PLATELET-AGGREGATION, CORONARY-ARTERY DISEASE PROGRESSION AND FUTURE CORONARY EVENTS

The platelet-aggregatory response, platelet-release factors and marker s of thrombin generation in vivo were studied prospectively in 53 pati ents participating in a randomized clinical trial evaluating the influ ence of nicardipine on the progression of coronary atherosclerosis. Co ronary lesions were measured quantitatively and progression was define d as a decrease in minimum diameter by greater than or equal to 0.4 mm . At repeat angiography 24 months after study entry, 20 of the 53 pati ents had progression of 28 coronary narrowings. Only thrombin-induced enhanced platelet aggregation differentiated patients with from those without coronary disease progression, with an estimated adds ratio of 2.49 (95% confidence interval 1.10 to 5.66). The aggregatory response to adenosine diphosphate, collagen, epinephrine and platelet-activatin g factor were not different in the 2 groups of patients, nor were meas urements of platelet fao tor 4, beta-thromboglobulin, thromboxane B-2, 6-keto-prostaglandin F-1 alpha and fibrinopeptide A. During 46.8 mont hs of follow-up after repeat angiography, coronary events occurred in 11 of the 20 with and 6 of the 33 without progression (difference 37%, p = 0.013, confidence interval 11 to 63%). Those with coronary diseas e progression and an enhanced thrombin-induced platelet aggregation ha d a worse prognosis than those with no disease progression and a low t hrombin-induced platelet aggregation. Thus, patients with coronary dis ease progression and future coronary events have an enhanced thrombin- induced platelet aggregation. This platelet abnormality may be a marke r of increased risk and may play a causative role in the development o f coronary events.