Substrate and Ventricular Tachyarrhythmias in Brugada Syndrome

Apr 10, 2018
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Authors:
Pappone C, Ciconte G, Manguso F, et al.
Citation:
Assessing the Malignant Ventricular Arrhythmic Substrate in Patients With Brugada Syndrome. J Am Coll Cardiol 2018;71:1631-1646.
Summary By:
Thomas C. Crawford, MD, FACC

Study Questions:

What are the clinical and electrophysiological predictors of malignant ventricular tachyarrhythmia inducibility in Brugada syndrome?

Methods:

A total of 191 consecutive selected patients with (group 1; n = 88) and without (group 2; n = 103) Brugada syndrome–related symptoms were prospectively enrolled in the registry. Patients underwent electrophysiological study and substrate mapping or ablation before and after ajmaline testing (1 mg/kg/5 min).

Results:

Overall, before ajmaline testing, 53.4% of patients had ventricular tachyarrhythmia inducibility, which was more frequent in group 1 (65.9%) than in group 2 (42.7%; p < 0.001). Regardless of clinical presentation, larger substrates with more fragmented long-duration ventricular potentials were found in patients with inducible arrhythmias than in patients without inducible arrhythmias (p < 0.001). After ajmaline, patients without arrhythmia inducibility had arrhythmia inducibility without a difference in substrate characteristics between the two groups. The substrate size was the only independent predictor of inducibility (odds ratio, 4.51; 95% confidence interval, 2.51-8.09; p < 0.001). A substrate size of 4 cm2 best identified patients with inducible arrhythmias (area under the curve, 0.98; p < 0.001). Substrate ablation prevented ventricular tachyarrhythmia reinducibility.

Conclusions:

In Brugada syndrome, the arrhythmogenic substrate dynamic and its size is independently associated with arrhythmia inducibility. Substrate ablation is associated with electrocardiogram normalization and noninducibility.

Perspective:

Although Brugada syndrome has traditionally been considered an arrhythmogenic disorder in structurally normal hearts, recent studies demonstrated complex arrhythmogenic substrates in the right ventricular (RV) outflow tract or the anterior RV wall. The present study shows that after ajmaline, both the substrate area and the duration of abnormal potentials correspondingly increased. The dynamic nature of the arrhythmogenic substrate in Brugada syndrome may be one reason for conflicting reports regarding the usefulness of programmed ventricular stimulation in risk stratification in this condition.

Keywords: Ajmaline, Arrhythmias, Cardiac, Brugada Syndrome, Cardiac Electrophysiology, Catheter Ablation, Electrocardiography, Secondary Prevention, Tachycardia, Ventricular


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