Abstract

ACUTE CORONARY SYNDROME AS A POST-COVID-19 COMPLICATION: A REVIEW ON ITS PREVALENCE, POTENTIAL MECHANISMS, AND TREATMENT

Priyanka Sri Betha*, Amrutha Valli Dasari, Tabitha Sharon, Kantamaneni Padmalatha

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Abstract

Coronavirus disease (COVID-19) is a major medical concern worldwide. The lung infection and respiratory failure that are linked to SARS-CoV-2 can result in considerable mortality and morbidity. Moreover, it has a similar inflammatory effect on different organ systems. The S proteins bind through the S1 subunit to angiotensinconverting enzyme 2 (ACE2) expressed on host cells, but merely binding to ACE2 is not sufficient for cell infection.22 Viral cell entry requires the transmembrane serine protease 2 (TMPRSS2) expressed on host cells to perform critical protein priming that leads to conformational changes, viral cell entry, and cell infection. Several COVID-19 individuals have been documented to have acute coronary syndrome (ACS). Even though the underlying pathophysiology is yet unknown. The most well-known mechanisms include oxygen supply/demand imbalance, endothelial dysfunction, prothrombotic activation of the coagulation cascade, and systemic inflammatory response mediated by cytokines. In addition, viral respiratory infections have been linked to a higher risk of MI due to gene expression that is prone to stimulating platelet activation. Further in-depth research on the relationship between COVID-19 and ACS is required to see whether there is a direct causative or instigating link between them. Although many experimental therapies are used, standard therapy should be established. Acknowledging this connection could result in fresh research and ACS patient treatment alternatives.

Keywords: Covid -19, Cytokine storm, ACE -2 Receptor, inflammatory response, transmembrane serine protease 2.