**2.2 Pathophysiology**

The mechanisms leading to AAS arise from many sources, although preexisting medial degeneration is proven to be an important risk factor for acute aortic dissection. Cystic medial necrosis is a hallmark of the histology, especially in aortic aneurysm patients. Microscopic features include decreased amount of vascular smooth-muscle cells, mucoid deposits and elastin deficiency [7]. However, over 80% of acute dissections occur in absence of a pre-existing aneurysm. The International Registry of Acute Aortic Dissection (IRAD) has collected an impressive amount of data for the demography of patients who present with AAS. The most commonly associated factors are:


Improvements in the resolution of aortic imaging has led to the identification of pathological submodalities, i.e. intramural haematoma or penetrating atherosclerotic ulcer. Histological findings of these lesions generally demonstrate significant intimal atherosclerosis, which is not a constant finding in aortic dissection biopsies. Studies suggest that aortic dissection is an end process with a wide pathological spectrum, many of which facilitate weakening and/or increased stress of the aortic wall. The chain of pathological events might begin with a small superficial intimal rupture; atherosclerotic ulcers may provide a good millieu for development of such a tear. Alternatively, disruption of vasa vasorum might result in an intramural haematoma, which later ruptures into the aortic lumen or leads to dissection. However, it is likely that many aortic dissections develop without having a pre-stage of intramural haematoma or penetrating ulcer [8].
