Heart failure & cardiomyopathiesCohort study
Proteomic insights into troponin elevation following COVID-19 infection
- prospective, multicentre cohort study
Authors' conclusion
Troponin elevation, exemplified here by COVID-19, could reflect systemic vascular injury. Recognising this mechanism may refine interpretation of cardiac biomarkers in viral illness and supports the investigation of vascular injury in future therapeutic strategies and biomedical studies.
Study context
- Population
- Hospitalised PCR-confirmed COVID-19 participants211 had baseline plasma proteomic data, 185 completed follow-up sampling, matched proteomic and imaging data for 155
- Participants
- 267 participants
Main finding
As reported in the abstract
High likelihood of myocarditis
High likelihood of myocarditis
13.2% (N=21/159)
Observational data: associations, not effects.
Further findings
High-sensitivity troponin-I · enrolment
- median
- 3 ng/L; IQR 2-6; n=159
- Among males (n=90), exceeded 34 ng/L
- 9.3%
- Among females (n=69), exceeded 16 ng/L
- 4.5%
Smooth muscle myosin light chain proteins · follow-up
- Downregulated, log2 fold change
- −0.12 to −0.6; all adjusted p<0.02
- Positively correlated with high-sensitivity troponin-I, but not N-terminal brain natriuretic peptide or cardiac MRI indices (n=155)
Original publication
Proteomic insights into troponin elevation following COVID-19 infection. Heart. Published 9 March 2026. doi:10.1136/heartjnl-2025-326786
Summarised from the published abstract; every number is checked against it