Introduction: Flecainide is a class Ic antiarrhythmic agent available in Europe since 1982. The clinical development program of flecainide provided good data on its antiarrhythmic effect for the prevention of ventricular and supraventricular arrhythmias. The Cardiac Arrhythmia Suppression Trial (CAST), conducted to test whether the arrhythmia suppression translates into prevention of sudden death, assessed the impact of flecainide and encainide therapy in patients with frequent ventricular ectopics and reduced left ventricular function who had survived an infarction. In that population, flecainide and encainide increased mortality. Consequently, sodium channel blockers are now rarely used to prevent sudden death and are not recommended in patients with heart failure. Current European and North American guidelines recommend the use of flecainide in carefully selected patients with atrial fibrillation (AF) and no documented structural heart disease.
Areas Covered: The aim of this review is to evaluate the available data on efficacy and safety of flecainide in all the spectrum of its indications including cardioversion of recent-onset AF, sinus rhythm maintenance in paroxysmal AF and management of ventricular tachyarrhythmias.
Expert Opinion: In the setting of AF and in carefully selected patients without structural heart disease, flecainide has shown a good efficacy and safety for both cardioversion and sinus rhythm maintenance.
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http://dx.doi.org/10.1517/14656566.2013.759212 | DOI Listing |
Front Pharmacol
December 2024
Department of Pediatrics, University of Missouri-Kansas City School of Medicine, Kansas City, MO, United States.
Flecainide acetate is a Class 1c anti-arrhythmic with a potent sodium voltage gated channel blockade which is utilized for the second-line treatment of tachyarrhythmias in children and adults. Given its narrow therapeutic index, the individualization of drug therapy is of utmost importance for clinicians. Despite efforts to improve anti-arrhythmic drug therapy, there remain knowledge gaps regarding the impact of variation in the genes relevant to flecainide's disposition and response.
View Article and Find Full Text PDFFront Cardiovasc Med
December 2024
Department of Paediatrics and Adolescent Medicine, The University of Hong Kong, Pok Fu Lam, Hong Kong SAR, China.
Background: Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare inherited arrhythmia disorder characterized by ventricular arrhythmia triggered by adrenergic stimulation.
Case Presentation: A 9-year-old boy presented with convulsions following physical exertion. Bidirectional ventricular tachycardia (VT) during a treadmill test led to the diagnosis of catecholaminergic polymorphic ventricular tachycardia (CPVT).
Korean Circ J
December 2024
Department of Pediatrics, Seoul National University Children's Hospital, Seoul National University College of Medicine, Seoul, Korea.
Background And Objectives: Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a life-threatening inherited arrhythmogenic disorder. Recently, , the major CPVT-causative gene, was associated with neuropsychiatric manifestations. We aimed to analyze the clinical presentations, neuropsychiatric manifestations, and treatment outcomes of children with CPVT.
View Article and Find Full Text PDFAnn Noninvasive Electrocardiol
January 2025
Department of Paediatrics and Adolescent Medicine, The University of Hong Kong, Pok Fu Lam, Hong Kong.
Background: Brugada syndrome (BrS) is an inherited channelopathy characterized by right precordial ST-segment elevation. This study investigates the clinical and genetic characteristics of children with BrS in Hong Kong.
Methods: A retrospective review was conducted at the only tertiary pediatric cardiology center in Hong Kong from 2002 to 2022, including all pediatric BrS patients under 18 years old.
J Am Heart Assoc
January 2025
Graduate Program in Translational Biology Medicine and Health, Virginia Tech Roanoke VA USA.
Background: Previous studies suggest the relationship between activation time (AT) and action potential duration (APD) in the heart is dependent on electrotonic coupling, but this has not been directly tested. This study assessed whether acute changes in electrical coupling, or other determinants of conduction or repolarization, modulate APD heterogeneity.
Methods And Results: Langendorff-perfused guinea pig hearts were epicardially paced and optically mapped after treatment with the gap junction uncoupler carbenoxolone, ephaptic uncoupler mannitol, ephaptic enhancer dextran 2MDa, sodium channel inhibitor flecainide, or rapid component of the delayed rectifier potassium channel inhibitor E4031.
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