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  • br Algorithm of treatment approach in Brugada syndrome

    2019-04-25


    Algorithm of treatment approach in Brugada syndrome patients with electrical storm Fig. 4 shows the flow diagram of how we treat BrS patients with ES. Patients are admitted to the ICU and should be well sedated, and some may require general anesthesia with endotracheal intubation. The patients are evaluated to determine if there are precipitating factors to be eliminated or treated. In the acute phase of ES when patients continue to have recurrent VF episodes, Steps 1 and 2, as described below, should be carrried out simultaneously.
    Conclusions
    Conflict of interest Dr. Koonlawee Nademanee has Consulting Agreements, Research Grants and Royalties from Biosense Webster.
    The review article of Veerakul and Nademanee entitled “Treatment of electrical storms in Brugada syndrome” has a wide range of coverage, from the cellular mechanism to the clinical management of electrical storms in Brugada syndrome (BrS) . Part of the study aimed to investigate the electrophysiological mechanisms of specific electrocardiographic manifestations and the substrate for ventricular fibrillation (VF) from different aspects of depolarization and repolarization abnormalities in BrS patients. However, in the paragraph under the section “Mechanism of Ventricular Fibrillation/Electrical Storm in the Brugada Syndrome,” the authors seem to place more emphasis on the depolarization theory by partly quoting their previous study in which an epicardial catheter ablation technique was used to eliminate electrical storms in BrS patients . We express our sincere admiration for how they have successfully braved through their challenges; however, we should be aware that their cases might have had extremely severe substrates facilitating VF because they had multiple VF episodes that required aggressive interventions. We previously demonstrated a “notch and dome” configuration of monophasic hcv protease inhibitors recordings from the right ventricular epicardium in 3 BrS patients . From our experience, a significant activation delay such as those shown in Figures 2 and 6 of this article could not be recorded, possibly because we obtained the epicardial electrograms from BrS patients without any electrical storms. Two recent studies in Japan and Europe reported that a fragmented QRS (multiple spikes within the QRS) can be a marker of a substrate for spontaneous VF in BrS patients and a predictor of high-risk patients . These studies concluded that the fragmented QRS was related to the underlying conduction disturbance and played an important role in the spontaneous occurrence of VF. A concomitant depolarization abnormality may develop into a more malignant pathophysiological condition in BrS patients. However, the repolarization theory is still a powerful and useful consideration when we see a pathognomonic response of the electrocardiographic manifestations in BrS patients, such as a pause-dependent elevation of the ST-segment and suppression of electrical storms by isoproterenol infusion .
    Introduction Sudden cardiac death (SCD) in the absence of structural heart diseases accounts for 5–10% of all sudden cardiac deaths and is caused by primary electrical disorders or ion channel diseases [1,2]. Identification of the ion channels and their genetic mutations responsible for SCDs has opened a new area of translational research in cardiac electrophysiology [3–8]. Long QT syndrome has been recognized as an important cause of SCD [3]. The genetic mutation and the basic electrophysiologic mechanisms in SCD were elucidated recently, long after the recognition of its clinical entity [4]. In contrast, key cellular electrophysiologic features underlying the development of ventricular fibrillation (VF) associated with Brugada syndrome (BS) and early repolarization syndrome (ERS) were described well before the recognition of clinical entities [9–11]. Unlike other ion channel diseases, BS and ERS share many electrocardiographic and clinical features [5,12]. Both syndromes are represented by electrocardiographic J waves that demonstrate similar dynamic behavior such as a pause or bradycardia dependence and short-coupled extrasystole-induced polymorphic ventricular arrhythmia [13]. J waves can be suppressed in both ERS and BS with the administration of isoproterenol and quinidine and with pacing. ERS and BS have been reported to occur simultaneously in the same individual or in different members of the same family [14]. In this review, we describe similarities and differences in the cellular electrophysiology and clinical features of BS and ERS.