Reports suggest that the Middle East respiratory syndrome-related coronavirus (MERS-CoV) can cause acute myocarditis and heart failure5. SARS-CoV-2 and MERS-CoV have similar pathogenicity, and the myocardial damage caused by infection with these viruses undoubtedly increases the difficulty and complexity of patient treatment. Myocardial injury associated with the SARS-CoV-2 occurred in 5 of the first 41 patients diagnosed with COVID-19 in Wuhan, which mainly manifested as an increase in high-sensitivity cardiac troponin I (hs-cTnI) levels (>28 pg/ml)3. In this study, four of five patients with myocardial injury were admitted to the intensive-care unit (ICU), which indicates the serious nature of the myocardial injury in patients with COVID-19. Blood-pressure levels were significantly higher in patients treated in the ICU than in those not treated in the ICU (mean systolic blood pressure 145 mmHg versus 122 mmHg; P < 0.001)3. In another report of 138 patients with COVID-19 in Wuhan, 36 patients with severe symptoms were treated in the ICU1. The levels of biomarkers of myocardial injury were significantly higher in patients treated in the ICU than in those not treated in the ICU (median creatine kinase (CK)-MB level 18 U/l versus 14 U/l, P < 0.001; hs-cTnI level 11.0 pg/ml versus 5.1 pg/ml, P = 0.004), suggesting that patients with severe symptoms often have complications involving acute myocardial injury1. In addition, among the confirmed cases of SARS-CoV-2 infection reported by the National Health Commission of China (NHC), some of the patients first went to see a doctor because of cardiovascular symptoms. The patients presented with heart palpitations and chest tightness rather than with respiratory symptoms, such as fever and cough, but were later diagnosed with COVID-19. Among the people who died from COVID-19 reported by the NHC, 11.8% of patients without underlying CVD had substantial heart damage, with elevated levels of cTnI or cardiac arrest during hospitalization. Therefore, in patients with COVID-19, the incidence of cardiovascular symptoms is high, owing to the systemic inflammatory response and immune system disorders during disease progression.

The mechanism of acute myocardial injury caused by SARS-CoV-2 infection might be related to ACE2. ACE2 is widely expressed not only in the lungs but also in the cardiovascular system and, therefore, ACE2-related signalling pathways might also have a role in heart injury. Other proposed mechanisms of myocardial injury include a cytokine storm triggered by an imbalanced response by type 1 and type 2 T helper cells3,6, and respiratory dysfunction and hypoxaemia caused by COVID-19, resulting in damage to myocardial cells.