The Pathophysiologic Basis of Fractionated and Complex Electrograms and the Impact of Recording Techniques on Their Detection and Interpretation

Bakker, Jacques M.T. de; Wittkampf, Fred H.M.

doi:10.1161/circep.109.904763

Cited by 162 publications

(142 citation statements)

References 73 publications

(57 reference statements)

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“…44,45 With low resolution mapping, poor local tissue-electrode contact and heavy signal processing and interpolation, it is possible that cause slowed, dyssynchronous, and/or anisotropic local conduction. 50,51 In human AF it has been proposed that fractionated electrograms may be caused by local collision of multiple wavelets, zones of slow conduction, local reentry, areas adjacent to high frequency sites where wavebreak and fibrillatory conduction occur or direct autonomic innervation. 51,52 Fractionated electrograms can be fixed and caused by anatomic barriers such as scar or inhomogeneous tissue, or they may be functional, dynamic and related to changes in wavefront propagation throughout the myocardium.…”

Section: Limitations Of Targeting Rotors With Ablation For the Treatmmentioning

confidence: 99%

“…50,51 In human AF it has been proposed that fractionated electrograms may be caused by local collision of multiple wavelets, zones of slow conduction, local reentry, areas adjacent to high frequency sites where wavebreak and fibrillatory conduction occur or direct autonomic innervation. 51,52 Fractionated electrograms can be fixed and caused by anatomic barriers such as scar or inhomogeneous tissue, or they may be functional, dynamic and related to changes in wavefront propagation throughout the myocardium. It has been further proposed that these fractionated sites are important in sustaining AF, 53 and that targeting fractionated electrograms with ablation can terminate AF and prevent its re-induction or recurrence.…”

Section: Limitations Of Targeting Rotors With Ablation For the Treatmmentioning

confidence: 99%

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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: Limitations Of Targeting Rotors With Ablation For the Treatmmentioning

confidence: 99%

Section: Limitations Of Targeting Rotors With Ablation For the Treatmmentioning

confidence: 99%

Mechanisms of Atrial Fibrillation – Reentry, Rotors and Reality

Waks

Josephson²

2014

Arrhythmia &Amp; Electrophysiology Review

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“…6,14,30 There are data that suggest that such electrograms are frequently identified at sites where catheter ablation does not terminate VT. 19,20 Conversely, only 50% of central, proximal, or exit sites of re-entry isthmuses have abnormal electrograms. 15 The present study confirms these results that while abnormal electrograms were prevalent within ventricular scar, only a small proportion was related to VT supporting channels.…”

Section: Scar-related Electrograms and Vt Channelsmentioning

confidence: 99%

High-Density Mapping of Ventricular Scar

Nayyar

Wilson

Ganesan

et al. 2014

Circ: Arrhythmia and Electrophysiology

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Background-Surviving myocytes within scar may form channels that support ventricular tachycardia (VT) circuits. There are little data on the properties of channels that comprise VT circuits and those that are non-VT supporting channels. Methods and Results-In 22 patients with ischemic cardiomyopathy and VT, high-density mapping was performed with the PentaRay catheter and Ensite NavX system during sinus rhythm. A channel was defined as a series of matching pacemaps with a stimulus (S) to QRS time of ≥40 ms. Sites were determined to be part of a VT channel if there were matching pace-maps to the VT morphology. This was confirmed with entrainment mapping when possible. Of the 238 channels identified, 57 channels corresponded to an inducible VT. Channels that were part of a VT circuit were more commonly located within dense scar than non-VT channels (97% versus 82%; P=0.036). VT supporting channels were of greater length (mean±SEM, 53±5 versus 33±4 mm), had higher longest S-QRS (130±12 versus 82±12 ms), longer conduction time (103±14 versus 43±13 ms), and slower conduction velocity (0.87±0.23 versus 1.39±0.21 m/s) than non-VT channels (P<0.001). Of all the fractionated, late, and very late potentials located in scar, only 21%, 26%, and 29%, respectively, were recorded within VT channels. Conclusions-High-density mapping shows substantial differences among channels in ventricular scar. Channels supporting VT are more commonly located in dense scar, longer than non-VT channels, and have slower conduction velocity. Only a minority of scar-related potentials participate in the VT supporting channels. MethodsThis study was approved by the Human Research Ethics Committee of the Royal Adelaide Hospital and the University of Adelaide. Patient PopulationTwenty-two consecutive patients with ICM with recurrent VT or VT storm (≥3 episodes or implantable cardioverter defibrillator therapies for VT in 24 hours) undergoing a clinically indicated catheter ablation procedure were studied. Patients with a previous VT ablation, acute coronary event within the preceding 1 month, intracardiac thrombus, mechanical prosthetic valve, and severe aortoiliac peripheral vascular disease were excluded. Electrophysiological StudyThe procedure was done in the postabsorptive state under conscious sedation. Briefly, a quadripolar catheter and decapolar catheter were positioned at the right ventricular apex and coronary sinus, respectively. Programmed ventricular stimulation was performed from the right ventricular apex at 2 drive cycle lengths (600 and 400 ms) with ≤3 extrastimuli. All sustained monomorphic VTs induced at baseline, during the course of the study, and after ablation were considered clinical VT. 21 A 20-pole catheter (PentaRay; 2-6-2 mm interelectrode spacing, 1 mm electrodes; Biosense-Webster Inc, Diamond Bar, CA) was introduced either retrogradely using standard sheaths or transeptally using the Agilis NxT steerable introducer (St Jude Medical Inc, St Paul, MN) into the left ventricle (LV) for mapping. Activated clotting time was...

