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(Circulation. 1995;92:1465-1472.)
© 1995 American Heart Association, Inc.

Articles

Intramural Hemorrhage of the Thoracic Aorta

Diagnostic and Therapeutic Implications

Christoph A. Nienaber, MD; Yskert von Kodolitsch, MD; Ben Petersen, MD; Roger Loose, MD; Udo Helmchen, MD; Axel Haverich, MD; Rolf P. Spielmann, MD

From the Department of Internal Medicine, Division of Cardiology, and Departments of Diagnostic Radiology (R.P.S.) and Human Pathology (U.H.), University Hospital Eppendorf, Hamburg, and the Department of Cardiovascular Surgery (R.L., A.H.), Christian-Albrechts-University, Kiel, Germany.

Correspondence to Christoph A. Nienaber, MD, Department of Internal Medicine, Division of Cardiology, University Hospital Eppendorf, Martinistr 52, 20246 Hamburg, Germany.

	Abstract

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Background Intramural hemorrhage (IMH) was recently identified at necropsy and anecdotally in vivo as a unique aortic syndrome (without entry and with no flap-like intraluminal component, such as overt aortic dissection). However, little is known about diagnosis, prognosis, and outcome of IMH.

Methods and Results Between 1983 and 1993, 360 patients from two medical centers with clinical indications of aortic dissection were prospectively evaluated; they presented to the emergency department a median of 3.5 hours after onset of back or chest pain or other suggestive symptoms. Among 195 patients with aortic syndromes, 25 patients (12.8%) were diagnosed to have IMH of the thoracic aorta with no evidence of a primary intimal tear, flap, or overt dissection by multiple noninvasive imaging modalities, including magnetic resonance imaging (n=12), contrast-enhanced computed tomography (n=14), and transesophageal echocardiography (n=3) in random order. There were 16 men and 9 women with a median age of 56±13 years (range, 15 to 80 years). Arterial hypertension was present in the majority (84%), and Marfan's syndrome was present in 3 patients (12%). IMH was diagnosed within 4 days of hospital admission (median, 2.5 hours). IMH involved the ascending aorta (type A) in 12 cases (48%), the aortic arch in 2 (8%), and the descending aorta (type B) in 11 cases (44%); imaging results were validated by crossmatching with intraoperative, pathomorphological, and/or angiographic findings. IMH was 8.5±5 cm in length and 2.0±1.2 cm in aortic wall thickness. Aortic regurgitation and pericardial and mediastinal effusion were present in 5 of 12 patients (42%) with type A IMH and 2 of 11 patients (18%) with type B IMH. IMH progression to overt dissection, rupture, and/or acute tamponade occurred in 8 of 25 patients (32%) within 24 to 72 hours, indicating the need for urgent intervention. The 30-day mortality rate of IMH afflicting the ascending aorta was 80% (4 of 5 cases) with medical treatment (sedation and blood pressure control) versus no mortality in 7 cases with early surgical repair (P<.01); after 1 year, 71.4% of surgically treated patients were alive versus 20% in the medical group (P<.05). IMH of the aortic arch resulted in an early mortality of 50% (1 of 2 patients) with medical treatment. In IMH confined to the descending thoracic aorta, survival with medical treatment was not different from surgical therapy; there was 1 early death among 6 patients with medical therapy and none out of 5 patients with surgery (P=NS). At 1-year follow-up, medical and surgical therapy groups had survival rates of 80% and 83%, respectively (P=NS).

Conclusions IMH is associated with a clinical profile and prognosis similar to classic dissection and may be considered an ominous precursor of overt aortic dissection. Tomographic noninvasive imaging ensures rapid, nontraumatic diagnosis of IMH. The outcome of IMH of the ascending aorta appears favorable only with immediate surgical repair.

Key Words: aorta • imaging • prognosis • magnetic resonance imaging • tomography

	Introduction

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Aortic dissections typically originate from a primary intimal tear, separation of the aortic wall components, and propagation of blood between wall layers. With increasing use of modern high-resolution imaging modalities, however, it has become a challenge not only to diagnose overt dissection but to image very early stages, identify subgroups of dissection, and possibly assess the initiating mechanism.^{1 2 3 4} Intramural hemorrhage (IMH), or localized hematoma forming in the aortic wall, has previously been reported both at necropsy and in vivo.^{5 6 7 8 9 10} The focus of this study was both the interpretation of diagnostic findings in IMH and the subsequent management of patients with medical or surgical treatment.

