title: Atherogenic, hemostatic, and other potential risk markers in subjects with previous isolated myocardial infarction compared with long-standing uncomplicated stable angina.
abstract: BACKGROUND
  Several atherogenic, hemostatic, inflammatory, and genetic parameters and markers have been implicated as risk factors in coronary artery disease, although whether they are risk factors for acute as opposed to chronic coronary disease is unclear.
  
  
  RESULTS
  Fifty subjects with an isolated myocardial infarction >3 months previously were compared with 50 subjects with a minimum 3-year history of stable angina, documented coronary artery disease, normal electrocardiogram and normal ventricular wall motion, and no episode suggesting infarction or unstable angina. Biologic variables analyzed included apolipoprotein B (apo B), lipoprotein (a), C-reactive protein (CRP), fibrinogen, factor VII, tissue plasminogen activator (TPA) and inhibitor (PAI-1), thrombin-antithrombin (TAT), fragment 1+2 (F1+2), von Willebrand factor (vWF), activated protein C resistance, homocyst(e)ine, anticardiolipin antibodies, blood group, and the angiotensin-converting enzyme insertion/deletion (I/D) and angiotensin II receptor gene polymorphisms. There were no significant differences between the 2 groups for any of the variables studied, although fibrinogen and F 1+2 tended to be slightly higher in the angina group (P = .09 for each). These significant correlations were present: age with fibrinogen, homocyst(e)ine, and vWF; factor VII with apo B, homocyst(e)ine, and TPA; apo B with TPA and CRP; CRP with fibrinogen, TPA, PAI-1, and factor VII; fibrinogen with vWF.
  
  
  CONCLUSIONS
  Examination of atherogenic, hemostatic, inflammation, and genetic variables in the clinically quiescent state permitted no distinction between subjects with a previous isolated myocardial infarction in contrast to those with long-standing uncomplicated stable angina, favoring the notion that acute coronary events occur at random on a varying background of atherosclerosis. The multiple correlations found among these variables also underscore their complex interaction in the atherosclerotic process.
authors.affiliation: Quebec Heart Institute/Laval Hospital, Laval University, Ste-Foy, Canada.
authors.forename: P
authors.initials: P
authors.lastname: Bogaty
authors.forename: N M
authors.initials: NM
authors.lastname: Robitaille
authors.forename: S
authors.initials: S
authors.lastname: Solymoss
authors.forename: L
authors.initials: L
authors.lastname: Boyer
authors.forename: D
authors.initials: D
authors.lastname: Auger
authors.forename: L
authors.initials: L
authors.lastname: Labbé
authors.forename: S
authors.initials: S
authors.lastname: Simard
authors.forename: J
authors.initials: J
authors.lastname: Rail
authors.forename: J
authors.initials: J
authors.lastname: Genest
authors.forename: J
authors.initials: J
authors.lastname: Turgeon
mesh_terms: D000328:Adult; D000367:Age Factors; D000368:Aged; D000787:Angina Pectoris / Q000097:blood / Q000150:complications*; D015415:Biomarkers / Q000097:blood*; D015986:Confounding Factors, Epidemiologic; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000209:etiology*; D011446:Prospective Studies; D012307:Risk Factors
chemical_list: D015415:Biomarkers