Effect of Sodium Channel Blockers on ST Segment, QRS Duration, and Corrected QT Interval in Patients with Brugada Syndrome

Shimizu, Wataru; Antzelevitch, Charles; Suyama, Kazuhiro; Kurita, Takashi; Taguchi, Atsushi; Aihara, Naohiko; Takaki, Hiroshi; Sunagawa, Kenji; Kamakura, Shiro

doi:10.1046/j.1540-8167.2000.01320.x

Cited by 215 publications

(136 citation statements)

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“…This difference was greater for flecainide in the study by Shimizu et al 9 The difference may be explained by the fact that the patients reported by Shimizu et al revealed mean baseline STsegment elevations of 0.39 mV, which already is diagnostic of Brugada syndrome, compared to a mean 0.16 ± 0.09 mV in our series. Of note, our series included patients with suspicion of Brugada syndrome and normal baseline ECG.…”

Section: Comparison To Previous Reportscontrasting

confidence: 67%

Intravenous drug challenge using flecainide and ajmaline in patients with Brugada syndrome

et al. 2005

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OBJECTIVES-The purpose of this study was to compare the effect of intravenous flecainide and ajmaline with respect to their ability to induce or accentuate the typical ECG pattern of Brugada syndrome.BACKGROUND-Brugada syndrome is associated with a high incidence of sudden cardiac death. The typical ECG pattern of ST-segment elevation in the right precordial leads often is concealed, but it can be unmasked with sodium channel blockers such as flecainide and ajmaline. Little is known about the relative effectiveness of these provocative agents in unmasking Brugada syndrome.

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Section: Comparison To Previous Reportscontrasting

confidence: 67%

Intravenous drug challenge using flecainide and ajmaline in patients with Brugada syndrome

et al. 2005

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“…It has been previously reported that a class Ic blocker test is not always positive in patients with Brugada syndrome (12). Thus, the value of the class Ic blocker test in Brugada syndrome is still being debated, and the specificity of sodium channel blockers in identifying patients at risk is currently not clear (13)(14)(15)(16). The fact that the ST elevations are dynamic is a well-established phenomenon in Brugada syndrome patients (17), but difficulties in their recognition make the Brugada syndrome difficult to diagnose.…”

Section: Discussionmentioning

confidence: 99%

Ventricular tachycardia in a Brugada syndrome patient caused by a novel deletion in SCN5A

Tfelt-Hansen

Jespersen

Hofman-Bang

et al. 2009

Canadian Journal of Cardiology

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“…1996;. Sodium channel blockers, including flecainide, ajmaline, procainamide, disopyramide, propafenone, and pilsicainide are used to aid in a differential diagnosis when ST segment elevation is not diagnostic under baseline conditions (Brugada et al 2000c;Shimizu et at. 2000a;Priori et at.…”

Section: Clinical Characteristics and Diagnostic Criteriamentioning

confidence: 99%

“…a Control, BCL 800 ms. b Terfenadine (5 μM) induces ST segment elevation as a result of heterogeneous loss of the epicardial action potential dome, leading to phase 2 reentry3 which triggers a closely coupled extrasystole (BCL = 800 ms). c Addition of AVEO 118 (7 μM) prevents loss of the epicardial action potential dome and phase 2 reentry-induced arrhythmias (BCL = 800 ms) Table 2 Device nad pharmacologic apaproach to therapy of the Brugada syndrome Devices and Ablation ICD (Brugada et al 2000a) ?Ablation or Cryosurgery (Haissaguerre et l. 2003) ?Pacemaker (vn den Berg et al 2001) Pharmcaologic Approach to Therapy Ineffective Amiodarone β-Blockers (Brugadaa et al 1998) Class iC antiarrhythmics Flecainide (Shimizu et al 2000a) Propafenone (Matana et al 2000) ?Disopyramide (Chinushi et al 1997) Class IA aaantiarrhythmics Procainaamide (Brugada et al 2000c) Effective for treatment of electrical storms β-Adrenergic agonists-isoproterenol (Miyazaki et al 1996;Shihmizu et al 2000b) Phosphodiesterase III inhibitors-cilostazol (Tsuchiya et al 2002) Effective general therapy Class IA antiarrythmics Quinidine (Belhassen and Viskin 2004;Alings et al 2001;Belhassen et al 1999Belhassen et al , 2002Yan and Antzelevitch 1999;Hermida et al 2004;Mok et al 2004) Experimental therapy I to blockers-cardioselective and ion channel specific Quinidine (Yan and Antzelevitch 1999) 4-Aaminopyridine (Yan and Antzelevitch 1999) Tedisamil (Fish et al 2004b) AVE0118 (Fish et al 2004a) …”

