The study investigated whether patients hospitalized for unstable angina pectoris (UAP), who subsequently develop complete coronary thrombosis (acute transmural myocardial infarction (AMI)) despite medical treatment, exhibit platelet hyperaggregability in an assay system that does not employ agonist stimulation. The study comprised 89 patients with UAP (Braunwald type B). Unfractionated heparin and nitrate were administered to all patients via continuous intravenous drip together with aspirin taken orally. Citrated platelet-rich plasma (230-250x 10(3)/microl) was obtained on admission and again, in some patients, following the AMI. Platelet aggregability was measured in an optically modified cone-plate viscometer that enables the detection of platelet aggregation without agonist stimulation. A continuous shear rate of 1,200/s was employed. Of the 89 patients, 85 were finally stabilized, while 4 developed an AMI accompanied by persistent ST-segment elevation with increased levels of plasma creatine kinase within 3 h after starting the treatment. The extent of platelet aggregation on admission was significantly greater in these 4 patients compared with the 85 who were stabilized (87.8+/-6.8%, n=4 vs 26.8+/-9.1%, n=85; mean+/-SD). These data suggest that platelet hyperaggregability mediated mainly by fibrinogen binding to the activated glycoprotein IIb/IIIa complex occurs before a complete thrombotic occlusion and this evaluation may provide important information before the onset of myocardial infarction.