(Circulation. 1995;92:1376-1378.)
© 1995 American Heart Association, Inc.
Articles |
Acute Aortic Dissection and Its Variants
Toward a Common Diagnostic and Therapeutic Approach
From Harvard Medical School and the Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital (P.T.O'G.), and the Cardiac Unit, Medical Services, Massachusetts General Hospital (R.W.DeS.), Boston, Mass.
Correspondence to Patrick T. O'Gara, MD, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115.
Key Words: editorials • aortic dissection
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Acute dissection of the aorta is an uncommon yet potentially catastrophic clinical event that mandates prompt recognition and expeditious treatment. Diagnosis begins with a high clinical index of suspicion in a patient presenting with chest pain and one or more predisposing risk factors, most notably, hypertension or an inherited disorder of connective tissue. Verification can be rapidly achieved with a high degree of accuracy using one of several noninvasive imaging techniques and, when necessary, contrast angiography. Involvement of the ascending aorta (type A) requires surgical intervention, whereas clinically stable dissection limited to the descending thoracic aorta (type B) can in general be treated medically. Negative inotropic andantihypertensive medical therapy is provided to all patients. Hospital and long-term survival has improved substantially over the past 40 years, yet there remains ample room for continued progress. For centers with an active interest in the evaluation and management of acute dissection, hospital mortality rates have been lowered to 15% to 25%.1 2 3 Five-year actuarial survival rates range between 50% and 70%,2 4 5 with a 7% to 20% incidence of late reoperation, usually for aneurysmal enlargement or redissection.2 6 7
There has long been some debate over the pathogenesis of aortic dissection. In the majority of cases, the initiating event is a tear in the intima of the aorta through which blood surges into the middle to outer third of the media.8 9 10 Intimal disease, such as that associated with atherosclerosis, is not a prerequisite, although underlying medial disease due to both elastic fiber and smooth muscle cell degeneration is the rule.11 12 13 Intimal tears are most commonly located a few centimeters above the aortic valve, along the right anterolateral aspect of the aorta, where hydrodynamic and torsional forces are greatest.9 The second most frequent site of entry is in the descending thoracic aorta just beyond the insertion of the ligamentum arteriosum, where the relatively mobile arch becomes anchored to the thoracic cage.9 The dissecting column of bloodpropagates most often in an anterograde direction under the influence of systolic forces, although retrograde extension can and does occur. Blood in this false channel can reenter the true lumen of the aorta anywhere along its length. Alternatively, the dissecting hematoma can rupture through the adventitia, which, depending on its location, can result in any one of several well-recognized clinical complications: hemopericardium with cardiac tamponade (type A involvement) or hemothorax with circulatory collapse (type A or B involvement). Distortion or disruption of the aortic valve may lead to varying degrees of aortic regurgitation. Compromise of a major aortic branch vessel can result in a wide variety of coronary, neurological, or visceral ischemic syndromes. In the process of propagation, the dissection shears the intima from the adventitia, thus creating an oscillating flap of tissue that separates the true from the false lumen. The diagnosis of classic dissection by any imaging technique hinges critically on the identification of this intimal flap, although exceptions do occur when, for example, the false lumen becomes completely thrombosed with varying degrees of true luminal compression.
The alternative mechanism for the initiation and propagation of an aortic dissection is embodied in the vasa vasorum hypothesis, which attributes the formation of the intramural hematoma to the spontaneous rupture of these nutritive vessels within the diseased aortic wall.14 15 16 Autopsy studies of patients with aortic dissection have described a minority (4% to 13%) in whom an entry tear was not identified.8 15 16 Criticisms levied against these studies have included the lack of personal inspection of specimens by the reporting authors, problems related to sampling errors or preparation, or both.17 However, the recent careful application of increasingly more-refined noninvasive imaging techniques (in particular, contrast-enhanced computed tomography [CT], magnetic resonance imaging [MRI], and transesophageal echocardiography [TEE] with Doppler interrogation) as well as direct surgical inspection21 22 have resurrected this hypothesis. These noninvasive techniques have greatly improved the ability to detect aortic pathology and have expanded the understanding of the natural history of a spectrum of disorders, the common expression of which is an intramural hematoma.
