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      Cardiac troponin I in patients with coronavirus disease 2019 (COVID-19): Evidence from a meta-analysis

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          Abstract

          To the Editor: Coronavirus disease 2019 (COVID-19) is an emerging outbreak caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). According to updated statistics released by the World Health Organization (WHO), COVID-19 has already affected over 93,000 people from over 75 countries worldwide, causing >3200 deaths. 1 In up to 15% of infected patients the clinical course of this pathology may be complicated by the onset of a severe form of intestinal pneumonia, which may then progress towards acute respiratory distress syndrome (ARDS) and/or multi organ failure (MOF) and death. 2 People with underlying cardiovascular disease are among the highest risk individuals for severe disease and death. Importantly, among the COVID-19 knowledge gaps are laboratory and diagnostics issues as well as the clinical management of severe and critically ill patients. 3 Since major cardiac complications have been reported to develop in a considerable number of patients with pneumonia, 4 we performed an analysis of the current scientific literature to investigate whether the measurement of cardiac troponin I (cTnI) or cardiac troponin T (cTnT) may help predict clinical severity in patients with COVID-19. An electronic search was carried out in Medline (PubMed interface), Scopus and Web of Science, using the keywords “laboratory” OR “troponin” AND “coronavirus 2019” OR “2019-nCoV” OR “SARS-CoV-2”, between 2019 and present time (i.e., March 4, 2020), without applying language restrictions. The title, abstract and full text of all documents identified with these search criteria were assessed, and those reporting information on cTnT or cTnI values in COVID-19 patients with or without severe disease (i.e., those needing mechanical ventilation, ICU admission or those who died), were included in a meta-analysis. The reference lists of all documents were also analyzed for identifying additional eligible studies. A meta-analysis was finally carried out, with calculation of standardized mean difference (SMD) and 95% confidence interval (95% CI) of cTnI or cTnT values in COVID-19 patients with or without severe disease. The statistical analysis was performed with MetaXL, software Version 5.3 (EpiGear International Pty Ltd., Sunrise Beach, Australia). Mean and standard deviation of cTnI or cTnT values were extrapolated from sample size, median and interquartile range (IQR), according to Hozo et al. 5 Overall, 81 documents could be initially identified based on our search criteria, 78 of which ought to be excluded after title, abstract or full text reading, since they were review articles (n = 6), commentaries or other editorial materials (n = 1), they did not deal with COVID-19 disease (n = 65), or did not expressly report the values of cTnI or cTnT in COVID-19 patients with or without severe disease (n = 6). One additional study could be identified from reading the reference list of the three selected documents, so that 4 studies were finally included in our meta-analysis.6., 7., 8., 9. All these clinical studies used cTnI (the specific method was not described in the published articles), and all except one 7 reported the use of high-sensitivity immunoassays. All studies were set in China, included a total number of 341 patients (123 with severe disease; 36%), the sample size varied between 12 and 150, whilst the clinical outcome was defined as intensive care unit (ICU) admission in 2 studies 6 , 8 onset of ARDS in another study, 7 and death in the remaining investigation. 9 The SMD of the four studies is summarized in Fig. 1 . Although the heterogeneity was considerably high (i.e., I2, 98%; p < 0.001), the values of cTnI were found to be significantly increased in COVID-19 patients with severe disease than in those without (SMD, 25.6 ng/L; 95% CI, 6.8–44.5 ng/L). Fig 1 Standardized mean difference (SMD) and 95% confidence interval (95% CI) of cardiac troponin I (cTnI) values in coronavirus disease 2019 (COVID-19) patients with or without severe disease. Fig 1 Recent literature data has shown that cTnI concentration is only marginally increased in all patients with SARS-CoV-2 infection, whereby values exceeding the 99th percentile in the upper reference limit (URL) can only be observed in 8–12% of positive cases. 10 Nonetheless, what seems to emerge from our results is that cTnI values are significantly increased in patients with severe SARS-CoV-2 infection compared to those with milder forms of disease. It is hence reasonable to hypothesize that initial measurement of cardiac damage biomarkers immediately after hospitalization for SARS-CoV-2 infection, as well as longitudinal monitoring during hospital stay, may help identifying a subset of patients with possible cardiac injury and thereby predict the progression of COVID-19 towards a worse clinical picture. Urgent studies shall also be planned to define whether or not echocardiographic testing and other adjunctive cardioprotective therapies such as corticosteroids, other anti-inflammatory agents, immunosuppressants, antivirals (antiviral agents and/or interferons) and/or immunomodulatory therapy (immunoglobulins) may be advisable in patients with significant elevation of cardiac injury biomarkers. Statement of conflict of interest None of the authors have any conflicts of interests with regard to this publication.

