Key result
Epicardial adipose tissue is implicated in the pathophysiology of obesity-related HFpEF, with ongoing studies evaluating if GLP-1 receptor agonists and SGLT2 inhibitors can attenuate these changes.
Why the study?
The magnitude of effect that epicardial adipose tissue plays on myocardial dysfunction in obesity-related heart failure remains unclear.
Epicardial adipose tissue is a unique visceral fat deposit implicated in the pathophysiology of obesity-related HFpEF, with ongoing research into its quantification via imaging and modification by GLP-1 RAs and SGLT2 inhibitors.
May inform future EAT-targeted HFpEF therapies; leaves open causal confirmation in prospective trials.
Obesity is associated with the development of heart failure and is a major risk factor for heart failure with preserved ejection fraction (HFpEF). Epicardial adipose tissue (EAT) is a unique visceral fat in close proximity to the heart and is of particular interest to the study of cardiac disease. Small poorly differentiated adipocytes with altered lipid:water content are associated with a proinflammatory secretome and may contribute to the pathophysiology observed in HFpEF. Multimodality imaging approaches can be used to quantify EAT volume and characterise EAT composition. Current research studies remain unclear as to the magnitude of effect that EAT plays on myocardial dysfunction and further work using multimodality imaging techniques is ongoing. Pharmacological interventions, including glucagon-like peptide 1 receptor agonists and sodium-dependent glucose linked transporter 2 inhibitors have shown promise in attenuating the deleterious metabolic and inflammatory changes seen in EAT. Clinical studies are ongoing to explore whether these therapies exert their beneficial effects by modifying this unique adipose deposit.
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Ayton et al. (2021) conducted a review in Obesity-related cardiac dysfunction and heart failure with preserved ejection fraction (HFpEF). Epicardial adipose tissue (EAT) was evaluated. Epicardial adipose tissue is implicated in the pathophysiology of obesity-related HFpEF, with ongoing studies evaluating if GLP-1 receptor agonists and SGLT2 inhibitors can attenuate these changes.
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