ALCOHOL AND STROKE - PATHOPHYSIOLOGIC MECHANISMS

Epidemiological evidence indicates that recent heavy alcohol consumpti on increases the risk for all major types of stroke, whereas light-to- moderate alcohol intake is associated with a decreased risk of ischemi c stroke. Although heavy drinking elevates blood pressure, there is no firm evidence to indicate that alcohol consumption causes the formati on of aneurysms, microaneurysms or other lesions in human arteries. Al cohol has been reported to precipitate vasoconstriction and rupture of small cerebral arteries in experimental animals. Alcohol-induced neck trauma has been shown to precipitate traumatic strokes,and alcohol-in duced cardiac arrhythmias have been observed in patients with embolic brain infarction. The effects of alcohol on hemostasis, fibrinolysis a nd blood clotting are variable and could either prevent or promote the occurrence of strokes. The antiatherogenic effects of regular light-t o-moderate alcohol consumption could be mediated by inhibition of low- density lipoprotein oxidation, and by elevated estrogen levels.