Site-Dependent Intra-Atrial Conduction Delay

Papageorgiou, Panos; Monahan, Kevin M.; Boyle, Noel G.; Seifert, Mark J.; Beswick, Philippa; Zebede, Joseph; Epstein, Laurence M.; Josephson, Mark E.

doi:10.1161/01.cir.94.3.384

Cited by 198 publications

(32 citation statements)

References 22 publications

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“…Large atria and small reentrant circuits (short wavelength due to a short atrial refractory period and/or slow conduction velocity) allow multiple reentrant circuits to form and increase the probability of sustaining AF, while small atria (or surgically partitioned atria as in the maze procedure) and large reentrant circuits (long wavelengths) are unlikely to be able to sustain reentry and AF. 4 These observations also complement experimental human studies which have demonstrated increased rates of AF in patients with enlarged left atria 17 , intra-atrial conduction defects, [18][19][20] or abnormal atrial refractory periods. 18,20,21 Recent experimental data have suggested, however, that although functional reentry may be of critical importance in initiating and sustaining AF, it is significantly more complex than can be accounted for by only leading circle reentry with multiple simultaneous wavelets.…”

Section: Functional Reentry and The Leading Circle Modelsupporting

confidence: 76%

Mechanisms of Atrial Fibrillation – Reentry, Rotors and Reality

Waks

Josephson²

2014

Arrhythmia &Amp; Electrophysiology Review

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Atrial fibrillation (AF), the most common sustained arrhythmia, is a leading cause of stroke, and is associated with significant morbidity and mortality worldwide. Despite its frequency, clinical importance, and advances in technology and our knowledge of the molecular, ionic and physiological fundamentals of cardiac electrophysiology, our limited understanding of the mechanisms that initiate and sustain AF has prevented us from being able to truly cure this arrhythmia with antiarrhythmic drugs and/or ablation. This contrasts with other arrhythmias, such as AV nodal tachycardia or circus movement tachycardia using an accessory pathway, which have well-defined mechanisms and circuits that can be safely targeted with high rates of cure. The observations that AF may have different mechanisms in different patients, and that paroxysmal, persistent and permanent forms of AF may differ in how they are initiated and sustained, only serves to reinforce our lack of understanding of this ubiquitous arrhythmia. Historical Mechanisms of Atrial Fibrillation and the Multiple Wavelet HypothesisInterest and understanding of the mechanism of AF began to take form in the early 1900s. Given the chaotic and irregular nature of AF on the surface electrocardiogram, rapid firing of automatic atrial foci was considered a potential mechanism. However, after the seminal work of Mayer 1 , Mines 2 and Garrey 3 in laying the foundation for describing and understanding reentrant arrhythmias, atrial reentrant circuits emerged as the likely drivers of AF.4-7 Although these theories were conceptually sound, it was impossible to prove a specific mechanism with the technology of the time. Moe et al. demonstrated that it was probabilistically unlikely that a large number of simultaneous wavefronts would all die out simultaneously, and AF would therefore perpetuate. However, if the number of simultaneous wavelets were small and/or below a critical value (between 15 and 30 in Moe's computer model), 9 at some point all reentrant wavefronts would be simultaneously extinguished, and AF would therefore terminate. 8,9 Allessie et al. provided experimental evidence supporting this mechanism in a canine heart model of AF where four to six simultaneous reentrant wavelets were needed to sustain arrhythmia. 10 Further evidence supporting multiple wavelets in AF was demonstrated in a separate model, which evaluated the effect of various antiarrhythmic drugs on canine myocardium. This model demonstrated that termination of AF was associated with a reduction AbstractAtrial fibrillation (AF) is the most common sustained arrhythmia encountered in clinical practice, yet our understanding of the mechanisms that initiate and sustain this arrhythmia remains quite poor. Over the last 50 years, various mechanisms of AF have been proposed, yet none has been consistently observed in both experimental studies and in humans. Recently, there has been increasing interest in understanding how spiral waves or rotors -which are specific, organised forms of functional reentry -su...

