Ann Thorac Surg 2006;81:1587-1592
© 2006 The Society of Thoracic Surgeons
Original article: Cardiovascular
Clinical Analysis of Acute Type A Intramural Hematoma: Comparison Between Two Different Pathophysiological Types
Kunihide Nakamura, MD, PhD
*
,
Toshio Onitsuka, MD, PhD,
Mitsuhiro Yano, MD, PhD,
Yoshikazu Yano, MD, PhD,
Masakazu Matsuyama, MD,
Kazushi Kojima, MD, PhD
Department of Surgery 2, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan
Accepted for publication December 8, 2005.
* Address correspondence to Dr Nakamura, Department of Surgery 2, Faculty of Medicine, University of Miyazaki, Kihara 5200, Kiyotake, Miyazaki 889-1692, Japan (Email: shiori{at}med.miyazaki-u.ac.jp).
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Abstract
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BACKGROUND: Type A intramural hematoma (IMH) has two different etiologies, which are rupture of vasa vasorum and penetrating atherosclerotic ulcer (PAU); however, it is difficult to know which is the initiating event.
METHODS: Between January 1993 and August 2004, 28 patients of acute type A IMH were treated in our department and were divided into two groups, 20 patients with IMH probably caused by rupture of vasa vasorum (non-PAU group) and 8 patients with IMH probably caused by PAU (PAU group), according to pathologic specimen and atherosclerotic findings on computed tomography. Background factors, radiographic findings, and prognosis were analyzed retrospectively.
RESULTS: Surgery was performed in 15 patients (75%) in non–PAU group and 4 patients (50%) in PAU group during the first admission. Late progression was noted in 3 patients, and operation was required. Finally, operation was performed in 22 patients (78.6%). The history of myocardial infarction (p = 0.026) and chronic renal failure (p = 0.026) were more associated with PAU group than with non-PAU group. Ascending aortic diameter at the onset was significantly larger in non-PAU group (50.3 ± 6.6 mm) than in PAU group (43.9 ± 9.0 mm; p = 0.046), and there were significantly more ulcer lesions in PAU group (1.9 ± 0.4) than in non-PAU group (1.1 ± 0.4; p = 0.0004). There was no significant difference in long-term survival rates between them.
CONCLUSIONS: The PAU group patients have more coexisting atherosclerotic diseases and multiple aortic ulcer lesions with significantly mild ascending aortic dilatation compared with non-PAU group patients.
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Introduction
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Although aortic dissection is considered to be the result of cystic medial necrosis or degeneration with an associated intimal tear or medial hemorrhage leading to the false lumen formation separating the media, aortic dissection without intimal tear or noncommunicating aortic dissection is thought to begin with rupture of the vasa vasorum (intramural hemorrhage) and is considered a variant of dissection [1, 2]. Occasionally, the defects in the intima are seen as ulcerlike projections of contrast agent from an otherwise smooth contour in patients with clotted false channel [3], and it may be a precursor sign of classic dissection [4]. Penetrating atherosclerotic ulcer (PAU) was first described by Stanson and colleagues [5] as an atheromatous ulceration that disrupts the internal elastic lamina and underlying media, and sometimes progresses to aortic rupture, medial hemorrhage, which was called intramural hematoma, and pseudoaneurysm. There are some discussions that noncommunicating aortic dissection should be differentiated from intramural hematoma, as the latter is localized in circumscribed parts of aortic wall and can lead to both communicating and noncommunicating dissections [6]. However, these subtypes of dissection have so similar clinical and radiologic findings that it is difficult to know which is an initiating event, so that they may be misclassified. Furthermore, the management of these patients involving ascending aorta (type A) still has room for debate [7].
The purpose of this study was to document the clinical features, computed tomography (CT) findings, and prognosis of type A IMH (intramural hemorrhage and hematoma). We treated type A IMH in a similar manner in disregard of the etiology, and there is no knowledge whether the treatment should be modified by the etiology. Appropriate correlates regarding the optimal treatment of these patients are also discussed.
