Remarkable progress has been made in recent years

Intramural Hematoma and Penetrating Atherosclerotic Ulcer of the Aorta Thoralf M. Sundt, MD Division of Cardiovascular Surgery, Mayo Clinic, Rochester, Minnesota Intramural hematoma and penetrating aortic ulcer are uncommon but potentially lethal thoracic aortic pathologies. Despite incomplete understanding of their natural history, they have emerged as anatomically appealing targets of endovascular therapy. Appropriate application of these technologies, however, must be predicated on an understanding of the fate of these lesions left untreated, and predictors of their misbehavior. We briefly review the current understanding of these entities. (Ann Thorac Surg 2007;83:S835 41) 2007 by The Society of Thoracic Surgeons Remarkable progress has been made in recent years with regard to both diagnostic and therapeutic modalities pertinent to thoracic aortic disease. The speed with which computed tomography can be performed has increased just as has its resolution, with 64 detector scanners able to image vessels only millimeters in diameter, and 128 detector scanners being brought into clinical use even as this manuscript is written. Advances are being made in magnetic resonance imaging as well, as more powerful magnets similarly permit faster image acquisition with higher resolution. Of equal if not greater importance, the availability of these technologies throughout the community permits their widespread application to a variety of clinical scenarios. As this has transpired, previously unrecognized aortic pathologies are being diagnosed. Just as diagnostic modalities are bringing the wide spectrum aortic disease to our awareness, therapeutic advances such as endovascular stent graft technologies as well as improvements in conventional approaches to aortic surgery, are encouraging a more aggressive posture towards their treatment. Appropriate indications for intervention on these entities, however, rely upon an appreciation of their natural history. The aim of this review is to focus on two such enties that have attracted considerable attention as potential targets for endovascular stent grafting: intramural hematoma (IMH) and penetrating aortic ulcer (PAU). We will discuss acute dissection, a far more common cause of acute aortic syndrome [1] only as it relates directly to these entities. Material and Methods The English language literature was searched using PubMed and Medline through the Mayo Clinic library. Presented at Aortic Surgery Symposium X, New York, NY, April 27 28, 2006. Address correspondence to Dr Sundt, Division of Cardiovascular Surgery, Mayo Clinic, 200 First St SW, Rochester, MN 55905; e-mail: sundt.thoralf@mayo.edu. Searches were conducted using the keywords acute aortic syndrome, penetrating aortic ulcer, and intramural hematoma. Relevant references derived from review of these articles were also searched at the discretion of the author. Results General Comments Several points of general discussion pertinent to both IMH and PAU are worthy of note. First, while traditional thinking places the entities acute dissection, IMH, and PAU along a spectrum of disease reflecting their overlap in some circumstances (Fig 1A), several differences in clinical presentation are worthy of note. Patients with PAU are typically somewhat older than those with acute dissection, and more commonly exhibit exhibit extensive and diffuse atherosclerotic disease involving both the aorta and coronary arteries [2 4]. It is curious but common clinical observation that patients with aortic dissection tend to have little systemic atherosclerosis [5]. That accounts in part for the trend away from routine preoperative coronary arteriography in patients presenting with acute aortic dissection [6]. This is manifest to the operating surgeon, who typically observes a calcified aorta with a thickened and cratered intima in the patient with PAU (Fig 2A), in contrast to the usually smooth intima apparent on the septum of an acute dissection (Fig 2B). The pathogenetic relationship between these entities remains unclear, although both likely share common mechanisms with inflammation and expression of matrix metalloproteinases [7] likely playing a role as well as medial proliferative changes with transformation of smooth muscle cells from contractile to synthetic phenotypes [8]. Medial degeneration with apoptosis is likely common to both as well [9]. These clinical differences, however, as well as the common observation of PAU without dissection and conversely dissection without PAU, suggests that there may be some utility in considering these entities as related and overlapping in a two 2007 by The Society of Thoracic Surgeons 0003-4975/07/$32.00 Published by Elsevier Inc doi:10.1016/j.athoracsur.2006.11.019

