Critical Isthmus Research Articles

CMR–Based Identification of Critical Isthmus Sites of Ischemic and Nonischemic Ventricular Tachycardia

ObjectivesThis study evaluates whether contrast-enhanced (CE) cardiac magnetic resonance (CMR) can be used to identify critical isthmus sites for ventricular tachycardia (VT) in ischemic and nonischemic heart disease. BackgroundFibrosis interspersed with viable myocytes may cause re-entrant VT. CE-CMR has the ability to accurately delineate fibrosis. MethodsPatients who underwent VT ablation with CE-CMR integration were included. After the procedure, critical isthmus sites (defined as sites with a ≥11 of 12 pacemap, concealed entrainment, or VT termination during ablation) were projected on CMR-derived 3-dimensional (3D) scar reconstructions. The scar transmurality and signal intensity at all critical isthmus, central isthmus, and exit sites were compared to the average of the entire scar. The distance to >75% transmural scar and to the core-border zone (BZ) transition was calculated. The area within 5 mm of both >75% transmural scar and the core-BZ transition was calculated. ResultsIn 44 patients (23 ischemic and 21 nonischemic, left ventricular ejection fraction 44 ± 12%), a total of 110 VTs were induced (cycle length 290 ± 67 ms). Critical isthmus sites were identified for 78 VTs (71%) based on ≥11 of 12 pacemaps (67 VTs), concealed entrainment (10 VTs), and/or termination (30 VTs). The critical isthmus sites, and in particular central isthmus sites, had high scar transmurality and signal intensity compared with the average of the entire scar. Of the pacemap, concealed entrainment, and termination sites, 74%, 100%, and 84% were within 5 mm of >75% transmural scar, and 67%, 100%, and 94% were within 5 mm of the core-BZ transition, respectively. The areas within 5 mm of both >75% transmural scar and the core-BZ transition (median 13% of LV) contained all concealed entrainment sites and 77% of termination sites. ConclusionsBoth in ischemic and nonischemic VT, critical isthmus sites are typically located in close proximity to the CMR-derived core-BZ transition and to >75% transmural scar. These findings suggest that CMR-derived scar characteristics may guide to critical isthmus sites during VT ablation.

Radiofrequency ablation of left atrial flutter mediated with double potentials in a seemingly normally structured heart

BackgroundLeft atrial flutter (left AFL) is common in patients who undergo atrial fibrillation ablation and cardiac surgery; however, few reports describe left AFL in detail in a seemingly normally structured heart, and the mechanisms of the occurrence of such arrhythmia are still not clear. We describe left AFL in patients without prior cardiac surgery or catheter ablation and discuss the electrophysiological characteristics that may explain the preferential generation and perpetuation of such tachycardia. Methods and resultsEleven patients with left AFL, who had no history of cardiac surgery or interventions, underwent electrophysiological studies and 3-dimensional electroanatomic mapping studies. Echocardiography revealed a relatively mild dilation of the left atrium, mild to moderate mitral regurgitation, and a normal left ventricular ejection fraction. The electroanatomic mapping during tachycardia showed a “reentrant” activation pattern in all patients. The mean tachycardia cycle length was 266±17ms. A single-loop reentrant circuit was identified in 7 patients. A counterclockwise left atrial flutter evolved around the mitral valve annulus in 6 patients. The tachycardia rotated around the left atrial anterior wall in 1 patient. Four patients exhibited a double-loop reentrant circuit with a “figure of 8” pattern reentry. Double potentials as the critical isthmus of the circuit were identified in the left atrial anterior wall near the mitral annulus which displayed a low-voltage area matched with the left atrium–aorta contiguity. The conduction velocity was significantly slower in the double-potential recording area than in the lateral mitral annulus (0.36±0.03m/s vs 0.74±0.12m/s; P<0.05). Successful ablation around the double-potential recording site caused an interruption of the tachycardia, and remained free of recurrence during a 12-month follow-up in all patients. ConclusionLeft AFL in patients without a history of surgery or ablation is rarely observed in clinical practice. The successful site of ablation was within the anterior wall near the mitral annulus showing the double potentials as the critical part of the reentrant circuit. This suggests that perhaps a double potential-targeted ablation may be effective for these patients.

