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Heart, Lung and Circulation

Cardiac Injury and Outcomes of Patients With COVID-19 in New York City

  • Author Footnotes
    1 Drs. Maeda and Obata contributed equally to this article.
    Tetsuro Maeda
    Footnotes
    1 Drs. Maeda and Obata contributed equally to this article.
    Affiliations
    Department of Medicine, Mount Sinai Beth Israel, Icahn School of Medicine at Mount Sinai, NY, USA
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  • Author Footnotes
    1 Drs. Maeda and Obata contributed equally to this article.
    Reiichiro Obata
    Footnotes
    1 Drs. Maeda and Obata contributed equally to this article.
    Affiliations
    Department of Medicine, Mount Sinai Beth Israel, Icahn School of Medicine at Mount Sinai, NY, USA
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  • Dahlia Rizk
    Affiliations
    Department of Medicine, Mount Sinai Beth Israel, Icahn School of Medicine at Mount Sinai, NY, USA
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  • Toshiki Kuno
    Correspondence
    Corresponding author at: Department of Medicine, Mount Sinai Beth Israel, Icahn School of Medicine at Mount Sinai, First Avenue, 16th Street, New York, NY, 10003, USA
    Affiliations
    Department of Medicine, Mount Sinai Beth Israel, Icahn School of Medicine at Mount Sinai, NY, USA
    Search for articles by this author
  • Author Footnotes
    1 Drs. Maeda and Obata contributed equally to this article.
Published:November 23, 2020DOI:https://doi.org/10.1016/j.hlc.2020.10.025

      Background

      Prior studies demonstrated that elevated troponin in patients with COVID-19 was associated with increased in-hospital mortality. However, the association of cardiac injury and electrocardiogram (ECG) changes remains unclear. The aim of this study was to investigate the association of cardiac injury with ECG abnormality and with in-hospital mortality.

      Methods

      We conducted a retrospective cohort study of patients who were hospitalised with COVID-19 between 13 March and 31 March 2020. Those patients with troponin I measurement were included in the study and divided into those who had elevated troponin I (cardiac injury group) and those who did not (no cardiac injury group). Statistical analyses were performed to compare differences between the groups, and a multivariate logistic regression model was constructed to assess the effect of cardiac injury on in-hospital mortality.

      Results

      One hundred and eight-one (181) patients were included, 54 of whom were in the cardiac injury group and 127 in the no cardiac injury group. The mean age was 64.0±16.6 years and 55.8% were male. The cardiac injury group was more likely to be older, have a history of coronary artery disease, atrial fibrillation and congestive heart failure compared to the no cardiac injury group (all p<0.05); there was no difference in presence of chest pain (cardiac injury group versus no cardiac injury group: 17.0% versus 22.5%, p=0.92); the cardiac injury group had a significantly higher value of brain natriuretic peptide, procalcitonin, interleukin-6 and D-dimer (all p<0.05); they had numerically more frequent ECG abnormalities such as T wave inversion (13.2% versus 7.5%, p=0.23) and ST depression (1.9% versus 0.0%, p=0.13) although statistically not significant; they had significantly higher in-hospital mortality (42.3% versus 12.6%, p<0.001). With a multivariate logistic regression model, age (odds ratio [95% confidence interval]: 1.033 [1.002–1.065], p=0.034) and cardiac injury (3.25 [1.40–7.54], p=0.006) were independent predictors of in-hospital mortality.

      Conclusions

      Patients with COVID-19 with elevated troponin I had a relatively low proportion of chest pain and ECG abnormality. Cardiac injury was independently associated with in-hospital mortality.

