Aspirin therapy in angina pectoris: Effects on platelet aggregation, exercise tolerance, and electrocardiographic manifestations of ischemia

If altered platelet function contributes to poorly perfused zones of myocardium in patients with angina pectoris, then specific antiplatelet therapy might improve cardiovascular function and exercise performance. Exercise tolerance on a bicycle ergometer, heart rate-blood pressure product, and ischemic ECG changes at exercise end-point were compared before and during oral aspirin therapy (2.4 Gm. per day for 2 weeks) in 11 normal subjects and in 11 patients with stable angina pectoris. Platelet aggregation threshold in response to ADP and epinephrine was measured. Untreated patients had increased platelet aggregability when compared to normal subjects. Mean concentration of ADP for aggregation threshold was 1.80 μM^* in patients and 4.1 μM^* in normal subjects (p<0.01); with epinephrine mean concentration for aggregation was 1.86 μM^* in patients and 11.0 μM^* in normal subjects (p<0.01). After aspirin, platelet release of ADP in response to aggregating agents was abolished in both patients and normal subjects, completely inhibiting irreversible aggregation. No change in exercise tolerance was observed in either group following aspirin and heart rate-blood pressure product was unchanged. In patients, total work performance was 810±122 k.p.m. before and 872±119 k.p.m. after aspirin (p=NS). Heart rate-blood pressure product was 15,700±425 before and 16,200±400 after aspirin. Exercise-induced ischemic ECG changes were not altered by aspirin. Thus, aspirin significantly reduces platelet aggregability in patients with angina pectoris but does not improve exercise tolerance, change pain threshold, or alter ischemic ECG abnormalities.*Geometric mean.