In patients with coronavirus disease 2019 (COVID-19), myocardial injury is prevalent and is associated with an adverse prognosis and increased mortality. This finding comes from two retrospective studies involving cohorts of patients from New York, USA, and Sichuan, China.

A total of 2,736 patients with laboratory-confirmed COVID-19 were admitted to one of five hospitals in the Mount Sinai Health System in New York between 27 February and 12 April 2020 and had their plasma level of troponin I measured within 24 h of hospital admission. Overall, 36% of patients had a troponin I level greater than the normal level (defined as 30 pg/ml), and elevated troponin I levels were associated with a higher prevalence of cardiovascular disease. Mildly elevated troponin I levels (30–90 pg/ml), indicative of small amounts of myocardial injury, were associated with an increased risk of death (HR 1.75, 95% CI 1.37–2.24, P < 0.001). This risk was further increased (HR 3.03, 95% CI 2.42–3.80, P < 0.001) in patients with a marked elevation in troponin I levels (>90 pg/ml).

Similarly, in a study of 101 patients admitted to one of two designated COVID-19 treatment centres in Sichuan between 16 January and 10 March 2020, 15.8% had a plasma troponin I level greater than the normal upper limit (14 pg/ml), indicative of acute myocardial injury. These patients had a higher prevalence of pre-existing cardiovascular disease and were more likely to require admission to an intensive care unit and mechanical ventilation.

Hypothesized mechanisms of myocardial injury in patients with COVID-19 include myocarditis related to the SARS-CoV-2 infection, systemic release of inflammatory cytokines, coronary microvascular damage from thrombosis, direct entry of the virus into myocardial cells via ACE2 receptors, hypoxaemia and acute coronary syndrome owing to destabilized atheromas.