Exercise training and high-sensitivity cardiac troponin T in patients with heart failure with reduced ejection fraction

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  • Elias Koppen
  • Torbjørn Omland
  • Alf Inge Larsen
  • Trine Karlsen
  • Axel Linke
  • Prescott, Eva
  • Martin Halle
  • Håvard Dalen
  • Charles Delagardelle
  • Torstein Hole
  • Emeline M. van Craenenbroeck
  • Paul Beckers
  • Øyvind Ellingsen
  • Patrick Feiereisen
  • Torstein Valborgland
  • Vibeke Videm
  • SMARTEX-HF Study Group

Aims: Whether an exercise training intervention is associated with reduction in long-term high-sensitivity cardiac troponin T (hs-cTnT) concentration (a biomarker of subclinical myocardial injury) in patients with heart failure with reduced ejection fraction (HFrEF) is unknown. The aims were to determine (i) the effect of a 12 week endurance exercise training intervention with different training intensities on hs-cTnT in stable patients with HFrEF (left ventricular ejection fraction ≤ 35%) and (ii) associations between hs-cTnT and peak oxygen uptake (VO2peak). Methods and results: In this sub-study of the SMARTEX-HF trial originally including 261 patients from nine European centres, 213 eligible patients were included after withdrawals and appropriate exclusions [19% women, mean age 61.2 years (standard deviation: 11.9)], randomized to high-intensity interval training (HIIT; n = 77), moderate continuous training (MCT; n = 63), or a recommendation of regular exercise (RRE; n = 73). Hs-cTnT measurements and clinical data acquired before (BL) and after a 12 week exercise training intervention (12 weeks) and at 1 year follow-up (1 year) were analysed using multivariable mixed models. Baseline hs-cTnT was above the 99th percentile upper reference limit of 14 ng/L in 35 (48%), 35 (56%), and 49 (64%) patients in the RRE, MCT, and HIIT groups, respectively. Median hs-cTnT was 16 ng/L at BL, 14 ng/L at 12 weeks, and 14 ng/L at 1 year. Hs-cTnT was statistically significantly reduced at 12 weeks in a model adjusted for randomization group, centre and VO2peak, and after further adjustment in the final model that also included age, sex, creatinine concentrations, N-terminal pro-brain natriuretic peptide, smoking, and heart failure treatment. The mean reduction from BL to 12 weeks in the final model was 1.1 ng/L (95% confidence interval: 1.0–1.2 ng/L, P < 0.001), and the reduction was maintained at 1 year with a mean reduction from BL to 1 year of 1.1 ng/L (95% confidence interval: 1.0–1.1 ng/L, P = 0.025). Randomization group was not associated with hs-cTnT at any time point (overall test: P = 0.20, MCT vs. RRE: P = 0.81, HIIT vs. RRE: P = 0.095, interaction time × randomization group: P = 0.88). Independent of time point, higher VO2peak correlated with lower hs-cTnT (mean reduction over all time points: 0.2 ng/L per increasing mL·kg−1·min−1, P = 0.002), without between-group differences (P = 0.19). Conclusions: In patients with stable HFrEF, a 12 week exercise intervention was associated with reduced hs-cTnT in all groups when adjusted for clinical variables. Higher VO2peak correlated with lower hs-cTnT, suggesting a positive long-term effect of increasing VO2peak on subclinical myocardial injury in HFrEF, independent of training programme.

OriginalsprogEngelsk
TidsskriftESC heart failure
Vol/bind8
Udgave nummer3
Sider (fra-til)2183-2192
Antal sider10
ISSN2055-5822
DOI
StatusUdgivet - 2021

Bibliografisk note

Funding Information:
Dr Ellingsen reports grants from St. Olavs University Hospital, grants from NTNU ‐ Norwegian University of Science and Technology, grants from Norwegian Health Association, and grants from Simon Fougner Hartmanns Familiefond during the conduct of the study; Dr Omland reports personal fees and non‐financial support from Roche Diagnostics, personal fees and non‐financial support from Abbott Diagnostics, personal fees from Siemens, non‐financial support from SomaLogic, non‐financial support from Novartis, and personal fees from CardiNor outside the submitted work; Dr Halle reports grants from Novartis and Roche outside the submitted work; Dr Valborgland reports grants from Western Norway Regional Health Authority during the conduct of the study; Dr Linke reports grants from Novartis, personal fees from Medtronic, Abbott, Edwards Lifesciences, Boston Scientific, Astra Zeneca, Novartis, Pfizer, Abiomed, Bayer, Boehringer, and other from Picardia, Transverse Medical, and Claret Medical, and grants from Edwards Lifesciences outside the submitted work.

Funding Information:
This work was supported by St. Olavs University Hospital; Faculty of Medicine and Health Sciences, NTNU – Norwegian University of Science and Technology; Norwegian Health Association; Danish Research Council; Central Norwegian Health Authorities; Western Norway Health Authorities; Simen Fougner Hartmanns Familiefond; Else Kröner‐Fresenius‐Stiftung; and Société Luxembourgeoise pour la recherche sur les maladies cardio‐vasculaires.

Funding Information:
This work was supported by St. Olavs University Hospital; Faculty of Medicine and Health Sciences, NTNU ? Norwegian University of Science and Technology; Norwegian Health Association; Danish Research Council; Central Norwegian Health Authorities; Western Norway Health Authorities; Simen Fougner Hartmanns Familiefond; Else Kr?ner-Fresenius-Stiftung; and Soci?t? Luxembourgeoise pour la recherche sur les maladies cardio-vasculaires. Contributors to the main SMARTEX-HF study are given in Ellingsen (2017).13 For the present study, Heidi Strand performed the hs-cTnT analyses.

Publisher Copyright:
© 2021 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.

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