Localizing the critical isthmus of postinfarct ventricular tachycardia: The value of pace-mapping during sinus rhythm

Most postinfarct ventricular tachycardias (VTs) are sustained by a reentrant mechanism. The "protected isthmus" of the reentrant circuit is critical for the maintenance of VTs and the target for catheter ablation. Various techniques based on conventional electrophysiology and/or detailed three-dimensional (3D) reconstruction of the VT circuit are used to unmask this isthmus. The purpose of this study was to assess pace-maps (PMs) to identify postinfarct VT isthmuses. We hypothesized that an abrupt change in paced QRS morphology may be used to identify a VT isthmus and be targeted for successful ablation. High-density 3D PMs were matched to the subsequent 3D endocardial reentrant VT activation mapping in 10 patients (8 men; age 70.7 ± 10.8 years) who underwent successful postinfarct VT ablation. At each pacing site in a given patient, the 12-lead ECG recorded during pacing was compared to that of VT, with the resulting matching percentage (up to 100% for perfect matches) allocated to this point to generate color-coded PMs. With respect to VT isthmuses, the best percentages of matching were found in the exit zones and isthmus exit part (89% ± 8% and 84% ± 7%, respectively) and the poorest adjacent to scar border in the outer entrance zones (23% ± 28%), in the entrance zones (39% ± 34%), and in the entrance part of the isthmus (32% ± 26%). The color-coded sequence (from the best to the poorest matching sites) on the PMs revealed figure-of-eight pictures matching the VT activation time maps and identifying VT isthmuses. Pace-mapping is useful for unmasking VT isthmuses in patients with well-tolerated postinfarct endocardial reentrant VTs.

Simplified progressive approach for the ablation of scar related atrial macroreentrant tachycardias

Radiofrequency ablation of scar related right atrial flutter is challenging. Long procedures, prolonged fluoroscopic times and high percentages of recurrences are of concern. We present a simple and progressive approach based on a single electroanatomic map of the right atrium. Twenty-two consecutive patients with atrial flutter and history of cardiac surgery were included. An electrophysiologic study was performed to define localization (left or right) and cavo-tricuspid isthmus participation using entrainment mapping. After a critical isthmus was localized, ablation was performed with an external irrigated tip catheter with a power limit of 30 W. Potential ablation sites were confirmed by entrainment. The predominant cardiopathy was atrial septal defect. All arrhythmias were localized in the right atrium; mean cycle length of the clinical flutter was 274 ± 31 ms. Only 40% had cavo-tricuspid isthmus participation. None of the patients with successful ablation had recurrences after 13 ± 9.4 months of follow-up. A progressive approach with only one activation/voltage CARTO(®) map of the atrium and ablation of all potential circuits is a highly effective method for ablating scar related macroreentrant atrial arrhythmias.

Pseudo-postpacing interval of diastolic potential after entrainment pacing of remote bystander pathway in reentrant ventricular tachycardia

After entrainment pacing, the postpacing interval of a diastolic potential may be misinterpreted if the distal tip of the ablation catheter captures a remote bystander pathway adjacent to the critical isthmus of a complex reentrant circuit in a structurally diseased heart. We discuss this possible pitfall of entrainment mapping of reentrant ventricular tachycardia, observed after a healed myocardial infarction.

Unusual response to entrainment of ventricular tachycardia: In or out?

