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      ST-Segment Elevation in Patients with Covid-19 — A Case Series

      letter
      , M.D., M.H.A. , , M.D., , M.D. , M.D. , M.D. , M.D. , M.D. , M.D. , M.D. , M.D. , M.D. , M.D., , M.D. , M.D. , M.D.
      The New England Journal of Medicine
      Massachusetts Medical Society
      Keyword part (code): 10Keyword part (keyword): Emergency MedicineKeyword part (code): 10_1Keyword part (keyword): Emergency Medicine General , 10, Emergency Medicine, Keyword part (code): 10_1Keyword part (keyword): Emergency Medicine General, 10_1, Emergency Medicine General, Keyword part (code): 14Keyword part (keyword): CardiologyKeyword part (code): 14_4Keyword part (keyword): Coronary Disease/Myocardial Infarction , 14, Cardiology, Keyword part (code): 14_4Keyword part (keyword): Coronary Disease/Myocardial Infarction, 14_4, Coronary Disease/Myocardial Infarction, Keyword part (code): 18Keyword part (keyword): Infectious DiseaseKeyword part (code): 18_6Keyword part (keyword): Viral Infections , 18, Infectious Disease, Keyword part (code): 18_6Keyword part (keyword): Viral Infections, 18_6, Viral Infections

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          Abstract

          To the Editor: Myocardial injury with ST-segment elevation has been observed in patients with coronavirus disease 2019 (Covid-19). Here, we describe our experience in the initial month of the Covid-19 outbreak in New York City. Patients with confirmed Covid-19 who had ST-segment elevation on electrocardiography were included in the study from six New York hospitals. Patients with Covid-19 who had nonobstructive disease on coronary angiography or had normal wall motion on echocardiography in the absence of angiography were presumed to have noncoronary myocardial injury. We identified 18 patients with Covid-19 who had ST-segment elevation indicating potential acute myocardial infarction (Fig. S1 in the Supplementary Appendix, available with the full text of this letter at NEJM.org). The median age of the patients was 63 years, 83% were men, and 33% had chest pain around the time of ST-segment elevation (Table 1). A total of 10 patients (56%) had ST-segment elevation at the time of presentation, and the other 8 patients had development of ST-segment elevation during hospitalization (median, 6 days) (Fig. S2A). Of 14 patients (78%) with focal ST-segment elevation, 5 (36%) had a normal left ventricular ejection fraction, of whom 1 (20%) had a regional wall-motion abnormality; 8 patients (57%) had a reduced left ventricular ejection fraction, of whom 5 (62%) had regional wall-motion abnormalities. (One patient did not have an echocardiogram.) Of the 4 patients (22% of the overall population) with diffuse ST-segment elevation, 3 (75%) had a normal left ventricular ejection fraction and normal wall motion; 1 patient had a left ventricular ejection fraction of 10% with global hypokinesis. A total of 9 patients (50%) underwent coronary angiography; 6 of these patients (67%) had obstructive disease, and 5 (56%) underwent percutaneous coronary intervention (1 after the administration of fibrinolytic agents) (Fig. S3). The relationship among electrocardiographic, echocardiographic, and angiographic findings are summarized in Figure S4. The 8 patients (44%) who received a clinical diagnosis of myocardial infarction had higher median peak troponin and d-dimer levels than the 10 patients (56%) with noncoronary myocardial injury (Fig. S2B and S2C). A total of 13 patients (72%) died in the hospital (4 patients with myocardial infarction and 9 with noncoronary myocardial injury). In this series of patients with Covid-19 who had ST-segment elevation, there was variability in presentation, a high prevalence of nonobstructive disease, and a poor prognosis. Half the patients underwent coronary angiography, of whom two thirds had obstructive disease. Of note, all 18 patients had elevated d-dimer levels. In contrast, in a previous study involving patients who presented with ST-segment elevation myocardial infarction, 64% had normal d-dimer levels. 1 Myocardial injury in patients with Covid-19 could be due to plaque rupture, cytokine storm, hypoxic injury, coronary spasm, microthrombi, or direct endothelial or vascular injury. 2 Myocardial interstitial edema has been shown on magnetic resonance imaging in such patients. 3

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          Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19)

