A variety of platelet function tests were performed in patients with four forms of obstructive
cerebrovascular disease (CVD);
transient ischemic attacks (TIA), reversible ischemic neurological deficit (RIND),
cerebral infarct, and
cerebral embolism of cardiac source in rheumatic
valvular heart disease (RVHD). Platelet studies included platelet aggregation induced by
ADP and
ristocetin,
spontaneous platelet aggregation,
von Willebrand factor (VIII:vWF),
platelet aggregation enhancing factor (PAEF), and percentage of large platelets (megathrombocytes). Serial testing was carried out in
acute stroke patients. The effect of
aspirin therapy was also evaluated. A clear difference in results was observed between patients with cardiogenic
embolism and those with other forms of CVD. In patients with TIA, RIND, and
cerebral infarct, platelet aggregation, both induced and spontaneous, was enhanced along with elevation of plasma VIII:vWF and PAEF, and increased percentage of megathrombocytes. In patients with cardiogenic
embolism, however, these studies were negative except for percent megathrombocytes. This value was increased in the embolic patients with RVHD in comparison with non-embolic patients with RVHD. Increase in platelet aggregation to
ADP and percent megathrombocytes developed slowly over a week following
stroke. Induced and
spontaneous platelet aggregation, and percent megathrombocytes could be normalized with 600 mg
aspirin p.o. These studies suggest that a systemic increase of hyperaggregable platelets and of plasma activators of platelet function exists in thrombotic CVD and may be related to its pathogenesis, while local hemodynamic factors may be more important in the thrombogenesis of cardiogenic
embolism.