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Patients and Methods
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Institutional Review Board approval was obtained for this study. Between January 1993 and January 2005, 82 symptomatic patients with type A acute aortic dissection were treated in the Department of Surgery 2, Faculty of Medicine, at hte University of Miyazaki. Of these 82 patients, 54 (65.9%) had a classic double-barreled dissection and 28 (34.1%) had IMH. We performed a retrospective analysis of these 28 symptomatic type A IMH patients. The diagnosis was confirmed from CT imaging, which was completed within 24 hours of hospital admission, and nonopacified crescentic or circular areas along the aortic wall that showed absence of false lumen flow were prerequisites for IMH [8]. Angiography was performed in 18 of 28 patients at the onset, and no entry and no false lumen flow were found. Radiographic diagnosis made by radiologists was aortic dissection without intimal tear, and ulcer lesions were diagnosed as ulcerlike projections in all patients. There were 9 male and 19 female patients with an average age of 65.7 ± 8.9 years (range, 45 to 81).
Treatment
Four patients with cardiac tamponade, aortic rupture, or aortic valve regurgitation underwent emergent operation, and the others were treated medically. The patients were bed rested for 7 days after the onset and transferred to a referral hospital 1 month later when no cardiac and aortic complications occurred, and further hospitalization for 2 months was required for healing of diseased aorta. Fourteen patients with medical treatment were promptly converted to surgical treatment because of progression to classic double-barreled dissection (5 patients, 55.0 ± 45.0 days after the onset), size increasing of aortic diameter (4 patients, 46.0 ± 25.6 days after the onset), and appearance or size increasing of ulcer lesion (5 patients, 59.9 ± 43.0 days after the onset). Recently, 1 patient with pericardial effusion and aortic diameter greater than 50 mm underwent early elective operation. Surgery was performed in 19 patients during the initial hospitalization and 9 patients discharged with uneventful hospital course. Of these 9 patients, late progression was noted in 3, and the operation was required 4, 7, and 8 years after the onset, respectively. Finally, surgical intervention was performed in 22 patients (78.6%).
Distinctive Diagnosis
Patients were divided into two groups: the patients with IMH probably caused by rupture of vasa vasorum (non-PAU group), and the patients with IMH probably caused by PAU (PAU group) according to pathologic specimen first, then according to atherosclerotic findings of CT imaging. Pathologic specimens were obtained in 20 of 22 operative patients. Six patients with cystic medial necrosis on pathologic specimens were diagnosed as non-PAU group (Fig 1). Seven patients with neither cystic medial necrosis nor atherosclerosis on pathologic specimens had no atherosclerotic findings on CT scan, so they were diagnosed as non-PAU group. Seven patients with atherosclerosis not accompanied by cystic medial necrosis were classified by CT findings; and 2 patients with no aortic calcification were diagnosed as non-PAU group, and 5 patients with extensive aortic calcification were diagnosed as PAU group (Fig 2). In 6 patients with thorough medical treatment and 2 operative patients without pathologic specimen, the distinctive diagnosis was made by CT findings; and 5 patients were diagnosed as non-PAU group, and 3 were diagnosed as PAU group. Finally, 20 patients were diagnosed as non-PAU group and 8 patients were diagnosed as PAU group.
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Fig 1. Computed tomography images from a patient in the non–penetrating atherosclerotic ulcer group (a 65-year-old woman with severe chest pain). She received only medical treatment thoroughly. (a) Initial computed tomography scan at the onset demonstrates nonopacified crescentic areas along the wall of the ascending aorta and the descending aorta. The diameter of the ascending aorta is 49 mm. (b) There was no calcification in the transverse aortic wall. (c) One month later, the nonopacified crescentic area has decreased in size, and the ascending aortic diameter is 47 mm. (d) Five years later, the nonopacified crescentic area has totally absorbed, and the ascending aortic diameter is 42 mm.
