Role of Progressive Widening of the Temporal Excitable Gap for Perpetuation of Atrial Fibrillation in the Goat

Shan, Zhaoliang; Yan, J S; Jun-yan, Zhou; Shi, Xiaorui; Guo, Jianping; Hu, Yuan; Allessie, Maurits A.; Wang, Yutang

doi:10.1253/circj.cj-09-0596

Cited by 7 publications

(2 citation statements)

References 22 publications

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“…This constitutes an AF induced, paradoxical physiological adaptation of the atrial APD to changes in heart rate. This maladaptation of the atrial APD had also been observed in prior human investigation [41,57,70,71] as well as animal models [54,[72][73][74].…”

Section: Atrial Electrophysiological Properties and Atrial Fibrillationsupporting

confidence: 76%

Monophasic Action Potential Recordings in Atrial Fibrillation and Role of Repolarization Alternans

2012

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Atrial fibrillation (AF) affects millions of people worldwide and is associated with increased rates of death, stroke and other thromboembolic events, heart failure, diminished quality of life, reduced exercise capacity and left ventricular dysfunction. While mechanisms of AF have been described, the current focus has been to uncover both triggers and substrate. Atrial electrical remodeling is a recognized substrate for the perpetuation of AF. Monophasic action potential (MAP) recordings provide a unique method to investigate localized myocardial depolarization and repolarization, and have been central to descriptions of atrial electrical properties in both physiological and AF states. Electric heterogeneity in AF manifested as rate maladaptation and repolarization alternans is posited to be mechanistically involved in AF development. Epidemiology of atrial fibrillationAtrial fibrillation (AF) affects 1-2% of the population with increases expected over the next several decades [1]. AF is associated with increased rates of death, stroke and other thrombo-embolic events, heart failure events, diminished quality of life, reduced exercise capacity and left ventricular dysfunction [1]. The prevalence of AF increases in each decade of life, as does the number of strokes attributable to AF [2,3]. The prevalence of AF-related hospitalizations in the USA is predicted to surpass 3.8 and 5.6 million by 2025 and 2050, respectively [4]. Mechanisms of AFSeveral mechanisms of AF have been described. The prevailing concept has focused on interplay between triggers that induce and substrate that maintain arrhythmia [5]. Pulmonary vein triggers are thought to contribute heavily to the development of AF. Studies support the fact that episodes of AF can be initiated by focal impulses within the pulmonary veins that propagate to atrial tissue, and radio-frequency ablation of these foci can terminate AF [6]. Other triggers, including non-pulmonary vein focal triggers [7], autonomic nervous system modulation [8] and atrial stretch [9] have been implicated in development of AF [10,11].Electrical remodeling of the atria, along with structural changes, is recognized as essential substrate for persistence of AF. To appreciate the effect of electrical remodeling on AF, normal atrial electrophysiological properties will be reviewed. Recording of monophasic action potentials (MAPs) by the "Franz" contact electrode catheter facilitated the investigation of both normal and pathologic properties of the atria. MAP recordingRecording of MAPs provides the only method to investigate localized myocardial depolarization and repolarization [12,13]. Under optimal conditions, MAPs record the repolarization time course of transmembrane action potentials (TAPs)

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Section: Atrial Electrophysiological Properties and Atrial Fibrillationsupporting

confidence: 76%

Monophasic Action Potential Recordings in Atrial Fibrillation and Role of Repolarization Alternans

2012

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“…The efficacy of I Na blockers to inhibit I Na (and therefore prolong atrial ERP) seems to be reduced in persistent versus paroxysmal AF, which may, in turn, contribute to a reduced effectiveness of I Na blockers in suppressing persistent versus paroxysmal AF. Several factors may decrease the ability of I Na blockers to inhibit I Na in long-lasting versus short-lasting AF, ie, (1) 2–5 mV more negative RMP 14 , 149 (consistent with augmentation of I K1 31 ), (2) shorter atrial APD, 47 , 48 (3) longer DI (including during AF), 150 and (4) a right-ward shift of the steady-state inactivation curve for the sodium channel (increasing the availability of the sodium channel). 149 In patients with persistent AF, inhibition of I K1 should act to normalize atrial RMP (shifting RMP to a more positive potential) and shorten DI (secondary to prolongation of late repolarization), enhancing the inhibition of the sodium channel.…”

Section: Af Maintenance: Reentry or Focal? Insight From Pharmacologicmentioning

confidence: 99%

Investigational Anti–Atrial Fibrillation Pharmacology and Mechanisms by Which Antiarrhythmics Terminate the Arrhythmia: Where Are We in 2020?

Burashnikov

2020

Journal of Cardiovascular Pharmacology

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: Antiarrhythmic drugs remain the mainstay therapy for patients with atrial fibrillation (AF). A major disadvantage of the currently available anti-AF agents is the risk of induction of ventricular proarrhythmias. Aiming to reduce this risk, several atrial-specific or -selective ion channel block approaches have been introduced for AF suppression, but only the atrial-selective inhibition of the sodium channel has been demonstrated to be valid in both experimental and clinical studies. Among the other pharmacological anti-AF approaches, “upstream therapy” has been prominent but largely disappointing, and pulmonary delivery of anti-AF drugs seems to be promising. Major contradictions exist in the literature about the electrophysiological mechanisms of AF (ie, reentry or focal?) and the mechanisms by which anti-AF drugs terminate AF, making the search for novel anti-AF approaches largely empirical. Drug-induced termination of AF may or may not be associated with prolongation of the atrial effective refractory period. Anti-AF drug research has been largely based on the “suppress reentry” ideology; however, results of the AF mapping studies increasingly indicate that nonreentrant mechanism(s) plays an important role in the maintenance of AF. Also, the analysis of anti-AF drug-induced electrophysiological alterations during AF, conducted in the current study, leans toward the focal source as the prime mechanism of AF maintenance. More effort should be placed on the investigation of pharmacological suppression of the focal mechanisms.

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Pathophysiology of Atrial Fibrillation

Burashnikov¹,

Antzelevitch²

2017

Cardiac Arrhythmias, Pacing and Sudden Death

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Role of Progressive Widening of the Temporal Excitable Gap for Perpetuation of Atrial Fibrillation in the Goat

Cited by 7 publications

References 22 publications

Monophasic Action Potential Recordings in Atrial Fibrillation and Role of Repolarization Alternans

Monophasic Action Potential Recordings in Atrial Fibrillation and Role of Repolarization Alternans

Investigational Anti–Atrial Fibrillation Pharmacology and Mechanisms by Which Antiarrhythmics Terminate the Arrhythmia: Where Are We in 2020?

Pathophysiology of Atrial Fibrillation

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