ID-19 and consequently the exact pathophysiological mechanisms of myocardial injury secondary to COVID-19 remain elusive. However, direct damage by the virus, exaggerated uncontrolled inflammatory responses, instability of coronary plaques, thrombosis and hypoxia have been proposed as possible mechanisms (Guo et al., 2020; Zheng et al., 2020; Zhou, Yu, et al., 2020). Importantly, the severity of infection, patient characteristics and host reaction all partici