Jayakumar Sahadevan

Role of Functional Block Extension in Lesion-Related Atrial Flutter

Background —A line of block in the right atrium (RA) between the venae cavae is necessary to obtain classic atrial flutter (AFL). We tested the hypothesis that the location of that line of block would determine whether the AFL reentrant circuit would be due to single-loop reentry or figure-of-8 reentry. Methods and Results —Simultaneous mapping from 392 sites (both atria and the atrial septum) was performed in 13 normal dogs before and after creating a linear lesion on the RA free wall. The lesion was 1 to 1.5 cm anterior and parallel to the crista terminalis (7 dogs) or posterior and close to the crista terminalis region (6 dogs). Sustained AFL (>2 minutes) was then induced. In 4 dogs with an anterior lesion, the AFL reentrant circuit traveled around the lesion (lesion reentry). In 9 dogs (3 with anterior lesions and 6 with posterior lesions), the AFL reentrant circuit included the anterior RA free wall, the atrial septum, and Bachmann’s bundle (single-loop reentry). In these 9 dogs, the fixed line of block was extended to the superior and/or inferior vena cava by a functional line of block, thereby preventing lesion reentry. No figure-of-8 reentry was induced. Conclusions —In this model, the location of a fixed line of block and its functional extension determine the type of AFL reentry. These data provide an explanation for the chronic AFL that occurs in some patients after surgical repair of congenital heart lesions.

Confirmation of novel noninvasive high-density electrocardiographic mapping with electrophysiology study: Implications for therapy

Background—Twelve lead ECGs have limited value in precisely identifying atrial and ventricular activation during arrhythmias, including accessory atrioventricular conduction activation. The aim of this study was to report a single center’s clinical experience validating a novel, noninvasive, whole heart, beat-by-beat, 3-dimensional mapping technology with invasive electrophysiological studies, including ablation, where applicable. Methods and Results—Using an electrocardiographic mapping (ECM) system in 27 patients, 3-dimensional epicardial activation maps were generated from >250 body surface ECGs using heart–torso geometry obtained from computed tomographic images. ECM activation maps were compared with clinical diagnoses, and confirmed with standard invasive electrophysiological studies mapping. (1) In 6 cases of Wolff–Parkinson–White syndrome, ECM accurately identified the ventricular insertion site of an accessory atrioventricular connection. (2) In 10 patients with premature ventricular complexes, ECM accurately identified their ventricular site of origin in 8 patients. In 2 of 10 patients transient premature ventricular complex suppression was observed during ablation at the site predicted by ECM as the earliest. (3) In 10 cases of atrial tachycardia/atrial flutter, ECM accurately identified the chamber of origin in all 10, and distinguished isthmus from nonisthmus dependent atrial flutter. (4) In 1 patient with sustained exercise induced ventricular tachycardia, ECM accurately identified the focal origin in the left ventricular outflow tract. Conclusions—ECM successfully provided valid activation sequence maps obtained noninvasively in a variety of rhythm disorders that correlated well with invasive electrophysiological studies.

Variable Clinical Features and Ablation of Manifest Nodofascicular/Ventricular Pathways

Background—Manifest nodofascicular/ventricular (NFV) pathways are rare. Methods and Results—From 2008 to 2013, 4 cases were identified with manifest NFV pathways from 3 centers. The clinical findings and ablation sites are reported. All 4 cases presented with a wide complex tachycardia but with different QRS morphologies. Case 1 showed a left bundle branch block/superior axis, case 2 showed a right bundle branch block/inferior axis, case 3 showed a left bundle branch block/inferior axis, and case 4 showed a narrow QRS tachycardia and a wide complex tachycardia with a left bundle branch block/inferior axis. Three of the 4 tachycardias had atrioventricular dissociation ruling out extranodal accessory pathways, including atriofascicular pathways. Programmed extrastimuli showed evidence of a decremental accessory pathway in 3 of the 4 cases. Coexisting tachycardia mechanisms were seen in 3 of the 4 cases (atrioventricular nodal reentry tachycardia [2] and atrioventricular reentrant tachycardia [1]). Ablation in the slow pathway region eliminated the NFV pathway in 3 (transient in 1) with the other responding to surgical closure of a large atrial septal defect. The NFV pathway was a critical part of the tachycardia circuit in 1 and proved to be a bystander in the other 3 cases. Conclusions—Manifest NFV pathways presented with variable QRS expression dependent on the ventricular insertion site and often coexisted with other tachycardia mechanisms (atrioventricular nodal reentry tachycardia and atrioventricular reentrant tachycardia). In most cases, the atrial insertion of the pathway was in or near the slow pathway region. The NFV pathways were either critical to the tachycardia circuit or served as bystanders.

Response to Letter Regarding Article, “Variable Clinical Features and Ablation of Manifest Nodofascicular/Ventricular Pathways”

We thank Drs Papagiannis and Kanter1 for their interest and keen attention to our recent article. We shall address each of the points raised in their letter. Case 1: There is no difference between your description of the mechanism of case I and that provided in the article. Case 2: There is again no substantive difference with regards to tachycardia mechanism. You are correct. Figure 4A shows an obvious error in that we clearly show that stim A-V increases with A2. Thank you for pointing out this oversight. Case 3: We are well aware of the differential diagnoses of mechanisms resulting in reverse activation of the His bundle,2 but these points are moot …

Noninvasive diagnostic mapping of supraventricular arrhythmias (wolf-parkinson-white syndrome and atrial arrhythmias)

The 12-lead electrocardiogram has limited value in precisely identifying the origin of focal or critical component of reentrant arrhythmias during supraventricular arrhythmias, as well as precisely locating accessory atrioventricular conduction pathways. Because of these limitations, efforts have been made to reconstruct epicardial activation sequences from body surface measurements obtained noninvasively. The last decade has registered significant progress in obtaining clinically useful data from the attempts to noninvasively map the epicardial electrical activity. This article summarizes the recent advances made in this area, specifically addressing the clinical outcomes of such efforts relating to atrial arrhythmias and Wolf-Parkinson-White syndrome.