S836 AORTIC SURGERY SYMPOSIUM X SUNDT Ann Thorac Surg INTRAMURAL HEMATOMA AND PAU OF THE AORTA 2007;83:S835 41 than IMH of the descending aorta, and most western authors agree that, as is the case in dissection, patients with type A IMH are at high risk of death without surgical intervention [10 14]. Although there are fewer data concerning type A versus type B PAU given the infrequency of this entity, anecdotal evidence suggests that distinction between those involving the ascending Fig 1. (A) The traditional concept of acute aortic syndromes places the three entities acute dissection, intramural hematoma (IMH), and penetrating ulcer (PAU), along a one-dimensional spectrum of disease. (B) An alternative view characterizes these entities on a two-dimensional spectrum descriptive of medial and intimal disease. dimensional plane defined by intimal and medial changes (Fig 1B). Any practical utility to this unproven alternative concept remains to be seen; however, it might serve as a framework for more detailed clinical classification and more precise risk stratification. At a minimum, it suggests that the tendency to lump these entities together in the literature should be resisted as we attempt to define their behavior more precisely. A second general point pertinent to clinical behavior and natural history is the increasing identification of these entities in settings other than as components of a true acute aortic syndrome. Given the widespread application of advanced axial imaging modalities, significant numbers of PAU and IMH are found incidentally in asymptomatic patients undergoing imaging for other conditions. It remains to be determined whether the behavior of these asymptomatic entities is similar to or disparate from that of the symptomatic forms. Third, a complete understanding of the behavior of these entities is complicated by confusion generated in the literature, in which many series combine analysis of those lesions involving the ascending aorta with those involving the descending aorta. It is widely accepted that acute dissection involving the ascending aorta (type A) has a far different clinical behavior than that restricted to the descending thoracic and abdominal aorta (type B). There is also substantial evidence to suggest that IMH involving the ascending aorta is similarly a worse actor Fig 2. The gross appearance of the intimal surface is strikingly different between the typical patient with (A) penetrating aortic ulcer and (B) acute dissection. In the case of the former, marked thickening of the intima with multiple ulcerlike craters is appreciated, whereas in the latter, the typical thin, pliable septum with a smooth intima is apparent.

Ann Thorac Surg AORTIC SURGERY SYMPOSIUM X SUNDT 2007;83:S835 41 INTRAMURAL HEMATOMA AND PAU OF THE AORTA S837 dissection [15 18]. The most commonly cited explanation for IMH is rupture of vasa vasora with intramural hemorrhage, although data to support this contention are thin. It is assumed, but again unproven, that progression of IMH to acute dissection occurs when the intramural component ruptures into the lumen. Clinically, IMH may be virtually indistinguishable from acute dissection. Chest and back pain is reportedly even more severe with IMH [15]. Patients with IMH are also typically somewhat older than those with classic dissection, supporting the notion that degenerative changes in the media are of particular importance in the evolution of this pathology [19]. Malperfusion and pulse deficit are decidedly rare in IMH, however [15, 19]. Discrimination between IMH and acute dissection with thrombosis of the false lumen may be difficult despite current imaging technologies. Transesophageal echocardiography will demonstrate localized thickening of the aorta with a thrombuslike appearance characterized by Fig 3. Intraoperative inspection of segmental intramural hematoma may provide convincing proof of (A) an intact intima, consonant with (B) the impression from computed tomography scanning. aorta and those involving the descending aorta is appropriate for this pathology as well. Accordingly, reports in which type A and type B pathologies are combined should be interpreted with caution. Intramural Hematoma By definition, IMH is distinguished from acute dissection with thrombosis of the false lumen by the absence of direct communication between the thrombus in the false lumen and the true lumen of the aorta. Given that this definition demands proof of a negative, some question the very existence of the entity. One s confidence in the proof of absence of an entry site is entirely dependent upon the adequacy of imaging. The direct observation of segmental IMH at surgical exploration, however, confirms that in at least some cases it can occur (Fig 3). Intramural hematoma is generally held to account for between 5% and 20% of patients admitted to hospital with the diagnosis of acute aortic syndrome or acute Fig 4. (A) A crescentic intramural hematoma involving the ascending aorta (Ao) may demonstrate areas of lucency (arrows) by transepsophageal echocardiography. (B) Intramural hematoma can also appear as a concentric thrombus involving the ascending aorta, as shown on this computed tomography scan.

