doi: 10.1161/01.CIR.0000023453.90533.82
(Circulation. 2002;106:284.)
© 2002 American Heart Association, Inc.
Intramural Hematoma in Acute Aortic Syndrome
More Than One Variant of Dissection?
From the Division of Cardiology at the University Hospital Rostock (C.A.N.), Rostock School of Medicine, Rostock, and University Hospital Lübeck, Division of Cardiovascular and Thoracic Surgery (H.H.S.), Lübeck, Germany.
Correspondence to Christoph A. Nienaber, MD, FACC, FESC, Department of Internal Medicine, Division of Cardiology, Rostock School of Medicine, Ernst-Heydemann-Str. 6, 18057 Rostock, Germany. E-mail christoph.nienaber@med.uni-rostock.de
Key Words: Editorials • aorta • cardiovascular diseases
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Intramural hematoma (IMH) of the aorta came onto the clinical horizon with its recognition as a variant of aortic dissection and with the early diagnostic use of modern tomographic imaging modalities in the evaluation of acute thoracic pain syndromes. IMH, which is a precursor of dissection, cannot be reliably distinguished from classic dissection on clinical grounds and is considered to represent about 10% to 20% of all cases of acute aortic syndromes. Other syndromes include symptomatic aneurysm, penetrating ulcerations, and dissection.
See p 342
Despite recent diagnostic advances, the complexities of aortic dissection remain the major challenge to cardiovascular medicine, with 30-day mortality rates of 27% for proximal and 29% for distal dissection even after surgery.1 In contrast to classic dissection, IMH is characterized by the absence of an aortic entry tear2–4 and the separation of media wall layers created by hematoma from rhexis of aortic vasa vasorum, which eventually leads to a secondary tear or to communication to the adventitial space. In both scenarios of progressive IMH, the evolution to overt dissection or even rupture may occur suddenly or be heralded by ongoing acute aortic syndrome. Unlike classic aortic dissection, IMH has no mechanisms of intramural decompression by a re-entry tear, but rather reveals intramural (intramedial) thickening or echolucent pockets of noncommunicating blood with potential for rupture or, at times, regression and resorption of the hematoma over time.4–9 Although the diagnostic implications of IMH continue to attract attention in the field of vascular medicine, predictions of both natural course
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