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CLINICAL STUDY

Interaction between smoking and the glycoprotein IIIa P1^A2 polymorphism in Non–ST-elevation acute coronary syndromes

^* Department of Cardiology, Bart’s and the London NHS Trust, London, United Kingdom
^b Department of Clinical Biochemistry, Bart’s and the London NHS Trust, London, United Kingdom
^c Department of Diabetes and Metabolic Medicine, St. Bartholomew’s and The Royal London School of Medicine and Dentistry, Queen Mary, University of London, London, United Kingdom
^d Department of Psychological Medicine, St. Bartholomew’s and The Royal London School of Medicine and Dentistry, Queen Mary, University of London, London, United Kingdom
^|| Department of Cardiology, Newham Healthcare Trust, London, United Kingdom

Manuscript received April 9, 2001; revised manuscript received July 20, 2001, accepted August 15, 2001.

^* Reprint requests and correspondence: Dr. Khalid Barakat, The London Chest Hospital, Bonner Road, London E2 9JX, United Kingdom
k.barakat{at}mds.qmw.ac.uk

OBJECTIVES

The goal of this study was to determine the interaction between smoking and the glycoprotein IIIa P1^A2 polymorphism in patients admitted with non–ST-elevation acute coronary syndromes (ACS).

BACKGROUND

An increased incidence of the P1^A2 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 P1^A2 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 P1^A2 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 P1^A2 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 P1^A2 polymorphism in smokers admitted with non–ST-elevation ACS compared with nonsmokers, which suggests an interaction between smoking and this polymorphism.

Abbreviations and Acronyms   ACS = acute coronary syndromes   AMI = acute myocardial infarction   GP = glycoprotein   STAMI = ST-elevation acute myocardial infarction   Tn I = troponin I

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