      Keywords

      Introduction

      Coronavirus disease 2019 (COVID-19), caused by a novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has emerged as a global public health emergency since December 2019 [
      • Zhu N.
      • Zhang D.
      • Wang W.
      • Li X.
      • Yang B.
      • Song J.
      • et al.
      A novel coronavirus from patients with pneumonia in China, 2019.
      ]. Prior studies demonstrated that 12–28% of patients with COVID-19 presented with acute cardiac injury defined as elevated troponin I, and that cardiac injury was associated with increased in-hospital mortality [
      • Huang C.
      • Wang Y.
      • Li X.
      • Ren L.
      • Zhao J.
      • Hu Y.
      • et al.
      Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China.
      ,
      • Shi S.
      • Qin M.
      • Shen B.
      • Cai Y.
      • Liu T.
      • Yang F.
      • et al.
      Association of cardiac injury with mortality in hospitalized patients with COVID-19 in Wuhan, China.
      ,
      • Guo T.
      • Fan Y.
      • Chen M.
      • Wu X.
      • Zhang L.
      • He T.
      • et al.
      Cardiovascular implications of fatal outcomes of patients with coronavirus disease 2019 (COVID-19).
      ,
      • Kuno T.
      • Takahashi M.
      • Obata R.
      • Maeda T.
      Cardiovascular comorbidities, cardiac injury, and prognosis of COVID-19 in New York City.
      ]. Guo et al. noted that 64% of patients had evidence of myocardial ischaemia on electrocardiogram (ECG), although only 27% of patients with cardiac injury were assessed with ECG [
      • Guo T.
      • Fan Y.
      • Chen M.
      • Wu X.
      • Zhang L.
      • He T.
      • et al.
      Cardiovascular implications of fatal outcomes of patients with coronavirus disease 2019 (COVID-19).
      ]. It is hypothesised that elevation of troponin in patients with COVID-19 stems from direct damage of cardiomyocytes from SARS-CoV-2 or inflammatory pathogenesis [
      • Inciardi R.M.
      • Lupi L.
      • Zaccone G.
      • Italia L.
      • Raffo M.
      • Tomasoni D.
      • et al.
      Cardiac involvement in a patient with coronavirus disease 2019 (COVID-19).
      ,
      • Siripanthong B.
      • Nazarian S.
      • Muser D.
      • Deo R.
      • Santangeli P.
      • Khanji M.
      • et al.
      Recognizing COVID-19-related myocarditis: the possible pathophysiology and proposed guideline for diagnosis and management.
      ,
      • Coyle J.
      • Igbinomwanhia E.
      • Sanchez-Nadales A.
      • Danciu S.
      • Chu C.
      • Shah N.
      A recovered case of COVID-19 Myocarditis and ARDS treated with corticosteroids, tocilizumab, and experimental AT-001.
      ,
      • Cizgici A.Y.
      • Zencirkiran Agus H.
      • Yildiz M.
      COVID-19 myopericarditis: it should be kept in mind in today's conditions.
      ,
      • Paul J.F.
      • Charles P.
      • Richaud C.
      • Caussin C.
      • Diakov C.
      Myocarditis revealing COVID-19 infection in a young patient.
      ] rather than typical large coronary artery occlusion; however, the exact mechanism remains unclear. The aim of this study was to investigate the association of cardiac injury with ECG abnormality as well as in-hospital mortality in our diverse multi-ethnic population in New York City, the global epicentre of this pandemic to date.

