Stroke, Vol 18, 268-271, Copyright © 1987 by American Heart Association
PB Gorelick
Alcohol might contribute to stroke in several ways: induction of cardiac
arrhythmias and cardiac wall motion abnormalities which predispose to
cerebral embolism, induction of hypertension, enhancement of platelet
aggregation and activation of the clotting cascade, and reduction of
cerebral blood flow by stimulation of cerebral vascular smooth muscle
contraction or by altering cerebral metabolism. While these
pathophysiological mechanisms have gained enthusiastic experimental and
theoretical support, the findings are preliminary and will require further
large-scale clinical and epidemiological analyses to substantiate their
roles as causal factors or potentiators of stroke. Documentation of
measurable platelet and coagulation cascade abnormalities reported in
healthy volunteers who have ingested alcohol will need to be confirmed on a
broader scale in stroke patients with recent ethanol consumption. The risk
of stroke in those with alcohol- induced atrial fibrillation and
cardiomyopathy must be ascertained for the general population. While the
experimental evidence is exciting and provocative, epidemiological evidence
also suggests a link between alcohol consumption and stroke. Regular
alcohol ingestion is associated with hypertension, fatal and nonfatal
intracranial hemorrhage, cerebral infarction, and increased risk of death
from stroke. Recent, less stringently controlled studies suggest that
alcohol consumption is a risk factor for cerebral infarction in young
adults with occasional ethanol intoxication and middle-aged women and young
men with occasional alcohol intoxication and regular heavy drinking.
Alcohol may also be a risk factor for subarachnoid hemorrhage.
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