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(Circulation. 2000;102:1901.)
© 2000 American Heart Association, Inc.

Clinical Investigation and Reports

Platelet Pl^A2 Allele and Incidence of Coronary Heart Disease

Results From the Atherosclerosis Risk In Communities (ARIC) Study

Nena Aleksic, PhD; Harinder Juneja, MD; Aaron R. Folsom, MD; Chul Ahn, PhD; Eric Boerwinkle, PhD; Lloyd E. Chambless, PhD; Kenneth K. Wu, MD, PhD

From the Division of Hematology and Vascular Biology Research Center, University of Texas-Houston Medical School, Houston, Tex (N.A., H.J., C.A., K.K.W.); the Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis (A.R.F.); Human Genetics Center, University of Texas-Houston Health Science Center, Houston, Tex (E.B.); and the Department of Biostatistics, University of North Carolina, Chapel Hill (L.E.C.).

Correspondence to Kenneth K. Wu, MD, PhD, Division of Hematology, University of Texas-Houston Medical School, 6431 Fannin, MSB 5.016, Houston, TX 77030. E-mail Kenneth.K.Wu{at}uth.tmc.edu

Background—The major platelet integrin glycoprotein IIb-IIIa plays a primary role in platelet aggregation and acute thrombus formation at the site of vascular injury. A genetic polymorphism of glycoprotein IIb-IIIa (Pl^A) has recently been proposed as a potential genetic factor linking to platelet hyperaggregability and increased risk of myocardial infarction. Despite numerous, mostly nonprospective studies, the role of this polymorphism as a clinically relevant, inherited risk factor for coronary heart disease (CHD) is still controversial. The purpose of this study was to determine whether Pl^A2 is a risk factor for incident CHD and whether it is correlated with increased platelet activation in a case-cohort study nested within a prospective epidemiologic investigation.

Methods and Results—Blood samples were collected and processed from the Atherosclerosis Risk in Communities Study cohort at the baseline examination (1987 to 1989). They were stored at -80°C. Pl^A1/A2 genotype and plasma ß-thromboglobulin levels were determined in 439 incident CHD cases and a reference cohort sample of 544 (of whom 18 were also CHD cases). The prevalence of the Pl^A2 allele was not different in cases versus noncases. No significant correlation between CHD risk factors and the Pl^A2 allele was noted either. Platelet activation, as measured by plasma ß-thromboglobulin levels, was not enhanced in individuals with the Pl^A2 allele.

Conclusions—This prospective study indicates that healthy individuals carrying the Pl^A2 allele do not have an increased risk of CHD.

Key Words: platelets • glycoproteins • coronary disease

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