FEATURED ARRHYTHMIA Unusual response to entrainment of ventricular tachycardia: In or out? Roderick Tung, MD, FHRS, Kalyanam Shivkumar, MD, PhD, FHRS From the UCLA Cardiac Arrhythmia Center, David Geffen School of Medicine at UCLA, Los Angeles, California. Case presentation A 70-year-old man with history of inferior myocardial infarction with an ejection fraction of 25% was urgently transferred for ablation of incessant slow ventricular tachycardia (VT). Electroanatomic mapping revealed extensive inferolateral scar extending to the inferior septum. Entrainment mapping demonstrated an entrance in periannular inferolateral scar with an exit anterior to the aortomitral continuity. Entrain- ment mapping was performed in the scar at a site in between these 2 regions. Is this response in or out of the circuit? (Figure 1) Commentary Entrainment mapping, or continuous resetting of VT, is the gold standard technique for characterizing the components within a reentrant circuit. Demonstration of an isthmus requires the presence of (1) concealed fusion, (2) postpacing interval within 30 ms of the tachycardia cycle length, and (3) stimulus-QRS (S-QRS) interval equal to electrogram-QRS (EGM-QRS) interval. 1 The presence of these responses is highly predictive of termination with ablation. 2,3 In this case, overdrive pacing of the slow VT (680 ms) is performed at 620 ms (10 mA @ 2 ms). Two distinct diastolic potentials are seen during VT, and it is important to distinguish the near-field EGM captured from far-field components in order to accurately measure the postpacing interval. 4 Disappearance of a local EGM during pacing represents either direct capture or saturation of the channel from pacing. Two features confirm that the early diastolic EGM is not captured during entrainment: (1) the S-QRS interval would be longer as the EGM-QRS occurs in early diastole and (2) analysis of the onset of pacing reveals KEYWORDS Ventricular tachycardia; Entrainment ABBREVIATIONS EGM-QRS ¼ electrogram-QRS; MES ¼ multiple exit site; S-QRS ¼ stimulus-QRS; VT ¼ ventricular tachycardia (Heart Rhythm Address reprint requests and correspondence: Dr Roderick Tung, UCLA Cardiac Arrhythmia Center, David Geffen School of Medicine at UCLA, 100 Medical Plaza, Suite 660, Los Angeles, CA 90095. E-mail address: rtung@mednet.ucla.edu. 1547-5271/$-see front matter B 2014 Heart Rhythm Society. All rights reserved. saturation (Figure 2, dashed circle) from the pacing current in the absence of local and QRS capture. The last entrained beat demonstrates overt or manifest fusion. The postpacing interval measured to the peak component of the return sensed EGM is within 30 ms of the tachycardia cycle length (680 ms). The S-QRS interval appears to match the EGM-QRS interval when measuring the peak deflection of the late diastolic EGM. These responses suggest entrainment from an outer loop site on the periphery of the reentrant circuit with antidromic fusion outside the circuit. However, careful analysis of the first 2 paced beats on the tracing demonstrates a QRS morphology with an exact 12-lead match for the VT. The possibility of transient loss of capture during these 2 complexes is ruled out by acceleration of the VT to the pacing cycle length (620 ms). These 2 beats represent concealed fusion with a perfect match for the VT, and the S-QRS interval (145 ms) matches the EGM-QRS interval when the EGM is timed to the onset of the return diastolic potential rather than the peak. Analysis of the diastolic EGM before pacing is useful because the EGM is not yet saturated by the pacing channel, which allows more detailed analysis of multicomponent local EGMs (Figure 2). Closer analysis of this EGM confirms a fractionated compo- nent of the late diastolic potential 35 ms before the peak deflection (EGM-QRS interval 145 ms). Note that the first entrained beat after the onset of pacing has the same morphology as the last entrained beat. Interpretation of this entrainment response using the first 2 complexes in Figure 1 suggests a critical isthmus site. Ablation at this site resulted in the abrupt termination of VT within 4 seconds (Figure 3). We have previously reported the observation of multiple exit site (MES) morphologies when pace mapping within scar during sinus rhythm. 5 These sites are likely specific for reentrant isthmuses and importantly can be identified as surrogates for critical sites in sinus rhythm. However, pacing during sinus rhythm from a point-like source is likely to have a radial spread of activation in contrast to a broad reentrant wave front with a preferential exit during VT. Therefore, activation through MESs out of scar is more likely to be seen during pace mapping. The entrainment response in this case likely represents an alternate exit site from a common http://dx.doi.org/10.1016/j.hrthm.2013.09.006

Characterization of Anatomic Ventricular Tachycardia Isthmus Pathology After Surgical Repair of Tetralogy of Fallot

Although catheter ablation has been used to target the critical isthmuses for re-entrant monomorphic ventricular tachycardia in tetralogy of Fallot, the anatomy and histology of these regions have not been fully characterized. Autopsy hearts with tetralogy of Fallot were evaluated to clarify the pathological substrate. Twenty-seven hearts with the diagnosis of tetralogy of Fallot were examined. Anatomically defined isthmuses included (1A) ventriculotomy-to-tricuspid annulus, (1B) ventriculotomy-to-ventricular septal defect patch, (2) ventriculotomy-to-pulmonary annulus, (3) pulmonary annulus-to-ventricular septal defect patch, and (4) ventricular septal defect patch-to-tricuspid annulus. Length and wall thickness were measured for all specimens, and light microscopy was performed for those surviving surgery. For subjects≥5 years at death, isthmuses 1A and 1B were present in 88%, isthmus 2 in 25%, isthmus 3 in 94%, and isthmus 4 in 13%. Isthmus 1A had the greatest dimensions (mean length, 3.9±1.08; thickness, 1.5±0.3 cm), isthmus 1B intermediate dimensions (mean length, 2.4±0.8; thickness, 1.1±0.4 cm), and isthmuses 2, 3, and 4 the smallest dimensions (mean length, 1.5±0.5, 1.4±0.8, and 0.6±0.4 cm; thickness, 0.5±0.2, 0.6±0.2, and 0.3±0.04 cm, respectively). Histological examination (n=7) revealed increased fibrosis in anatomic isthmuses relative to nonisthmus controls. Consistencies in isthmus dimensions and histology are found among patients with repaired tetralogy of Fallot. Isthmus 1A is associated with the largest morphological dimensions, whereas the nearby newly described isthmus 1B is significantly smaller. Of isthmuses with the smallest dimensions, isthmus 3 is the most common.

