Moment-by-moment reports exhibit the pandemic outbreak of new emerging coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which leads to over 4.55 million deaths worldwide. 1 There is no doubt that different cell types, particularly type II pneumocytes, with the ability to express transmembrane receptors, so-called angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2), are at the centre of a SARS-COV-2 attack (Figure 1A). 2,3 Considering the relatively high expression levels of ACE2 and TMPRSS2 in cardiomyocytes, it should come as no surprise that a significant proportion of the COVID-19 mortality is associated with cardiovascular disease (CVD), in which morbidity and mortality rates can increase in individuals with a history of cardiovascular (CV) co-morbidities. 4 In this sense, Razeghian-Jahromi et al. also emphasized the importance