many years. Symptoms usually appear late in the course of this disease. The manifestations of AS are angina pectoris, syncope, and congestive heart failure. Coexisting coronary artery disease is c o m m o n in older patients, but more than one half of all patients with AS and angina pectoris have normal coronary arteries. The myocardial ischemia in these patients is the result of a combination of increased oxygen demands by the hypertrophic myocardium and a reduction of oxygen delivery resulting from the excessive compression of the coronary arteries. 26 Syncope is usually the result of cerebral hypoperfusion, but it can also be a result of arrhythmias such as transient ventricular fibrillation, atrial fibrillation, or transient heart block. Symptoms of congestive heart failure often occur late in the course of this disease. Patients with AS are at risk for sudden death, but it seldom occurs in asymptomatic patients. 27,28 Other less c o m m o n symptoms are gastrointestinal bleeding (idiopathic or caused by angiodysplasia), infective endocarditis, and arterial thromboembolism. On auscultation these patients have a harsh systolic murmur, sometimes with a thrill along the left sternal border, often radiating to the neck. The second heart sound ($2) is soft, absent, or paradoxically split. The carotid pulses are diminished and delayed. The electrocardiogram reveals left ventricular hypertrophy in most patients with severe AS. Echocardiography establishes the diagnosis; provides information regarding the ventricular function, ventricular thickness, pulmonary hypertension; and estimates the aortic valve area and transvalvular gradient. Coronary angiography to identify concomitant coronary artery disease is important in patients aged 40 years and older. Aortic Insufficiency. The clinical presentation is determined by the rapidity with which AI develops. Patients with chronic AI remain asymptomatic for many years while the heart slowly enlarges. Palpitations and head pounding may occur during exertion. Angina pectoris may occur, but it is not as common as with AS. Syncope is rare. Symptoms of congestive heart failure are usually an indication of left ventricular dysfunction. Acute AI is frequently associated with cardiovascular collapse, with extreme fatigue, dyspnea, and hypotension resulting from reduced stroke volume and elevated left atrial pressure. The major physical findings relate to the wide pulse pressure caused by the large stroke volume. The pulse is the water-hammer or collapsing type with a rapid rise and fall (Corrigan's pulse). The patient's head may bob with each heart beat (de Mussers sign). The systolic pressure is elevated and the diastolic pressure is low. A variety of peripheral artery auscultatory signs may 442

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be present in patients with AI: Traube's sign (also known as "pistol shot sounds"), Muller's sign (pulsations of the uvula), and Duroziez's sign (systolic murmur over the femoral artery when it is compressed proximally to where the stethoscope is placed). The apical impulse is prominent and displaced laterally. The aortic diastolic murmur is high pitched and decrescendo. The electrocardiogram usually demonstrates left ventricular hypertrophy. Chest radiographs demonstrate cardiomegaly. Echocardiography confirms the diagnosis and provides information regarding the cause of AI. Radionuclide imaging is useful in assessing the left ventricular function at rest and during exercise, valuable information in asymptomatic patients.

Natural History Aortic Stenosis Several studies showed that asymptomatic patients with AS have a good prognosis. 27,28 Sudden death in asymptomatic patients is rare. 28 In one study of 229 asymptomatic patients with severe AS only 5 (2%) died suddenly. 28 Once symptoms develop (eg, angina, syncope, or heart failure), the prognosis with medical treatment becomes poor. The average survival time is 2 to 3 years for patients with angina or syncope and 1 to 2 years for those with heart failure. 29,3°

Aortic Insufficiency In a classic series of the natural history of patients with chronic AI, approximately 75% survived 5 years and 50% survived 10 years after diagnosis. 3~ Symptomatic patients had a poor prognosis: death occurred within 4 years after development of angina and within 2 years after the onset of congestive heart failure. 32 Because of the deleterious effects of AI on the left ventricle, asymptomatic patients should undergo operation before irreversible myocardial changes develop.

Indications for Surgery Aortic Stenosis Patients with asymptomatic AS should be offered operation when either the aortic valve area is less than 0.8 cm z or the mean systolic gradient is greater than 50 mm Hg or when there is severe left ventricular hypertrophy. An echocardiographic flow velocity across the aortic valve greater than 4 m/s is associated with poor prognosis and surgery should be considered. 33 Curr Probl Surg, June 1999

443

Advanced age and comorbid conditions must be weighed in the decision to offer operation. Patients with AS, acute congestive heart failure, and serious associated diseases may be best treated with percutaneous balloon valvotomy as definitive treatment or as a bridge to A V R . 34

Aortic Insufficiency Asymptomatic patients with chronic AI should have AVR when the left ventricular function begins to deteriorate.3537 Radionuclide angiography at rest and during maximum exercise for measurements of left ventricular size, performance, and end-systolic wall stress is useful for determining the timing of operation in asymptomatic patients. 38 Operation should be performed if the ejection fraction falls during exercise. Echocardiography is also useful to follow up asymptomatic patients. When the left ventricular end-systolic diameter exceeds 55 mm, AVR should be performed. Operation is recommended for all symptomatic patients. Left ventricular function often improves after AVR even in patients with a depressed left ventricular ejection fraction. 39

Aortic Root Aneurysm The effects of AI and the diameter of the aortic root and ascending aorta should be taken into account in the assessment of patients with aortic root aneurysm. Patients with Marfan syndrome should undergo operation when the transverse diameter of the aortic root reaches 55 Iill/1. 40-42 However, if the aortic valve can be saved or if the patient has a family history of acute type A aortic dissection, a more aggressive approach is justifiable. 4°,41 For patients without Marfan syndrome operation is indicated when the transverse diameter exceeds 60 nlnq. 43,44 Here, again, if the aortic valve is tricuspid and repairable, we believe that it is justifiable to recommend operation when the aneurysm reaches 55 mm or even less. 4°

Prosthetic Valve Dysfunction Patients with biologic aortic valves should have a transthoracic Doppler echocardiographic study every year to assess the function of the valve and ventricle. Aortic valve homografts and stentless porcine valves develop AI as the mode of failure. 18,45,46 The timing of reoperation should be based on symptoms, left ventricular function, and the echocardiographic appearance of the valve. Unlike native aortic valve incompetence, AI caused by a bioprosthetic valve can increase rapidly and cause acute heart failure. Because it is safer to reoperate electively, earlier operation may improve the overall outcome.47-49Stented porcine valves and the first generation of pericardial valves fail because of calcification or leaflet tears, whereas the 444

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newer pericardial valves usually fail because of calcification that causes AS. 5°,51 Mechanical aortic valve failure is uncommon. These valves may fail because of strut fracture, pannus, thrombosis, or infection.

Surgical Options to Treat Aortic Valve Disease Percutaneous balloon valvotomy is useful in children with AS. 52 It is also useful in elderly patients in acute heart failure or in cardiogenic shock as a palliative treatment or as a bridge to A V R . 34'53 This technique also has been used in pregnant women with A S . 54 The operative mortality rate in elderly patients in cardiogenic shock resulting from critical AS is very high. The mortality rate can be reduced by performing a percutaneous balloon valvotomy to improve the cardiac output, renal function, and pulmonary function, and AVR can be performed electively at a later date. Aortic valve repair is feasible in certain patients with AI. 55 Aortic valve replacement is the treatment of choice in patients with AS. Decalcification of a mildly or moderately stenotic tricuspid aortic valve is sometimes possible in patients in whom the primary indication for operation is myocardial revascularization. The calcific deposits should be only along the aortic annulus; the leaflets should be pliable and without calcification. Ultrasonic decalcification of aortic valves leaflets has given disappointing results. 56 Therefore, if the leaflets are calcified, AVR should be performed even if the gradient is only moderate. Newer stentless porcine aortic valves are ideally suited for elderly patients with a relatively small aortic a n n u l u s . 46,57 The standard incision for AVR has been median sternotomy. A right parastemal anterior thoracotomy with excision of the third and fourth cartilages, a transverse or a limited median sternotomy with extension into an intercostal space, and other variations of these incisions have been used to expose the aortic root and ascending aorta. 58-6° It remains to be proved that limited thoracotomies to perform aortic valve operations are superior to the standard median sternotomy. The standard median sternotomy was compared with a limited upper median sternotomy for AVR in a prospective randomized trial by Afis and colleagues, 6~ and they could not demonstrate an advantage of one incision over the other. It is important not to compromise the safety and quality of AVR in favor of a small incision in the skin or sternum. 62 Although surgeons continue to use different methods of myocardial protection during aortic cross-clamping for AVR, we believe that the best protection is offered by continuous blood cardioplegia. It can be delivered directly into the coronary arteries, through vein grafts if the patient needs concomitant coronary artery grafting, or retrograde through the coronary sinus. We have used continuous antegrade blood cardioplegia for myocarCurt Probl Surg, June 5.999

445

dial protection during AVR since 1984. We place Polystan coronary artery cannulas (Polystan A/S, Vaerlose, Denmark) into the coronary artery oririces and give blood cardioplegia at 150 to 250 mL/min, depending on the degree of left ventricular hypertrophy. We used to administer cold cardioplegia, but during the past 5 years we have administered it at room temperature. In patients with coronary artery disease we have also used combined antegrade and retrograde routes to deliver cardioplegia.

