title: Interaction between smoking and the glycoprotein IIIa P1(A2) polymorphism in non-ST-elevation acute coronary syndromes.
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Cardiology, Bart's and the London NHS Trust, London, United Kingdom. k.barakat@mds.qmw.ac.uk
authors.forename: K
authors.initials: K
authors.lastname: Barakat
authors.forename: S
authors.initials: S
authors.lastname: Kennon
authors.forename: G A
authors.initials: GA
authors.lastname: Hitman
authors.forename: E
authors.initials: E
authors.lastname: Aganna
authors.forename: C P
authors.initials: CP
authors.lastname: Price
authors.forename: P G
authors.initials: PG
authors.lastname: Mills
authors.forename: K
authors.initials: K
authors.lastname: Ranjadayalan
authors.forename: B
authors.initials: B
authors.lastname: North
authors.forename: H
authors.initials: H
authors.lastname: Clarke
authors.forename: A D
authors.initials: AD
authors.lastname: Timmis
mesh_terms: D000208:Acute Disease; D000789:Angina, Unstable / Q000097:blood / Q000235:genetics*; D016009:Chi-Square Distribution; D005260:Female; D005838:Genotype; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000235:genetics*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000235:genetics*; D011110:Polymorphism, Genetic; D011446:Prospective Studies; D012907:Smoking / Q000009:adverse effects*; D018709:Statistics, Nonparametric; D013577:Syndrome; D044465:White People
chemical_list: D019039:Platelet Glycoprotein GPIIb-IIIa Complex