Adenosine-Insensitive Focal Atrial Tachycardia

Markowitz, Steven M.; Nemirovksy, Dmitry; Steín, Kenneth M.; Mittal, Suneet; Iwai, Sei; Shah, Bindi K.; Dobesh, David P.; Lerman, Bruce B.

doi:10.1016/j.jacc.2006.11.037

Cited by 70 publications

(17 citation statements)

References 16 publications

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“…Focal AT was subclassified as caused by triggered activity, enhanced automaticity, or microreentry. Triggered activity was diagnosed if AT was inducible and terminated with programmed stimulation, and a discrete electrogram (<20% of TCL) 9 was recorded from the site of earliest activation and successful ablation. Enhanced automaticity was diagnosed if AT was not inducible with programmed stimulation, induction was facilitated by catecholamine stimulation in nonincessant ATs (usually in association with warm-up of tachycardia rate during initiation and a cool-down period during termination), and a discrete electrogram was recorded from the site of earliest activation and successful ablation.…”

Section: Baseline Electrophysiology Studymentioning

confidence: 99%

“…Enhanced automaticity was diagnosed if AT was not inducible with programmed stimulation, induction was facilitated by catecholamine stimulation in nonincessant ATs (usually in association with warm-up of tachycardia rate during initiation and a cool-down period during termination), and a discrete electrogram was recorded from the site of earliest activation and successful ablation. AT due to microreenty was defined as AT that was inducible with programmed stimulation, showed electrogram fractionation (≥35% of TCL) 9 at a focal site of successful ablation, and had ≥75% of TCL mapped. Entrainment was attempted in all cases of AT that fulfilled criteria for microreentry.…”

Section: Baseline Electrophysiology Studymentioning

confidence: 99%

“…9,[13][14][15] However, the presence of fractionated electrograms alone is not entirely sufficient for validating the diagnosis of microreentry because fractionated electrograms are also associated with macroreentry and, in rare instances, of triggered activity. 4,13 Patients with microreentrant AT are also more likely to have undergone previous ablation (65%), which in approximately half the patients provided the substrate for AT in this study.…”

Section: Focal At: Microreentry Versus Triggered Activity and Enhancementioning

confidence: 99%

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Unifying Algorithm for Mechanistic Diagnosis of Atrial Tachycardia

Liu

Cheung

et al. 2016

Circ: Arrhythmia and Electrophysiology

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Background-No existing criteria unequivocally differentiate focal atrial tachycardia (AT) caused by microreentry, triggered activity, or enhanced automaticity. Although macroreentrant AT is readily diagnosed based on entrainment criteria, the smaller circuit dimension associated with microreentrant AT makes it challenging to validate the presence of reset with fusion. An algorithm was, therefore, developed that is independent of entrainment but which reliably identifies specific mechanisms of focal AT. Methods and Results-Fifty-nine patients with AT underwent adenosine testing after mapping of tacycardia. Ten ATs had nonfocal activation, with ≥90% of tachycardia cycle length identified with electroanatomical mapping, findings consistent with macroreenty. All ATs were insensitive to adenosine. Forty-nine patients had focal AT with centrifugal activation. In 32/49 (67%) ATs, electrograms were nonfractionated, and <50% of tachycardia cycle length could be mapped. Based on programmed stimulation, 26/32 (81%) of these ATs were classified as due to triggered activity and 6/32 (19%) as due to enhanced automaticity. Adenosine terminated 100% of triggered ATs and transiently slowed or suppressed 100% of automatic ATs. The remaining 17 focal ATs had localized fractionated electrograms (≥35% of tachycardia cycle length) at the site of successful ablation and were classified as microreentrant. Adenosine had no effect in these ATs. The response to adenosine accurately differentiated all subtypes of focal AT, P<0.05. Conclusions-Adenosine-sensitivity (termination or transient slowing/suppression) in response to adenosine was 100% sensitive and specific for identifying focal AT mechanisms due to triggered activity or automaticity, respectively. Absence of adenosine effect on focal AT identifies tachycardia due to microreentry. Methods Study PopulationWe studied 59 consecutive patients who presented for invasive electrophysiological evaluation and catheter ablation of AT and received adenosine during tachycardia. The presence of structural heart disease was based on a diagnosis of cardiomyopathy, valvular disease, coronary artery disease (> 60% stenosis), or prior myocardial infarction. All procedures were performed after informed consent was obtained for a study approved by the Institutional Review Board of Weill Cornell Medical College. Baseline Electrophysiology StudyAll patients underwent electrophysiology study in a postabsorptive state. Antiarrhythmic drugs were held for 5 half-lives before the study. Quadripolar catheters were positioned at the His bundle position and right ventricular apex. Right atrial electrogram recordings were obtained with either a quadripolar catheter positioned in the high right atrium or a 7-Fr duodecapolar catheter positioned along the tricuspid annulus. A 6-Fr decapolar catheter was positioned in the coronary sinus to record left atrial and left ventricular activity. In selected patients, a 5-spline mapping catheter configured as radial spokes was deployed (PentaRay Nav; Biosense-Webster, Dia...

