Hemodynamic and Functional Impact of Epicardial Adipose Tissue in Heart Failure With Preserved Ejection Fraction

This study determined the impact of excess epicardial adipose tissue (EAT) in patients with the obese phenotype of heart failure with preserved ejection fraction (HFpEF).

Patients with HFpEF and an elevated body mass index differ from nonobese patients, but beyond generalized obesity, fat distribution may be more important. Increases in EAT are associated with excess visceral adiposity, inflammation, and cardiac fibrosis, and EAT has been speculated to play an important role in the pathophysiology of HFpEF, but no study has directly evaluated this question.

Patients with HFpEF and obesity (n = 169) underwent invasive hemodynamic exercise testing with expired gas analysis and echocardiography. Increased EAT was defined by echocardiography (EAT thickness ≥9 mm).

Compared with obese patients without increased EAT (HFpEF_EAT-, n = 92), obese patients with HFpEF with increased EAT (HFpEF_EAT+; n = 77) displayed a higher left ventricular eccentricity index, indicating increased pericardial restraint, but similar resting biventricular structure and function. In contrast, hemodynamics were more abnormal in patients with HFpEF_EAT+, with higher right atrial, pulmonary artery, and pulmonary capillary wedge pressures at rest and during exercise compared with those of patients with HFpEF_EAT-. Peak oxygen consumption (VO₂) was reduced in both groups but was 20% lower in patients with HFpEF_EAT+ (p < 0.01).

Among patients with the obese phenotype of HFpEF, the presence of increased EAT is associated with more profound hemodynamic derangements at rest and exercise, including greater elevation in cardiac filling pressures, more severe pulmonary hypertension, and greater pericardial restraint, culminating in poorer exercise capacity. Further study is needed to understand the biology and treatment of excessive EAT in patients with HFpEF.