Direct invasion of pathogens to the cardiac tissue has been confirmed in patients with severe pneumonia. For example, Streptococcus pneumoniae was identified in the myocardium of patients with severe pneumococcal disease, leading to local inflammatory reactions and consequently cardiac injury (Xu, Shi, et al., 2020). Oudit et al. reported SARS-CoV RNA was detected in 35% (7/20) of autopsied human heart samples obtained from SARS patients during the Toronto SARS outbreak, suggesting the likelihood of direct damage to cardiomyocytes by the virus (Oudit et al., 2009). In the same report, a study in mice infected with the human strain of the SARS-CoV demonstrated that pulmonary infection with SARS-CoV also precipitated myocardial infection (Oudit et al., 2009). As SARS-CoV-2 is genetically related to SARS-CoV, there is a high potential that it shares a similar mechanism and the same functional host-cell receptor, angiotensin-converting enzyme 2 (ACE2) for cell entry (Gheblawi et al., 2020). Importantly, ACE2 is highly expressed in both the heart and the lung (Patel, Zhong, Grant, & Oudit, 2016) and evidence indicates the affinity of SARS-CoV-2 to ACE2 is approximately 10- to 20-fold higher than that for SARS-CoV which may account for both the greater pathogenicity of SARS-CoV-2 and the rapid spread (Gheblawi et al., 2020; Hoffmann et al., 2020). Altogether, SARS-CoV-2 might directly infect the myocardial tissue leading to severe cardiac injury (Wu et al., 2020). However, large-scale biopsy studies are still warranted to further confirm the direct myocardial infection by SARS-CoV-2.