Epicardial fat in HFmrEF and HFpEF patients

Epicardial fat in heart failure patients with mid-range and preserved ejection fraction

News - Dec. 3, 2018

Introduction and methods

No therapies with proven benefit in reducing morbidity and mortality are available for heart failure with left ventricular ejection fraction (LVEF) >40%, possibly because of heterogeneous presentation of the condition [1]. Many of the patients in this category are obese, and increasing evidence suggests that adipose tissue and the associated inflammation may play a role in the pathophysiology of HF [2,3].

In obese patients, epicardial fat excretes several pro-inflammatory chemokines and cytokines, collectively called adipokines [4]. Epicardial fat volume has been related to several systemic diseases, such as the metabolic syndrome and obesity, which both induce a systemic pro-inflammatory state [5-7]. It is conceivable that epicardial fat has local inflammatory and mechanical effects on the myocardium and the coronary arteries.

This study therefore investigated the extent and location of epicardial fat volume using Cardiac Magnetic Resonance (CMR). Both patients with LVEF 40-50% (HF with mid-range EF, HFmrEF) and with LVEF >50% (HF with preserved EF, HFpEF) were enrolled. Patients enrolled were symptomatic (NYHA class ≥II), had LVEF >40% on echocardiography, and had NT-proBNP >125 ng/L and echocardiographic evidence of LV diastolic dysfunction and/or left ventricular hypertrophy. 64 HF patients with LVEF >40% and 20 controls were enrolled.

Main results

  • While BMI was similar, total and ventricular epicardial fat volume was significantly increased in HF patients, as compared with controls (total fat: 107 mL/m² vs. 77mL/m² and ventricular fat: 80 mL/m² vs. 53mL/m²; all P <0.001).
  • BMI and body surface area were not associated with the amount of epicardial fat volume in HF patients. Nor were other patient characteristics significantly correlated with atrial epicardial fat.
  • In controls, no associations between patient characteristics or CMR parameters and total epicardial fat were noted.
  • HF patients with T2DM and/or atrial fibrillation showed higher epicardial fat volumes than HF patients without these co-morbidities (120 mL/m² vs. 97mL/m², P =0.001; and 116mL/m² vs. 100 mL/m², P =0.03, respectively).
  • Left ventricular end-systolic volume showed a positive association with total epicardial fat (R=0.28, P=0.03) and LVEF showed an inverse association with total epicardial fat (R=-0.27, P=0.03). Global longitudinal and circumferential strain were negatively correlated with total epicardial fat (R=-0.34, P=0.006 and R=-0.32, P=0.009, respectively).
  • The only right ventricular parameter with a significant association with total epicardial fat volume, was right ventricular end-diastolic mass index (R=0.34, P=0.005).
  • Both higher left and right atrial volumes were associated with higher total epicardial fat volume (left and right atrial end-systolic volume index, both R=0.28, P=0.03). Only left atrial end-systolic volume showed a significant association with atrial epicardial fat volume (R=0.26, P=0.04).

Conclusion

These data demonstrate that HF patients with LVEF >40% had more epicardial fat than non-HF controls, even though they had similar BMI. Higher epicardial fat volume was seen in patients with T2DM and in patients with atrial fibrillation. Further research may focus on the potential cause-effect relationship between epicardial fat, co-morbidities and myocardial damage in HF.

References

1. Ponikowski P, Voors AA, Anker SD, et al., 2016 ESC Guidelines for the diagnosis and treatment

of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur J Heart Fail 2016;18:891–975.

2. Obokata M, Reddy YN, Pislaru SV, et al.. Evidence supporting the existence of a distinct obese phenotype of heart failure with preserved ejection fraction. Circulation 2017;136:6–19.

3. Packer M, Kitzman DW. Obesity-related heart failure with a preserved ejection fraction: the mechanistic rationale for combining inhibitors of aldosterone, neprilysin, and sodium-glucose cotransporter-2. JACC Heart Fail 2018;6:633–639.

4. Iacobellis G, Bianco AC. Epicardial adipose tissue: emerging physiological, pathophysiological and clinical features. Trends Endocrinol Metab 2011;22:450–457.

5. Iacobellis G. Epicardial adipose tissue in endocrine and metabolic diseases. Endocrine 2014;46:8–15.

6. Guglielmi V, Sbraccia P. Epicardial adipose tissue: at the heart of the obesity complications. Acta Diabetol 2017;54:805–812.

7. Doesch C, Haghi D, Fluchter S, et al. Epicardial adipose tissue in patients with heart failure. J Cardiovasc Magn Reson 2010;12:40.

Find this article online at Eur J Heart Fail

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