	Methods

Top Abstract Introduction Methods Results Discussion References

 
Between 1983 and 1993, 360 patients (251 men and 109 women) were evaluated at two medical centers for clinical indications of aortic dissection.^{11 12} Patients presented to the emergency department within 48±44 hours (median, 3.5 hours) after onset of symptoms. Dissection was ruled out in 165 individuals, revealing 100 patients with symptomatic (true) aortic aneurysm, 10 with coronary syndromes (myocardial infarction or unstable angina), 4 with pulmonary embolism, and 51 with pleuritic, pancreatic, or chest pain of unknown origin. Of the remaining 195 patients, 170 had overt aortic dissection and 25 had IMH with no evidence of an intimal tear or dissecting membrane (16 men, 9 women; median age, 56±13 years; range, 15 to 80 years). Follow-up was obtained in 23 of 25 patients with IMH (92%) by direct patient contact and/or by communication with the primary physician.

Diagnostic Evaluation
Routine clinical and diagnostic evaluation was performed by noninvasive and/or invasive modalities,^{2 3 13 14} consisting of random combinations of contrast-enhanced x-ray computed tomography (CT), magnetic resonance imaging (MRI), transesophageal echocardiography (TEE), and digital angiography. Imaging diagnoses were validated by crossmatching with findings at surgery, autopsy, and, for the exclusion of dissection, by combined use of independent tomographic and follow-up imaging and an angiogram negative for dissection (Table 2); thus, in 8 cases the diagnosis of IMH was based on independent confirmatory tomographic imaging with CT or MRI in the presence of normal angiographic findings.

View this table: [in this window] [in a new window]   Table 2. Diagnostic Procedures

Echocardiographic Evaluation
Initial surface echocardiograms using conventional and suprasternal cross-sectional projections were obtained with 2.25- and 3.5-MHz transducers and V3400 R CV60 (Diasonics Inc), HP 77065 (Hewlett-Packard Co), or Sonos 1000 sector scanners (Hewlett-Packard Co). TEE with color Doppler flow mapping was performed with a wide-angle transducer at 5.0 MHz (model HP 21362A, Hewlett-Packard Co) and recorded on a 0.5-in VHS tape. Procedural details are described elsewhere^{2 3} (Fig 1). With hemodynamic monitoring and sedation, studies were safely completed within 10±6 minutes.

View larger version (18K): [in this window] [in a new window]   Figure 1. Schematic of the thoracic and abdominal aorta subdivided into four segments: the ascending aorta (A), the arch (B), the descending thoracic aorta (C), and the abdominal segment of the aorta (D). This representation also illustrates the spatial relation between the transesophageal ultrasound probe and the thoracic structures. AV indicates aortic valve; LA, left atrium; LV, left ventricle; and P, probe.

X-Ray Computed Tomography
Third-generation scanners (Somatom Plus and 2, Siemens AG) and intravenous boluses of 80 to 150 mL of nonionic contrast medium (Ultravist 370, Schering AG) were used for x-ray CT. Transverse scans were obtained during shallow respiratory excursions from the arch to the aortic bifurcation in 2-cm intervals.^{15 16}

Magnetic Resonance Imaging
A whole-body magnet was used for MRI at 1.5 T (Gyroscan S15, Philips) while patients were monitored by telemetric ECG, continuous blood pressure measurement, and voice communication. Gated spin-echo sequences using a trigger delay of 100 ms from the R wave were performed (TE=30 ms). Guided by scout images, transverse scans (8 mm thick) were obtained encompassing the ascending aorta, the arch, and the descending aorta. The size of the acquisition matrix was 256x192 to 256 phase-encoding steps; longitudinal planes were also obtained. In the event that aortic pathology was not visible either on transverse images or coronal images, oblique sagittal scans were added. In 2 symptomatic patients, T2-weighted spin-echo sequences were obtained by triggering every second heartbeat and using a TE of 60 ms. In selected cases, cine-MRI was performed to assess flowing blood in thickened aortic wall segments using a TE of 12 ms^{3 17 18} ; in 6 cases, phase images were obtained for identification of slow blood flow. Spin-echo sequences were completed within 23±3 minutes; with cine-MRI studies, completion was extended to 40±14 minutes.

