Is the Optimal Management of Acute Type A Aortic Intramural Hematoma Evolving?
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Aortic intramural hematoma (IMH) has been considered a variant or precursor of aortic dissection with no entry tear or false lumen flow; however, the pathophysiological mechanism, risk factors, and evolution are rather different from those of classic dissection. Hematoma forms within the aortic wall as a result of either hemorrhage of the vasa vasorum or, less commonly, an intimal fracture of an atherosclerotic plaque. The marked relationship between IMH and atherosclerotic disease explains the older age of these patients compared with those with aortic dissection, the higher incidence of arterial hypertension, and the tendency for descending aorta involvement (50% to 60%).1–5
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Evolution of the IMH in the acute phase may be highly dynamic, with bleeding of the aorta wall increasing progressively, stabilizing or provoking disruption of the intima, which may lead to a classic or localized dissection. This intimal disruption may be seen in the early hours of presentation or some months after the intramural bleeding has occurred2,5–8 (Figure 1). For this reason, IMH has been considered a precursor of aortic dissection. However, 2 significant differences between IMH and aortic dissection appear to be well defined. First, IMH might regress spontaneously with time4,5,7,9 (Figure 2). Second, fewer severe cardiovascular complications, valvular aortic regurgitation, and visceral or peripheral ischemia are present.2,8 Therefore, IMH almost resembles an aortic dissection, but with a distinct, unique pathological nature.