Long-Term Outcome of Type B Aortic Intramural Hematoma: Comparison With Classic Aortic Dissection Treated by the Same Therapeutic Strategy

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Long-Term Outcome of Type B Aortic Intramural Hematoma: Comparison With Classic Aortic Dissection Treated by the Same Therapeutic Strategy Eijun Sueyoshi, MD, Ichiro Sakamoto, MD, Masatoshi Fukuda, MD, Kuniaki Hayashi, MD, and Tatsuya Imada, MD Department of Radiology, Nagasaki University School of Medicine, Sakamoto, Nagasaki, and Department of Radiology and Cardiovascular Surgery, Omura Municipal Hospital, Omura, Nagasaki, Japan

Background. The long-term clinical course and therapeutic strategy of patients with type B aortic intramural hematoma (IMH) are not completely known. The purpose of this study was to clarify long-term prognosis of patients with type B IMH by comparison with type B classic aortic dissection (AD). Methods. Clinical data were compared retrospectively between 37 patients with acute type B IMH (IMH group) and 69 patients with acute type B AD (AD group). Our therapeutic strategy for all patients was medical therapy with frequent follow-up imaging studies and timed surgical repair in cases with progression. Results. Initially, medical therapy was selected for 104 of 106 (98%) patients. In two patients of the AD group, immediate surgical treatment was performed because of aortic rupture. As for complications, no significant dif-

ference was seen between the two groups. There was no significant difference in the incidence of the total number of deaths; early death, late death, or causes of deaths. The actuarial survival rates for the IMH group at 1, 2, 5, and 10 years were 97 ⴞ 3, 97 ⴞ 3, 85 ⴞ 9, and 85 ⴞ 9%, respectively; the values were 96 ⴞ 1, 96 ⴞ 1, 89 ⴞ 4, and 71 ⴞ 9%, for the AD group. The actuarial survival rates of the two groups were not significantly different from each other (p ⴝ 0.398). Conclusions. Patients with type B IMH have similar long-term prognosis to patients with type B AD. Medical therapy with frequent follow-up imaging studies and timed surgical repair in cases with progression can be a rational therapeutic strategy in patients with type B IMH. (Ann Thorac Surg 2004;78:2112–7) © 2004 by The Society of Thoracic Surgeons

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IMH and AD, a similar therapeutic strategy is usually selected for both conditions [2– 6, 17–19]. Recently, the long-term prognosis of patients with type B AD has been good, but we have found no report to clarify whether the same therapeutic strategy as that for patients with type B AD is proper for patients with type B IMH [15, 20 –23]. In this study, we evaluated the clinical features of both type B IMH and AD during the follow-up period. The purpose of this study was to clarify the long-term prognosis and therapeutic strategy of patients with type B IMH by comparison with classic AD.

ecently, using noninvasive imaging techniques such as computed tomography (CT), magnetic resonance (MR), and transesophageal echocardiography (TEE), aortic intramural hematoma (IMH) has been recognized and characterized primarily by aortic wall hematoma without demonstrable intimal disruption or penetrating ulcer [1–7]. Several studies suggested that IMH may cause morbidity and mortality that are similar to those of classic aortic dissection (AD) [2, 3, 5, 8 –13]. Moreover, recent studies suggested indications of therapeutic strategy and prognostic factors for patients with IMH [14, 15]. Kaji and colleagues [16] reported that patients with type A IMH have better long-term prognosis than patients with type A AD. The long-term clinical course of patients with type B IMH is not completely known. Several studies reported the midterm outcome of IMH including type B. However, there was only one report focusing on the long-term outcome of patients with type B IMH [17]. Although there may be some differences of aortic pathology between Accepted for publication May 17, 2004. Address reprint requests to Dr Sueyoshi, Department of Radiology, Nagasaki University School of Medicine, 1–7–1 Sakamoto, Nagasaki 852– 8501, Japan; e-mail: [email protected].