Three-Dimensional Architecture of Scar and Conducting Channels Based on High Resolution ce-CMR

Background— Conducting channels are the target for ventricular tachycardia (VT) ablation. Conducting channels could be identified with contrast enhanced–cardiac magnetic resonance (ce-CMR) as border zone (BZ) corridors. A 3-dimensional (3D) reconstruction of the ce-CMR could allow visualization of the 3D structure of these BZ channels. Methods and Results— We included 21 patients with healed myocardial infarction and VT. A 3D high-resolution 3T ce-CMR was performed before CARTO-guided VT ablation. The left ventricular wall was segmented and characterized using a pixel signal intensity algorithm at 5 layers (endocardium, 25%, 50%, 75%, epicardium). A 3D color-coded shell map was obtained for each layer to depict the scar core and BZ distribution. The presence/characteristics of BZ channels were registered for each layer. Scar area decreased progressively from endocardium to epicardium (scar area/left ventricular area: 34.0±17.4% at endocardium, 24.1±14.7% at 25%, 16.3±12.1% at 50%, 13.1±10.4 at 75%, 12.1±9.3% at epicardium; P &lt;0.01). Forty-five BZ channels (2.1±1.0 per patient, 23.7±12.0 mm length, mean minimum width 2.5±1.5 mm) were identified, 85% between the endocardium and 50% shell and 76% present in ≥1 layer. The ce-CMR–defined BZ channels identified 74% of the critical isthmus of clinical VTs and 50% of all the conducting channels identified in electroanatomic maps. Conclusions— Scar area in patients with healed myocardial infarction decreases from the endocardium to the epicardium. BZ channels, more commonly seen in the endocardium, display a 3D structure within the myocardial wall that can be depicted with ce-CMR. The use of ce-CMR–derived maps to guide VT ablation warrants further investigation.

Relationship Between Voltage Map “Channels” and the Location of Critical Isthmus Sites in Patients With Post-Infarction Cardiomyopathy and Ventricular Tachycardia

The goal of this study was to determine the relationship of the ventricular tachycardia (VT) isthmus to channels of preserved voltage on an electroanatomic voltage map in postinfarction cardiomyopathy. Substrate mapping in patients with postinfarction cardiomyopathy and VT may involve lowering the voltage cutoff that defines the scar (<1.5 mV) to identify "channels" of relative higher voltage within the scar. However, the prevalence of channels within the scar identified by using electroanatomic mapping and the relationship to the protected VT isthmus identified by entrainment mapping is unknown. Detailed bipolar endocardial voltage maps (398 ± 152 points) from 24 patients (mean age 69 ± 9 years) with postinfarction cardiomyopathy (ejection fraction 33 ± 9%) and tolerated VT were reviewed. Endocardial scar was defined according to voltage <1.5 mV. Isolated late potentials (ILPs) were identified and tagged on the electroanatomic voltage map. The baseline voltage cutoffs were then adjusted until all channels were identified. The VT isthmus was identified using entrainment mapping. Inferior and anterior/lateral infarction was present by voltage mapping in 18 and 6 patients, respectively (scar area 44 ± 24 cm(2)). By adjusting voltage cutoffs, 37 channels were identified in 21 (88%) of 24 patients. The presence of ILPs within a channel was seen in 11 (46%) of 24 patients and 17 (46%) of 37 channels. A VT isthmus site was contained within a channel in only 11 of 24 patients or 11 of 37 channels. No difference in voltage characteristics was identified between clinical and nonclinical channels. Voltage channels with ILPs harbored the clinical isthmus with a sensitivity and specificity of 78% and 85%, respectively. Channels were identified in 88% of patients with VT by adjusting the voltage limits of bipolar maps; however, the specificity of those channels in predicting the location of VT isthmus sites was only 30%. The presence of ILPs inside the voltage channel significantly increases the specificity for identifying the clinical VT isthmus.

