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Case Reports
. 2020 Oct;48(5):773-777.
doi: 10.1007/s15010-020-01424-5. Epub 2020 Apr 10.

First case of COVID-19 complicated with fulminant myocarditis: a case report and insights

Jia-Hui Zeng  1 , Ying-Xia Liu  2 , Jing Yuan  3 , Fu-Xiang Wang  3 , Wei-Bo Wu  3 , Jin-Xiu Li  4 , Li-Fei Wang  5 , Hong Gao  6 , Yao Wang  1 , Chang-Feng Dong  1 , Yi-Jun Li  1 , Xiao-Juan Xie  1 , Cheng Feng  7 , Lei Liu  8
Affiliations
Case Reports

First case of COVID-19 complicated with fulminant myocarditis: a case report and insights

Jia-Hui Zeng et al. Infection. 2020 Oct.

Abstract

Background: Coronavirus disease 2019 (COVID-19) has been demonstrated to be the cause of pneumonia. Nevertheless, it has not been reported as the cause of acute myocarditis or fulminant myocarditis.

Case presentation: A 63-year-old male was admitted with pneumonia and cardiac symptoms. He was genetically confirmed as having COVID-19 according to sputum testing on the day of admission. He also had elevated troponin I (Trop I) level (up to 11.37 g/L) and diffuse myocardial dyskinesia along with a decreased left ventricular ejection fraction (LVEF) on echocardiography. The highest level of interleukin-6 was 272.40 pg/ml. Bedside chest radiographs showed typical ground-glass changes indicative of viral pneumonia. Laboratory test results for viruses that cause myocarditis were all negative. The patient conformed to the diagnostic criteria of the Chinese expert consensus statement for fulminant myocarditis. After receiving antiviral therapy and mechanical life support, Trop I was reduced to 0.10 g/L, and interleukin-6 was reduced to 7.63 pg/mL. Moreover, the LVEF of the patient gradually recovered to 68%. The patient died of aggravation of secondary infection on the 33rd day of hospitalization.

Conclusion: COVID-19 patients may develop severe cardiac complications such as myocarditis and heart failure. This is the first report of COVID-19 complicated with fulminant myocarditis. The mechanism of cardiac pathology caused by COVID-19 needs further study.

Keywords: COVID-19; Coronavirus; Echocardiography; Fulminant myocarditis; Infection.

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Conflict of interest statement

On behalf of all authors, the corresponding author states that there are no conflicts of interest.

Figures

Fig. 1
Fig. 1
a Bedside chest radiograph on the day of admission; b, c computerized tomography on the ninth day showing typical ground-glass changes indicative of viral pneumonia
Fig. 2
Fig. 2
The line chart of the markers of myocardial injury. Trop I troponin I, MYO myoglobin, NTBNP n-terminal brain natriuretic peptide. Trop I and NTBNP decreased gradually, while no significant decrease in MYO was observed
Fig. 3
Fig. 3
The electrocardiogram showing sinus tachycardia and no ST-segment elevation
Fig. 4
Fig. 4
The echocardiographic left ventricular M-mode images on the first day, 10th day, and 17th day after admission. a The left ventricular diameter was enlarged, and the ejection fraction was decreased on first day of admission; b this figure shows edema of left ventricular wall and improvement of LVEF. c The last bedside echocardiography examination showing a normal LVEF and wall thickness. LVEF left ventricular ejection fraction
Fig. 5
Fig. 5
Line chart of the echocardiography measurements. a The patients showed thickened IVSd and enlarged LVDd during treatment. TAPSE showed a sudden decline on the 29th day, suggesting impaired right cardiac function. The IVSd gradually thickened to a maximum thickness of 14 mm. b A LVEF decrease appeared early during hospitalization and gradually returned to normal after treatment. c The PASP gradually increased as the disease progressed; however, a sudden drop in pulmonary artery pressure occurred on the 26th day. LVDd left ventricular end-diastolic diameter, IVSd interventricular septum dimension, TAPSE tricuspid annular plane systolic excursion, LVEF left ventricular ejection fraction, PASP pulmonary artery systolic pressure
See this image and copyright information in PMC

Comment in

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