Intracellular calcium dynamics and acetylcholine-induced triggered activity in the pulmonary veins of dogs with pacing-induced heart failure

Chou, Chung Chuan; Nguyen, Bich Lien; Tan, Alex Y.; Chang, Po Cheng; Lee, Hui Ling; Lin, Fun‐Chung; Yeh, San Jou; Fishbein, Michael C.; Lin, Shien Fong; Wu, Delon; Wen, Ming; Chen, Peng Sheng

doi:10.1016/j.hrthm.2008.04.009

Cited by 43 publications

(42 citation statements)

References 17 publications

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“…Ablation of highfrequency sites results in AF termination in a significant proportion of patients with paroxysmal AF, even if the underlying mechanisms remain unresolved (9). We previ- ously showed that PV focal discharge sites were colocated with the DF max sites during acetylcholineinduced AF (5). Infusion of ryanodine and thapsigargin suppressed PV focal discharge and resulted in noninducibility of sustained AF in 4 of 6 preparations, suggesting that inhibition of intracellular calcium accumulation may suppress the triggers of AF within the PVs.…”

Section: Discussionmentioning

confidence: 93%

“…We have previously shown that the left superior pulmonary vein (LSPV)-LA junction is a privileged site for anisotropic re-entry (4). Acetylcholine infusion facilitates both PV focal discharge and micro-reentry at the LSPV-LA junction to perpetuate AF, and pharmacological suppression of PV focal discharge may inhibit the AF inducibility in a heart failure canine model (5). Whether radiofrequency ablation (RFA) targeting at the rotor anchoring sites is effective in suppressing AF inducibility remains unknown.…”

confidence: 99%

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Epicardial Ablation of Rotors Suppresses Inducibility of Acetylcholine-Induced Atrial Fibrillation in Left Pulmonary Vein–Left Atrium Preparations in a Beagle Heart Failure Model

Chou

Wen

Lee

et al. 2011

Journal of the American College of Cardiology

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Section: Discussionmentioning

confidence: 93%

confidence: 99%

Epicardial Ablation of Rotors Suppresses Inducibility of Acetylcholine-Induced Atrial Fibrillation in Left Pulmonary Vein–Left Atrium Preparations in a Beagle Heart Failure Model

Chou

Wen

Lee

et al. 2011

Journal of the American College of Cardiology

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“…2,13,19 The study by de Groot et al 2 postulates transmural conduction of fibrillation waves as the leading mechanism of epicardial breakthrough, whereas many others use radial spread of activation as criterion to identify ectopic focal discharges during AF. [20][21][22][23][24] Using radial spread of activation and QS electrogram morphology as criterion for ectopy, Lee et al 25 recently demonstrate that AF in dogs undergoing vagal stimulation can be maintained by multiple ectopic foci.…”

Section: Discussionmentioning

confidence: 99%

Transmural Conduction Is the Predominant Mechanism of Breakthrough During Atrial Fibrillation