Understanding atrial arrhythmia mechanisms by mapping and ablation

strate for the arrhythmia. It is perhaps pertinent to note the limitations of the electrocardiogram diagnosis. The term ‘flutter’ is used to describe rapid atrial tachycardias (AT) with an undulating waveform without isoelectric baseline; however, this has been overlooked by many groups reporting left AT that, as in Coffey’s paper, show rather long cycle lengths, around 300 ms, and longer isoelectric baselines between P-waves. Since the term ‘flutter’ is so closely related to typical flutter, depending on the cavotricuspid isthmus, it tends to suggest a macroreentrant mechanism, and the term ‘atrial tachycardia’ would appear more appropriate, as it does not pre-judge the mechanism. 2 In fact, around one-third of the mechanisms described in this study were focal discharges. The mapping technique, leading to ablation of the critical isthmus or the focus responsible for the arrhythmia, is remarkable because it creates excellent activation maps on the virtual atrial anatomy and allows, with some limitations, better understanding of the arrhythmia mechanism. Reduction of pacing manoeuvres to the minimum necessary to confirm the role of critical areas of the circuit minimizes the chances of altering activation sequences, a significant concern in left atrial macroreentrant AT, in which complex combinations of anatomic and functional obstacles can support multiple reentrant circuits and/or focal mechanisms. The average number of AT mechanisms encountered was 1.9 per patient, and 21 patients had three or more AT mechanisms, underlining the importance of this method. Another point of interest is the extremely low voltage recorded at some of the critical isthmuses that would suggest that activation could course over thin epicardial layers of atrial myocardium over endocardial scars. The interpretation of these local electrograms would be very difficult in the absence of the full activation maps supported with critical entrainment runs to confirm participation of adjacent areas in the circuit. The complexity and low amplitude of the electrograms would make quite impossible to reliably measure local post-pacing intervals at these critical isthmuses. Atrial tachycardia mechanisms were based in both atria and one-third were called septal. Two-thirds of the AT had a macroreentrant mechanism, and about one-third were focal. It is not clear from the paper if combinations of focal and macroreentrant mechanisms were found in the same patient and if more than one AT could be localized at distant sites in the same patient, but the report does give the general impression of dealing with severely diseased (remodelled? injured?) atria. The worse performance with ‘septal’ AT raises questions about the ability to precisely locate foci or critical isthmuses in this anatomically complex area. This seems particularly relevant because fragmented electrograms are often recorded from the septal atrial walls 3 and this

A new approach for catheter ablation of atrial tachycardia following atrial fibrillation ablation

The origin and mechanisms of focal and macro-re-entrant atrial tachycardia occurring after ablation of paroxysmal or persistent atrial fibrillation are difficult to determine and are often the cause of distress for both patients and electrophysiologists. The purpose of this study was to describe a novel practical approach which would be helpful in planning the treatment of atrial tachycardia in patients who had received prior atrial fibrillation ablation. We used an algorithm which aims to facilitate mapping and ablation strategies, using both conventional electrophysiological tools and a three-dimensional electroanatomic approach. We investigated a series of 40 patients with atrial tachycardia who had undergone a prior ablation procedure for paroxysmal or persistent atrial fibrillation with a step-wise approach. This approach consisted of four steps: the use of a decapolar catheter to assess the coronary sinus and an entrainment map to evaluate the cavotricuspid isthmus (CTI). If the CTI was not involved, we used a 20-pole dual-loop circular mapping catheter, AFocusII DL, to map the left atrium chamber rapidly during the rhythm of interest. We identified the target entrainment at the putative channels and performed catheter ablation at the critical isthmus of these macrocircuits until the restoration of sinus rhythm. Seventy-five atrial tachycardias were identified in 40 consecutive patients (1.9 ± 1.6 per patient). In 48, the mechanism was macro-re-entry, and the remaining 27 were focal. During 18 months of follow-up, the treated arrhythmia recurred in only three patients, whereas in another four patients, a different atrial tachycardia was observed. The remaining 33 patients maintained sinus rhythm. The increased acquisition speed by AFocusII DL facilitated the reconstruction of the geometric chamber, and the generation of an isochronal activation map reduced processing time and fluoroscopy time per patient, together with the radiation exposure and patient radiation dose. A novel algorithm combining both conventional electrophysiology and a three-dimensional electroanatomic approach for rapid diagnosis, accurate mapping and ablation of iatrogenic atrial tachycardias showed high reproducibility and a satisfactory overall success rate.

Temporary Percutaneous Left Ventricular Support for Ablation of Untolerated Ventricular Tachycardias

Catheter ablation is increasingly recognized as an important option for the treatment of ventricular tachycardia (VT) in the serious clinical settings of frequent implantable cardioverter defibrillator shocks, and arrhythmia storms, in a variety of structural heart diseases.1 The high incidence of VTs that are not hemodynamically tolerated forces challenges to the traditional approaches of using activation and entrainment mapping to localize the ablation target area, in favor of a strategy of substrate modification that can be performed during sinus rhythm. In some patients, however, a clear target cannot be detected during sinus rhythm; this frequently occurs in some forms of nonischemic cardiomyopathies. More recently, interest is growing in the possibility of making VT tolerable through cardiopulmonary support. Article see p 1202 In this issue of Circulation: Arrythmia and Electrophysiology , Ostadal et al2 provide experimental data on the different capabilities offered by 3 commercially available support systems. It should be kept in mind, however, that these systems are Food and Drug Administration–approved only to support temporary high-risk situations. The data offered in this study are limited in that they provide only information related to systemic arterial pressure in healthy animals and do not allow any evaluation of the different levels of perfusion attained at individual critical organs, ie, brain or kidney. The study does, however, offer a comparative evaluation of the performances of these different systems and offers the opportunity to discuss advantages and limitation of their use. Percutaneous left ventricular assist devices (pLVAD) are increasingly used in few high-volume and skilled centers around the world in an attempt to achieve hemodynamic support during previously nontolerated ventricular arrhythmias to allow use of electrophysiological maneuvers to identify the critical isthmus of the circuit where an effective ablation will produce a permanent interruption of the VT. It is hoped that …