Aortic Valve Repair The mechanism of AI must be determined before an aortic valve can be repaired. Aortic insufficiency is caused by anatomic abnormalities of 1 or more components of the aortic root. Dilatation of the sinotubularjunction causes outward displacement of the commissures of the aortic leaflets and prevents central coaptation, resulting in AI (Fig 7). This is the mechanism of AI in patients with ascending aortic aneurysms, megaaorta syndrome, and long-standing hypertension and a mildly dilated and elongated ascending aorta. Depending on the duration of AI, the rapidity of dilatation, and leaflet strength, the leaflets may remain normal or the free margin of 1 or more leaflets may become elongated or fenestrations may develop in the commissural areas. These changes in the leaflets are probably the result of increased mechanical stress caused by the lack of coaptation. Dilatation of the sinuses of Valsalva does not cause AI if the aortic annulus and the sinotubular junction remain normal. That is the reason patients with ruptured sinus of Valsalva aneurysms may not have AI. Patients with Marfan syndrome and those with the forma frusta of Marfan initially have only dilatation of the aortic sinuses with no change in the diameters of the sinotubular junction and aortic annulus. Most of these patients do not have AI until the diameter of the sinuses of Valsalva reaches 45 to 50 ram, at which point the sinotubular junction dilates, the aortic leaflets can no longer coapt, and central AI develops. The aortic annulus may also dilate, contributing to the mechanism of AI in these patients. The fibrous components of the left ventricular outflow tract become enlarged and the normal relationship between muscular (45% of the circumference) and fibrous components (55% of the circumference) is altered in favor of the fibrous components. Bicuspid aortic valve causes AI because of leaflet prolapse. The free margin of the larger of the 2 leaflets, usually the 1 that contains the raphe, becomes elongated and prolapses. These patients often have dilatation of the aortic root with increased diameters of the aortic annulus and sinotubular junction. 446

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FIG 7. Dilatation of the sinotubular junction causes outward displacement of the commissures of the aortic valve and prevents the leaflets from coapting, with resulting central aortic insufficiency.

Type A aortic dissection causes AI because of detachment of 1 or both commissures of the noncoronary leaflet of the aortic valve with resulting prolapse. In addition, most of these patients have preexisting dilatation of the aortic root, which contributes to the development of AI. Rheumatic valvulitis of the aortic valve can cause commissural fusion, thickening, scarring, and contraction of the leaflets, which are inadequate to seal the aortic valve orifice. Some degree of aortic stenosis is almost always present in these cases. Rheumatic AI is commonly associated with rheumatic mitral valve disease. Although infective endocarditis of the aortic valve is far more common in patients with than in those without preexisting aortic valve disease, a normally functioning tricuspid aortic valve can become infected with leaflet destruction and consequent AI. A subaortic membranous ventricular septal defect may cause AI because of downward and outward displacement of the aortic annulus along the right leaflet that with time may become elongated and increase the degree of leaflet prolapse. Curr Probl Surg, June 1999

447

Selection of Patients for Aortic Valve Repair Early operation may be justifiable if the AI can be corrected by an aortic valve repair. Therefore it is important to determine preoperatively whether the valve is repairable. Transesophageal echocardiography is the best tool to study the aortic root and the mechanism of AI. The echocardiographer must understand the functional anatomy of the aortic root and the principles of aortic valve repair to obtain the information needed to determine the possibility of aortic valve repair. Each component of the aortic root must be examined--in particular the leaflets. Calcification of the aortic annulus and subannular regions indicates a more advanced degenerative process that often precludes aortic valve repair. A subaortic membranous ventricular septal defect deforms the aortic annulus of the right aortic leaflet, and in the adult patient this leaflet may become calcified. The number of leaflets, their thickness, the appearance of their free margins, and the excursion of each leaflet during the cardiac cycle must be carefully examined. The coaptation areas of the leaflets should also be interrogated by Doppler imaging in multiple views. Information regarding the morphologic features of the aortic sinuses, sinotubular junction, and ascending aorta is also important. The diameters of the aortic annulus, aortic sinuses, and sinotubular junction and the heights of the leaflets should be measured. The lengths of the free margins of the leaflets should be estimated if possible. Dilatation of the sinotubular junction is easily diagnosed by echocardiography. If the aortic sinuses, leaflets, and annulus appear to be normal by echocardiography and the AI is central, reconstruction of the aortic root with preservation of the aortic valve will restore normal valve function.14'ls Patients with a dilated sinotubular junction are frequently in their sixth and seventh decades of life, often have a history of hypertension, and have degenerative aneurysms of the ascending aorta or the mega-aorta syndrome. Dilatation of the entire aortic root with A_I, as found in patients with Marfan syndrome or its forma frusta, is also a correctable lesion as long as the leaflets are normal or near normal. In patients with large aortic root aneurysms (ie, diameter of the aortic sinuses >60 mm) the leaflets may be overstretched and thinned and may have large stress fenestrations in the commissural areas. Although fenestrations are not detected by echocardiography, a regurgitant jet in a commissural area in these patients usually indicates a large fenestration. The leaflets are often normal or minimally stretched in patients with aortic root aneurysms of 55 mm or less in diameter. However, even in patients with larger aneurysms if the AI is only central and no leaflet prolapses, a valve-sparing operation may be possible. 448

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Aortic insufficiency caused by prolapse of a single leaflet in patients with a normal aortic root is uncommon but easily repairable. Prolapse of one leaflet in patients with a bicuspid aortic valve is more common and also amenable to repair as long as the other leaflet does not prolapse and both leaflets are thin, mobile, and free from calcification. Echocardiography has not been useful in predicting the feasibility of repair of rheumatic aortic valves but it is useful for excluding the possibility of repair.

Operative Techniques for Aortic Valve Repair Aortic valve repair must be performed with intraoperative transesophageal Doppler echocardiography. An attempt should be made to establish the mechanism of AI by Doppler echocardiography, and all diameters of the aortic root are obtained before the patient is placed on cardiopulmonary bypass. The patient is placed on cardiopulmonary bypass and the aorta is clamped and opened through a transverse aortotomy 1 to 2 cm above the sinotubular junction or 4 to 5 cm above the origin of the right coronary artery. We administer continuous antegrade blood cardioplegia directly into the coronary artery orifices or retrograde through the coronary sinus. A left ventricular vent is inserted through the right superior pulmonary vein. Intraoperatively, the mechanism of AI is established by careful inspection of each component of the aortic root. Because the feasibility of aortic valve repair is highly dependent on the quality and morphologic features of the aortic leaflets, they are inspected first. If the aortic valve has 3 leaflets that are thin and pliable and inspection reveals that they have the typical crescent shape, aortic valve repair is probably feasible. Next, the arterial wall immediately above the 3 commissures should be suspended gently with forceps or sutures at approximately the same level and equidistantly to allow the leaflets to coapt to determine whether the free margin of any of the 3 leaflets is elongated. If the 3 leaflets coapt normally, the AI must be caused by dilatation of the sinotubular junction. If 1 leaflet coapts at a lower level than the other 2, its free margin is elongated and it should be shortened before proceeding with the next step of the valve repair. The same patient may have AI caused by leaflet prolapse and dilatation of the sinotubular junction or of the aortic annulus.

Repair of Leaflet Prolapse Prolapse of a single leaflet in patients with a tricuspid aortic valve is corrected either by a triangular resection or by plication of the central portion of the leaflet to shorten its free margin. The degree of shortening Curt Probl Surg, June 1999

449

FIG 8. AI caused by leaflet prolapse. Free margin of 1 leaflet is longer than other 2 (left). Triangular resection of central portion of prolapsing leaflet and reapproximation of resected margins with horizontal mattress sutures correct prolapse (right). Alternatively, plication of triangular segment of central portion can also be performed.

is based on the length of the free margins of the other 2 leaflets to allow them to coapt at the same level. If the leaflet is myxomatous and thickened, we perform a triangular resection and approximate the margins with interrupted horizontal mattress sutures of 5-0 polypropylene buttressed on 2 small strips of autologous pericardium. If the leaflet is thin and overstretched, we perform a triangular plication with the same type of suture (Fig 8). Minor elongation of the free margin of a leaflet can also be corrected with a double layer of 6-0 Gore-tex expanded polytetrafluoroethylene suture (W. L. Gore, Langstaff, Ariz) passed along the free margin from commissure to commissure (Fig 9). This technique allows for a fine band of fibrous tissue to grow along the suture and surrounding leaflet tissue, reinforcing its free margin. We often use this technique in patients with AI caused by dilatation of the aortic root in whom 1 leaflet is slightly more elongated than the other 2 and it is thin and overstretched. We also use it to reinforce the free margins when large fenestrations are found. If the aortic root is normal, repair of the leaflet prolapse is all that is required to correct the AI. If the aortic root is dilated, remodeling of the aortic root is also necessary. 450

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FIG 9. The free margin of the leaflet can be reinforced and mild prolapse corrected with a double layer of 6-0 Gore-tex suture passed in and out its Free margin from commissure to commissure.

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451

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FIG 10. Repair of an incompetent bicuspid aortic valve_The raphe is resected and the prolapsing leaflet is shortened by triangular resection or plication of the central portion of the free margin.

FIG 11. Repair of bicuspid aortic valve. Plication of the subcommissuraltriangles increases the coaptation areas of 2 leaflets and reduces the diameter of the aortic annulus.

Repair of Incompetent Bicuspid Aortic Valve An incompetent bicuspid aortic valve can be satisfactorily repaired when both leaflets are pliable without calcification, the AI is caused by prolapse of only 1 leaflet, and the aortic root is only mildly dilated. The leaflet that contains the raphe is the larger of the 2 and often the 1 that prolapses. The raphe should be resected and a triangular plication of the central portion of the free margin is performed to shorten its length (Fig 10). If the aortic annulus is mildly dilated, plication of the triangular spaces underneath the commissures reduces the diameter of the aortic annulus and increases the coaptation area of the 2 leaflets (Fig 11). 452

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Palient~ With a Normal Aortic Annulus

I

FIG 12. Remodeling of the aortic root by correcting a dilated sinotubular junction. This is accomplished by replacing the ascending aorta with a tubular Dacron gra~tof diameter 5% to 10% smaller than the average lengths of the free margins of the leaflets. (From David TE, Feindel CM, Bos J. Repair of the aortic valve in patients with aortic insufficiency and aortic root aneurysm. J Thorac Cardiovasc Surg 1995;109:345-52. Used by permission.)

