The mild but persistent non-ischemic cardiac inflammation that we describe in this study was not associated with overt structural heart disease or troponin release. Although it is triggered by a viral infection, profound myocardial injury or functional impairment is not typical, contrary to the classical definition of viral myocarditis2. Its pathophysiology is more reminiscent of findings in other chronic diffuse inflammatory syndromes that occur post-virally (for example, human immunodeficiency virus–associated cardiomyopathy)3 or as a result of autoimmunity (for example, systemic lupus erythematosus4,5). In these cases, persistent subclinical cardiovascular inflammation seems to predispose people to a poor prognosis and the development of heart failure. Non-ischemic cardiac inflammatory involvement is therefore emerging as an important risk factor, and the long-term prognostic relevance of post-acute COVID-19 cardiac involvement in previously healthy people with mild initial COVID-19 illness requires further investigation.

There are some limitations to our study. Although mapping techniques provide valuable pathophysiological insights, transferability of these findings is limited by a lack of standardization and methodological variations. Furthermore, we note that these results are based on a selected population of people who had recovered from COVID-19, and thus an extrapolation of prevalence of symptoms or findings onto the general population is not possible. Although it was most likely driven by an autoimmune process, the underlying pathophysiology remains only partially understood.

Valentina Puntmann and Eike Nagel

University Hospital Frankfurt, Frankfurt am Main, Germany.