Hyperhomocysteinemia and hyperlipidemia in coronary heart disease

Objective To examine the relationship between coronary heart disease (CHD) and serum lipid, plasma homocysteine (HCY) as well as the factors related t o HCY metabolisms. Methods The mutation of the 677C-->T transition of 5, 10-methylenetetrahydr ofolate reductase (MTHFR) was determined by PCR-based assay. Whole-blood an d plasma folate and plasma vitamin B-12, as cofactors of MTHFR, were determ ined by radio-immunologic assay. Plasma HCY was determined by HPLC. Results Patients with CHD had elevated plasma HCY concentrations (17.38 +/- 1.94 mu mol/L vs 10.25 +/- 1.57 mu mol/L, P < 0.01). In patients with myoc ardial infarction (MI) and family history (FH) of CHD, plasma HCY were elev ated even higher (P < 0.05). Plasma HCY concentrations had significant non- linear inverse correlation with plasma folate and B-12 concentrations, i.e. the lower the serum folate or B-12 concentrations, the higher the plasma H CY concentrations (P < 0.01). Patients with homozygous mutants had higher p lasma HCY concentrations. Patients with CHD had increased serum Chol and LD L-C and Apo-B levels (P < 0.01, P < 0.05 and P < 0.05 respectively). But pl asma HCY concentrations had no correlation with serum lipid levels. 24.1% o f the patients had high lipid and high HCY level, 25.9% had high lipid leve l 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 pl asma folate and B-12 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 mec hanisms and can be classified into hyperlipidemia, HH (e) normolipidemia, a nd normohomocys-teinemia.