Dataset Information

Cardiac troponin and COVID-19 severity: Results from BIOCOVID study.

ABSTRACT:

Background

Myocardial injury is a common finding in COVID-19 strongly associated with severity. We analysed the prevalence and prognostic utility of myocardial injury, characterized by elevated cardiac troponin, in a large population of COVID-19 patients, and further evaluated separately the role of troponin T and I.

Methods

This is a multicentre, retrospective observational study enrolling patients with laboratory-confirmed COVID-19 who were hospitalized in 32 Spanish hospitals. Elevated troponin levels were defined as values above the sex-specific 99th percentile upper reference limit, as recommended by international guidelines. Thirty-day mortality was defined as endpoint.

Results

A total of 1280 COVID-19 patients were included in this study, of whom 187 (14.6%) died during the hospitalization. Using a nonspecific sex cut-off, elevated troponin levels were found in 344 patients (26.9%), increasing to 384 (30.0%) when a sex-specific cut-off was used. This prevalence was significantly higher (42.9% vs 21.9%; P < .001) in patients in whom troponin T was measured in comparison with troponin I. Sex-specific elevated troponin levels were significantly associated with 30-day mortality, with adjusted odds ratios (ORs) of 3.00 for total population, 3.20 for cardiac troponin T and 3.69 for cardiac troponin I.

Conclusion

In this multicentre study, myocardial injury was a common finding in COVID-19 patients. Its prevalence increased when a sex-specific cut-off and cardiac troponin T were used. Elevated troponin was an independent predictor of 30-day mortality, irrespective of cardiac troponin assay and cut-offs to detect myocardial injury. Hence, the early measurement of cardiac troponin may be useful for risk stratification in COVID-19.

SUBMITTER: Garcia de Guadiana-Romualdo L

PROVIDER: S-EPMC7995181 | biostudies-literature | 2021 Jun

REPOSITORIES: biostudies-literature

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Publications

Cardiac troponin and COVID-19 severity: Results from BIOCOVID study.

García de Guadiana-Romualdo Luis L Morell-García Daniel D Rodríguez-Fraga Olaia O Morales-Indiano Cristian C María Lourdes Padilla Jiménez Ana A Gutiérrez Revilla José Ignacio JI Urrechaga Eloísa E Álamo José María JM Hernando Holgado Ana María AM Lorenzo-Lozano María Del Carmen MDC Sánchez Fdez-Pacheco Silvia S de la Hera Cagigal Patricia P Juncos Tobarra María Ángeles MÁ Vílchez Juan A JA Vírseda Chamorro Isabel I Gutiérrez Garcia Irene I Pastor Murcia Yolanda Y Sahuquillo Frías Laura L Altimira Queral Laura L Nuez-Zaragoza Elisa E Adell Ruiz de León Juan J Ruiz Ripa Alicia A Salas Gómez-Pablos Paloma P Cebreiros López Iria I Fernández Uriarte Amaia A Larruzea Álex Á López Yepes María Luisa ML Sancho-Rodríguez Natalia N Zamorano Andrés María Consuelo MC Pedregosa Díaz José J Acevedo Alcaraz Cristina C Blázquez Manzanera Alfonso-L AL Pérez Sanmartín Sonia S Baamonde Calzada María Del Carmen MDC Vera Marina M Valera Nuñez Elena E Canalda Campás Magdalena M García Muñoz Sara S Bauça Josep Miquel JM Vicente Gutiérrez Luis L Jiménez Añón Laura L Pérez Martínez Alfonso A Pons Castillo Aurelio A González Tamayo Ruth R Férriz Vivancos Jorge J José Alcaide Martín María M Ferrer Díaz de Brito Fernández Vicente V Aguadero Vicente V García Arévalo María Gloria MG Arnaldos Carrillo María M González Morales Mercedes M Núñez Gárate María M Ruiz Iruela Cristina C Esteban Torrella Patricia P Vila Pérez Martí M Egea-Caparrós Jose Manuel JM Sáenz Luis L Galán Ortega Amparo A Consuegra-Sánchez Luciano L

European journal of clinical investigation 20210315 6

<h4>Background</h4>Myocardial injury is a common finding in COVID-19 strongly associated with severity. We analysed the prevalence and prognostic utility of myocardial injury, characterized by elevated cardiac troponin, in a large population of COVID-19 patients, and further evaluated separately the role of troponin T and I.<h4>Methods</h4>This is a multicentre, retrospective observational study enrolling patients with laboratory-confirmed COVID-19 who were hospitalized in 32 Spanish hospitals. ...[more]

PMID: 33660278

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Project description:Using RNA-seq and high-resolution mass spectrometry we performed a comprehensive systems analysis on 128 plasma and leukocyte samples from hospitalized patients with or without COVID-19 (n=102 and 26 respectively) and with differing degrees of disease severity. We generated abundance measurements for over 17,000 transcripts, proteins, metabolites, and lipids and compiled them with clinical data into a curated relational database. This resource offers the unique opportunity to perform systems analysis and cross-ome correlations to both molecules and patient outcomes. In total 219 molecular features were mapped with high significance to COVID-19 status and severity, including those involved in processes such as complement system activation, dysregulated lipid transport, and B cell activation. In one example, we detected a trio of covarying molecules – citrate, plasmenyl-phosphatidylcholines, and gelsolin (GSN) – that offer both pathophysiological insight and potential novel therapeutic targets. Further, our data revealed in some cases, and supported in others, that several biological processes were dysregulated in COVID-19 patients including vessel damage, platelet activation and degranulation, blood coagulation, and acute phase response. For example, we observed that the coagulation-related protein, cellular fibronectin (cFN), was highly increased within COVID-19 patients and provide new evidence that the upregulated proteoform stems from endothelial cells, consistent with endothelial injury as a major activator of the coagulation cascade. The abundance of prothrombin, which is cleaved to form thrombin during clotting, was significantly reduced and correlated with severity and might help to explain the hyper coagulative environment of SARS-CoV-2 infection. From transcriptomic analysis of leukocytes, we concluded that COVID-19 patients with acute respiratory distress syndrome (ARDS) demonstrated a phenotype that overlapped with, but was distinct from, that found in patients with non-COVID-19-ARDS. To aid in the global efforts toward elucidation of disease pathophysiology and therapeutic development, we created a web-based tool with interactive visualizations allowing for easy navigation of this systems-level compendium of biomolecule abundance in relation to COVID-19 status and severity. Finally, we leveraged these multi-omic data to predict COVID-19 patient outcomes with machine learning, which highlighted the predictive power of these expansive molecular measurements beyond the standardized clinical estimate of 10-year survival Charlson score.

Dataset Information

Cardiac troponin and COVID-19 severity: Results from BIOCOVID study.

Background

Methods

Results

Conclusion

Publications

Cardiac troponin and COVID-19 severity: Results from BIOCOVID study.

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