Endovascular management of acute aortic dissections

From the Eastern Vascular Society

Endovascular management of acute aortic dissections Sean O’Donnell, MD,a Ann Geotchues, MD,a Frederick Beavers, MD,a Cameron Akbari, MD,a Robert Lowery, MD,a Sherif Elmassry, MD,b and John Ricotta, MD,a Washington, DC; and Richmond, British Columbia, Canada Introduction: Acute aortic dissection (AAD) is one of the most common aortic emergencies that vascular specialists are asked to manage. Traditional surgical interventions for cases complicated by malperfusion have resulted in significant morbidity and mortality. With increasing availability of thoracic endografts, endovascular interventions for complicated AAD have become more acceptable. We reviewed our experience with endovascular treatment of AAD since January 2005. Methods: Medical records of patients admitted for AAD from January 1, 2005, to December 31, 2008, were entered into our vascular registry and analyzed for risk factors, extent of dissection, type of management, fate of the false lumen, complications, and survival. There were 249 admissions for aortic dissections during the study period. Our study group included 28 patients with complicated AAD who underwent endovascular intervention. Results: During the study interval, 28 patients (16 male) underwent 44 procedures. The average age was 54 years. Risk factors differed from the typical atherosclerotic patient and were dominated by an 89.3% incidence of hypertension. Five patients (17.9%) presented with a history of recent cocaine use. The average length of stay was 25.1 days (range, 1-196 days). Stanford type B dissections were present in all but one patient. Twenty-six thoracic endografts were placed in 25 patients. Eight patients required multiple procedures in addition to a thoracic endograft. Morbidity occurred in 17 (60.7%) patients, with renal insufficiency occurring in 11 patients (39.3%) and one requiring permanent dialysis. Four neurologic events occurred: three strokes (10.7%) and one patient (3.6%) with temporary paraplegia. Three patients (10.7%) died in the periprocedural period, with ruptured dissection in one and pericardial tamponade in another. Eight of 10 computed tomography scans (80%) available for review in follow-up showed complete thrombosis of the thoracic false lumen. Conclusions: Complicated AAD remains a challenging problem, with significant morbidity and mortality rates. However, our early experience with endovascular management offers a favorable reduction in mortality from historic controls. ( J Vasc Surg 2011;54:1283-9.)

Acute aortic dissection (AAD) is one of the most frequent aortic emergencies that confronts the vascular specialist.1 Most are Stanford type A, and early surgery is well established as the preferred treatment.2 Type A dissections with distal extension have higher mortality rates.3 The treatment of Sanford type B dissections has been largely medical, with surgical intervention reserved for patients developing complications. Mortality has been 8% to 10% for medical management and 21% to 34% for surgical treatment.1,4-6 Interventional options for the treatment of complicated type B AAD during the last 2 decades have changed the landscape, and numerous reports have demonstrated significant improvement in mortality rates compared with open surgery.7-9 a

From the Center For Vascular Care, Washington Hospital Center ; and Consensus Medical System, Inc, Richmond, British Columbia, Canada.b Competition of interest: none. Presented at the Twenty-third Annual Meeting of the Eastern Vascular Society, September 24-26, 2009, Philadelphia, Pa. Reprint requests: Sean D. O’Donnell, Center For Vascular Care, Washington Hospital Center, 106 Irving St, NW, POB, Suite 3150 N, Washington, DC 20010-2975 (e-mail: sean.o’[email protected]). The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a competition of interest. 0741-5214/$36.00 Copyright © 2011 Published by Elsevier Inc. on behalf of the Society for Vascular Surgery. doi:10.1016/j.jvs.2011.04.025

