Myocardial injury is one of the important pathogenic features of COVID-19. As a surrogate for myocardial injury, multiple studies have shown increased cardiac biomarkers mainly cardiac troponins I and T in the infected patients especially those with severe disease. Myocarditis is depicted as another cause of morbidity amongst COVID-19 patients. The exact mechanisms of how SARS-CoV-2 can cause myocardial injury are not clearly understood. The proposed mechanisms of myocardial injury are direct damage to the cardiomyocytes, systemic inflammation, myocardial interstitial fibrosis, interferon mediated immune response, exaggerated cytokine response by Type 1 and 2 helper T cells, in addition to coronary plaque destabilization, and hypoxia. This is a 62-year-old M.K with a poorly monitored type 2 diabetes and hypertension as ATCDS who was admitted to the emergency department for syncope, a complete AVB responding to the bolus of atropine and the sternal punch. After electro systolic training probe we were able to find a regular sinus rhythm with gradual recovery of consciousness Evidence of myocardial injury is common among adults hospitalized with COVID-19. Possible causes of myocardial injury in patients with COVID-19 include myocarditis, hypoxic injury, stress (Takotsubo) cardiomyopathy, ischemic injury caused by cardiac microvascular damage or coronary artery disease, right heart strain (acute cor pulmonale) and systemic inflammatory response syndrome. COVID-19 infection has been associated with myocardial injury, which has been implicated with more severe disease courses and even death. Remarkable efforts are being done to elaborate underlying mechanisms of myocardial injury. Due to the acuteness of this pandemic, the scientific world currently lacks randomized controlled trials in order to fully elucidate the pathophysiological mechanisms and therapeutic measures.