Effects of Electrophysiologic‐Guided Therapy with Class IA Antiarrhythmic Drugs on the Long‐Term Outcome of Patients with Idiopathic Ventricular Fibrillation with or without the Brugada Syndrome

Belhassen, Bernard; Viskin, Sami; Fish, Roman; Glick, Aharon; Setbon, Israel; Eldar, Michael

doi:10.1111/j.1540-8167.1999.tb00183.x

Cited by 189 publications

(106 citation statements)

References 33 publications

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“…SPVT / VT were induced in 27 (76%) patients without and in all 5 (100%) patients with the Brugada syndrome. 10) Our results demonstrate that VF was induced in 5 of 7 (71.4%) patients with right bundle-branch block with ST elevation and positive LP in the baseline study. On the other hand, VF was induced in 3 of 6 (50.0%) patients with right bundle-branch block with ST elevation and negative LP in the baseline study, although LP became positive after induction of VF in 2 of 3 (67%) patients in whom SAECG was recorded just after or 1 day after electrophysiological study.…”

Section: -Lead Ecgmentioning

confidence: 49%

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Role of Signal-Averaged Electrocardiograms for Predicting the Inducibility of Ventricular Fibrillation in the Syndrome Consisting of Right Bundle Branch Block and ST Segment Elevation in Leads V1-V3.

et al. 2002

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SUMMARYRight bundle branch block and ST segment elevation (RBBB-STE) in the right precordial leads have been reported as a distinct clinical and electrocardiographic syndrome in patients prone to ventricular fibrillation (VF) in the absence of structural heart disease (Brugada syndrome). The purpose of the study was to investigate the role of signal averaged electrocardiogram (SAECG) in identifying patients at high risk among asymptomatic RBBB-STE patients. Thirteen patients with the RBBB-STE ECG were identified. Symptoms were: syncope (n=3, cases 1, 3, and 11), atypical chest pain (n=3, cases 4, 10, and 12) and palpitations (n=2, cases 6, and 7). The other 5 patients were asymptomatic. SAECG and programmed electrical stimulation (PES) were conducted in all patients. Body surface late potentials (LPs) were present in 7 of 13 patients before PES. Vf was induced in 6 of 7 LP positive patients. Vf was induced in 3 of 6 LP negative patients, but LP became positive in 2 of 3 patients in whom Vf was induced. One patient with syncope due to VF (case 1), 1 patient without symptoms who died suddenly during follow up (case 2), and 1 asymptomatic patient (case 9) showed reproducibly positive LP. In a patient (case 9) with positive LP at baseline, LP transiently became negative during follow up. In RBBB-STE patients, reproducibly positive LP is at risk for malignant ventricular arrhythmias and sudden death. Repeated SAECG recording may be useful for screening high-risk patients who should receive electrophysiological study among asymptomatic RBBB-STE patients. (

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Section: -Lead Ecgmentioning

confidence: 49%

“…10) Thus, a randomized prospective study of electrophysiologic-guided antiarrhythmic drug therapy in right bundle-branch block and ST segment elevation on V 1 through V 3 in patients with an ICD seems warranted. Study limitations: The number of patients included in the present study (n=13) was relatively small.…”

Section: -Lead Ecgmentioning

confidence: 99%

Role of Signal-Averaged Electrocardiograms for Predicting the Inducibility of Ventricular Fibrillation in the Syndrome Consisting of Right Bundle Branch Block and ST Segment Elevation in Leads V1-V3.

et al. 2002

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“…Only under backup with ICD therapy, should adjunctive pharmacological treatment be considered in symptomatic Brugada patients to reduce the incidence of VF episodes. Quinidine is the only oral antiarrhythmic agents which may be of therapeutic value [92,93]. Although quinidine is classified as a IA sodium channel blocker, it improves ST segment elevation as a result of its relatively strong I to blocking effect [94].…”

Section: Specific Therapy Based On Cellular Mechanismsmentioning

confidence: 99%

Specific Therapy Based on the Genotype and Cellular Mechanism in Inherited Cardiac Arrhythmias. Long QT Syndrome and Brugada Syndrome

Shimizu

Aiba²,

Antzelevitch

2005

CPD

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Seven forms of congenital long QT syndrome (LQTS) caused by mutations in ion channel genes have been identified. Genotype-phenotype correlation in clinical and experimental studies involving arterially-perfused canine left ventricular wedges suggest that ,β-blockers are protective in LQT1, less so in LQT2, but not protective in LQT3. A class IB sodium channel blocker, mexiletine, is most effective in abbreviating QT interval in LQT3, but effectively reduces transmural dispersion of repolarization (TDR) and prevents the development of Torsade de Pointes (TdP) in all 3 models, suggesting its potential as an adjunctive therapy in LQT1 and LQT2. High concentrations of intravenous nicorandil, a potassium channel opener, have been shown to be capable of decreasing QT and TDR, and preventing TdP in LQT1 and LQT2 but not in LQT3. The calcium channel blocker, verapamil, has also been suggested as adjunctive therapy for LQT1, LQT2 and possibly LQT3.Experimental data using right ventricular wedge preparations suggest that a prominent transient outward current (I to )-mediated action potential (AP) notch and a loss of AP dome in epicardium, but not in endocardium, give rise to a transmural voltage gradient, resulting in ST segment elevation and the induction of ventricular fibrillation (VF), characteristics of the Brugada syndrome. Since the maintenance of the AP dome is determined by the balance of currents active at the end of phase 1 of the AP, any intervention that reduces the outward current or boosts inward current at the end of phase I may normalize the ST segment elevation and suppress VF. Such interventions are candidates for pharmacological therapy of the Brugada syndrome. The infusion of isoproterenol, a β-adrenergic stimulant, strongly augments L-type calcium current (I Ca-L ), and is the first choice for suppressing electrical storms associated with Brugada syndrome. Quinidine, by virtue of its actions to block I to , has been proposed as adjunctive therapy, with an implantable cardioverter defibrillator as backup. Oral denopamine, atropine or cilostazol all increase I Ca-L , and for this reason may be effective in reducing episodes of VF.

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“…Thus, other therapeutic alternatives, such as quinidine, have not been properly evaluated despite some interesting data. 8,9 In this issue, Belhassen et al 2 reported their experience in the management of patients affected by the Brugada syndrome over a period of >30 years.…”

Section: Article See P 1393mentioning

confidence: 99%

Quinidine in Brugada Syndrome

Probst

Gourraud

2015

Circ: Arrhythmia and Electrophysiology

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Effects of Electrophysiologic‐Guided Therapy with Class IA Antiarrhythmic Drugs on the Long‐Term Outcome of Patients with Idiopathic Ventricular Fibrillation with or without the Brugada Syndrome

Abstract: Our results suggest that EP-guided therapy with Class IA agents is a reasonable, safe, and effective approach for the long-term management of patients with idiopathic VF. A randomized prospective study of EP-guided Class IA therapy in patients with ICDs seems warranted.

Cited by 189 publications

References 33 publications

Role of Signal-Averaged Electrocardiograms for Predicting the Inducibility of Ventricular Fibrillation in the Syndrome Consisting of Right Bundle Branch Block and ST Segment Elevation in Leads V1-V3.

Role of Signal-Averaged Electrocardiograms for Predicting the Inducibility of Ventricular Fibrillation in the Syndrome Consisting of Right Bundle Branch Block and ST Segment Elevation in Leads V1-V3.

Specific Therapy Based on the Genotype and Cellular Mechanism in Inherited Cardiac Arrhythmias. Long QT Syndrome and Brugada Syndrome

Quinidine in Brugada Syndrome

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