With the recognition that exclusion of the entry tear reliably restores the true lumen pressure and that thoracic endografts are available to accomplish this goal, vascular surgeons have found themselves increasingly involved in the management of AAD with distal extension.10,11 This is also true for type A dissections with distal extension, with endovascular techniques being used in this group as well.12,13 We have used endovascular methods for treating complicated type A and B AADs since 2005, and this report details our experience with the management of AAD since that time. METHODS Patients. Medical records of patients admitted for AAD from January 1, 2005, to December 31, 2008, were entered into our vascular registry and analyzed for risk factors, extent of dissection, type of management, fate of the false lumen, complications, and survival. There were 249 admissions for aortic dissections during the study period. In July 2005, an acute aortic service was established, with treatment protocols for acute aortic pathology. The cardiac surgery and vascular surgery services both admitted patients, with the other service consulting. Our study group included 28 patients with complicated AAD who underwent endovascular intervention. Indications. All patients with type A AAD were referred emergently for surgical repair. If the aorta distal to 1283

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the subclavian artery was involved, the patient was assessed for evidence of visceral or extremity ischemia and, if present, was treated with endovascular interventions. All patients with type B AAD with evidence of malperfusion shown by overt visceral or extremity ischemia underwent urgent endovascular intervention. All patients with type B AAD were admitted to the surgical intensive care unit and initially managed with a standing protocol for medical management of AAD and observed for evidence of visceral or extremity malperfusion. Patients with evidence of malperfusion who did not respond to medical management underwent endovascular intervention. Rising serum lactate levels, persistent abdominal pain, inability to advance to an oral diet, rising serum creatinine levels, and inability to wean intravenous antihypertensive medication were all considered evidence of persistent malperfusion. Pain alone was not used as an indication for endovascular intervention. Procedural techniques. The principle goals of endovascular management are: 1. Establish access to the true lumen. 2. Cover the entry tear with an endograft. The Gore TAG (W. L. Gore and Associates, Flagstaff, Ariz) was used as the endograft to cover the entry site in all patients during this study period. 3. Correct any static or dynamic obstruction to the aortic true lumen and the visceral, renal, and lower extremity arteries (Fig 1). Frequently, after accomplishing the first and second goals of covering the aortic entry tear, the third goal was fulfilled by a windsock effect when true lumen flow was restored. Stents were not placed in fenestrated visceral orifices unless a significant static or dynamic obstruction was noted. Intravascular ultrasound (IVUS) was used in all patients as an aid in identifying the anatomy and gaining access to the true lumen. Endografts were sized by two anatomic measurements made on the admission computed tomography (CT) scan and intraoperative IVUS: the diameter of the normal aorta proximal to the dissection and the diameter of the crescent formed by the true lumen collapse in the descending aorta. Adequate true lumen and visceral flow was verified by completion angiography and IVUS. No attempt was made to completely exclude the false lumen. Medical management was continued after the procedure, and patients were weaned to oral antihypertensive agents. Spinal drainage was not used prophylactically but was instituted emergently if evidence of lower extremity weakness developed. Access for endograft delivery was primarily a femoral cutdown and confirmation of true-lumen position. Although not required in this series, we do not hesitate to use a limited retroperitoneal approach to the iliac artery for device delivery if the external iliac artery is not clearly suitable. The contralateral femoral artery is usually accessed percutaneously for diagnostic angiography and

Table I. A, Demographics Age

Type

Variable

No.

Mean ⫾ SD

Procedures

A

B

Male Female Total

16 12 28

51 ⫾ 14.4 58 ⫾ 14.7 54 ⫾ 14.7

23 21 44

1 0

15 12 28

SD, Standard deviation.

Table I. B, Comorbidities Variable

Yes (n)

No (n)

%

0 25 10 3 0 4 0 2 4 5 2

28 3 18 25 28 24 28 26 24 23 26

0 89.3 35.7 10.7 0 14.3 0 7.1 14.3 17.9 7.1

Cardiac Hypertension Smoking Hyperlipidemia Pulmonary Renal PAD Cerebral Diabetes Cocaine Obesity PAD, Peripheral arterial disease.

