Key result
Combined troponin elevation linked to ~18-fold higher odds of critical COVID-19 disease.
Why the study?
Cardiovascular and respiratory involvement significantly contributes to COVID-19 severity, motivating an evaluation of cardiorespiratory phenotypes, troponin-defined myocardial injury patterns, Holter rhythm findings, and early post-discharge outcomes in severe and critical disease.
Are troponin-defined myocardial injury patterns and inflammatory biomarkers such as transferrin associated with progression to critical disease, in-hospital mortality, and new-onset atrial fibrillation in patients hospitalized with severe or critical COVID-19?
Cohort (n=172)
No
Are troponin-defined myocardial injury patterns and inflammatory biomarkers such as transferrin associated with progression to critical disease, in-hospital mortality, and new-onset atrial fibrillation in patients hospitalized with severe or critical COVID-19?
In hospitalized patients with severe or critical COVID-19, concurrent hs-cTnT and TnI elevation strongly predicts critical illness and mortality, while low transferrin levels are inversely associated with new-onset atrial fibrillation burden.
Answers are grounded in this paper and cite their sources.
Troponin elevations were associated with critical COVID-19; hypothesis-generating for risk stratification and requires prospective validation before clinical use.
Introduction Cardiovascular and respiratory involvement significantly contributes to COVID-19 severity. This study evaluated cardiorespiratory phenotypes in severe and critical COVID-19, including troponin-defined myocardial injury patterns, Holter rhythm findings, and early post-discharge outcomes. Material and Methods We conducted a prospective cohort study of 172 patients hospitalized with severe or critical COVID-19, analyzing clinical, inflammatory, thrombotic, and myocardial injury biomarkers (hs-cTnT, TnI, IL-6, hs-CRP, transferrin, D-dimers) on days 3–5. Troponin-defined injury patterns were analyzed in patients with both troponins available. An exploratory Holter substudy (n=24) and a 3-week post-discharge re-evaluation assessed early cardiac and respiratory outcomes. Results Among 132 patients with both troponins available, the proportion of critical disease increased progressively across troponin phenotypes (normal, isolated hs-cTnT, combined elevation: 27.9%, 62.5%, 84.6%; p<0.001). After adjustment for age, chronic kidney disease, and cardiovascular disease, isolated hs-cTnT (aOR 4.34; 95% CI 1.67–11.29) and combined elevation (aOR 17.96; 95% CI 3.16–102.04) remained independently associated with critical disease. Newly detected AF occurred in 6/24 patients; transferrin was inversely correlated with AF burden (ρ=–0.638; p=0.001; n=23), persisting after adjustment (partial ρ=–0.649; p=0.002). Each additional 5 days of oxygen therapy increased odds of fibrotic-like pulmonary changes (aOR 1.60; 95% CI 1.04–2.47; p=0.034). At re-evaluation, biological improvement coexisted with residual pulmonary changes in 14/25 (56%) patients. Conclusions Troponin elevation patterns, largely reflecting differing assay sensitivity, were associated with cardiorespiratory severity. Myocardial injury, hypoxemia, pulmonary involvement, and new-onset atrial fibrillation may define high-risk phenotypes, and transferrin warrants validation as a marker of arrhythmic vulnerability.
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Negrea et al. (2026) conducted a cohort in Severe or critical COVID-19 (n=172). Combined hs-cTnT and TnI elevation (myocardial injury) vs. Normal hs-cTnT and TnI levels was evaluated on Maximum COVID-19 severity reached during hospitalization (critical vs. severe disease) (OR 17.96, 95% CI 3.16-102.04, p=<0.001). Combined hs-cTnT and TnI elevation (aOR 17.96, p<0.001) and isolated hs-cTnT elevation (aOR 4.34, p=0.003) were independently associated with critical disease in hospitalized COVID-19 patients.
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