title: Influence of cigarette smoking on rate of reopening of the infarct-related coronary artery after myocardial infarction: a multivariate analysis.
abstract: OBJECTIVE
  This study sought to determine whether the reopening of the infarct-related vessel is related to clinical characteristics or cardiovascular risk factors, or both.
  
  
  BACKGROUND
  In acute myocardial infarction, thrombolytic therapy reduces mortality by restoring the patency of the infarct-related vessel. However, despite the use of thrombolytic agents, the infarct-related vessel remains occluded in up to 40% of patients.
  
  
  METHODS
  We studied 295 consecutive patients with an acute myocardial infarction who underwent coronary angiography within 15 days (mean [+/- SD] 6.7 +/- 3.2 days) of the onset of symptoms. Infarct-related artery patency was defined by Thrombolysis in Myocardial Infarction trial flow grade > or = 2. Four cardiovascular risk factors--smoking, hypertension, hypercholesterolemia and diabetes mellitus--and eight different variables-age, gender, in-hospital death, history of previous myocardial infarction, location of current myocardial infarction, use of thrombolytic agents, time interval between onset of symptoms, thrombolytic therapy and coronary angiography--were recorded in all patients.
  
  
  RESULTS
  Thrombolysis in current smokers and anterior infard location on admission were the three independent factors highly correlated with the patency of the infarct-related vessel (odds ratios 3.2, 3.0 and 1.9, respectively). In smokers, thrombolytic therapy was associated with a higher reopening rate of the infard vessel, from 35% to 77% (p < 0.001). Nonsmokers did not benefit from thrombolytic therapy, regardless of infarct location.
  
  
  CONCLUSIONS
  These observational data, if replicated, suggest that in patients with acute myocardial infarction, thrombolytic therapy may be most effective in current smokers, whereas nonsmokers and ex-smokers may require other management strategies, such as emergency percutaneous transluminal coronary angioplasty.
authors.affiliation: Service de Cardiologie, Centre Hospitalier Universitaire, Nancy, France.
authors.forename: C
authors.initials: C
authors.lastname: de Chillou
authors.forename: P
authors.initials: P
authors.lastname: Riff
authors.forename: N
authors.initials: N
authors.lastname: Sadoul
authors.forename: G
authors.initials: G
authors.lastname: Ethevenot
authors.forename: L
authors.initials: L
authors.lastname: Feldmann
authors.forename: K
authors.initials: K
authors.lastname: Isaaz
authors.forename: J P
authors.initials: JP
authors.lastname: Simon
authors.forename: M
authors.initials: M
authors.lastname: Boursier
authors.forename: K
authors.initials: K
authors.lastname: Khalifé
authors.forename: J Y
authors.initials: JY
authors.lastname: Thisse
authors.forename: E
authors.initials: E
authors.lastname: Aliot
mesh_terms: D000368:Aged; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy*; D010960:Plasminogen Activators / Q000627:therapeutic use*; D012008:Recurrence; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects*; D013300:Streptokinase / Q000627:therapeutic use*; D013318:Stroke Volume; D015912:Thrombolytic Therapy; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use*; D017211:Treatment Failure; D014654:Vascular Patency
chemical_list: D013300:Streptokinase; D010960:Plasminogen Activators; D010959:Tissue Plasminogen Activator