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Section: Functional Reentry and The Leading Circle Modelsupporting

confidence: 76%

Mechanisms of Atrial Fibrillation – Reentry, Rotors and Reality

Waks

Josephson²

2014

Arrhythmia &Amp; Electrophysiology Review

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“…The relative spatial distributions of atrial rate maladaptation and remodeling 4 may increase APD dispersion to facilitate the transition to and maintenance of AF. These spatially nonuniform repolarization dynamics may help to explain why repolarization sequence is less responsive to activation sequence in the atrium 9,11,24 than the ventricle. 25 Although we studied APD during Afl, the majority of prior studies have been made after electrical cardioversion from tachycardia, 8,15,17,24 meaning that those APDs were often measured at slower (nontachycardia) rates and may also have been influenced by the electrical shock.…”

Section: Nonuniformity and Rate Maladaptation Of Atrial Apdmentioning

confidence: 99%

Alternans of Atrial Action Potentials During Atrial Flutter as a Precursor to Atrial Fibrillation

et al. 2002

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Background-The mechanisms underlying the transition of typical atrial flutter (Afl) to fibrillation (AF) remain unclear.We set out to test the hypothesis that Afl disorganizes to AF via alternans of atrial action potentials. Methods and Results-In 38 patients with Afl, monophasic action potentials (MAPs) were recorded at the isthmus and either high or low right atrium (HRA, LRA) during overdrive pacing to 160 ms or to the initiation of AF, whichever came first. MAP duration measured at 90% repolarization was longer at the isthmus in all patients, and failed to shorten with rate, compared with the HRA (nϭ38) or LRA (nϭ5). In 20 patients who developed AF, progressive pacing first caused alternans of isthmus MAP duration and amplitude at mean cycle length of 219Ϯ45 ms, followed by AF at a mean onset cycle length of 184Ϯ38 ms. Subsets of this group showed spontaneous action potential duration alternans at the isthmus (11 of 20 patients) and 2:1 isthmus conduction block immediately preceding AF (4 of 20 patients). In the 18 patients who did not develop AF, MAP alternans was less common (9 of 18 patients; PϽ0.0003), and occurred only at faster pacing (cycle lengthϭ169Ϯ25 ms; PϽ0.05). Conclusions-In patients with typical Afl, action potential duration rate maladaptation at the isthmus may lead to action potential duration alternans and conduction block preceding the transition to AF. These isthmus characteristics may enable the spontaneous initiation of AF through wavefront fractionation and may explain the benefits of isthmus ablation in preventing AF recurrence.

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“…Evidence suggesting that alternate and multiple sites of atrial pacing may result in less site-dependent conduction delay 16 and AF 17 has stimulated the development of pacing techniques for the prevention of atrial arrhythmias. 18 The effects of alternate and multiple pacing sites on atrial mechanical function are unknown.…”

Section: Effect Of Pacing Sitementioning

confidence: 99%

Reversal of Atrial Mechanical Stunning After Cardioversion of Atrial Arrhythmias

et al. 2002

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Background-Atrial mechanical stunning develops on termination of chronic atrial arrhythmias and is implicated in the genesis of thromboembolic complications after cardioversion. The mechanisms responsible for atrial mechanical stunning are unknown. The effects of atrial rate, isoproterenol, and calcium on atrial mechanical function in patients with atrial stunning have not been evaluated, and it is not known if atrial stunning can be reversed. Methods and Results-Thirty-five patients with chronic atrial flutter (AFL) undergoing radiofrequency ablation were studied. Fifteen patients in sinus rhythm undergoing ablation for paroxysmal AFL were studied as control for effects of the procedure. Left atrial appendage emptying velocities (LAAEVs) and spontaneous echocardiographic contrast (LASEC) were assessed by transesophageal echocardiography during AFL, after reversion to sinus rhythm, during atrial pacing at cycle lengths of 750 to 250 ms, after a postpacing pause, and with isoproterenol or calcium. PϽ0.0001). No change in LAAEV was observed in the paroxysmal AFL group. Conclusion-Atrial mechanical stunning can be reversed by pacing at increased rates and through the administration of isoproterenol or calcium. These findings suggest a functional contractile apparatus in the mechanically remodeled atrium as a result of chronic atrial flutter.

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Site-Dependent Intra-Atrial Conduction Delay

Cited by 198 publications

References 22 publications

Mechanisms of Atrial Fibrillation – Reentry, Rotors and Reality

Mechanisms of Atrial Fibrillation – Reentry, Rotors and Reality

Alternans of Atrial Action Potentials During Atrial Flutter as a Precursor to Atrial Fibrillation

Reversal of Atrial Mechanical Stunning After Cardioversion of Atrial Arrhythmias

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