Key result
Greater epicardial fat in HFpEF is linked to increased LV septal thickness and inflammatory proteins.
Why the study?
Epicardial adipose tissue may play a role in the pathophysiology of HFpEF, but its associations with proteomics, coronary flow reserve, cardiac structure and function, and quality of life were unclear.
Is epicardial adipose tissue associated with proteomics, coronary flow reserve, cardiac structure and function, and quality of life in patients with HFpEF?
Cohort
Yes
Is epicardial adipose tissue associated with proteomics, coronary flow reserve, cardiac structure and function, and quality of life in patients with HFpEF?
Increased epicardial adipose tissue in HFpEF is associated with adverse cardiac structural alterations and proteomic profiles reflecting inflammation and endothelial dysfunction.
EAT may mark adverse remodeling and inflammation in HFpEF; leaves open whether targeting it alters outcomes.
AIM: Epicardial adipose tissue (EAT) may play a role in the pathophysiology of heart failure with preserved ejection fraction (HFpEF). We investigated associations of EAT with proteomics, coronary flow reserve (CFR), cardiac structure and function, and quality of life (QoL) in the prospective multinational PROMIS-HFpEF cohort. METHODS AND RESULTS: ; p < 0.001), lower N-terminal pro-B-type natriuretic peptide (466 [193-1133] vs. 1120 [494-1990] pg/ml; p < 0.001), smaller indexed left ventricular (LV) end-diastolic and left atrial (LA) volumes and tendency to lower KCCQ score. Non-indexed LV/LA volumes did not differ between groups. When adjusted for body mass index, EAT remained associated with LV septal wall thickness (coefficient 1.02, 95% confidence interval [CI] 1.00-1.04; p = 0.018) and mitral E wave deceleration time (coefficient 1.03, 95% CI 1.01-1.05; p = 0.005). Increased EAT was associated with proteomic markers of adipose biology and inflammation, insulin resistance, endothelial dysfunction, and dyslipidaemia but not significantly with CFR. CONCLUSION: Increased EAT was associated with cardiac structural alterations and proteins expressing adiposity, inflammation, lower insulin sensitivity and endothelial dysfunction related to HFpEF pathology, probably driven by general obesity. Potential local mechanical or paracrine effects mediated by EAT remain to be elucidated.
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Venkateshvaran et al. (2022) conducted a cohort in Heart failure with preserved ejection fraction (HFpEF). Epicardial adipose tissue (EAT) was evaluated on Left ventricular septal wall thickness (adjusted for body mass index) (coefficient 1.02, 95% CI 1.00-1.04, p=0.018). Increased epicardial adipose tissue in HFpEF was associated with LV septal wall thickness (coefficient 1.02; 95% CI 1.00-1.04; p=0.018) and proteins expressing adiposity and inflammation.
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