Exercise training and high‐sensitivity cardiac troponin‐I in patients with heart failure with reduced ejection fraction

• Published in: ESC Heart Failure 2024-04, Vol.11 (2), p.1121-1132
• Main Authors: Riveland, Egil, Valborgland, Torstein, Ushakova, Anastasia, Skadberg, Øyvind, Karlsen, Trine, Hole, Torstein, Støylen, Asbjørn, Dalen, Håvard, Videm, Vibeke, Koppen, Elias, Linke, Axel, Delagardelle, Charles, Van Craenenbroeck, Emeline M., Beckers, Paul, Prescott, Eva, Halle, Martin, Omland, Torbjørn, Ellingsen, Øyvind, Larsen, Alf Inge
• Format: Article
• Language: English
• Subjects: Biomarkers; Cardiac arrhythmia; Cardiac rehabilitation; Chronic heart failure; Ejection fraction; Exercise; Fitness equipment; Fitness training programs; Heart failure; HFrEF; Hypertension; Intervention; Ischemia; Original; Peptides; Physical fitness; Troponin I
• ISSN: 2055-5822; 2055-5822
• DOI: 10.1002/ehf2.14674

Aims The aims of this sub‐study of the SMARTEX trial were (1) to evaluate the effects of a 12‐week exercise training programme on serum levels of high sensitivity cardiac troponin I (hs‐cTnI) in patients with moderate chronic heart failure (CHF), in New York Heart Association class II‐III with reduced ejection fraction (HFrEF) and (2) to explore the associations with left ventricular remodelling, functional capacity and filling pressures measured with N‐terminal pro brain natriuretic peptide (NT‐proBNP). Methods and results In this sub‐study, 196 patients were randomly assigned to high intensity interval training (HIIT, n = 70), moderate continuous training (MCT, n = 59) or recommendation of regular exercise (RRE), (n = 67) for 12 weeks. To reveal potential difference between structured intervention and control, HIIT and MCT groups were merged and named supervised exercise training (SET) group. The RRE group constituted the control group (CG). To avoid contributing factors to myocardial injury, we also evaluated changes in patients without additional co‐morbidities (atrial fibrillation, hypertension, diabetes mellitus, and chronic obstructive pulmonary disease). The relationship between hs‐cTnI and left ventricular end‐diastolic diameter (LVEDD), VO2peak, and NT‐proBNP was analysed by linear mixed models. At 12 weeks, Hs‐cTnI levels were modestly but significantly reduced in the SET group from median 11.9 ng/L (interquartile ratio, IQR 7.1–21.8) to 11.5 ng/L (IQR 7.0–20.7), P = 0.030. There was no between‐group difference (SET vs. CG, P = 0.116). There was a numerical but not significant reduction in hs‐cTnI for the whole population (P = 0.067) after 12 weeks. For the sub‐group of patients without additional co‐morbidities, there was a significant between‐group difference: SET group (delta −1.2 ng/L, IQR −2.7 to 0.1) versus CG (delta −0.1 ng/L, IQR −0.4 to 0.7), P = 0.007. In the SET group, hs‐cTnI changed from 10.9 ng/L (IQR 6.0–22.7) to 9.2 ng/L (IQR 5.2–20.5) (P = 0.002), whereas there was no change in the CG (6.4 to 5.8 ng/L, P = 0.64). Changes in hs‐cTnI (all patients) were significantly associated with changes in; LVEDD, VO2peak, and NT‐proBNP, respectively. Conclusions In patients with stable HFrEF, 12 weeks of structured exercise intervention was associated with a modest, but significant reduction of hs‐cTnI. There was no significant difference between intervention group and control group. In the sub‐group of patients without additional co‐morbidit