Plasma beta-thromboglobulin (beta TG), platelet procoagulant activity (PPA) and malondialdehyde were evaluated in a control group and in 59 patients with chronic coronary heart disease (CHD) undergoing long-term anticoagulant therapy (ACT) with acenocoumarol, and within 2 months after its termination. The patients were clinically stabilized after more than 1 year of an acute myocardial infarction. An increase in beta TG and PPA was found in the patients, both with or without ACT, when compared to the control group. In addition, PPA was found to be higher in older and hypercholesterolemic patients on ACT. After ACT suppression, PPA activity increased significantly, particularly in younger and normocholesterolemic patients. The results of the present study suggest that CHD patients on ACT have some platelet hyperactivity and that the termination of ACT induces an increase in platelet function, particularly in PPA.