Homocysteine, Cardiovascular Inflammation, and Myocardial Remodeling

Jennifer      M. Finch; Jacob      Joseph

doi:10.2174/187152910793743887

Abstract

Chronic heart failure is a major public health problem causing considerable morbidity and mortality. Recent studies have shown that an elevated plasma level of homocysteine is a strong independent risk factor for heart failure, in addition to atherosclerotic disease. Preclinical studies have demonstrated that induced hyperhomocysteinemia acts via multiple pathogenic mechanisms, including inflammation and oxidative stress, to promote adverse cardiac remodeling and failure. However, clinical studies have not conclusively shown a causative relation between hyperhomocysteinemia and cardiovascular disease. This article will review current data concerning homocysteine and its pathogenic relationship to heart failure.

Keywords: Homocysteine, Heart Failure, Remodeling, Cardiovascular Disease, morbidity, mortality, atherosclerotic disease, oxidative stress, atherothrombotic, spironolactone, hypertension, diabetes mellitus, obesity, B-type, natriuretic peptide, hyperuricaemia, echocardiographic signs, diastolic diameter, methionine, cystathionine, methyltetrahydrofolate, adenosylmethionine, neurohormonal model, angiotensin-converting enzyme, fibrosis, tumor necrosis, myocardium, Interleukins-1, matrix metalloproteinases, Cathepsin G, anti-oxidant vitamin, Coronary artery disease