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 Printable version |
Homocysteine and cardiovascular risk |
Sang Thrombose Vaisseaux. Volume 19, Number 3, 143-9, Mars 2007, Mini-revue
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 Résumé
Article gratuit
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Author(s) : Claire Vesin, Marie-Hélène Horellou, Sandrine Mairesse, Jacqueline Conard, Michel Safar, Jacques Blacher |
Summary : For the past thirty years, homocysteine has been considered a potential cause of atherosclerosis. Mild hyperhomocysteinemia, which is sometimes associated with a low plasma level of vitamin B9, B12 and folic acid, is a proven cardiovascular risk marker, if not factor. Its level is closely related to experimental and clinical events as diverse as acute myocardial infarction, stroke, dementia, and venous thrombo-embolic disease. Its direct incrimination in causing these events remains uncertain and controversal. Indeed, even if vitamin supplementation has clearly proven its efficiency on lowering plasma levels of homocysteine, recent studies do not show any positive effect of vitamin therapy on cardio-vascular events. The hypothesis that this therapy is inefficient has been recently reinforced by three randomized trials, two on the arterial effects of vitamin supplementation (the NORVIT and HOPE 2 studies) and one on its effects on thrombo-embolic venous disease (the VITRO study).Several hypotheses still need to be explored: that of total uselessness of vitamin supplementation\; the possible need to complete the actual data with further, more powerful studies in order to prove a clinical effect of vitamin therapy\; or even the exploration other metabolic paths that could lower homocysteine levels. |
Keywords : homocysteine, hyperhomocysteinemia, vitamin supplementation, atherosclerosis |
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