title: Contemporaneous carrier-state of two or three "proatherosclerotic" variants of APOE, ICAM1, PPARA and PAI-1 genes differentiate CAD patients from healthy individuals.
abstract: BACKGROUND
  Atherosclerosis is the most important cause of coronary artery disease (CAD). Genetic predisposition to CAD is related to polymorphisms of genes encoding products functionally involved in pathogenesis of atherosclerosis. Polymorphisms of genes participating in monocyte adhesion and diapedesis, lipid metabolism and fibrinolysis regulation may be partially responsible for this process. The aim of our study was to assess the polymorphic variants frequencies of ICAM1, APOE, PPARA and PAI-1 genes in CAD patients and healthy blood donors and to find specific arrangement of polymorphic variants which would differentiate both groups.
  
  
  METHODS
  We studied 146 CAD patients and 121 healthy blood donors. Polymorphisms in analyzed genes were examined using PCR-RFLP analysis.
  
  
  RESULTS
  We found significantly higher frequency of 5G allele of PAI-1 gene in patients than in control subjects (p = 0.038, OR = 1.44). We observed also a considerably higher frequency of contemporaneous carriers of two or three "proatherosclerotic" variants: 1) PPARA and PAI-1, 2) APOE and ICAM1 and 3) PPARA, ICAM1 and PAI-1 in CAD group comparing to control subjects. The number of "proatherosclerotic" variants carriers differentiate studied groups also independently of specific genotype arrangement.
  
  
  CONCLUSIONS
  In conclusion, contemporaneous carrier-state of two or three polymorphic variants within analyzed genes is associated with CAD.
authors.affiliation: Department of Biochemistry and Medical Genetics, Medical University of Silesia, Katowice, Poland. izak@slam.katowice.pl
authors.forename: Iwona
authors.initials: I
authors.lastname: Zak
authors.forename: Anna
authors.initials: A
authors.lastname: Balcerzyk
authors.forename: Beata
authors.initials: B
authors.lastname: Sarecka
authors.forename: Paweł
authors.initials: P
authors.lastname: Niemiec
authors.forename: Zbigniew
authors.initials: Z
authors.lastname: Ciemniewski
authors.forename: Stanisław
authors.initials: S
authors.lastname: Dylag
mesh_terms: D000328:Adult; D000483:Alleles; D001057:Apolipoproteins E / Q000235:genetics*; D050197:Atherosclerosis / Q000150:complications / Q000235:genetics*; D003324:Coronary Artery Disease / Q000150:complications / Q000235:genetics*; D005260:Female; D006262:Health; D006579:Heterozygote; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D047493:PPAR alpha / Q000235:genetics*; D017395:Plasminogen Activator Inhibitor 1 / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics
chemical_list: D001057:Apolipoproteins E; D047493:PPAR alpha; D017395:Plasminogen Activator Inhibitor 1; D018799:Intercellular Adhesion Molecule-1