RT Journal Article SR Electronic T1 COVID-19 pandemic and troponin: indirect myocardial injury, myocardial inflammation or myocarditis? JF Heart JO Heart FD BMJ Publishing Group Ltd and British Cardiovascular Society SP 1127 OP 1131 DO 10.1136/heartjnl-2020-317186 VO 106 IS 15 A1 Massimo Imazio A1 Karin Klingel A1 Ingrid Kindermann A1 Antonio Brucato A1 Francesco Giuseppe De Rosa A1 Yehuda Adler A1 Gaetano Maria De Ferrari YR 2020 UL http://heart.bmj.com/content/106/15/1127.abstract AB The initial mechanism for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection is the binding of the virus to the membrane-bound form of ACE2, which is mainly expressed in the lung. Since the heart and the vessels also express ACE2, they both could become targets of the virus. However, at present the extent and importance of this potential involvement are unknown. Cardiac troponin levels are significantly higher in patients with more severe infections, patients admitted to intensive care units or in those who have died. In the setting of COVID-19, myocardial injury, defined by an increased troponin level, occurs especially due to non-ischaemic myocardial processes, including severe respiratory infection with hypoxia, sepsis, systemic inflammation, pulmonary thrombosis and embolism, cardiac adrenergic hyperstimulation during cytokine storm syndrome, and myocarditis. At present, there are limited reports on definite diagnosis of myocarditis caused by SARS-CoV-2 in humans and limited demonstration of the virus in the myocardium. In conclusion, although the heart and the vessels are potential targets in COVID-19, there is currently limited evidence on the direct infection of the myocardium by SARS-CoV-2. Additional pathological studies and autopsy series will be very helpful to clarify the potentiality of COVID-19 to directly infect the myocardium and cause myocarditis.