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Hyperhomocysteinemia and hyperlipidemia in coronary heart disease.
Chin Med J (Engl). 1999 Jul; 112(7):586-9.CM

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+Show Affiliations

Department of Cardiology, First Teaching Hospital of Beijing Medical University, Beijing 100034, China.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

11601248

Citation

Gao, W, et al. "Hyperhomocysteinemia and Hyperlipidemia in Coronary Heart Disease." Chinese Medical Journal, vol. 112, no. 7, 1999, pp. 586-9.
Gao W, Jiang N, Meng Z, et al. Hyperhomocysteinemia and hyperlipidemia in coronary heart disease. Chin Med J. 1999;112(7):586-9.
Gao, W., Jiang, N., Meng, Z., & Tang, J. (1999). Hyperhomocysteinemia and hyperlipidemia in coronary heart disease. Chinese Medical Journal, 112(7), 586-9.
Gao W, et al. Hyperhomocysteinemia and Hyperlipidemia in Coronary Heart Disease. Chin Med J. 1999;112(7):586-9. PubMed PMID: 11601248.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hyperhomocysteinemia and hyperlipidemia in coronary heart disease. AU - Gao,W, AU - Jiang,N, AU - Meng,Z, AU - Tang,J, PY - 2001/10/17/pubmed PY - 2002/1/5/medline PY - 2001/10/17/entrez SP - 586 EP - 9 JF - Chinese medical journal JO - Chin. Med. J. VL - 112 IS - 7 N2 - 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. SN - 0366-6999 UR - https://www.unboundmedicine.com/medline/citation/11601248/Hyperhomocysteinemia_and_hyperlipidemia_in_coronary_heart_disease_ L2 - http://www.diseaseinfosearch.org/result/130 DB - PRIME DP - Unbound Medicine ER -