endograft positioning and also with caution to ensure true lumen position. Left brachial artery access was occasionally used to establish the true lumen position and endograft positioning. Statistical analysis. The statistical software that is part of our clinical database was used to perform life-table analysis using the Kaplan-Maier technique and bivariant analysis in addition to the descriptive statistics of the group. Risk factors were compared with the outcome of death by using the log-rank test for bivariant analysis. Follow-up. Our clinical database and hospital records were used to determine patient status and length of followup. CT scans were routinely performed at 3 months, 6 months, and yearly after the intervention. Survival, false lumen thrombosis, and aortic measurements were reviewed when available. RESULTS Demographics. During the study period, 249 patients were admitted with an AAD, and 28 (16 men) underwent endovascular interventions. The average age was 54 years. Risk factors differed from the typical atherosclerotic patient and were dominated by an 89.3% incidence of hypertension (Table I). Five patents (17.9%) presented with a history of recent cocaine use. The average length of stay was 25.1 days (range, 1-196; mode, 7 days). Stanford type B dissections were present in all but one patient. The patient with a type A dissection is worth special mention. This patient presented with distal extension and profound visceral and lower extremity ischemia. After considerable discussion, this patient underwent endograft coverage of the entry site in the proximal descending thoracic

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Fig 1. Drawings show how side branches are affected by acute aortic dissections. A, Static obstruction. B, Fenestration. C, Dynamic obstruction.

Table II. Endovascular procedures performed Procedure

Table III. Complications

No. Complication

Thoracic endograft Renal stent Celiac stent Superior mesenteric artery stent Iliac stent Aortic stent Total

26a 9 1 1 5 1 43b

a Eight patients required mesenteric, renal, or iliac artery stenting in addition to the endograft. b Six procedures were performed on two patients during follow-up.

aorta, with resolution of his ischemia. Repair of his ascending aorta was deferred because of myoglobinuria and renal insufficiency. The patient died suddenly on postoperative day 3, and the postmortem examination revealed pericardial tamponade as the cause of death. Interventions. The 28 patients underwent 43 endovascular procedures. One patient had a left carotid to

No. (%) (n ⫽ 28)

Renal failure 11 (39.3%) Stroke 3 (10.7) Intestinal ischemia 2 (7.1) Cardiac arrest 1 (3.6) Aortic rupture 1 (3.6) Pericardial tamponade 1 (3.6) Lymphocele 1 (3.6) Respiratory failure 1 (3.6) Paraplegia 1 (3.6) Total 22 in 17 (60.7) pts

Outcome 1 permanent dialysis 1 permanent deficit 1 colon resection Died Died Died Resolved Ventilator-dependant Resolved

subclavian artery bypass for a total of 44 procedures during the study period. All patients were initially treated during the acute phase, defined as ⬍2 weeks after the onset of AAD.1 Three patients were treated with endovascular stenting without a thoracic endograft. Time to treatment

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Fig 2. Life-table shows survival after endovascular repair for acute aortic dissections.

averaged 2.9 days, ranging from day of admission to 10 days. Seven patients (25%) were treated in ⬍24 hours, eight were treated 24 to 48 hours after admission, and 13 were treated after the second day of admission. Of the seven treated in ⬍24 hours, the average time to treatment was 4.8 hours (range, 1-10.5 hours). These patients had severe visceral malperfusion, and one patient also had an ischemic lower extremity. A total of 26 thoracic endograft procedures were performed in 25 patients (Table II). The left subclavian was covered in four patients. Ten patients (35.7%) required 12 additional interventions during the initial hospitalization, 8 patients at the same time as the thoracic endograft, which included seven renal, two superior mesenteric, one celiac, and two aortic stents. Three patients did not have thoracic endografting. These included two patients who received an isolated renal artery stents when intravenous antihypertensives could not be weaned, associated with static renal artery obstruction. In the other patient, an infrarenal aortic stent and iliac stent were placed for lower extremity ischemia. Complications. A total of 22 complications occurred in 17 patients (60.7%). Renal insufficiency occurred in 11 patients (39.3%), with one patient requiring permanent dialysis (Table III). Four neurologic events occurred, comprising three strokes (10.7%), of which two were minor. Temporary paraplegia developed in one patient (3.6%) after an onset of lower extremity weakness on postoperative day

