Related Experiment Videos

Homocysteine and coronary risk

N Seshadri1, K Robinson

  • 1Desk F15, Department of Cardiology, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA.

Current Cardiology Reports
|September 12, 2000
PubMed

Insights

High homocysteine levels are a risk factor for coronary artery disease. Folic acid may help lower homocysteine and reduce this risk, with ongoing studies investigating its therapeutic potential.

Area of Science:

  • Cardiovascular Medicine
  • Nutritional Biochemistry

Background:

  • Hyperhomocysteinemia is increasingly recognized as a significant risk factor in coronary artery disease (CAD) pathogenesis.
  • Plasma homocysteine levels are influenced by diverse genetic and non-genetic factors.
  • The precise mechanisms linking hyperhomocysteinemia to atherosclerosis remain under investigation, though potential adverse effects on vascular endothelium are noted.

Purpose of the Study:

  • To explore the role of hyperhomocysteinemia as a risk factor in coronary artery disease.
  • To investigate the potential of folic acid in ameliorating the adverse effects of elevated homocysteine.
  • To summarize current research on homocysteine-lowering therapy with folic acid for atherosclerotic vascular disease risk.

Main Methods:

  • Review of existing literature on homocysteine metabolism and cardiovascular risk.
  • Analysis of studies investigating the impact of folic acid on plasma homocysteine levels.
  • Examination of epidemiological and clinical trial data related to homocysteine-lowering therapy.

Main Results:

  • Hyperhomocysteinemia is associated with an increased risk of atherosclerotic vascular disease.
  • Folic acid, even in low doses, demonstrates potential in reducing homocysteine levels.
  • Ongoing research aims to confirm the efficacy of folic acid therapy in mitigating cardiovascular events.

Conclusions:

  • Hyperhomocysteinemia represents a modifiable risk factor for coronary artery disease.
  • Folic acid supplementation shows promise as a therapeutic strategy to lower homocysteine and potentially reduce vascular disease risk.
  • Further clinical studies are warranted to establish definitive treatment guidelines.

Related Concept Videos