© 2004 by The Society of Thoracic Surgeons Published by Elsevier Inc

Patients and Methods Patients The study group consisted of 37 patients with Stanford type B IMH and 69 patients with Stanford type B AD in two hospitals (Omura Municipal Hospital and Nagasaki University Hospital) between 1992 and December, 2001. All patients experienced sudden back or chest pain. Diagnosis of type B IMH and AD was established with CT scan within 24 hours from the onset of pain. The initial and follow-up CT studies were performed with nonenhanced and enhanced CT in all patients. Enhanced 0003-4975/04/$30.00 doi:10.1016/j.athoracsur.2004.05.048

CT was done with a bolus injection of 100 mL of ionic or nonionic contrast material. Computed tomography was performed with a 9800, high speed advantage, light speed Qx/i scanner (GE Medical Systems, Milwaukee, WI) or a Somatom Plus 4 scanner (Simens Medical Systems, Erlagen, Germany) generating axial images with contiguous 5-mm-thick sections from the top of the aortic arch to the abdominal aorta. In the spiral CT scanner, a power injector was used and scanning began at 20 to 30 seconds and 120 to 150 seconds (two phases) after the start of the injection of the contrast material. Diagnosis of type B IMH was established with CT scan using the following criteria: (1) a crescent-shaped or circumferential area along the wall of the aorta having higher attenuation than blood at precontrast CT; (2) a noncontrast enhancement effect within the area seen on postcontrast CT; (3) a nonintimal-flaplike component; and (4) no intimal tear or a penetrating atherosclerotic ulcer (PAU) [1, 7, 24]. In addition, the initial diagnosis of IMH was reconfirmed in all cases with TEE and/or MR imaging. There were 67 males and 39 females between the ages of 37 and 86 years, with a mean age of 64 ⫾ 12 years at onset. Patients with Marfan’s syndrome and traumatic IMH or AD were excluded from this study. Ninety-two of 106 (87%) patients had a history of hypertension. At admission, hypertension was present in all patients. Our therapeutic strategy for patients with type B IMH was the same as that for patients with type B AD. Patients without complications, such as rupture, organ ischemia, or severe pain, were treated with hypotensive drugs during the acute phase. Surgical treatment was selected if the aortic diameter (including ulcerlike projection) became enlarged progressively (⬎ 6 cm in diameter or an expanding rate ⬎ 1 cm/yr) or a new complication appeared during the chronic phase [25, 26]. Those complications typically include severe pain and organ ischemia. Initially, medical therapy was selected for 104 of 106 (98%) patients. In two patients, immediate surgical treatment was performed because of aortic rupture. During the acute phase, a calcium channel antagonist, nitrate, and ␤-blocker were administered intravenously to reduce systolic blood pressure (100 to 120 mm Hg). In the chronic phase, several antihypertensive drugs, such as a calcium channel antagonist, angiotensin-converting enzyme inhibitors, or ␤-blocker, were administered orally to adequately control the blood pressure (⬍ 130 mm Hg). After discharge, all patients were followed up at regular intervals, and were controlled (⬍ 130 mm Hg) during the follow-up period. Follow-up periods were 54 ⫾ 27 (IMH group) and 55 ⫾ 33 months (AD group). There was no significant difference in the follow-up period between the two groups (p ⫽ 0.955) Regular follow-up CT studies were also performed every week during the first month and two or three times per year after the second month. The patients without complications after two years from the onset had been excluded from the regular CT follow-up series. However, in all cases, follow-up CT studies were performed at least once per year after regular CT follow-up series. In

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Table 1. Patient Characteristics Characteristics Age, years Gender, male/female Hypertension, n (%) Diabetes mellitus, n (%) Hyperlipidemia, n (%) History of smoking (⬎20 years), n (%) Cerebrovascular disease, n (%) Ischemic heart disease, n (%) Hemodialysis, n (%) Mean systolic BP ⬎ 140 mm Hg during follow-up period, n (%) AD ⫽ aortic dissection; hematoma.

IMH (n ⫽ 37)

AD (n ⫽ 69)

p

69 ⫾ 11 22/15 30 (81) 3 (8) 2 (5) 14 (28)

62 ⫾ 12 45/24 62 (90) 5 (7) 5 (7) 17 (25)

0.005 0.558 0.364 0.340 0.999 0.181

1 (3) 2 (5) 2 (5) 2 (5)

3 (4) 4 (6) 1 (1) 4 (6)

0.999 0.999 0.279 0.999

BP ⫽ blood pressure;

IMH ⫽ intramural

patients with a new episode suggesting complications during the follow-up period, additional studies were performed.

Statistical Analysis All values are expressed as means ⫾ 1 standard deviation except for survival rates and event free rates. Differences between categorical factors were assessed using ␹2 analysis or Fisher’s exact test when appropriate. Continuous variables were compared using the Mann-Whitney U test. Analysis of freedom from aortic rupture and survival analysis were performed with Kaplan-Meier analysis, and differences in survival and the event-free rate between groups were examined with the log-rank test. Variabilities of survival rate and event-free rate were expressed as ⫾ 1 standard error of the mean. A p less than 0.05 was considered statistically significant. Data analysis was performed with the use of Stat-View J-5.0 for Windows (Abacus Concepts, Berkeley, CA).

