Myocardial injury and COVID-19: Possible mechanisms
Myocardial injury and COVID-19: Possible mechanisms
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DOI：
10.1016/j.lfs.2020.117723
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发表时间：
2020-07-15
期刊：
影响因子：
6.1
通讯作者：
Amanullah, Aman
中科院分区：
文献类型：
--
作者：
Babapoor-Farrokhran, Savalan;Gill, Deanna;Amanullah, Aman
2019冠状病毒病（COVID - 19）已迅速发展成为全球卫生紧急事件。呼吸系统疾病是这些患者发病和死亡的主要原因，疾病谱从无症状的亚临床感染到进展为急性呼吸窘迫综合征的重症肺炎不等。越来越多的证据表明，新冠病毒（SARS - CoV - 2）感染在病理生理上与其他冠状病毒感染，如严重急性呼吸综合征冠状病毒和中东呼吸综合征冠状病毒（MERS - CoV）相似。血管紧张素转换酶2受体在该病毒的发病机制中起着关键作用。这种受体的破坏会导致心肌病、心功能障碍和心力衰竭。心血管疾病患者更有可能感染新冠病毒，也更有可能出现严重症状。高血压、心律失常、心肌病和冠心病是COVID - 19重症病例中常见的主要心血管疾病合并症。越来越多的文献探讨了新冠病毒感染中的心脏受累情况。心肌损伤是COVID - 19的重要致病特征之一。作为心肌损伤的替代指标，多项研究表明，感染患者尤其是重症患者的心脏生物标志物主要是心肌肌钙蛋白I和T升高。心肌炎被认为是COVID - 19患者发病的另一个原因。新冠病毒如何导致心肌损伤的确切机制尚不清楚。提出的心肌损伤机制包括对心肌细胞的直接损伤、全身炎症、心肌间质纤维化、干扰素介导的免疫反应、1型和2型辅助性T细胞过度的细胞因子反应，以及冠状动脉斑块不稳定和缺氧。
Coronavirus Disease 2019 (COVID-19) has quickly progressed to a global health emergency. Respiratory illness is the major cause of morbidity and mortality in these patients with the disease spectrum ranging from asymptomatic subclinical infection, to severe pneumonia progressing to acute respiratory distress syndrome. There is growing evidence describing pathophysiological resemblance of SARS-CoV-2 infection with other coronavirus infections such as Severe Acute Respiratory Syndrome coronavirus and Middle East Respiratory Syndrome coronavirus (MERS-CoV). Angiotensin Converting Enzyme-2 receptors play a pivotal role in the pathogenesis of the virus. Disruption of this receptor leads to cardiomyopathy, cardiac dysfunction, and heart failure. Patients with cardiovascular disease are more likely to be infected with SARS-CoV-2 and they are more likely to develop severe symptoms. Hypertension, arrhythmia, cardiomyopathy and coronary heart disease are amongst major cardiovascular disease comorbidities seen in severe cases of COVID-19. There is growing literature exploring cardiac involvement in SARS-CoV-2. Myocardial injury is one of the important pathogenic features of COVID-19. As a surrogate for myocardial injury, multiple studies have shown increased cardiac biomarkers mainly cardiac troponins I and T in the infected patients especially those with severe disease. Myocarditis is depicted as another cause of morbidity amongst COVID-19 patients. The exact mechanisms of how SARS-CoV-2 can cause myocardial injury are not clearly understood. The proposed mechanisms of myocardial injury are direct damage to the cardiomyocytes, systemic inflammation, myocardial interstitial fibrosis, interferon mediated immune response, exaggerated cytokine response by Type 1 and 2 helper T cells, in addition to coronary plaque destabilization, and hypoxia.