Heart Failure and Obesity: The Latest Pandemic

The marked rise in rates of obesity, which is most prominent among individuals from socio-economically disadvantaged circumstances, has been a powerful contributor to the rising prevalence of heart failure (HF). Obesity has indirect effects on HF through the development of several metabolic risk factors, but also direct adverse effects on the myocardium. Obesity contributes to myocardial dysfunction and HF risk through multiple mechanisms, including hemodynamic changes, neurohormonal activation, endocrine and paracrine effects of adipose tissue, ectopic fat deposition and lipotoxicity. These processes principally result in concentric left ventricular (LV) remodeling and predominant increase in the risk for HF with preserved LV ejection fraction (HFpEF). Despite the excess risk for HF associated with obesity, there is a well described obesity paradox in which individuals with overweight and grade I obesity have better survival than those with normal weight and underweight. Despite the obesity paradox among individuals with prevalent HF, intentional weight loss is associated with improvements in metabolic risk factors, myocardial dysfunction and quality of life, in a dose-response fashion. In matched observational studies of bariatric surgery patients, marked weight loss is associated with decreased risk for developing HF, as well as improved cardiovascular disease (CVD) outcomes in those with existing HF. Ongoing clinical trials using powerful new obesity pharmacotherapies in individuals with obesity and CVD may provide definitive information regarding the cardiovascular impact of weight loss. Given the powerful contribution of rising obesity prevalence to rates of HF, addressing these intertwined epidemics is a clinical and public health priority.