This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Aleksic, N. Articles by Wu, K. K. Search for Related Content PubMed PubMed Citation Articles by Aleksic, N. Articles by Wu, K. K. Related Collections Clinical genetics Epidemiology Genetics of cardiovascular disease Risk Factors

(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

This article has been cited by other articles:

				S. E. Bojesen, K. Juul, P. Schnohr, A. Tybjaerg-Hansen, and B.o. G. Nordestgaard Platelet glycoprotein IIb/IIIa PlA2/PlA2 homozygosity associated with risk of ischemic cardiovascular disease and myocardial infarction in young men: The Copenhagen City Heart Study J. Am. Coll. Cardiol., August 20, 2003; 42(4): 661 - 667. [Abstract] [Full Text] [PDF]

				J. B. Braunstein, D. W. Kershner, P. Bray, G. Gerstenblith, S. P. Schulman, W. S. Post, and R. S. Blumenthal Interaction of Hemostatic Genetics With Hormone Therapy : New Insights To Explain Arterial Thrombosis in Postmenopausal Women Chest, March 1, 2002; 121(3): 906 - 920. [Abstract] [Full Text] [PDF]

				K. K. Wu and J. T. Willerson Monitoring Platelet Function in Glycoprotein IIb/IIIa Inhibitor Therapy Circulation, May 29, 2001; 103(21): 2528 - 2530. [Full Text] [PDF]