Key result
Epicardial adipose tissue measures ~52% thicker in HFpEF and links to new-onset HF via A-FABP.
Why the study?
It was unclear how epicardial adipose tissue associates with A-FABP, a cytokine implicated in cardiometabolic syndrome, and whether A-FABP mediates links between EAT and cardiac structure, function, and HFpEF outcomes.
Does epicardial adipose tissue thickness correlate with metabolic abnormalities, A-FABP levels, and heart failure with preserved ejection fraction?
Cohort (n=252)
Does epicardial adipose tissue thickness correlate with metabolic abnormalities, A-FABP levels, and heart failure with preserved ejection fraction?
Answers are grounded in this paper and cite their sources.
Excessive epicardial adipose tissue is associated with metabolic syndrome, renal insufficiency, and HFpEF, with A-FABP mediating the link between EAT and new-onset heart failure.
Epicardial adipose tissue (EAT) as a source of pro-inflammatory cytokines tightly linked to metabolic abnormalities. Data regarding the associations of EAT with adipocyte fatty acid-binding protein (A-FABP), a cytokine implicated in the cardiometabolic syndrome, might play an important part in mediating the association between EAT and cardiac structure/function in preserved ejection fraction heart failure (HFpEF). We conducted a prospective cohort study comprising 252 prospectively enrolled study participants classified as healthy (n = 40), high-risk (n = 161), or HFpEF (n = 51). EAT was assessed using echocardiography and compared between the three groups and related to A-FABP, cardiac structural/functional assessment utilizing myocardial deformations (strain/strain rates) and HF outcomes. EAT thickness was highest in participants with HFpEF (9.7 ± 1.7 mm) and those at high-risk (8.2 ± 1.5 mm) and lowest in healthy controls (6.4 ± 1.9 mm, p < 0.001). Higher EAT correlated with the presence of cardiometabolic syndrome, diabetes and renal insufficiency independent of BMI and waist circumference (pinteraction for all > 0.1), and was associated with reduced LV global longitudinal strain (GLS) and LV mass-independent systolic/diastolic strain rates (SRs/SRe) (all p < 0.05). Higher A-FABP levels were associated with greater EAT thickness (pinteraction > 0.1). Importantly, in the combined control cohort, A-FABP levels mediated the association between EAT and new onset HF. Excessive EAT is independently associated with the metabolic syndrome, renal insufficiency, and higher A-FABP levels. The association between EAT and new onset HF is mediated by A-FABP, suggesting a metabolic link between EAT and HF.
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Lin et al. (2021) conducted a cohort in Preserved ejection fraction heart failure (HFpEF) (n=252). Epicardial adipose tissue (EAT) thickness vs. Healthy controls was evaluated on EAT thickness (p=<0.001). Epicardial adipose tissue thickness was highest in HFpEF (9.7 mm) and high-risk patients (8.2 mm) versus healthy controls (6.4 mm, p<0.001), with A-FABP mediating its link to new onset HF.
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