Long-term results of catheter ablation for ventricular tachycardia in arrhythmogenic right ventricular cardiomyopathy/dysplasia

AimsThis study analyzed the arrhythmogenic substrates and mechanisms of ventricular tachycardia (VT), and long-term outcomes of catheter ablation in patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D). MethodsNine patients (1 female, 40±17 years) with ARVC/D and sustained monomorphic VT (SMVT) exhibiting left bundle branch block morphology of the QRS complex were studied. The diagnosis of ARVC/D was confirmed by means of echocardiography, magnetic resonance imaging, and electroanatomic mapping in all patients. ResultsThe patients underwent 10 ablation procedures. At the initial ablation, the mean VT rate was 196±21 (170–240)bpm. In total, 17 VT types were observed. One VT type with left axis (+I, aVL), or right axis (+II,III,aVF) of the QRS complex was present in 3 and 1 patient, respectively. Two VT types of left and intermediate (+I, II, aVL) axis or of left and right axis of the QRS complex were observed in 3 and 2 patients, respectively. Multiple VT types with left axis QRS complex recurred in 1 patient. One VT displayed characteristics of focal arrhythmia, the mechanism of remaining VTs was clearly macroreentrant. The critical slow-conducting isthmus of the reentry circuit was located at the infero-lateral aspect of tricuspid annulus and was bounded by the annulus and baso-lateral wall scar in 7 VTs; the isthmus was located within the scars in the remaining VTs. During 52±31 (12–93) month follow-up since the last ablation, 8 (89%) patients remained free from any VT recurrence without antiarhythmic drug. ConclusionsPatients with ARVC/D frequently presented ≥1 SMVT type. The critical isthmus of reentry circuit was dominantly located close to the tricuspid annulus. Long-term outcome of extensive endocardial ablation was favorable with isolated VT recurrences in one patient.

Incisional Atrial Flutter in a Patient with Repaired Tetralogy of Fallot

A 40-year-old man with a history of tetralogy of Fallot and multiple cardiac surgeries presented for mapping and ablation of an incessant atrial tachyarrhythmia. Activation and entrainment mapping in conjunction with an electroanatomic mapping system defined the mechanism of the tachycardia as a dual-loop incisional reentry atrial flutter around previous atriotomy scars in the lateral right atrium. A line of ablation lesions transecting the critical isthmus of both loops of the dual-loop circuit successfully terminated the atrial flutter.

Letter by Obeyesekere Regarding Article, “Functional Pace-Mapping Responses for Identification of Targets for Catheter Ablation of Scar-Mediated Ventricular Tachycardia”

HomeCirculation: Arrhythmia and ElectrophysiologyVol. 5, No. 5Letter by Obeyesekere Regarding Article, “Functional Pace-Mapping Responses for Identification of Targets for Catheter Ablation of Scar-Mediated Ventricular Tachycardia” Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBLetter by Obeyesekere Regarding Article, “Functional Pace-Mapping Responses for Identification of Targets for Catheter Ablation of Scar-Mediated Ventricular Tachycardia” Manoj N. Obeyesekere, MBBS Manoj N. ObeyesekereManoj N. Obeyesekere Mildura Cardiology, Victoria, Australia Search for more papers by this author Originally published1 Oct 2012https://doi.org/10.1161/CIRCEP.112.974055Circulation: Arrhythmia and Electrophysiology. 2012;5:e100To the Editor:The elegant study by Tung et al1 presents additional sites for ablation of scar-based ventricular tachycardia (VT). Pace-mapped induction sites predicted successful sites of termination during ablation. This study raises a hypothesis that pace-mapped induction may be viewed as a surrogate for entrainment.At induction as with at the end of entrainment, when pacing from within the scar and the exit site after the last paced impulse at induction is the same as the induced/entrained VT, conduction follows the same route, and the return cycle to the site of pacing may also be similar. Thus, the postpacing interval after entrainment may be the same as the postpacing interval measured from the last pacing stimulus that initiates VT (postpacing intervalInitiation). Similarly, the stimulus-QRS interval that initiates VT or during pacing is because of the same distance as the stimulus-QRS interval during entrainment if the exit is the same. In fact, the authors report that 71% of critical isthmus sites had a stimulus-QRS during pacing minus electrogram-QRS interval of <30 ms. Thus, the cycle at induction may provide comparable information to that derived after entrainment.2 This assumption can be confounded by decrement and concealed conduction at initiation, and remote site pace mapping may match VT morphology in up to 29% of sites.3 Could the authors provide data on analysis of the postpacing intervalInitiation minus tachycardia cycle length at pace-mapped induction sites, both when the last paced beat matched the VT and when it did not? Data on analysis of entrainment mapping at the 21 pace-mapped induction sites would also be valuable.DisclosuresNone.Manoj N. Obeyesekere, MBBSMildura CardiologyVictoria, Australia

