ABSTRACT
Three mechanisms have been implicated in the development o f aortic dissection.4,5,8 Firstly, aortic dissection often results from an initial intimal tear with secondary extension into the media, thereby separating the intima from adventitia. Once blood enters the aortic media, the time required for the pulsatile flow to dissect the entire aorta may be extremely brief. Multiple hemodynamic and physical factors
Fig. 4.1. Illustrations of different types of aortic dissections. Examples a, c, and fare considered Stanford type A aortic dissections (involvement of the ascending aorta). Note that the primary intimal tear may be located in the ascending aorta (a-1), transverse arch (a-2, c-2) or proximal descending thoracic aorta (f-3). Examples b, d, and e are considered Stanford type B dissections; that is, the ascending aorta is not involved. The intimal tear may originate in the arch (b-2, d-2, e-2) or the de scending thoracic aorta (b-3). (Modified from Miller DC. Surgical management of aortic dissections: Indications, perioperative management, and long-term results. In: Doroghazi RM, Slater EE, eds. Aortic Dissection. New York: McGraw-Hill, 1983: 193-243.)
lead to the initial development and subsequent propagation of the dissection. These include the rate of rise of systolic pressure, diastolic recoil pressure, mean arterial pressure, and structural integrity o f the media. Extension of the dissection requires underlying medial laxity and/or degeneration.4,5 Although this particular mechanism is common and thought to be the main cause o f aortic dissection, an intimal tear by itself does not necessarily lead to aortic dissection, and a dissecting hematoma may develop without a defined intimal tear. An important, but less common, etiology for the development o f aortic dissection is hemorrhage due to ruptured vasa vasorum
into a diseased media followed by propagation along the course of the aorta; a sec ondary intimal may or may not develop.4,5,8 Hirst et al found that 4% of patients had no identifiable intimal tear in a series of 505 autopsy cases o f aortic dissection.7 Distinct features o f “aortic dissection without intimal rupture” on imaging studies, such as computer tomographic scan (CT), magnetic resonance imaging (MRI) and/or transesophageal echocardiography (TEE), are the lack of an intimal tear and the presence of an intramural hematoma (IMH).8 The natural history of IMH is unpre dictable; it can heal with little evidence of a previous medial disruption, or it can progress to frank aortic dissection years later. Finally, a third and rare mechanism of localized aortic dissection is the result of penetrating atherosclerotic ulcer extending through the intima with resultant hematoma formation within the media. C T dem onstrates intimal disruption with an ulcer, a localized hematoma and limited propa gation o f the false lumen. In contrast to conventional type B aortic dissection, where the intimal defect is typically located immediately distal to the left subclavian artery, dissection due to a penetrating atherosclerotic ulcer usually originates in the mid or distal descending thoracic aorta.
