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Ann Thorac Surg 2008;85:982-986. doi:10.1016/j.athoracsur.2007.11.041
© 2008 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Intermediate-Term Results of Surgical Treatment of Acute Intramural Hematoma Involving the Ascending Aorta

Tomoki Shimokawa, MDa,*, Naomi Ozawa, MDa, Shuichiro Takanashi, MDa, Tsuyoshi Itoh, MDb

a Department of Cardiovascular Surgery, Sakakibara Heart Institute, Tokyo, Japan
b Department of Thoracic and Cardiovascular Surgery, Saga University, Saga, Japan

Accepted for publication November 13, 2007.

* Address correspondence to Dr Shimokawa, Department of Cardiovascular Surgery, Sakakibara Heart Institute, 3-16-1 Asahicho, Fuchu City, Tokyo, 183-0003, Japan (Email: tshimokawa-circ{at}umin.ac.jp).


    Abstract
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
Background: The treatment strategy of acute intramural hematoma involving the ascending aorta remains uncertain. The objective of this study was to evaluate the effectiveness of surgical treatment for this condition.

Methods: A total of 41 patients underwent operation for acute intramural hematoma involving the ascending aorta between 2000 and 2006. Mean age was 67.2 ± 10.1 years, with 26 female patients and 10 in cardiogenic shock at presentation. Early and midterm results, including mortality, morbidity, survival, event-free rates, and the persistence of residual hematoma, were analyzed retrospectively in all patients. Mean follow-up period was 29.7 ± 18.1 months.

Results: All but one patient underwent operation within 72 hours from the onset of symptoms. Thirty-four patients underwent isolated ascending aortic replacement, three had hemiarch repair, and four required total arch replacement. There were no in-hospital deaths. Stroke occurred in two patients and transient neurologic dysfunction in one. Postoperative computed tomographic scan showed residual distal hematoma progression to classical double-barrel dissection in two patients. At five years follow-up, survival was 100%. During the follow-up period, one patient had a new type B aortic dissection. A follow-up study confirmed hematoma resorption in 29 patients (70.7%). The estimated freedom from intramural hematoma-related events was 92.6 ± 4.1% at five years. No independent predictor of intramural hematoma-related events was found on multivariate analysis.

Conclusions: Immediate surgical treatment of acute aortic intramural hematoma involving the ascending aorta with open distal replacement of ascending aorta results in lower mortality rates and excellent midterm survival.


    Introduction
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
Advances in vascular imaging technology have led to increasing recognition of aortic intramural hematoma (IMH). Two different pathophysiologic processes are currently believed to lead to the occurrence of IMH. One is IMH without intimal disruption; according to this hypothesis, spontaneous rupture of aortic vasa vasorum is responsible for hematoma formation within the aortic wall [1]. The other type of IMH is associated with an atherosclerotic ulcer that penetrates into the internal elastic lamina and allows hematoma formation within the media of the aortic wall [2]. However, these subtypes of dissection have similar clinical and radiologic findings, and the optimal treatment strategy for these patients remains ill-defined [3]. Based on the concept of the Stanford classification, IMH can be classified as either involving (type A) or not involving (type B) the ascending aorta. It is generally accepted that patients with type B IMH can be managed conservatively in the absence of disease progression. However, the treatment of patients with type A IMH is controversial. Some reports have recommended early surgery for all patients with type A IMH because of their poor prognoses with medical treatment [4–6].

We believe that the risk of surgical management is lower than that of medical therapy, and that patients with type A IMH should be managed with a similar therapeutic strategy, as is currently indicated for patients with type A aortic dissection. The objective of this study was to evaluate the effectiveness of this surgical strategy by analyzing operative results, midterm survival, and event-free rates, as well as persistence of residual hematoma on postdischarge computed tomographic (CT) scan, in order to establish the optimal therapeutic approach.


    Patients and Methods
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
Between January 2000 and December 2006, 147 symptomatic patients with type A acute aortic dissection were treated at Sakakibara Heart Institute. Of these patients, 47 (31.9%) had IMH. This study retrospectively focuses on the 41 patients who underwent operation during the acute stage (within two weeks after the onset of pain). The remaining six patients, who were initially treated with medical therapy, were excluded. In the early series one patient was treated medically because maximum aortic diameter was 48 mm on admission, but developed classical dissection two weeks after onset. Two patients refused operation because of their advanced age and one of the two died from aortic rupture 15 days after onset. In the remaining three, the ascending aorta was normal aortic size (<40 mm). The indication of the surgical therapy was cardiac tamponade, aortic rupture, diameter of the ascending aorta 45 mm or greater, or presence of the ulcerlike projection (ULP). Institutional Review Board approval was obtained for this study and the Board waived the need for patient consent.