S838 AORTIC SURGERY SYMPOSIUM X SUNDT Ann Thorac Surg INTRAMURAL HEMATOMA AND PAU OF THE AORTA 2007;83:S835 41 echolucent areas, and compression of the true lumen (Fig 4A) [11]. Intimal displacement of calcium may be demonstrable with this technology, just as it may be with other imaging modalities. Sensitivity of transesophageal echocardiography has been reported to be as high as 100% with a specificity of 91%, although this will be somewhat operator dependent [20]. The capability of this modality to rule out an intimal defect and thereby distinguish this entity from dissection with thrombosis, is obviously limited. Findings by computed tomography may be quite similar with a hyperdense, crescentic, or circumferential thickening of the wall with a smooth wall distinguishing it from intraluminal thrombus or atherosclerotic disease (Fig 4B) [21]. Intimal displacement of calcium will also help distinguish intramural thickening from intraluminal clot. No dissection flap should be seen. Magnetic resonance imaging may be superior to computed tomography scanning in differentiating IMH from atherosclerotic plaque [22]. Magnetic resonance imaging will demonstrate the thickening of the wall, with hyperintese foci indicative of hemorrhage on T1-weighted images, although the signal intensity characteristics depend in part on the age of the hematoma [11, 23]. Regardless of the technology employed, the extent and thickness of the IMH is important for comparison with subsequent studies. In contrast to classic dissection, IMH is far more often observed in the descending than ascending aorta [18]. The acute prognosis of IMH appears somewhat less grave than that of acute dissection, although again the behavior is highly dependent on location [12, 15, 18, 24]. The acute mortality rate of IMH involving the ascending aorta was more than four times that for IMH involving the arch and descending thoracic aorta in the recently published International Registry of Acute Dissection (IRAD) study (42% versus 8%) [15], supporting the aggressive approach to type A lesions espoused by Robbins and colleagues [13] more than a decade ago. Although some data from investigators in the Far East have suggested that a nonoperative, expectant approach may be taken to IMH involving the ascending aorta when the Fig 5. Meta-analysis by Maraj and colleagues [12] of the outcome of 143 cases of intramural hematoma reported in the literature confirms the appropriateness of operative therapy for those involving the ascending aorta, and nonoperative management of those sparing the ascending aorta. The risk ratios (RR) and 95% confidence intervals (CI) are provided. Fig 6. Both early and late survival of intramural hematoma is superior to that for acute dissection in this study by Kaji and associates [24]. maximum diameter is less than 5 cm [25 27], and indeed a somewhat superior outcome of type A IMH versus acute dissection has been shown in a series reported by von Kodolitsch and colleagues [14], most data from the West support the Stanford philosophy, as has been borne out in a recent meta-analysis by Maraj and colleagues [12] (Fig 5). Progression to frank dissection heralded by persistent or recurrent chest pain has been reported to occur even while the patient is under observation. In the IRAD study reported by Evangelista and colleagues [15], this occurred in as many as 16% of patients, although this report did not distinguish between type A and type B locations. Just as type A IMH is treated in a manner directly analogous with acute type A dissection, type B IMH is generally treated nonoperatively as one would type B dissection. Data from both the East [27] and the West [15] suggest a lower early mortality rate associated with IMH than dissection, perhaps in part due to the infrequency with which IMH is associated with malperfusion syndromes [3, 15]. In a direct comparison of the outcome of 57 patients with acute type B dissection with that of 53 patients with type B IMH, all of whom were initially treated medically, Kaji and associates [27] observed no early deaths in the IMH group but 14 in the dissection group (Fig 6). Indications for surgical intervention on type B IMH would include recurring, refractory chest pain and evidence of increasing extent or diameter of the hematoma. The role of endovascular stent grafts in the repair of IMH and PAU is in evolution. Notably, successes in the treatment of IMH and dissection have been reported in the literature [28, 29]. The late fate of IMH is variable, although it too is likely superior to that of classic dissection (Fig 5). Complete resolution of type B IMH has been documented in 50% to 80% of patients [25, 30, 31]; however, so has progression to frank dissection or late aneurysm [14, 22]. Accordingly, long-term follow-up is recommended by all [3, 14]. Predictors of resolution include younger age [30], aortic