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Fig 2. Computed tomography images from a patient in the penetrating atherosclerotic ulcer group (a 65-year-old man with severe chest pain and hypotension). Emergent operation was performed, and no intimal tear was found in the ascending aorta and the aortic arch. Pathology specimens showed medial hemorrhage with moderate atherosclerosis, and there was no evidence of cystic medial necrosis or degeneration. (a) A nonopacified crescentic area can be observed in the ascending aorta, and the descending aorta has multiple atheromatous ulcers. (b) Multiple calcifications are visible in the wall of the aortic arch. (c) Hemopericardium is evident, and calcification is visible in the descending aortic wall. (d) A contrast-filled ulcer is seen in the abdominal aorta.
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Study Variables
Medical records for the patients were reviewed for demographic, medical history, and hospital courses. Specifically, preadmission comorbidities (hypertension, diabetes mellitus, smoking, a history of myocardial infarction, chronic renal failure defined as a serum creatinine levels greater than 2 mg/dL, chronic obstructive pulmonary disease, and a history of cerebrovascular disease) and CT findings (presence of calcification, maximum diameter of the ascending aorta at the onset and the operation, location and number of ulcer lesions) were studied. Follow-up was 100% complete, ranging from 3 months to 12 years (average, 54.1 ± 45.6 months).
Statistics
Continuous variables were expressed as the mean ± 1 SD, and categorical variables were expressed as percentages. All variables were analyzed by univariate analysis (Student's t test, 
2 method, or Fisher exact tests when appropriate) to make comparison between PAU group and non-PAU group. Survival rate was analyzed with standard Kaplan-Meier actuarial technique for estimation of survival probabilities. Statistical analysis was performed with SPSS 6.1 for UNIX (SPSS, Chicago, Illinois). A p value of less than 0.05 was considered significant.
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Results
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Clinical characteristics and radiographic findings of the patients are presented in Table 1. Patients in PAU group were slightly older than those in non-PAU group, but there was no significant difference (PAU group, 69.6 ± 5.5 years old; non-PAU group, 64.2 ± 9.6 years old; p = 0.14). The majority of patients in non-PAU group were female (non-PAU group, female 17 and male 3; PAU group, female 2 and male 6; p = 0.009). The maximum diameter of the ascending aorta was significantly greater in PAU group than in non-PAU group (non-PAU group, 50.3 ± 6.6 mm; PAU group, 43.9 ± 9.0 mm; p = 0.046). There were significantly more ulcer lesions in PAU group than in non-PAU group (PAU group, 1.9 ± 0.4; non-PAU group, 1.1 ± 0.4; p = 0.0004), and all patients of PAU group had ulcer in descending or abdominal aorta. Ulcers in non-PAU group were tiny projections of contrast agent from an otherwise smooth contour, and these projections were considered to be the defects in intima leading to a clotted false lumen (Fig 3). There was no significant difference in incidence of pericardial effusion and aortic valve regurgitation.
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Fig 3. Ulcer lesions (arrows) in patients of the non-penetrating atherosclerotic ulcer group. (a) In a 60-year-old woman, ascending aortic replacement was performed 48 days after the onset because of progression to type A double-barreled aortic dissection. (b) In a 71-year-old woman, ascending and transverse aorta replacement was performed 41 days after the onset because of progression to type A double-barreled aortic dissection. (c) A 54-year-old woman received only medical treatment, and the intramural hematoma was absorbed and disappeared. (d) In an 81-year-old woman, urgent operation was performed because of dilatation of ascending aorta (60 mm) and pericardial effusion. Pathology specimens showed medial dissection with cystic medial degeneration.
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Associated diseases of the patients in PAU and non-PAU group are listed in Table 2. History of myocardial infarction and chronic renal failure was seen in 3 patients of PAU group, with an apparent difference in the incidence between PAU and non-PAU groups (p = 0.026). There was no significant difference in incidence of smoking, hypertension, diabetes, the history of cerebrovascular disease, and chronic obstructive pulmonary disease between PAU and non-PAU groups.
