In early December 2019, a series of cases of pneumonia emerged in Wuhan, Hubei, China. Respiratory tract samples revealed a novel coronavirus that was named 2019 novel coronavirus (2019-nCoV) and then Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), based on the clinical presentation in the symptomatic cases(1). On March 11, 2020, the World Health Organization (WHO) declared the SARS-CoV-2 outbreak a pandemic due to the increasing number of cases outside of China. Patients with SARS-CoV-2 infection can develop coronavirus disease 2019 (COVID-19), which has resulted in high rates of hospitalization and intensive care unit (ICU) admissions. According to the WHO daily report, we are facing a global pandemic with nearly all countries affected, over 5 million cases, and over 330.000 deaths. This viral outbreak is worrisome because of the enormous pressure it exerts on health and economic systems. Despite lack of understanding of the exact pathophysiological mechanisms of SARS-CoV-2, cardiac involvement appears to be a prominent feature in symptomatic patients. Furthermore, it has been demonstrated that cardiac involvement, even when subclinical, is both prevalent and a prognostic factor for affected patients(2). It has been noted that elevated cytokine levels (3,4) and hypercoagulable disorders and severe thrombo-embolic complications are frequent in patients with more severe COVID-19. It has been acknowledged that the primary infective mechanism occurs with engagement of the SARS-CoV-2 spike proteins onto the Angiotensin-converting enzyme 2 (ACE2). Therefore, it is reasonable to assume that direct myocardial involvement in COVID disease could be mediated by these receptors, particularly expressed in myocardial pericytes, which spread outside the endothelium of venules and capillaries.