Open AccessFibroblast growth factor 21 in patients with cardiac cachexia: a possible role of chronic inflammation
Author(s) -
Refsgaard Holm Maria,
Christensen Heidi,
Rasmussen Jon,
Johansen Marie Louise,
Schou Morten,
Faber Jens,
Kistorp Caroline
Publication year - 2019
Publication title -
esc heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.787
H-Index - 25
ISSN - 2055-5822
DOI - 10.1002/ehf2.12502
Subject(s) - medicine , ejection fraction , wasting , cachexia , heart failure , inflammation , fgf21 , cardiac function curve , systemic inflammation , endocrinology , cardiology , gastroenterology , fibroblast growth factor , cancer , receptor
Abstract Aims Cardiac cachexia is a wasting syndrome characterized by chronic inflammation and high mortality. Fibroblast growth factor 21 (FGF‐21) and monocyte chemoattractant protein 1 (MCP‐1) are associated with cardiovascular disease and systemic inflammation. We investigated FGF‐21 and MCP‐1 in relations to cardiac function, inflammation, and wasting in patients with heart failure with reduced ejection fraction (HFrEF) and cardiac cachexia. Methods and results Plasma FGF‐21 and MCP‐1 were measured in a cross‐sectional study among the three study groups: 19 patients with HFrEF with cardiac cachexia, 19 patients with HFrEF without cachexia, and 19 patients with ischaemic heart disease and preserved ejection fraction. Patients with HFrEF and cardiac cachexia displayed higher FGF‐21 levels median (inter quantile range) 381 (232–577) pg/mL than patients with HFrEF without cachexia 224 (179–309) pg/mL and ischaemic heart disease patients 221 (156–308) pg/mL ( P = 0.0496). No difference in MCP‐1 levels were found among the groups ( P = 0.345). In a multivariable regression analysis, FGF‐21 (logarithm 2) was independently associated with interleukin 6 (logarithm 2) ( P = 0.015) and lower muscle mass ( P = 0.043), while no relation with N‐terminal pro‐hormone brain natriuretic peptide was observed. Conclusions Fibroblast growth factor 21 (FGF‐21) levels were elevated in patients with HFrEF and cardiac cachexia, which could be mediated by increased inflammation and muscle wasting rather than impaired cardiac function.