Confirmation of Novel Noninvasive High-Density Electrocardiographic Mapping With Electrophysiology StudyClinical Perspective

Background—Twelve lead ECGs have limited value in precisely identifying atrial and ventricular activation during arrhythmias, including accessory atrioventricular conduction activation. The aim of this study was to report a single center’s clinical experience validating a novel, noninvasive, whole heart, beat-by-beat, 3-dimensional mapping technology with invasive electrophysiological studies, including ablation, where applicable. Methods and Results—Using an electrocardiographic mapping (ECM) system in 27 patients, 3-dimensional epicardial activation maps were generated from >250 body surface ECGs using heart–torso geometry obtained from computed tomographic images. ECM activation maps were compared with clinical diagnoses, and confirmed with standard invasive electrophysiological studies mapping. (1) In 6 cases of Wolff–Parkinson–White syndrome, ECM accurately identified the ventricular insertion site of an accessory atrioventricular connection. (2) In 10 patients with premature ventricular complexes, ECM accurately identified their ventricular site of origin in 8 patients. In 2 of 10 patients transient premature ventricular complex suppression was observed during ablation at the site predicted by ECM as the earliest. (3) In 10 cases of atrial tachycardia/atrial flutter, ECM accurately identified the chamber of origin in all 10, and distinguished isthmus from nonisthmus dependent atrial flutter. (4) In 1 patient with sustained exercise induced ventricular tachycardia, ECM accurately identified the focal origin in the left ventricular outflow tract. Conclusions—ECM successfully provided valid activation sequence maps obtained noninvasively in a variety of rhythm disorders that correlated well with invasive electrophysiological studies.

Confirmation of Novel Noninvasive High-Density Electrocardiographic Mapping With Electrophysiology StudyClinical Perspective: Implications for Therapy

Background—Twelve lead ECGs have limited value in precisely identifying atrial and ventricular activation during arrhythmias, including accessory atrioventricular conduction activation. The aim of this study was to report a single center’s clinical experience validating a novel, noninvasive, whole heart, beat-by-beat, 3-dimensional mapping technology with invasive electrophysiological studies, including ablation, where applicable. Methods and Results—Using an electrocardiographic mapping (ECM) system in 27 patients, 3-dimensional epicardial activation maps were generated from >250 body surface ECGs using heart–torso geometry obtained from computed tomographic images. ECM activation maps were compared with clinical diagnoses, and confirmed with standard invasive electrophysiological studies mapping. (1) In 6 cases of Wolff–Parkinson–White syndrome, ECM accurately identified the ventricular insertion site of an accessory atrioventricular connection. (2) In 10 patients with premature ventricular complexes, ECM accurately identified their ventricular site of origin in 8 patients. In 2 of 10 patients transient premature ventricular complex suppression was observed during ablation at the site predicted by ECM as the earliest. (3) In 10 cases of atrial tachycardia/atrial flutter, ECM accurately identified the chamber of origin in all 10, and distinguished isthmus from nonisthmus dependent atrial flutter. (4) In 1 patient with sustained exercise induced ventricular tachycardia, ECM accurately identified the focal origin in the left ventricular outflow tract. Conclusions—ECM successfully provided valid activation sequence maps obtained noninvasively in a variety of rhythm disorders that correlated well with invasive electrophysiological studies.

Actively rethinking the reentrant circuit

t m C w T t s i i Common atrial flutter (AFL), a macrorentrant circuit nvolving the right atrium (RA), is characterized by its ependence on the cavotricuspid isthmus (CTI), the latter emonstrated by concealed entrainment and successful terination of AFL during its ablation. Most components of he AFL reentrant circuit have been well described. Using arious forms of activation sequence mapping, including he techniques of entrainment mapping and postpacing inervals (PPIs), the anterior and the posterior boundaries of FL have been well defined. From these prior observaions, it has been considered that the tricuspid annulus erves as the anterior boundary and the line of block beween the superior and inferior vena cava as the posterior oundary of the AFL reentrant circuit. However, the supeior portion of the reentrant circuit of AFL has been less ell defined. The study published in this issue of Heart Rhythm by antucci et al characterized the AFL reentrant circuit not olely or primarily by its activation sequence pattern but ather by defining “active” and “passive” portions of the ircuit using the PPI technique. By defining further the uperior and anterior aspects of the reentrant circuit, they ave advanced our understanding of RA flutter. Their study also has made us rethink what constitutes the ctual reentrant circuit, especially when the wave front of he reentrant circuit courses between wide boundaries. oundaries are critical to a reentrant circuit, as they are equired to preserve its integrity. Without boundaries, short ircuiting will occur, and stable reentry will not be possible. hat, then, do “active” and “passive” portions of a reenrant circuit mean in this context? To address this question, it is useful to consider the xperience of ablation in the presence of reentrant circuits. fter creating AFL in their canine intercaval crush lesion odel, Rosenblueth and Garcia-Ramos introduced another rush lesion in the RA free wall separate from the intercaval rush lesion. This lesion did not affect the AFL cycle length. owever, when they made another crush lesion that con-