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

Novel coronavirus (nCoV-19) infection has been declared a pandemic by WHO. More than 223 countries are under the attack of this emergency situation. Primarily, pneumocytes encountered by the nCoV-19 via ACE-2 receptor cause 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 to the 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. The hypothesis of this study 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 cardiotoxic 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.