HOMOCYST(E)INE AND CORONARY-ARTERY DISEASE - CLINICAL-EVIDENCE AND GENETIC AND METABOLIC BACKGROUND

Many studies have demonstrated a strong association between elevated p lasma total homocyst(e)ine levels and vascular diseases. Consequently, hyperhomocyst(e)inemia is now generally accepted as an independent ri sk factor for coronary artery disease. We critically reviewed the resu lts of 35 human studies in which the levels of plasma total homocystei ne were measured in patients with atherosclerotic diseases (n=4338) an d in controls (n=22593). Total homocysteine levels were consistently h igher in patients than in controls. The average of this increment amon g 23 case-control studies was 26%. New insights into the biochemical p athways of total homocysteine metabolism, the factors that influence t otal homocysteine levels, genetic contributions to hyperhomocyst(e)ine mia, the pathogenesis of homocyst(e)ine-induced vascular damage, and c urrent recommendations for treatment of hyperhomocyst(e)inemia were al so reviewed. Various lines of evidence now link hyperhomocyst(e)inemia with vascular diseases. Although there are no data from double-blind, placebo-controlled clinical trials of treatment for hyperhomocyst(e)i nemia, the strong epidemiologic and experimental evidence argues for t reatment of hyperhomocyst(e)inemia; in fact, its treatment with low do ses of vitamins is thought to be safe and is inexpensive.