[Homocysteine and cerebrovascular disease]
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Published on: May 17, 2024
J M Sepúlveda-Sánchez1, R Matía-Francés, A Martínez-Salio
1Servicio de Neurología, Hospital Universitario 12 de Octubre, Madrid, España. sepulveda25@mundofree.com
Insights
The link between high homocysteine (Hc) levels and cerebrovascular disease (CVD) is controversial. While some studies suggest a connection, others indicate it may be weak or non-existent, requiring further research.
Area of Science:
- Cardiovascular Science
- Neurology
- Metabolic Disorders
Context:
- Elevated total homocysteine (tHc) is a recently proposed vascular risk factor.
- The hypothesis stems from observations of early atherosclerosis in individuals with inborn errors of homocysteine metabolism.
- This paper reviews existing literature on the association between homocysteine (Hc) and cerebrovascular disease (CVD).
Purpose:
- To analyze the published studies investigating the relationship between homocysteine levels and cerebrovascular disease.
- To critically evaluate the evidence for and against homocysteine as a causal factor in atherothrombosis.
- To contextualize the ongoing clinical trials assessing vitamin therapy for vascular risk reduction.
Summary:
- Retrospective studies report a strong, dose-dependent link between plasma Hc levels and thromboembolic events (cerebrovascular, cardiac, peripheral).
- Prospective studies, however, show a weak or no association between Hc and CVD.
- Alternative explanations for retrospective findings include Hc increase post-stroke or due to other vascular risk factors.
Impact:
- The role of Hc in CVD remains debated.
- Further research, including clinical trials on vitamin therapy (folic acid, B12, pyridoxine), is crucial to elucidate the Hc-CVD relationship.
- Findings will inform future strategies for managing vascular risk.
Aims:
In the search for new, potentially treatable, vascular risk factors, one of the most recent to be put forward is the presence of increased total homocysteine (tHc) levels in blood plasma and this has also given rise to a large amount of literature and controversy. The origin of this hypothesis lies in the observation that patients with congenital disorders affecting homocysteine (Hc) metabolism suffered from early atherosclerosis. In this paper we analyse the studies that have been published about Hc and cerebrovascular disease (CVD).
Development:
An important number of retrospective case control studies have found a strong dose dependent link between levels of Hc in plasma and cerebrovascular, heart and peripheral thromboembolic disease. Yet the prospective studies that have been published to date note only a weak or inexistent link between homocysteine and CVD. Moreover, some observations question the causal relationship between hyperhomocysteinemia and atherothrombosis and account for the findings in the retrospective studies as being a result of the rise in Hc following a stroke or its increasing because of classical vascular risk factors. In any case, knowing that the ingestion of folic acid, vitamin B12 and pyridoxine lowers tHc levels in plasma has led to clinical trails being set up that evaluate the effects of this treatment on vascular risk.
Conclusion:
The relation between Hc levels in plasma and CVD is open to controversy. New studies and the findings of clinical studies with vitamin therapy will allow this relation to be fully explained in coming years.
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