(Circulation. 1995;92:1465-1472.)
© 1995 American Heart Association, Inc.
Articles |
Intramural Hemorrhage of the Thoracic Aorta
Diagnostic and Therapeutic Implications
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.
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Abstract |
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 Top Abstract IntroductionMethods Results Discussion References |
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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
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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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.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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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.
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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
elsewhere2 3 (Fig 1). With
hemodynamic monitoring and sedation, studies were
safely completed within 10±6 minutes.
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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
ms3 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.
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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).
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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
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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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%).
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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.
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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).
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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.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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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.
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Acknowledgments |
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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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