Value of Dynamic Substrate Mapping to Identify the Critical Diastolic Pathway in Postoperative Ventricular Reentrant Tachycardias After Surgical Repair of Tetralogy of Fallot

Characterization of the Critical Isthmus in VT in TOF. The complexity of postoperative ventricular reentrant tachycardias may limit success of catheter ablation. The objective of this analysis was to compare the usefulness of dynamic substrate mapping (DSM) versus color-coded isopotential mapping of the noncontact mapping system for the identification of the critical diastolic pathway of postoperative ventricular reentrant tachycardias (VT) after surgical repair of tetralogy of Fallot (TOF). Postoperative VT had been studied applying isopotential maps with the noncontact mapping system EnSite in 7 patients, and radiofrequency current lesion lines had been applied across the shortest isthmus to target during sinus rhythm. Data of the noncontact mapping system were reanalyzed applying the DSM algorithm. For DSM, a 2-Hz filter and color settings between 0 mV and 50% of peak negative voltage (PNV) with autofocus turned off were used. DSM was initially applied over the QRS complex duration during sinus rhythm. Abnormal myocardium was defined as <35-40% of PNV. DSM was subsequently applied to ventricular diastole during the final 33% of VT cycle length. Areas with >70% of PNV within this time frame were to identify the critical diastolic pathway. Applying DSM, the critical diastolic pathway of the VT was identified in all 7 patients that corresponded to the regions targeted for ablation. By focusing the time reference to electrical diastole, when the VT wavefront is moving through the low-voltage area, the region of greatest relative voltage could be highlighted, which corresponded to the diastolic pathway. (J Cardiovasc Electrophysiol, Vol. 23, pp. 930-937, September 2012).

Showing Up Channels for Postinfarct Ventricular Tachycardia Ablation

The number of scar-related ventricular tachycardia (VT) ablation procedures is increasing worldwide. This is certainly due to the ever growing number of patients implanted with an implantable cardioverter defibrillator in whom an ablation procedure may be required to better control the ventricular arrhythmia burden, but is also likely related to our better understanding of the arrhythmias mechanisms as well as the improvement of the mapping techniques during the last 15 years. Most VTs, especially those arising after myocardial infarction, depend on a critical isthmus. Defining precisely the critical isthmus of postinfarct VT may be challenging, particularly when the arrhythmia is poorly tolerated. In the literature, there are extensive data concerning the value of conventional electrophysiological techniques, especially entrainment mapping in association with postpacing interval measurements, regarding the identification of postinfarct VT isthmuses. There are, however, other--sometimes emerging--approaches to image critical postinfarct VT channels. We have summarized these, reviewing data from the published literature as well as our own experience.

Role of the coronary sinus ostium musculature in reentrant formation

Radiofrequency ablation of focal atrial tachycardias (AT) is a validated technique with high success rates. However, electrophysiological (EP) characteristics and ablation strategy of localized reentrant AT originating from the coronary sinus ostium (CSo) have not been reported in detail so far. From January 2009 to July 2010, 1,453 patients underwent clinically motivated EP studies. Four patients were diagnosed with localized reentrant AT originating from the CSo. P wave morphology and consistency of tachycardia cycle length were studied. Subsequently, if reentry was suggested as an underlying mechanism for AT, color-coded 3-dimensional (3D) entrainment mapping was performed to localize the reentrant circuit or differentiate a localized reentrant AT from macroreentant AT, and also confirm reentry as an underlying mechanism of AT by evaluating consistency of return cycles after entrainment at multiple sites in both atria. Finally, activation mapping was performed to localize the earliest activation site. The P wave morphologies and isoelectric line between the P waves suggested most likely an AT originating from the CSo with a centrifugal activation pattern, which was confirmed by activation mapping. Consistency of return cycles and continuously fragmented local electrograms at successful ablation sites suggested reentry as an underlying AT mechanism. Color-coded 3D entrainment mapping in all 4patients located the reentrant circuit in the CSo. There were also two specific features observed. One was fragmented and/or double potentials recorded in the CSo with prominent prolonged electrogram duration compared to those during sinus rhythm. The other is a significant conduction delay within the CS. The myocardium of the CSo was suggested as a part of the critical isthmus within the reentrant circuit, while the rest of atria distal to the CSo and myocardial coat of the distal CS were not involved in the tachycardia circuit, which was confirmed by entrainment mapping. Although CSo myocardium has been implicated to be a part of atrioventricular nodal reentrant tachycardia, to the best of our knowledge, this is the first report showing the localized reentrant AT confined to the CSo. Three of our patients (75%) had concomitant atrial fibrillation (AF). Further studies should be warranted to clarify the role of AT from the CS in triggering AF.