Results Table 1 summarizes the clinical features of all patients. The mean age of patients in the IMH group was significantly higher than that in the AD group (p ⫽ 0.005). The prevalence of hypertension, diabetes mellitus, hyperlipidemia, history of smoking (⬎ 20 years), cerebrovascular disease, ischemic heart disease, hemodialysis, and hypertension during the follow-up period (⬎ 140 mm Hg) did not show any significant differences between the two groups. Table 2 summarizes the complications of all patients. For complications related to IMH or AD, there was no significant difference between the two groups in the incidence of the total number of patients with complications; redissection, aneurysmal dilatation (maximum diameter ⬎ 5 cm or maximum diameter of the affected aorta increased greater than 1 cm from the onset), rupture, or others (including organ ischemia, coagulopathy, and/or severe pain). The causes of surgical treatment

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Table 2. Complications and Surgical Interventions During the Follow-Up Period

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Patients with complications, n (%) Redissection, n (%) Aneurysmal dilatation, n (%) Rupture, n (%) Others, n (%) AD ⫽ aortic dissection;

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Table 3. Early Death, Late Death, and Cause of Death

IMH (n ⫽ 37)

AD (n ⫽ 69)

p

16 (43) 3 (8) 12 (32) 3 (8) 1 (3)

42 (61) 2 (3) 34 (49) 11 (16) 9 (13)

0.082 0.340 0.095 0.370 0.160

IMH ⫽ intramural hematoma.

(n ⫽ 6) in the IMH group were: aortic rupture in one, redissection (progression to type A) in 2, and progressive aneurysmal dilatation in 3 (⬎ 6 cm in 3). The causes of surgical treatment (n ⫽ 26) in the AD group were: aortic rupture in 4, redissection (progression to type A) in 1, organ ischemia (renal ischemia) in 1, and progressive aneurysmal dilatation in 20 (⬎ 6 cm in 14 and/or an expansion rate greater than 1 cm/yr in 7). Figure 1 shows the event-free curves from aortic rupture in the IMH and AD groups during the follow-up period. The values from freedom from aortic rupture for the IMH group at 1, 2, 5, and 10 years were 97 ⫾ 3, 97 ⫾ 3, 86 ⫾ 8, and 86 ⫾ 8%, respectively; values were 94 ⫾ 3, 94 ⫾ 3, 91 ⫾ 4, and 73 ⫾ 9% for the AD group. The event-free rates of the two groups were not significantly different from each other (p ⫽ 0.547). Mortality and the cause of deaths related to IMH or AD are summarized in Table 3. In the IMH group, no patient died after surgery and 3 patients died without surgery. In

The total number of early deaths, n (%) Rupture, n (%) The total number of late deaths, n (%) Rupture, n (%) Multiorgan failure caused by organ ischemia, n (%) Postoperative complication, n (%)

IMH (n ⫽ 37)

AD (n ⫽ 69)

P

1 (3)

1 (1)

0.999

1 (3) 2 (5)

1 (1) 11 (16)

0.999 0.135

2 (5) 0 (0)

6 (9) 2 (3)

0.710 0.541

0 (0)

3 (4)

0.550

Early death is defined as death within 30 days from the onset. Late death is defined as death later than 30 days after the onset. AD ⫽ aortic dissection;

IMH ⫽ intramural hematoma.

the AD group, 3 patients died after surgery and 9 patients died without surgery. There were 2 (2%) early deaths (within 30 days from the onset) in all 106 patients: 1 (3%) in the IMH group and 1 (1%) in the AD group (p ⫽ 0.999) [25]. The cause of early death was aortic rupture in both the IMH and AD group. There were 13 (12%) late deaths (greater than 30 days from the onset) in all 106 patients: 2 (5%) in the IMH group and 11 (16%) in the AD group (p ⫽ 0.135) [25]. The cause of late death in the IMH group were aortic rupture due to dilatation in 2 (2 patients refused surgery). The cause of late deaths in the AD group were: aortic rupture in 4 (3 patients refused surgery; surgery was contraindicated due to severe asthma in 1 patient), spontaneous rupture of nondilatated aorta in 2, multiorgan failure caused by organ ischemia (mesenteric ischemia) in 2, and postoperative complication in 3 (complications of uncontrollable bleeding in 1, acute renal failure in 1, and pneumonia in 1). Except for these 3 patients, no patient died after surgery in this study. During the follow-up period, 2 patients with IMH and 1 patient with AD died of lung cancer, hepatoma, and oral cancer, which were unrelated to the IMH and AD. There was no significant difference between the two groups in the incidence of the total number of deaths, early death, late death, or in causes of deaths. Figure 2 shows the actuarial survival curves for the IMH group and the AD group. Considering death related to IMH or AD, the actuarial survival rates for the IMH group at 1, 2, 5, and 10 years were 97 ⫾ 3, 97 ⫾ 3, 85 ⫾ 9, and 85 ⫾ 9%, respectively; values were 96 ⫾ 1, 96 ⫾ 1, 89 ⫾ 4, and 71 ⫾ 9%, for the AD group. The actuarial survival rates of the two groups were not significantly different from each other (p ⫽ 0.398).

