Proteomic insights into troponin elevation following COVID-19 infection
Anna Kamdar1,2, Daniel Tze Yee Ang1,2, Kenneth Mangion1,2
1Department of Cardiology, Golden Jubilee National Hospital, Clydebank, UK.
Insights
Cardiac troponin-I elevation in viral infections like COVID-19 may indicate systemic vascular injury, not just heart damage. Understanding this mechanism can improve biomarker interpretation and guide future treatments.
Area of Science:
- Cardiology
- Infectious Diseases
- Proteomics
Background:
- Elevated cardiac troponin-I is common in acute viral infections, including COVID-19.
- The cause of troponin elevation without overt myocardial injury is unclear.
- This presents a diagnostic challenge in clinical practice.
Purpose of the Study:
- To investigate the mechanisms of troponin elevation in hospitalized COVID-19 patients.
- To correlate proteomic data with cardiac biomarkers and imaging.
- To explore potential systemic vascular injury as a cause.
Main Methods:
- Prospective, multicentre CISCO-19 study (NCT04403607) of 267 COVID-19 patients.
- Inclusion of plasma proteomics (SOMAscan V.4.1), cardiovascular MRI, and clinical biomarkers.
- Multi-system evaluation at enrolment and 28-60 days post-infection.
Main Results:
- 13.2% of participants showed a high likelihood of myocarditis.
- Elevated high-sensitivity troponin-I levels were observed, with sex-specific thresholds.
- Downregulation of smooth muscle myosin light chain proteins correlated with troponin-I levels.
Conclusions:
- Troponin elevation in COVID-19 may signify systemic vascular injury.
- Recognizing vascular injury can refine cardiac biomarker interpretation in viral illnesses.
- This finding supports investigating vascular injury in future therapeutic strategies.
Background:
Raised cardiac troponin-I is a common finding in patients hospitalised with acute viral infections, including but not limited to COVID-19. This often occurs in the absence of overt myocardial injury presenting a challenge for interpretation. The mechanisms underlying troponin elevation are uncertain.
Methods:
The CISCO-19 (Cardiovascular Imaging in SARS-CoV-19) study (NCT04403607) is a prospective, multicentre cohort study, in which hospitalised PCR-confirmed COVID-19 participants (N=267) underwent multisystem evaluation at enrolment and at 28-60 days. The study incorporated plasma proteomics (SOMAscan V.4.1), cardiovascular MRI and clinical biomarkers. Of these, 211 had baseline plasma proteomic data and 185 completed follow-up sampling. Matched proteomic and imaging data were available for 155 participants (mean age: 55 years (SD 12); 43% female).
Results:
A high likelihood of myocarditis was identified in 13.2% (N=21/159) of participants. High-sensitivity troponin-I was modestly elevated at enrolment (median 3 ng/L; IQR 2-6; n=159). Among males (n=90), 9.3% had a high-sensitivity troponin that exceeded 34 ng/L. Among females (n=69), 4.5% exceeded 16 ng/L. Smooth muscle myosin light chain proteins were downregulated at follow-up (log2 fold change -0.12 to -0.6; all adjusted p<0.02) and positively correlated with high-sensitivity troponin-I, but not N-terminal brain natriuretic peptide or cardiac MRI indices (n=155).
Conclusions:
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.
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