Cardiopulmonary Profiles in Severe and Critical COVID-19: Troponin Patterns, Transferrin-Linked Atrial Fibrillation, and Early Pulmonary Recovery
DOI:
https://doi.org/10.62838/jccm-2026-0053Keywords:
myocardial injury, COVID-19, troponin T, troponin I, atrial fibrillation, electrocardiography, transferrinAbstract
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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Copyright (c) 2026 Valentina Negrea, Andreea Varga, Ioan Tilea, Tudor Fleseriu, Anca Meda Vasiesiu (Author)
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