[Adhesive activity of blood platelets in patients with stable or unstable angina pectoris and acute myocardial infarct].

Platelet adhesive activity was assayed in patients with stable angina (SA) or unstable angina (UA) and acute myocardial infarction (AMI). With scanning electron microscopy, platelet adhesions to Type IV collagen (C-IV) and plastic material, which had been stimulated by low-dose ADP, epinephrine and U-46 619, a stable thromboxane A2 analogue (agonist-induced adhesion) were determined. As compared with the control group, patients with SA or UA, showed significantly higher adhesion of platelets to the collagen substrate, whereas UA patients alone displayed a significantly increased agonist-induced adhesion when epinephrine was employed as an agonist. A sharp enhancement of platelet adhesion was characteristic of patients with AMI on days 1-3 of the onset. On days 4-5, the adhesive activity slightly dropped, and on day 7-10, it returned to the control level of healthy volunteers. The time course of adhesive activity decrease correlated with lower blood levels of creatine phosphokinase in patients with AMI. A high correlation was established between the alterations found in all the types of platelet adhesion during the course of AMI, which suggests there is an unspecific nature of increase and subsequent decrease platelet responses to all the inductors used. A comparison of patients taking and not taking aspirin (250 mg/day) revealed no differences both in the magnitude of an increase in platelet adhesion in the first 3 days and in that of its decrease on days 7-10 of AMI.