Remodeling of the Aortic Root for Dilatation of the Sinotubular Junction Dilatation of the sinotubular junction displaces the commissures outward and prevents the leaflets from coapting during diastole (Fig 7). The dilatation of the sinotubular junction is often more severe along the area of the noncoronary aortic sinus. Patients with a dilated sinotubular junction and AI frequently have an aneurysm of the ascending aorta. The AI can be corrected by reducing the sinotubular junction to its normal diameter. This is accomplished by replacing the ascending aorta with a tubular Dacron polyester graft with a diameter slightly smaller than the average length of the free margins of the 3 leaflets and suturing the graft right at the sinotubular junction (Fig 12). The 3 commissures of the aortic valve should be equidisCurr Probl Surg, June 1999

453

FIG 13. Remodeling ofthe aortic root by correcting the dilated sinotubular junction and replacing the noncoronary aortic sinus. (From David TE, Feindel CM, Bos J. Repair of the aortic valve in patients with aortic insufficiency and aortic root aneurysm.J Thorac Cardiovasc Surg 1995; 109:345-52. Used by permission.)

tantly placed in the Dacron graft if all 3 leaflets have similar sizes. If 1 leaflet is larger than the others, the space between its commissures should be proportionally larger. The Dacron graft should lie against the intima of the aortic root along the suture line at the level of the sinotubular junction and be secured to it with a simple continuous 4-0 polypropylene suture with a fine cardiovascular needle. This suture should be interrupted at each commissure. We have not used Teflon felt to buttress this suture line. If the estimated diameter of the sinotubular junction is less than 24 mm, it is preferable to use a Dacron graft of larger diameter (eg, 26 or 28 mm) and reduce one of its ends to the desirable diameter before suturing it to the sinotubular junction of the aortic root to avoid mismatch between the size of the graft and the size of patient. Grafts of small diameters in the ascending aorta can be obstructive and can cause an increase in left ventricular aftedoad. In addition to a dilated sinotubular junction, 1 or more sinuses of Valsalva may also be aneurysmal. The noncoronary sinus of Valsalva is the most 454

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FIG 14. Remodeling of the aortic root by correcting the dilated sinotubular junction and replacing the noncoronary and right aortic sinuses. (From David TE, Feindel CM, Bos J. Repair of the aortic valve in patients with aortic insufficiency and aortic root aneurysm. J Thorac Cardiovasc Surg 1995;109:345-52. Used by permission.)

commonly affected in patients with ascending aortic aneurysms arid a dilated sinotubular junction. If the other 2 sinuses are fairly normal, only the dilated aortic sinus needs replacement. A graft of appropriate diameter (5% to 10% smaller than the average lengths of the free margins of the 3 aortic leaflets) is selected, and 1 of its ends is tailored to replace the noncoronary aortic sinus. If all 3 leaflets have similar sizes, 1 of the ends of the graft is divided into 3 equal parts and a sinus is tailored in 1 of the ends of the Dacron graft (Fig 13). The height of the Dacron sinus is approximately equal to the diameter of the graft. The graft is sutured to the sinotubular junction of the aortic root along the left and right aortic sinuses and to the remnants of the noncoronary sinus and part of the aortic annulus. The graft should lie against the intima of the aortic root along the suture line, The right aortic sinus is the second most commonly involved by the dilatation process and it may need replacement during remodeling of the aortic root. In this case the right coronary artery must be reimplanted (Fig 14). In most patients with aortic root aneurysm all 3 aortic sinuses are dilatCurr Probl Surg, June 1999

455

FIG 15. Remodeling of the aortic root in patients with aortic root aneurysm (A). All 3 aortic sinuses are excised (B). (From David TE. Remodeling of the aortic root and preservation of the native aortic valve. Op Tech Cardiac Thorac Surg 1996;1:44-56. Used by permission.)

ed and need replacement. This is performed by excising all 3 aortic sinuses and replacing them with a properly tailored Dacron graft (Figs 15 to 17).

Remodeling of the Aortic Root and Correction of Dilated Aortic Annulus Dilatation of the aortic annulus or annuloaortic ectasia is seldom encountered in isolation in patients with AI. It is often associated with dilatation of the sinotubular junction and aortic root aneurysm. These patients may or may not have Marfan syndrome. The aortic leaflets are often normal or near normal in these patients when the aortic root is not excessively large. We believe that remodeling of the aortic root must include correction of the dilated aortic annulus. The diameter of the aortic annulus should not exceed the average length of the free margins of the aortic leaflets. Dilatation of the aortic annulus occurs along its fibrous 456

Curr Probl Surg, June 1999

A

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FIG 16. Remodeling of the aortic root by replacing all 3 aortic sinuses. Properly tailored tubular Dacron graft is used to resuspend the 3 aortic commissures (A) and replace the aortic sinuses (B). (From David TE. Remodeling of the aortic root and preservation of the native aortic valve. Op Tech Cardiac Thorac Surg 1996;1:44-56. Used by permission.)

components. Correction of dilatation of the aortic annulus can be accomplished by an aortic annuloplasty. This is performed by passing multiple horizontal mattress sutures of 4-0 or 3-0 polyester from the inside to the outside of the fibrous components of the left ventricular outflow tract immediately below the lowest level of the insertion of the leaflets through a single horizontal plane (Fig 18). These sutures are then passed through a strip of Dacron fabric to reduce the diameter of the aortic annulus, espeCurr Probl Surg, June 1999

457

FIG 17. Remodeling of the aortic root with replacement of all 3 aortic sinuses. Coronary arteries are reimplanted in their respective aortic sinuses. (From David TE. Remodeling of the aortic root and preservation of the native aortic valve. Op Tech Cardiac Thoroc Surg 1996;1:44-56. Used by permission.)

cially underneath the commissures of the noncoronary leaflet. The length of the strip of Dacron fabric is based on the desired diameter of the aortic annulus calculated by measuring the lengths of the free margins of the aortic leaflets. The aortic sinuses and ascending aorta are replaced as described above (Figs 16 and 17). The coronary arteries are reimplanted on their respective sinuses, as shown in Fig 19. 458

Curr Probl Surg, June 1999

[

C FIG 18. Aortic annuloplasty to correct annuloaortic ectasia in patients with dilated aortic annulus and aortic root aneurysm. Multiple horizontal mattress sutures are passed through the fibrous components of the left ventricular outflow tract, through a single horizontal plane immediately below the lowest level of the leaflets (A and B). These sutures are passed through a strip of Dacron fabric (C) and sutures are tied outside the aortic root (D). (From David TE. Remodeling of the aortic root and preservation of the native aortic valve. Op Tech Cardiac Thorac Surg 1996;1:44-56. Used by permission.)

Reimplantation of the Aortic Valve This is another method to correct annuloaortic ectasia and AI. The aortic root is dissected circumferentially and all 3 dilated aortic sinuses are excised, leaving a small button of arterial wall around the coronary artery orifices and some arterial wall attached to the aortic annulus. Multiple sutures of 4-0 or 3-0 polyester are passed from the inside to the outside of the left ventricular outflow tract. This suture line is in a single horizontal plane along the fibrous components of the left ventricular outflow tract and it follows the scalloped shape of the aortic annulus in its muscular component (Fig 20). A tubular Dacron graft of diameter equal to the average length of the free margins of the 3 aortic leaflets is selected. Three equidistant marks are made in 1 of its ends, and the scalloped shape of the suture line in the left ventricular outflow tract is tailored in the Dacron graft (Fig 20). These sutures are then passed from the inside to the outside of the Dacron graft. They must be equidistantly distributed, and a reducCurr Probl Surg, June 1999

459

FIG 19. Aortic root remodeling in patients with annuloaortic ectasia. Three aortic sinuses are replaced as illustrated in Figs 16 and 1Z Note the Dacron band below the sinuses used to correct the dilated aortic annulus. (From David TE. Remodeling of the aortic root and preservation of the native aortic valve. Op Tech Cardiac Thorac Surg 1996;1:44-56. Used by permission.)

tion in the diameter of the aortic annulus is accomplished underneath the commissures of the noncoronary leaflet (ie, the sutures are spaced closer together in the graft than they are spaced in the left ventricular outflow tract). The valve is placed inside the graft and all sutures are tied on the outside. Next, the 3 commissures are resuspended inside the graft and secured with horizontal mattress sutures of 4-0 polypropylene. These sutures are then used to secure the remnants of the aortic sinuses to the Dacron graft with a continuous in-and-out suture line. The coronary arteries are reimplanted in their respective sinuses.

Repair of the Aortic Valve in Aortic Dissections Patients with aortic dissections may have AI because of dilatation of the aortic root or detachment of 1 or more commissures of the aortic 460

Curr Probl Surg, June 1999

FIG 20. Reimplantation of the aortic valve for aortic root aneurysm with annuloaortic ectosia. Multiple sutures are placed all around the left ventricular outflow tract and then through a tailored Dacron graft. The aortic valve is placed inside the graft and sutures are tied on the outside. The three commissures are resuspended in the Dacron graft and remnants of the sinuses wall are sutured to graft. The coronary arteries are reimplanted in their respective new sinuses.

valve. If the aortic root is dilated but the leaflets are normal, remodeling of the aortic root is performed as described above. In the case of acute type A aortic dissection without aortic root aneurysm, resuspension of the detached commissures and replacement of the ascending aorta with a tubular Dacron graft of appropriate diameter sutured right Curr Probl Surg, June 1999

461

at the sinotubular restores normal aortic valve function. In cases of extensive dissection of the aortic sinuses, reimplantation of the aortic valve is an ideal operative procedure because all dissected tissues are excised and the aortic valve is secured within a tubular Dacron graft as described above (Fig 20). This technique is associated with a very low risk of bleeding along the proximal suture line in comparison with the remodeling procedure. Ten percent to 15% of patients with acute type A aortic dissection have a bicuspid aortic valve. This valve does not need to be replaced if the leaflets are normal and the root is not aneurysmal. However, if the root is dilated, we believe that composite replacement of the aortic valve and the ascending aorta is better than a valve-sparing procedure.

Subaortic Membranous Ventricular Septal Defect A subaortic membranous ventricular septal defect is often associated with prolapse of the right aortic leaflet and AI. Most surgeons repair the aortic valve by closing the ventricular septal defect with a patch and by plicating the free margin of the prolapsing right aortic leaflet. 63 Yacoub and colleagues64 recently described a technique that uses a transaortic approach whereby the subaortic membranous ventricular septal defect is closed primarily with multiple mattress sutures passed from the crest of the ventricular septum through the aortic annulus and into the thinned portion of the sinus of Valsalva. These stitches are supposed to elevate the aortic annulus of the right aortic leaflet and correct the AI. If this maneuver does not correct the prolapse entirely because the leaflet has become elongated, plication of the free margin is added.

