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Published on: September 5, 2016
Homocysteine and arterial thrombosis: Challenge and opportunity
Matteo N D Di Minno1, Elena Tremoli, Antonio Coppola
1Department of Experimental and Clinical Medicine, Federico II University, Naples, Italy. diminno@unina.it
Insights
Elevated homocysteine (Hcy) is linked to vascular disease, but current evidence does not support routine screening or vitamin treatment for cardiovascular risk prevention.
Area of Science:
- Cardiovascular Medicine
- Metabolic Disorders
- Vascular Biology
Background:
- Elevated plasma total homocysteine (tHcy) is an independent risk factor for atherosclerotic vascular disease.
- Homocysteine metabolism disorders range from rare enzyme deficiencies to common milder abnormalities.
- Homocysteine-mediated oxidant stress can activate platelets, promoting thrombosis in severe hyperhomocysteinemia.
Purpose of the Study:
- To review the role of homocysteine in vascular disease.
- To clarify whether hyperhomocysteinemia is causal or merely a marker of vascular disease.
- To assess the impact of vitamin supplementation on cardiovascular risk in relation to homocysteine levels.
Main Methods:
- Review of clinical and experimental studies on homocysteine and vascular disease.
- Examination of the relationship between hyperhomocysteinemia, oxidant stress, and thrombosis.
- Analysis of data regarding vitamin supplementation (folic acid, B12, B6) and cardiovascular outcomes.
- Evaluation of lipid-modifying treatments' effects on homocysteine levels and cardiovascular risk in diabetics.
Main Results:
- Homocysteine's role in vascular disease is supported by its association with oxidant stress and thrombosis.
- Vitamin supplementation trials failed to show significant cardiovascular risk reduction despite lowering homocysteine levels.
- No evidence suggests that increased homocysteine levels from lipid-modifying treatments negate their cardiovascular benefits in diabetics.
Conclusions:
- The causal role of hyperhomocysteinemia in vascular disease and whether tHcy is solely a metabolic indicator requires further clarification.
- Current data do not support routine screening for elevated homocysteine or its treatment with vitamins to prevent cardiovascular disease.
- Further research is needed to fully understand homocysteine's complex relationship with cardiovascular health and disease prevention strategies.
Abstract:
The correlation between homocysteine and vascular disease has been assessed in several clinical studies that demonstrated that elevation of plasma total homocysteine (tHcy) was an independent risk factor for atheriosclerotic disease. Major advances of homocysteine metabolism disorders have been made during the last few years, encompassing the rare homozygous enzyme deficiencies, as well as more common milder abnormalities. In experimental and clinical studies, a homocysteine-mediated oxidant stress has been shown to trigger platelet activation, in turn leading to a tendency to thrombosis, in patients with severe hyperhomocysteinaemia. Likewise, the hypomethylation hypothesis on acquired hyperhomocysteinaemia (chronic renal disease) and the interrelationship between hyperhomocysteinaemia and impaired fibrinolysis, have added further biological plausibility to the role for hyperhomocysteinaemia in vascular medicine. However, whether hyperhomocysteinaemia is causal or a marker of vascular disease, and whether plasma tHcy is only an indicator of the metabolic status remains to be clarified. The role of the intake of some vitamins (folic acid, vit.B12, vit.B6) on cardiovascular disease (CVD) is poorly understood: in spite of the lowering of homocysteine (Hcy) levels, vitamin supplementation failed to exert significant effects on cardiovascular risk. On the other hand, although some lipid-modifying treatments increase Hcy levels in diabetics, there is no evidence that this attenuates the beneficial effects of such treatments on the cardiovascular risk. Because of these uncertainties in the area, the data available do not provide support for routine screening and treatment for elevated Hcy to prevent CVD.
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