Epicardial adipose tissue expansion in obese and diabetic patients with HFpEF represents a specific phenotype that may benefit from targeted interventions like statins, SGLT2 inhibitors, and GLP-1 agonists.
Epicardial adipose tissue expansion represents a specific, targetable pathophysiological mechanism in obese and diabetic patients with HFpEF that may benefit from therapies such as SGLT2 inhibitors and GLP-1 receptor agonists.
Graphical Abstract Epicardial adipose tissue (EAT)-related heart failure with preserved ejection fraction (HFpEF). Obesity and type 2 diabetes mellitus (T2DM) are common triggers of HFpEF, frequently associated with EAT expansion. EAT plays metabolic and mechanical roles in HFpEF development via para/vasocrine factors and pericardial restrain, respectively. Life-style modifications including healthy diet and regular exercise can quash the EAT expansion. Statins, proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors and fat-modulating antidiabetics including metformin, sodium-glucose cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide-1 (GLP-1) agonists can target EAT. FFA, free fatty acids; AGEs, advanced glycation end-products; NO, nitric oxide; ROS, reactive oxygen species; Ang-II, angiotensin II; TGF-β, Transforming growth factor beta; MCP-1, monocyte chemoattractant protein 1; IL-6, interleukin 6; TNF-α, tumor necrosis factor alpha. Figure created via Servier Medical Art and BioRender tools.
Elsanhoury et al. (2021) conducted a review in Heart failure with preserved ejection fraction (HFpEF). Epicardial fat modifying interventions was evaluated. Epicardial adipose tissue expansion in obese and diabetic patients with HFpEF represents a specific phenotype that may benefit from targeted interventions like statins, SGLT2 inhibitors, and GLP-1 agonists.
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