Oxidant stress mechanisms in heart failure

Evidences clearly indicate that HF is accompanied by excessive generation of OFRs and depletion of endogenous antioxidant system. The resultant oxidant stress depresses myocardial contractility and function by decreasing Ca++ uptake in sarcoplasmic reticulum and by impaired Ca(++)-ATPase in cardiac tissue. The various sources of OFRs production in HF include increased production of nitric oxide, cytokines, prostaglandins, auto-oxidation of catecholamines, activation of polymorph leucocytes and ischemia induced xanthine-xanthine oxidase. The prevention of oxidative stress by antioxidant translates into better metabolism and function of myocytes. It appears that antioxidant drugs may represent a novel adjunct to the existing therapeutic armamentarium in patients of HF irrespective of its etiology and severity.