Homocysteine and cerebrovascular disease

• Published in: Revista de neurologiá Vol. 38; no. 4; pp. 347 - 358
• Main Authors: Sepúlveda-Sánchez, J M, Matía-Francés, R, Martínez-Salio, A, González-de la Aleja-Tejera, J, Rodríguez-Peña Marín, M, Porta-Etessam, J
• Format: Journal Article
• Language: Spanish
• Published: Spain 16.02.2004
• Subjects: Arteriosclerosis - blood; Arteriosclerosis - drug therapy; Cardiovascular Diseases - blood; Cardiovascular Diseases - drug therapy; Case-Control Studies; Cerebrovascular Disorders - blood; Cerebrovascular Disorders - drug therapy; Homocysteine - blood; Humans; Hyperhomocysteinemia - metabolism; Methylenetetrahydrofolate Reductase (NADPH2) - genetics; Methylenetetrahydrofolate Reductase (NADPH2) - metabolism; Retrospective Studies; Risk Factors; Thrombosis - blood; Thrombosis - drug therapy; Vitamins - therapeutic use
• ISSN: 0210-0010
• DOI: 10.33588/rn.3804.2003605

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). 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. 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.