PLATELET ACTIVATION IN STABLE CORONARY-ARTERY DISEASE

To elucidate the role of physical activity in the pathogenesis of acute ischemic syndromes in patients with coronary artery disease (CAD), we hypothesized that platelet activation occurs when coronary blood flew velocity and shear stress increase across an atherosclerotic vascular bed. We measured platelet aggregation by using angiologic catheterization to obtain simultaneous samples of whole blood from the coronary sinus and the aorta while at rest, 2 minutes after the onset of rapid atrial pacing and 10 minutes after termination of pacing. Of 82 consecutive patients included in our study, 36 had stenosis of the left coronary artery, 12 had stenosis of the right coronary artery only, and 34 had no evidence of CAD. Samples taken at rest revealed no arteriovenous difference in platelet aggregation between patients with CAD and those without CAD. In patients with significant stenosis (greater than or equal to 80%) of the left coronary artery, atrial pacing caused platelet aggregation to increase in samples from the coronary sinus (64 +/- 9% increase; p <0.01) but not in blood from the aorta (2 +/- 8% decrease; difference not significant). This increase was transient, with aggregation returning almost to resting values 10 minutes after pacing ended. Atrial pacing elicited no change in platelet aggregation in samples from either the coronary sinus or aorta of patients with nonsignificant stenosis (<50%) of the left coronary artery, patients with significant stenosis of the right coronary artery only, and patients free of CAD. Thus, under resting conditions, no evidence of platelet activation across the coronary bed was seen regardless of CAD status. However, significant stenosis was associated with heightened platelet activation and aggregation when coronary blood flow was increased with atrial pacing.