Altered Levels of Fatty Acids and Inflammatory and Metabolic Mediators in Epicardial Adipose Tissue in Patients With Systolic Heart Failure

Linn E Fosshaug; Christen P Dahl; Ivar Risnes; Pavol Bohov; Rolf K Berge; Ståle Nymo; Odd Geiran; Arne Yndestad; Lars Gullestad; Pål Aukrust; Leif E Vinge; Erik Øie

doi:10.1016/j.cardfail.2015.07.014

Altered Levels of Fatty Acids and Inflammatory and Metabolic Mediators in Epicardial Adipose Tissue in Patients With Systolic Heart Failure

J Card Fail. 2015 Nov;21(11):916-23. doi: 10.1016/j.cardfail.2015.07.014. Epub 2015 Jul 29.

Authors

Linn E Fosshaug¹, Christen P Dahl², Ivar Risnes³, Pavol Bohov⁴, Rolf K Berge⁵, Ståle Nymo⁶, Odd Geiran⁷, Arne Yndestad⁸, Lars Gullestad⁹, Pål Aukrust¹⁰, Leif E Vinge¹¹, Erik Øie¹¹

Affiliations

¹ Department of Internal Medicine, Diakonhjemmet Hospital, Oslo, Norway; Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Center for Heart Failure Research, University of Oslo, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway. Electronic address: l.e.lillerud@medisin.uio.no.
² Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Center for Heart Failure Research, University of Oslo, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway; Department of Cardiology, Oslo University Hospital Rikshospitalet, Oslo, Norway; K. G. Jebsen Inflammatory Research Center, University of Oslo, Oslo, Norway.
³ Department of Thoracic and Cardiovascular Surgery, Oslo University Hospital Rikshospitalet, Oslo, Norway.
⁴ Department of Clinical Science, University of Bergen, Bergen, Norway.
⁵ Department of Clinical Science, University of Bergen, Bergen, Norway; Department of Heart Disease, Haukeland University Hospital, Bergen, Norway.
⁶ Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Center for Heart Failure Research, University of Oslo, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway.
⁷ K. G. Jebsen Inflammatory Research Center, University of Oslo, Oslo, Norway; Department of Thoracic and Cardiovascular Surgery, Oslo University Hospital Rikshospitalet, Oslo, Norway.
⁸ Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Center for Heart Failure Research, University of Oslo, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway; K. G. Jebsen Inflammatory Research Center, University of Oslo, Oslo, Norway.
⁹ Center for Heart Failure Research, University of Oslo, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway; Department of Cardiology, Oslo University Hospital Rikshospitalet, Oslo, Norway.
¹⁰ Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway; K. G. Jebsen Inflammatory Research Center, University of Oslo, Oslo, Norway; Section of Clinical Immunology and Infectious Diseases, Oslo University Hospital Rikshospitalet, Oslo, Norway.
¹¹ Department of Internal Medicine, Diakonhjemmet Hospital, Oslo, Norway; Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Center for Heart Failure Research, University of Oslo, Oslo, Norway; Department of Cardiology, Oslo University Hospital Rikshospitalet, Oslo, Norway.

PMID: 26231517
DOI: 10.1016/j.cardfail.2015.07.014

Abstract

Background: Adipose tissue has endocrine properties, secreting a wide range of mediators into the circulation, including factors involved in cardiovascular disease. However, little is known about the potential role of adipose tissue in heart failure (HF), and the aim of this study was to investigate epicardial (EAT) and subcutaneous (SAT) adipose tissue in HF patients.

Methods and results: Thirty patients with systolic HF and 30 patients with normal systolic function undergoing thoracic surgery were included in the study. Plasma was sampled and examined with the use of enzyme-linked immunosorbent assays, whereas SAT and EAT biopsies were collected and examined by means of reverse-transcription polymerase chain reaction and gas chromatography. Significantly higher expressions of mRNA encoding interleukin-6, adrenomedullin, peroxisome proliferator-activated receptor α, and fatty acid (FA)-binding protein 3, as well as higher levels of monounsaturated FA and palmitoleic acid, were seen in the EAT of HF patients, whereas the levels of docosahexaenoic acid were lower. Palmitoleic acid levels in EAT were correlated with 2 parameters of cardiac remodeling: increasing left ventricular end-diastolic diameter and N-terminal pro-B-type natriuretic peptide.

Conclusions: Our results demonstrate adipose tissue depot-specific alterations of synthesis of FA and inflammatory and metabolic mediators in systolic HF patients. EAT may be a source of increased circulatory and myocardial levels of these mediators through endocrine actions.

Keywords: Heart failure; adipose tissue; fatty acids; palmitoleic acid.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Adipose Tissue / metabolism
Adult
Aged
Biomarkers / analysis
C-Reactive Protein / metabolism*
Cardiac Surgical Procedures / methods
Case-Control Studies
Chi-Square Distribution
Elective Surgical Procedures
Enzyme-Linked Immunosorbent Assay
Fatty Acids / metabolism*
Female
Heart Failure, Systolic / diagnostic imaging
Heart Failure, Systolic / metabolism*
Heart Failure, Systolic / surgery
Humans
Linear Models
Male
Middle Aged
Natriuretic Peptide, Brain / blood*
Peptide Fragments / blood*
Pericardium / metabolism
RNA, Messenger / analysis
Real-Time Polymerase Chain Reaction / methods
Statistics, Nonparametric
Subcutaneous Fat / metabolism
Ultrasonography

Substances

Biomarkers
Fatty Acids
Peptide Fragments
RNA, Messenger
pro-brain natriuretic peptide (1-76)
Natriuretic Peptide, Brain
C-Reactive Protein