Calcium channel blockers are known to inhibit platelet aggregation in vitro and ex vivo. We studied the influence of a single oral dose of diltiazem (60 mg), nifedipine (10 mg) and verapamil (80 mg) on ADP-, collagen-, and epinephrine-induced platelet aggregation, malondialdehyde formation, serum thromboxane B2and platelet sensitivity to PGI2in 24 patients with coronary artery disease. Ninety minutes after drug intake most platelet function parameters were clearly decreased. Only collagen-stimulated platelet aggregation showed no significant drug effect. Malondialdehyde formation was more affected than ADP-induced platelet aggregation. Platelet sensitivity to PGI2was enhanced after nifedipine. These results suggest an alteration of the prostaglandin system as one of the underlying mechanisms. Diltiazem seems to be the most effective drug with a potent influence on platelet function ex vivo.