Long-term prognosis of patients with type B IMH is better than in patients with aortic dissection. However, survival at five years reported in different series ranges from 43% to 90%, depending on the population characteristics32,33,42. Several studies have shown important dynamic changes in IMH during evolution, mainly during the six first months31,33,37. Regression occurred within six months in 30% of cases, progression to dissection was observed in 40%, with classical dissection in 12% and focal dissection in 28%, and 30% reabsorbed with aortic dilatation33. In our series33, 50 patients with IMH were followed by clinical and imaging techniques for 45 ± 31 months. At the end of follow-up, the IMH had reabsorbed completely in 34% (Figure 14.10), progressed to classical dissection in 12% (Figure 14.11), evolved to fusiform aneurysm in 22% (Figure 14.12), evolved to saccular aneurysm in 8% (Figure 14.13), and evolved to pseudoaneurysm in 24% (Figure 14.14). Therefore, the most frequent morphological long-term evolution of IMH is to aortic aneurysm or pseudoaneurysm formation (54% of cases).
Maximum aortic diameter in the acute phase is the variable of greatest prognostic yield for IMH regression, showing smaller maximum aortic diameter than in the group that evolved to aortic aneurysm or dissection.
It has been reported that IMH with PAU or penetrating atherosclerotic ulcer was associated with a progressive disease course32. Sueyoshi et al.37 reported that 12 of 17 projections progressed to complications such as enlargement or evolution to classical dissection. Ganaha et al.31 reported that IMH with PAU was significantly associated with a progressive disease course and concluded that it was important to make a clear distinction between IMH with or without PAU. Kaji et al.40 showed that older age and appearance of an ulcerlike projection are predictive for progression with type B IMH. Literature results seem to confirm that one of the important complications of IMH is the localized dissection which is identified as an ulcerlike image43 (Figure 14.15). However, little is known about the long-term evolution of this complication.
Other variables (such as echolucency and IMH extension) predict progression to aortic dissection. Song et al.27 found no prognostic significance between echo-free space detected in IMH and progression to dissection. In that
study, only TEE was performed during a short follow-up period, and some localized dissections therefore may have gone unnoticed.
Long-term evolution to fusiform aneurysm is related to greater aortic diameter in the acute phase because structural weakness of the media and mechanical stress may favor fusiform dilatation44. On the other hand, patients evolving to fusiform or saccular aneurysm had higher frequency of atherosclerotic disease and ulcerated plaque in the aorta, which points to the atherosclerotic process as a leading cause of aneurysm formation. These findings suggest that IMH might be involved in the pathogenesis of chronic aneurysm. In patients with aortic atherosclerosis, some aorta wall hemorrhages may be symptomatic and be diagnosed as IMH within acute aortic syndrome, whereas others might be asymptomatic with silent progression to aortic aneurysm. In our follow-up studies, five asymptomatic aortic rebleeding were found, and all cases evolved to aneurysm formation. Moizumi et al.41 showed that thickness at two to four weeks after admission (cutoff value > 16 mm) was the only predictor of IMH-related events because of enlargement of the ulcerlike images or classical type B dissection. On the other hand, the maximum aortic diameter on admission
and two to four weeks later (cutoff value >53 mm) was also a significantly correlated variable for IMH-related events because of progressive aortic dilatation or rupture.
Was this article helpful?