Reference Techniques
Inspection of the aorta and adjacent tissues at surgery or autopsy, including histology of wall segments, was performed by two experienced surgeons or pathologists; findings were recorded at the time of visual or histological examination (Fig 2). Digital aortography was used to confirm or exclude aortic dissection by evidence of a double lumen or dissecting flap with aortic root injections of 20 to 40 mL contrast dye. Since IMH cannot be directly visualized, it was diagnosed in the presence of a thickened wall segment by two independent tomographic procedures in patients 13 and 22 and at late follow-up in patients 1, 18, 19, and 20.

View larger version (0K): [in this window] [in a new window]   Figure 2. Photomicrograph of histological section of the aortic media layer of a subject whose x-ray computed tomographic scan is shown in Fig 3. Light microscopy reveals a slit-like intramural dissection within the aortic media with intramural accumulation of erythrocytes as evidence of an early stage of intramural hemorrhage. Focal media necroses are present adjacent to the dissection with focal disappearance of nuclear staining, swelling of the matrix, and intensively stained, spot-like cellular degeneration. There is no evidence of inflammatory infiltration. (Hematoxylin-eosin, original magnification x75.)

Imaging Criteria for Intramural Hemorrhage
Exclusion of dissecting flap or intimal disruption was a prerequisite for diagnosis of IMH by any imaging modality. Regional thickening of the aortic wall >7 mm in a circular or crescent shape and/or evidence of intramural accumulation of blood was considered diagnostic of IMH.^{7 19} On TEE, IMH was visualized by a typical reflection pattern of sequestered blood that changes with formation of intramural thrombus between the intima and the adventitia.²⁰ Similarly, on CT images, fresh hematoma was evidenced by higher density compared with adjacent aortic layers, usually between 60 and 70 Hounsfield units (HU) (Fig 3); conversely, partial or complete thrombosis is reflected by a multilayered pattern of increasing density.²¹ On MRI, acute IMH is isodense on T1-weighted images and may not be separated from the embedding aortic wall.^{8 22} However, on T2-weighted images, fresh blood has a high signal intensity, whereas IMH between 1 and 5 days of age has a low signal intensity. Subacute IMH reveals a high signal intensity on both T1 and T2 images due to formation of methemoglobin (Fig 4).

View larger version (127K): [in this window] [in a new window]   Figure 3. Transverse horizontal x-ray computed tomographic (CT) section at the level of the aortic root and pulmonary trunk. Arrow marks a discrete localized wall thickening of high density (60 to 70 Hounsfield units); this is considered strong evidence of fresh intramural hematoma in a patient presenting with acute symptoms clinically suggestive of aortic dissection. There is no evidence of any luminal component such as a flap, tear, or dissecting membrane. This patient died within 20 hours of the CT scan of sudden rupture and fulminant pericardial tamponade before surgical intervention. Histopathology of the aortic media in this patient is displayed in Fig 2.

View larger version (115K): [in this window] [in a new window]   Figure 4. Transverse horizontal T1-weighted magnetic resonance image at the level just below the pulmonary artery bifurcation acquired 7 days after the initial presentation with acute symptoms suggestive of aortic dissection. The descending aorta reveals a crescent-shaped wall thickening suggestive of recent intramural accumulation of blood. There is no evidence of progression of the intramural hemorrhage to a luminal component such as a flap, tear, or dissecting membrane. The crescent-shaped intramural hematoma displays a characteristic high signal intensity consistent with the subacute stage of the hemorrhage due to formation of methemoglobin.