1, presumably caused by relative hypotension. The patient had a thoracic endograft without coverage of the subclavian artery and was treated with spinal drainage for 48 hours and was able to ambulate at the time of discharge. Perioperative mortality was 10.7%, with three patients dying ⱕ30 days. Causes of death, in one patient each, were a ruptured dissection, cardiac arrest, and pericardial tamponade. When death was analyzed by risk factors, age ⬎70 was the only significant factor (P ⫽ .028). Two patients were aged ⬎80, and both died perioperatively. Two patients (7.1%) had bowel ischemia, and one required a colon resection. One was ventilator-dependent at discharge because of pulmonary failure. Of the 25 patients who survived the perioperative period, 18 (72%) were discharged home, and seven (28%) were discharged to rehabilitation centers. Follow-up. The average follow-up was 21 months (range, 1-45 months). Overall survival was 85%, with only one death during follow-up (Fig 2). Eight of the 10 CT scans (80%) available for review in follow-up showed complete thrombosis of the thoracic false lumen. Two patients (7.1%) required elective reinterventions. The indication in the first patient was short-distance claudication, which was treated with iliac stenting. The second patient is of particular interest. A baremetal Wallstent (Boston Scientific, Natick, Mass) was placed across the distal descending thoracic aorta and mesenteric arteries after a proximal thoracic endograft failed to

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Fig 3. Computed tomography angiography at 3 years after reintervention shows distal graft extension.

resolve the true lumen collapse across the visceral segment. At 5 months after the initial intervention, back pain developed, associated with recurrent flow in the thoracic false lumen. This appeared to be caused by separation of the proximal endograft and the distal stent, resulting in a large tear in the dissection septum. The patient’s original endograft covered her left subclavian artery, and the recurrent symptoms were coincident to the return of her left radial pulse on examination. She underwent placement of a distal extension to the endograft that covered the new tear in the septum, along with coiling of the proximal left subclavian artery (Fig 3). She was again readmitted with vertebral basilar insufficiency and left hand numbness, which resolved after a left carotid-to-subclavian bypass. Endograft erosion through the dissection septum has been described, mandating long-term follow-up.14,15 This problem may be related to oversizing as well as to grafts with bare metal extensions. DISCUSSION Management of AADs complicated by malperfusion remains one of the most dreaded conditions faced by vascular surgeons. Conventional open surgical treatment has produced poor results, with a mortality rate of 34% in a recent review from the International Registry of Acute Aortic Dissection database.6 Although surgery for type A dissection is the standard of care, mortality is still high, and patients with distal extension present with challenges that are similar to those with type B dissections.16,17 For this reason, we included type A dissections in our review. Although not included in this study, we have intervened on a number of type A dissections outside of the acute period and have made it a practice to evaluate all type

Fig 4. Treatment algorithm for acute aortic dissections (AADs). CTA, Computed tomography angiography. *Transesphageal echocardiogram considered for patients with renal insufficiency.

A dissections with a distal aortic component immediately after the ascending aortic repair. The patient with a type A dissection included in our study, whose details were noted in the Results, represents a particularly lethal set of anatomic features. From our experience and limited data, we currently recommend sequential endovascular distal repair, followed by open surgical repair of the ascending and arch components, with as minimal as possible delay between the two procedures in patients with visceral or peripheral ischemia as the major presenting symptoms. Cocaine ingestion immediately before the onset of symptoms was noted in 17.9% of our patients. This is a recognized risk factor described by other reports.18-23 The rapid catecholamine surge after cocaine ingestion, especially in a patient with poorly treated hypertension, can result in AAD. Community awareness of this catastrophic complication of cocaine use may be an opportunity that has not been emphasized.24 Hypertension continues to be the dominant risk factor.25,26 The cardiac and cerebrovascular complications of untreated hypertension have been well recognized, and public awareness of this fact is high. AAD does not enjoy the same status, however. Vascular specialists as well as primary care physicians and physician extenders should emphasize this point when counseling patients with hypertension. Thoracic endografts have evolved considerably since this study. We have more recently favored the available

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Table IV. Comparison of series using endovascular treatment for complicated acute aortic dissections First author

Year

No.