Ann Thorac Surg AORTIC SURGERY SYMPOSIUM X SUNDT 2007;83:S835 41 INTRAMURAL HEMATOMA AND PAU OF THE AORTA S839 Fig 7. Representative axial images obtained by computed tomography without intravenous contrast demonstrate heavy, concentric calcification of the ascending aorta surrounding the area of a penetrating ulcer that has evolved to a large pseudoanerysm. diameter less than 4.0 to 4.5 cm [15, 30, 33], thickness of the hematoma less than 1 cm [15, 33, 34], and postoperative -blocker use [14]. Some authors have identified presence of a PAU as a predictor of progression as well [16]. Resolution of ulcer associated hematoma has been reported in 85% of patients, however, in one study [2]. Penetrating Aortic Ulcer Like IMH, the entity now recognized as PAU has become a part of the medical community s general consciousness thanks to high-resolution imaging. The true incidence of PAU is unclear, ulcers were identifiable retrospectively among 7.6% of patients admitted with a diagnosis of acute dissection in a study from the Yale University database leading to the suggestion that they are far more commonly the cause of dissection than previously recognized [19]. Regardless, seemingly coincident with the advent of stent grafting, the frequency with which PAU are identified appears anecdotally to be on the rise. Although the entity now understood to be PAU was likely described by Dr Shannon Schumacher, it was the publication of a series of such cases in 1986 by Stanson and colleagues [35] in which the hallmarks of the entity by angiographic and computed tomography imaging were described that stimulated significant interest in the entity and debate over it s management. These authors described the histopathology as...an atherosclerotic lesion with ulceration that penetrates the internal elastic lamina and allows hematoma formation within the medial layer of the aortic wall. It is now apparent that a penetrating ulcer may appear as an ulcerlike projection into the media with or without associated IMH or psuedoaneurysm [21]. It is well documented that PAU may lead to IMH, although this is not universally the case. In the Mayo Clinic series almost 20% of patients with PAU had no associated IMH [2]. Presumably medial fibrosis secondary to chronic atherosclerotic disease prevents propagation of the hematoma. Like IMH, PAU is more frequently observed in the descending thoracic aorta. Ulcers are often multiple, and may range in size from 2 to 25 mm in diameter and 4 to 30 mm in depth [36]. Extensive aortic atherosclerosis is often obvious during the imaging study with calcifications noted throughout the aorta (Fig 7). By transesophageal echocardiography, PAU may appear as a craterlike ulcer with jagged edges. Angiography is not a first choice examination for diagnosis of PAU today, as the ulcer may not be obvious depending on the projection of the image obtained. Even less common than IMH, there is considerably more controversy over the natural history of PAU and, accordingly, indications for open or endovascular repair. The clinical presentation is variable. Lesions are most often symptomatic, however asymptomatic lesions also being identified during axial imaging for other indications. In the Mayo Clinic series, 26 of 105 PAU involving the descending thoracic aorta were asymptomatic [2]. An aggressive surgical approach was advocated in

