新型冠状病毒肺炎心肌损伤的病理生理机制探讨

<正>新型冠状病毒肺炎(coronavirus disease 2019, COVID-19)自2019年12月爆发流行以来,截至2020年3月9日,已迅速蔓延至包括我国在内的世界99个国家和地区。全球累计确诊111 044例,累计死亡3 876例[1],成为了全球性的公众健康威胁。肺组织是新型冠状病毒的主要攻击靶器官,常见的临床症状为发热、干咳、乏力;少数伴有鼻塞、流涕、咽痛等。近期研究发现,在新型冠状病毒肺炎感染的患者中,16.7%的患者

Potential pathophysiological mechanisms underlying COVID-19-induced myocardial injury

The outbreak of coronavirus disease 2019(COVID-19) has rapidly spread to 99 countries and regions including China(update on March 9, 2020). Although patients with COVID-19 mainly manifest as pneumonia, some of them have clinical manifestations of myocardial injury. Recent histopathological results showed myocardial injury which is characterized by cardiomyocyte degeneration/necrosis, infiltration of monocytes, lymphocytes and/or neutrophils into the myocardial interstitium, endothelial cell detachment, intimal inflammation and microthrombus formation. These results indicate that the myocardium might be an important attack target of severe acute respiratory syndrome coronavirus 2(SARS-CoV-2), the virus that causes COVID-19. Therefore, investigation of the pathophysiological process of COVID-19-induced myocardial injury is of great significance to reduce the mortality and increase the cure rate of the patients. In this review, we focus on the current understanding of COVID-19-induced myocardial injury involving vasculitis and hypoxemia as well as their underlying potential mechanisms.