Interaction between smoking and the glycoprotein IIIa P1A2 polymorphism in Non–ST-elevation acute coronary syndromes

OBJECTIVES The goal of this study was to determine the interaction between smoking and the glycoprotein IIIa P1A2 polymorphism in patients admitted with non–ST-elevation acute coronary syndromes (ACS). BACKGROUND An increased incidence of the P1A2 polymorphism in smokers presenting with ST-elevation acute myocardial infarction (AMI) has recently been reported. We, therefore, postulated that, as a consequence of this interaction, fewer smokers with the P1A2 polymorphism would present with non–ST-elevation ACS. METHODS We performed a prospective cohort analysis of 220 white Caucasoid patients admitted with non–ST-elevation ACS fulfilling Braunwald class IIIb criteria for unstable angina who were stratified by smoking status. RESULTS There were twice as many nonsmokers as smokers. Nonsmokers compared with smokers were older (mean [SD]; 63.9 [11.2] vs. 57.6 [10.3]; p < 0.0001), more likely to have had a previous admission with unstable angina (24.3% vs. 13.2%; P = 0.051) and AMI (45.8% vs. 30.3%; p < 0.026), more likely to have undergone revascularization (24.3% vs. 1.8%; P = 0.028) and were more likely to be on aspirin on admission (60.4% vs. 44.7%; P = 0.026). The proportion of nonsmokers positive for the P1A2 polymorphism was equivalent to that expected for this population but was significantly reduced in smokers (28.7% vs. 10%; Pearson CHI-SQUARE = 9.09, P = 0.0026). In a logistic regression model, the odds ratio (OR) for being positive for the P1A2 polymorphism was significantly reduced by smoking (OR [interquartile range]: 0.26 [0.11 to 0.62]; P = 0.0026). CONCLUSIONS There is a significant reduction in the P1A2 polymorphism in smokers admitted with non–ST-elevation ACS compared with nonsmokers, which suggests an interaction between smoking and this polymorphism.