Author + information
- Received March 11, 2020
- Revision received April 15, 2020
- Accepted April 16, 2020
- Published online July 27, 2020.
- Katlyn E. Koepp, BS,
- Masaru Obokata, MD, PhD,
- Yogesh N.V. Reddy, MBBS,
- Thomas P. Olson, PhD and
- Barry A. Borlaug, MD∗ ()
- ↵∗Address for correspondence
: Dr. Barry A. Borlaug, Mayo Clinic and Foundation, 200 First Street SW, Rochester, Minnesota 55905.
Objectives This study determined the impact of excess epicardial adipose tissue (EAT) in patients with the obese phenotype of heart failure with preserved ejection fraction (HFpEF).
Background Patients with HFpEF and an elevated body mass index differ from nonobese patients, but beyond generalized obesity, fat distribution may be more important. Increases in EAT are associated with excess visceral adiposity, inflammation, and cardiac fibrosis, and EAT has been speculated to play an important role in the pathophysiology of HFpEF, but no study has directly evaluated this question.
Methods Patients with HFpEF and obesity (n = 169) underwent invasive hemodynamic exercise testing with expired gas analysis and echocardiography. Increased EAT was defined by echocardiography (EAT thickness ≥9 mm).
Results Compared with obese patients without increased EAT (HFpEFEAT−, n = 92), obese patients with HFpEF with increased EAT (HFpEFEAT+; n = 77) displayed a higher left ventricular eccentricity index, indicating increased pericardial restraint, but similar resting biventricular structure and function. In contrast, hemodynamics were more abnormal in patients with HFpEFEAT+, with higher right atrial, pulmonary artery, and pulmonary capillary wedge pressures at rest and during exercise compared with those of patients with HFpEFEAT−. Peak oxygen consumption (VO2) was reduced in both groups but was 20% lower in patients with HFpEFEAT+ (p < 0.01).
Conclusions Among patients with the obese phenotype of HFpEF, the presence of increased EAT is associated with more profound hemodynamic derangements at rest and exercise, including greater elevation in cardiac filling pressures, more severe pulmonary hypertension, and greater pericardial restraint, culminating in poorer exercise capacity. Further study is needed to understand the biology and treatment of excessive EAT in patients with HFpEF.
Dr. Borlaug is supported by the National Institutes of Health (NIH) (R01 HL128526, R01 HL 126638, U01 HL125205, and U10 HL110262). Ms. Koepp is supported by the NIH (F31 HL143952). The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Heart Failure author instructions page.
- Received March 11, 2020.
- Revision received April 15, 2020.
- Accepted April 16, 2020.
- 2020 American College of Cardiology Foundation
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