The diagnosis was confirmed by clinical and diagnostic evaluations consisting of enhanced CT and transesophageal echocardiography. The IMH was defined as thickened aortic wall (>7 mm) caused by intramural hemorrhage, with crescent or circular high attenuation area along the aortic wall without enhancement on the contrast-enhanced CT scan, signifying noncommunication with the aortic lumen. Earlier reports have defined IMH as the absence of an intimal tear, but because we cannot recognize the existence or absence of intimal tear in the entire aorta without complete aortography or autopsy, we did not utilize this definition. Penetrating atherosclerotic ulcer (PAU) that may lead to IMH was defined as a deep ulcerated lesion in the thickest part of the IMH within the involved aorta by CT scan [7]. Radiographic diagnosis was made by a Board Certified Radiologist (K.F.) in all patients.

There were 15 male and 26 female patients, with an average age of 67.2 ± 10.1 years (range, 39 to 84). Preoperative characteristics of the patients are shown in Table 1. Seventeen patients (41.5%) were admitted within three hours after onset of symptoms, and 31 (75.6%) were admitted within six hours. At admission, ten patients (24.4%) were in cardiogenic shock, with a systolic blood pressure of 80 mm Hg or less. Three patients (7.3%) were intubated, and 5 (12.2%) had drainage for cardiac tamponade before operation. On preoperative CT scan, the maximal external diameter and maximal hematoma thickness in the ascending aorta were 47.3 ± 5.7 mm and 11.4 ± 5.2 mm, respectively. Patients with cardiac tamponade or aortic rupture underwent emergent operation, and the remainder underwent urgent surgical repair within three days after admission.


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Table 1 Preoperative Patient Characteristics
 
Surgical Technique
Our general technique included femoral artery and right atrium venous cannulation and perfusion of cardiopulmonary bypass. Ascending aortic replacement with an open distal anastomosis was performed through a median sternotomy in 34 patients (82.9%). The proximal and distal aortic anastomoses were reinforced with Teflon felt strips and gelatin-resorcinol-formaldehyde glue. Using hypothermic circulatory arrest (25°C) and retrograde cerebral perfusion, a beveled presealed Dacron graft (Hemashield, Boston Scientific, Natick, MA; UB, Ube Medical, Tokyo, Japan; Intergard, Interwascular, La Ciotat, France) was sutured to the distal aortic stump. Antegrade systemic perfusion was then reinstituted through the side branch of the graft, and rewarming was started. Finally, the proximal anastomosis was completed. If the patients had giant PAU in the aortic arch or distal arch, extended aortic arch replacement was indicated: hemiarch replacement in three (7.3%) and total arch replacement using antegrade cerebral perfusion in four (9.8%).

Follow-Up
Follow-up CT studies were obtained before discharge, six months after surgery, and annually thereafter. Analysis was complete for all patients to an endpoint of either death or completion of the study (May 30, 2007). Mean follow-up period was 29.7 ± 18.1 months (range, 5 to 84). The IMH-related events were defined as follows: (1) new IMH or dissection; (2) progression to classical dissection; (3) need for further surgical treatment; (4) death from aortic rupture; (5) sudden unexplained death.

Statistical Analysis
All statistical analyses were performed using a statistical software program (SPSS Inc, Chicago, IL). The Kaplan-Meier method was used to calculate the cumulative survival rate. Continuous data were expressed as mean ± standard deviation. Univariate analysis was performed using the Fisher 2-tailed exact test. All variables showing a p value less than 0.1 on the exact test were included in the multivariate analysis. Independent risk factors for IMH-related events were examined using a stepwise multiple logistic regression analysis. All p values less than 0.05 were taken as significant.


    Results
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
Operative Data
The mean time from admission to the start of the operation was 7.8 ± 14.4 hours, and all but one patient underwent operation within 72 hours of symptom onset. According to preoperative CT scan, intraoperative transesophageal echocardiography, and surgical findings, 16 patients (39.0%) had deep PAU. Location of the PAU was in the ascending aorta in six patients, aortic arch in five, distal aortic arch in five, descending aorta in three, and in the abdominal aorta in two. Multiple deep ulcers existed in three patients. The IMH involved the arch vessels in 14 patients and aortic root in 31. Preoperative and operative findings are shown in Table 2. The mean operative time, cardiopulmonary bypass time, and aortic cross-clamp time were 251.4 ± 71.4, 131.5 ± 36.3, and 91.3 ± 29.5 minutes, respectively. Operative times are shown in Table 3.


