title: CHRNA5 variant predicts smoking cessation in patients with acute myocardial infarction.
abstract: BACKGROUND
  While smoking is a major modifiable risk factor for secondary prevention of myocardial infarction (MI), active smoking is common among patients hospitalized with acute MI. Recent studies suggest that nicotinic receptor variants, and specifically the high-risk CHRNA5 rs16969968 A allele, are associated with cessation failure among noncardiac patients. This study investigates the association between CHRNA5 rs16969968 and smoking cessation in patients hospitalized with acute MI.
  
  
  METHODS
  Using data from the TRIUMPH study, we ascertained smoking status at the time of index hospitalization for acute MI and 1 year after hospitalization. After adjusting for age and sex, we used logistic regression to model the association between smoking cessation and CHRNA5 rs16969968.
  
  
  RESULTS
  At index admission, 752 Caucasian subjects were active smokers and 699 were former smokers. Among these ever-smokers, the A allele was associated with significantly decreased abstinence (45.0% abstinence for A allele carriers vs. 51.7% for GG homozygotes; odds ratio [OR] = 0.70, 95% confidence interval [CI] = 0.56-0.88, p = .0027). The A allele was also significantly associated with decreased abstinence at 1 year (69.1% abstinence for A allele carriers vs. 76.0% for GG homozygotes; OR = 0.70, 95% CI = 0.53-0.94, p = .0185).
  
  
  CONCLUSIONS
  Among patients who have smoked and who are hospitalized with acute MI, the high-risk CHRNA5 allele was associated with lower likelihood of quitting before hospitalization and significantly less abstinence 1 year after hospitalization with MI. The CHRNA5 rs16969968 genotype may therefore identify patients who would benefit from aggressive, personalized smoking cessation intervention.
authors.affiliation: Department of Psychiatry, Washington University School of Medicine, St. Louis, MO;
authors.forename: Li-Shiun
authors.initials: LS
authors.lastname: Chen
authors.affiliation: Department of Medicine, Washington University School of Medicine, St. Louis, MO;
authors.forename: Richard G
authors.initials: RG
authors.lastname: Bach
authors.affiliation: Department of Genetics, Washington University School of Medicine, St. Louis, MO;
authors.forename: Petra A
authors.initials: PA
authors.lastname: Lenzini
authors.affiliation: Mid-America Heart Institute, University of Missouri-Kansas City, Kansas City, MO.
authors.forename: John A
authors.initials: JA
authors.lastname: Spertus
authors.affiliation: Department of Psychiatry, Washington University School of Medicine, St. Louis, MO;
authors.forename: Laura Jean
authors.initials: LJ
authors.lastname: Bierut
authors.affiliation: Department of Medicine, Washington University School of Medicine, St. Louis, MO; Department of Genetics, Washington University School of Medicine, St. Louis, MO; scresci@dom.wustl.edu.
authors.forename: Sharon
authors.initials: S
authors.lastname: Cresci
mesh_terms: D000368:Aged; D000483:Alleles; D005260:Female; D005838:Genotype; D006760:Hospitalization; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications*; D009419:Nerve Tissue Proteins / Q000235:genetics*; D016017:Odds Ratio; D011978:Receptors, Nicotinic / Q000235:genetics*; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects / Q000235:genetics*; D016540:Smoking Cessation / Q000706:statistics & numerical data*; D044465:White People / Q000235:genetics
chemical_list: C447158:CHRNA5 protein, human; D009419:Nerve Tissue Proteins; D011978:Receptors, Nicotinic
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