Institute of Cardiology, Department of Medical and Surgical Specialties, Radiological Sciences, and Public Health, University of Brescia, Brescia, Italy.
Institute of Radiology, Department of Medical and Surgical Specialties, Radiological Sciences, and Public Health, University of Brescia, Brescia, Italy.
JAMA Cardiol. 2020 Jul 1;5(7):819-824. doi: 10.1001/jamacardio.2020.1096.
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.
DESIGN, SETTING, AND PARTICIPANT: 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.
病毒感染已被广泛描述为心肌炎最常见的原因之一。然而,对于严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)感染作为并发症导致的心脏受累,人们知之甚少。
描述一名患有 2019 年冠状病毒病(COVID-19)的患者出现急性心肌炎症的表现,该患者从流感样综合征中康复,在上呼吸道症状出现一周后出现疲劳和心力衰竭的体征和症状。
设计、地点和参与者:本病例报告描述了一名 53 岁健康女性,她的 COVID-19 检测呈阳性,并于 2020 年 3 月因急性心肌心包炎和收缩功能障碍被收入心脏监护病房,这是在 COVID-19 出现发热和干咳后一周通过心脏磁共振成像(CMR)证实的。在整个临床过程中,该患者没有任何呼吸道受累的迹象。
COVID-19 导致的心脏受累。
通过 N 末端脑钠肽前体(NT-proBNP)和高敏肌钙蛋白 T 水平升高、超声心动图变化以及 CMR 上弥漫性双心室心肌水肿和晚期钆增强检测到心脏受累。
一名健康的 53 岁白人女性因严重疲劳到急诊就诊。她描述说,一周前出现发热和干咳。她体温正常但血压低;心电图显示弥漫性 ST 段抬高,检测到高敏肌钙蛋白 T 和 NT-proBNP 水平升高。胸部 X 线检查结果正常。冠状动脉造影未发现阻塞性冠状动脉疾病。根据 COVID-19 疫情,进行了鼻咽拭子检测,实时逆转录-聚合酶链反应(RT-PCR)检测 SARS-CoV-2 呈阳性。CMR 显示心室壁增厚,弥漫性双心室运动功能减退,尤其是心尖段,左心室收缩功能严重受损(左心室射血分数为 35%)。短tau反转恢复(short tau inversion recovery,STIR)和 T2 映射序列显示双心室心肌间质水肿明显,整个双心室壁均有弥漫性晚期钆增强。心包周围有环形心包积液,主要围绕右心腔。所有这些发现均与急性心肌炎一致。她接受了多巴酚丁胺、抗病毒药物(洛匹那韦/利托那韦)、皮质类固醇、氯喹和心力衰竭的药物治疗,临床和仪器状况逐渐稳定。
本病例强调了 COVID-19 可导致心脏受累,即使没有间质性肺炎的症状和体征也是如此。