Statistical Analysis
Results of each imaging procedure were interpreted by two experienced readers blinded to any other imaging findings. Conflicting results were resolved by consensus with a third blinded observer. Comparisons between groups (of patients or characteristics) or frequency ratios were performed with the ² or McNemar test with continuity correction, if appropriate; a value of P<.05 was considered significant.²³ Actuarial survival was analyzed according to published guidelines.²⁴

	Results

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Of 360 patients evaluated for clinically suspected thoracic aortic dissection, a group of 195 patients was identified as having acute or subacute aortic syndrome, including 25 cases of IMH. Their demographic data and anatomic and risk profiles are summarized in Table 1. IMH was confined to the ascending thoracic aorta (type A) in 12 patients (48%), to the aortic arch in 2 (8%), and to the descending thoracic aorta (type B) in 11 (44%), 6 of whom presented with acute onset and 5 with subacute. Eight patients (32%) developed evidence of progression to dissection. Patients with IMH of the ascending aorta were 52±10 years old and thus younger than those with IMH of the descending thoracic aorta (60±13 years; P<.05). Regardless of the anatomic location, IMH was associated with chronic hypertension in 21 cases (84%) and with Marfan's syndrome in 3 cases (12%). Diabetes mellitus, pregnancy, history of continuous heavy smoking, or abdominal aortic disease was present in 7 patients (28%).

View this table: [in this window] [in a new window]   Table 1. Demographics and Anatomic and Risk Profile of 25 Patients With Intramural Hemorrhage

Clinical Signs and Symptoms
Nineteen individuals (76%) presented with severe central thoracic or upper abdominal pain not responsive to nitroglycerin and without radiation to either arm or to the chin. Eleven patients complained of radiating interscapular back pain; 6 patients had subacute nonspecific chest pain. One patient with IMH of the descending aorta developed spinalis anterior syndrome, and another with arch-type IMH presented with sudden hoarseness and a diminished left carotid pulse. Renal function was acutely compromised in one case of descending aorta IMH. Chest x-ray film on admission revealed evidence of mild to moderate upper mediastinal enlargement from a prominent aortic silhouette in 22 patients (87%) and pleural effusion in 3 (12%). The ECG was nondiagnostic, with evidence of fluctuating ST segments in 12 patients (48%); Q waves were present on 2 ECGs. Aortic regurgitation was found in 6 patients (24%), 5 of whom were diagnosed as IMH of the ascending aorta; ultrasound screening revealed pericardial effusion in 5 cases (20%).

Diagnostic Imaging of Intramural Hemorrhage
Contrast-enhanced x-ray CT was diagnostic in 14 patients, MRI in 12, and TEE in 3. Angiographic evaluation was used to exclude overt classic dissection in 14 of 25 patients (56%). IMH was confirmed by surgery in 12 patients (48%) and necropsy in 5 (20%); the remaining 8 patients showed a typical IMH pattern with CT or MRI that was subsequently confirmed by a second noninvasive modality in 2 patients and by follow-up imaging by both MRI and CT in 4 patients. One patient (patient 6) had chronic type B dissection in segment C and separate acute IMH in segment A. Whereas transthoracic ultrasound was not useful, TEE, x-ray CT, and MRI had diagnostic potential for IMH, with sensitivities of 100% each. In one segment, however, false-positive evidence of IMH was seen both with TEE (patient 23, segment C) and x-ray CT (patient 13, segment A); one arch segment (patient 3) was missed by TEE, and two abdominal segments (patients 13 and 18) were missed on x-ray CT. High-density subintimal blood or localized thickening of the aorta was present in all 14 individuals subjected to x-ray CT (56%), with additional displacement of intimal calcification in 3. Two patients had signs of fluid extravasation; pericardial tamponade was diagnosed in 1 and periaortic hematoma in the other. A third patient had evidence of mediastinal hematoma at necropsy due to progression to aortic rupture barely visible on x-ray CT (Fig 3). Similarly, MRI findings of IMH consistently revealed abnormal thickness of the aortic wall up to 30 mm (asymmetrical or symmetrical in circumference) ranging from 3 to 30 cm in extent. One patient with subacute back pain revealed high signal intensity within the aortic wall on T1 spin-echo images consistent with postacute IMH (Fig 4). In 2 acutely symptomatic patients, T2 images showed high signal intensity at the site of abnormal wall thickening. IMH was identified by TEE in 3 patients by localized thickening of the aortic wall but a smooth surface.