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“…Venkatachalam KL,et al 9 The pathophysiologic basis of fractionated and complex electrograms and the impact of recording techniques on their detection and interpretation. de Bakker JM et al 10 Recording and interpreting electrograms is fundamental to electrophysiologic studies and mapping. An understanding of how recording techniques influence electrograms, including discussion of artifacts is provided by Venkatachalam and coworkers.…”

Section: Arrhythmogenic Implications Of Fibroblast-myocyte Interactiomentioning

confidence: 99%

Fundamental Concepts in Electrophysiology in Cases and Reviews

Stevenson

Asirvatham²

2013

Circ: Arrhythmia and Electrophysiology

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A ssimilating the increasing body of knowledge required for the treatment of patients with cardiac arrhythmias is a substantial task. The trainee is bombarded with chapters and reviews that are important for providing the frame work from which to develop a detailed and nuanced knowledge acquired from clinical experience and ongoing education. Images and Case Reports provide succinct observations of not only a novel or unusual finding, but often of the fundamentals that must be appreciated to place novel findings in context. The Teaching Points series in Circulation Arrhythmia and Electrophysiology provides a more indepth synthesis of case-based learning building on common and uncommon clinical findings. The purpose of this Casebased Curriculum in Clinical Electrophysiology is to provide the clinician and trainee with an easily accessible body of current reviews, cases and Teaching Points that cover a broad range of the field. Links to the individual articles are provided to facilitate using this article as a spring board for review. Fundamentals of Electrophysiology, Mapping, Ablation, and ElectrocardiographyEmergence of complex behavior: An interactive model of cardiac excitation provides a powerful tool for understanding electric propagation. Spector PS, et al. 1 To facilitate an understanding of the relations between electrophysiologic properties and geometry that govern conduction, block and reentry, Spector and colleagues have developed an interactive model that allows the student to study the effects of varying parameters on conduction, block, reentry and even entrainment (http://circep.ahajournals.org/cgi/content/full/CIRCEP.110.961524/DC1). Munoz F, et al. 4 Teaching points with 3-dimensional mapping of cardiac arrhythmia: Mechanism of arrhythmia and accounting for the cycle length. Del Carpio Munoz F, et al. 5 Accurate activation sequence mapping of cardiac arrhythmias is a fundamental skill in cardiac electrophysiology. For complex arrhythmias an electroanatomic mapping system, which allows the mapping data to be displayed on a representation of the anatomy is often employed, as discussed in a series of articles Del Carpio Munoz and colleagues. [3][4][5][6] Accurate mapping requires selecting an appropriate reference point and mapping window and identification of the electrogram that indicates local activation. In applying a mapping strategy it is important to recognize features of macroreentrant, as compared to focal arrhythmias, and to recognize that seemingly small errors in assigning activation times, reference electrograms, or mapping windows, can render a map uninterpretable or meaningless. These issues are discussed in detail. Munoz F, et al. 6 Endocardial unipolar voltage mapping to detect epicardial ventricular tachycardia substrate in patients with nonischemic left ventricular cardiomyopathy. Hutchinson MD, et al. 7 Substrate mapping is a term that refers to localization of the likely arrhythmia substrate, during sinus or paced rhythm rather than during VT, and is of...

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The Pathophysiologic Basis of Fractionated and Complex Electrograms and the Impact of Recording Techniques on Their Detection and Interpretation

Cited by 162 publications

References 73 publications

Mechanisms of Atrial Fibrillation – Reentry, Rotors and Reality

Mechanisms of Atrial Fibrillation – Reentry, Rotors and Reality

High-Density Mapping of Ventricular Scar

Fundamental Concepts in Electrophysiology in Cases and Reviews

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