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Section: Baseline Electrophysiology Studymentioning

confidence: 99%

Section: Baseline Electrophysiology Studymentioning

confidence: 99%

Section: Focal At: Microreentry Versus Triggered Activity and Enhancementioning

confidence: 99%

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Unifying Algorithm for Mechanistic Diagnosis of Atrial Tachycardia

Liu

Cheung

et al. 2016

Circ: Arrhythmia and Electrophysiology

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“…Termination of micro-reentrant AT with localized ablation without connecting to non-conducting obstacles or limiting critical mass 19 - a common result - offers a similar conundrum.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms for the Termination of Atrial Fibrillation by Localized Ablation

Rappel

Zaman

Narayan

2015

Circ: Arrhythmia and Electrophysiology

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Background Human atrial fibrillation (AF) can terminate after ablating localized regions, that supports the existence of localized rotors (spiral waves) or focal drivers. However, it is unclear why ablation near a spiral wave tip would terminate AF and not anchor reentry. We addressed this question by analyzing competing mechanisms for AF termination in numerical simulations, referenced to clinical observations. Methods and Results Spiral wave reentry was simulated in monodomain 2D myocyte sheets using clinically realistic rate-dependent values for repolarization and conduction. Heterogeneous models were created by introduction of parameterized variations in tissue excitability. Ablation lesions were applied as non-conducting circular regions. Computational models confirmed localized ablation may anchor spiral wave reentry, producing organized tachycardias. Several mechanisms also explained termination of AF to sinus rhythm. First, lesions may create an excitable gap vulnerable to invasion by fibrillatory waves. Second, ablation of rotors in regions of low-excitability (from remodeling) produced reentry in more excitable tissue allowing collision of wave-front and back. Conversely, ablation of rotors in high-excitability regions migrated spiral waves to less excitable tissue, where they detached to collide with non-conducting boundaries. Third, ablation may connect rotors to non-conducting anatomic orifices. Fourth, reentry through slow conducting channels may terminate if ablation closes these channels. Conclusions Limited ablation can terminate AF by several mechanisms. These data shed light on how clinical AF may be sustained in patients’ atria, emphasizing heterogeneities in tissue excitability, slow-conducting channels and obstacles that are increasingly detectable in patients and should be the focus of future translational studies.

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“…Adenosine will usually terminate AVJRT as well as some types of AT (making it less specific than carotid sinus massage). [8] Intravenous verapamil should be avoided in the emergency setting.…”

Section: Management Of Tachycardia Acute Management Of Svtmentioning

confidence: 99%

An approach to the patient with a suspected tachycardia in the emergency department

et al. 2015

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Patients present to the emergency department with either an ongoing tachycardia or a history suspicious of a tachycardia. Either way, the tachycardia needs to be documented, preferably on a 12-lead electrocardiogram (ECG) for diagnosis and management. If a tachycardia is not documented, a careful history of the palpitations should be taken to see if further monitoring and investigations are required. If a tachycardia is confirmed on an ECG, the clinician needs to classify it according to two variables: (i) regularity of the rhythm; and (ii) QRS width. This will allow a differential diagnosis to be made.

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Adenosine-Insensitive Focal Atrial Tachycardia

Abstract: ObjectivesThe purpose of this work was to describe the entity and mechanism of adenosine-insensitive focal atrial tachycardia (AT).

Cited by 70 publications

References 16 publications

Unifying Algorithm for Mechanistic Diagnosis of Atrial Tachycardia

Unifying Algorithm for Mechanistic Diagnosis of Atrial Tachycardia

Mechanisms for the Termination of Atrial Fibrillation by Localized Ablation

An approach to the patient with a suspected tachycardia in the emergency department

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