Rheumatic Aortic Insufficiency Repair of the aortic valve in patients with rheumatic disease and severe AI is usually not possible without leaflet augmentation with glutaraldehyde-fixed autologous or bovine pericardium. 65 Rheumatic patients who need mitral valve surgery and have mild or moderate AI sometimes have enough leaflet tissue to correct the AI without leaflet augmentation. Commissurotomy, shaving the leaflets to make them thinner and more pliable, plication of the subcommissural triangles, and reduction of the diameter of the sinotubular junction are maneuvers used in these cases.

Results of Aortic Valve Repair for Aortic Insufficiency The results of aortic valve-sparing operations for dilated aortic root or ascending aorta and AI have been excellent.4°,66-68 There are 2 reports on premature failure of the reconstructed aortic root, but we believe those 462

Curr Probl Surg, June 1999

failures were the result of technical e r r o r s . 69,70 We have performed aortic valve-sparing operations in almost 200 patients. In our last report we described the outcomes of the first 126 patients. 67 Thirty-two patients had Marfan syndrome (8 with severe mitral insufficiency), 17 had chronic or acute type A aortic dissection, 23 had transverse aortic arch aneurysm, and 26 had coronary artery disease. The aortic valve repair consisted of simple adjustment of the sinotubular junction in 33 patients, remodeling of the aortic root in 60, and reimplantation of the aortic valve in 33. Fifteen patients also had prolapse of 1 aortic leaflet, which was repaired with Gore-tex sutures. There were 3 operative deaths. During a follow-up period that extended up to 117 months (mean, 31 months), the repair failed in only 2 patients. The freedom from AVR was 97% at 7 years. There were no differences in the outcomes of patients who had remodeling of the aortic root or reimplantation of the aortic valve. Yacoub and colleagues 66 reported their results with aortic root remodeling in 158 patients with ascending aortic aneurysms and AI, including 68 with Marfan syndrome. The actuarial survival at 10 years was approximately 80%, and the freedom from reoperation was 89%. Schafers and colleagues 68 compared the results of remodeling of the aortic root with those of reimplantation of the aortic valve in patients with aortic root aneurysm and found similar clinical and echocardiographic outcomes. Some investigators have expressed concerns regarding the appropriateness of preserving the aortic valve in patients with Marfan syndrome because they have abnormal fibrillin. 71,72 However, our experience 65 and that of Yacoub and colleagues 66 suggest that aortic valve repair in these patients is durable. Patients with myxomatous mitral valves also have abnormal fibrillin in the leaflets. 72 The experience with mitral valve repair in these patients indicates that recurrence of the prolapse is rare during the first decade of follow-up. 73 By analogy, stabilization of the aortic annulus and sinotubular junction with a properly tailored Dacron graft may prevent or retard the degenerative changes of the connective tissue of the aortic leaflets. Cosgrove and colleagues 74-76 demonstrated that incompetent bicuspid aortic valves could be repaired satisfactorily by a triangular resection of the leaflet with prolapse, resection of the raphe, and plication of the subcommissural triangles if the annulus was dilated. Those investigators recently reported their experience with 94 patients. 76 Most of their patients were men (93%), with a mean age of 38 years. The freedom from reoperation was 84% at 7 years. The only predictive factor for reoperation was residual AI after the repair. There were no operative or late deaths in that series. 76 Curr Probl Surg, June 1999

463

Resuspension of detached commissures during repair of acute type A aortic dissection has provided good long-term results in most patients77-79; however, most surgeons replace the aortic root and aortic valve when it is dilated. 79 We believe that the aortic valve can be spared in patients with dissection and root dilatation by use of a remodeling procedure or reimplantation of the aortic valve. The second procedure is ideal for patients with acute type A aortic dissection and a dilated aortic root because it is associated with a low risk of bleeding along the proximal suture line. A congenital subaortic ventricular septal defect is frequently associated with prolapse of the right coronary cusp and m][. 63'64'80 Patients with this lesion often undergo operation before reaching adulthood. Most surgeons have used the technique of closing the ventricular septal defect with a patch and plicating the free margin of the right cusp to correct its prolapse. 63,8° Trusler and colleagues 63 reported a freedom from aortic valve replacement of 85% at 10 years with use of the above technique. Yacoub and colleagues 64 recently reported a new approach to this syndrome in which the septal defect is closed primarily with the same sutures used to remodel the aortic annulus and the dilated sinus of Valsalva. These investigators described 46 patients with this syndrome. During a mean followup period of 8.4 years, only 5 patients required AVR. Aortic valve repair for AI caused by rheumatic disease is seldom feasible because the leaflets are often fibrotic, thickened, and fused. Thus patients with advanced rheumatic changes in the aortic valve are not candidates for aortic valve repair. Repair of these valves requires leaflet augmentation with glutaraldehyde-fixed autologous or heterologous pericardium. 65 This operative procedure has been performed since the early days of cardiac surgery. 81 This technique has been used largely in young rheumatic patients but most reports provide only short-term results. 65 The only rheumatic aortic valves we have repaired are in patients who need mitral valve surgery and who have moderate AI, and at surgery the leaflets are found to be mildly fibrotic but still pliable. We have occasionally shaved them to increase their pliability, but more often we simply plicate the subcommissural triangles and sinotubular junction to increase leaflet coaptation. These maneuvers seem to reduce or eliminate AI in patients with mild or moderate rheumatic involvement of the aortic valve. However, the long-term results appear to be disappointing according to a recent report by Bernal and colleagues. 82 These investigators followed up for almost 2 decades a group of 55 patients who underwent, at the time of mitral valve surgery, aortic valve repair for mild or moderate rheumatic aortic valve disease. The freedom from aortic valve deterioration at 20 years was 25%. 464

Curr Probl Surg, June 1999

We believe that aortic valve repair for AI should be reserved for straightforward cases with normal or minimally diseased leaflets in which the mechanism of AI is prolapse of a single leaflet, dilatation of the sinotubular junction, or dilatation of the aortic annulus. Aortic valve repair should also be performed in patients with bicuspid aortic valves with minimally dilated aortic roots in whom the AI is caused by prolapse of only 1 of the 2 leaflets. Patients with degenerative disease of the aortic valve with overstretched, thinned, and prolapsing leaflets and those with rheumatic disease with fibrotic and fused leaflets are better served by AVR.

Aortic Valve Replacement Types of Heart Valves for Aortic Valve Replacement A variety of biologic and mechanical valves is available for AVR. Biologic valves can be stented or stentless. Stentless biologic valves include the pulmonary autograft, aortic valve homograft, and aortic valve xenografts. Stented bioprostheses include glutaraldehyde-fixed porcine aortic valves and bovine pericardial valves. It is often difficult to decide which valve is best suited for an individual patient. Mechanical valves are very durable but require lifelong anticoagulation with warfarin sodium. AVR with mechanical valves is associated with a small but constant risk of valve thrombosis and thromboembolic and hemorrhagic complications. 83,84 The linearized rates for these valve-related complications for the most commonly used mechanical valves are shown in Figs 21 to 23. The risk of thrombosis of mechanical aortic valves is relatively low, ranging from 0% to 1.1% per year for an average of 0.2% per year in most series. 83,84 Thromboembolic complications (ie, stroke and transient ischemic attacks [TIA]) are more common. The linearized rates range from 0% to 5.1% per year in various reports, yielding a composite average of 2% per year.83,84The risk of major hemorrhagic complications ranges from 0% to 7.9% per year, a composite average of 2% per year.83,84 In a recent review of multiple reports on thrombotic, thromboembolic, and hemorrhagic complications of mechanical valves, we found a wide range of incidences for every type of valve with no statistical advantage of 1 valve over another. 83 Biologic valves do not require oral anticoagulation. The risk of thromboembolism with stentless biologic valves is very low. 45'46'85-90Stroke and TIA after AVR with pulmonary autografts and aortic homografts are rare. 85-9° Thromboembolic complications are uncommon with stentless porcine valves implanted in the subcoronary position. 45,91 Because these valves are usually implanted in elderly patients, strokes can occur but when Curr Probl Surg, June 3_999

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investigated they are often found to be unrelated to the bioprosthesis. 45 Porcine aortic roots and stented xenograft valves are associated with low thromboembolic rates. 2t,22,92-96 Sintek and colleagues 92 observed a higher thromboembolic rate early after implantation of porcine aortic roots in elderly patients and recommended low-level oral anticoagulation to avoid 466

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this complication. We have not anticoagulated patients who have had AVR with porcine roots and have not observed an increased risk of thromboembolic complications during the first few years after operation. Westaby and colleagues93 also reported a low risk of thromboembolism in these patients. Stented xenografts do not require oral anticoagulation in the aortic position and the risk of thromboembolism is l o w . 21'22'94-96 We believe that aspirin should be administered to these patients because it appears to reduce the risk of stroke and T I m . 97 The combined risk of stroke plus TIA in patients with stented xenograft aortic valves ranges from 1.1% to 1.8% per year, although these valves are usually used in older patients. 21,22,94-97 The major drawback of biologic valves is their limited durability, particularly in young patients. The pulmonary autograft conceivably could be a permanent aortic valve in patients who need AVR, but clinical experience varies and the results have not been perfect. 85-87,98 In addition, these patients have a semilunar homograft valve in the pulmonary position that is likely to fail with time. Ross and colleaguesY who have the longest experience with this procedure, reported a freedom from reoperation rate on the pulmonary autograft of 75% and on the homograft in the pulmonary position of 80% at 20 years. Elkins and colleagues 86 reported a freedom from reoperation rate on the pulmonary autograft of 89% at 8 years in 146 children. Stelzer and colleagues 98reported a freedom from reoperation rate of 88.6% at 7 years in a group of 145 patients with a mean age of 43 years. Curr Probl Surg, June 1999

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Grunkemeier GL, Bodnar E. Comparison of structural valve failure among different "models" of homograft valves. J Heart Valve Dis 1994;3:556-60. Used by permission.)