Clinical Outcome and Follow-up
Twelve patients underwent surgical interventions between 3 hours and 20 days (median, 5.5 days) after diagnostic evaluation. In 8, the affected segment of the aorta was replaced by a polyester tube prosthesis of adjusted length. In 4 patients with ascending aortic IMH, a composite graft (with an integrated aortic valve prosthesis) was used; in 1, additional coronary bypass graft surgery was performed. Thirteen patients (2 with IMH of the aortic arch, 5 with ascending aortic IMH, and 6 with descending aortic IMH) were treated by sedation and atenolol titration to control arterial blood pressure. Four of 5 patients died before surgical repair could be performed (patients 6, 10, 11, and 12) on day 1, 3, or 7 (Tables 2 and 3), whereas patient 1 refused any intervention.

View this table: [in this window] [in a new window]   Table 3. Location of Intramural Hemorrhage, Therapeutic Strategy, and Outcome

No deaths occurred within 30 days of undelayed surgical intervention in cases of IMH of the ascending aorta; conversely, the 30-day mortality rate was 80% with medical treatment (P<.01). At 1-year follow-up, 71.4% of surgically treated patients were alive versus 20% with medical treatment (P<.05). IMH of the aortic arch had an early mortality of 50% with medical treatment. In IMH confined to the descending thoracic aorta, survival after medical treatment was not different from survival after surgical therapy; there was 1 early death with medical treatment and none with surgical repair (P=NS). At 12-month follow-up, surgical and medical treatment of IMH of the descending aorta revealed survival rates of 80% and 83%, respectively (P=NS), with 1 late death after surgical intervention (Table 4).

View this table: [in this window] [in a new window]   Table 4. Survival of Intramural Hemorrhage by Type of Treatment

The actuarial survival rate of all patients with IMH (Fig 5A) was not different from survival of overt dissection; overall IMH mortality is high in the first month after the acute onset of symptoms and is confined to IMH of the ascending aorta, similar to the survival pattern of classic aortic dissection.^{1 25 26 27} Within a follow-up period of 6.5 years, 6 of 11 patients (54%) with IMH of the ascending aorta died; only 2 of these 6 patients had undergone surgical repair, and 1 death after 2 months was related to surgery (patient 9). All survivors, however, except for patient 1, underwent placement of either composite or aortic wall grafts. Separate actuarial survival analysis of both type A and type B IMH showed no prognostic advantage for either type within 5 years (Fig 5B). In contrast, surgical repair of IMH (regardless of location) had a beneficial prognostic impact (Fig 5C). Five patients after surgery and 4 given medical treatment (patients 1, 18, 19, and 20) underwent follow-up imaging by CT and/or MRI confirming either a satisfactory postoperative result, partial retraction of wall thickening and no evidence of new hemorrhage or dissection, or the initial diagnosis of IMH.

View larger version (20K): [in this window] [in a new window]   Figure 5. A, Overall actuarial survival curves of patients with the diagnosis of intramural hemorrhage (IMH) of the aorta and of patients with true aortic dissection (types A and B), including hospital deaths and late mortality during follow-up after both medical and surgical therapy in both subsets. The actuarial survival of IMH and classic dissection are not different. B, Separate actuarial survival curves of patients with type A IMH and type A dissection (afflicting the ascending aorta) and of patients with type B IMH and type B dissections (afflicting the descending aorta without participation of the ascending segment). The mortality rate of type A IMH is slightly higher both early (within 1 week) and late (after both 1 and 7 years) compared with type B IMH and type B dissection. There is a marginal trend to better survival of type A dissection than type A IMH, most likely as the result of undelayed surgical intervention in >95% of cases of typical type A dissection. The sample size, however, is too small to allow a comparative survival analysis between groups of IMH. C, Actuarial survival analysis separated for medical treatment and surgical interventions in IMH. In contrast to medical treatment, early surgical interventions are associated with better survival in the first 3 years of the diagnosis, even considering the small sample size. w indicates week; m, month; y, year; and t, time.

