title: Combined effect of hemostatic gene polymorphisms and the risk of myocardial infarction in patients with advanced coronary atherosclerosis.
abstract: BACKGROUND
  Relative little attention has been devoted until now to the combined effects of gene polymorphisms of the hemostatic pathway as risk factors for Myocardial Infarction (MI), the main thrombotic complication of Coronary Artery Disease (CAD). The aim of this study was to evaluate the combined effect of ten common prothrombotic polymorphisms as a determinant of MI.
  
  
  RESULTS
  We studied a total of 804 subjects, 489 of whom with angiographically proven severe CAD, with or without MI (n = 307; n = 182; respectively). An additive model considering ten common polymorphisms [Prothrombin 20210G>A, PAI-1 4G/5G, Fibrinogen beta -455G>A, FV Leiden and "R2", FVII -402G>A and -323 del/ins, Platelet ADP Receptor P2Y12 -744T>C, Platelet Glycoproteins Ia (873G>A), and IIIa (1565T>C)] was tested. The prevalence of MI increased linearly with an increasing number of unfavorable alleles (chi(2) for trend = 10.68; P = 0.001). In a multiple logistic regression model, the number of unfavorable alleles remained significantly associated with MI after adjustment for classical risk factors. As compared to subjects with 3-7 alleles, those with few (</=2) alleles had a decreased MI risk (OR 0.34, 95%CIs 0.13-0.93), while those with more (>/=8) alleles had an increased MI risk (OR 2.49, 95%CIs 1.03-6.01). The number of procoagulant alleles correlated directly (r = 0.49, P = 0.006) with endogenous thrombin potential.
  
  
  CONCLUSIONS
  The combination of prothrombotic polymorphisms may help to predict MI in patients with advanced CAD.
authors.affiliation: Department of Clinical and Experimental Medicine, University of Verona, Verona, Italy.
authors.forename: Nicola
authors.initials: N
authors.lastname: Martinelli
authors.forename: Elisabetta
authors.initials: E
authors.lastname: Trabetti
authors.forename: Mirko
authors.initials: M
authors.lastname: Pinotti
authors.forename: Oliviero
authors.initials: O
authors.lastname: Olivieri
authors.forename: Marco
authors.initials: M
authors.lastname: Sandri
authors.forename: Simonetta
authors.initials: S
authors.lastname: Friso
authors.forename: Francesca
authors.initials: F
authors.lastname: Pizzolo
authors.forename: Claudia
authors.initials: C
authors.lastname: Bozzini
authors.forename: Pier Paolo
authors.initials: PP
authors.lastname: Caruso
authors.forename: Ugo
authors.initials: U
authors.lastname: Cavallari
authors.forename: Suzanne
authors.initials: S
authors.lastname: Cheng
authors.forename: Pier Franco
authors.initials: PF
authors.lastname: Pignatti
authors.forename: Francesco
authors.initials: F
authors.lastname: Bernardi
authors.forename: Roberto
authors.initials: R
authors.lastname: Corrocher
authors.forename: Domenico
authors.initials: D
authors.lastname: Girelli
mesh_terms: D000368:Aged; D000483:Alleles; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000150:complications*; D005260:Female; D020022:Genetic Predisposition to Disease; D006487:Hemostasis / Q000235:genetics*; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000175:diagnosis / Q000209:etiology* / Q000235:genetics; D011110:Polymorphism, Genetic; D011237:Predictive Value of Tests; D012307:Risk Factors; D019851:Thrombophilia / Q000235:genetics