First of all, we would like to thank Miranda-Arboleda et al. for their interest in our article.1 Their thoughtful comments have given us the opportunity to clarify certain clinical aspects of our case that could affect its interpretation.

Indeed, the case report describes electrocardiographic (ECG) findings consistent with a Brugada pattern in the context of fever and clinical findings compatible with COVID–19-associated multisystem inflammatory syndrome in children (MIS-C). The pattern, however, persisted for approximately 4 days after the fever had subsided. While fever is a precipitating factor for ECG abnormalities in Brugada syndrome, afebrile patients with this disorder often have normal findings.2 The Brugada pattern disappeared on day 5 of admission, although the ECG did show repolarization abnormalities, possibly indicative of myocardial involvement.

MIS-C can cause inflammation and myocardial involvement3 with reduced ejection fraction and increased N-terminal pro-B-type natriuretic peptide (NT-proBNP) and troponin levels (observed in our patient). This myocardial involvement could be in keeping with conditions that have been linked to Brugada phenocopy. The improvements in cardiac function and clinical and biochemical parameters (reduction in NT-proBNP and troponin levels) in our patient all coincided with the disappearance of the Brugada pattern.

Because the boy had a Brugada type 1-like pattern that resolved on improvement of the acute inflammation, in addition to a negative flecainide challenge and genetic study and, above all, a very low pretest probability of Brugada syndrome (no compatible clinical manifestations or family history of the syndrome), we believe he met al.l the criteria for Brugada phenocopy. We also believe, however, that close long-term monitoring is warranted, and if the patient shows any additional symptoms, we will, as suggested, perform a provocation test with incremental doses of sodium channel blockers, assuming of course that the benefits outweigh any possible risks.