• acute myocardial infarction
• myocardial disease

In the span of a few months, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has permeated the mindset and overshadowed priorities throughout the world. Within public health and clinical hospital systems, the persistent and surging threat of the coronavirus disease 2019 (COVID-19) pandemic dictates patient care. Concurrently, the focus of many researchers has transformed into a race against the pandemic to mitigate the spread of disease, and to recognise high-risk cohorts and characterise underlying mechanistic pathways of disease progression in efforts to discover effective treatments.

In the current study by Wei and colleagues,1 the authors evaluated a consecutive cohort of 101 patients with COVID-19, admitted between 10 January and 10 March 2020 in Sichuan, China. They found that 15.8% of the hospitalised COVID-19 cohort demonstrated elevations in high-sensitivity troponin T, which was correlated with an increased risk for adverse outcomes including mortality. This study provides a snapshot of myocardial injury in cases of COVID-19 from a region not as overwhelmed by the pandemic as Wuhan, China. With less competition for scarce resources, thresholds for hospital admission, testing and level of care likely differed considerably between the two provinces.

There is substantial variation in case fatality rates between countries, ranging from 0.3% in Germany to 8.6% in Italy.2 Although data across countries are lacking for cardiac biomarkers, rates of myocardial injury in patients with COVID-19 will likely exhibit similar variation between countries as well. To date, the majority of existing data on myocardial injury are from Wuhan—but even within the same region, reported rates of myocardial injury have varied from 7.2% to 27.8%3–7 (table 1).

Several explanations for this variability exist. The foremost lies within case ascertainment driven by testing availability. The true denominator of individuals with COVID-19 …