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Homocysteine and arterial occlusive disease: a concise review
F Andreotti1, F Burzotta, A Mazza
1Istituto di Cardiologia, Università Cattolica del Sacro Cuore, Roma. felicita.andreotti@iol.it
Insights
High homocysteine levels increase the risk of arterial diseases. Lowering homocysteine with folate supplements may reduce cardiovascular events, offering potential therapeutic benefits.
Area of Science:
- Cardiovascular Science
- Metabolic Disease Research
- Vascular Biology
Background:
- Elevated serum/plasma total homocysteine is a recognized risk factor for coronary, cerebral, and peripheral artery disease.
- The risk is concentration-dependent and independent of traditional cardiovascular risk factors.
- Mild hyperhomocysteinemia affects 5-10% of the general population.
Purpose of the Study:
- To review the evidence linking elevated homocysteine levels to arterial occlusive disease.
- To discuss the factors influencing homocysteine levels and potential interventions.
- To highlight the need for interventional studies to confirm causality.
Main Methods:
- Review of cross-sectional and prospective studies on homocysteine and arterial disease.
- Analysis of factors affecting plasma homocysteine concentrations.
- Evaluation of in vitro and in vivo studies on homocysteine's endothelial effects.
Main Results:
- A 5 mumol/l increase in total plasma homocysteine is associated with an odds ratio of 1.4 for ischemic heart disease.
- Factors increasing homocysteine include age, male gender, renal dysfunction, low vitamin B intake, and genetic defects.
- Folate supplementation can decrease total homocysteine levels by approximately 25%.
Conclusions:
- Hyperhomocysteinemia is a significant risk factor for atherothrombosis.
- Further interventional trials lowering homocysteine are needed to establish direct causality and reduce cardiovascular events.
- Genetic studies may also elucidate the causal role of hyperhomocysteinemia in arterial disease.
Abstract:
Many cross-sectional and prospective studies have shown that raised serum/plasma levels of total homocysteine increase the risk of coronary, cerebral, and peripheral artery disease. The risk associated with hyperhomocysteinemia appears to be concentration-dependent and not attributable to traditional risk factors. The odds ratio for ischemic heart disease has been estimated to be 1.4 for every 5 mumol/l increase of total plasma homocysteine. Median fasting total plasma homocysteine in adult males is approximately 10 mumol/l. Mild hyperhomocysteinemia is estimated to occur in 5-10% of the general population. Plasma concentrations are increased as a result of age, male gender, impaired renal function, low vitamin B intake, and genetically-determined defects of the enzymes involved in homocysteine metabolism. Folate supplements can reduce total homocysteine levels by approximately 25%. Studies in vitro and in vivo indicate that homocysteine can impair endothelial function. Despite increasing recognition of hyperhomocysteinemia as a risk factor for arterial occlusive disease, irrefutable proof that mild hyperhomocysteinemia contributes directly to the pathogenesis of atherothrombosis will come if interventions to lower total homocysteine reduce cardiovascular events. Family studies may also provide evidence of causality if genetic causes of hyperhomocysteinemia are found to segregate with disease.