Resting energy expenditure and the effects of muscle wasting in patients with chronic heart failure: results from the Studies Investigating Comorbidities Aggravating Heart Failure (SICA-HF)

Matthias Tacke, Nicole Ebner, Michael Boschmann, Annett Jarius, Miroslava Valentova, Susann Fülster, Anja Sandek, Lutz Schomburg, Stefan D Anker, Wolfram Doehner, Stephan von Haehling
Journal of the American Medical Directors Association 2013, 14 (11): 837-41

OBJECTIVES: Muscle wasting is common in patients with chronic heart failure (HF) and worsens functional status. Protein catabolism is characteristic of muscle wasting and contributes to resting energy expenditure (REE). Glucagonlike peptide 1 (GLP-1) is linked to REE in healthy individuals. We aimed to evaluate (1) whether REE is elevated in patients with HF with muscle wasting, and (2) whether basal GLP-1 levels are linked to REE in HF.

DESIGN: Cross-sectional study.

SETTING: Ambulatory patients with HF were recruited at the Charité Medical School, Campus Virchow-Klinikum, Berlin, Germany.

PARTICIPANTS: A total of 166 patients with HF and 27 healthy controls participating in the Studies Investigating Co-morbidities Aggravating Heart Failure (SICA-HF) were enrolled. GLP-1 was measured in 55 of these patients.

MEASUREMENTS: Body composition was measured by dual-energy X-ray absorptiometry (DEXA). Muscle wasting was defined as appendicular lean mass of at least 2 SDs below values of a healthy young reference group. REE was measured by indirect calorimetry. GLP-1 was assessed by ELISA.

RESULTS: Thirty-four of 166 patients (mean age 67.4 ± 10.2 years, 77.7% male, New York Heart Association class 2.3 ± 0.6) presented with muscle wasting. REE in controls and patients with muscle wasting was significantly lower than in patients without muscle wasting (1579 ± 289 and 1532 ± 265 vs 1748 ± 359 kcal/d, P = .018 and P = .001, respectively). REE normalized for fat-free mass (FFM) using the ratio method (REE/FFM) and analysis of covariance was not different (P = .23 and .71, respectively). GLP-1 did not significantly correlate with REE (P = .49), even not after controlling for FFM using multivariable regression (P = .15).

CONCLUSIONS: Differences in REE are attributable to lower FFM. GLP-1 does not relate to REE in patients with HF, possibly because of HF-related effects on REE.

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