We thank Dr. Bertini and colleagues for their thoughtful response to our paper (1). Specifically, the authors comment on the relative dearth of electrocardiographic (ECG) data in the study of the novel coronavirus disease-2019 (COVID-19). They further suggest that ECG information could have offered incremental insight in determining the underlying pathophysiology of elevated troponin levels, representing myocardial injury.
We agree that ECG data are additive in helping to understand the nature of myocardial involvement and also holds prognostic relevance. Unfortunately, reviewing ECG data in our large cohort of patients (nearly 3,000) was not feasible within a reasonable timeframe to allow the dissemination of information that was of importance during a surge in COVID-19 cases across the globe. Furthermore, data were collected during the peak of the pandemic in New York City (February 27 to April 12, 2020), with variable uses of antiviral therapy, anticoagulation, and hydroxychloroquine, which may have influenced ECG information. Nonetheless, the message of our paper was simple and still holds true: myocardial injury is common, and when present, it portends worse prognosis among patients hospitalized with COVID-19. Myocardial injury is represented by elevated troponin concentrations based on the fourth universal definition of myocardial infarction (2). We acknowledge that understanding the underlying pathophysiology of myocardial injury in the setting of COVID-19 was beyond the scope of our paper. Indeed, several months after our data were collected, the causal relationship between severe acute respiratory syndrome-coronavirus-2 and cardiac involvement remains elusive and requires further study (3). Systematic study of ECGs among affected patients is of interest.
Another important point raised by Bertini et al. is the frequently inappropriate invocation of severe acute respiratory syndrome-coronavirus-2 myocarditis as a diagnosis based on elevated troponin levels. In fact, as we have seen in recent studies, this diagnosis requires the presence of histologic findings and viral particles within myocytes as well as the exclusion of other cardiotropic viruses within the appropriate clinical setting, and has proven to be quite rare (4).
Footnotes
Dr. Lala has received speaker honoraria from Zoll. Dr. Januzzi is a Trustee of the American College of Cardiology; has received grant support from Novartis Pharmaceuticals and Abbott Diagnostics; has received consulting income from Abbott, Janssen, Novartis, MyoKardia, and Roche Diagnostics; and participates in clinical endpoint committees/data safety monitoring boards for Abbott, AbbVie, Amgen, CVRx, Janssen, and Takeda. Dr. Pinney has received consulting fees from Abbott, CareDx, Medtronic, and Procyrion; has participated in clinical endpoint committees for Abbott, Axon, SoniVie, and Transmedics; and has received honoraria from Boston Scientific. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Patrick O'Gara, MD, served as Guest Associate Editor for this paper. P.K. Shah, MD, served as Guest Editor-in-Chief for this paper.
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACCauthor instructions page.
References
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