Aortic valve homografts may not be more durable than stented glutaraldehyde-preserved xenograft valves. 99 Grunkemeier and Bodnar99 reviewed the results of the published series on AVR with homografts prepared and implanted by different methods and found a wide variation in the probability of tissue degeneration. Fig 24 shows the freedom from valve degeneration after AVR with a homograft. 99 Those investigators also reported on the freedom of valve degeneration after AVR with stented xenograft valves (Fig 25). Yacoub and colleagues 89 reported a freedom from reoperation rate of 91% at 10 years after AVR with a homograft. Those investigators found that the determinants of degeneration of the aortic valve homograft were age (P = .007) and previous AVR with a xenograft valve (P = 0.05). Doty and colleagues 88reported a freedom from valve explantation rate of 92% at 10 years. McGriffm and colleagues ~°° found that the probability of reoperation after AVR with an aortic homograft is similar to that of stented xenograft valves in patients older than age 60 years but it was much lower in younger patients. The freedom from primary tissue failure of various stented xenograft valves is shown in Fig 25.99 Age is the principal determinant of primary tissue failure in these valves. 2294-96,101 In a recent review of clinical outcomes after AVR with the Hancock II bioprosthesis at 12 years, we found a free468

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dom from primary tissue failure rate of 100% in patients older than age 65 years and a rate of 86% in younger patients. 22,1°I Similar results have been reported with the Carpentier-Edwards pericardial valve. 21,]°2 Banbury and colleagues21 reported a freedom from primary tissue failure rate of 96% at 12 years in patients older than 65 years and of 86% in younger patients. The durability of stentless porcine aortic valves remains unknown because of limited follow-up periods in most reports. 45,46,91-93 However, AVR with stentless porcine valves is a more complicated operation than AVR with stented bioprostheses and reoperations may occur more often because of the learning curve with those procedures. In addition, poorly aligned commissures and leaflets of a stentless valve may increase mechanical stress and actually cause premature tissue degeneration.45 Two independent prospective randomized clinical trials comparing the Hancock porcine bioprosthesis with the Bj6rk-Shiley valve showed that the type of valve had no effect on the long-term survival rate after AVR. 1°3,1°4 Although it is possible that stentless biologic valves may enhance survival after AVR because of their superior hemodynamic performance, 1°5 this remains unproved, and this argument should not be entered in the decisionmaking process about the type of valve for AVR in an individual patient. Curr Probl Surg, June 1999

469

Patients must be informed of the pros and cons of mechanical and biologic valves. Ideally, the patient should decide what type of valve he or she wishes to have. The patient must accept the responsibility of taking warfarin sodium permanently if he or she chooses to have a mechanical valve or accept the probability of valve failure and reoperation if he or she chooses a biologic valve. Unfortunately, surgeons and cardiologists often have their own bias toward 1 or another type of valve and they are the ones often responsible for selecting the type of valve for AVR because most patients leave this decision to their physicians. This is a serious and often difficult decision to make.

Hemodynamic Performanceof ProstheticHeart Valves Prosthetic heart valves (ie, mechanical and stented bioprostheses) are obstructive and cause transvalvular gradients after AVR. In most patients with these valves the mean systolic gradients range from 15 to 25 mm Hg at rest. However, in certain patients the gradients can be much higher, particularly during exercise. 1°6-n2 Patients with high transvalvular gradients after AVR are said to have prosthesis-patient mismatch. 113-116 Pibarot and colleagues u4 defined prosthesis-patient mismatch to be present when the effective valve orifice index was <0.85 cm2/m2. To avoid prosthesis-patient mismatch, the largest possible prosthetic heart valve should be implanted in the aortic position. However, this is not possible in patients with a small aortic root, and a patch enlargement of the aortic annulus is often necessary. 117-121 Because patch enlargement of the aortic annulus may increase the operative mortality rate for AVR, 121 most surgeons have been reluctant to perform this additional procedure and prefer to implant small prosthetic valves. 122-124Their argument is that size of the prosthetic valve has no effect on the long-term results ofAVR.122-125 Sawant and colleagues 192reported on a series of 104 patients, mostly women, with a mean age of 66 years who underwent AVR with a St. Jude Medical valve of 19 mm. The follow-up was 100% complete and the authors reported extremely low rates of valve-related complications (linearized rates of 0.3% for paravalvular leak, no mention of endocarditis, 0.85% for hemorrhagic complications, and only 0.4% for thromboembolism) and spectacular functional results (most patients were in New York Heart Association functional class I and 11). Medallion and colleagues 124 compared the results of AVR with 19 mm valves with larger ones in an octogenarian population. Although the operative mortality rate was higher for the patients receiving 19 m m valves (12.5% vs 7.7%), the difference did not reach significance. 124 The size of valve had no effect on the long-term survival rate either. 124 Other investigators have found that small valves have a detrimental effect on the operative and late survival 470

Curr Probl Surg, June 3_999

rates. 106,107,126,127 Unfortunately,

there has been no randomized clinical trial in patients with a small aortic annulus who need AVR. We compared the clinical outcomes of AVR in patients who had patch enlargement with those who did not and could not find an obvious benefit of patch enlargement of the aortic annulus, t21 Other investigators claim that patch enlargement of the aortic annulus had a beneficial effect on the functional result of A V R ) °7'118-12° Mismatch has been associated with a lack of symptomatic improvement but has not had a statistically significant effect on the survival rate during the first 5 years after AVR.115 However, in a long-term study by He and colleagues 126 on 404 patients who underwent AVR with small aortic prostheses (<21 mm), mismatch was found to be an independent predictor of late mortality by multivariate analysis. In addition, data from Lund and colleagues 127indicated that suboptimal hemodynamic results after AVR increased the mortality rate from sudden death and congestive heart failure. The left ventricular mass regresses after AVR. 128-136 DePaulis and colleagues 13° measured transvalvular gradients and left ventricular mass by echocardiography before and 1 year after AVR with various types of stented and stentless valves. Although the mean transvalvular gradients were lower in patients with stentless than in those with stented valves, left ventricular mass and interventricular septal thickness decreased in all patients but remained abnormal after the first year after operation. ~30It is possible that it takes longer than 1 year for resorption of the increased amount of connective tissue that is present in the hypertrophic myocardium. We have observed in AVR with stentless porcine aortic valves that the left ventricular mass continues to decline up to the fifth postoperative year) 35A36 Stentless biologic valves have excellent h e m o d y n a m i c performance.90,91,~35,136A pulmonary autograft leaves practically no residual gradient across the left ventricular outflow tract and it is an ideal valve substitute for athletes, children, and young adults from the hemodynamic standpoint. 134 Stentless porcine aortic valves have similar hemodynamics to aortic valve homografts) 31,133 These valves are minimally obstructive and leave mean transvalvular gradients below 10 mm Hg in most patients. 45,9~,~3z-~36In addition, left ventricular function after AVR is probably better with a stentless valve than with a stented one. ~32,~33 This improvement in left ventricular function may have a beneficial effect on the late survival rate. 1°5 In a case-match study of AVR with the Hancock II and the Toronto SPV bioprostheses, we found an enhanced late survival rate with the stentless valve.~°5 There are several prospective randomized clinical trials on AVR with stented versus stentless bioprostheses in progress, and we will learn whether a hemodynamically superior valve has a positive effect on the survival rate. Curr Probl Surg, June "1999

471

Operative Techniques Aortic Valve Replacement With Mechanical and Stented Bioprostheses The aortotomy to expose the aortic valve can be oblique or transverse and should be 2 to 3 cm above the level of the right coronary artery. The diseased aortic valve is excised. Calcific deposits in the aortic annulus, anterior leaflet of the mitral valve, and interventricular septum should be debrided completely until soft tissue is encountered. An aggressive debridement is important to prevent prosthetic valve dehiscence and also to allow a larger valve to be implanted. If the aortic annulus or anterior leaflet of the mitral valve is disrupted during debridement, a small patch of autologous pericardium should be sutured around the defect with a continuous polypropylene suture. Care must be exercised to prevent calcium debris from entering the ventricular cavity and embolizing later. It has been our practice to perform a septal myectomy in patients with a hypertrophic interventricular septum that protrudes into the left ventricular outflow tract. We believe this maneuver decreases the systolic gradient after AVR. The diameter of the aortic annulus should be measured with the sizer provided by the manufacturer of the valve to be used because of size variation among different valves. 137'138 We believe that mechanical valves are best secured to the aortic annulus with multiple simple interrupted 2-0 polyester sutures. These sutures should be spaced 4 to 5 mm apart. A total of 20 to 25 sutures are used. Mechanical valves can also be secured to the aortic annulus with the use of multiple interrupted horizontal mattress sutures with pledgets. The pledgets can be left on the ventricular or the aortic side of the annulus. If they are left on the ventricular side of the annulus, care must be exercised to prevent the pledgets from interfering with the disc of the valve. Stented xenograft valves should be secured to the aortic annulus with interrupted pledgeted sutures, leaving the pledgets on the ventricular side of the aortic annulus. There is no evidence that any orientation is better than another when a bileaflet mechanical valve is implanted. However, when a single disc valve is implanted, the largest opening should be oriented toward the noncoronary sinus of Valsalva. This orientation is supposed to offer the lowest resistance to flow. Patients with aortic valve disease, particularly those with a bicuspid aortic valve, may have aneurysms of the ascending aorta. If the aortic sinuses are normal, a supracoronary replacement of the ascending aorta is performed. If the aortic sinuses are dilated, composite replacement of the aortic valve and ascending aorta should be performed. 472

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FIG 26. Aortic root replacement with a valved conduit containing a mechanical valve. The valve is secured to the aortic annulus with inverted horizontal mattress sutures with pledgers.

Aortic root replacement can be performed with commercially available valved conduits or the surgeon can make one in the operating room. I believe that both coronary arteries should be detached from their aortic sinuses and mobilized to allow a tension-free anastomosis after reimplantation in the Dacron graft. When mechanical valves are used for root replacement, the valved conduit should be secured to the aortic annulus with multiple interrupted horizontal mattress sutures with pledgets. The pledgets should be left on the outside of the aortic annulus (Fig 26). When stented porcine or pericardial valves are used, they should be secured to the Dacron graft a few millimeters above the anastomosis between the Dacron and the aortic annulus (Fig 27). This technique permits future rereplacement of the bioprosthesis without taking down the coronary arteries from the Dacron graft.

