[Role of molsidomine on platelet activation in coronary ischemia]

Abstract

Platelet suppressive agents have been shown to improve the prognosis of coronary diseases such as myocardial infarction and unstable angina. Several markers of platelet activation during myocardial ischemia have been found to be increased. Platelet granule constituents (beta thromboglobulin or platelet factor 4) or thromboxane B2 have been reported to be enhanced and, in some studies, to be correlated with the ischemia. Molsidomine or its active metabolite SIN-1 have antithrombotic properties in experimental models. This effect seems to be at least partly related to their antiplatelet activities. SIN-1A inhibited platelet aggregation and release reaction. Specific investigations have demonstrated that SIN-1A acts at a early stage of platelet activation inhibiting calcium influx and phospholipase activity which lead to inhibition of thromboxane formation and fibrinogen binding. Antiplatelet properties were also observed after oral administration of molsidomine but the extent of inhibition appeared to vary with the subjects.