Key result
Procainamide provocation in suspected Brugada syndrome prolongs QRS duration but fails to aid risk stratification.
Why the study?
The effects of procainamide on the signal averaged ECG in Brugada syndrome and the significance of procainamide-induced late potentials are unknown.
Does procainamide provocation alter SAECG parameters and unmask late potentials in patients with suspected Brugada syndrome?
Observational (n=150)
Does procainamide provocation alter SAECG parameters and unmask late potentials in patients with suspected Brugada syndrome?
Procainamide provocation alters SAECG parameters and can unmask late potentials in suspected Brugada syndrome, but these induced late potentials do not provide additional diagnostic or risk stratification value.
Should not yet guide Brugada risk stratification; leaves open SAECG utility during procainamide provocation.
Background Late potentials (LPs) identified on the signal averaged electrocardiogram (SAECG) are a marker for an increased risk of arrhythmias in Brugada syndrome (BrS). Procainamide is a sodium channel blocker used to diagnose BrS. The effects of Procainamide on the SAECG in those with BrS and the significance of Procainamide‐induced LPs are unknown. Methods Procainamide provocation was performed for suspected BrS with 12‐lead and SAECG pre‐ and post‐infusion. Filtered QRS duration (fQRSd), duration of low amplitude signals <40 μV (LAS40) and root‐mean‐square voltage in the terminal 40 ms (RMS40) were determined. Results Data from 150 patients were included in the analysis (mean age 44.5 years, 109 males). Procainamide increased fQRSd (Pre 118.8 ± 10.5 ms, post 121.2 ± 10.2 ms, p < 0.001) and LAS40 (Pre 38.7 ± 9.8 ms, post 40.2 ± 10.5 ms, p = 0.005) and decreased RMS40 (Pre 24.6 ± 12 ms, post 22.8 ± 12 ms, p = 0.002). LPs were present in 68/150 (45%) at baseline. Fifteen patients with negative baseline SAECGs had LPs unmasked by Procainamide, but six patients had LPs at baseline that were no longer present following Procainamide. Comparing those with normal hearts ( n = 48) to those with a final diagnosis of BrS ( n = 38), Procainamide prolonged fQRSd to a greater extent in those with BrS. Comparing those with Procainamide‐induced LPs to those with no LPs at any time did not highlight any aspect of phenotype and did not correlate with a history of ventricular arrhythmias. Conclusions Procainamide influences the SAECG, provoking LPs in a small proportion of patients. However, there is no evidence that Procainamide‐induced LPs provide additional diagnostic information or aid risk stratification.
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Pearman et al. (2021) conducted an observational in Suspected Brugada syndrome (n=150). Procainamide provocation vs. Baseline (pre-infusion) was evaluated on Filtered QRS duration (fQRSd) (p=<0.001). Procainamide provocation in suspected Brugada syndrome significantly increased filtered QRS duration (121.2 vs 118.8 ms, p<0.001) but procainamide-induced late potentials did not aid risk stratification.
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