Pacing induced angina and platelet reactivity.

Platelet function was studied during pacing-induced angina pectoris in nine patients with coronary heart disease. Blood was sampled via catheters from the coronary sinus and the aorta at rest and during angina. The influence of the sampling procedures on the platelet function was evaluated in blood collected via catheters and via short venflons. The catheter induced pseudopod formation in the platelets. The aggregation response was similar, while platelet retention as measured with Hellem's method for native blood, was slightly lower in blood collected via catheters than via venflons. At rest the maximal rate of primary, ADP-induced aggregation was lower in blood from the coronary sinus than from the aorta, as was the percentage of platelets retained in glass bead columns. The ability of platelets to produce prostaglandin metabolites, estimated from malondialdehyde formation after thrombin stimulation was also moderately, but significantly lower in coronary sinus blood. During pacing-induced angina primary, ADP-induced aggregation and platelet retention values remained significantly lower in blood that had passed the coronary circulation than the aortic blood. There were no differences between aortic or coronary sinus samples collected at rest than during pacing. Unchanged platelet counts indicates that trapping of platelets did not occur. Thus, platelet reactivity was lower in coronary sinus than aortic blood at rest in patients with coronary heart disease, and a moderate pacing-induced angina did not influence this pattern.