Impact of Epicardial Adipose Tissue in Heart Failure with Preserved Ejection Fraction

Abstract

IntroductionObesity is a strong risk factor for heart failure (HF) with preserved ejection fraction (HFpEF). HFpEF patients with obesity display distinct structural and functional changes in the heart compared to non-obese HFpEF. In addition to generalized obesity, fat distribution may also be important. Prior studies have shown that epicardial adipose tissue (EAT) is associated with inflammation, atrial fibrillation and cardiac fibrosis. Based upon its location, EAT might also influence hemodynamics and ventricular interaction via direct mechanical effects. However, no study has directly evaluated the impact of EAT content in HFpEF.HypothesisWe hypothesized that among patients with obesity and HFpEF, those with excess EAT (EAT+, n=77) would display more deranged hemodynamics compared to obese HFpEF patients without excess EAT (EAT−, n=92).MethodsPatients underwent invasive hemodynamic cardiopulmonary exercise testing and echocardiography. Obesity was defined by BMI≥30 kg/m2 and excess EAT was defined by EAT thickness ≥9mm by echocardiography. Ventricular interaction was assessed by the left ventricular eccentricity index (LVecc), where higher values indicate greater interdependence.ResultsEAT+ and EAT− patients displayed similar cardiac structure and function (Table). However, compared to EAT−, LVecc were elevated in EAT+. Right atrial (RA), pulmonary artery (PA), and pulmonary capillary wedge pressures (PCWP) were higher at rest and during exercise in EAT+ compared to EAT−, despite similar diastolic chamber stiffness (β) among EAT+ and EAT−. Peak VO2 was reduced in both groups, but was significantly lower in EAT+ compared to EAT−.ConclusionAmong patients with the obese phenotype of HFpEF, the presence of increased EAT is associated with more profound hemodynamic derangements at rest and exercise, greater pericardial restraint, and poorer exercise capacity (VO2). Further study is needed to understand the biology and potential treatment of excessive EAT in patients with HFpEF. Obesity is a strong risk factor for heart failure (HF) with preserved ejection fraction (HFpEF). HFpEF patients with obesity display distinct structural and functional changes in the heart compared to non-obese HFpEF. In addition to generalized obesity, fat distribution may also be important. Prior studies have shown that epicardial adipose tissue (EAT) is associated with inflammation, atrial fibrillation and cardiac fibrosis. Based upon its location, EAT might also influence hemodynamics and ventricular interaction via direct mechanical effects. However, no study has directly evaluated the impact of EAT content in HFpEF. We hypothesized that among patients with obesity and HFpEF, those with excess EAT (EAT+, n=77) would display more deranged hemodynamics compared to obese HFpEF patients without excess EAT (EAT−, n=92). Patients underwent invasive hemodynamic cardiopulmonary exercise testing and echocardiography. Obesity was defined by BMI≥30 kg/m2 and excess EAT was defined by EAT thickness ≥9mm by echocardiography. Ventricular interaction was assessed by the left ventricular eccentricity index (LVecc), where higher values indicate greater interdependence. EAT+ and EAT− patients displayed similar cardiac structure and function (Table). However, compared to EAT−, LVecc were elevated in EAT+. Right atrial (RA), pulmonary artery (PA), and pulmonary capillary wedge pressures (PCWP) were higher at rest and during exercise in EAT+ compared to EAT−, despite similar diastolic chamber stiffness (β) among EAT+ and EAT−. Peak VO2 was reduced in both groups, but was significantly lower in EAT+ compared to EAT−. Among patients with the obese phenotype of HFpEF, the presence of increased EAT is associated with more profound hemodynamic derangements at rest and exercise, greater pericardial restraint, and poorer exercise capacity (VO2). Further study is needed to understand the biology and potential treatment of excessive EAT in patients with HFpEF.