The pathobiology of aortic aneurysms.

Aneurysmal disease of the aorta, defined as a focal dilation exceeding 150% of the normal arterial diameter [1], is a potentially fatal disease occurring with increasing frequency in our aging population. Its prevalence is estimated at 3% in individuals over the age of 50 [2], with a peak incidence in the eighth decade of life [3, 4]. Although a definite etiology of this disease has not been identified, it has been associated with numerous, although nonspecific risk factors, including male gender, hypertension, smoking, coronary artery occlusive disease, concurrent peripheral aneurysms, a family history of aneurysm disease, and the presence of inguinal hernia(e) or emphysema [5–11]. Early studies regarding the pathobiology of aneurysms have indicated that they originate from a degenerative disorder of the arterial wall that is often found in conjunction with atherosclerotic change [12]. These observations led to the conclusion that atherosclerotic plaque resulted in a weakening of the arterial wall either because of lipid infiltration and direct disruption of normal wall architecture or to compression and reduction of flow through the vasa vasorum causing medial ischemia [13]. However, despite this strong association, clinical and histochemical differences between these diseases did not support a causative link. Tilson and Stansel outlined features of aneurysmal and occlusive disease, which suggested distinct etiologies. They noted that aneurysms occurred in an older demographic population with a greater degree of gender specificity, that they were infrequently associated with evidence of significant occlusive disease, that they tended to affect the proximal to mid infrarenal aorta rather than follow the more distal distribution of atherosclerosis, and that the natural history of arterial