疑似COVID-19引起的急性病毒性心肌炎

C. Song, V. Bedi, B. C. Buragamadagu, J. Nair
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Tenderness in the left chest wall, left upper and lower extremities was elicited on physical examination. Labs obtained were significant for a creatine kinase of 37,000 IU/L and troponin I of 9.93ng/mL. EKG showed nonspecific T wave abnormalities, and prolonged QTC of 548ms. Chest x-ray showed multifocal pneumonia with no features suggestive of trauma. She was admitted to telemetry for further management of COVID-91 pneumonia and cardiac work up. Her troponin I peaked to 12.52ng/mL and she was treated with empiric intravenous heparin and aspirin. Echocardiogram shows global hypokinesis with left ventricular ejection fraction of 35-40%. Heart failure regimen with beta blocker and aldosterone receptor blocker were started. Rhabdomyolysis normalized with intravenous fluids. For COVID-19 pneumonia, she received dexamethasone and remdesivir and was weaned to 4L oxygen on discharge. 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引用次数: 0

摘要

导言:已知COVID-19病毒是细胞因子风暴和呼吸衰竭继发死亡的主要原因。其他表现包括胃肠道症状、味觉和嗅觉丧失以及血栓栓塞。我们在此报告一例疑似COVID-19引起的病毒性心肌炎,患者为86岁女性。病例介绍:86岁女性,无既往病史报告,无日常用药,跌倒后被救护车送来,数小时无法起床。入院时,她因左侧肌肉骨骼疼痛,发热,心动过速,呼吸过速,室内空气饱和度达93%而出现轻微窘迫。病人在住院期间否认胸痛。体格检查发现左胸壁、左上肢和下肢有压痛。实验结果表明,肌酸激酶为37,000 IU/L,肌钙蛋白I为9.93ng/mL。心电图显示非特异性T波异常,QTC延长548ms。胸部x线显示多灶性肺炎,无外伤征象。她接受了遥测治疗,以进一步治疗COVID-91肺炎和心脏检查。她的肌钙蛋白I峰值为12.52ng/mL,并给予经验性静脉注射肝素和阿司匹林治疗。超声心动图显示全身运动不足,左室射血分数35-40%。开始使用-受体阻滞剂和醛固酮受体阻滞剂治疗心力衰竭。横纹肌溶解经静脉输液恢复正常。因COVID-19肺炎,她接受地塞米松和瑞德西韦治疗,出院时断奶至4L吸氧。讨论:病毒性心肌炎通常是由直接的病毒损伤和随后的细胞免疫激活共同引起的。对COVID-19相关病毒性心肌炎的了解有限;大多数记录的病例来自现有病例报告,其中大多数患者为男性,年龄在70岁以下。诊断通常具有挑战性,因为在持续的大流行和感染风险增加的情况下,经常放弃心肌膜活检。病毒性心肌炎的治疗包括心衰管理,随后根据疑似病因进行定向治疗。在COVID-19的情况下,淋巴细胞性心肌炎通常涉及糖皮质激素和静脉注射免疫球蛋白的免疫抑制,尽管这些方案尚未在COVID-19相关心肌炎中进行广泛研究。由于关于这种感染的文献正在迅速发展,识别和记录疑似病例至关重要。本病例有助于确定COVID-19诱导的病毒性心肌炎的表现,促进未来的理解,并提高对这种肺外表现的认识。
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Suspected COVID-19 Induced Acute Viral Myocarditis
Introduction: COVID-19 virus has been known to be a major cause of mortality secondary to cytokine storm and respiratory failure. Other manifestations include GI symptoms, loss of taste and smell and thromboembolism. Here we introduce a case of suspected COVID-19 induced viral myocarditis in an 86 year old woman. Case presentation: An 86-year-old female with no reported past medical history, not on daily medications, was brought in by ambulance after fall and unable to get up for many hours. On presentation, she was in mild distress due to left sided musculoskeletal pain, afebrile, tachycardic, tachypneic, and saturating at 93% on room air. Patient denied chest pain throughout her hospitalization. Tenderness in the left chest wall, left upper and lower extremities was elicited on physical examination. Labs obtained were significant for a creatine kinase of 37,000 IU/L and troponin I of 9.93ng/mL. EKG showed nonspecific T wave abnormalities, and prolonged QTC of 548ms. Chest x-ray showed multifocal pneumonia with no features suggestive of trauma. She was admitted to telemetry for further management of COVID-91 pneumonia and cardiac work up. Her troponin I peaked to 12.52ng/mL and she was treated with empiric intravenous heparin and aspirin. Echocardiogram shows global hypokinesis with left ventricular ejection fraction of 35-40%. Heart failure regimen with beta blocker and aldosterone receptor blocker were started. Rhabdomyolysis normalized with intravenous fluids. For COVID-19 pneumonia, she received dexamethasone and remdesivir and was weaned to 4L oxygen on discharge. Discussion:Viral myocarditis often results from a combination of direct viral injury and subsequent cellular immune activation. There is limited knowledge for COVID-19 associated viral myocarditis;most documented cases are from existing case reports, where most patients are male, and under the age of 70 years. Diagnosis is often challenging, as endomyocardial biopsy is often forgone in the setting of the ongoing pandemic and increased infection risk. Treatment for viral myocarditis involves heart failure management followed by directed therapy based on suspected etiology. Lymphocytic myocarditis, as seen in the setting of COVID-19, would typically involve immunosuppression in the form of glucocorticoids and intravenous immunoglobulin;although these regimens have yet to be extensively studied in COVID-19 associated myocarditis. As literature on this infection is rapidly evolving, it is vital to recognize and document suspected cases. This case helps to establish presentation of COVID-19 induced viral myocarditis and facilitate future understanding and raises awareness of this extrapulmonary presentation.
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