      Materials and Methods

      This study was a retrospective cohort study using the data of patients hospitalised from 13 March to 31 March 2020 with diagnosis of COVID-19 at Mount Sinai Beth Israel, an urban academic medical centre in downtown Manhattan [
      • Jangi S.
      Facing uncertainty--dispatch from Beth Israel Medical Center, Manhattan.
      ]. Of note, the first case of hospitalisation occurred on 13 March 2020. The study protocol was approved by the institutional review board and conducted in accordance with the principles of the Declaration of Helsinki. Diagnosis of COVID-19 required detection of SARS-CoV-2 in a nasopharyngeal swab specimen using reverse transcriptase polymerase chain reaction. The decision whether to admit the patients diagnosed with COVID-19 was provider dependent and not based on any specific predetermined criteria. Since our study was a retrospective observational study, it did not require specific tests including troponin I, ECG, or any other treatments.
      A retrospective review of patient electronic medical records was conducted mainly by two authors (R.O. and T.M.) for demographics, comorbidities, and clinical outcomes including troponin I and ECG findings. Regarding ECG findings, T wave inversions were subdivided into inferior (II, III, aVF), anterior (V1-V4), lateral (I, aVL), and apex (V5, V6); we also collected the data of upright T wave in aVR [
      • Kosuge M.
      • Ebina T.
      • Hibi K.
      • Tsukahara K.
      • Iwahashi N.
      • Gohbara M.
      • et al.
      Differences in negative T waves among acute coronary syndrome, acute pulmonary embolism, and Takotsubo cardiomyopathy.
      ].
      Among the patients who were admitted with COVID-19, those who had troponin I measured upon admission were included in our study. They were divided into two groups: those with cardiac injury (cardiac injury group) and those without cardiac injury (no cardiac injury group). Cardiac injury was defined as troponin I greater than 0.031 ng/ml, which was the institutional cut-off and the 99th percentile upper reference limit [
      • Huang C.
      • Wang Y.
      • Li X.
      • Ren L.
      • Zhao J.
      • Hu Y.
      • et al.
      Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China.
      ,
      • Hartikainen T.S.
      • Sorensen N.A.
      • Haller P.M.
      • Gobling A.
      • Lehmacher J.
      • Zeller T.
      • et al.
      Clinical application of the 4th Universal Definition of Myocardial Infarction.
      ]. Laboratory data, radiographic findings reviewed by attending radiologists, and characteristics of hospital stay such as total length of stay and ICU stay were collected. Our institution initially used hydroxychloroquine for moderate cases which was defined as radiologic evidence of pneumonia or oxygen saturation <94%.
      Continuous variables were presented as mean±standard deviation or median (interquartile range), as appropriate for the data distribution; categorical variables were expressed as percentages. The changes from baseline in continuous variables were evaluated using Student’s t-test or Mann-Whitney U test; the χ2 or Fisher’s exact t-test was used for analysing categorical variables. A multivariate logistic regression model was constructed in order to assess the association of cardiac injury with in-hospital mortality. We included age and troponin as variables because they have been reported as independent predictors of mortality in patients with COVID-19 [
      • Shi S.
      • Qin M.
      • Shen B.
      • Cai Y.
      • Liu T.
      • Yang F.
      • et al.
      Association of cardiac injury with mortality in hospitalized patients with COVID-19 in Wuhan, China.
      ,
      • Zhou F.
      • Yu T.
      • Du R.
      • Fan G.
      • Liu Y.
      • Liu Z.
      • et al.
      Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study.
      ]. Then, we performed a stepwise multivariate analysis including age and cardiac injury, and other baseline characteristics such as hypertension, diabetes mellitus, history of coronary artery disease, congestive heart failure, peripheral vascular disease, cerebrovascular disease, chronic obstructive pulmonary disease, and end-stage renal disease on dialysis. All statistical calculations and analyses were performed using SPSS (version 24, SPSS, Armonk, NY, USA), with p-values <0.05 considered statistically significant.

      Results

      Two hundred and twenty-four (224) patients were hospitalised with a diagnosis of COVID-19, 181 (80.8%) of whom had measurement of troponin I upon admission and were included in the study. Among the 181 patients, the mean age was 64.0±16.6 and 55.8% were male; 36.4% were Caucasian, 21.0% were African American, 43.9% were Hispanic. Fifty-four (54) patients were categorised into the cardiac injury group and 127 into the no cardiac injury group.
      Detailed baseline characteristics are shown in Table 1. The cardiac injury group was more likely to be older and have hypertension, and end-stage renal disease on dialysis, coronary artery disease as a previously known comorbidity (all p-value <0.05). Prior coronary revascularisation and known atrial fibrillation and congestive heart failure were also more frequently compared to no cardiac injury group (all p-value <0.05). Notably, both groups had non-significantly different, relatively low rates of chest pain (cardiac injury group versus no cardiac injury group: 17.0% versus 22.5%, p=0.92).
      Table 1Baseline characteristics at admission.
      No Cardiac Injury Group N=127Cardiac Injury Group N=54P-value
      Age60 [49, 71]73.5 [67, 83]<0.001
      Male54.3% (69/127)59.3% (32/54)0.54
      Body mass index28.7 [25.1, 33.2]28.1 [25.6, 31.9]0.79
      RaceWhite 38.6% (49/127)

      Black 19.7% (25/127)

      Asian 10.2% (13/127)

      Others 29.1% (37/127)
      White 31.5% (17/54)

      Black 24.1% (13/54)

      Asian 11.1% (6/54)

