Possible atrial proarrhythmic effects of class 1C antiarrhythmic drugs

doi:10.1016/0002-9149(90)90856-V

The American Journal of Cardiology

Volume 66, Issue 3, 1 August 1990, Pages 378-383

https://doi.org/10.1016/0002-9149(90)90856-V Get rights and content

Abstract

The class IC antiarrhythmic drugs encainide and flecainide have been used to treat ventricular arrhythmias.^1,2 Although not currently approved, they are also being used in the treatment of atria1 arrhythmias.^3,4 This antiarrhythmic action results from a marked depressant effect on conduction velocity and a moderate effect on prolonging refractoriness in the myocardium.^5,6 This marked depression of conduction velocity also results in the highest incidence of ventricular proarrhythmic effects observed with any class of antiarrhythmic drug.^7,8 However, less is known regarding their potential to produce atria1 proarrhythmic effects.^3,4 Recently we observed 6 patients who were being treated with flecainide or encainide for preexisting ventricular or atria1 arrhythmias, and who developed new or modified symptomatic atria1 arrhythmias with a rapid ventricular response. In 2 cases, life-threatening consequences arose from the arrhythmia. The clinical details of these cases are presented and the potential mechanisms of the atria1 proarrhythmic effects of the 1C drugs are discussed.

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Cited by (146)

