Platelet aggregation, coronary artery disease progression and future coronary events.
The platelet-aggregatory response, platelet-release factors and markers of thrombin generation in vivo were studied prospectively in 53 patients participating in a randomized clinical trial evaluating the influence of nicardipine on the progression of coronary atherosclerosis. Coronary lesions were measured quantitatively and progression was defined as a decrease in minimum diameter by > or = 0.4 mm. At repeat angiography 24 months after study entry, 20 of the 53 patients had progression of 28 coronary narrowings. Only thrombin-induced enhanced platelet aggregation differentiated patients with from those without coronary disease progression, with an estimated odds ratio of 2.49 (95% confidence interval 1.10 to 5.66). The aggregatory response to adenosine diphosphate, collagen, epinephrine and platelet-activating factor were not different in the 2 groups of patients, nor were measurements of platelet factor 4, beta-thromboglobulin, thromboxane B2, 6-keto-prostaglandin F1 alpha and fibrinopeptide A. During 46.8 months 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 disease progression and an enhanced thrombin-induced platelet aggregation had a worse prognosis than those with no disease progression and a low thrombin-induced platelet aggregation. Thus, patients with coronary disease progression and future coronary events have an enhanced thrombin-induced platelet aggregation. This platelet abnormality may be a marker of increased risk and may play a causative role in the development of coronary events.
Lam
J Y
JY
Department of Medicine, Montreal Heart Institute, Québec, Canada.
Latour
J G
JG
Lespérance
J
J
Waters
D
D
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D017023:Coronary Angiography; D003327:Coronary Disease / Q000097:blood* / Q000503:physiopathology* / Q000517:prevention & control; D004311:Double-Blind Method; D005260:Female; D005344:Fibrinopeptide A / Q000032:analysis; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D009529:Nicardipine / Q000627:therapeutic use; D010919:Placebos; D010974:Platelet Aggregation / Q000187:drug effects / Q000502:physiology*; D010978:Platelet Factor 4 / Q000032:analysis; D011446:Prospective Studies; D015996:Survival Rate; D013917:Thrombin / Q000494:pharmacology; D013929:Thromboxane B2 / Q000097:blood; D001620:beta-Thromboglobulin / Q000032:analysis
D010919:Placebos; D001620:beta-Thromboglobulin; D005344:Fibrinopeptide A; D010978:Platelet Factor 4; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D009529:Nicardipine; D013917:Thrombin