As the COVID-19 pandemic goes on, we continue to identify the long-term complications or symptoms among patients who recovered from this infection, be it mild or severe.

 These complications are collectively recognized as “COVID-19 long-hauler syndrome”.

 It is crucial to understand the factors leading to the development of these long-term sequelae to identify, prevent and manage them using appropriate interventions.

Acute cardiac injury (ACI), marked by elevation of troponin levels in the blood over the 99th percentile, is an important phenomenon shown to occur in nearly 30% of patients admitted to the hospital with COVID-19 infection.

 ACI has been shown to be associated with an elevated risk of critical illness, increased duration of hospital stay and mortality.

 Multiple processes, both ischaemic and non-ischaemic, have been shown to contribute to the development of ACI in COVID-19 patients. The most important among them is the direct myocardial injury caused by SARS-CoV-2.

 Tavazzi et al. demonstrated direct viral infection in the interstitial cells of the myocardium on endomyocardial biopsy, accompanied by low-grade inflammation.

 But to date, there has been no demonstration of COVID-19 genome in the cardiac tissue in patients with clinical myocarditis. Other mechanisms postulated to increase myocardial injury include systemic inflammation, vascular endothelial damage, cardiomyocyte apoptosis, abnormal myocardial strain, microthrombi formation and supply-demand mismatch (Figure 1).

 The precise mechanisms of myocardial injury in patients with COVID-19 are still unclear. It is also unknown if the myocardial injury is a direct effect of the virus or a response to systemic inflammation or both.