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Hyperhomocysteinemia and hyperlipidemia in coronary heart disease
1Department of Cardiology, First Teaching Hospital of Beijing Medical University, Beijing 100034, China.
Insights
Elevated homocysteine (HCY) levels are strongly associated with coronary heart disease (CHD). Low folate and vitamin B12 levels contribute to high HCY, suggesting HCY is an independent risk factor for CHD.
Area of Science:
- Cardiovascular Science
- Biochemistry
- Genetics
Background:
- Coronary heart disease (CHD) is a leading cause of mortality worldwide.
- Serum lipids and homocysteine (HCY) are implicated in CHD pathogenesis.
- Understanding factors influencing HCY metabolism is crucial for CHD prevention.
Purpose of the Study:
- To investigate the association between coronary heart disease (CHD) and serum lipid profiles, plasma homocysteine (HCY) levels.
- To identify factors related to HCY metabolism, including MTHFR gene mutations and vitamin cofactor levels.
Main Methods:
- Genotyping for the MTHFR 677C-->T mutation using PCR.
- Quantification of whole-blood and plasma folate, plasma vitamin B12 via radio-immunologic assay.
- Measurement of plasma HCY concentrations using High-Performance Liquid Chromatography (HPLC).
Main Results:
- Patients with CHD exhibited significantly higher plasma HCY concentrations compared to controls.
- Elevated HCY levels were observed in patients with myocardial infarction and a family history of CHD.
- Plasma HCY showed a significant inverse correlation with plasma folate and vitamin B12 levels, indicating lower vitamin levels lead to higher HCY.
- Patients with homozygous MTHFR 677C-->T mutation had higher plasma HCY.
- While CHD patients had elevated cholesterol and LDL-C, plasma HCY showed no correlation with serum lipid levels.
- A significant portion of patients presented with combinations of high lipid and high HCY, high lipid/normal HCY, or normal lipid/high HCY.
Conclusions:
- Homocysteine (HCY) is strongly associated with the development of coronary heart disease (CHD).
- Low plasma folate and vitamin B12 concentrations are identified as key contributors to hyperhomocysteinemia (HH(e)).
- Plasma HCY levels are independent of serum lipid profiles, positioning HCY as a distinct risk factor for CHD.
- CHD may arise from diverse mechanisms, potentially classifiable into hyperlipidemic, hyperhomocysteinemic, and normolipidemic/normohomocysteinemic subtypes.
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.