Abstract
ADP-induced platelet aggregation was examined in patients with a history of ischemic cerebral vascular disease (CVD). When a threshold concentration of ADP for production of the secondary platelet aggregation was taken as a marker of platelet function, no remarkable difference was observed between CVD patients and control subjects. However, when thrombosis of perforating arteries diagnosed from computotomography findings was compared with that of main trunks of cerebral arteries, enhanced platelet aggregation was noted in the patients of perforating artery occulsion. The role of platelet aggregability in thrombogenesis thus seems to be manifested more readily in this type of vessel branching. As previously reported, platelet aggregation is remarkably enhanced in the presence of red blood cells. Our results also suggested that higher platelet aggregability might be compensated for by a lower hematocrit value.
β-Thromboglobulin (βTG), a new indicator of intravascular platelet activation, was determined in plasma of CVD patients but no increase was observed in the chronic phase after the attack. In patients with Ménière's disease, the BTG level was elevated during the attack, but was within normal range in the intermittent periods.
