title: Stromelysin-1 promoter 5A/6A polymorphism is an independent genetic prognostic risk factor and interacts with smoking cessation after index premature myocardial infarction.
abstract: OBJECTIVE
  To evaluate the prognostic roles of multiple polymorphisms and smoking cessation for premature myocardial infarction (MI).
  
  
  METHODS
  We studied 170 patients with MI onset before the age of 45 years (range 27-45 years, 84% men) and analyzed the traditional risk factors and several candidate genes' associations with their subsequent coronary events.
  
  
  RESULTS
  Follow-up data were available for a total of 162 individuals (95.3%) with the other 38 individuals (4.7%) being lost-to-follow-up premature MI patients. During a mean period of 4.43 years' follow-up, diabetes mellitus (DM), hypertension, hypercholesterolemia and Killip's status > or =II were more frequent among patients with subsequent cardiac events (all P-values <0.05). The frequency of 5A allele of stromelysin-1 gene was significantly higher among event group (P = 0.01). Smoking cessation after MI, use of beta-blocker or angiotensin-converting enzyme inhibitor (ACEI) could improve outcome (all P-values <0.05). After multivariate analysis, we found that DM was an independent risk factor for survival [Hazard ratio (HR) 2.45, P = 0.01]. Successful smoking cessation and therapy with ACEI could have a protective effect (HR 0.33 and 0.09, P = 0.01 and <0.01, respectively). The stromelysin-1 5A gene polymorphism was also an independent survival predictor (HR 2.51, P = 0.03). In addition, smoking cessation could significantly modify the risk, especially among patients with 5A allele polymorphism (HR 6.75 vs. 1.50).
  
  
  CONCLUSIONS
  We thus conclude that the stromelysin-1 gene polymorphism alone or in combination with smoking cessation can influence the prognosis after index premature MI.
authors.affiliation: Department of Internal Medicine, Division of Cardiology, National Cheng-Kung University Medical Center, Tainan, Taiwan.
authors.forename: P-Y
authors.initials: PY
authors.lastname: Liu
authors.forename: Y-H
authors.initials: YH
authors.lastname: Li
authors.forename: W-C
authors.initials: WC
authors.lastname: Tsai
authors.forename: L-M
authors.initials: LM
authors.lastname: Tsai
authors.forename: T-H
authors.initials: TH
authors.lastname: Chao
authors.forename: H-L
authors.initials: HL
authors.lastname: Wu
authors.forename: J-H
authors.initials: JH
authors.lastname: Chen
mesh_terms: D000328:Adult; D017668:Age of Onset; D000483:Alleles; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D005260:Female; D005500:Follow-Up Studies; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D019278:Matrix Metalloproteinase 3 / Q000235:genetics*; D008875:Middle Aged; D009203:Myocardial Infarction / Q000453:epidemiology / Q000235:genetics*; D011110:Polymorphism, Genetic; D011379:Prognosis; D011401:Promoter Regions, Genetic / Q000235:genetics; D012307:Risk Factors; D016540:Smoking Cessation
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D019278:Matrix Metalloproteinase 3