[Platelets and coronary artery disease (CAD) (author's transl)].
During recent years, platelets have been increasingly implicate in the pathogenesis of coronary artery disease and its complications. This is based on new knowledge of platelet physiology as well as on clinical observations. Experimentally, it can be demonstrated that platelet vessel wall interaction is important in atherogenesis. In animal, platelet aggregates in the arterial circulation may cause ischemic myocardial lesions. In patients who died suddenly platelet thrombi can often be found in the microcirculation at autopsy. Compounds released during platelet aggregation may cause a spasm of the coronary arteries. Hyperactive platelets can be demonstrated in patients with CAD as well as in patients with the known risk factors of CAD. In some clinical trials, platelet function inhibitors reduced death from cardiac causes. Here we review the theoretical and experimental basis of the "platelet hypothesis" of CAD and its complications as well as the rationale for treating patients with CAD with "'antiplatelet" drugs.
D000818:Animals; D001241:Aspirin / Q000627:therapeutic use; D001344:Autopsy; D001792:Blood Platelets / Q000502:physiology; D009202:Cardiomyopathies / Q000150:complications; D002473:Cell Wall / Q000502:physiology; D002986:Clinical Trials as Topic; D002994:Clofibrate / Q000627:therapeutic use; D003327:Coronary Disease / Q000188:drug therapy / Q000209:etiology*; D004176:Dipyridamole / Q000627:therapeutic use; D006494:Heparin Antagonists / Q000627:therapeutic use; D006801:Humans; D010974:Platelet Aggregation; D012306:Risk; D013442:Sulfinpyrazone / Q000627:therapeutic use
D006494:Heparin Antagonists; D004176:Dipyridamole; D002994:Clofibrate; D001241:Aspirin; D013442:Sulfinpyrazone
Thrombozyten und koronare Herzkrankheit.