Obesity increases the risk of heart failure (HF), which continues to be a significant proportion of all cardiovascular diseases and affects increasingly younger populations. The cross-talk between adipose and the heart involves insulin resistance, adipokine signaling and inflammation, with the capacity of adipose tissue to mediate hemodynamic signals, promoting progressive cardiomyopathy. Areas covered: From a therapeutic perspective, there is not yet a single obesity-related pathway that when addressed, can ameliorate cardiomyopathy in obese patients and this is a matter of ongoing research. There is poor evidence of the beneficial long-term effect of small nonsurgical intentional weight loss on HF outcomes, in contrast to the field of HF accompanying severe obesity where observational studies have shown that bariatric surgery is associated with improved cardiac structure/function in severely obese patients with HF and preserved ejection fraction (HFpEF) as well as with improved cardiac structure/function in those with HF and reduced ejection fraction (HFrEF). Few studies report positive outcomes in subjects with obesity and HF, both severe, who underwent bariatric surgery as a rescue treatment, including bridge to heart transplantation. Expert commentary: The fast growing prevalence of obesity will continue to require the development of appropriate interventions directed at controlling or slowing pathways of cardiac damage in these patients, but at present, bariatric surgery should be considered an option to try to decrease morbidity associated with HF in severely obese adults.
Keywords: Severe obesity; bariatric surgery; heart failure; morbidity; mortality.