Heart Failure Results in Inspiratory Muscle Dysfunction Irrespective of Left Ventricular Ejection Fraction.


Journal

Respiration; international review of thoracic diseases
ISSN: 1423-0356
Titre abrégé: Respiration
Pays: Switzerland
ID NLM: 0137356

Informations de publication

Date de publication:
Historique:
received: 10 03 2020
accepted: 04 07 2020
pubmed: 11 11 2020
medline: 11 11 2021
entrez: 10 11 2020
Statut: ppublish

Résumé

Exercise intolerance in heart failure with reduced ejection fraction (HFrEF) or heart failure with preserved ejection fraction (HFpEF) results from both cardiac dysfunction and skeletal muscle weakness. Respiratory muscle dysfunction with restrictive ventilation disorder may be present irrespective of left ventricular ejection fraction and might be mediated by circulating pro-inflammatory cytokines. To determine lung and respiratory muscle function in patients with HFrEF/HFpEF and to determine its associations with exercise intolerance and markers of systemic inflammation. Adult patients with HFrEF (n = 22, 19 male, 61 ± 14 years) and HFpEF (n = 8, 7 male, 68 ± 8 years) and 19 matched healthy control subjects underwent spirometry, measurement of maximum mouth occlusion pressures, diaphragm ultrasound, and recording of transdiaphragmatic and gastric pressures following magnetic stimulation of the phrenic nerves and the lower thoracic nerve roots. New York Heart Association (NYHA) class and 6-min walking distance (6MWD) were used to quantify exercise intolerance. Levels of circulating interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured using ELISAs. Compared with controls, both patient groups showed lower forced vital capacity (FVC) (p < 0.05), maximum inspiratory pressure (PImax), maximum expiratory pressure (PEmax) (p < 0.05), diaphragm thickening ratio (p = 0.01), and diaphragm strength (twitch transdiaphragmatic pressure in response to supramaximal cervical magnetic phrenic nerve stimulation) (p = 0.01). In patients with HFrEF, NYHA class and 6MWD were both inversely correlated with FVC, PImax, and PEmax. In those with HFpEF, there was an inverse correlation between amino terminal pro B-type natriuretic peptide levels and FVC (r = -0.77, p = 0.04). In all HF patients, IL-6 and TNF-α were statistically related to FVC. Irrespective of left ventricular ejection fraction, HF is associated with respiratory muscle dysfunction, which is associated with increased levels of circulating IL-6 and TNF-α.

Sections du résumé

BACKGROUND BACKGROUND
Exercise intolerance in heart failure with reduced ejection fraction (HFrEF) or heart failure with preserved ejection fraction (HFpEF) results from both cardiac dysfunction and skeletal muscle weakness. Respiratory muscle dysfunction with restrictive ventilation disorder may be present irrespective of left ventricular ejection fraction and might be mediated by circulating pro-inflammatory cytokines.
OBJECTIVE OBJECTIVE
To determine lung and respiratory muscle function in patients with HFrEF/HFpEF and to determine its associations with exercise intolerance and markers of systemic inflammation.
METHODS METHODS
Adult patients with HFrEF (n = 22, 19 male, 61 ± 14 years) and HFpEF (n = 8, 7 male, 68 ± 8 years) and 19 matched healthy control subjects underwent spirometry, measurement of maximum mouth occlusion pressures, diaphragm ultrasound, and recording of transdiaphragmatic and gastric pressures following magnetic stimulation of the phrenic nerves and the lower thoracic nerve roots. New York Heart Association (NYHA) class and 6-min walking distance (6MWD) were used to quantify exercise intolerance. Levels of circulating interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured using ELISAs.
RESULTS RESULTS
Compared with controls, both patient groups showed lower forced vital capacity (FVC) (p < 0.05), maximum inspiratory pressure (PImax), maximum expiratory pressure (PEmax) (p < 0.05), diaphragm thickening ratio (p = 0.01), and diaphragm strength (twitch transdiaphragmatic pressure in response to supramaximal cervical magnetic phrenic nerve stimulation) (p = 0.01). In patients with HFrEF, NYHA class and 6MWD were both inversely correlated with FVC, PImax, and PEmax. In those with HFpEF, there was an inverse correlation between amino terminal pro B-type natriuretic peptide levels and FVC (r = -0.77, p = 0.04). In all HF patients, IL-6 and TNF-α were statistically related to FVC.
CONCLUSIONS CONCLUSIONS
Irrespective of left ventricular ejection fraction, HF is associated with respiratory muscle dysfunction, which is associated with increased levels of circulating IL-6 and TNF-α.

Identifiants

pubmed: 33171473
pii: 000509940
doi: 10.1159/000509940
doi:

Substances chimiques

Interleukin-6 0
Tumor Necrosis Factor-alpha 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

96-108

Informations de copyright

© 2020 S. Karger AG, Basel.

Auteurs

Jens Spiesshoefer (J)

Institute of Life Sciences, Scuola Superiore Sant'Anna, Pisa, Italy, jspiesshoefe@ukaachen.de.
Department of Pneumology and Intensive Care Medicine, University Hospital RWTH Aachen, Aachen, Germany, jspiesshoefe@ukaachen.de.
Department of Neurology with Institute for Translational Neurology, University of Muenster, Muenster, Germany, jspiesshoefe@ukaachen.de.

Carolin Henke (C)

Department of Neurology, Herz-Jesu-Krankenhaus Hiltrup, Muenster, Germany.

Hans Joachim Kabitz (HJ)

Department of Pneumology, Cardiology and Intensive Care Medicine, Klinikum Konstanz, Konstanz, Germany.

Philipp Bengel (P)

Clinic for Cardiology and Pneumology/Heart Center, University Medical Center Goettingen, DZHK (German Centre for Cardiovascular Research), Goettingen, Germany.

Katharina Schütt (K)

Department of Internal Medicine I, University Hospital Aachen, RWTH Aachen University, Aachen, Germany.

Jerzy-Roch Nofer (JR)

Center for Laboratory Medicine, University Hospital Muenster, University of Muenster, Muenster, Germany and Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Maximilian Spieker (M)

Division of Cardiology, Pulmonology and Vascular Medicine, University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.

Stefan Orwat (S)

Department of Cardiology III, University Hospital Muenster, Muenster, Germany.

Gerhard Paul Diller (GP)

Department of Cardiology III, University Hospital Muenster, Muenster, Germany.

Jan Kolia Strecker (JK)

Department of Neurology with Institute for Translational Neurology, University of Muenster, Muenster, Germany.

Alberto Giannoni (A)

Institute of Life Sciences, Scuola Superiore Sant'Anna, Pisa, Italy.

Michael Dreher (M)

Department of Pneumology and Intensive Care Medicine, University Hospital RWTH Aachen, Aachen, Germany.

Winfried Johannes Randerath (WJ)

Institute for Pneumology at the University of Cologne, Solingen, Germany.
Bethanien Hospital gGmbH Solingen, Solingen, Germany.

Matthias Boentert (M)

Department of Neurology with Institute for Translational Neurology, University of Muenster, Muenster, Germany.
Department of Medicine, UKM Marienhospital Steinfurt, Steinfurt, Germany.

Izabela Tuleta (I)

Department of Cardiology I, University Hospital Muenster, Muenster, Germany.

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