Alves31 Feezor32 Khoynezhad33 O’Donnell Patel34 Chang7

2009 2009 2009 2011 2009 2008

73 33 28 28 69 47

Follow-up (months)

Mortality (%)

Morbidity (%) Stroke/paraplegia

35.9

6.8 21 11 10.7 17.4 12.8

5.5/1.4 12/15

36 21 28.2

Dacron grafts, which have more reliable proximal positioning and less propensity for infolding than the grafts that were used during this study.27-29 In addition, the new grafts frequently do not require ballooning, which may contribute to retrograde dissection and neurologic complications. Although supporting data are limited, proximal positioning of the endograft in normal aorta may reduce retrograde dissection. For this reason, and the imperative to perform all interventions from within the true lumen, we have found the use IVUS mandatory. Instances of the wire starting in the true lumen and ending up in the false lumen have occurred; if unrecognized, this could prove disastrous. It is essential to ensure wire access in the true lumen from the femoral artery to the ascending thoracic aorta, because placement of an endograft in the false lumen could occlude the true lumen, and endovascular salvage would be extremely difficult, if not impossible. Multiple tears and reentry sites are traps for the unexpecting operator to think he or she has access in the true lumen, only to find that part way up the aorta, the wire has gone through a secondary tear and into the false lumen. The length of dissected aorta that requires endografting is unknown.14 The initial goal of treatment is to correct malperfusion. Prevention of aneurysmal dilatation awaits further data, and with paraplegia being a continuing concern, as seen in this series, it is not unreasonable to continue with a conservative approach and treat the length required to resolve malperfusion.30 This same logic applies to the treatment of visceral and lower extremity arteries involved in the dissection. In our series, 35.7% of patients underwent additional branched artery interventions with the goal of doing only what was necessary to correct malperfusion and not just to restore normal anatomy. Although the long-term outcome of AAD treated with endovascular approaches is waiting further study, the dramatic difference between surgical and endovascular treatments for complicated AAD would seem to justify the continued use of an endovascular approach in these patients.6 Our current treatment algorithm is shown in Fig 4. We use CT angiography as our first-line imaging modality to confirm the diagnosis of AAD and determine the extent. The only exception to this are patients who present with renal insufficiency and creatinine levels ⬎2.0 mg/dL. In these instances, we often use transesophageal echo to distinguish between type A and B dissections. If a type A is

Reintervention (%)

10.7/3.6 4.3/2.9

37 7.1

Survival (%) 80 78 85 84.3

seen on echo, then those patients go directly to the operating room for an ascending aortic repair. If a type B dissection is seen and the patient requires urgent intervention, we use IVUS to determine the extent of distal aortic involvement and use contrast only as needed for the correction of the malperfusion. The patients who require emergency repair of their type A dissections are evaluated immediately after the repair for resolution of any visceral or extremity ischemia. If present, they are treated by endovascular interventions. The results of recent series also appear to justify an endovascular approach first for the treatment of the thoracic and abdominal component of AAD (Table IV).7,31-34 Although it is often difficult to compare retrospective series, we tried to identify common ground in contemporary reports (Table IV). The average rates for mortality and morbidity approach that of medical management.1 Although the midterm results reported in this article appear favorable, the long-term benefits with regard to aneurysmal progression and aortic-related deaths may not prove to be as beneficial as the management of the acute malperfusion states.35 CONCLUSIONS Complicated AAD remains a challenging problem with significant morbidity and mortality. However, our early experience with endovascular management offers a favorable reduction in mortality rates from historical controls. Appropriately applied endovascular interventions may provide similar mortality to that of medical management. The high incidence of additional procedures at presentation, during initial hospitalization, and after discharge places a particular importance on imaging to delineate the anatomy and close follow-up of patients with AAD throughout their course for successful outcomes. The success of endovascular interventions in preventing long-term aortic-related deaths will require further investigation. The authors especially thank Shawn McMahon for his artwork in Fig 1. AUTHOR CONTRIBUTIONS Conception and design: SO Analysis and interpretation: SO, AG, FB, CA, RL, JR Data collection: SO, AG, FB Writing the article: SO, RL