      Others 33.3% (18/54)
      0.78
      Hispanic 46.3% (57/123)Hispanic 46.3% (25/54)0.996
      Symptoms
       Fever70.9% (90/127)42.3% (22/52)<0.001
       Myalgia19.7% (25/127)3.8% (2/53)0.38
       Chest pain22.8% (29/127)17.0% (9/53)0.92
       Malaise27.6% (35/127)32.1% (17/53)0.54
       Sore throat8.7% (11/127)0.0% (0/53)0.027
       Runny nose7.9% (10/126)5.7% (3/53)0.59
       Dyspnoea66.9% (85/127)56.6% (30/53)0.19
       Cough74.0% (94/127)60.4% (32/53)0.069
       Sputum25.4% (32/126)8.7% (4/46)0.049
       Abdominal pain11.8% (15/127)7.5% (4/53)0.47
       Nausea/Vomiting29.1% (37/127)22.6% (12/53)0.37
       Diarrhoea28.3% (36/127)13.2% (7/53)0.030
      Initial Vital Signs
       Temperature (°C)36.8 [36.3, 37.7]36.9 [36.2, 37.5]0.71
       Heart rate (beat/min.)97 [86, 110]86.5 [75.5, 109]0.074
       SBP (mmHg)133 [117, 148]137 [109, 155]0.90
       DBP (mmHg)77 [68, 86]75 [64, 88]0.57
       MAP (mmHg)94.7 [86.7, 106]93.5 [80.8, 111]0.97
       RR (/min.)20 [18, 24]20 [18, 24]0.59
       SpO2 (%) at room air95 [93, 98]95 [92, 97.3]0.71
      Altered mental status5.6% (7/126)26.4% (14/53)<0.001
      Aspirin18.9% (24/127)41.5% (22/53)0.002
      Anticoagulation6.3% (8/127)28.3% (15/53)<0.001
      ACEI15.0% (19/127)24.5% (13/53)0.13
      ARB15.1% (19/126)26.4% (14/53)0.074
      Steroid use at home0.8% (1/126)5.6% (3/54)0.047
      Comorbidities
       Hypertension53.5% (68/127)90.7% (49/54)<0.001
       Hyperlipidaemia36.2% (46/127)63.0% (34/54)0.001
       DM29.1% (37/127)46.3% (25/54)0.026
       COPD5.5% (7/127)14.8% (8/54)0.038
       Asthma11.0% (14/127)12.5% (6/48)0.99
       CVA3.9% (5/127)14.8% (8/54)0.010
       PVD4.7% (6/127)13.0% (7/54)<0.001
       Dialysis0.8% (1/127)9.3% (5/54)0.004
       Cirrhosis1.6% (2/127)3.7% (2/54)0.37
       CAD10.0% (9/127)44.4% (27/54)<0.001
       Previous PCI3.1% (4/127)33.3% (18/54)<0.001
       Previous CABG0.8% (1/127)14.8% (8/54)<0.001
       Previous PE/DVT7.9% (10/127)3.7% (2/54)0.30
       History of AF3.9% (5/127)25.9% (14/54)<0.001
       Previous CHF4.0% (5/126)35.2% (19/54)<0.001
      History of cancer9.4% (12/127)5.6% (3/54)0.39
      HIV4.7% (6/127)5.6% (3/54)0.81
      Smoker0.065
       Never smoker73.8% (93/126)58.8% (30/51)
       Former smoker22.2% (28/126)39.2% (20/51)
       Current smoker4.0% (5/126)2.0% (1/51)
      Abbreviations: SBP, systolic blood pressure; DBP, diastolic blood pressure; MAP, mean arterial pressure; RR, respiratory rate; SIRS, systematic inflammatory response syndrome; ACEI, angiotensin converting enzyme inhibitor; ARB, angiotensin receptor blocker; DM, diabetes mellitus; COPD, chronic obstructive pulmonary disease; CVA, cerebrovascular accident; PVD, peripheral vascular disease; CKD, chronic kidney disease; CAD, coronary artery disease; PCI, percutaneous coronary intervention; CABG, coronary artery bypass grafting; PE/DVT, pulmonary embolism/deep vein thrombosis; AF, atrial fibrillation; CHF, congestive heart failure; HIV, human immunodeficiency virus.