Aortic Valve Replacement With StentlessBiologic Valves There are various techniques to implant stentless biologic valves. They are technically more demanding than AVR with stented valves and the surgeon must have a good knowledge of the functional anatomy of the semilunar valves. The key concept to know during implantation of these valves is that the diameter of a semilunar valve annulus and the diameter Curr Probl Surg, June 1999

473

FIG 27. Aortic root replacement with a stented xenograft valve sutured inside a Dacron graft. Note that the bioprosthesis is secured to the Dacron graft above the aortic annulus-graft anastomosis.

of its sinotubular junction are a function of the size of the leaflets. Mismatch between the size of the leaflets of the donor valve and the size of the aortic root of the recipient causes AI and premature failure of the stentless biologic valve. This is 1 of the reasons aortic valve homografts fail prematurely. Stentless biologic valves do not necessarily have the same geometry as the recipient's aortic root. Therefore, to compensate for these differences, tailoring of the aortic root during implantation of stentless biologic valves is often necessary. Pulmonary Autografl. The selection of technique for implantation of the pulmonary autograft should be made intraoperatively. A generous ~ansverse aortotomy is performed 2 to 3 cm above the level of the origin of the right coronary artery. The diseased aortic valve is excised. The diameters of the aortic annulus and the sinotubular junction are measured. A transverse pulmonary arteriotomy is made and the pulmonary leaflets are carefully inspected for abnormalities. If the valve is normal, the pulmonary root is excised. Care must be taken to avoid damage to the first septal perforator artery. The diameter of the sinotubular junction of the pulmonary root is measured. The pulmonary annulus is assumed to be 10% to 15% larger in diameter. If the aortic annulus has similar dimensions, a subcoronary implantation of the pulmonary autograft can be performed. The pulmonary autograft is sutured to the left ventricular outflow tract with multiple interrupted simple 4-0 polyester sutures (Fig 28). The pulmonary annulus should lie at the same level as the aortic annulus after this layer of sutures is tied down. The pulmonary arterial wall immediately above each commissure of the autograft is suspended and sutured to the aortic root with horizontal mattress sutures of 5-0 polypropylene with small pledgets. The left and right sinuses of the autograft are partially excised and their remnants are sutured to the aortic sinuses with a continuous 474

Curr Probl Surg, June 1999

f IJ

FIG 28. Aortic valve replacement with a pulmonary autografl with the use of the subcoronary implantation technique. The right and left aortic sinuses of the pulmonary root are excised and the remnants are sutured to the recipient's aortic sinuses. The noncoronary aortic sinus of the pulmonary autografl is left intact.

5-0 polypropylene suture. The noncoronary sinus of the autograft is left intact, and the arterial wall of the pulmonary autograft immediately above its sinotubular junction is sutured to the aortic wall. After completion of the implantation, the spatial relationship of the 3 commissures must be the same as when the pulmonary autograft functioned as a pulmonary valve. The pulmonary autograft can also be implanted with the use of the root inclusion technique. The arteriotomy can be extended into the nonCurr Probl Surg, June 1 9 9 9

475

FIG 29. Aortic valve replacement with a pulmonary autografl by use of the root inclusion technique. Openings are made in the right and left aortic sinuses of the pulmonary root and these sinuses are sutured around the coronary artery orifices.

coronary aortic sinus to increase exposure of the aortic annulus and coronary artery orifices. The pulmonary autograft is sutured to the left ventricular outflow tract as described above. Its 3 commissures are suspended with horizontal mattress sutures, but the sutures are not tied (Fig 29). A round opening is made in the left sinus of the autograft at the level of the left coronary artery orifice and the sinus wall of the pulmonary autograft is sutured to the sinus wall around the left main coronary artery with a continuous 5-0 polypropylene suture. The right coronary artery is attached to the autograft with the same technique. The 3 commissural stitches are tied and the pulmonary arterial wall immedi476

Curr Probl Surg, June 1999

ately above its sinotubular junction is sutured to the aortic wall. The extended aortotomy into the noncoronary aortic sinus is left opened until the aorta is unclamped and hemostasis along all suture lines is secured. Implantation of the pulmonary autograft with the root inclusion technique may prevent dilatation of the pulmonary sinuses that have become aneurysmal in a small proportion of patients who had a congenital bicuspid aortic valve and AI. Finally, the pulmonary autograft can be used for complete aortic root replacement. In this case the coronary arteries are detached from the aortic root and reanastomosed to the pulmonary root after it is sutured to the aortic annulus (Fig 30). The fixation of the pulmonary root to the aortic annulus is done as described above. Some surgeons use either a strip of Teflon felt or autologous pericardium to buttress this suture line. We use the remnants of the aortic sinuses to cover the suture line between the autograft and left ventricular outflow tract by suturing the aortic sinuses to the adventitia of the pulmonary autograft. The autograft is sutured to the ascending aorta in an end-to-end fashion. If the diameter of the aortic annulus is larger than the calculated diameter of the pulmonary annulus by 3 mm or more, plication of the aortic annulus should be performed before the autograft is sutured to the left ventricular outflow tract.139 This annular reduction can be easily accomplished by plicating the fibrous triangles underneath the commissures of the noncoronary aortic sinus (Fig 31). If the diameter of the ascending aorta is larger than the diameter of the sinotubular junction of the pulmonary autograft by 3 mm or more, the ascending aorta should be reduced to the diameter of the pulmonary autograft in the anastomotic area (Fig 30). In patients with a bicuspid aortic valve and dilated ascending aorta to more than 40 mm, it may be safer to replace or wrap the ascending aorta with a tubular Dacron graft. If the Dacron graft is sutured to the pulmonary autograft, the diameter of the graft must not exceed that of the sinotubular junction of the pulmonary autograft at the level of the anastomosis (Figs 7 and 12). Continuity between the right ventricular outflow tract and the pulmonary artery is re-established with a valved conduit. Aortic and pulmonary valve homografts are ideal for this reconstruction. A pulmonary valve homograft may be more durable than an aortic homograft. 14°,m We perform the distal anastomosis first. Both proximal and distal anastomoses are performed with continuous 4-0 polypropylene sutures (Fig 30). Aortic Valve Homografl. Aortic valve replacement with an aortic valve homograft can be performed with the use of 1 of the 3 techniques described above. Unlike the pulmonary valve annulus, which is attached entirely to Curr Probl Surg, June 1999

477

FIG 30. Aortic root replacement with a pulmonary autograft.

thin right ventricular muscle, which is very distensible, the aortic valve homograft annulus is attached to fibrous structures in 55% of its circumference and to interventricular muscle in 45%. For this reason the aortic valve homograft is more forgiving as far as discrepancies in diam478

Curr Probl Surg, June 1999

FIG 31. Reduction of the diameter of the aortic annulus by plic'ation of the subcommissuraltriangles of its noncoronary portion.

eter between the donor and recipient aortic roots. However, to obtain perfect functional results, the diameter of the aortic annulus of the recipient should be reduced if the difference is greater than 2 mm. The aortic homograft can be secured to the left ventricular outflow tract with interrupted or continuous sutures. I believe that an aortic valve homograft should be implanted in its anatomic orientation (ie, the annulus and sinuses of the homograft should be oriented in the same direction as the native aortic valve). Stentless Porcine Aortic Valves. There are 2 commercially available stentless porcine aortic valves in North America: the Medtronic Freestyle valve (Medtronic, Minneapolis, Minn) and the Toronto SPV valve (St Jude Medical, St Paul, Minn). The Medtronic Freestyle valve is an intact porcine aortic root and can be implanted with the same operative techniques described above for the pulmonary autograft. The Toronto SPV valve is a scalloped porcine valve that can be used only for subcoronary implantation. This valve was designed in such a way that its external diameter is like a cylinder (ie, the external diameter at the level of the aortic annulus is the same at the level of the sinotubular junction). Thus, after its implantation, the diameter of the sinotubular junction of the patient must be identical to the diameter of the valve used. If the sinotubular junction of the patient is larger, it should be reduced to that of the Toronto SPV bioprosthesis. Curr Probl Surg, June 1999

479

Results of Aortic Valve Replacement

Operative Mortality The operative mortality rate for AVR in large series ranges from 1% to 8%. 21'22'45'57'94-96'101'102 The following factors have been associated with increased operative risk in these series: advanced age, female gender, emergency operation, left ventricular dysfunction, coronary artery disease, New York Heart Association functional class IV, active infective endocarditis, previous valve replacement, and renal dysfunction. 94-96'101'102'142"146 Elective isolated AVR in a middle-aged patient without comorbidities carries an operative mortality rate of 1%, whereas AVR together with coronary artery bypass in an elderly patient with unstable angina, impaired left ventricular function, and increased creatinine levels carries an operative mortality rate in excess of 10%. The operative mortality rate for composite replacement of the aortic valve and ascending aorta in experienced hands is not higher than for AVR. 42'147 The operative mortality rate in the International Registry of the Ross Procedure was 3.1 t7~.134 The operative mortality rate for AVR with aortic homografts and stentless porcine valves has been reported from 1% to 3 o~.45,46.88,90-93,148

Postoperative Complications In spite of improved methods of myocardial preservation during aortic cross-clamp periods, 149.15°low cardiac output after AVR occurs in approximately 10% of patients. 151 This may be the result of inadequate myocardial protection, perioperative myocardial infarction, right ventricular dysfunction, an obstructive aortic valve prosthesis, and systolic anterior motion of the mitral valve. Intraoperative transesophageal echocardiography is extremely helpful in the management of these patients because it often determines the reason for the low cardiac output syndrome. Patients with severe triple-vessel coronary artery disease are at a higher risk of inadequate myocardial protection and perioperative myocardial infarction. 151 Retrograde cardioplegia is useful in these cases, but it does not solve the problem entirely. 149-152Most patients with a bicuspid aortic valve have a nondominant right coronary artery, and delivery of cardioplegia to protect the right ventricle may be difficult by antegrade or retrograde routes, iSl.lS2Mechanical problems with the right coronary artery may also be the cause of low output syndrome after aortic root surgery. ~53 Small prosthetic aortic valves are obstructive and have been associated with higher operative mortality rates.151,154We have had to reoperate on several patients who had intractable congestive heart failure soon after AVR 480

