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Comment & Response
October 28, 2020

Cardiac Involvement After Recovering From COVID-19

Author Affiliations
  • 1Department of Cardiology, Centre hospitalier régional et universitaire de Nancy, Nancy, France
  • 2Centre hospitalier régional et universitaire de Nancy, Université de Lorraine, Nuclear Medicine and Nancyclotep Platform, Nancy, France
  • 3Université de Lorraine, INSERM, UMR-1116, Nancy, France
JAMA Cardiol. 2021;6(2):243-244. doi:10.1001/jamacardio.2020.5279

To the Editor We read with great interest the article by Puntmann et al1 on a cohort of German patients affected by coronavirus disease 2019 (COVID-19) and investigated by cardiovascular magnetic resonance (CMR) imaging. The authors’ observations are very similar to our own findings from a region of eastern France that was also severely affected by COVID-19. However, the interpretation of the results by Puntmann et al,1 particularly concerning the potential long-term persistence of myocardial inflammation, seems very alarmist, and in any case excessive, given the current state of understanding.

The most prevalent abnormality reported in the article by Puntmann et al1 was myocardial inflammation, which was predominantly characterized by moderate increases in myocardial T1 and T2. However, criteria for true myocarditis were not met on the endomyocardial biopsies obtained in a few patients with severe cardiac involvement,1 a finding that is concordant with results from previous autopsy studies.2

Moreover, rises in myocardial T2 and T1 are not specific to inflammation and may relate to a noninflammatory edema, as already documented in patients with chronic kidney disease.3 In our university hospital, myocardial extracellular volume, computed with the additional recording of postcontrast T1 sequences,4 was found to be constantly increased on CMR imaging recorded in 4 patients with a recent history of COVID-19 and presenting significant increases in blood cardiac enzymes. This fluid overload could explain the concomitant observation of small increases in myocardial T2 and T1 as well as in myocardial mass, similar to that documented in the article by Puntmann et al.1 However, in our recent experience, all these increases are much more unusual when patients are investigated during the later course of COVID-19 (this part of our study is still ongoing).

The mechanism underpinning cardiac involvement in patients with COVID-19 is currently poorly understood and surely complex. In general terms, tissue damage related to COVID-19 is not only the result of local inflammatory mechanisms but also possibly the result of vascular-related damage, such as capillary leakage and vessel thrombosis.5

The CMR imaging study by Puntmann et al1 makes a significant contribution to the description of myocardial damage associated with COVID-19, but it does so over a relatively short time frame (less than 3 months) and without establishing the inflammatory nature of this involvement and its potentially deleterious consequences over the longer term. As stated by Puntmann et al,1 we are currently in urgent need of longitudinal studies to improve our understanding of this particular aspect of COVID-19.

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Article Information

Corresponding Author: Pierre-Yves Marie, MD, PhD, Médecine Nucléaire, Hôpital de Brabois, CHRU-Nancy, rue Morvan, 54500 Vandoeuvre-les-Nancy, France (py.marie@chru-nancy.fr).

Published Online: October 28, 2020. doi:10.1001/jamacardio.2020.5279

Conflict of Interest Disclosures: None reported.

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