      Table 2 describes baseline laboratory, ECG and radiographic findings. The cardiac injury group had significantly higher blood urea nitrogen, creatinine, creatine kinase, brain natriuretic peptide, D-dimer and inflammatory markers such as procalcitonin and interleukin-6, and lower haemoglobin compared to the no cardiac injury group (all p-value <0.05). Electrocardiograph was obtained in 95.6% of individuals. Electrocardiograph findings including T wave inversion and ST depression appeared numerically more frequent in the cardiac injury group but were not statistically significantly different (cardiac injury group versus no cardiac injury group; T wave inversion: 13.2% versus 7.5%, p=0.23; ST depression: 1.9% versus 0.0%, p=0.13). There was no significant difference of multifocal pneumonia on chest X-ray in both groups (cardiac injury group versus no cardiac injury group: 56.6% versus 59.3%, p=0.73).
      Table 2Baseline laboratory findings.
      No Cardiac Injury Group N=127Cardiac Injury Group N=54P-value
      Complete blood count
       White blood cell, K/μL7.0 [4.9, 9.2]7.5 [5.5, 10.2]0.28
       Neutrophil, K/μL5.2 [3.3, 7.1]5.5 [3.9, 7.2]0.31
       Lymphocyte, K/μL1.0 [0.8, 1.4]0.80 [0.63, 1.38]0.076
       Haemoglobin, g/dL14.1 [13.1, 15.2]12.6 [11.0, 13.6]<0.001
       Platelet, K/μL177 [133, 233]148 [123, 171]0.005
      Biochemistry panel
       Glucose, mg/dL116 [99, 149]122 [103.8, 154]0.50
       BUN, mg/dL15 [11, 22]26 [17.8, 43]<0.001
       Creatinine, mg/dL0.9 [0.71, 1.13]1.41 [0.9, 2.16]<0.001
       AST, U/L41.5 [28, 60.3]44 [27, 68]0.82
       ALT, U/L31.5 [19.3, 49.8]26 [19, 44.5]0.25
       Total bilirubin, mg/dL0.5 [0.4, 0.7]0.6 [0.4, 0.9]0.030
       Albumin, g/dL3.4 [3.1, 3.7]3.2 [2.8, 3.6]0.003
       LDH, U/L374 [271, 509]409 [380, 545]0.15
       CPK, U/L174 [65, 376]140 [69, 441]0.83
       Coagulation
      PT-INR1.0 [1.0, 1.1]1.1 [1.0, 1.3]0.004
      APTT (s)31.4 [28.4, 36.2]33.3 [29.6, 38.4]0.27
      D-dimer, μg/mL0.82 [0.58, 1.33]2.03 [0.97, 3.08]<0.001
       Inflammation marker
      CRP or hsCRP, mg/L70.7 [37.8, 141]99.3 [42.8, 167]0.21
      Procalcitonin, ng/mL0.11 [0.05, 0.24]0.42 [0.11, 0.74]<0.001
      Ferritin, ng/mL525 [303, 1,315]670 [253, 1,428]0.66
      IL-6, pg/L47.1 [22.1, 110]87.9 [48.0, 140]0.020
      Others
       pH (venous blood gas)7.41 [7.38, 7.44]7.40 [7.33, 7.42]0.026
       Lactate, mmol/L1.31 [1.08, 1.80]1.50 [1.15, 1.95]0.11
       BNP, pg/mL13.6 [10.0, 40.4]191 [78, 720]<0.001
       Troponin I, ng/mL0.01 [0.01, 0.01]0.096 [0.059, 0.14]<0.001
      ECG
       AF1.7% (2/119)13.2% (7/53)0.002
       PAC2.5% (3/120)5.7% (3/53)0.30
       PVC0.0% (0/120)13.2% (7/53)<0.001
       CRBBB3.3% (4/120)11.3% (6/53)0.038
       CLBBB0.8% (1/120)3.8% (2/53)0.172
       TWI7.5% (9/120)13.2% (7/53)0.23
      TWI inferior0.8% (1/120)3.8% (2/53)0.17
      TWI anterior5.8% (7/120)1.9% (1/53)0.26
      TWI lateral1.7% (2/120)7.5% (4/53)0.051
      TWI apex0.0% (0/120)5.7% (3/53)0.009
       Upright T wave in aVR0.0% (0/120)0.0% (0/53)-
       ST depression0.0% (0/120)1.9% (1/53)0.13
       ST elevation in aVR0.0% (0/120)0.0% (0/53)-
