The role of increased levels of homocysteine in the development of cardiovascular diseases

Abstract

Introduction. Homocysteine is a sulphur amino acid produced by demethylation of the essential amino acid methionine. Dysfunction of certain enzymes or insufficient intake of nutrients may cause increase of intracellular homocysteine, which is then exported into plasma. Etiopathogenesis of cardiovascular diseases accompanied with higher level of homocysteine. McCully's theory suggests that high levels of homocysteine are associated with cardiovascular diseases, arteriosclerosis and endothelial dysfunction. Harmful effects of homocysteine are associated with LDL cholesterol oxidation, increased production of collagen, lower availability of nitric oxide as well as prothrombotic activity. Reduction of homocysteine levels. The most recent researches show that hyperhomocysteinemia is responsible for about 10% of total risk of cardiovascular diseases. Vitamin BJ2 plays a major role in the remethylation of homocysteine. Reducing the homocysteine concentration in blood by 3 mol/l (with daily intake of 0.8 mg of folic acid) reduces the risk of ishemic heart diseases by 16%, vein thrombosis by 25%, and stroke by 24%. A six-month therapy with folic acid (Img/d), vitamin B12 (400g/d) and vitamin B6 (10mg/d), reduces the frequency of cardiovascular occurrences after successful PTCA. Plasma homocysteine concentration over 12/1 doubles the risk of myocardial infarction. Conclusion. A lack of folates, vitamin B6 and vitamin B12 increases the level of homocysteine and thus increases the risk of cardiovascular diseases. Changes in lifestyle and diet, as well as intake of food supplements, are of great importance in reducing homocysteine levels in plasma and therefore in reducing the occurrence and acceleration of arteriosclerosis. .