Summary
Elevated levels of shear stress that occur in stenotic arteries may induce platelet
aggregation and initiate thrombosis. Shear-induced platelet aggregation (SIPA) was
studied in groups of ischemic stroke patients and normal subjects using a viscometric-flow
cytometric technique. Twenty-three patients who sustained an ischemic stroke that
was not of cardiac origin were included in this study, and were classified either
as atherosclerotic (n = 15) or as lacunar (n = 8) stroke patients. The results show
that shear stresses at the levels which occur in arteries partially occluded by atherosclerosis
or vascular spasm strongly activate and aggregate platelets, and this response is
much more pronounced in non-lacunar stroke patients who had documented atherosclerotic
disease of their cerebral vessels. SIPA is not affected by the time of blood drawing
after the onset of stroke suggesting that these platelet abnormalities are not transient
but chronic. Furthermore, the extent of platelet activation detected by an anti-P-selectin
monoclonal antibody and the proportion of neutrophil-platelet aggregates circulating
in vivo are significantly higher in the atherosclerotic stroke patients studied at
least one month after the onset of stroke. The results indicate that the enhanced
platelet responses observed in atherosclerotic stroke patients are not consequences
of ischemia, and therefore both platelet activation and elevated SIPA may be considered
as important risk factors for stroke. The methodology developed in this work may be
useful for characterization of platelet reactivity, and may contribute to our understanding
of thrombotic mechanisms.