Drug Therapy in Adult Congenital Heart Disease
2017, Cardiac Electrophysiology Clinics
Citation Excerpt :
Although they have minimal effect on the action potential duration, they cause marked conduction slowing, resulting in electrical heterogeneity and proarrhythmia, with consequent development of ventricular arrhythmias and increased mortality when they are used in patients with structurally abnormal hearts. Similarly, slowing of conduction can organize atrial fibrillation into a slow atrial flutter20 (which can potentially conduct in a 1:1 ratio to the ventricle) and hence AV nodal blocking agents should always be used with class IC agents. These agents are predominantly used in the treatment of atrial arrhythmias, but are also effective in the treatment of ventricular arrhythmias when the benefits outweigh their proarrhythmic risks.
Flecainide-induced incessant orthodromic atrioventricular reentrant tachycardia in Wolff-Parkinson-White syndrome: Uneven depression of accessory pathway conduction
2016, HeartRhythm Case Reports
Citation Excerpt :
A similar proarrhythmic effect has not been described with antiarrhythmic drugs in patients with an AP. In fact, the literature only describes the proarrhythmic effect of flecainide causing atrial flutter or ventricular tachycardia,5,6 but not the development of incessant supraventricular tachycardia in subjects with an AP. In the present report we describe a patient with Wolff-Parkinson-White syndrome due to a right paraseptal AP in whom the administration of flecainide resulted in an incessant form of AVRT resembling the permanent form of junctional reciprocating tachycardia.
1:1 atrial-flutter. Prevalence and clinical characteristics
2013, International Journal of Cardiology
Citation Excerpt :
It is however not possible to reproduce the same 1:1 conduction obtained during 1: 1 atrial flutter by atrial pacing [14,17]. The role of antiarrhythmic drugs has also been previously reported [19–21] mainly with class I antiarrhythmic drugs and this factor was also noted in the present study. The ventricular response during atrial flutter is determined by the refractory period of the AV node, the degree of concealed conduction within the AV node, and the level of autonomic tone.
Little is known about the epidemiology of 1:1 atrial flutter (AFL). Our objectives were to determine its prevalence and predisposing conditions.
1037 patients aged 16 to 93 years (mean 64 ± 12) were consecutively referred for AFL ablation. 791 had heart disease (HD). Patients admitted with 1/1 AFL were collected. Patients were followed 3 ± 3 years.
1:1 AFL-related tachycardiomyopathy was found in 85 patients, 59 men (69%) with a mean age of 59 ± 12 years. The prevalence was 8%. They were compared to 952 patients, 741 men (78%, 0.04), with a mean age of 65 ± 12 years (0.002) without 1:1 AFL. Factors favoring 1:1 AFL was the absence of HD (35 vs 23%, 0.006), the history of AF (42 vs 30.5%)(0.025) and the use of class I antiarrhythmic drugs (34 vs 13%)(p < 0.0001), while use of amiodarone or beta blockers was less frequent in patients with 1:1 AFL (5, 3.5%) than in patients without 1:1 AFL (25, 15%) (p < 0.0001, 0.03). The failure of ablation (9.4 vs 11%), ablation-related complications (2.3 vs 1.4%), risk of subsequent atrial fibrillation (AF) (20 vs 24%), risk of AFL recurrences (19 vs 13%) and risk of cardiac death (5 vs 6%) were similar in patients with and without 1:1 AFL.
The prevalence of 1:1 AFL in patients admitted for AFL ablation was 8%. These patients were younger, had less frequent HD, had more frequent history of AF and received more frequently class I antiarrhythmic drugs than patients without 1:1 AFL. Their prognosis was similar to patients without 1:1 AFL.
Clinical approach to atrial tachycardia and atrial flutter from an understanding of the mechanisms. Electrophysiology based on anatomy
2012, Revista Espanola de Cardiologia
En el año 2009 se llevaron a cabo en España 2.343 procedimientos de ablación con catéter de aleteo, taquicardia macrorreentrante atípica o taquicardia auricular focal, con un crecimiento del 8% sobre el año anterior, lo que da una idea de la importancia clínica de estas arritmias. La clasificación tradicional que distingue la taquicardia auricular del aleteo auricular basándose en criterios de frecuencia y morfología de ondas ha dejado de ser relevante, en un momento en que el desarrollo de la electrofisiología clínica puede permitir una intervención curativa sobre la arritmia, basada en su mecanismo, y se hace muy necesario acercar la experiencia del laboratorio a la clínica. En esta revisión se dibuja el panorama actual de los mecanismos de taquicardias auriculares, tanto focales como reentrantes, procurando establecer lazos con los conceptos clásicos que permitan al clínico enfrentarse a los diagnósticos diferenciales y hacer las indicaciones correctas de tratamiento, incluido el estudio electrofisiológico. Algunos de los conceptos expuestos son complejos, pero creemos que es necesario apuntar la perspectiva de los métodos electrofisiológicos que permiten dibujar las bases anatómicas de las arritmias, que hoy resultan más fácilmente comprensibles gracias a la construcción de moldes anatómicos con sistemas computarizados de navegación.
In 2009, 2343 catheter ablation procedures were performed in Spain for focal atrial tachycardia or atrial flutter (typical and atypical), with a yearly growth rate of 8%, indicating the clinical importance of these arrhythmias. The classic categorization of atrial tachycardia and atrial flutter based on rate and morphological criteria has become almost irrelevant at a time when clinical electrophysiology may lead to curative intervention based on a definition of the mechanism, making it necessary to bring laboratory experience closer to clinical practice. In this review we outline our present understanding of atrial tachycardia mechanisms, both focal and macroreentrant, and attempt to establish the conceptual links with classic concepts that may help the clinician to make a differential diagnosis and establish therapeutic indications, including that of an electrophysiologic study. Some of the concepts may seem complex, but we thought it important to provide an overview of the electrophysiological methods that may eventually lead to the description of the anatomic bases of the arrhythmias; currently, these are easier to understand thanks to the virtual anatomic casts built using computerized navigation systems.
Full English text available from: www.revespcardiol.org
Cardiac Arrhythmias
2010, Brocklehurst's Textbook of Geriatric Medicine and Gerontology
Aggravation of Arrhythmia by Antiarrhythmic Drugs (Proarrhythmia)
2010, Cardiac Electrophysiology Clinics
Citation Excerpt :
As a result of this, among other factors, including blockade of multiple ionic channels (as discussed in “Risk factors for arrhythmia aggravation” in the section on electrocardiographic changes), amiodarone and dronedarone do not generally produce torsade des pointes.40–44 Although antiarrhythmic drugs may provoke new ventricular tachyarrhythmia in patients being treated for a supraventricular tachyarrhythmia, this form of arrhythmia aggravation should be distinguished from drug-induced rate-related aberration of ventricular conduction or prolongation of the QRS complex duration during a supraventricular tachyarrhythmia (see Fig. 4).45–47 In this situation the wide complex tachycardia may be confused with a new ventricular tachyarrhythmia.

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^☆: This work was done during the tenure of Clinician Scientist Award 88 414 from the American Heart Association to Dr. Chen.

¹: Dr. Fleck was a Fellow in Cardiac Electrophysiology at the University of California at San Diego Medical Center, from Balboa Naval Hospital, San Diego, California.

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Brief reportPossible atrial proarrhythmic effects of class 1C antiarrhythmic drugs☆

Abstract

JACC

Am J Cardiol

Am J Cardiol

Am Heart J

Am Heart J

Am J Cardiol

Brief report
Possible atrial proarrhythmic effects of class 1C antiarrhythmic drugs☆