Epicardial Adipose Tissue and Outcome in Heart Failure With Mid-Range and Preserved Ejection Fraction

Abstract

Background: Epicardial adipose tissue (EAT) accumulation is thought to play a role in the pathophysiology of heart failure (HF) with mid-range and preserved ejection fraction, but its effect on outcome is unknown. We evaluated the prognostic value of EAT volume measured with cardiac magnetic resonance in patients with HF with mid-range ejection fraction and HF with preserved ejection fraction. Methods: Patients enrolled in a prospective multicenter study that investigated the value of implantable loop-recorders in HF with mid-range ejection fraction and HF with preserved ejection fraction were analyzed. EAT volume was quantified with cardiac magnetic resonance. Main outcome was the composite of all-cause mortality and first HF hospitalizations. Hazard ratios (HR) and 95% CI are described per SD increase in EAT. Results: We studied 105 patients (mean age 72±8 years, 50% women, and mean left ventricular ejection fraction 53±8%). During median follow-up of 24 (17–25) months, 31 patients (30%) died or were hospitalized for HF. In univariable analysis, EAT was significantly associated with a higher risk of the composite outcome (HR, 1.76 [95% CI, 1.24–2.50], P =0.001), and EAT remained associated with outcome after adjustment for age, sex, and body mass index (HR, 1.61 [95% CI, 1.13–2.31], P =0.009), and after adjustment for New York Heart Association functional class and N-terminal of pro-brain natriuretic peptide (HR, 1.53 [95% CI, 1.04–2.24], P =0.03). Furthermore, EAT was associated with all-cause mortality alone (HR, 2.06 [95% CI, 1.26–3.37], P =0.004) and HF hospitalizations alone (HR, 1.54 [95% CI, 1.04–2.30], P =0.03). Conclusions: EAT accumulation is associated with adverse prognosis in patients with HF with mid-range ejection fraction and HF with preserved ejection fraction. This finding supports the importance of EAT in these patients with HF. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01989299.

Connecting epicardial adipose tissue and heart failure with preserved ejection fraction: mechanisms, management and modern perspectives

“…However, some longitudinal studies have shown that higher EAT at baseline is associated with new‐onset HFpEF, 6,30 as well as a worse prognosis in those with established HFpEF, 7 independent of overall obesity and important comorbidities. An overview of the recent studies that investigated EAT in relation to HFpEF is shown in Table 1 6,7,23,25–27,30–41 . Of note, one study by Haykowsky et al 32 .…”

Diabesity in Elderly Cardiovascular Disease Patients: Mechanisms and Regulators

“…Epicardial fat accumulation is a risk of HF with mildly reduced ejection fraction (HFmrEF) and HF preserved ejection fraction (HFpEF). In these patients, a high epicardial fat volume is also a predictor of death and/or hospitalization for HF [ 147 ]. Greater total EATs in HFpEF is associated with myocardial fibrosis markers but not in HFrEF [ 148 ].…”

Underestimation of congestion in very obese heart failure with preserved ejection fraction patients: EAT your heart out…?!

“…Unfortunately, the current study by Obokata et al did not include cardiac MRI scanning to further bolster their findings. Recent cardiac MRI studies in patients with HFpEF have already demonstrated that the site of EAT accumulation is associated with structural changes that induce haemodynamic and electrical changes, 11 and that in these patients higher EAT volume is associated with worse outcomes, including all‐cause mortality and HF hospitalizations 12 …”

“…Recent cardiac MRI studies in patients with HFpEF have already demonstrated that the site of EAT accumulation is associated with structural changes that induce haemodynamic and electrical changes, 11 and that in these patients higher EAT volume is associated with worse outcomes, including all-cause mortality and HF hospitalizations. 12 We therefore hypothesize that, apart from local proinflammatory and pro-fibrotic changes due to increased EAT volumes, build-up of EAT itself may also act as an important disease modifier that increasing volumes of EAT may form a dense . and compact layer around the myocardium that prevents the heart from passive filling, resulting in higher intracardiac pressures and lower natriuretic peptide levels due to limited left ventricular (and right ventricular) stretch, and thus uncoupling of intracavitary and intravascular pressures.…”