title: Interactions between fibrinolysis, lipoproteins and leptin related to a first myocardial infarction.
abstract: BACKGROUND
  The summarized importance of haemostatic and metabolic variables (insulin, lipids including lipoprotein (a) [Lp(a)] and leptin) in predicting first myocardial infarction, as well as possible interactions among these variables, have not been reported.
  
  
  METHODS
  A prospective case-control study nested within the Northern Sweden Health and Disease Cohort.
  
  
  METHODS
  Sixty-two men diagnosed with a first myocardial infarction were sex- and age-matched with 124 controls. Conditional logistic regression was conducted including established risk factors, plasma levels of plasminogen activator inhibitor-1 (PAI-1), tissue plasminogen activator (tPA) mass concentration, von Willebrand factor, insulin, proinsulin, specific insulin, apolipoprotein A-I (apo A-I), Lp(a), and leptin. Interaction analysis was also performed for tPA, apo A-I, Lp(a), leptin and proinsulin.
  
  
  RESULTS
  Smoking, low plasma levels of apo A-I and high plasma levels of cholesterol, Lp(a), tPA, PAI-1, proinsulin and leptin were associated with myocardial infarction in univariate conditional logistic regression analysis. High tPA [odds ratio (OR), 21.3; 95% confidence interval (CI), 2.04-222] and Lp(a) (OR, 7.21; 95% CI, 1.31-39.8) and low apo A-I (OR, 0.15; 95% CI, 0.02-0.93) remained significant risk determinants in multivariate analysis with smoking habits, body mass index, hypertension, cholesterol, and diabetes included as covariates. There were non-significant synergic interactions between high Lp(a) and leptin and tPA, respectively, and between high Lp(a) and low apo A-I.
  
  
  CONCLUSIONS
  Plasma levels of tPA, Lp(a), and apo A-I are independently associated with subsequent development of a first myocardial infarction in men.
authors.affiliation: Department of Medicine and Public Health, Umeå University Hospital, Umeå, Sweden. amt@rh.dk
authors.forename: Anna M
authors.initials: AM
authors.lastname: Thøgersen
authors.forename: Stefan
authors.initials: S
authors.lastname: Söderberg
authors.forename: Jan-Håkan
authors.initials: JH
authors.lastname: Jansson
authors.forename: Gösta
authors.initials: G
authors.lastname: Dahlén
authors.forename: Kurt
authors.initials: K
authors.lastname: Boman
authors.forename: Torbjörn K
authors.initials: TK
authors.lastname: Nilsson
authors.forename: Bernt
authors.initials: B
authors.lastname: Lindahl
authors.forename: Lars
authors.initials: L
authors.lastname: Weinehall
authors.forename: Hans
authors.initials: H
authors.lastname: Stenlund
authors.forename: Vivan
authors.initials: V
authors.lastname: Lundberg
authors.forename: Owe
authors.initials: O
authors.lastname: Johnson
authors.forename: Bo
authors.initials: B
authors.lastname: Ahrén
authors.forename: Göran
authors.initials: G
authors.lastname: Hallmans
mesh_terms: D001055:Apolipoproteins B / Q000097:blood; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000502:physiology; D015992:Body Mass Index; D016022:Case-Control Studies; D003971:Diastole / Q000502:physiology; D005260:Female; D005342:Fibrinolysis / Q000502:physiology*; D006801:Humans; D020738:Leptin / Q000097:blood*; D017270:Lipoprotein(a) / Q000097:blood; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009203:Myocardial Infarction / Q000097:blood* / Q000503:physiopathology*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011446:Prospective Studies; D013223:Statistics as Topic; D013548:Sweden; D013599:Systole / Q000502:physiology; D010959:Tissue Plasminogen Activator / Q000097:blood; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D001055:Apolipoproteins B; D015415:Biomarkers; D020738:Leptin; D017270:Lipoprotein(a); D008074:Lipoproteins; D017395:Plasminogen Activator Inhibitor 1; D014841:von Willebrand Factor; D010959:Tissue Plasminogen Activator