ENHANCED PLATELET AGGREGABILITY UNDER HIGH SHEAR STRESS IN CORONARY CIRCULATION OF PATIENTS WITH UNSTABLE ANGINA

Abstract

Mechanical forces, including high shear stress, have been found to cause platelet aggregation. Although increased platelet aggregation is also associated with the pathophysiology of unstable angina, it is not known whether platelet aggregation induced by high shear stress occurs in the coronary circulation of patients with unstable angina. We assayed high shear stress induced platelet aggregation (h-SIPA) in each of 25 patients with unstable angina and a severe stenotic lesion of the left coronary artery, and in 5 patients with chest pain syndrome as controls. We obtained blood from the coronary ostium and coronary sinus of each subject during angiography and measured h-SIPA of each sample with a modified cone-and-plate type viscometer set at 108 dyne/cm^2. In the patients with unstable angina, h-SIPA of the samples from the coronary sinus was significantly higher than in those from the coronary ostium (p＜0.01). However, we detected no differences between blood from the coronary ostium and coronary sinus in samples from the control subjects. Although h-SIPA has been known to be mediated by the interaction between platelets and von Willebrand factor (vWF), we found no differences in the concentrations of vWF antigen or ristocetin cofactor activity between plasma from coronary ostium and coronary sinus of the patients with unstable angina. Platelet aggregation under conditions of high shear stress is enhanced in the coronary circulation of patients with unstable angina. These results suggest that treatment of these patients with an agent that prevents h-SIPA may be beneficial.