title: Hyperhomocysteinemia and hyperlipidemia in coronary heart disease.
abstract: OBJECTIVE
  To examine the relationship between coronary heart disease (CHD) and serum lipid, plasma homocysteine (HCY) as well as the factors related to HCY metabolisms.
  
  
  METHODS
  The mutation of the 677C-->T transition of 5, 10-methylenetetrahydrofolate reductase (MTHFR) was determined by PCR-based assay. Whole-blood and plasma folate and plasma vitamin B12, as cofactors of MTHFR, were determined by radio-immunologic assay. Plasma HCY was determined by HPLC.
  
  
  RESULTS
  Patients with CHD had elevated plasma HCY concentrations (17.38 +/- 1.94 mumol/L vs 10.25 +/- 1.57 mumol/L, P < 0.01). In patients with myocardial infarction (MI) and family history (FH) of CHD, plasma HCY were elevated even higher (P < 0.05). Plasma HCY concentrations had significant non-linear inverse correlation with plasma folate and B12 concentrations, i.e. the lower the serum folate or B12 concentrations, the higher the plasma HCY concentrations (P < 0.01). Patients with homozygous mutants had higher plasma HCY concentrations. Patients with CHD had increased serum Chol and LDL-C and Apo-B levels (P < 0.01, P < 0.05 and P < 0.05 respectively). But plasma HCY concentrations had no correlation with serum lipid levels. 24.1% of the patients had high lipid and high HCY level, 25.9% had high lipid level and normal HCY level, 20.4% had normal lipid and high HCY level, and 29.6% had normal lipid and HCY level.
  
  
  CONCLUSIONS
  HCY may have strong association with the genesis of CHD. Low plasma folate and B12 concentrations may induce Hyperhomocysteinemia [HH(e)]. Plasma HCY concentrations have no correlation with serum lipid levels, so HCY may be an independent risk factor. CHD may be induced by different mechanisms and can be classified into hyperlipidemia, HH (e) and normolipidemia, and normohomocysteinemia.
authors.affiliation: Department of Cardiology, First Teaching Hospital of Beijing Medical University, Beijing 100034, China.
authors.forename: W
authors.initials: W
authors.lastname: Gao
authors.forename: N
authors.initials: N
authors.lastname: Jiang
authors.forename: Z
authors.initials: Z
authors.lastname: Meng
authors.forename: J
authors.initials: J
authors.lastname: Tang
mesh_terms: D045103:5,10-Methylenetetrahydrofolate Reductase (FADH2); D000328:Adult; D000368:Aged; D003327:Coronary Disease / Q000097:blood* / Q000209:etiology; D005260:Female; D005492:Folic Acid / Q000097:blood; D006710:Homocysteine / Q000097:blood; D006801:Humans; D020138:Hyperhomocysteinemia / Q000150:complications*; D006949:Hyperlipidemias / Q000150:complications*; D008297:Male; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D008875:Middle Aged; D010088:Oxidoreductases / Q000235:genetics; D017354:Point Mutation; D012307:Risk Factors; D014805:Vitamin B 12 / Q000097:blood
chemical_list: D006710:Homocysteine; D005492:Folic Acid; D010088:Oxidoreductases; D045103:5,10-Methylenetetrahydrofolate Reductase (FADH2); D042965:Methylenetetrahydrofolate Reductase (NADPH2); D014805:Vitamin B 12