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          Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China

          Summary Background A recent cluster of pneumonia cases in Wuhan, China, was caused by a novel betacoronavirus, the 2019 novel coronavirus (2019-nCoV). We report the epidemiological, clinical, laboratory, and radiological characteristics and treatment and clinical outcomes of these patients. Methods All patients with suspected 2019-nCoV were admitted to a designated hospital in Wuhan. We prospectively collected and analysed data on patients with laboratory-confirmed 2019-nCoV infection by real-time RT-PCR and next-generation sequencing. Data were obtained with standardised data collection forms shared by WHO and the International Severe Acute Respiratory and Emerging Infection Consortium from electronic medical records. Researchers also directly communicated with patients or their families to ascertain epidemiological and symptom data. Outcomes were also compared between patients who had been admitted to the intensive care unit (ICU) and those who had not. Findings By Jan 2, 2020, 41 admitted hospital patients had been identified as having laboratory-confirmed 2019-nCoV infection. Most of the infected patients were men (30 [73%] of 41); less than half had underlying diseases (13 [32%]), including diabetes (eight [20%]), hypertension (six [15%]), and cardiovascular disease (six [15%]). Median age was 49·0 years (IQR 41·0–58·0). 27 (66%) of 41 patients had been exposed to Huanan seafood market. One family cluster was found. Common symptoms at onset of illness were fever (40 [98%] of 41 patients), cough (31 [76%]), and myalgia or fatigue (18 [44%]); less common symptoms were sputum production (11 [28%] of 39), headache (three [8%] of 38), haemoptysis (two [5%] of 39), and diarrhoea (one [3%] of 38). Dyspnoea developed in 22 (55%) of 40 patients (median time from illness onset to dyspnoea 8·0 days [IQR 5·0–13·0]). 26 (63%) of 41 patients had lymphopenia. All 41 patients had pneumonia with abnormal findings on chest CT. Complications included acute respiratory distress syndrome (12 [29%]), RNAaemia (six [15%]), acute cardiac injury (five [12%]) and secondary infection (four [10%]). 13 (32%) patients were admitted to an ICU and six (15%) died. Compared with non-ICU patients, ICU patients had higher plasma levels of IL2, IL7, IL10, GSCF, IP10, MCP1, MIP1A, and TNFα. Interpretation The 2019-nCoV infection caused clusters of severe respiratory illness similar to severe acute respiratory syndrome coronavirus and was associated with ICU admission and high mortality. Major gaps in our knowledge of the origin, epidemiology, duration of human transmission, and clinical spectrum of disease need fulfilment by future studies. Funding Ministry of Science and Technology, Chinese Academy of Medical Sciences, National Natural Science Foundation of China, and Beijing Municipal Science and Technology Commission.
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            Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus–Infected Pneumonia in Wuhan, China

            In December 2019, novel coronavirus (2019-nCoV)-infected pneumonia (NCIP) occurred in Wuhan, China. The number of cases has increased rapidly but information on the clinical characteristics of affected patients is limited.
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              Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China