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Critical revision of the article: SO Final approval of the article: SO Statistical analysis: SE Obtained funding: SO Overall responsibility: SO REFERENCES 1. Hagan PG, Nienaber CA, Isselbacher EM, Bruckman D, Karavite DJ, Russman PL, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA 2000;283:897903. 2. Daily PO, Trueblood HW, Stinson EB, Wuerflein RD, Shumway NE. Management of acute aortic dissections. Ann Thorac Surg 1970;10: 237-47. 3. Tamiya Y, Itoh M, Komatsu K Ichimiya Y, Takagi N, Tanaka T, et al. Operative results and long-term prognosis of type A acute aortic dissection. Kyobu Geka 1998;51:626-9. 4. Bozinovski J, Coselli JS. Outcomes and survival in surgical treatment of descending thoracic aorta with acute dissection. Ann Thorac Surg 2008;85:965-70. 5. Trimarchi S, Nienaber CA, Rampoldi V, Myrmel T, Suzuki T, Bossone E, T et al. Role and results of surgery in acute type B aortic dissection: insights from the International Registry of Acute Aortic Dissection (IRAD). Circulation 2006;114:I357– 64. 6. Fattori R, Tsai TT, Myrmel T, Evangelista A, Cooper JV, Trimarchi S, et al. Complicated acute type B dissection: is surgery still the best option?: a report from the International Registry of Acute Aortic Dissection. JACC Cardiovasc Interv 2008;1:395-402. 7. Chang GQ, Li XX, Chen W, Li JP, Hu ZJ, Yao C, et al. Early to mid-term results of endovascular repair of aortic dissection: report of 165 cases. Zhonghua Wai Ke Za Zhi 2008;46:752-5. 8. Eggebrecht H, Nienaber CA, Neuhäuser M, Baumgart D, Kische S, Schmermund A, et al. Endovascular stent-graft placement in aortic dissection: a meta-analysis. Eur Heart J 2006;27:489-98. 9. Dake MD, Wang DS. Will stent-graft repair emerge as treatment of choice for acute type B dissection? Semin Vasc Surg 2006;19:40-7. 10. Chung JW, Elkins C, Sakai T, Kato N, Vestring T, Semba CP, et al. True-lumen collapse in aortic dissection: part II. Evaluation of treatment methods in phantoms with pulsatile flow. Radiology 2000;214: 99-106. 11. Chung JW, Elkins C, Sakai T, Kato N, Vestring T, Semba CP, et al. True-lumen collapse in aortic dissection: part I. Evaluation of causative factors in phantoms with pulsatile flow. Radiology 2000;214:87-98. 12. Fujita W, Taniguchi S, Daitoku K, Fukuda I. Stenting for acute aortic dissection with malperfusion as “bridge therapy”. Tex Heart Inst J 2010;37:691-4. 13. Shiiya N, Matsuzaki K, Kunihara T, Murashita T, Matsui Y. Management of vital organ malperfusion in acute aortic dissection: proposal of a mechanism-specific approach. Gen. Thorac Cardiovasc Surg 2007;55: 85-90. 14. Manning BJ, Dias N, Ohrlander T, Malina M, Sonesson B, Resch T, et al. Endovascular treatment for chronic type B dissection: limitations of short stent-grafts revealed at midterm follow-up. J Endovasc Ther 2009;16:590-7. 15. Yuan L, Bao J, Zhao Z, Jing Z. Repeat endovascular exclusion for distal tear after treatment of primary aortic dissection by endovascular exclusion. Vascular 2010;18:288-91.

