Mechanism of Cardiac Pathogenesis and Cardiotoxicity of Anti- COVID-19 Drugs

(E-pub Ahead of Print)

Author(s): Ashif Iqubal, Farazul Hoda, Abul Kalam Najmi, Syed Ehtaishamul Haque*

Journal Name: Coronaviruses
The World's First International Journal Dedicated to Coronaviruses


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Abstract:

Novel coronavirus (nCoV-19) infection has been declared epidemic by the WHO. More than 223 countries are under the attack of this emergency situation. Primarily, pneumocytes encountered by the nCoV-19 via ACE-2 receptor causes pulmonary edema, damage to alveolar cells, production of inflammatory cells and hypoxia. It has been found that patients with co-existing cardiovascular diseases are more prone towards infection and severe cardiovascular dysfunction was further observed when infected with nCoV-19. There is no substantial mechanism available for the pathogenesis of this cardiovascular dysfunction, therefore, we herein, present a possible mechanistic approach of cardio-toxicity by nCov-19 infection.This hypothesis is based on immunopathology of nCoV-19 in pneumocytes, presence of ACE-2 on cardiomyocytes membrane, cytokine storm, genomic analysis of virus in cardiac tissue and several reports published on the cardiovascular complications in nCoV-19 across the globe. We have also analyzed the cardio toxic profile of recently used repurposed and investigational drugs and highlighted their possible cardiotoxic consequences and drug interactions with cardiovascular medicines, such as statins and anti-coagulants.

Keywords: COVID-19, cardiac complications, cytokine storm, pneumocytes, immunopathology, inflammation, cardiac troponin T and ACE-2 receptor

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(E-pub Ahead of Print)
DOI: 10.2174/2666796701999201222113227

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