Hyperhomocyst(e)inemia: is this a novel risk factor in hypertension?

Homocysteine is an intermediate sulfur-containing amino acid formed during intracellular metabolism of methionine. Circulating homocyst(e)ine can be increased by genetic deficiency of enzymatic pathways involved in its catabolism as well as by environmental factors including nutritional deficiencies, life style factors, physiological conditions, drugs and some diseases, which mainly induce deficiency of folate, vitamin B12 and vitamin B6. Therefore plasma homocyst(e)ine can be reduced by vitamin therapy with folate and vitamin B12. Although hyperhomocyst(e)inemia exerts a prothrombotic and proatherosclerotic effect, its relevance in the genesis of the atherosclerotic lesions, as well in the first occurrence of cardiovascular events in normotensive and even more so in hypertensive patients is still to be established. However available data indicate that hyperhomocyst(e)inemia could be an independent risk factor for the recurrence of cardiovascular events in patients with coronary artery disease and in elderly high risk patients. Finally, the possibility that a reduction in plasma homocyst(e)ine induced by vitamin therapy can diminish the risk of cardiovascular events is under evaluation in several controlled longitudinal studies focusing mainly on secondary prevention.