Abstract
Purpose of Review: Cardiac myosin inhibitors (CMIs) and activators are emerging therapies for hypertrophic cardiomyopathy (HCM) and heart failure with reduced ejection fraction (HFrEF), respectively. However, their effects on cardiac troponin levels, a biomarker of myocardial injury, are incompletely understood. Recent Findings: In patients with HCM, CMIs cause substantial reductions in cardiac troponin levels which are reversible after stopping treatment. In patients with HFrEF, cardiac myosin activator (omecamtiv mecarbil) therapy cause modest increases in cardiac troponin levels which are reversible following treatment cessation and not associated with myocardial ischaemia or infarction. Summary: Transient changes in cardiac troponin levels might reflect alterations in cardiac contractility and mechanical stress. Such transient changes might not indicate cardiac injury and do not appear to be associated with adverse outcomes in the short to intermediate term. Longitudinal changes in troponin levels vary depending on the population and treatment. Further research is needed to elucidate mechanisms underlying changes in troponin levels.
Original language | English (US) |
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Pages (from-to) | 504-518 |
Number of pages | 15 |
Journal | Current heart failure reports |
Volume | 20 |
Issue number | 6 |
DOIs | |
State | Published - Dec 2023 |
Keywords
- Biomarkers
- Cardiac myosin activator
- Cardiac myosin inhibitor
- Heart failure
- Hypertrophic cardiomyopathy
- Troponin
ASJC Scopus subject areas
- Emergency Medicine
- Cardiology and Cardiovascular Medicine
- Physiology (medical)