Catheter ablation of three macroreentrant atrial tachycardias after surgical repair of Double-Outlet Right Ventricle

A 54-year-old man with a surgically repaired double-outlet right ventricle (DORV) presented with palpitations and worsening right heart failure. His 12-lead ECG showed atrial tachycardia (AT) with an atrial cycle length (CL) of 300ms and an inverted saw-tooth F-wave pattern in the inferior leads II, III, and aVF typical of atrial flutter. Electrophysiological study and radiofrequency catheter ablation were performed. A total of 3 sustained ATs (AT1–AT3) were induced. Using the electroanatomical mapping system, CARTO3, and conventional mapping techniques, the ATs were identified as macroreentrant tachycardias circling around an incisional line on the free wall of the right atrium (AT1), the tricuspid annulus (AT2), and low voltage area in the lateral wall including the right septum (AT3). Accuracy of CARTO3 in three-dimensional reconstruction was sufficient to elucidate anatomical features (including catheter sites, incision, and low voltage areas) and macroreentrant circuits. However, conventional mapping techniques were also necessary to identify the mechanism of the tachycardias, and therefore to eliminate all of them successfully. This case demonstrates that the use of combined conventional and electroanatomical mapping techniques, such as CARTO3, can be helpful in identifying the critical isthmus for catheter ablation of macroreentrant AT in patients with surgically corrected congenital heart disease (CHD).

Atrial Flutter with Alternating Cycle Lengths: Mechanism and Mapping

A 69-year-old woman with a 10-year history of paroxysmal atrial fibrillation was initially treated with propafenone and amiodarone. Four years ago her arrhythmia burden worsened and she developed recurrent episodes of symptomatic persistent atrial fibrillation. After several cardioversions, she was referred to our institution for radiofrequency catheter ablation. Her amiodarone was discontinued, and 1 year ago she underwent radiofrequency catheter ablation using a pulmonary vein antral isolation approach. Unfortunately, she developed recurrent atrial fibrillation and remained extremely symptomatic despite adequate control of her heart rate. Six months ago, she underwent a second radiofrequency catheter ablation procedure. Electrophysiology study revealed recurrent conduction between all four pulmonary veins and the left atrium, and the veins were reisolated and linear ablations were performed on the roof of the left atrium and the cavotricuspid isthmus. After the ablation, no atrial tachycardia or atrial fibrillation could be induced with aggressive pacing protocols. Unfortunately, she developed recurrent persistent atrial fibrillation within 1 week of the procedure. Four months later she underwent cardioversion with initiation of dofetilide. Two days after starting dofetilide she developed atypical atrial flutter and was referred for a third electrophysiology study. Surface ECG revealed upright P waves in leads V1 and V2 but were poorly seen in the other leads. At electrophysiology study, a circular mapping catheter placed in the four pulmonary veins demonstrated no electrical activity during atrial tachycardia, confirming adequate pulmonary vein isolation. At baseline the atrial tachycardia had stable alternating cycle lengths of 365 ms and 410 ms. Initial pacing maneuvers from the anterolateral right atrium and the proximal and distal coronary sinus yielded post-pacing intervals with long return cycle lengths. In addition, constant fusion and progressive fusion during pacing from the right atrium and the coronary sinus were observed. In order to delineate the tachycardia circuit a 64-electrode basket catheter was placed in the posterior left atrium (Figure 1). At baseline, electrograms could be recorded for 318 ms of the 363-ms and 411-ms cycle lengths (88% and 77% respectively) over a large area in the posterior left atrium. The deflection of the P wave corresponded to activation of the superior and anterior portions of the left atrium. We mapped the tachycardia circuit by identifying the initial site of cycle length change that localized the critical isthmus to the posterior roof of left atrium near the right superior pulmonary vein (Figure 2). When the mapping catheter was moved septally or laterally, split potentials suggestive of a line of conduction block were observed and a 20-electrode catheter revealed a fractionated electrogram that was the first site of cycle length change. Unfortunately, adequate capture could not be obtained despite pacing at maximal outputs from either electrode pair 17 and 18 of the 20-electrode reference catheter or an ablation catheter placed at the same fluoroscopic site. In addition, despite maximal gains, low amplitude electrograms could not be recorded with the The authors report no conflicts of interest for the published content. Manuscript received January 23, 2012, final version accepted February 13, 2012. Address correspondence to: Fred M. Kusumoto, MD, Electrophysiology and Pacing Service, Division of Cardiovascular Disease, Mayo Clinic, 4500 San Pablo Ave, Jacksonville, FL 32224. E-mail: Kusumoto.fred@mayo.edu The Journal of Innovations in Cardiac Rhythm Management, 3 (2012), 727–730