Section: Pharmacologic Approach To Therapymentioning

confidence: 99%

“…Class IC drugs [Elecainide (Krishnan and Josephson 1998;Fujiki et al 1999;Shimizu et al 2000a;Brugada et al 2000c;Gasparini et al. 2003), Pilsicainide (Takenaka et al 1999;Shimizu et al 2001), Propafenone (Matana et al 2000)] Class IA drugs [Ajmaline (Brugada et al 2000c;Rolf et al 2003), Procainamide (Miyazaki et al 1996;Brugada et al 2000c), Disopyramide (Miyazaki et al 1996;Wilde et al 2002a), Cibenzoline (Tada et al 2000 …”

Section: Imentioning

confidence: 99%

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Therapy for the Brugada Syndrome

Antzelevitch

Fish

Basis and Treatment of Cardiac Arrhythmias

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The Brugada syndrome is a congenital syndrome of sudden cardiac death first described as a new clinical entity in 1992. Electrocardiographically characterized by a distinct coved-type ST segment elevation in the right precordial leads, the syndrome is associated with a high risk for sudden cardiac death in young and otherwise healthy adults, and less frequently in infants and children. The ECG manifestations of the Brugada syndrome are often dynamic or concealed and maybe revealed or modulated by sodium channel blockers. The syndrome may also be unmasked or precipitated by a febrile state, vagotonic agents, α-adrenergic agonists, β-adrenergic blockers, tricyclic ortetracyclic antidepressants, a combination of glucose and insulin, and hypokalemia, as well as by alcohol and cocaine toxicity. An implantable cardioverter-defibrillator (ICD) is the most widely accepted approach to therapy. Pharmacological therapy aimed at rebalancing the currents active during phase 1 of the right ventricular action potential is used to abort electrical storms, as an adjunct to device therapy, and as an alternative to device therapy when use of an ICD is not possible. Isoproterenol and cilostazol boost calcium channel current, and drugs like quinidine inhibit the transient outward current, acting to diminish the action potential notch and thus suppress the substrate and trigger for ventricular tachycardia/fibrillation (VT/VF). KeywordsBrugada syndrome; Phase 2 reentry; ST segment elevation; I Na ; I to ; Implantable cardioverterdefibrillator (ICD); VT; SCN5A mutations; Sudden death; Bradycardia Clinical Characteristics and Diagnostic CriteriaThe Brugada syndrome typically manifests in the third or fourth decade of life (average age of 41±15 years), although patients have been diagnosed with the syndrome at an age as young as 2 days and as old as 84 years. The prevalence of the disease is estimated to be at least 5 per 10,000 inhabitants in Southeast Asia, where the syndrome is endemic (Nademanee et al. 1997). In Japan, a Brugada syndrome ECG (type 1) is observed in 12 per 10,000 inhabitants; type 2 and type 3 ECGs, which are not diagnostic of Brugada syndrome, are much more prevalent, appearing in 58 per 10,000 inhabitants (Miyasaka et al. 2001). The true prevalence of the disease in the general population is difficult to estimate because the ECG pattern is often concealed (Brugada et al. 2003). Sudden unexplained nocturnal death syndrome (SUNDS also known as SUDS) and Brugada syndrome have been shown to be phenotypically, genetically, and functionally the same disorder (Vatta et al. 2002).Although syncope and sudden death are a consequence of ventricular tachycardia/fibrillation (VT/VF), approximately 20% of Brugada syndrome patients also develop supraventricular arrhythmias (Morita et al. 2002). Atrial fibrillation (AF) is reported in approximately 10%-20% of cases. Atrio-ventricular (AV) nodal reentrant tachycardia (AVNRT) and Wolf-ParkinsonWhite (WPW) syndrome have been described as well (Eckardt et al. 2001 et al. 2004)...

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Effect of Sodium Channel Blockers on ST Segment, QRS Duration, and Corrected QT Interval in Patients with Brugada Syndrome

Cited by 215 publications

References 34 publications

Intravenous drug challenge using flecainide and ajmaline in patients with Brugada syndrome

Intravenous drug challenge using flecainide and ajmaline in patients with Brugada syndrome

Ventricular tachycardia in a Brugada syndrome patient caused by a novel deletion in SCN5A

Therapy for the Brugada Syndrome

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