Type B

There is a paucity of information regarding the evolution of type B IMH and maximum aortic diameter. In a recent study, Sueyoshi et al.37 reported that in the follow-up of 35 type B IMH, maximum aortic diameter over 40 mm predicted IMH progression. Although normal descending aorta diameter is smaller than that of the ascending aorta, the lower risk of descending aorta rupture could justify 50 mm being an adequate cutoff value for both type A and type B. A possible explanation for the prognostic value of maximum aortic diameter in short-term IMH evolution is that when intramural bleeding weakens the aorta wall, the greater stress on the wall of the dilated aorta implies a greater risk of rupture than that of the nondilated aorta.

Ganaha et al.31 suggested the presence of penetrating atherosclerotic ulcer in acute phase as the factor predicting IMH progression, with maximum aortic diameter lacking prognostic value. The high incidence of aortic ulcers

Figure 14.5. CT study showed a type A IMH, which evolved at six months to type B dissection with total reabsorption of ascending aorta IMH (arrowhead).

Figure 14.5. CT study showed a type A IMH, which evolved at six months to type B dissection with total reabsorption of ascending aorta IMH (arrowhead).

Figure 14.6. TEE visualized a localized dissection in the descending aorta (arrow) at one month of evolution of IMH. Arrow shows a short intimal flap.

(52%) in this retrospective series could be explained by the inclusion of IMH cases in a subacute or chronic phase with ulcerlike images due to localized dissections during IMH evolution. Thus, these localized dissections would constitute a complication rather than a prognostic variable in an acute phase. In our series33, TEE showed localized dissections with ulcerlike images in the study conducted prior to discharge in 28% of patients (Figure 14.6). TEE is the technique of choice for differentiating penetrating atherosclerotic ulcers from ulcerlike images (Figure 14.7). Although some focal dissection evolved to pseudoaneurysm formation, most remain stable without enlargement and others disappear.

Several published series showed that periaortic bleeding is more frequent in IMH than in classical dissection12,16,17. Although this bleeding is not necessarily the equivalent of aortic rupture, and most IMH tend to reabsorb without complications (Figure 14.8)12, the mortality of our patients with these complications was high (35-43%), particularly in the subgroup of patients who presented anemia on biochemical analysis (47%). However, progressive accumulation of a large amount of pleural effusion is not in itself an indication for surgical treatment.

Risk stratification based on clinical and diagnostic imaging findings in patients with IMH is very useful38. Some of the current predictive factors of disease progression proposed for patients with IMH include persistent and recurrent pain despite aggressive medical treatment31 , difficult blood pressure control32, ascending aorta involvement12, maximum aortic diameter 50 mm or more on initial CT scan34, progressive maximal aortic wall thickness

Figure 14.7. Differential diagnosis of aortic ulcers by TEE. In the left image, a penetrating aortic ulcer with thrombosis within is observed. In the right image, the ulcer is secondary to a localized dissection from a IMH.

Figure evolve follow

; 14.8. Type B IMH (arrows) with hemothorax and hemomediastinum (asteriscs), which to total regression of IMH, periaortic hemorrhage, and hemotorax, at eight months of -up.

(>11 mm)35, enlarging aortic diameter32, repetitive pleural effusion31, and presence of an associated penetrating ulcer or ulcerlike projection in the involved segment31.

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