Surgery was required in 15 non-PAU patients (75%) and 4 PAU patients (50%) during the first hospital admission, and late operation was required in 1 non-PAU patient 8 years after the onset and in 2 PAU group patients 4 and 7 years after the onset. In total, 16 patients (80%) of non-PAU group and 6 patients (75%) of PAU group required operation, and there was no significant difference in incidence of surgery (Table 3). In terms of replacement portion, ascending aorta was replaced in 8 patients, ascending aorta and aortic arch in 11 patients, descending aorta in 1 patients, thoracoabdominal aorta in 1 patient, and stent-graft repair of PAU in the descending aorta was performed in 1 patient. The operative and in-hospital mortality rate was none in this series, and there was no significant difference in aortic diameter at the surgical intervention in the operative cases between two groups: the PAU group, 53.5 ± 9.2 mm; the non-PAU group, 54.9 ± 7.8 mm (p = 0.7176). During a mean follow-up period of 58.9 ± 47.2 months (range, 8 to 148), there were 3 late deaths resulting from cerebral bleeding, pneumonia, and accidental death. Survival rate of acute type A IMH including PAU group and non-PAU group was 90.5%, 84.0%, and 84.0% at 3, 5, and 10 years after the operation, respectively, and it showed significantly better result than acute type A classic dissection (Fig 4). There was no significant difference in long-term survival rates between PAU group and non-PAU group.
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Fig 4. Comparison of actuarial survival curves in patients with acute type A classic aortic dissection (open circles [n = 54]) and acute type A noncommunicating aortic dissection (solid circles [n = 28]; p = 0.0284).
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Comment
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The medical term IMH is in confusion whether it is an early or incomplete stage of the classic dissection or medial hemorrhage caused by ulcer rupture. In Japan, Yamada and colleagues [8] described noncommunicating dissection as aortic dissection without intimal rupture in 1988, and they regarded it as an early or incomplete aortic dissection. Rubbins and associates [9] managed 13 patients with IMH between 1983 and 1992, and the diagnosis of IMH was established by exclusion; they excluded the IMH caused by giant PAU and described IMH as a distinct subgroup of patients who presented with neither intimal tear nor deeply penetrating ulcer. Vilacosta and colleagues [10] described in 1997 that two types of aortic IMH can be distinguished: traumatic, with a good prognosis; and nontraumatic, which can be an early stage of the classic dissection, with a bad prognosis in cases involving the ascending aorta. Because PAU is found almost exclusively in the descending aorta [5, 11, 12], IMH caused by PAU most often involves the descending aorta. Rarely, IMH caused by PAU extends the ascending aorta [5]. Between 1993 and 2005, 73 patients with symptomatic type A acute aortic dissection were operated on in our department during the first admission, and of these patients, 19 patients (26.0%) were IMH, including only 4 patients of PAU group (5.1%).
Penetrating atherosclerotic ulcers significantly affect elderly patients more commonly than they do patients with classic aortic dissection, and accompanying medical problems are more common in the former group [13], especially hypertension and coronary artery disease are found in the majority of patients with PAU [5, 14]. Previous reports have described that clinical signs of pulse asymmetry, neuroligic deficit, pericardial effusion, aortic regurgitation, or visceral vessel compromise were not present in PAU patients [5, 12]. In our study, the patients in PAU group were slightly older than patients in non-PAU group, and coexisting atherosclerotic diseases (myocardial infarction and chronic renal failure) were more frequent in PAU group. These results of ours were consistent with previous reports; however, aortic regurgitation appeared in 25% and 10%, and pericardial effusion appeared in 62.5% and 75% in PAU group and non-PAU group, respectively. Our findings suggest that the behavior of IMH involving ascending aorta is similar to Stanford type A classic aortic dissection, whether the initial event is cystic medial necrosis or PAU.
