title: Relationship of classical and non-classical risk factors with genetic variants relevant to coronary heart disease.
abstract: BACKGROUND
  In addition to the well established cardiovascular risk factors, evidence suggests a possible role of genetic and non-classical risk factors in the development and progression of atherothrombosis. We aimed to determine the relationship of classical and non-classical cardiovascular risk factors with candidate gene polymorphisms potentially involved in cardiovascular risk in the general Mediterranean population.
  
  
  METHODS
  Cross-sectional study.
  
  
  METHODS
  We have determined the prevalence of classical (lipid profile, blood pressure, glycaemia, diabetes, smoking, body mass index, menopause and family history of coronary heart disease) and non-classical cardiovascular risk factors (infectious processes, homocysteinaemia, oxidative status, C-reactive protein, lipoprotein (a) and fibrinogen) in a population-based study. We analysed the relationship of these risk factors with the following five gene polymorphisms potentially involved in cardiovascular risk: ATP-binding cassette transporter A1-R219K, Peroxisome proliferator-activated receptor (PPAR)-alpha-L162V, Lipoprotein lipase (LPL)-HindIII, Paraoxonase (PON)1-Q192R, and Tumour necrosis factor (TNF)-alpha-G-308A.
  
  
  RESULTS
  We found PPAR-alpha-V and LPL-H alleles to be associated with decreased high-density lipoprotein-cholesterol (HDL-c) concentration and with increased total cholesterol : HDL-c and triglyceride : HDL-c ratios. Regarding the non-classical risk factors, C-reactive protein concentration was higher for the PPAR-alpha-V allele. A higher oxidative status was shown in homozygotes for LPL-H and TNF-alpha-G alleles, although the latter also had lower homocysteinaemia.
  
  
  CONCLUSIONS
  Three of the genetic variants analysed, PPAR-alpha-L162V, LPL-HindIII, and TNF-alpha-G-308A, were associated with non-classical risk factors, specifically lipid profile, inflammation, and oxidative status.
authors.affiliation: Unitat de Lípids i Epidemiologia Cardiovascular, Institut Municipal d'Investigació Mèdica, Barcelona, Spain.
authors.forename: Josep Maria
authors.initials: JM
authors.lastname: Manresa
authors.forename: Alberto
authors.initials: A
authors.lastname: Zamora
authors.forename: Marta
authors.initials: M
authors.lastname: Tomás
authors.forename: Mariano
authors.initials: M
authors.lastname: Sentí
authors.forename: Montserrat
authors.initials: M
authors.lastname: Fitó
authors.forename: María Isabel
authors.initials: MI
authors.lastname: Covas
authors.forename: Mercedes
authors.initials: M
authors.lastname: Alcántara
authors.forename: Glòria
authors.initials: G
authors.lastname: Latorre
authors.forename: Verónica
authors.initials: V
authors.lastname: Escurriol
authors.forename: Sophie
authors.initials: S
authors.lastname: Domingues
authors.forename: Jaume
authors.initials: J
authors.lastname: Marrugat
mesh_terms: D064286:ATP Binding Cassette Transporter 1; D018528:ATP-Binding Cassette Transporters / Q000235:genetics; D000328:Adult; D000368:Aged; D043303:Aryldialkylphosphatase / Q000235:genetics; D003327:Coronary Disease / Q000175:diagnosis* / Q000453:epidemiology / Q000235:genetics*; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D008071:Lipoprotein Lipase / Q000235:genetics; D008297:Male; D008875:Middle Aged; D047493:PPAR alpha / Q000235:genetics; D011110:Polymorphism, Genetic; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D064286:ATP Binding Cassette Transporter 1; D018528:ATP-Binding Cassette Transporters; D047493:PPAR alpha; D014409:Tumor Necrosis Factor-alpha; D008071:Lipoprotein Lipase; D043303:Aryldialkylphosphatase; C468406:PON1 protein, human