Diverging role of epicardial adipose tissue across the entire heart failure spectrum

Author:

Rossi Valentina A.12ORCID,Nebunu Delia1,Haider Thomas1,Laptseva Natallia12,Naegele Matthias P.1,Ruschitzka Frank123,Sudano Isabella12,Flammer Andreas J.123ORCID

Affiliation:

1. Department of Cardiology University Heart Centre, University Hospital of Zurich Raemistrasse 100 Zurich 8091 Switzerland

2. Centre for Translational and Experimental Cardiology Schlieren Switzerland

3. University of Zurich Zurich Switzerland

Abstract

AbstractAimsEpicardial adipose tissue (EAT) is a metabolically highly active tissue modulating numerous pathophysiological processes. The aim of this study was to investigate the association between EAT thickness and endothelial function in patients with heart failure (HF) across the entire ejection fraction spectrum.Methods and resultsA total of 258 patients with HF with an ejection fraction across the entire spectrum [HF with reduced ejection fraction (HFrEF), n = 168, age 60.6 ± 11.2 years; HF with preserved ejection fraction (HFpEF), n = 50, mean age 65.1 ± 11.9 years; HF with mildly reduced ejection fraction (HFmrEF), n = 32, mean age 65 ± 12] were included. EAT was measured with transthoracic echocardiography. Vascular function was assessed with flicker‐light‐induced vasodilation of retinal arterioles (FIDart%) and flow‐mediated dilatation (FMD%) in conduit arteries. Patients with HFrEF have less EAT compared with patients with HFpEF (4.2 ± 2 vs. 5.3 ± 2 mm, respectively, P < 0.001). Interestingly, EAT was significantly associated with impaired microvascular function (FIDart%; r = −0.213, P = 0.012) and FMD% (r = −0.186, P = 0.022), even after multivariate correction for confounding factors (age, body mass index, hypertension, and diabetes; standardized regression coefficient (SRC) = −0.184, P = 0.049 for FIDart% and SRC = −0.178, P = 0.043 for FMD%) in HFrEF but not in HFpEF.ConclusionsAlthough less EAT is present in HFrEF than in HFpEF, only in HFrEF EAT is associated with vascular dysfunction. The diverging role of EAT in HF and its switch to a functionally deleterious tissue promoting HF progression provide the rationale to specifically target EAT, in particular in patients with reduced ejection fraction.

Publisher

Wiley

Subject

Cardiology and Cardiovascular Medicine

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