Abstract
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.
Highlights
Owing to excessive adiposity, obesity is an important key clinical risk in the pathophysiology of heart failure with preserved ejection fraction (HFpEF), an emerging HF phenotype worldwide in both Western and Asian populations [1,2]
By using multi-variate linear regression models adjusted for age, sex, body mass, and LV mass in multivariable models, we further examined the mechanistic effects of greater Epicardial adipose tissue (EAT) on a variety of echocardiography-defined cardiac structural and functional measures including Tissue-Doppler imaging (TDI) and myocardial speckle-tracking parameters
Subjects in the second EAT tertile group (7.6–9.0 mm) without phenotypic obesity almost doubled and tripled the risk of having metabolic syndrome (MetS) compared to first EAT tertile despite having a lower body mass index (BMI) (60% vs. 31%) and normal waist circumference (28% vs. 9%), respectively
Summary
Obesity is an important key clinical risk in the pathophysiology of heart failure with preserved ejection fraction (HFpEF), an emerging HF phenotype worldwide in both Western and Asian populations [1,2]. Accumulating data proposed that excessive visceral adiposity, rather than BMI, is a central pathological player mediating metabolic derangements and may serve as a major source of pro-inflammatory cytokines, leading to cardiovascular disorders [3,4,5]. Epicardial adipose tissue (EAT), as visceral adiposity confined within the pericardial sac that tightly regulates myocardial structural and functional homeostasis [6], has recently emerged as an attractive research topic in the pathogenetic mechanisms of HFpEF. Emerging evidence reveals that adipocyte fatty acid-binding protein (A-FABP), a circulating marker enriched in and released from visceral adipose tissue, increases correspondingly with incident MetS [12] and may suppress cardiomyocyte contractility and contribute to HF development [13]. To investigate whether EAT may distribute differently in concert with the degree of cardiometabolic myocardial dysfunction, we aimed to compare EAT across a broad spectrum of cardiovascular disease (CVD) categories comprising healthy and high metabolic risk subjects
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