Stroke, Vol 16, 643-647, Copyright © 1985 by American Heart Association
AB Shah, N Beamer and BM Coull
It remains uncertain whether platelet activation in ischemic stroke is
contributory or secondary to brain ischemia. The efficacy of aspirin (ASA)
in stroke prevention suggests that platelet activation contributes to the
occurrence of stroke. On the other hand, platelet activation may be simply
a generalized consequence of cerebral ischemic damage. To examine this
issue, plasma levels of the platelet specific proteins beta-thromboglobulin
(beta-TG) and platelet factor 4 (PF4) were measured in fifty-eight patients
with various defined types of acute ischemic strokes. beta-TG was a broader
indicator of platelet activation than PF4. Compared with an age-matched
control group, thromboembolic and cardioembolic stroke patients had
significantly elevated beta-TG levels (p less than 0.001). Also, beta-TG
levels in these stroke categories were significantly higher in samples
drawn within the first week after the event than in those drawn later (p
less than 0.001). In contrast, beta-TG levels in lacunar stroke patients
and in most TIA patients were normal. beta-TG levels did not correlate with
the volume of cerebral infarction as measured by planimetry from CT scans.
Moreover, beta-TG levels in patients on chronic ASA therapy at the time of
stroke did not differ from those in patients of the same diagnostic
categories not taking aspirin. These data indicate that platelet activation
may be important in some, but not all, subtypes of ischemic stroke and that
platelet activation can occur in stroke even though the platelet
cyclooxygenase pathway is suppressed.
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