title: Homocysteine, traditional risk factors and impaired renal function in coronary artery disease.
abstract: BACKGROUND
  To establish whether the frequent finding of a moderate-intermediate increase in plasma total homocysteine (tHcy) causes coronary artery disease (CAD), the authors evaluated the number of coexisting major traditional risk factors, as well as the major tHcy determinants, in patients with the same degree of CAD but different tHcy levels.
  
  
  METHODS
  The authors studied 180 patients with CAD, who were divided into three groups according to tHcy levels: 60 patients with normal tHcy, 60 patients with moderate (15-30 micromol L(-1)) and 60 patients with intermediate hyperhomocysteinaemia (30-100 micromol L(-1)). The patient groups were matched for gender, age and number of affected coronary vessels. All patients were checked for the presence of traditional risk factors for CAD (i.e. hypertension, diabetes, hyperlipidaemia, smoking habit, familial history, obesity), as well as determinants of tHcy levels. The population was subdivided into those having, or not, a substantial burden of traditional risk factors (i.e. < 4 and > or = 4, respectively).
  
  
  RESULTS
  There was a significant trend towards a reduced number of subjects within the group with > or = 4 risk factors across increasing tHcy levels (51.7%, 37.8%, 26%, for normal, moderate, intermediate tHcy, respectively, chi2 for linear-trend = 0.006). Folate and vitamin B12 concentrations, estimated glomerular filtration rate (GFR), MTHFR 677C > T polymorphism were the major determinants of tHcy in this population.
  
  
  CONCLUSIONS
  In patients with the same degree of CAD, those with hyperhomocysteinaemia had a reduced burden of traditional risk factors as compared with those with normal tHcy levels. Hyperhomocysteinaemia was significantly associated with an emerging non-traditional risk factor such as lower GFR.
authors.affiliation: Department of Clinical and Experimental Medicine, University of Verona School of Medicine, Verona, Italy. fracesca.pizzolo@unimib.it
authors.forename: F
authors.initials: F
authors.lastname: Pizzolo
authors.forename: S
authors.initials: S
authors.lastname: Friso
authors.forename: O
authors.initials: O
authors.lastname: Olivieri
authors.forename: N
authors.initials: N
authors.lastname: Martinelli
authors.forename: C
authors.initials: C
authors.lastname: Bozzini
authors.forename: P
authors.initials: P
authors.lastname: Guarini
authors.forename: E
authors.initials: E
authors.lastname: Trabetti
authors.forename: G
authors.initials: G
authors.lastname: Faccini
authors.forename: R
authors.initials: R
authors.lastname: Corrocher
authors.forename: D
authors.initials: D
authors.lastname: Girelli
mesh_terms: D000368:Aged; D003324:Coronary Artery Disease / Q000097:blood* / Q000503:physiopathology; D003920:Diabetes Mellitus / Q000097:blood / Q000453:epidemiology; D005260:Female; D005919:Glomerular Filtration Rate; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000097:blood; D006949:Hyperlipidemias / Q000097:blood / Q000453:epidemiology; D006973:Hypertension / Q000097:blood / Q000453:epidemiology; D008297:Male; D042965:Methylenetetrahydrofolate Reductase (NADPH2) / Q000235:genetics; D008875:Middle Aged; D009765:Obesity / Q000097:blood / Q000453:epidemiology; D011110:Polymorphism, Genetic; D012307:Risk Factors; D014803:Vitamin B Complex / Q000097:blood
chemical_list: D006710:Homocysteine; D014803:Vitamin B Complex; D042965:Methylenetetrahydrofolate Reductase (NADPH2)