Homocyst(e)ine, atherosclerosis, and thrombosis

Area of Science:

• Cardiovascular Medicine
• Biochemistry
• Epidemiology

Background:

• Homocysteine is an established risk factor for atherosclerotic vascular disease and thrombosis.
• The exact mechanisms linking homocysteine to vascular injury are not fully understood but involve endothelial dysfunction and a prothrombotic state.
• Elevated plasma homocysteine concentration (PHC) is associated with increased risk of cardiovascular events.

Purpose of the Study:

• To review the evidence implicating homocysteine in vascular disease.
• To discuss the potential mechanisms of homocysteine-induced vascular injury.
• To evaluate the efficacy of folic acid in reducing PHC and the potential role of vitamins B6 and B12.

Main Methods:

• Review of clinical and epidemiologic evidence.
• Discussion of proposed pathogenetic mechanisms.
• Assessment of the impact of folic acid supplementation on PHC.

Main Results:

• Clinical and epidemiologic data strongly suggest homocysteine is a risk factor for vascular disease.
• Folic acid effectively reduces plasma homocysteine concentration.
• The necessity of vitamins B6 and B12 for homocysteine reduction in non-deficient individuals is uncertain.

Conclusions:

• Homocysteine is implicated in atherosclerotic vascular disease and thrombosis through mechanisms involving endothelial injury and a prothrombotic state.
• Folic acid is effective in lowering plasma homocysteine.
• Further research is needed to determine if reducing homocysteine levels translates to decreased clinical vascular events and the role of other B vitamins.