          What are the cardiac complications associated with the emerging outbreak of coronavirus disease 2019 (COVID-19)? In this case report, an otherwise healthy 53-year-old patient developed acute myopericarditis with systolic dysfunction confirmed on cardiac magnetic resonance imaging a week after onset of fever and dry cough due to COVID-19. The patient was treated with inotropic support, antiviral drugs, corticosteroids, and chloroquine, with progressive stabilization of the clinical course. The emerging outbreak of COVID-19 can be associated with cardiac involvement, even after the resolution of the upper respiratory tract infection. This case report describes the presentation of acute myocardial inflammation in a patient with coronavirus disease 2019 (COVID-19) who recovered from influenzalike syndrome and developed fatigue and signs and symptoms of heart failure a week after upper respiratory tract symptoms. Virus infection has been widely described as one of the most common causes of myocarditis. However, less is known about the cardiac involvement as a complication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. To describe the presentation of acute myocardial inflammation in a patient with coronavirus disease 2019 (COVID-19) who recovered from the influenzalike syndrome and developed fatigue and signs and symptoms of heart failure a week after upper respiratory tract symptoms. This case report describes an otherwise healthy 53-year-old woman who tested positive for COVID-19 and was admitted to the cardiac care unit in March 2020 for acute myopericarditis with systolic dysfunction, confirmed on cardiac magnetic resonance imaging, the week after onset of fever and dry cough due to COVID-19. The patient did not show any respiratory involvement during the clinical course. Cardiac involvement with COVID-19. Detection of cardiac involvement with an increase in levels of N-terminal pro–brain natriuretic peptide (NT-proBNP) and high-sensitivity troponin T, echocardiography changes, and diffuse biventricular myocardial edema and late gadolinium enhancement on cardiac magnetic resonance imaging. An otherwise healthy 53-year-old white woman presented to the emergency department with severe fatigue. She described fever and dry cough the week before. She was afebrile but hypotensive; electrocardiography showed diffuse ST elevation, and elevated high-sensitivity troponin T and NT-proBNP levels were detected. Findings on chest radiography were normal. There was no evidence of obstructive coronary disease on coronary angiography. Based on the COVID-19 outbreak, a nasopharyngeal swab was performed, with a positive result for SARS-CoV-2 on real-time reverse transcriptase–polymerase chain reaction assay. Cardiac magnetic resonance imaging showed increased wall thickness with diffuse biventricular hypokinesis, especially in the apical segments, and severe left ventricular dysfunction (left ventricular ejection fraction of 35%). Short tau inversion recovery and T2-mapping sequences showed marked biventricular myocardial interstitial edema, and there was also diffuse late gadolinium enhancement involving the entire biventricular wall. There was a circumferential pericardial effusion that was most notable around the right cardiac chambers. These findings were all consistent with acute myopericarditis. She was treated with dobutamine, antiviral drugs (lopinavir/ritonavir), steroids, chloroquine, and medical treatment for heart failure, with progressive clinical and instrumental stabilization. This case highlights cardiac involvement as a complication associated with COVID-19, even without symptoms and signs of interstitial pneumonia.
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            Myocardial localization of coronavirus in COVID‐19 cardiogenic shock

            Abstract We describe the first case of acute cardiac injury directly linked to myocardial localization of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) in a 69‐year‐old patient with flu‐like symptoms rapidly degenerating into respiratory distress, hypotension, and cardiogenic shock. The patient was successfully treated with venous‐arterial extracorporeal membrane oxygenation (ECMO) and mechanical ventilation. Cardiac function fully recovered in 5 days and ECMO was removed. Endomyocardial biopsy demonstrated low‐grade myocardial inflammation and viral particles in the myocardium suggesting either a viraemic phase or, alternatively, infected macrophage migration from the lung.
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              Is Open Access

              D-Dimer Levels Predict Myocardial Injury in ST-Segment Elevation Myocardial Infarction: A Cardiac Magnetic Resonance Imaging Study

              Objectives Elevated D-dimer levels on admission predict prognosis in patients undergoing primary percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI), but the association of D-dimer levels with structural markers of myocardial injury in these patients is unknown. Methods We performed cardiac magnetic resonance (CMR) imaging in 208 patients treated with primary PCI for STEMI. CMR was performed a median of 3 days after the index procedure. Of the 208 patients studied, 75 patients had D-dimer levels above the normal range on admission (>0.5 μg/mL; high D-dimer group) while 133 had normal levels (≤0.5 μg/mL; low D-dimer group). The primary outcome was myocardial infarct size assessed by CMR. Secondary outcomes included area at risk (AAR), microvascular obstruction (MVO) area, and myocardial salvage index (MSI). Results In CMR analysis, myocardial infarct size was larger in the high D-dimer group than in the low D-dimer group (22.3% [16.2–30.5] versus 18.8% [10.7–26.7]; p = 0.02). Compared to the low D-dimer group, the high D-dimer group also had a larger AAR (38.1% [31.7–46.9] versus 35.8% [24.2–45.3]; p = 0.04) and a smaller MSI (37.7 [28.2–46.9] versus 47.1 [33.2–57.0]; p = 0.01). In multivariate analysis, high D-dimer levels were significantly associated with larger myocardial infarct (OR 2.59; 95% CI 1.37–4.87; p<0.01) and lower MSI (OR 2.62; 95% CI 1.44–4.78; p<0.01). Conclusions In STEMI patients undergoing primary PCI, high D-dimer levels on admission were associated with a larger myocardial infarct size, a greater extent of AAR, and lower MSI, as assessed by CMR data. Elevated initial D-dimer level may be a marker of advanced myocardial injury in patients treated with primary PCI for STEMI.
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                Author and article information

                Journal
                N Engl J Med
                N. Engl. J. Med
                nejm
                The New England Journal of Medicine
                Massachusetts Medical Society
                0028-4793
                1533-4406
                17 April 2020
                : NEJMc2009020
                Affiliations
                New York University Grossman School of Medicine, New York, NY sripalbangalore@ 123456gmail.com
                New York City Health and Hospitals–Elmhurst, New York, NY
                New York University Grossman School of Medicine, New York, NY
                VA New York Harbor Healthcare System, New York, NY
                New York University Grossman School of Medicine, New York, NY
                St. Francis Hospital, Roslyn, NY
                New York University Grossman School of Medicine, New York, NY
                New York City Health and Hospitals–Bellevue, New York, NY
                Brookdale University Hospital and Medical Center, New York, NY
                New York University Grossman School of Medicine, New York, NY
                New York City Health and Hospitals–Bellevue, New York, NY
                New York University Grossman School of Medicine, New York, NY
                Article
                NJ202004173820006
                10.1056/NEJMc2009020
                7182015
                32302081
                e755cf1f-7037-4578-a134-f8ad16eaebaa
                Copyright © 2020 Massachusetts Medical Society. All rights reserved.

                This article is made available via the PMC Open Access Subset for unrestricted re-use, except commercial resale, and analyses in any form or by any means with acknowledgment of the original source. These permissions are granted for the duration of the Covid-19 pandemic or until revoked in writing. Upon expiration of these permissions, PMC is granted a license to make this article available via PMC and Europe PMC, subject to existing copyright protections.

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