This article confirms the existence of two variants of acute aortic pathology, the penetrating atherosclerotic ulcer (PAU) and the intramural hematoma (IMH), which are radiologically distinct from classic aortic dissection. Table 4 reviews the characteristics distinguishing PAU from classic aortic dissection and IMH. We took as a matter of definition that classic aortic dissection involves a flap which traverses the aortic lumen. We defined PAU and IMH as nonflap lesions, with PAU demonstrating a crater extending from the aortic lumen into the space surrounding the aortic lumen. This categorization can be summarized with the expression, "no flap, no dissection." With these definitions made, re-review of the imaging studies for the present report identified 36 such lesions out of 214 cases originally read as aortic dissection. Therefore, these variant lesions accounted for over 1 out of 8 acute aortic pathologies. Besides confirming the existence of the conditions, PAU and IMH, as distinct radiographic lesions, this series strongly suggests that these two conditions constitute distinct clinical entities as well. Table 4 summarizes the clinical patterns of these two entities as apparent from the present study, and contrasts them with classic aortic dissections. In particular, the following observations, some of which are consonant findings in smaller series, can be made regarding the typical patient profiles of PAU and IMH from the present study: The patients with PAU and IMH are distinctly older than those with type A aortic dissection (74.0 and 73.9 versus 56.5 years, P = 0.0001). Although not statistically significant, PAU and IMH patients tend to be older than patients with type B aortic dissections as well. For PAU and IMH, unlike aortic dissection, the concentration in the elderly is manifested in a very small standard deviation of the mean age (see Fig. 13); these two entities, PAU and IMH, are essentially diseases of the seventh, eighth, and ninth decades of life. Patients with PAU and IMH are almost invariably hypertensive (about 94% of cases). The pain of PAU and IMH mimics that of classic aortic dissection, with anterior symptoms in the ascending aortic lesions and intrascapular or back pain with descending aortic lesions. Unlike classic dissection, PAU and IMH do not produce branch vessel compromise or occlusion and do not result in ischemic manifestations in the extremities or visceral organs. PAU and IMH are more focal lesions than classic aortic dissection, which frequently propagates for much or the entire extent of the thoracoabdominal aorta. PAU is uniformly associated with severe aortic arteriosclerosis and calcification, whereas classic dissection often occurs in aortas with minimal arteriosclerosis and calcification. PAU and IMH tend to occur in even larger aortas than classic aortic dissection (6.2 and 5.5 versus 5.2 cm, P = 0.01). PAU and IMH are strongly associated with AAA, which is seen concomitantly in 42.1% of PAU patients and 29.4% of IMH patients. PAU and IMH are largely diseases of the descending aorta (90% for PAU and 71% for IMH). Although our pathology data is limited, we do feel that an inherent difference in the histologic intramural level of the hematoma may underlie the pathophysiologic process that determines which patient develops a typical dissection and which develops an intramural hematoma. In particular, we feel that the level of blood collection is more superficial, closer to the adventitia, in IMH than in typical aortic dissection. This may explain why the inner layer does not prolapse into the aorta on imaging studies or when the aorta is opened in the operating room. This more superficial location would also explain the high rupture rates as compared to classic aortic dissection (Fig. 14, Table 3). We did find PAU and IMH to behave much more malignantly than typical descending aortic dissection. As seen in Figure 6, the rupture rate is much higher than for aortic dissection. Docume