Key result
Ajmaline testing in Brugada syndrome significantly increased right ventricular outflow tract activation time (105.9 vs 65.8 ms; P<0.001), which was a strong predictor of aborted sudden cardiac death.
Why the study?
Noninvasive electrocardiographic imaging assesses Brugada syndrome depolarization and repolarization abnormalities, but its parameters during ajmaline testing required analysis.
Does noninvasive electrocardiographic imaging during ajmaline testing identify predictors of sudden cardiac death in patients with Brugada syndrome?
Observational (n=39)
Does noninvasive electrocardiographic imaging during ajmaline testing identify predictors of sudden cardiac death in patients with Brugada syndrome?
Absolute Event Rate: 105.9% vs 65.8%
p-value: p=<0.001
Noninvasive electrocardiographic imaging during ajmaline testing reveals distinct depolarization and repolarization abnormalities that strongly correlate with a history of aborted sudden cardiac death in Brugada syndrome.
Background The rate of sudden cardiac death (SCD) in Brugada syndrome (BrS) is ≈1%/y. Noninvasive electrocardiographic imaging is a noninvasive mapping system that has a role in assessing BrS depolarization and repolarization abnormalities. This study aimed to analyze electrocardiographic imaging parameters during ajmaline test (AJT). Methods and Results All consecutive epicardial maps of the right ventricle outflow tract (RVOT‐EPI) in BrS with CardioInsight were retrospectively analyzed. (1) RVOT‐EPI activation time (RVOT‐AT); (2) RVOT‐EPI recovery time, and (3) RVOT‐EPI activation‐recovery interval (RVOT‐ARI) were calculated. ∆RVOT‐AT, ∆RVOT‐EPI recovery time, and ∆RVOT‐ARI were defined as the difference in parameters before and after AJT. SCD‐BrS patients were defined as individuals presenting a history of aborted SCD. Thirty‐nine patients with BrS were retrospectively analyzed and 12 patients (30.8%) were SCD‐BrS. After AJT, an increase in both RVOT‐AT [105.9 milliseconds versus 65.8 milliseconds, P <0.001] and RVOT‐EPI recovery time [403.4 milliseconds versus 365.7 milliseconds, P <0.001] was observed. No changes occurred in RVOT‐ARI [297.5 milliseconds versus 299.9 milliseconds, P =0.7]. Before AJT no differences were observed between SCD‐BrS and non SCD‐BrS in RVOT‐AT, RVOT‐EPI recovery time, and RVOT‐ARI ( P =0.9, P =0.91, P =0.86, respectively). Following AJT, SCD‐BrS patients showed higher RVOT‐AT, higher ∆RVOT‐AT, lower RVOT‐ARI, and lower ∆RVOT‐ARI ( P <0.001, P <0.001, P =0.007, P =0.002, respectively). At the univariate logistic regression, predictors of SCD‐BrS were the following: RVOT‐AT after AJT (specificity: 0.74, sensitivity 1.00, area under the curve 0.92); ∆RVOT‐AT (specificity: 0.74, sensitivity 0.92, area under the curve 0.86); RVOT‐ARI after AJT (specificity 0.96, sensitivity 0.58, area under the curve 0.79), and ∆RVOT‐ARI (specificity 0.85, sensitivity 0.67, area under the curve 0.76). Conclusions Noninvasive electrocardiographic imaging can be useful in evaluating the results of AJT in BrS.
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A 2022 study conducted an observational in Brugada syndrome (n=39). Ajmaline test vs. Baseline (before ajmaline test) was evaluated on Right ventricle outflow tract activation time (RVOT-AT) (p=<0.001). Ajmaline testing in Brugada syndrome significantly increased right ventricular outflow tract activation time (105.9 vs 65.8 ms; P<0.001), which was a strong predictor of aborted sudden cardiac death.
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