K. Barakat et al., Interaction between smoking and the glycoprotein IIIa Pl(A2) polymorphism in non-ST-elevation acute coronary syndromes, J AM COL C, 38(6), 2001, pp. 1639-1643
Citations number
22
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
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 pre
senting with ST-elevation acute myocardial infarction (AMI) has recently be
en reported. We, therefore, postulated that, as a consequence of this inter
action, fewer smokers with the P1(A2) polymorphism would present with non-S
T-elevation ACS.
METHODS We performed a prospective cohort analysis of 220 white Caucasoid p
atients 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 < 0.000
1), 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 t
o have undergone revascularization (24.3% vs. 1.8%; p = 0.028) and were mor
e likely to be on aspirin on admission (60.4% vs. 44.7%; p = 0.026). The pr
oportion of nonsmokers positive for the P1(A2) polymorphism was equivalent
to that expected for this population but was significantly reduced in smoke
rs (28.7% vs. 10%; Pearson chi-square = 9.09, p = 0.0026). In a logistic re
gression model, the odds ratio (OR) for being positive for the P1(A2) polym
orphism was significantly reduced by smoking (OR [interquartile range]: 0.2
6 [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. (C) 2001 by
the American College of Cardiology.