Why the study?
Are platelet coagulant activities altered in patients with angiographically proven coronary artery disease compared to those with normal angiograms?
Are platelet coagulant activities altered in patients with angiographically proven coronary artery disease compared to those with normal angiograms?
Patients with coronary artery disease exhibit enhanced platelet coagulant hyperactivity and reduced antithrombin III activity, suggesting a role of platelets in CAD pathogenesis.
Hypothesis-generating for prothrombotic platelet activity in CAD; leaves open causality and therapeutic relevance.
Platelets have been implicated in the pathogenesis of coronary artery disease, and a number of studies have examined platelet function and coagulation parameters in such patients. We have examined platelet coagulant activities, volumes, and aggregate ratios in 23 patients with chest pain, seven of whom had normal coronary angiograms (group I) and 16 of whom had angiographically proven coronary artery disease (group II). There were no significant differences in the mean values for platelet volume or platelet aggregate ratios between the two groups. The platelet coagulant activities concerned with initiation and the early stages of intrinsic coagulation were significantly increased in patients in group II as compared with those in group I. No significant differences were noted between the two groups with respect to prothrombin time, partial thromboplastin time, and plasma levels of fibrinogen and coagulation factors V and VIII. However, the mean activity in plasma of antithrombin III (but not the level of antithrombin III antigen) was significantly lower in patients of group II compared with group I. Overall, our observations provide evidence for an enhanced contribution of platelets to the intrinsic coagulation system in patients with coronary artery disease. The platelet coagulant hyperactivity noted in these patients may reflect a role of platelets in the pathogenesis of coronary artery disease or may be secondary to the underlying arterial disease.
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Rao et al. (1984) studied this question.
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