	Discussion

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IMH was first described in 1920 as "dissection without intimal tear" and was considered a distinct entity at necropsy.²⁸ However, with high-resolution tomographic imaging, the in vivo diagnosis of IMH is now feasible²⁹ and suggestive of IMH as a precursor of dissection, particularly with the high rate of progression to overt dissection. In this series, noninvasive imaging procedures identified IMH in 12.8% of patients with acute aortic syndromes; this percentage is almost identical to autopsy results from 204 patients with aortic dissection, 27 of whom (13.2%) had no identifiable intimal tear.³⁰

Pathogenesis of Intramural Hemorrhage
Arterial hypertension is the most frequent predisposing factor for IMH, present in 84% of our patient cohort and similar to the 67% incidence reported in a postmortem study of 161 cases of overt dissection.^{31 32} Nevertheless, as in aortic dissection, the initiating event of acute IMH is still unclear. Gore³³ suggested that spontaneous rupture of aortic vasa vasorum may initiate aortic wall disintegration, eventually leading to dissection with or without an intimal tear. Similarly, rupture of the nutrient vasa vasorum of the media layer may cause hematoma without a tear.³⁴ Others have proposed intimal fracture of an atherosclerotic plaque as the primary event, which then allows propagation of blood into the aortic media. Moreover, discrete penetrating atheromatous ulcers ("giant ulcers") were also discussed as a prerequisite for intramural bleeding.¹⁹ In such a chronic setting, however, the hematoma is confined to the area adjacent to an atherosclerotic ulcer. Although some uncertainty exists concerning how to distinguish IMH from limited aortic dissection with a thrombosed false lumen, IMH pathology has been recognized as the very early stages of dissection with impending risk of rupture.^{9 29}

Distinction From Aortic Dissection and Atherosclerotic Ulcers
With clinical signs and symptoms as well as a risk profile virtually identical to classic aortic dissection,³⁵ IMH appears more likely to be a precursor of dissection than a separate entity (Table 1). Typical complications of dissection, such as fluid extravasation with pericardial or pleural effusion or periaortic and mediastinal hematoma, were seen in 7 cases of IMH (28%) and are considered typical features²⁰ ; acute aortic valve regurgitation was also often associated with IMH confined to an aneurysmal segment of the ascending aorta. Therefore, urgent diagnosis (and distinction from normal) by use of sensitive imaging modalities is of utmost importance.

In contrast to IMH, aortic ulcers are characterized by focal contrast enhancement (or filling defects) beyond the confines of the aortic lumen but communicating with the aortic lumen.^{34 36} Both IMH and ulcers are unrelated to intimal lacerations, as in acute aortic dissection.³⁷ Lacerations and IMH usually occur at points of greatest hydraulic stress (right lateral wall of the ascending aorta or in the vicinity of the ligamentum arteriosum), whereas penetrating ulcers are typically found in the descending thoracic or abdominal aorta and are of a chronic nature.^{38 39}

Diagnostic Approach
In ascending aortic IMH, aortic regurgitation (found in 42% of our patients with IMH) and pericardial effusion are common, whereas other physical findings of classic dissection (pulse differential, ischemic and neurological symptoms) are seen less frequently. Nonspecific ST-segment changes in the acute symptomatic phase of IMH lack a plausible explanation. Contrast angiography is rarely diagnostic because a luminal component is a missing feature in IMH. The diagnosis relies on the visualization of intramural blood or evidence of localized increased wall thickness (sometimes less than 7 mm). The high density of fresh hematoma on CT scans appears specific for IMH. MRI techniques allow the age of the hematoma to be assessed based on the formation of methemoglobin.⁴⁰ TEE has been emphasized as a primary diagnostic tool; however, differentiation from severe atherosclerosis with local wall thickening may be difficult, and IMH may only be diagnosed retrospectively with serial evaluation (resolution or progression of IMH). Moreover, false-positive findings of local thickening on tangential scans and around the hemiazygos vein may be more likely with TEE. Both TEE and CT had one false-positive and one false-negative segmental finding (pathological wall thickness without hematoma), whereas the segmental extent of IMH was correctly assessed with MRI (Table 2). Although TEE has an excellent sensitivity to detect aortic dissection,^{2 3 27} the definite distinction between IMH and normal findings may require a second tomographic modality such as CT or MRI because a false-negative result (or false exclusion of IMH) is more likely to be avoided with independent morphological information.

