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Review
. 2024 Dec 26;13(1):27.
doi: 10.3390/biomedicines13010027.

Epicardial Ablation for Arrhythmogenic Disorders in Patients with Brugada Syndrome

Affiliations
Review

Epicardial Ablation for Arrhythmogenic Disorders in Patients with Brugada Syndrome

Andrea Matteucci et al. Biomedicines. .

Abstract

Brugada syndrome (BrS) is an inherited arrhythmogenic disorder characterized by distinct electrocardiographic patterns and an increased risk of sudden cardiac death due to ventricular arrhythmias. Effective management of BrS is essential, particularly for high-risk patients with recurrent arrhythmias. While implantable cardioverter-defibrillator (ICD) is effective in terminating life-threatening arrhythmias, it does not prevent arrhythmia onset and can lead to complications such as inappropriate shocks. Epicardial ablation has emerged as a promising treatment option for patients with recurrent ventricular arrhythmias and frequent ICD interventions. This review examines the latest advancements in the management of Brugada syndrome, focusing on the role and rationale of epicardial ablation for the treatment of patients at risk of sudden cardiac death.

Keywords: Brugada syndrome; epicardial ablation; sudden cardiac death.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Comparison between standard chest electrode placement and high-lead placement in patients with BrS. (Left): Standard precordial lead placement, with V1 and V2 positioned in the fourth intercostal space. (Right): High-lead placement to enhance diagnostic sensitivity in Brugada Syndrome. In this configuration, V1 and V2 are shifted to the second or third intercostal space, remaining parasternal, while V3 and V4 are similarly elevated to corresponding higher positions along the chest.
Figure 2
Figure 2
Epicardial electroanatomic mapping of a patient with Brugada syndrome, comparing baseline conditions with the effects of ajmaline administration. On the left, the surface ECG leads (I, II, III, aVR, aVL, aVF, hV1–hV4) demonstrate the transformation induced by ajmaline, with the emergence of a coved-type ST-segment elevation. On the right, the electroanatomic maps display the distribution of epicardial potentials, color-coded by bipolar voltage amplitude (PDM range: 110–160). Under baseline conditions, a localized region of fractionated, low-voltage electrograms is observed near the right ventricular outflow tract (RVOT). Following the ajmaline challenge, this area expands significantly, with a prominent enlargement of the low-voltage zone, corresponding to the arrhythmogenic substrate, extending to the pulmonary valve (PV).

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