Sensitivity and specificity of sodium channel blocking test in the diagnosis of Brugada syndrome

Gavrielatos, Gerasimos; Letsas, Κonstantinos P.; Pappas, Loukas K.; Efremidis, Michalis; Sideris, Antonios; Kardaras, Fotios

doi:10.1016/j.ijcard.2008.11.147

Cited by 8 publications

(6 citation statements)

References 11 publications

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“…Previous studies looking at the use of sodium channel blockers (procainamide, ajmaline, flecainide, and pilsicainide) suggest that in general they have a high sensitivity and specificity for unmasking ST-segment elevation, 12,24 although some differences have been reported, 25 the varied potency of inhibition of I to and I Na by these agents is believed to contribute to the varied effectiveness in unmasking the Brugada pattern ECG. In SCN5A-positive subjects with Brugada syndrome and their relatives, the class 1C agent flecainide has been reported to have sensitivity of 77%, specificity of 80%, and positive and negative predictive values of 96% and 36%, respectively.…”

Section: Discussionmentioning

confidence: 99%

Procainamide infusion in the evaluation of unexplained cardiac arrest: From the Cardiac Arrest Survivors with Preserved Ejection Fraction Registry (CASPER)

et al. 2014

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Section: Discussionmentioning

confidence: 99%

Procainamide infusion in the evaluation of unexplained cardiac arrest: From the Cardiac Arrest Survivors with Preserved Ejection Fraction Registry (CASPER)

et al. 2014

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“…negative predictive value of flecainide-testing is 36%). 40, 42 Ajmaline and pilsicainide seem to be more effective tools in unmasking BrS, compared to flecainide 43, 44 or procainamide 38 . The electrocardiographic manifestations of the Brugada syndrome when concealed can be also be unmasked by bradycardia, febrile state or with vagotonic agents.…”

Section: Clinical Characteristics and Diagnostic Criteriamentioning

confidence: 94%

Brugada Syndrome: Clinical, Genetic, Molecular, Cellular, and Ionic Aspects

Antzelevitch¹,

Patocskai²

2016

Current Problems in Cardiology

104

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The Brugada syndrome (BrS) is an inherited cardiac arrhythmia syndrome first described as a new clinical entity in 1992. Electrocardiographically characterized by 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 adults, and less frequently in infants and children. The ECG manifestations of the BrS are often concealed and may be unmasked or aggravated by sodium channel blockers, a febrile state, vagotonic agents, as well as by tricyclic and tetracyclic antidepressants. An implantable cardioverter defibrillator (ICD) is the most widely accepted approach to therapy. Pharmacological therapy is designed to produce an inward shift in the balance of currents active during the early phases of the right ventricular action potential and can be used to abort electrical storms or as an adjunct or alternative to device therapy when use of an ICD is not possible. Isoproterenol, cilostazol and milrinone boost calcium channel current and drugs like quinidine, bepridil and the Chinese herb extract Wenxin Keli inhibit the transient outward current, acting to diminish the action potential (AP) notch and thus to suppress the substrate and trigger for VT/VF. Radiofrequency ablation of the right ventricular outflow tract epicardium of BrS patients has recently been shown to reduce arrhythmia-vulnerability and the ECG-manifestation of the disease, presumably by destroying the cells with more prominent AP notch. This review provides an overview of the clinical, genetic, molecular and cellular aspects of the BrS as well as the approach to therapy.

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“…However a negative I Na -block test does not exclude a latent forms of BrS. 13, 14 The electrocardiographic manifestations of Brugada syndrome when concealed can also be unmasked by a febrile state as well as with vagotonic agents. 9, 15–20 …”

Section: Clinical Characteristicsmentioning

confidence: 99%

Novel therapeutic strategies for the management of ventricular arrhythmias associated with the Brugada syndrome

Patocskai

Antzelevitch

2015

Expert Opinion on Orphan Drugs

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Introduction Brugada syndrome (BrS) is an inherited cardiac arrhythmia syndrome characterized by prominent J waves appearing as distinct coved type ST segment elevation in the right precordial leads of the ECG. It is associated with a high risk for sudden cardiac death. Areas Covered We discuss 1) ECG manifestations of BrS which can be unmasked or aggravated by sodium channel blockers, febrile states, vagotonic agents, as well as tricyclic and tetracyclic antidepressants; 2) Genetic basis of BrS; 3) Ionic and cellular mechanisms underlying BrS; 4) Therapy involving devices including an implantable cardioverter defibrillator (ICD); 5) Therapy involving radiofrequency ablation; and 6) Therapy involving pharmacological therapy which is aimed at producing an inward shift in the balance of the currents active during phase 1 of the right ventricular action potential either by boosting calcium channel current (isoproterenol, cilostazol and milrinone) or by inhibition of transient outward current Ito (quinidine, bepridil and the Chinese herb extract Wenxin Keli). Expert Opinion This review provides an overview of the clinical and molecular aspects of BrS with a focus on approaches to therapy. Available data suggest that agents capable of inhibiting the transient outward current Ito can exert an ameliorative effect regardless of the underlying cause.

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Sensitivity and specificity of sodium channel blocking test in the diagnosis of Brugada syndrome

Cited by 8 publications

References 11 publications

Procainamide infusion in the evaluation of unexplained cardiac arrest: From the Cardiac Arrest Survivors with Preserved Ejection Fraction Registry (CASPER)

Procainamide infusion in the evaluation of unexplained cardiac arrest: From the Cardiac Arrest Survivors with Preserved Ejection Fraction Registry (CASPER)

Brugada Syndrome: Clinical, Genetic, Molecular, Cellular, and Ionic Aspects

Novel therapeutic strategies for the management of ventricular arrhythmias associated with the Brugada syndrome

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