Epicardial Fat in Heart Failure with Preserved Ejection Fraction: Bad Actor or Just Lying Around?

Abstract

Heart failure with preserved ejection fraction (HFpEF) is increasingly recognised to be strongly associated with obesity and abnormalities in fat distribution. Epicardial fat has been associated with abnormal haemodynamics in HFpEF, with potential for direct mechanical effects on the heart causing constriction-like physiology and local myocardial remodelling effects from secretion of inflammatory and profibrotic mediators. However, patients with epicardial fat generally have more systemic and visceral adipose tissue making determination of causality between epicardial fat and HFpEF complex. In this review, we will summarise the evidence for epicardial fat being either directly causal in HFpEF pathogenesis or merely being a correlate of worse systemic inflammatory and generalised adiposity. We will also discuss therapies that directly target epicardial fat and may have potential for treating HFpEF and elucidating the independent role of epicardial fat in its pathogenesis.

The Impact of SGLT2 Inhibitors on Cardiovascular Outcomes in Patients With Heart Failure With Preserved Ejection Fraction

“…29 Obese individuals with HFpEF have higher amounts of EAT leading to increased pericardial restraint. 17,30 Reduction of EAT may provide an additional mechanism for CV benefits in patients with HFpEF. 31 At present, both dapagliflozin and empagliflozin, in a broad population of heart failure patients including, HFrEF, HFmrEF, HFpEF, have shown consistent improvement in the combined outcome of CV death and hospitalization for heart failure along with symptomatic improvement based on KCCQ quality of life scores (Table 3).…”

“…29 Obese individuals with HFpEF have higher amounts of EAT leading to increased pericardial restraint. 17,30 Reduction of EAT may provide an additional mechanism for CV benefits in patients with HFpEF. 31…”

New Mechanisms to Prevent Heart Failure with Preserved Ejection Fraction Using Glucagon-like Peptide-1 Receptor Agonism (GLP-1 RA) in Metabolic Syndrome and in Type 2 Diabetes: A Review

“…EAT may lead to an increase in myocardial fat content and interstitial fibrosis, which can reduce myocardial diastolic function and contractility, as evidenced by reduced global longitudinal strain [101]. In patients with substantial obesity with cardiomegaly and increased epicardial fat volume, the pericardial sac is stretched to a steeper pressure-volume relationship and there is enhanced diastolic ventricular interaction and pericardial restraint [102]. This exerts an exaggerated compressive force on the heart, resulting in higher left-and rightsided filling pressures for any degree of left ventricular (LV) end diastolic volume-the true LV preload [103].…”

“…Most abdominal visceral adipose tissue and EAT loss (43% and 14%, respectively p < 0.0001) occurred within the first 212 days, with non-significant reductions thereafter [105]. Currently, bariatric surgery is the most effective weight loss therapy available and also has independent benefits for epicardial fat deposits, which may have advantages in terms of relieving pericardial restraint [102].…”