S840 AORTIC SURGERY SYMPOSIUM X SUNDT Ann Thorac Surg INTRAMURAL HEMATOMA AND PAU OF THE AORTA 2007;83:S835 41 Fig 8. (A) Survival of patients with penetrating aortic ulcer managed medically at Mayo Clinic has been superior to that of patients treated surgically. (B) As a consequence, the institutional practice has shifted to favor nonoperative management. (Open bars total cases; shaded bars surgically treated; solid bars operative mortality.) Stanson s early report, with particular attention to the important clinical observation that such ulcers often arise in the mid-descending thoracic aorta and, therefore, any surgical resection should include this portion of the aorta [35, 37]. Very shortly thereafter, however, this view was challenged by Hussain and colleagues [38], who presented convincing evidence that nonoperative management was successful in many cases, a view supported by Kazerooni and associates [39] as well, who demonstrated that 8 of 9 such ulcers treated with antihypertensives became asymptomatic. This debate has been renewed more recently by investigators at Yale University who reported their observations of 26 patients with PAU [3]. Of these, more than one third presented with rupture and two thirds underwent surgery during their hospitalization. Again an aggressive surgical approach was advocated. In counterpoint, however, a subsequent report from the Mayo Clinic suggested that an expectant approach was appropriate [2]. Of 107 patients identified retrospectively from the institutional databases, the majority (72%) were managed nonoperatively with success. As a result, the approach at this institution swung increasingly to an expectant one over time (Fig 8). Late survival was comparable between those operated and those treated medically, with only rupture at presentation and maximum aortic diameter being predictive of failure of medical management as defined by death due to an aortic cause or aortic surgery. The explanation for these disparate experiences is unclear, although part of the answer may be bias in the populations studied. Both institutions are quaternary referral centers; however, Mayo Clinic also draws a significant percentage of cases from the surrounding rural region in which there are few other centers providing cardiac surgical care. This may lead to a somewhat less screened population of patients in the Rochester study, with less bias for the highly symptomatic or gravely ill. Indeed, only 9% of the Mayo patients presented with rupture. Additionally, 46% of the Yale patients but only 2% of the Mayo patients had involvement of the ascending aorta, a recognized marker for bad behavior. Investigators from both institutions agree that patients with IMH or PAU should be followed over time by aortic specialists, just as dissection patients should be followed to monitor the development of aneurismal disease. When operative repair is required, it should consist of graft replacement of the involved aorta. Of particular note, when a PAU is identified, the site of the ulcer must be included in the resection. As PAU may occur anywhere in the thoracic aorta, one must be prepared to replace the mid and distal aorta as well as the proximal portion more typically replaced when repairing type B dissection [40]. In conclusion, intramural hematoma and penetrating aortic ulcer arguably should be the ideal entities for endovascular stent treatment given their segmental nature [41 45]. Unfortunately, it is unclear whether these treatments will truly impact long-term survival [46]. It is, therefore, critical that practitioners be thoughtful and data-driven in the application of this exciting new technology to this tempting target. References 1. Vilacosta I, Roman JA. Acute aortic syndrome. Heart 2001; 85:365 8. 2. Cho KR, Stanson AW, Potter DD, et al. Penetrating atherosclerotic ulcer of the descending thoracic aorta and arch. J Thorac Cardiovasc Surg 2004;127:1393 401. 3. Tittle SL, Lynch RJ, Cole PE, et al. Midterm follow-up of penetrating ulcer and intramural hematoma of the aorta. J Thorac Cardiovasc Surg 2002;123:1051 9. 4. Adler Y, Fisman EZ, Shemesh J, et al. Spiral computed tomography evidence of close correlation between coronary and thoracic aorta calcifications. Atherosclerosis 2004;176: 133 8. 5. Achneck H, Modi B, Shaw C, et al. Ascending thoracic aneurysms are associated with decreased systemic atherosclerosis. Chest 2005;128:1580 6. 6. Motallebzadeh R, Batas D, Valencia O, et al. The role of coronary angiography in acute type A aortic dissection. Eur J Cardiothorac Surg 2004;25:231 5. 7. Schneiderman J, Bordin GM, Adar R, et al. Patterns of expression of fibrinolytic genes and matrix metalloproteinase-9 in dissecting aortic aneurysms. Am J Pathol 1998;152: 703 10.

