Rasmi Yousef, Mosa Osama F, Alipour Shahriar, Heidari Nadia, Javanmard Farzaneh, Golchin Ali, Gholizadeh-Ghaleh Aziz Shiva
Cellular and Molecular Research Center, Urmia University of Medical Sciences, Urmia, Iran.
Department of Biochemistry, School of Medicine, Urmia University of Medical Sciences, Urmia, Iran.
Front Mol Biosci. 2022 Feb 24;9:821155. doi: 10.3389/fmolb.2022.821155. eCollection 2022.
Coronavirus disease 2019 (COVID-19) has rapidly developed as a global health emergency. Respiratory diseases are significant causes of morbidity and mortality in these patients with a spectrum of different diseases, from asymptomatic subclinical infection to the progression of severe pneumonia and subsequent acute respiratory distress syndrome. Individuals with cardiovascular disease are more likely to become infected with SARS-CoV-2 and develop severe symptoms. Hence, patients with underlying cardiovascular disease mortality rate are over three times. Furthermore, note that patients with a history of cardiovascular disease are more likely to have higher cardiac biomarkers, especially cardiac troponins, than infected patients, especially those with severe disease, making these patients more susceptible to cardiac damage caused by SARS-2-CoV. Biomarkers are important in decision-making to facilitate the efficient allocation of resources. Viral replication in the heart muscle can lead to a cascade of inflammatory processes that lead to fibrosis and, ultimately, cardiac necrosis. Elevated troponin may indicate damage to the heart muscle and may predict death. After the first Chinese analysis, increased cardiac troponin value was observed in a significant proportion of patients, suggesting that myocardial damage is a possible pathogenic mechanism leading to severe disease and death. However, the prognostic performance of troponin and whether its value is affected by different comorbidities present in COVID-19 patients are not known. This review aimed to assess the diagnostic value of troponin to offer insight into pathophysiological mechanisms and reported new assessment methods, including new biosensors for troponin in patients with COVID-19.
2019年冠状病毒病(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有一系列不同疾病患者发病和死亡的重要原因,从无症状亚临床感染到重症肺炎进展及随后的急性呼吸窘迫综合征。患有心血管疾病的个体更易感染严重急性呼吸综合征冠状病毒2(SARS-CoV-2)并出现严重症状。因此,患有基础心血管疾病的患者死亡率高出三倍多。此外,值得注意的是,有心血管疾病史的患者比感染患者,尤其是重症患者,更有可能出现更高的心脏生物标志物,特别是心肌肌钙蛋白,这使得这些患者更容易受到SARS-CoV-2所致心脏损伤的影响。生物标志物在决策过程中很重要,有助于有效分配资源。心肌中的病毒复制可引发一系列炎症过程,导致纤维化并最终导致心肌坏死。肌钙蛋白升高可能表明心肌受损,并可能预示死亡。在中国首次分析后,发现相当比例的患者心肌肌钙蛋白值升高,这表明心肌损伤可能是导致重症和死亡的一种致病机制。然而,肌钙蛋白的预后性能以及其值是否受COVID-19患者存在的不同合并症影响尚不清楚。本综述旨在评估肌钙蛋白的诊断价值,以深入了解病理生理机制,并报告新的评估方法,包括用于COVID-19患者肌钙蛋白检测的新型生物传感器。