Corresponding author:
Sergio Conti, MD, PhD
ARNAS Civico, Department of Cardiac Electrophysiology
P.zza Nicola Leotta, 4 – 90127 Palermo, Italy
Tel: (+39)0916665038; mail:
sergioconti.md@gmail.com
We thank Dr. Dendramis and Dr. Brugada for their interest in our paper
[1].
Overall, our population included a large and non-selected cluster of
patients previously diagnosed with Brugada syndrome (BrS). That said,
50.3% of patients in our analysis (164/326 patients) had a spontaneous
Brugada type 1 electrocardiogram (ECG). It is well-demonstrated that
patients with a spontaneous Brugada type 1 ECG have a worse arrhythmic
prognosis than patients with drug-induced Brugada type 1 ECG [2].
Previous data from large meta-analyses reported an arrhythmic risk three
to four times higher in asymptomatic patients with a spontaneous Brugada
type 1 ECG [3,4]. In addition, 20.1% of patients presenting with a
spontaneous type 1 ECG also had a history of documented ventricular
fibrillation/sudden cardiac death (VF/SCD), thus representing an even
higher risk population. In our population, 10.4% of patients had a
previous history of VF/SCD documented. Patients with a history of severe
ventricular arrhythmias or aborted SCD are considered at high risk, with
an estimated recurrence rate of arrhythmic events of 48% over ten years
[5].
Among the group of patients with drug-induced Brugada type 1 ECG
(162/326 patients, 49.7%), who are generally considered at lower risk
than subjects with spontaneous type 1 ECG, 23.4% had a positive
programmed electrical stimulation (PES). Although we acknowledge that
the role of PES in the risk stratification of asymptomatic patients
remains controversial, it may still have a role in selected patients
[7].
Considering only the ICD carriers (202/326 patients), the overall number
of patients that presented with ventricular arrhythmias in our
population was comparable between patients deemed at high risk and those
at low risk. During COVID infection, 1.4% of patients with drug-induced
Brugada type 1 had ventricular arrhythmias compared to 1.5% of patients
with spontaneous Brugada type 1. After the first and booster vaccine
dose, no sustained ventricular arrhythmias were recorded in patients
with drug-induced Brugada type 1 and spontaneous Brugada type 1. After
the second dose of vaccine, one VT episode was recorded in the group of
patients with spontaneous Brugada type 1 and one in the group of
patients with drug-induced Brugada type 1.
What surprised us the most was the peculiar timing of implantable
cardioverter-defibrillator (ICD) interventions. Indeed, in the two
patients that received ICD therapies (1 ATP and 1 shock), these episodes
were not related to acute infection or vaccine-related hyperpyrexia but
happened in the last window of the study observation (6 months after
COVID infection or 1-month after the last dose of vaccine). Moreover,
one of the two episodes was in a patient with drug-induced Brugada type
1 ECG, and the other was in a subject with spontaneous Brugada type 1
ECG and positive PES.
In our opinion, the added value of our study was the extensive use of
remote device monitoring and the vast amount of data collected and
analyzed to assess the arrhythmic burden, which strengthen our findings.
Finally, in this real-world analysis, we found that most BrS patients
followed the recommendations given for fever treatment and
pre-treatment. This may reconcile the apparent discrepancy between the
heterogeneous risk profile and the low observed incidence of ventricular
arrhythmia in our population.