ABC | Volume 115, Nº2, August 2020

Brief Communication Myocardial Injury Biomarkers and Cardiac Complications Associated with Mortality in Patients with COVID-19 Paulo Ricardo Martins-Filho, 1 J osé Augusto Soares Barreto-Filho, 1, 2 V ictor Santana Santos 3 Universidade Federal de Sergipe, 1 Aracaju, SE - Brazil Fundação São Lucas - Centro de Ensino e Pesquisa, 2 Aracaju, SE - Brazil Universidade Federal de Alagoas – Campus Arapiraca, 3 Arapiraca, Al – Brazil Mailing Address: Paulo Ricardo Martins-Filho • Universidade Federal de Sergipe - Hospital Universitário, Rua Claudio Batista, s/n. CEP 49060-108, Aracaju, SE – Brazil E-mail: saqmartins@hotmail.com Manuscript received April 28, 2020, revised manuscript May 22, 2020, accepted June 03, 2020 DOI: https://doi.org/10.36660/abc.20200372 Abstract Background: SARS-CoV-2 is an emerging RNA virus associated with a severe acute respiratory disease known as COVID-19. Although COVID-19 is predominantly a pulmonary disease, some patients have severe cardiovascular damage. We performed a quantitative evidence synthesis of clinical data, myocardial injury biomarkers, and cardiac complications associated with in-hospital death in patients with COVID-19. Methods: We searched the databases PubMed, Embase, and Google Scholar to identify studies comparing clinical data, myocardial injury biomarkers, and cardiac complications between non-survivors and survivors of COVID-19. Effect sizes were reported as mean difference or standardized mean difference for continuous variables and risk ratio for dichotomous variables with 95% confidence intervals. A random effects model was used to pool the results. Results: Six retrospective studies reporting data from 1,141 patients (832 survivors and 309 non-survivors) were included. We found that underlying cardiovascular conditions; elevation of high-sensitivity cardiac troponin I, N-terminal pro-B- type natriuretic peptide, and creatine kinase-MB; and cardiac complications were associated with increased risk of death for patients with SARS-CoV-2 infection. Conclusions: The confirmation that underlying cardiovascular conditions, elevation of myocardial injury biomarkers during COVID-19 infection, and acute cardiovascular decompensation are predictors for mortality in SARS-CoV-2 infection must encourage new research to clarify potential mechanisms and test appropriate treatments. (Arq Bras Cardiol. 2020; 115(2):273-277) Keywords: Coronavirus; COVID-19; SARS-CoV-2; Mortality. Introduction Severe acute respiratory syndrome coronavirus 2 (SARS- CoV-2) is a novel coronavirus that leads to an emerging infectious disease with remarkable pulmonary involvement, known as COVID-19. In addition to the hypothesis that cardiac patients are more susceptible to COVID-19 infection via ACE2 receptor dysregulation, preliminary individual reports have shown that patients with previous cardiovascular disease are at a higher risk of adverse outcomes. Moreover, patients who present any clinical or biological marker of acute cardiac involvement during COVID-19 infection are less likely to survive. 1 Although acute cardiac involvement, whether clinical or revealed by biomarkers, has been described as a common condition among patients hospitalized with COVID-19, and it is associated with a higher risk of in-hospital death, 2 current available evidence is based on individual studies with potentially overlapping data. 3 Therefore, a synthesis of evidence can help confirm these findings. In this study, we performed a quantitative evidence synthesis of clinical data, myocardial injury biomarkers, and cardiac complications associated with in-hospital death in patients with COVID-19. Methods This systematic review and meta-analysis was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. 4 Given the urgent need for this review, PROSPERO registration was not sought. We searched the databases PubMed, Embase, and Google Scholar to identify studies comparing clinical data, myocardial injury biomarkers, and cardiac complications between non-survivors and survivors of COVID-19. We included only studies with clinical data that provided, at least, concentrations of high-sensitivity cardiac troponin I (hs-cTnI). Patients were considered to have acute myocardial injury if serum levels of hs-cTnI were above the 99 th percentile upper reference limit (URL). Heart failure was defined when the serum level of N-terminal pro-B-type natriuretic peptide (NT-proBNP) exceeded the normal range and in the presence of associated symptoms, such as dyspnea, orthopnea, and lower extremity edema. Arrhythmia was defined as rapid ventricular tachycardia lasting more than 30 seconds, inducing 273