![]() Overall, these data support the hypothesis that COVID-19-associated myocardial injury can result from the direct infection of CMs and the cardiotoxic effect of SARS-CoV-2 and is not merely a secondary effect derived from hypoxia and systemic inflammation.Ī single-cell sequencing study has revealed that the expression of viral ACE2 receptors is noticeable in CMs from normal hearts and has suggested that ACE2 expression in the adult human heart is higher than that in the lung. Increasing concentrations of viral RNA were detected in the supernatants of infected CMs, and SARS-CoV-2 infection ability was confirmed in 3D cardiosphere tissue. successfully infected hiPS-derived CMs with SARS-CoV-2 and demonstrated the presence of intracellular double-strand viral RNA and viral spike glycoprotein protein expression. In addition, in vitro studies with human induced pluripotent stem cells (hiPS) and isolated adult CMs and in vivo experiments using animal models have confirmed that CMs are permissive for SARS-CoV-2 infection. Pathology reports from several studies have identified SARS-CoV-2 viral proteins and genetic material in CMs of patients with COVID-19, even in those with no clinical signs of cardiac involvement. Direct and indirect SARS-CoV-2 entry into CMs Given the rapid development of this field, in this review, we shed light on the updated mechanisms of CM impairment associated with direct SARS-CoV-2 invasion to provide a more comprehensive understanding of the cardiac manifestations in COVID-19. However, limited by insufficient evidence, myocardial injury caused by direct viral invasion of CMs was not fully understood earlier. We have previously proposed several pathogenic mechanisms explaining the association of COVID-19 with myocardial injury, including SARS-CoV-2 host cell invasion, myocardial oxygen supply/demand imbalance, abnormal coagulation, and excessive immune reaction. In addition, the long-term effects of COVID-19 on cardiovascular health are still a major global concern. Given the current convincing evidence that myocardial injury intensifies the severity of COVID-19, cardiac management should be a priority for physicians. This complication contributes to disease severity and mortality, with a hazard ratio ranging from 4.3 to 8.9 and an odds ratio from 6.6 to 26.9. According to clinical observations, increased myocardial biomarker levels unrelated to obstructive coronary artery disease, a condition generally diagnosed as myocardial injury, occurred in 7.2–40.9% of patients with COVID-19. Theoretically, cells expressing high ACE2 levels are more vulnerable to SARS-CoV-2 invasion and subsequent organ injury, including cardiomyocytes (CMs). With the COVID-19 pandemic entering the third year, the role of SARS-CoV-2 in the heart and the cardiovascular system has gained attention. obtained the trimeric S protein structure by 3D reconstruction technology based on the genomic sequence of SARS-CoV-2 and observed that the binding affinity of the S protein to ACE2 was 10–20 fold higher compared to that of SARS-CoV, partly explaining its high contagiousness. It recognizes and binds to the ACE2 receptor via the spike (S) protein. SARS-CoV-2 invades cells via angiotensin-converting enzyme 2 (ACE2), a membrane protein that counterbalances the adverse effects of the renin–angiotensin–aldosterone system (RAAS) by converting angiotensin II (Ang II) to Ang-(1–7). Although predominantly characterized by viral pneumonia, cardiac involvement could be prevalent during COVID-19 progression, which is reportedly associated with disease severity and mortality. Omicron has become the current dominant variant worldwide, including in China. ![]() Omicron’s R0 could be as high as 10, indicating a more contagious phenotype than earlier virus variants. Another new variant of the virus, Omicron, first originated in southern Africa (South Africa, Botswana) and later spread to Britain and other countries. The R0 of SARS-CoV-2 in the original strain was 2.5, whereas the number increased to approximately 7 in the delta variant (B.1.617.2). Coronavirus disease 2019 (COVID-19), a contagious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a worldwide pandemic.
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