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Table 2 Preoperative and Operative Findings
 

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Table 3 Operative Findings
 
In-Hospital Mortality and Morbidity
There was no operative and in-hospital mortality in this series. Two patients had a perioperative cerebrovascular deficit, confirmed on CT scan. One of the two patients required preoperative endotracheal intubation, not allowing for accurate identification of the time of onset of the cerebrovascular deficit. The other patient experienced a stroke five days after surgery in the setting of atrial fibrillation. One patient suffered early postoperative delirium, with complete resolution and absence of radiologic findings.

Postoperative complications are shown in Table 4, and included pulmonary failure (defined as need for mechanical ventilation for more than 48 hours postoperatively) in nine patients (22.0%), renal failure (defined as need for hemodialysis) in one (2.4%), pericardial effusion or bleeding requiring operation in three (7.3%), heparin-induced thrombocytopenia in one (2.4%), and mediastinitis in one (2.4%). Postoperative CT scan showed progression of a residual distal hematoma to a classical double-barreled dissection after surgery in two patients.


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Table 4 Postoperative Complications
 
Survival and IMH-Related Event-Free Rate
There were no late deaths. The five-year survival rate of acute type A IMH was 100%. During the follow-up period, one patient, who had IMH limited to the ascending aorta, had a new type B aortic dissection nine months after surgery, and underwent graft replacement 17 months after initial intervention because of dilatation of the descending aorta. Follow-up CT scan confirmed complete resorption of the IMH in 29 patients (70.7%). No patients developed aortic dissection in the late period. The diameter of the false lumen was not increased in the two patients with classical dissection just after surgery. The estimates of freedom from IMH-related events were 92.6 ± 4.1% at five years after the operation (Fig 1). On univariate and multivariate analysis, no independent predictors of IMH-related events were identified.


Figure 1
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Fig 1. Freedom from intramural hematoma (IMH)-related event.

 

    Comment
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
Recently, the term "acute aortic syndrome" has been proposed for a new cardiovascular condition clinically characterized by aortic pain [8]. Aortic dissection and intramural hematoma, two important causes of this syndrome, can be distinguished using noninvasive imaging modalities. This is essential because emergent surgical intervention is the standard treatment for proximal aortic dissection. Meanwhile, the treatment strategy and surgical indication of type A IMH remain controversial because clinical data are limited. This study was a retrospective analysis of outcome of immediate surgery in 41 patients with type A IMH. Approximately 90% of the entire type A IMH cohort underwent surgery during the acute phase, demonstrating the impact of an aggressive surgical strategy on the early and midterm results.

There are two pathophysiologic events that are currently believed to play a crucial role in the development of IMH: rupture of vasa vasorum and PAU [1–3]. However, it is difficult to know which is an initiating event because they have similar clinical and radiologic findings. Previous reports indicate that IMH commonly affects elderly patients with a history of hypertension, with an unexplained female predominance [5]. In this study, the diagnosis of IMH was based on the evidence of wall thickening in the absence of an intimal flap by excluding aortic dissection. We believe that the absence of evidence of direct-flow communication by CT scan or transesophageal echocardiography provides more important prognostic information than the pathologic findings in this syndrome.

Early reports have noted that medical treatment alone leads to poor outcome for patients with type A IMH [9]. In their metaanalysis of 143 reported cases of IMH, Maraj and colleagues [10] found that patients with type A IMH who underwent surgery had a significantly better prognosis than did those who received medical treatment (14% vs 36% mortality). They recommended prompt surgical intervention for the risk of progression of type A IMH to overt dissection or aortic rupture. However, recent studies have shown favorable results of type A IMH with medical therapy in Asia. Kaji and colleagues [11] reported that in-hospital mortality was 7% in 30 cases of type A IMH with initial medical treatment. Furthermore, IMH of the ascending aorta completely regressed in 12 patients (40%) but progressed in 13 (43%). The five-year survival rate was 90%. Song and colleagues [12] reported that in-hospital mortality was 7.3% in 41 cases managed conservatively. A follow-up imaging study in 36 patients confirmed resorption of the hematoma in 24 (67%) and development of aortic dissection in 9 (25%). The three-year survival rate was 78%. Finally, the mortality of medical treatment was 7.3% to 80% in previous reports [9, 12].

It is also important to clarify the predictive factors of progression of IMH and conversion from medical treatment to surgery. Maximum aortic diameter 50 mm or greater in initial CT images [13], hematoma thickness 11 mm or greater within 48 hours [14] or 12 mm at two weeks after admission [15], and presence of ULP in the ascending aorta [16] were proposed in previous studies. However Kodolitsch and colleagues [17] mentioned, in their multicenter study, that type A IMH was at high risk for early progression regardless of aortic diameter. In our experience, one of six patients who were treated medically developed classical dissection at two weeks after onset and had graft replacement. Maximum aortic diameter was 48 mm on admission. Evangelista and colleagues [18] identified a normal aortic diameter in the acute phase to be the best predictor of IMH regression without complication. However, the number of patients in these reports was limited, and further investigation might be needed to clarify predictors of progression or regression of IMH.