Ann Thorac Surg AORTIC SURGERY SYMPOSIUM X SUNDT 2007;83:S835 41 INTRAMURAL HEMATOMA AND PAU OF THE AORTA S841 8. Lesauskaite V, Tanganelli P, Sassi C, et al. Smooth muscle cells of the media in the dilatative pathology of ascending thoracic aorta: morphology, immunoreactivity for osteopontin, matrix metalloproteinases, and their inhibitors. Hum Pathol 2001;32:1003 11. 9. He R, Guo DC, Estrera AL, et al. Characterization of the inflammatory and apoptotic cells in the aortas of patients with ascending thoracic aortic aneurysms and dissections. J Thorac Cardiovasc Surg 2006;131:671 8. 10. Vilacosta I, San Roman JA, Ferreiros J, et al. Natural history and serial morphology of aortic intramural hematoma: a novel variant of aortic dissection. Am Heart J 1997;134:495 507. 11. Harris KM, Braverman AC, Gutierrez FR, et al. Transesophageal echocardiographic and clinical features of aortic intramural hematoma. J Thorac Cardiovasc Surg 1997;114:619 26. 12. Maraj R, Rerkpattanapipat P, Jacobs LE, et al. Meta-analysis of 143 reported cases of aortic intramural hematoma. Am J Cardiol 2000;86:664 8. 13. Robbins RC, McManus RP, Mitchell RS, et al. Management of patients with intramural hematoma of the thoracic aorta. Circulation 1993;88(suppl II):II1 10. 14. von Kodolitsch Y, Csosz SK, Koschyk DH, et al. Intramural hematoma of the aorta: predictors of progression to dissection and rupture. Circulation 2003;107:1158 63. 15. Evangelista A, Mukherjee D, Mehta RH, et al. Acute intramural hematoma of the aorta. A mystery in evolution 2005; 111:1063 70. 16. Ganaha F, Miller DC, Sugimoto K, et al. Prognosis of aortic intramural hematoma with and without penetrating atherosclerotic ulcer: a clinical and radiological analysis. Circulation 2002;106:342 8. 17. Nienaber CA, Eagle KA. Aortic dissection: new frontiers in diagnosis and management. Part I. From etiology to diagnostic strategies [see comment]. Circulation 2003;108:628 35. 18. Shimizu H, Yoshino H, Udagawa H, et al. Prognosis of aortic intramural hemorrhage compared with classic aortic dissection. Am J Cardiol 2000;85:792 5. 19. Coady MA, Rizzo JA, Elefteriades JA. Pathologic variants of thoracic aortic dissections. Penetrating atherosclerotic ulcers and intramural hematomas. Cardiol Clin 1999;17:637 57. 20. Kang DH, Song JK, Song MG, et al. Clinical and echocardiographic outcomes of aortic intramural hemorrhage compared with acute aortic dissection. Am J Cardiol 1998;81: 202 6. 21. Ledbetter S, Stuk JL, Kaufman JA. Helical (spiral) CT in the evaluation of emergent thoracic aortic syndromes. Traumatic aortic rupture, aortic aneurysm, aortic dissection, intramural hematoma, and penetrating atherosclerotic ulcer. Radiol Clin North Am 1999;37:575 89. 22. Hayashi H, Matsuoka Y, Sakamoto I, et al. Penetrating atherosclerotic ulcer of the aorta: imaging features and disease concept. Radiographics 2000;20:995 1005. 23. Macura KJ, Szarf G, Fishman EK, Bluemke DA. Role of computed tomography and magnetic resonance imaging in assessment of acute aortic syndromes. Semin Ultrasound CT MR 2003;24:232 54. 24. Kaji S, Akasaka T, Katayama M, et al. Long-term prognosis of patients with type B aortic intramural hematoma. Circulation 2003;108:9. 25. Song JK, Kim HS, Song JM, et al. Outcomes of medically treated patients with aortic intramural hematoma [Comment]. Am J Med 2002;113:181 7. 26. Moizumi Y, Komatsu T, Motoyoshi N, Tabayashi K. Management of patients with intramural hematoma involving the ascending aorta [Comment]. J Thorac Cardiovasc Surg 2002;124:918 24. 