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because of high transvalvular gradients. We also have had 5 cases of severe systolic anterior motion of the mitral valve (SAM) with obstruction of the left ventricular outflow tract and mitral regurgitation after isolated AVR. All 5 patients had severe concentric left ventricular hypertrophy and had undergone AVR with stentless biologic valves. None of the patients had asymmetric septal hypertrophy. Three patients were treated with a ~blocker and vasopressor and 2 required myectomy because they could not be separated from cardiopulmonary bypass. All 5 patients survived and the SAM decreased and eventually disappeared as the ventricular hypertrophy regressed. Postoperative bleeding has been reduced with the routine use of antifibrinolytic agents, but it is still a problem in patients undergoing complex reoperative aortic valve or aortic root surgery, in those with active endocarditis with aortic root abscess, and in cases requiring prolonged cardiopulmonary bypass. Transfusion of platelets, cryoprecipitate, and freshfrozen plasma is often needed in patients with coagulopathy. Stroke is a devastating complication of cardiac surgery. The incidence of stroke during valve surgery has decreased during the past 2 decades. 155 In a retrospective review of 5954 consecutive patients undergoing heart valve operations at our institution, the incidence of stroke decreased from 3.8% in the early 1980s to 2.6% in the mid-1990s) 55 Infective endocarditis, age greater than 74 years, urgent surgery, concomitant coronary artery bypass surgery, and reoperations were independent predictors of perioperative stroke. ]55 The principal cause of stroke during AVR is embolization of atherosclerotic, calcified, or septic debris. Meticulous operative technique and extreme care in handling diseased tissues reduce the risk of stroke. Sternal wound infection is a largely preventable complication of cardiac surgery, but it continues to occur in a small proportion of patients. In a retrospective review of 12,267 patients who had open-heart surgery through a median sternotomy, the incidence of deep sternal wound infection was 0 . 7 5 % . 156 The incidence of this complication was slightly higher in patients who had concomitant coronary artery bypass than in those who had isolated valve surgery. An additional 0.82% of the patients had superficial wound infection in our unit. Complete heart block occurs in approximately 3% to 5% of patients after AVR. 151 The incidence of this complication is much higher in reoperative AVR and in complex reconstructions of the aortic root and left ventricular outflow tract to treat patients with aortic root abscess or a small aortic annulus) 57 Postcardiotomy syndrome or pericarditis is common after AVR in young patients, particularly when homograft valves are implanted. Aspirin or Curr Probl Surg, June 1999

481

other anti-inflammatory agents decrease the symptoms and may prevent the development of pericardial effusion. Occasionally the effusion causes pericardial tamponade and requires drainage. Thrombosis of prosthetic aortic valves is rare. 83,84 The average linearized annual rate of prosthetic aortic valve thrombosis in various series is 0.2%. 83'84 Thrombosis of prosthetic mitral valves is more common than thrombosis of prosthetic aortic valves. 158-161 Thrombosis of a prosthetic valve is often the result of inadequate anticoagulation. 159Although thrombolysis is often effective in these patients, rethrombosis and embolization are serious problems associated with this form of treatment. 158-16° Thrombolysis should be reserved for critically ill patients who are poor surgical candidates. 16° Therefore patients with thrombosis of the aortic valve should undergo operation, and valve rereplacement is better than simple surgical thrombectomy.161 Patients with prosthetic aortic valves, including those with pulmonary autografts and aortic valve homografts, have a small but constant risk for development of infective endocarditis. 21.22,87-96,98,1°1,1°2The reported incidences of infective endocarditis are (1) with mechanical valves 0.24% to 1.4% per year, 109,123,143,144,162 (2) with stented bioprostheses 0.5% to 0.8% per year, 21,22,94-96,1°1A°2 (3) with stentless bioprostheses 0.2% to 0.4% per year, 45,91,93 (4) with aortic homografts 0.2% to 0.5% per year, 88-9°,148 and (5) with pulmonary autografts 0% to 0.5% per year. 86,87,98.139 Although appropriate antibiotics alone may sterilize an infected prosthetic aortic valve, operation is often necessary (see below). Paravalvular leakage occurs in a small percentage of patients who had AVR. 21'22A23'143 Patients with a heavily calcified aortic annulus, aortitis, or other connective tissue disorders are more likely to have paravalvular leakage. If a leakage is detected intraoperatively by Doppler echocardiography, it should be corrected because even small leakages may progress or may cause hemolysis. Late valve dehiscence is usually caused by inadequate debridement of calcium from the aortic annulus or by endocarditis.

Survival After Aortic Valve Replacement Survival after AVR is highly dependent on the patient's variables such as the age at the time of operation, gender, preoperative functional class, left ventricular function, the presence of coronary artery disease, and noncardiac comorbidities. ~°1 Table 2 shows the probability of survival at 5 and 10 years after AVR in various subsets of patients according to cardiac comorbidities. The 10-year actuarial survival rate ranged from 84% for a young patient with isolated aortic valve disease to 43% for an older 482

Curr Probl Surg, June 1999

TABLE 2. Survival probability calculated from accelerated time failure model with the use of log-logistic distribution for combinations of risk factors

Coronary artery disease

Age _>65 y

NYHA class IV

LV grades 3 or 4

89.1 83.4 84.5 83.6

¢" / •/

./ ¢" ,/ ,/

,/ ,/ ,/ / ,/

,/ ,/ /

,/ / ,/ ,/

/ ,/ ,/ ./ ,/

Predicted survival at 5 y (%)

¢" ./ ,/ / ,/

(73-100) (70-97) (71-98) (70-97)

Predicted survival at 10 y (%) 83.9 76.2 77.7 76.6

(73-95) (674]5) (69-86) (6885)

82.3 (69-96)

74.8 (66-84)

77.1 75.9 74.1 77.4 75.7 74.5 67.8 65.7 66.2 54.6

68.2 66.8 64.6 68.6 66.5 65.1 57.4 55.0 55.5 43.5

(6688) (65-87) (63-85) (66-88) (65.-86) (6485) ( 59-77) (57-75) (57-75) (47-62)

(61-75) (60-74) (58-72) (62-76) (59-74) (58-72) (52-63) (49-61) (5061) (39-48)

Each of these 4 risk factors was entered into the model as a dichotomous variable (ie, New York Heart Association class IV vs classes i, II. or III; left. ventricular grades 3 or 4 vs grades i or 2). These 4 risk factors are not present for the first row of estimates. Upper and lower 95% confidence intervals for predicted survival probabilities are given in parentheses. NYHA,New York Heart Association; LV, left ventricular; J, risk factor is present. (From Cohen G, David TE, Ivanov J, Armstrong S, Feindel CM. The impact of age, coronary artery disease, and cardiac comorbidity on late survival aRer bioprosthetic aortic valve replacement. J Thorac Cardiovasc Surg 1999;117:273-84. Used by permission.)

patient who is functionally class IV with impaired left ventricular function and coronary artery disease.l°1

Aortic Valve Endocarditis Infective endocarditis requires early diagnosis because it almost invariably leads to devastating complications and death if it is not treated properly. Although a myriad of micro-organisms can cause infective endocarditis, gram-positive cocci are responsible for the majority of cases. Staphylococcus aureus has become the most common organism, followed by Streptococcus viridans. 163'164 Staphylococcus is an extremely virulent bacteria that can cause endocarditis in normal heart valves. Prosthetic valve endocarditis has been arbitrarily classified as early when it occurs within the first 60 days after operation and late when it occurs after 60 days. 165 However, it is possible that many cases of endocarditis that occur during the first year after valve operation are acquired at the time of the operation. 166,167 Early infection is usually caused by contamination of the aortic valve at the time of operation or by perioperative bacteremia. S aureus, Staphylococcus epidermidis, and Enterococcus faecalis are among the most common micro-organisms in early prosthetic valve endoCurr Probl Surg, June 1 9 9 9

483

carditis.157.165-168 The sources of late prosthetic valve endocarditis are more difficult to determine. Bacteremia is probably the main cause of late prosthetic endocarditis. Streptococci and staphylococci are the most common micro-organisms in late prosthetic valve endocarditis. ~57,165-~68 Doppler echocardiography is an extremely useful tool in the diagnosis and management of infective endocarditis. 169 Echocardiography can detect vegetations as small as 1 to 2 rnm in size, but it is more reliable in native than in prosthetic valve endocarditis. It is also more accurate in biologic than in mechanical valves because of the acoustic shadowing and motion of the mobile components of the mechanical heart valves. Echocardiography is highly sensitive for the detection of paravalvular abscesses and cardiac fistulas. 170 Administration of appropriate antibiotics is the most important element in the treatment of infective endocarditis. Whenever the diagnosis is suspected, several blood cultures should be obtained and antibiotic therapy should be started immediately. Once the micro-organism has been identified by blood cultures and its sensitivity to specific antibiotics is known, the antibiotic therapy should be adjusted accordingly. Two or 3 antibiotics that potentiate each other are often needed for the treatment of endocarditis. Antibiotics alone can eradicate the infection in many patients with native aortic valve endoCarditis. 163"164 However, depending on the duration of the disease before the diagnosis is made and on the virulence of the micro-organism, large vegetations or abscess formation can develop and antibiotics alone become inadequate to eradicate the infection. Antibiotics and phagocytes cannot penetrate large vegetations (>1 cm) or paravalvular abscesses. Consequently, these patients require operation to cure the infection. 157"J63.164,168A71 Early operation is also recommended for aortic valve endocarditis caused by S aureus, Pseudomonas aeruginosa, Serratia marcescens, and fungi because these micro-organisms are extremely virulent and cause extensive damage to the aortic valve leaflets and paravalvular structures or form large vegetations (fungi) with systemic embolization, tSv.163,t64,168 Prosthetic valve endocarditis is also best treated by early operation. 168,172,173 Late prosthetic valve endocarditis in biologic valves often behaves like native valve endocarditis and the infection usually begins on the leaflets. For this reason, antibiotics can be effective in eradicating the infection. Early prosthetic valve endocarditis in biologic valves can start on the leaflets or on suture lines and the aortic annulus and often requires surgical intervention. Antibiotics alone seldom cure infective endocarditis in patients with mechanical Valves. 172'173 Patients with infective endocarditis must be monitored closely for signs of valve dysfunction, heart failure, embolization, and persistent infection. Operation is justifiable in most patients with mechanical 484

Curt Probl Surg, June 1999

valves or with any valve with large vegetations (>1 cm), and with certain micro-organisms such as S a u r e u s . Vegetations can embolize and cause metastatic abscesses. Anticoagulation is not effective in preventing embolization of vegetations and is associated with increased risk of neurologic complications. 174,175Patients with evidence of cerebral embolization should have a computerized tomography scan or magnetic resonance images of the brain to evaluate for ischemic or hemorrhagic s t r o k e . 174-176 Cerebral angiography may be warranted in patients with hemorrhagic stroke. 176 If possible, operation should be delayed for 2 or 3 weeks in patients with hemorrhagic stroke. There is no need to delay operation in patients who have had an ischemic stroke.

