Verapamil eliminates the hierarchical nature of activation frequencies from the pulmonary veins to the atria during paroxysmal atrial fibrillation

Kushiyama, Yasunori; Osaka, Toshiyuki; Yokoyama, Eriko; Hasebe, Hideyuki; Kuroda, Yusuke; Kamiya, Kaichiro; Kodama, Itsuo

doi:10.1016/j.hrthm.2010.01.008

Cited by 4 publications

(1 citation statement)

References 22 publications

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“…The ERP, wavelength and AFCL were not measured, and Ca 2+ channel blocker effects on AF were inconsistent. Thus, verapamil either increased atrial dominant frequency, suggestive of a pro-arrhythmic effect by promoting high frequency zones of activation (Kushiyama et al , 2010), or decreased the incidence of pulmonary vein ectopic activity and “burst AF” (Chen et al , 1999).…”

Section: Class IV Drugs (Ca2+ Channel Blockers): Electrophysiologimentioning

confidence: 99%

Mechanisms of termination and prevention of atrial fibrillation by drug therapy

Workman

Smith

Rankin

2011

Pharmacology & Therapeutics

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Atrial fibrillation (AF) is a disorder of the rhythm of electrical activation of the cardiac atria. It is the most common cardiac arrhythmia, has multiple aetiologies, and increases the risk of death from stroke. Pharmacological therapy is the mainstay of treatment for AF, but currently available anti-arrhythmic drugs have limited efficacy and safety. An improved understanding of how antiarrhythmic drugs affect the electrophysiological mechanisms of AF initiation and maintenance, in the setting of the different cardiac diseases that predispose to AF, is therefore required. A variety of animal models of AF has been developed, to represent and control the pathophysiological causes and risk factors of AF, and to permit the measurement of detailed and invasive parameters relating to the associated electrophysiological mechanisms of AF. The purpose of this review is to examine, consolidate and compare available relevant data on in-vivo electrophysiological mechanisms of AF suppression by currently approved and investigational anti-arrhythmic drugs in such models. These include the Vaughan Williams class I-IV drugs, namely Na + channel blockers, β-adrenoceptor antagonists, action potential prolonging drugs, and Ca 2+ channel blockers; the "upstream therapies", e.g., angiotensin converting enzyme inhibitors, statins and fish oils; and a variety of investigational drugs such as "atrial-selective" multiple ion channel blockers, gap junction-enhancers, and intracellular Ca 2+ -handling modulators. It is hoped that this will help to clarify the main electrophysiological mechanisms of action of different and related drug types in different disease settings, and the likely clinical significance and potential future exploitation of such mechanisms.

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Section: Class IV Drugs (Ca2+ Channel Blockers): Electrophysiologimentioning

confidence: 99%

Mechanisms of termination and prevention of atrial fibrillation by drug therapy

Workman

Smith

Rankin

2011

Pharmacology & Therapeutics

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Is verapamil a double-edged sword in rate control of paroxysmal atrial fibrillation?

Raatikainen

2010

Heart Rhythm

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Pharmacotherapy of Atrial Fibrillation: A Pathophysiological Perspective and Review

Jacob

Ali

Pidlaoan

et al. 2011

American Journal of Therapeutics

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Atrial fibrillation (AF) is one of the most common arrhythmia encountered in clinical practice. Although AF is due to the structural and electrophysiological alterations in the atria, its sustainability is multifactorial, and the actual mechanisms are still not clear. Despite the recent advances in catheter ablation technology and techniques, pharmacotherapy still remains the first-line therapy for the management of AF. Current pharmacotherapy targets ion channel alterations that in fact represent only one aspect of the management of this complex arrhythmia. Successful pharmacological treatment of AF and restoration of sinus rhythm is limited and is in part due to its potential deleterious side effects. Newer agents having diverse mechanisms acting on the recently uncovered pathophysiological processes are on the horizon. These include atrial repolarization delaying agents, newer class III agents, Na(+)-Ca(2+) channel blockers, stretch receptor blockers, I(KACH) blockers, gap junction modifiers, upstream therapies, and agents targeting ischemia-induced AF. Gene- and cell-specific therapies including 'tailored nanopharmacy,' newer rate control medications with minimal side effects and the emergence of novel drugs targeting multiple areas of AF arrhythmogenesis in tandem with electrical therapy may be the future direction in the management of AF.

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Verapamil eliminates the hierarchical nature of activation frequencies from the pulmonary veins to the atria during paroxysmal atrial fibrillation

Cited by 4 publications

References 22 publications

Mechanisms of termination and prevention of atrial fibrillation by drug therapy

Mechanisms of termination and prevention of atrial fibrillation by drug therapy

Is verapamil a double-edged sword in rate control of paroxysmal atrial fibrillation?

Pharmacotherapy of Atrial Fibrillation: A Pathophysiological Perspective and Review

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