There are few reports about the radiographic distinction between type A IMH patients caused by medial necrosis and those caused by PAU. Gabaha and associates [14] clarified differences between IMH coexisting with PAU and IMH not associated with PAU by comparing clinical features and outcome because of difficulty of distinction between IMH and PAU. They showed that IMH unaccompanied by PAU frequently involved the ascending aorta (26%); on the other hand, IMH associated with PAU had exclusive involvement of the descending aorta (91%) [14]. Mohr-Kahaly and associates [15] described two different transesophageal echocardiographic features of IMH, which were patients with smooth lumen surface and with rough lumen surface, and cystic medial necrosis and rupture of the vasa vasorum were considered the most probable etiologies in the former patients. Mohr-Kahaly and coworkers [15] found 4 patients with smooth lumen surface of 15 patients with IMH, but they suggested that differentiation between intramural hemorrhage and severe atherosclerotic changes of the aorta with associated wall thickening from a healing chronic type B dissection based on echocardiography alone may be difficult or even impossible. Other distinctive features of IMH caused by PAU were that the position of ulcer lesion was often mid and distal descending aorta, and sometimes these ulcer lesions were multiple [5, 13]. In our study, which was limited to type A IMH, the location and number of ulcer lesions in PAU group were compatible with previous reports, and new findings were that the ascending aortic diameter of non-PAU group was significantly greater than that of PAU group.
It seems likely that IMH is a heterogeneous condition, and its behavior may well depend on a variety of factors including its relationship to other aortic conditions, such as PAU, medial degeneration, or underlying genetic factors [7]. The optimal mode of management of patients with type A IMH remains controversial. In the case of type A classic aortic dissection, emergent operation should be performed; however, recent studies have shown favorable results of type A IMH with medical therapy in Japan [16, 17], and healing due to complete thrombus formation within the false lumen has been described [17]. Rubbins and associates [9] managed 13 patients with IMH involving descending thoracic aorta in 10 patients and the ascending/arch in 3, and all patients were initially treated aggressively with antihypertensive medications. In that report, all 3 patients with type A IMH ultimately required operative intervention, and 2 of them died; and Rubbins and associates [9] concluded that patients with IMH involving ascending/arch should probably undergo early graft replacement. Cho and associates [18] stated that type A IMH might be treated nonoperatively, but they do not endorse this approach. In our study, 16 patients (80%) of non-PAU group and 6 patients (75%) of PAU group required operation eventually, and there was no significant difference in incidence of surgery between them. Our findings confirmed that the Stanford classification for aortic dissection has to be applied to IMH, that is, early surgical intervention is recommended for type A IMH. When uncomplicated patients with type A IMH were observed and treated medically, frequent CT or magnetic resonance imaging investigations are necessary to assess progression to classic dissection or increasing aortic diameter; however, the inherent fatal risk remains, and after all, approximately 80% of patients required surgical intervention in our study.
Since 1993, we have treated patients with type A IMH as follows. Emergent or urgent operation is performed for patients with cardiac tamponade, impending rupture, rupture, and acute aortic regurgitation. Other patients were treated medically with intensive antihypertensive therapy, and the operation was performed for the reason of increasing aortic diameter, appearance or size increasing of ulcerlike lesion, and progression to classic double-barreled dissection. We would justify our strategy for IMH because of no operative and in-hospital mortality in this series. Another significant conclusion that we could draw from our study was that we ordinarily observed type A IMH without surgery unnecessarily long enough to allow them manifest their known poor prognostic sign, because almost 80% of the patients ended up requiring the operation. We would propose early surgery, because this approach is more cost efficient and lowers the overall cost of care, and because this approach eliminates unnecessary medical expense for hospitalization and repeat radiologic examinations.
Our data are limited, and further additional studies are clearly needed.
In conclusion, patients with type A IMH caused by PAU are of more advanced age, and have more coexisting atherosclerotic diseases and multiple ulcer lesions compared with patients who have IMH caused by cystic medial necrosis. There was no difference in the incidence of surgical intervention between the two groups, and almost 80% of type A IMH patients required operation. Urgent or early surgical intervention should be performed for patients with type A IMH because of shortage of medical resources.
