Key result
Epicardial fat in HFpEF may exert mechanical and inflammatory effects but systemic adiposity confounds causality.
Why the study?
Determining whether epicardial fat is directly causal in HFpEF pathogenesis or merely a correlate of systemic inflammation and generalized adiposity is complex.
This review highlights epicardial fat as a potential contributor to pericardial restraint and inflammation in obesity-related HFpEF, suggesting it may be a viable therapeutic target for weight-loss interventions and novel pharmacotherapies.
May identify epicardial fat as a target in obesity-related HFpEF; leaves open causal confirmation pending prospective studies.
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.
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Oduah et al. (2023) conducted a review in Heart failure with preserved ejection fraction (HFpEF). Epicardial fat in HFpEF may have direct mechanical and inflammatory effects, but its causal role remains complex due to confounding by systemic and visceral adiposity.
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