Nearly half of all patients with heart failure (HF) symptoms have HF with preserved ejection fraction (HFpEF) and the prevalence of this pathologic condition is rising being aging one of the most important risk factors. HFpEF is a very challenging syndrome vulnerable and frail affecting, in the most of cases, patients, with high health care costs due to high number of hospitalizations and medical cares.
More and more evidence are accumulating on the role of inflammation in the pathogenesis of HFpEF. The presence of multiple comorbidities in HFpEF may significantly contribute to a systemic pro-inflammatory state which negatively affects the myocardium.
Obesity promotes systemic inflammation and exacerbates the inflammatory burden imposed by many chronic extracardiac comorbidities. Importantly, the chronic systemic inflammation related to obesity is associated to a significant increase of the amount of epicardial adipose tissue (EAT), the cardiac visceral fat. The increase of EAT volume is associated to a pro-inflammatory state of this fat depot. Several observations support the hypothesis that the inflammation of EAT can act in a paracrine and vasocrine manner to influence the structure and function of the heart, thus contributing to the pathohenesis of HFpEF.
Given the recognized role of EAT in the pathophysiology of HFpEF, it should be desirable to identify specific therapies targeting the cardiac visceral fat and able to modulate its pro-inflammatory profile and the negative effect of the inflammatory burden on the neighboring myocardium.