COVID-19 could Disrupt Heart Muscle Contraction

A new study from Washington University School of Medicine in St. Louis published on a preprint server provides evidence that COVID-19 patients’ heart damage is caused by the virus invading and replicating inside heart muscle cells, leading to cell death and interfering with heart muscle contraction. The researchers used stem cells to engineer heart tissue that models the human infection and could help in studying the disease and developing possible therapies.

The study showed that cardiomyocytes are the targets of SARS-Co-V-2 infection and there is a link established between the cardiomyocyte infection and the SARS-Co-V-2 with help of the Engineered Heart Tissue model. An autopsy and endomyocardial biopsy specimens from 4 subjects with SARS-Co-V-2 showing a clinical diagnosis of myocarditis were taken. Postmortem Microscopic examination of myocardium revealed areas of myocardium necrosis, degenerative of cardiomyocytes cytoplasm with mononuclear cell infiltrate.

Examination of coronary arteries from COVID19 myocarditis autopsy showed mild atherosclerotic changes which were non-obstructive. SARS-Co-V -2 spike and Nucleocapsid RNA were detected in the myocardial tissue of the subjects. Macrophage infiltration and T-cell infiltration were also noted at the site of myocardial injury. These observations suggest that SARS-Co-V -2 can infect the human heart and contribute to myocardial injury, myocardial inflammation, and cell death. Further studies were conducted to check if SARS-Co-V-2 infects and replicates within human cardiomyocytes which concluded that cardiomyocytes are targets of SARS-Co-V-2 infection. ACE 2 is preferentially expressed in cardiomyocytes and is essential for SARS-Co-V- 2 entry into the cell.

This explains the expression of ACE2 in the human heart increases the risk factor of SARS-Co-V-2 in pre-existing cardiovascular disease. The study on the engineered heart tissue also revealed a reduction in contractile force, sarcomere death, and myocarditis with macrophage activation.

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