Two important radiological and pathological variants of aortic dissection are recognized: penetrating aortic ulcer23 24 25 26 27 and intramural hemorrhage (IMH) without an intimal flap.18 19 20 21 22 Patients with these variants cannot be distinguished reliably from those with classic dissection at initial presentation on clinical grounds alone. Chest or back pain on a substrate of chronic hypertension is the common theme. Abnormalities of either the size or contour of the thoracic aorta on plain chest radiographs are present in the vast majority (approximately 90%). A few distinctions, however, can be made. Patients with penetrating ulcers tend to be older, with a heavier burden of atherosclerotic disease, and are often active smokers.24 27 Preexistent disorders of connective tissue, as might occur in a minority of patients with classic dissection or IMH, are not a feature of patients with penetrating ulcers.24 27 The ulcers affect the mid to distal portion of the descending thoracic aorta almost exclusively and are not usually associated with extensive longitudinal propagation or branch vessel compromise. Accordingly, they are not accompanied by the valvular, pericardial, or neurovascular complications seen with classic dissection and IMH.24 27 By either cross-sectional or angiographic imaging techniques, the penetrating aortic ulcer is further distinguished by evidence of associated atherosclerotic disease and clear ulceration extending beyond the intimal border—often with a nipple-like projection—with subjacent hematoma formation.26 In contrast to classic aortic dissection and spontaneous IMH, medial hematoma formation in penetrating aortic ulcer derives from the continued erosion of an atherosclerotic plaque with eventual violation of the internal elastic membrane.23 The process may be spontaneously contained or progress to false aneurysm formation and/or rupture.
The article by Nienaber and colleagues in this issue of Circulation28 emphasizes the remarkable clinical similarities between patients with IMH and those with classic aortic dissection. In so doing, it further clarifies the management of patients with IMH and eliminates the ambiguity previously engendered by the inability to discern an intimal flap. The recognition and localization of intramural hematoma, rather than intimal disruption or oscillation per se, are the critical determinants of therapy.
Although previous reports have described an older cohort of patients (mean age, 70 years) with a marked predilection for the descending thoracic aorta,20 22 patients in the study of Nienaber et al were in general younger (mean age, 56 years), and approximately half had ascending aortic involvement.28 The frequent progression of IMH to either frank dissection or rupture, as well as the potential development of aortic regurgitation, pulse deficits, or neurological syndromes, accentuates the clinical similarities. Distinctions between IMH and classic aortic dissection are clinically artificial and should be abandoned so as not to delay appropriate treatment.
Nienaber et al have confirmed and extended the previous observation of Mohr-Kahaly et al20 and Robbins et al22 that patients with aortic IMH should be managed with the same empirical guidelines that have been successfully adopted for patients with classic dissection. Specifically, involvement of the ascending aorta should prompt urgent surgical repair, the ultimate extent of which will depend on the intraoperative findings. Initially stable patients with IMH of the descending thoracic aorta can be treated medically with frequent clinical and radiological reassessment. A similar strategy is appropriate for patients with penetrating aortic ulcers.27 Indications for surgery in lesions involving the descending thoracic aorta have traditionally included recurrent or intractable pain despite aggressive medical therapy; rapid, localized aortic expansion; leakage or threatened rupture, particularly in a previously aneurysmal aorta; major branch vessel compromise with vital organ ischemia; and a preexistent connective tissue abnormality.29 Lesions involving the aortic arch are inherently more complex, although advances in anesthetic techniques and cerebral protection have led to a more aggressive approach.30
It is equally important to note that in 8 of the 25 patients (32%) described by Nienaber et al,28 the contrast digital angiographic studies were described as normal despite the detection of IMH with corroborative cross-sectional imaging techniques. The inability to recognize IMH with contrast angiography likely contributed to the reduced sensitivity of this technique reported by Erbel et al31 in their investigation of 126 patients with suspected aortic dissection. More recently, Barnsal et al32 reported false-negative angiographic studies in 15 of 65 patients, 13 of whom had aortic intramural hematoma detected by TEE or CT scanning. In all studies, the sensitivity for either TEE, contrast-enhanced CT scanning, or MRI exceeded 96%.28 31 32 The relative usefulness of these noninvasive imaging modalities for the diagnosis of suspected aortic dissection has been well characterized in a cohort of 110 consecutive patients in an earlier report by Nienaber et al33 and have been reviewed elsewhere.34 35
In clinical practice, TEE or contrast-enhanced CT scanning has become the initially preferred diagnostic strategy for the assessment of patients with suspected acute aortic syndromes. The use of MRI has been limited by the restricted availability of the magnets and by considerations of patient safety while undergoing study. Decisions regarding the urgent need for surgery need not depend on contrast angiographic findings.3 22 28 32 Contrast angiography may be the least-sensitive imaging technique for the detection of IMH, an entity that may pertain to as many as 20% of patients with suspected dissection,20 yet has the same spectrum of potential complications. The particular strategy adopted at any institution involved in the evaluation and care of patients with acute aortic syndromes should be that for which there is the greatest local expertise. Vigilance, careful attention to detail, and a low threshold for repeat imaging of the same or complementary type are critical to any management plan.
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The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association, Inc.
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References |
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