      Chest X-ray96.9% (123/127)98.1% (53/54)1.00
       Multifocal pneumonia59.3% (73/123)56.6% (30/53)0.73
       Pleural effusion4.1% (5/123)17.0% (9/53)0.006
      Abbreviations: BUN, blood urea nitrogen; AST, aspartate aminotransferase; ALT, alanine aminotransferase; LDH, lactate dehydrogenase; CPK, creatine kinase; PT-INR, prothrombin time-international normalised ratio; APTT, activated partial thromboplastin time; CRP, C-reactive protein; hsCRP, high sensitivity C-reactive protein; IL-6, interleukin-6; BNP, B type natriuretic peptide; ECG, electrocardiogram; AF, atrial fibrillation; CRBBB, complete right bundle branch block; CLBBB, complete left bundle branch block; PAC, premature atrial contraction; PVC, premature ventricular contraction; TWI, T wave inversion.
      Table 3 shows in-hospital treatment and outcomes. 32.1% of patients in the cardiac injury group required invasive mechanical ventilation (18.2% of total cohort). The cardiac injury group had significantly higher in-hospital mortality than the no cardiac injury group (42.3% versus 12.6%, p<0.001). Only one patient died with ventricular fibrillation/pulseless ventricular tachycardia in the overall group (4.5% of deceased patients among cardiac injury, 1.9% of cardiac injury).
      Table 3In-hospital treatment and outcomes.
      No Cardiac Injury Group N=127Cardiac Injury Group N=54P-value
      ICU stay23.6% (30/127)40.7% (22/54)0.020
      Hydroxychloroquine86.6% (110/127)83.3% (45/54)0.57
      Azithromycin66.1% (84/127)63.0% (34/54)0.68
      Steroids29.9% (38/127)29.6% (16/54)0.97
      Vasopressor10.2% (13/127)20.8% (11/53)0.058
      Dobutamine1.6% (2/127)3.8% (2/53)0.36
      Milrinone0.8% (1/127)0.0% (0/53)0.52
      Oxygen69.3% (88/127)81.1% (43/53)0.10
       NPPV2.4% (3/127)9.4% (5/53)0.036
       IMV12.6% (16/127)32.1% (17/53)0.002
      New initiation of dialysis1.6% (2/125)7.7% (4/52)0.041
      Liver failure0.8% (1/127)1.9% (1/53)0.52
      Cardiac catheterisation0.0% (0/127)1.9% (1/53)0.12
      VF/Pulseless VT0.0% (0/127)1.9% (1/53)0.12
      CPR3.1% (4/127)13.2% (7/53)0.010
      Length of stay6 [4, 11]8 [4.5, 15]0.13
      In-hospital mortality12.7% (16/126)42.3% (22/52)<0.001
      Abbreviations: ICU, intensive care unit; NPPV, noninvasive positive pressure ventilation; IMV, invasive mechanical ventilator; VT, ventricular tachycardia; STEMI, ST elevation myocardial infarction; VF, ventricular fibrillation; CPR, cardiopulmonary resuscitation.
      The multivariate logistic regression analysis with stepwise method was performed with age, cardiac injury, hypertension, diabetes mellitus, history of coronary artery disease, congestive heart failure, peripheral vascular disease, cerebrovascular disease, chronic obstructive pulmonary disease, and end-stage renal disease on dialysis as variables. The final variables were age and cardiac injury. Age (odds ratio (OR) [95% confidence interval (CI)]: 1.033 [1.002–1.065], p=0.034) and cardiac injury (3.25 [1.40–7.54], p=0.006) were both independent predictors of in-hospital mortality.