27. Kaji S, Nishigami K, Akasaka T, et al. Prediction of progression or regression of type A aortic intramural hematoma by computed tomography. Circulation 1999;100(Suppl 2):281 6. 28. Dake MD, Kato N, Mitchell RS, et al. Endovascular stentgraft placement for the treatment of acute aortic dissection [Comment]. N Engl J Med 1999;340:1546 52. 29. Grabenwoger M, Fleck T, Czerny M, et al. Endovascular stent graft placement in patients with acute thoracic aortic syndromes. Eur J Cardiothorac Surg 2003;23:788 93. 30. Nishigami K, Tsuchiya T, Shono H, et al. Disappearance of aortic intramural hematoma and its significance to the prognosis. Circulation 2000;102(Suppl 3):243 7. 31. Song JK, Kang DH, Lim TH, et al. Different remodeling of descending thoracic aorta after acute event in aortic intramural hemorrhage versus aortic dissection. Am J Cardiol 1999;83:937 41. 32. Evangelista A, Dominguez R, Sebastia C, et al. Long-term follow-up of aortic intramural hematoma: predictors of outcome [see comment]. Circulation 2003;108:583 9. 33. Sueyoshi E, Imada T, Sakamoto I, et al. Analysis of predictive factors for progression of type B aortic intramural hematoma with computed tomography [Comment]. J Vasc Surg 2002; 35:1179 83. 34. Song JM, Kim HS, Song JK, et al. Usefulness of the initial noninvasive imaging study to predict the adverse outcomes in the medical treatment of acute type A aortic intramural hematoma. Circulation 2003;108(Suppl 1):II324 8. 35. Stanson AW, Kazmier FJ, Hollier LH, et al. Penetrating atherosclerotic ulcers of the thoracic aorta: natural history and clinicopathologic correlations. Ann Vasc Surg 1986;1: 15 23. 36. Troxler M, Mavor AI, Homer-Vanniasinkam S. Penetrating atherosclerotic ulcers of the aorta. Br J Surg 2001;88:1169 77. 37. Cooke JP, Kazmier FJ, Orszulak TA. The penetrating aortic ulcer: pathologic manifestations, diagnosis, and management. Mayo Clin Proc 1988;63:718 25. 38. Hussain S, Glover JL, Bree R, Bendick PJ. Penetrating atherosclerotic ulcers of the thoracic aorta. J Vasc Surg 1989;9: 710 7. 39. Kazerooni EA, Bree RL, Williams DM. Penetrating atherosclerotic ulcers of the descending thoracic aorta: evaluation with CT and distinction from aortic dissection. Radiology 1992;183:759 65. 40. Mohiaddin RH, McCrohon J, Francis JM, et al. Contrastenhanced magnetic resonance angiogram of penetrating aortic ulcer. Circulation 2001;103:E18 9. 41. Demers P, Miller DC, Mitchell RS, et al. Stent-graft repair of penetrating atherosclerotic ulcers in the descending thoracic aorta: mid-term results. Ann Thorac Surg 2004;77:81 6. 42. Eggebrecht H, Baumgart D, Schmermund A, et al. Endovascular stent-graft repair for penetrating atherosclerotic ulcer of the descending aorta. Am J Cardiol 2003;91:1150 3. 43. Sailer J, Peloschek P, Rand T, et al. Endovascular treatment of aortic type B dissection and penetrating ulcer using commercially available stent-grafts. AJR Am J Roentgenol 2001;177:1365 9. 44. Schoder M, Grabenwoger M, Holzenbein T, et al. Endovascular stent-graft repair of complicated penetrating atherosclerotic ulcers of the descending thoracic aorta. J Vasc Surg 2002;36:720 6. 45. Pitton MB, Duber C, Neufang A, Schlegel J. Endovascular repair of a non-contained aortic rupture caused by a penetrating aortic ulcer. Cardiovasc Intervent Radiol 2002;25: 64 7. 46. Umana JP, Miller DC, Mitchell RS. What is the best treatment for patients with acute type B aortic dissections medical, surgical, or endovascular stent-grafting? Ann Thorac Surg 2002;74(Suppl):1840 3;1857-63.