Pneumologie 2020; 74(S 01): 123-124
DOI: 10.1055/s-0039-3403345
Freie Vorträge (FV13) – Sektion Kardiorespiratorische Interaktion
Freie Vorträge der Sektion Kardiorespiratorische Interaktion
Georg Thieme Verlag KG Stuttgart · New York

Inspiratory muscle dysfunction with restrictive lung disease in heart failure: association with exercise intolerance and relation to IL-6 and TNF-alpha

J Spießhöfer
1   Respiratory Physiology Laboratory, Department of Neurology with Institute for Translational Neurology, University Hospital Muenster, Germany
,
HJ Kabitz
2   Medizinische Klinik II, Department of Pneumology, Cardiology and Intensive Care Medicine, Klinikum Konstanz, Germany
,
I Tuleta
3   Department of Cardiology I, University Hospital Muenster, Germany
,
E Fröb
3   Department of Cardiology I, University Hospital Muenster, Germany
,
M Boentert
4   Department für Neurologie, Klinik für Schlafmedizin und Neuromuskuläre Erkrankungen, Universitätsklinikum Münster
› Author Affiliations
Further Information

Publication History

Publication Date:
28 February 2020 (online)

 

Background: In patients with heart failure with reduced (HFrEF) and with preserved (HFpEF) ejection fraction the characteristics of respiratory muscle dysfunction and its association with clinical symptoms and circulating pro-inflammatory cytokines are incompletely understood. Therefore, the present study used a multimodal approach to evaluate the characteristics of inspiratory and expiratory muscle dysfunction in HFrEF and HFpEF while exploring its association with exercise intolerance and circulating pro-inflammatory cytokines.

Methods: 22 HFrEF (19 men and 3 women, 61 ± 14 years) and 8 HFpEF (7 men and 1 woman, 68 ± 8 years) patients as well as healthy controls matched for age, gender and body mass index underwent spiro-manometry, diaphragm ultrasound, and recording of transdiaphragmatic and gastric pressures (twPdi and twPgas) following magnetic stimulation of the phrenic nerves (inspiratory muscle strength) and the lower thoracic nerve roots (expiratory muscle strength), respectively. 6 minute walking distance (6 MWD) test and NYHA class were used to quantify exercise intolerance. Levels of circulating IL-6 and TNF α were measured using enzyme-linked immunosorbent assays.

Results: Both HFrEF and HFpEF patients showed the following respiratory abnormalities compared to controls: forced vital capacity (FVC), maximum inspiratory (PIMax) and expiratory (PEMax) pressures were reduced; diaphragm thickening ratio (HFrEF 2.0 ± 0.5 vs. 2.8 ± 0.8, p < 0.01 and HFpEF 1.8 [1.4 – 2.0] vs.3.1 [2.1 – 3.3], p = 0.01) and diaphragm strength were reduced (twPdi: HrEF 11.8 ± 7.4 vs. 18.7 ± 6.3 cmH2O, p = 0.05 and HFpEF 9.8 ± 3.4 vs. 23.8 ± 4.4 cmH2O, p = 0.01.). In HFrEF patients NYHA class showed a moderate-strong inverse correlation with FVC (r = − 0.60, p < 0.01), PImax (r = − 0.61, p = 0.03) and PEmax (r = − 0.56, p < 0.01). In HFpEF patients NT-proBNP levels correlated inversely with FVC (r = − 0.77, p = 0.04). In HFrEF and HFpEF, reduced FVC was systematically associated with higher levels of IL-6 and TNF α.

Conclusions: We conclude that in HF there is relevant inspiratory muscle dysfunction with restrictive lung disease independently from left ventricular ejection fraction.

In HFrEF the extents of restrictive lung disease is associated with exercise intolerance and is linked to increased levels of circulating IL-6 and TNF α.