Intracoronary thrombus formation is the essential pathogenic substrate for the development of the acute ischaemic coronary syndromes (unstable angina pectoris (UAP), acute myocardial infarction (MI) and sudden cardiac death). Rupture of an atherosclerotic plaque has been shown to be of major importance for initiation of the thrombogenic process, but the reactivity of the circulating platelets and their interaction with the coronary vessel wall are also important for the formation and propagation of the intracoronary thrombus. The evidence favouring the role of platelets is: 1) the aggregability of platelets is increased in the morning where the incidence of MI and sudden cardiac death has been shown to be high, 2) shortened bleeding time and increased mean platelet volume in the acute phase of MI, 3) the synthesis of proaggregatory thromboxane A2 is increased in the acute phase of MI and in UAP, 4) a high platelet count and an increased ADP-induced platelet aggregation predispose to MI and death in healthy males, 5) high mean platelet volume and increased spontaneous platelet aggregation are risk factors for MI and death in patients with a recent MI, 6) the platelet inhibitor, acetylsalicylic acid, has been shown to reduce the incidence of MI and mortality in patients with silent myocardial ischaemia, stable and unstable angina pectoris and in patients with MI.