              Dear Editor, The rapid emergence of COVID-19 in Wuhan city, Hubei Province, China, has resulted in thousands of deaths [1]. Many infected patients, however, presented mild flu-like symptoms and quickly recover [2]. To effectively prioritize resources for patients with the highest risk, we identified clinical predictors of mild and severe patient outcomes. Using the database of Jin Yin-tan Hospital and Tongji Hospital, we conducted a retrospective multicenter study of 68 death cases (68/150, 45%) and 82 discharged cases (82/150, 55%) with laboratory-confirmed infection of SARS-CoV-2. Patients met the discharge criteria if they had no fever for at least 3 days, significantly improved respiratory function, and had negative SARS-CoV-2 laboratory test results twice in succession. Case data included demographics, clinical characteristics, laboratory results, treatment options and outcomes. For statistical analysis, we represented continuous measurements as means (SDs) or as medians (IQRs) which compared with Student’s t test or the Mann–Whitney–Wilcoxon test. Categorical variables were expressed as numbers (%) and compared by the χ 2 test or Fisher’s exact test. The distribution of the enrolled patients’ age is shown in Fig. 1a. There was a significant difference in age between the death group and the discharge group (p < 0.001) but no difference in the sex ratio (p = 0.43). A total of 63% (43/68) of patients in the death group and 41% (34/82) in the discharge group had underlying diseases (p = 0.0069). It should be noted that patients with cardiovascular diseases have a significantly increased risk of death when they are infected with SARS-CoV-2 (p < 0.001). A total of 16% (11/68) of the patients in the death group had secondary infections, and 1% (1/82) of the patients in the discharge group had secondary infections (p = 0.0018). Laboratory results showed that there were significant differences in white blood cell counts, absolute values of lymphocytes, platelets, albumin, total bilirubin, blood urea nitrogen, blood creatinine, myoglobin, cardiac troponin, C-reactive protein (CRP) and interleukin-6 (IL-6) between the two groups (Fig. 1b and Supplementary Table 1). Fig. 1 a Age distribution of patients with confirmed COVID-19; b key laboratory parameters for the outcomes of patients with confirmed COVID-19; c interval from onset of symptom to death of patients with confirmed COVID-19; d summary of the cause of death of 68 died patients with confirmed COVID-19 The survival times of the enrolled patients in the death group were analyzed. The distribution of survival time from disease onset to death showed two peaks, with the first one at approximately 14 days (22 cases) and the second one at approximately 22 days (17 cases) (Fig. 1c). An analysis of the cause of death was performed. Among the 68 fatal cases, 36 patients (53%) died of respiratory failure, five patients (7%) with myocardial damage died of circulatory failure, 22 patients (33%) died of both, and five remaining died of an unknown cause (Fig. 1d). Based on the analysis of the clinical data, we confirmed that some patients died of fulminant myocarditis. In this study, we first reported that the infection of SARS-CoV-2 may cause fulminant myocarditis. Given that fulminant myocarditis is characterized by a rapid progress and a severe state of illness [3], our results should alert physicians to pay attention not only to the symptoms of respiratory dysfunction but also the symptoms of cardiac injury. Further, large-scale studies and the studies on autopsy are needed to confirm our analysis. In conclusion, predictors of a fatal outcome in COVID-19 cases included age, the presence of underlying diseases, the presence of secondary infection and elevated inflammatory indicators in the blood. The results obtained from this study also suggest that COVID-19 mortality might be due to virus-activated “cytokine storm syndrome” or fulminant myocarditis. Electronic supplementary material Below is the link to the electronic supplementary material. Supplementary material 1 (DOCX 38 kb)
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                Author and article information

                Contributors
                Journal
                Prog Cardiovasc Dis
                Prog Cardiovasc Dis
                Progress in Cardiovascular Diseases
                Elsevier Inc.
                0033-0620
                1873-1740
                10 March 2020
                10 March 2020
                :
                Affiliations
                [a ]Section of Clinical Biochemistry, Department of Neuroscience, Biomedicine and Movement, University of Verona, Verona, Italy
                [b ]John Ochsner Heart and Vascular Institute, Ochsner Clinical School - The University of Queensland School of Medicine, New Orleans, LA, USA
                [c ]Department of Physiology, Faculty of Medicine, University of Valencia and INCLIVA Biomedical Research Institute, Valencia, Spain
                [d ]Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, CA, USA
                Author notes
                [* ]Address reprint requests to Fabian Sanchis-Gomar, Department of Physiology, Faculty of Medicine, University of Valencia, Av. Blasco Ibañez, 15, 46010 Valencia, Spain. fabian.sanchis@ 123456uv.es
                Article
                S0033-0620(20)30055-4
                10.1016/j.pcad.2020.03.001
                7127395
                32169400
                0999fae0-4fd5-4dec-b971-6e4347d106c0
                © 2020 Elsevier Inc. All rights reserved.

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

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                coronavirus,covid-19,troponin,prognosis
                coronavirus, covid-19, troponin, prognosis

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