Comment Fig 1. Comparison of event-free curves from aortic rupture in patients with type B intramural hematoma (IMH) (n ⫽ 37) and type B aortic dissection (AD) (n ⫽ 69). The values from freedom from aortic rupture for the IMH group at 1, 2, 5, and 10 years are 97 ⫾ 3, 97 ⫾ 3, 86 ⫾ 8, and 86 ⫾ 8%, respectively; values are 94 ⫾ 3, 94 ⫾ 3, 91 ⫾ 4, and 73 ⫾ 9% for the AD group. The event-free rates of the two groups are not significantly different from each other (p ⫽ 0.547).

Recently, Kaji and colleagues [16] reported that patients with type A IMH were treated with supportive medical therapy with timed surgical repair. In their study, patients with type A IMH had better long-term prognosis than patients with AD. They suggested that supportive medical therapy with timed surgical repair in cases with progression can be a rational therapeutic strategy in

Fig 2. Comparison of actuarial survival curves in patients with type B intramural hematoma (IMH) (n ⫽ 37) and type B aortic dissection (AD) (n ⫽ 69). Considering death related to IMH or AD, the actuarial survival rates for the IMH group at 1, 2, 5, and 10 years are 97 ⫾ 3, 97 ⫾ 3, 85 ⫾ 9, and 85 ⫾ 9%, respectively; values are 96 ⫾ 1, 96 ⫾ 1, 89 ⫾ 4, and 71 ⫾ 9%, for the AD group. The actuarial survival rates of the two groups are not significantly different from each other (p ⫽ 0.398).

patients with type A IMH. However, some authors suggest that the Asian experience may attribute a more benign prognosis [12]. On the other hand, von Kodolitsch and colleagues recommended immediate surgical repair for type A IMH because type A IMH is at high risk for early progression [12]. The optimal treatment for patients with type A IMH remains a matter of debate. Generally, patients who have type B AD without complication, such as rupture or organ ischemia, should be treated with hypotensive drugs during the acute phase, because the mortality rate with this treatment was reported to be equal to or slightly better than that for surgical treatment during the acute phase [27–29]. Surgical treatment should be selected if the aortic diameter becomes enlarged or a new complication appears during the chronic phase. Such a therapeutic strategy for patients with type B AD results in good long-term prognosis. Most institutions may select a similar therapeutic strategy for patients with type B AD as for patients with type B IMH [2– 6, 18, 19]. In the present study, the 5-year actuarial survival rate for the type B IMH and AD group was 85 ⫾ 9% and 89 ⫾ 4%, respectively. Hence, the actuarial survival rates of the two groups were not significantly different from each other. According to our results, the incidence of aortic rupture (fatal complication) in the IMH group was lower than that in the AD group, but there was no significant difference between the two groups. Therefore, there was no significant difference in the actuarial survival rates between the two groups. According to previous findings, no significant differences are seen among patients with AD when comparing type A versus type B, acute versus

