Heart failure in patients with high homocysteine levels

Abstract

S-adenosyl-methionine; methyl group; S-adenosyl-homocysteine; S-adenosyl homocysteine Abstract Increased levels of homocysteine (HHcy) can induce both systolic and diastolic left ventricular (LV) dysfunction that may evolve until chronic heart failure (HF). It is known that HHcy acts as an independent risk factor for atherosclerosis and hypercoagulation. This condition may cause coronary artery disease (CAD. Chronic reduction of oxygen supply to the myocardium can induce a reduction in LV contractility. These conditions can further evolve towards HF with reduced ejection fraction (HFrEF). But, HHcy can be also responsible for adverse cardiac remodeling for accumulation and proliferation of interstitial collagen, increased fibrosis and myocardial stiffness and preserved LV ejection fraction (HFpEF). Both HF can be further favoured by the advanced age, hypertension, diabetes and others. The administration of some nutrients, such as folic acid and B 12 vitamin can delay or avoid these cardiac complications. However, the cellular mechanisms behind the adverse effects of Hcy on cardiac remodeling and pump function are not understood.