Heart failure with preserved ejection fraction (HFpEF) represents a significant and growing public health burden, with obesity and type 2 diabetes (T2D) emerging as major predisposing factors [1]. HFpEF pathogenesis results from a complex interplay of mechanisms, including systemic inflammation, insulin resistance, endothelial dysfunction, and myocardial fibrosis, ultimately leading to impaired ventricular relaxation and increased myocardial stiffness despite preserved contractile function [2]. Adipose tissue, particularly visceral fat, acts as an active endocrine organ, releasing pro-inflammatory cytokines and adipokines that promote adverse cardiac remodelling.