Surgery for Infective Endocarditis of the Aortic Valve Patients with infection limited to the leaflets of the native or a biologic aortic valve are treated by valve replacement. 157Any valve substitute can be used in patients with aortic valve endocarditis. Aortic valve homografts and pulmonary autografts are believed to be superior to bioprosthetic and mechanical valves, but no randomized clinical trial has ever been carried OUt 177-179

Patients with aortic root abscess or aortic fistulas require radical resection of all infected tissues. 157'~8°n83Aortic valve homografts are ideal valved conduits for these patients. ~82-~84The anterior leaflet of the mitral valve of the aortic valve homograft can be used to patch a defect in the left ventricular outflow tract created by the radical resection of the abscess. Radical resection is, however, far more important than the type of valve used. 157We have obtained very good results with operation for aortic root abscess by adopting an approach of radical resection of the abscess and reconstruction of the left ventricular outflow tract and surrounding structures with fresh autologous or glutaraldehyde-fixed bovine pericardium and by use of mechanical or bioprosthetic valves. ~57'185 Aortic valve homografts are probably more forgiving if the abscess is not extirpated entirely, but it cannot be sutured to necrotic or friable tissues, t84 Abscess limited to the aortic annulus can be treated by wide excision of the involved portion of the annulus and reconstruction with a patch of fresh autologous pericardium (Fig 32). Any type of heart valve can then be secured to the unaffected part of the aortic annulus and patch. ~68 More extensive abscesses may extend into the surrounding structures and rupture into the left atrium, pulmonary artery, right ventricle, or right atrium. These abscesses require more radical resection and reconstruction with multiple pericardial patches (Fig 33). The infection in patients who had previous aortic root replacement with Curr Probl Surg, June 1999

485

FIG 32. Abscess localized in the aortic annulus (A] is widely excised (B). Aortoventricular continuity is re-establishedby suturing a patch of autologous pericardium to healthy tissues around the defect (C).

a mechanical valve in a Dacron tube is always located in the suture line between the aortic annulus and the valved conduit. ~81 The graft is completely removed and the abscess is radically excised. Defects in the surrounding structures and in the left ventricular outflow tract can be repaired with flesh autologous or glutaraldehyde-fixed bovine pericardium, and a new valved conduit can be implanted (Fig 34). Aortic valve homografts are ideal in these circumstances. The coronary arteries may have to be extended with a short 8-ram tubular Dacron graft if they cannot be mobilized for reimplantation into the new valved conduit. If an aortic valve homograft is used, extension of the coronary arteries with saphenous veins may be preferable. The aortic root abscess may extend into the intervalvular fibrous body and mitral valve, t86.187 After removal of the native or prosthetic aortic valve, the aortotomy is extended into the intervalvular fibrous body and dome of the left atrium to expose the mitral valve (Figs 35 and 36). The abscess is radically excised and the mitral valve is repaired or replaced. A double patch of glutaraldehyde-fixed bovine pericardium is sutured to the mitral valve (to the anterior leaflet if it was repaired or to the sewing ring of a prosthetic valve if it was replaced) and to the lateral and medial fibrous trigones and aortic root (Figs 37 to 39). The outer patch is used to close the dome of the left atrium and the inner patch is used to reconstruct the aortic root. If an aortic valve homograft is used, the anterior leaflet of the mitral valve of the homograft replaces the native intervalvular fibrous body. Patients with aortic root abscess who had extensive reconstruction of the left ventricular outflow tract may have development of heart block and need a permanent pacemaker. We normally wait 1 week before implanting a permanent transvenous pacemaker in a patient who had an operation for active endocarditis, to make sure the infection has been eradicated. 486

Curr Probl Surg, June 1999

FIG 33. Reconstruction of the left atrial wall, anterior leaflet of the mitral valve, and aortic root after excision of an aortic root abscess.

FIG 34. Circumferential reconstruction of the aortic annulus and left atrium after excision of an infected valved conduit.

Cerebral, splenic, hepatic, and other metastatic abscesses rarely require surgical treatment. ~57,~68,tSH85 Large abscesses may have to be drained and splenectomy should be performed because of the risk of rupture. 187 Patients who have had operation for active infective endocarditis of the aortic valve need antibiotic therapy for 6 weeks from the start of the therapy. Curr Probl Surg, June 1 9 9 9

487

s

~

~

FIG 35. Reconstructionof the intervalvular fibrous body. The aortic valve is excised and the aortotomy is extended into the mitral valve and dome of the left atrium. (From David TE, Kuo J, Armstrong S. Aortic and mitral valve replacement with reconstruction of the intervalvular fibrous body. J Thorac Cardiovasc Surg 1997; 114:766-72. Used by permission.)

J

FIG 36. Reconstructionof the intervalvular fibrous body. The mitral valve is exposed through the dome of the left atrium and the valve is excised. (From David TE, Kuo J, Armstrong S. Aortic and mitral valve replacement with reconstructionof the intervalvular fibrous body. J Thorac Cardiovasc Surg 1997; 114:766-72. Used by permission.)

Results of Surgery for Infective Endocarditis of the Aortic Valve The results of surgery for infective endocarditis have improved substantially during the past 4 decades. In a series of 122 consecutive patients undergoing operation for active infective endocarditis in our unit, the operative mortality rate was 7.4%. 168A stepwise logistic regression analysis identified shock and renal failure as the only 2 predictors of operative 488

Curr Probl Surg, June 1999

FIG 37. Reconstructionof the intervalvulor fibrous body. A triangular patch is sutured to the medial and lateral fibrous trigone. (From David TE, Kuo J, Armstrong S. Aortic and mitral valve replacementwith reconstruction of the intervalvular fibrous body. J Thorac Cardiovasc Surg 1997;114:766-72. Used by permission.)

mortality in that series. 168At 10 years after operation the actuarial survival rate was 61%, and the freedom from recurrent endocarditis rate was 79%. 168 None of these events were early recurrences of the infection. In the series of 158 patients of Larbalestier and colleagues, 188 the operative mortality rate was 6% for native valve endocarditis and 22% for prosthetic valve endocarditis. Patients with prosthetic valve endocarditis have a more guarded prognosis than those with native valve endocarditis, and patients with early prosthetic valve endocarditis have a worse prognosis than those with late prosthetic valve endocarditis. 168,188 The outcome of patients with aortic root abscess has also improved considerably with the use of homograft valved conduits ~82,~83 and radical resection and reconstruction with pericardium. 157,~85 Operations can now be performed with a high probability of bacteriologic cure and mortality rates of 10% to 20%. 157'180"186 Patients in whom infective endocarditis develops are at a higher risk for development of endocarditis again than are those who never had it. 168'~88

Reoperative Aortic Valve Surgery Aortic valve and aortic root rereplacement are becoming increasingly more common procedures as the number of patients with prosthetic aortic valves increases. 47-49,172,173,181 The most common indication for reoperation is failed bioprosthetic v a l v e s . 47-49 Prosthetic valve endocarditis, paravalvular leakage with or without hemolysis, thrombosis, pannus, and prosthesisCurt Probl Surg, June 1999

489

FIG 38. Reconstructionof the intervalvular fibrous body. A prosthetic mitral valve is secured to the mitral annulus and patch. A second patch is used to close the dome of the left atrium. {From David TE, Kuo J, Armstrong S. Aortic and mitral valve replacement with reconstruction of the intervalvular fibrous body. J Thorac Cardiovasc Surg 1997;114:766-72. Used by permission.)

patient mismatch are other reasons for reoperation. 47-49,172.173,181 Structural failure of mechanical valves is extremely rare with newer valves. However, there are still many patients with Bjrrk-Shiley valves who can have strut failure and disc escape. The overall operative mortality rate for repeat AVR ranges from 8% to 11% in various reports. 47-49 The operative risk is highly dependent on patient variables such as the indication for reoperation, timing of operation, ventricular function, and associated cardiac and other diseases. 48,49 In an analysis of 2246 operations for valve rereplacement by Piehler and colleagues, 48 the overall mortality rate was 10.8%, but the risk-adjusted mortality for an elective reoperation in a good-risk patient was only 1.3%. The risk of stroke, heart block, and other perioperative complications is also higher in this patient population. 48,49 Aortic root rereplacements are also becoming increasingly more com490

Curr Probl Surg, June 1999

FIG 39. Reconstructionof the intervalvulor fibrous body. The prosthetic aortic valve is sutured to the aortic annulus and patch. The aortotomy is closed and the patch is incorporated in this closure. (From David TE, Kuo J, Armstrong S. Aortic and mitral valve replacement with reconstructionof the intervalvular fibrous body. J Thoroc Cardiovasc Surg 1997;114:766-72. Used by permission.)

mon operations, t8~,189 Reoperations in these patients are performed because of valve-related problems and false aneurysms or aneurysms of the remaining ascending aorta and transverse arch. 189 Although more complicated reoperations than repeat AVR, the operative mortality rate has been reported to be similar. 18~'~89 I thank Ms J. David for collecting hundreds of references and Ms C. Dunford for her assistance in preparing this manuscript.

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