      Discussion

      The salient findings of this cohort study are the following: 1) the cardiac injury group had higher rates of prior cardiac history as compared to the no cardiac injury group and also had higher inflammatory markers and D-dimer; 2) the cardiac injury group had a relatively low proportion of chest pain and ECG abnormality such as T wave inversion and ST depression; and 3) the cardiac injury group had a mortality rate of 42.3% and cardiac injury was an independent predictor of in-hospital mortality.
      As of 12 April 2020, New York City has been named the epicentre of the COVID-19 global pandemic and better understanding of the disease was highly desired [
      • Tanne J.H.
      Covid-19: New York City deaths pass 1000 as Trump tells Americans to distance for 30 days.
      ]. Most of the initial clinical data of COVID-19 came from China, including those regarding cardiac injury, which may not be applicable to a population with different ethnic and social backgrounds. In our study, the cardiac injury group was more likely to have a history of cardiovascular disease, similar to a prior study by Guo et al. [
      • Guo T.
      • Fan Y.
      • Chen M.
      • Wu X.
      • Zhang L.
      • He T.
      • et al.
      Cardiovascular implications of fatal outcomes of patients with coronavirus disease 2019 (COVID-19).
      ]. That study also revealed that the cardiac injury group had a higher rate of coronary artery disease, and that a combination of cardiovascular disease and cardiac injury was associated with greater mortality. Our study validates that cardiac injury is a predictor of in-hospital mortality even in a diverse multi-racial population. Several studies have reported the association of elevated troponin and poor outcomes in patients with COVID-19 [
      • Lala A.
      • Johnson K.W.
      • Januzzi J.L.
      • Russak A.J.
      • Paranjpe I.
      • Richter F.
      • et al.
      Prevalence and impact of myocardial injury in patients hospitalized with COVID-19 infection.
      ], but there have not been robust reports of ECG findings to our knowledge. Our study contained a detailed analysis of presenting symptoms and ECG findings, and did not show statistically significant difference in presence of chest pain or ECG changes; although T wave inversion and ST depression appeared numerically more frequent in the cardiac injury group. The small sample may have failed to show an increase in large vessel coronary artery disease and ischaemia, but this result suggests that cardiac injury with COVID-19 may be from other mechanisms. For instance, there are reports of myocarditis caused by direct myocardial invasion by SARS-CoV-2 and of takotsubo cardiomyopathy [
      • Inciardi R.M.
      • Lupi L.
      • Zaccone G.
      • Italia L.
      • Raffo M.
      • Tomasoni D.
      • et al.
      Cardiac involvement in a patient with coronavirus disease 2019 (COVID-19).
      ,
      • Cizgici A.Y.
      • Zencirkiran Agus H.
      • Yildiz M.
      COVID-19 myopericarditis: it should be kept in mind in today's conditions.
      ,
      • Tavazzi G.
      • Pellegrini C.
      • Maurelli M.
      • Belliato M.
      • Sciutti F.
      • Bottazzi A.
      • et al.
      Myocardial localization of coronavirus in COVID-19 cardiogenic shock.
      ,
      • Minhas A.S.
      • Scheel P.
      • Garibaldi B.
      • Liu G.
      • Horton M.
      • Jennings M.
      • et al.
      Takotsubo syndrome in the setting of COVID-19.
      ]; also, cytokine storm caused by systemic inflammation leading to coagulopathy, which may contribute to thrombus formation and ischaemia in microcoronary circulation [
      • Deng Q.
      • Hu B.
      • Zhang Y.
      • Wang H.
      • Zhou X.
      • Hu W.
      • et al.
      Suspected myocardial injury in patients with COVID-19: evidence from front-line clinical observation in Wuhan, China.
      ].
      There are several limitations in our study. This study was conducted in a single centre hospital with a relatively small sample size with approximately 80% of total consecutive hospitalised patients with a measurement of troponin I. Despite adjustment, we could not eliminate all unmeasured confounding factors. Moreover, higher rates of chronic kidney disease in cardiac injury group might affect elevation of troponin I [
      • Pang L.
      • Wang Z.
      • Zhao Z.L.
      • Guo Q.
      • Huang C.W.
      • Du J.L.
      • et al.
      Associations between estimated glomerular filtration rate and cardiac biomarkers.
      ]. Nonetheless, our study shows detailed information regarding symptoms and ECG abnormalities among patients with COVID-19.

      Conclusion

      Patients with COVID-19 with elevated troponin I had relatively low proportion of chest pain and ECG abnormality, which might suggest cardiac injury is just a reflection of systemic inflammation and coagulopathy due to COVID-19. Cardiac injury was an independent predictor of in-hospital mortality.

      Disclosures

      There are no conflicts of interest to disclose.

      Funding Sources

      None.

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