Therapeutic Approach
Of the 12 patients with IMH of the ascending aorta, 7 (58%) ultimately underwent a surgical intervention; there were 2 postoperative deaths (28%), at 2 months and 3.3 years, in this group. Five of these 12 patients received medical treatment, and 4 of them (80%) died between 24 hours and 7 days after the diagnosis, before surgical intervention (Table 3). This high mortality rate may suggest that ascending aortic IMH will benefit from early surgical repair. Even a slight intramural accumulation of blood carries the risk of progression to dissection, suggesting surgical repair as a preventive measure in IMH of the ascending aorta; recurrent episodes of pain or increasing outer aortic diameter should prompt undelayed ascending aortic and/or arch graft replacement.

Individuals with descending aortic IMH can probably be safely monitored without early surgical intervention (Table 4). However, frequent follow-up investigations for evidence of intimal disruption, tearing, or progression are advisable.²⁰ Surgical intervention may be avoided if resolution of intramural bleeding is documented and symptoms resolve with negative inotropic and antihypertensive therapy. Although the cumulative risk inherent in a conservative treatment policy is not known precisely, there is no clear advantage to a surgical strategy. Moreover, many patients with IMH confined to the descending aorta are not ideal candidates for surgery because of advanced age and/or comorbidity.^{7 20 40} Considering the prognostic impact related to both location of IMH and choice of treatment, similarities to the "prognostic" Stanford classification²⁶ for aortic dissection are obvious, and thus a formal distinction between type A and type B IMH may be justified with respect to both prognosis and treatment⁴¹ (Fig 5B).

This concept is supported by Yamada et al⁴⁰ ; in their report, of 14 patients with IMH of both the ascending (type A) and descending (type B) thoracic aorta, 2 patients with type A IMH died within 1 month of medical treatment. Autopsy revealed dissection of the entire aorta (from the ascending thoracic to the abdominal aorta) with no evidence of a primary intimal tear. Spontaneous progression of IMH to dissection may, however, occur in both type A and type B IMH.^{8 9 10} The risk of progression to dissection is substantiated by a recent collaborative study of 2 patients with type A IMH and 13 with type B IMH.²⁰ Four of 10 patients (40%) under medical treatment developed bona fide acute aortic dissection, with rupture in 3; 7 of the 15 patients in that study (47%) died within short-term follow-up. Cause of death was rupture in 3 patients, progression to acute dissection in 2, and unknown in 2. IMH remained unchanged in 5 patients and was completely resolved in only 1. This pooled experience supports our findings of 8 patients with documented progression to dissection (leading to 1 death and 6 emergency operations) and characterizes IMH as a precursor of imminent rupture and a harbinger of an unfavorable prognosis if recurrently symptomatic patients are treated only medically. Thus, similar to aortic dissection, immediate diagnosis of IMH is life saving.

Clinical Impact
As a potential precursor of aortic dissection, IMH requires careful diagnostic attention by use of high-resolution tomographic imaging such as MRI, x-ray CT, or serial TEE; angiography is not diagnostic. Moreover, the concept of the Stanford classification of aortic dissection appears valid for IMH as well. Given the poor experience with medical treatment, early surgical repair should be considered for all patients with ascending aortic involvement (type A IMH) and for any patient with persistent or recurrent pain. Conversely, surgery may not be required in all patients with IMH of the descending thoracic aorta. In particular, older, high-risk individuals in whom both hematoma of the descending aorta and pain can be controlled with antihypertensive therapy may benefit from a conservative approach. All patients, however, need serial follow-up imaging to rule out progression. Regardless of the treatment strategy, IMH is associated with a poor long-term prognosis in elderly hypertensive patients. In the presence of typical symptoms and with no visualization of a dissecting membrane, IMH should be suspected until ruled out by independent imaging modalities. Additional studies merging pathological, imaging, and clinical investigations are needed before firm treatment guidelines can be established.

	Acknowledgments

 
The authors want to express their appreciation to the academic and technical staff of the emergency room service, the coronary care units, and the divisions of diagnostic radiology, anesthesiology, thoracic surgery, and pathology at the University Hospital Eppendorf in Hamburg and the Christian-Albrechts-Universität in Kiel, Germany. We are also indebted to Dörte Oestreich for her help in preparing this manuscript.

Received December 27, 1994; revision received February 23, 1995; accepted February 25, 1995.

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