Eckstein

Zeemering

Linz

et al. 2013

Circ: Arrhythmia and Electrophysiology

137

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Present hypotheses on mechanisms underlying breakthrough events include transmural conduction from the opposing layer of the atrial wall (endo-epicardial or vice versa), transmural microreentry, or ectopic focal discharges. 2,[5][6][7][8][9][10][11][12] Electric dissociation between the endocardial bundle network and the epicardial layer (EED) during AF is a prerequisite condition for transmural conduction of fibrillation waves because only in the presence of EED electric activity in 1 layer of the atrial wall can encounter excitable tissue in the opposing layer.We recently demonstrated that in goats EED increases during the first 6 months of AF, 13 which might well explain the higher incidence of breakthrough in complex substrates for AF. However, increasing evidence for altered intracellular Ca 2+ handling in atrial myocytes of AF patients supports the hypothesis that ectopic focal discharges because of triggered activity might also occur during AF and contribute to its perpetuation. 9,12,14 © 2013 American Heart Association, Inc. Background-Endo-epicardial dissociation (EED) of electric activations resulting in transmural conduction of fibrillation waves (breakthroughs) has been postulated to contribute to the complexity of the substrate of atrial fibrillation (AF). The aim of this study was to elucidate the correlation between EED and incidence of breakthrough and to test the plausibility of transmural conduction versus ectopic focal discharges as sources of breakthrough. Methods and Results-We analyzed high-resolution simultaneous endo-epicardial in vivo mapping data recorded in left atrial free walls of goats with acute AF, 3 weeks and 6 months of AF (all n=7). Waves were analyzed for number, size, and width and categorized according to their origin outside (peripheral wave) or within the mapping area (breakthrough). Breakthrough incidence was lowest (2.1±1.0%) in acute AF, higher (11.4±6.1%) after 3 weeks (P<0.01 versus acute AF) and highest (14.2±3.8%) after 6 months AF (P<0.001 versus acute AF) and similar in the epicardium and endocardium. Most of the breakthroughs (86%; n=564) could be explained by transmural conduction, whereas only 13% (n=85) could be explained by ectopic focal discharges. Transmural microreentry did not play a role as source of breakthrough. Conclusions-This is the first study to present simultaneous endo-epicardial in vivo mapping data at sites of breakthrough events. Breakthrough incidence and degree of EED increased with increasing AF substrate complexity. In goat left atrial free walls, most of the breakthroughs can be explained by transmural conduction, whereas ectopic focal discharges play a limited role as source of breakthrough. (Circ Arrhythm Electrophysiol. 2013;6:334-341.) Circ Arrhythm Electrophysiol

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“…Autonomic hyperinnervation causes spontaneous paroxysmal AF in dogs (42), with sympathovagal nerve discharge immediately preceding AF paroxysms (43). Vagal activation may promote spontaneous arrhythmogenesis by reducing APD, allowing adrenergically induced afterdepolarizations to induce ectopic activity in susceptible regions such as pulmonary veins (44).…”

Section: Extracardiac Factors Contributing To Ectopic Activitymentioning

confidence: 99%

Recent advances in the molecular pathophysiology of atrial fibrillation

Wakili¹,

Voigt²,

Kääb³

et al. 2011

J. Clin. Invest.

477

461

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Atrial fibrillation (AF) is an extremely common cardiac rhythm disorder that causes substantial morbidity and contributes to mortality. The mechanisms underlying AF are complex, involving both increased spontaneous ectopic firing of atrial cells and impulse reentry through atrial tissue. Over the past ten years, there has been enormous progress in understanding the underlying molecular pathobiology. This article reviews the basic mechanisms and molecular processes causing AF. We discuss the ways in which cardiac disease states, extracardiac factors, and abnormal genetic control lead to the arrhythmia. We conclude with a discussion of the potential therapeutic implications that might arise from an improved mechanistic understanding.Authorship note: Reza Wakili and Niels Voigt contributed equally to this work.

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Intracellular calcium dynamics and acetylcholine-induced triggered activity in the pulmonary veins of dogs with pacing-induced heart failure

Abstract: BACKGROUND-Heart failure increases autonomic nerve activities and changes intracellular calcium (Ca i ) dynamics.

Cited by 43 publications

References 17 publications

Epicardial Ablation of Rotors Suppresses Inducibility of Acetylcholine-Induced Atrial Fibrillation in Left Pulmonary Vein–Left Atrium Preparations in a Beagle Heart Failure Model

Epicardial Ablation of Rotors Suppresses Inducibility of Acetylcholine-Induced Atrial Fibrillation in Left Pulmonary Vein–Left Atrium Preparations in a Beagle Heart Failure Model

Transmural Conduction Is the Predominant Mechanism of Breakthrough During Atrial Fibrillation

Recent advances in the molecular pathophysiology of atrial fibrillation

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