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References
|
|---|
- Krukenberg E. Beitrage zur frage des aneurysma dissecans Beitr Pathol Anat Allg Pathol 1920;67:329-351.
- Gore I, Seiwert VJ. Dissecting aneurysm of the aorta Arch Pathol 1952;53:121-141.
- Eyler WR, Clark MD. Dissectiong aneurysm of the aortaroentgen manifestations including a comparison with other types of aneyrysms. Radiology 1965;85:1047-1057.[Medline]
- Tisnado J, Cho S, Beachley MC, Vines FS. Ulcerlike projectionsa precursor angiographic sign to thoracic aortic dissection. Am J Radiol 1980;135:719-722.[Abstract]
- Stanson AW, Kazmier FL, Hollier LH, Edwarda WD. Penetrating atherosclerotic ulcers of the thoracic aortanatural history and clinicopathologic correlations. Ann Vasc Surg 1986;1:15-19.[Medline]
- Erbel R, Oelert H, Meyer J, et al. Effects of medical and surgical therapy on aortic dissection evaluated by transesophageal echocardiography. Implication for prognosis and therapy Circulation 1993;87:1604-1615.[Abstract/Free Full Text]
- Sundt TM. Management of intramural hematoma of the ascending aortastill room for debate. J Thorac Cardiovasc Surg 2002;124:894.[Free Full Text]
- Yamada T, Tada S, Harada J. Aortic dissection without intimal rupturediagnosis with MR imaging and CT. Radiology 1988;168:347-352.[Abstract/Free Full Text]
- Rubbins RC, McManus RP, Mitchell RS, et al. Management of patients with intramural hematoma of the thoracic aorta Circulation 1993;88(Suppl II):1-10.
- Vilacosta I, Roman JAS, Ferreiros J, et al. Natural history and serial morphology of aortic intramural hematomaa novel variant of aortic dissection. Am Heart J 1997;134:495-507.[Medline]
- Demers P, Miller C, Mitchell RS, Kee ST, Chagonjiian L, Dake MD. Stent-graft repair of penetrating atherosclerotic ulcers in the descending thoracic aortamid-term results. Ann Thorac Surg 2004;77:81-86.[Abstract/Free Full Text]
- Movsowitz HD, Lampert C, Jacobs LE, Kotler MN. Penetrating atherosclerotic aortic ulcers Am Heart J 1994;128:1210-1217.[Medline]
- Coady MA, Rizzo JA, Hammond GL, Pierce JG, Kopf GS, Elefteriades JA. Penetrating ulcers of the thoracic aorta: what is it? How do we recognize it? How do we manage it? J Vasc Surg 1998;27:1006-1016.[Medline]
- Ganaha F, Miller C, Sugimoto K, et al. Prognosis of aortic intramural hematoma with and without penetrating atherosclerotic ulcer. A clinical and radiographical analysis Circulation 2002;106:342-348.[Abstract/Free Full Text]
- Mohr-Kahaly S, Erbel R, Kearney P, Puth M, Meyer J. Aortic intramural hemorrhage visualized by transesophageal echocardiographyfindings and prognosis. J Am Coll Cardiol 1994;23:658-664.[Abstract]
- 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):281-286.
- Moizumi Y, Komatsu T, Motoyoshi N, Tabayashi K. Management of patients with intramural hematoma involving the ascending aorta J Thorac Cardiovasc Surg 2002;124:918-924.[Abstract/Free Full Text]
- Cho KR, Stanson AW, Potter DD, Cherry KJ, Schaff HV, Sundit TM. Penetrating atherosclerotic ulcer of the descending thoracic aorta and arch J Thorac Cardiovasc Surg 2004;127:1393-1401.[Abstract/Free Full Text]
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Abstract
Introduction
