Smoking and Cerebral Aneurysms—Potential Pathobiologic Mechanisms

Abstract

ubarachnoid hemorrhage, caused by a rupture of a saccular intracranial artery aneurysm (sIAA), is a devastating disease S with highmorbidity andmortality (6). Smoking, in addition to hypertension, female gender, alcohol abuse, and positive family history, is one of the most important risk factors for aneurysmal subarachnoid hemorrhage. Smoking is also an independent risk factor for sIAA formation and growth, the latter being related to an increased risk of aneurysm rupture (4). Although a small portion of sIAAs are diagnosed in children,most sIAAs occur during adult life. sIAA is considered an acquired disease, in which known risk factors play a significant role in pathogenesis, although the exact pathobiologic mechanisms are still largely unknown. As reviewed by Aoki and Nishimura (1), intracranial aneurysms can also be induced in cerebral vasculature of rodents in an experimental setting merely by changing the flow conditions by inducing hypertension and disrupting the collagen-elastin cross-linkages by administration of b-aminopropionitrile, which additionally supports the view of sIAA being an acquired disease by nature.