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16. Bachet J, Goudot B, Dreyfus G, Brodaty D, Dubois C, Delentdecker P, et al. Surgery of acute type A dissection: what have we learned during the past 25 years? Z Kardiol 2000;89(Suppl 7):47-54. 17. Bavaria JE, Brinster DR, Gorman RC, Woo YJ, Gleason T, Pochettino A. Advances in the treatment of acute type A dissection: an integrated approach. Ann Thorac Surg 2002;74:S1848-52. 18. Singh S, Trivedi A, Adhikari T, Molnar J, Arora R, Khosla S. Cocainerelated acute aortic dissection: patient demographics and clinical outcomes. Can J Cardiol 2007;23:1131-4. 19. Afonso L, Mohammad T, Thatai D. Crack whips the heart: a review of the cardiovascular toxicity of cocaine. Am J Cardiol 2007;100:1040-3. 20. Daniel JC, Huynh TT, Zhou W, Kougias P, El Sayed HF, Huh J, et al. Acute aortic dissection associated with use of cocaine. J Vasc Surg 2007;46:427-33. 21. Gadaleta D, Hall MH, Nelson RL. Cocaine-induced acute aortic dissection. Chest 1989;96:1203-5. 22. Cregler LL. Acute aortic dissection associated with cocaine abuse. Clin Cardiol 1988;11:806. 23. Grannis FW Jr, Bryant C, Caffaratti JD, Turner AF. Acute aortic dissection associated with cocaine abuse. Clin Cardiol 1988;11:572-4. 24. Virmani R. Cocaine-associated cardiovascular disease: clinical and pathological aspects. NIDA Res Monogr 1991;108:220-9. 25. De Gaudio AR, Chelazzi C, Villa G, Cavaliere F. Acute severe arterial hypertension: therapeutic options. Curr Drug Targets 2009; 10:788-98. 26. Patel PD, Arora RR. Pathophysiology, diagnosis, and management of aortic dissection. Ther adv. Cardiovasc Dis 2008;2:439-68. 27. Leung DA, Davis I, Katlaps G, Tisnado J, Sydnor MK, Komorowski DJ, et al. Treatment of infolding related to the Gore TAG thoracic endoprosthesis. J Vasc Interv Radiol 2008;19:600-5. 28. Sze DY, Mitchell RS, Miller DC, Fleischmann D, Frisoli JK, Kee ST, et al. Infolding and collapse of thoracic endoprostheses: manifestations and treatment options. J Thorac Cardiovasc Surg 2009;138:324-33. 29. Cheng SH, Kato N, Shimono T, Shinpo H, Ishida M, Hirano T, et al. Aneurysm shrinkage after endovascular repair of aortic diseases. Clin Img 2006;30:22-6. 30. Park KB, Do YS, Kim SS, Kim DK, Choe YH. Endovascular treatment of acute complicated aortic dissection: long-term follow-up of clinical outcomes and CT findings. J Vasc Interv Radiol 2009;20:334-41. 31. Alves CM, da Fonseca JH, de Souza JA, Kim HC, Esher G, Buffolo E. Endovascular treatment of type B aortic dissection: the challenge of late success. Ann Thorac Surg 2009;87:1360-5. 32. Feezor RJ, Martin TD, Hess PJ Jr, Beaver TM, Klodell CT, Lee WA. Early outcomes after endovascular management of acute, complicated type B aortic dissection. J Vasc Surg 2009;49:561-6. 33. Khoynezhad A, Donayre CE, Omari BO, Kopchok GE, Walot I, White RA. Midterm results of endovascular treatment of complicated acute type B aortic dissection. J Thorac Cardiovasc Surg 2009;138:625-31. 34. Patel HJ, Williams DM, Meerkov M, Dasika NL, Upchurch GR Jr, Deeb GM. Long-term results of percutaneous management of malperfusion in acute type B aortic dissection: implications for thoracic aortic endovascular repair. J Thorac Cardiovasc Surg 2009;138:300-8. 35. Chemelli-Steingruber IE, Chemelli A, Strasak A, Hugl B, Hiemetzberger R, Czermak BV. Evaluation of volumetric measurements in patients with acute type B aortic dissection⫺thoracic endovascular aortic repair (TEVAR) vs conservative. J Vasc Surg 2009;49:20-8. Submitted Nov 7, 2010; accepted Apr 11, 2011.