Department of Medical Ultrasonics, National Clinical Research Center for Infectious Disease, State Key Discipline of Infectious Disease, Shenzhen Third People's Hospital, Second Hospital Affiliated to Southern University of Science and Technology, No. 29 Bulan Road, Shenzhen, 518112, People's Republic of China.
National Clinical Research Center for Infectious Disease, State Key Discipline of Infectious Disease, Shenzhen Third People's Hospital, Second Hospital Affiliated to Southern University of Science and Technology, Shenzhen, China.
Infection. 2020 Oct;48(5):773-777. doi: 10.1007/s15010-020-01424-5. Epub 2020 Apr 10.
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.
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.
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.
新型冠状病毒病 2019(COVID-19)已被证实可导致肺炎。然而,尚未有报道称其可导致急性心肌炎或暴发性心肌炎。
一名 63 岁男性因肺炎和心脏症状入院。根据入院当天的痰检测,他被基因确认为 COVID-19 感染。他的肌钙蛋白 I(Trop I)水平升高(高达 11.37μg/L),且超声心动图显示弥漫性心肌运动障碍,左心室射血分数(LVEF)降低。白细胞介素-6 最高水平为 272.40pg/ml。床边胸部 X 光片显示典型的磨玻璃样改变,提示病毒性肺炎。引起心肌炎的病毒的实验室检测结果均为阴性。该患者符合暴发性心肌炎中国专家共识的诊断标准。接受抗病毒治疗和机械生命支持后,Trop I 降低至 0.10μg/L,白细胞介素-6 降低至 7.63pg/ml。此外,患者的 LVEF 逐渐恢复至 68%。患者在住院第 33 天因继发感染加重而死亡。
COVID-19 患者可能会发生严重的心脏并发症,如心肌炎和心力衰竭。这是首例 COVID-19 合并暴发性心肌炎的报告。COVID-19 引起的心脏病理机制需要进一步研究。