TNF inhibitors and Heart Failure

Chronic systemic inflammation yields a notable and proportional risk for myocardial infarction, coronary artery disease, heart failure and cardiovascular (CV) death. The role of tumor necrosis factor (TNF) in the pathogenesis of cardiovascular events and congestive heart failure (CHF) in rheumatoid arthritis (RA) has been well documented (1-4). TNFα mediates anorexia, cardiac cachexia and endotoxic shock, and also induces left ventricular hypertrophy (LVH), LV dysfunction/remodeling/dilation and has negative inotropic effects on the myocardium. Many studies have shown increased circulating levels of TNF in heart failure, especially in those with New York Heart Association (NYHA) class III and IV disease, which correlates with the morbidity and mortality of CHF. Finally, transgenic mice that over express TNFα tend to die prematurely from dilated cardiomyopathy. The vascular and myotoxic effects of TNF have led to th