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chronic AD, or medical versus surgical treatment. The 5-year survival rates for all these groups are typically high (75% to 82%) [20 –23]. In the present study, 5-year survival rates for both the IMH and AD groups were higher than this range. These results suggest that survival rates for patients with type B IMH are high if the same therapeutic strategy for type B AD is selected as for type B IMH. It is suggested that supportive medical therapy with timed surgical repair in cases with progression can also be a rational therapeutic strategy in patients with type B IMH. However, with this strategy, follow-up studies using diagnostic imaging modalities, including CT, MR, or TEE, are essential. Lately, Kaji and colleagues reported the long-term prognosis of patients with type B IMH [17]. Their study revealed that the actuarial survival rates in the IMH group were 100%, 97%, and 97% at 1, 2, and 5 years. In their study, patients with type B IMH have better longterm prognosis than patients with type B AD. Their results are different from our results. The reasons for these differences are unknown. However, there are a few differences in study design between the two studies. They described that their study evaluated patients with distal IMH involving the descending thoracic aorta. Therefore, their study might not include patients with isolated aortic arch involvement by IMH. On the other hand, this study included patients with all type B IMH (including isolated aortic arch involvement by IMH) [21]. In addition, their therapeutic strategy was slightly different from ours. These differences may be reasons for the different results . Intramural hematoma was first described in 1920 as “dissection without intimal tear” [30]. Although the exact mechanism of IMH formation remains to be clarified, one cause of IMH was suggested to be rupture of the vasa vasorum in the aorta resulting in hematoma formation [5, 9]. Intramural hematoma may not have any intimal disruptions (intimal tear or PAU) at the onset. Therefore, we excluded patients with a demonstrable intimal disruption from this study. In the present study, the prevalence of hypertension, diabetes mellitus, hyperlipidemia, history of smoking, cerebrovascular disease, ischemic heart disease, hemodialysis, and hypertension during the follow-up period did not show any differences between the two groups. However, the mean age of the patients in the IMH group was significantly higher than that in the AD group. This result suggests that IMH formation may be related to arteriosclerosis in some cases, because the severity of arteriosclerosis usually depends on age. However, further studies are required to clarify the exact mechanism of IMH formation. As for complications, there was no significant difference between the two groups. In this study, the aneurysmal dilatation was the most common cause of surgical treatment. Especially, 20 of 26 causes of surgical treatment in the AD group were progressive aneurysmal dilatation of the aorta. One reason for these results may be that the aneurysmal dilatation in the AD group increased in size more rapidly than in the IMH group. Since the AD wall is relatively thin and consists of only

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the outer half of the original aortic wall, aneurysmal dilatation may progress rapidly in the AD group [20, 31, 32]. In addition, hydraulic stress of the aneurysmal dilatation wall may be more severe in the AD group than in the IMH group [3]. Therefore, new cases of aortic rupture and death might be less in the IMH group than in the AD group greater than 5 years from the onset. In the present study, there was no significant difference between the two groups in the incidence of the total number of deaths, early death, late death, or in the cause of deaths. The values from freedom from aortic rupture between the two groups were not significantly different from each other, and the most common cause of death in both groups was aortic rupture. According to previous findings, the most common cause of death of type B AD is aortic rupture [20, 25, 31]. Neya and colleagues [25] reported the outcome of 58 patients with type B AD. They found aortic rupture in 19% of patients with type B AD during the follow-up period. In the present study, aortic rupture occurred in 3 of 37 patients (8%) with IMH and 10 of 69 patients (15%) with AD. Therefore, the incidence of aortic rupture in our series was lower than previous findings [25]. These results suggest that the incidence of aortic rupture in patients with IMH is low if proper surgical therapy is performed. However, the early deaths of the AD group in this study was less than those of previous reports [25, 33, 34]. This reason is not clear, and further studies are needed. In the present study, the actuarial survival rates for the IMH group at 10 years was 85 ⫾ 9%, and value was 71 ⫾ 9% for the AD group. The event-free rate from aortic rupture for the AD group decreased at 10 years. Although there was no significant difference between the IMH and AD groups, the actuarial survival rates for the IMH group might be less than that for the AD group more than 5 years from the onset. However, longer follow-up studies and analyses are needed to clarify longer prognosis of patients with IMH or AD. As a limitation of this study, diagnosis of IMH was only established by imaging methods. The radiologic findings of AD are sometimes very similar to those of IMH if the false lumen of AD is completely thrombosed. On imaging, IMH must be diagnosed by means of the findings of aortic IMH formation without intimal disruption or penetrating ulcer. However, the authors of some reports have suggested that small intimal disruption may be overlooked even at surgery and autopsy [18, 35, 36]. In the present study, we might have overlooked nondemonstrable intimal disruption. However, such cases may have similar prognoses to that of IMH, because aortic pathology and flow dynamics were very similar to each other. As other limitations of this study, our indications for operation remain a matter of debate. If the indications for operation were better, the prognosis of patients with AD or IMH might be more improved. As other limitations, the sample size was small, and we only studied patient groups with symptoms at the onset. Further studies involving larger numbers of patients with and without symptoms seem needed.

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Conclusion In conclusion, patients with type B IMH have similar long-term prognoses as compared with patients with type B AD, and have good long-term prognoses. There was no significant difference between the IMH and AD groups in the incidence of early death, late death, or complications. Medical therapy with frequent follow-up imaging studies and timed surgical repair in cases with progression can be a rational therapeutic strategy in patients with type B IMH.

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