When uncomplicated, patients with type A IMH have been observed and treated medically, with frequent imaging necessary to assess progression to classical dissection or increasing aortic diameter. Furthermore, 40% to 80% of medically managed patients will still require surgical intervention at late follow-up [11, 19]. In our study, the risk of immediate surgical treatment was quite low and midterm results were acceptable. We therefore advocate early surgery, with this approach being not only effective, but also more cost efficient.

Recent technical improvements in emergent surgery for acute aortic dissection have resulted in a marked decline in hospital mortality [20]. Unlike with typical dissection, ischemic vascular complications are rare in patients with IMH [5]. For prevention of rupture, ascending aortic replacement is adequate. In this study, only seven patients underwent hemiarch or total arch replacement; there was no evidence that hemiarch or total arch replacement provided better results if the patients had PAU in the aortic arch or distal arch. Similar to acute aortic dissection, we can currently reduce the surgical mortality with early recognition of the disease with noninvasive diagnostic modalities, with earlier referral, and with improvements in surgical techniques, including open distal anastomosis using hypothermic circulatory arrest with cerebral perfusion.

There are a few limitations of this study. First, the size of the cohort is relatively small and the follow-up period short. As there was a relatively small number of patients with IMH-related events, the study lacks adequate power to identify independent predictors for outcome. We speculate that the cause of classical dissection after graft replacement might be related to a technical problem. Second, this study was also a retrospective study and there was no control group. Therefore, the results of our aggressive strategy could not be compared with those of a conservative approach. For an accurate assessment of this strategy, a prospective randomized study comparing treatment modalities is needed.

In conclusion, immediate surgical treatment of acute type A aortic intramural hematoma with open distal replacement of ascending aorta results in lower mortality rates and acceptable midterm survival, and freedom from IMH-related events. We believe that, in experienced centers, surgical intervention should be offered to all patients presenting with IMH involving the ascending aorta.


    Acknowledgments
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
The authors thank Dr K. Fujimura for radiographic contribution to this study.


    References
 Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 

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  6. Uchida K, Imoto K, Takahashi M, et al. Pathologic characteristics and surgical indications of superacute type A intramural hematoma Ann Thorac Surg 2005;79:1518-1521.[Abstract/Free Full Text]
  7. 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;106:342-348.[Abstract/Free Full Text]
  8. Vilacosta I, Roman JA. Acute aortic syndrome Heart 2001;85:365-368.[Free Full Text]
  9. Nienaber CA, von Kodolitsch Y, Petersen B, et al. Intramural hemorrhage of the thoracic aorta. Diagnostic and therapeutic implications. Circulation 1995;92:1465-1472.[Abstract/Free Full Text]
  10. Maraj R, Rerkpattanapipat P, Jacobs LE, Makornwattana P, Kotler MN. Meta-analysis of 143 reported cases of aortic intramural hematoma Am J Cardiol 2000;86:664-668.[Medline]
  11. Kaji S, Akasaka T, Horibata Y, et al. Long-term prognosis of patients with type A aortic intramural hematoma Circulation 2002;106:I248-I252.[Medline]
  12. Song JK, Kim HS, Song JM, et al. Outcomes of medically treated patients with aortic intramural hematoma Am J Med 2002;113:181-187.[Medline]
  13. 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):II281-II286.[Medline]
  14. 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-II328.[Medline]
  15. Sueyoshi E, Matsuoka Y, Imada T, Okimoto T, Sakamoto I, Hayashi K. New development of an ulcerlike projection in aortic intramural hematoma: CT evaluation Radiology 2002;224:536-541.[Abstract/Free Full Text]
  16. 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]
  17. von Kodolitsch Y, Csösz SK, Koschyk DH, et al. Intramural hematoma of the aorta: predictors of progression to dissection and rupture Circulation 2003;107:1158-1163.[Abstract/Free Full Text]
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  19. Nakamura K, Onitsuka T, Yano M, Yano Y, Matsuyama M, Kojima K. Clinical analysis of acute type A intramural hematoma: comparison between two different pathophysiological types Ann Thorac Surg 2006;81:1587-1592.[Abstract/Free Full Text]
  20. Kazui T, Washiyama N, Bashar AHM, et al. Surgical outcome of acute type A aortic dissection: analysis of risk factors Ann Thorac Surg 2002;74:75-82.[Abstract/Free Full Text]



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