Activation Sequence Mapping Research Articles

High frame rate speckle tracking echocardiography for the mapping of cardiac mechanical activation sequence

Abstract Funding Acknowledgements Type of funding sources: Public Institution(s). Main funding source(s): KU Leuven. Background Cardiac arrhythmias are a leading cause of worldwide morbidity and mortality, with catheter ablation being an effective treatment. Current clinical practice includes performing an electrophysiological study in order to detect the focal source or the re-entrant circuit of the arrhythmia, i.e. the ablation target. This technique is invasive, with increased patient related risk and variable success rate. Conversely, echocardiography could be used to determine the correct ablation target. Indeed, high frame rate (HFR) ultrasound provides an adequately high temporal resolution, has proven helpful in detecting the onset of myocardial deformation and could be used for accurate localization of the arrhythmia sources. Purpose To test whether HFR speckle tracking echocardiography (STE) can be employed to construct cardiac mechanical activation maps. Methods 16 healthy volunteers (age: 30±6y; 69% males) and 11 heart failure patients treated with cardiac resynchronisation therapy (CRT) (age: 69±10y; 73% males) were included. All participants were scanned with a research high frame rate ultrasound scanner (frame rate: 848±101fps) and apical 4-, 2- and 3-chamber views were acquired. Patients were scanned with CRT on and after turning the device off, in order to allow native ventricular conduction. All patients had a left bundle branch block (LBBB) pattern of intrinsic activation on the surface ECG. For each apical view, a manually placed contour was tracked during the cardiac cycle by a custom-made 2D HFR STE algorithm; the contours were divided in a standard 16 segment model and segmental strain rate (SR) curves were computed and used to measure the temporal distance between electrical and mechanical activation (i.e. distance between the beginning of QRS and the first zero crossing in the SR curve representing the onset of segmental shortening). Finally, an activation map for each subject was created by placing the extracted timings in the middle of the corresponding segment of a bull’s-eye plot and interpolating values between them. Results Tracking was feasible in 96% of the segments; extracted curves showed a physiological pattern (Fig. 1A). For the healthy participants, mechanical activation started from the mid-anteroseptal (69%) or mid-inferoseptal (31%) segment at 22±5ms, spreading to the basal posterolateral segment at 50±8ms from the start of QRS, in all but two cases, where activation ended in the basal inferoseptal and basal inferior segment respectively (Fig. 1B). During CRT off, the septal wall was activated 31±9ms and the lateral wall 73±20ms after the beginning of QRS (p<0.01) (Fig. 1C), whereas during CRT on, the septal wall was activated 40±11ms and the lateral wall 37±7ms after the beginning of QRS (p = 0.3) (Fig. 1D). Conclusion Our findings comply with left ventricular activation as described in the literature and show that HFR STE could be a useful tool in defining the ablation target for arrhythmia treatment.

An Evaluation of Phase Analysis to Interpret Atrial Activation Patterns during Persistent Atrial Fibrillation for Targeted Ablation.

Background: Phase analysis has been used to identify and localize atrial fibrillation (AF) sources for targeted ablation. We previously demonstrated that repetitive wannabe reentry (incomplete reentry) often generated an apparent stable rotor using phase analysis. The misinterpretation caused by phase analysis using atrial electrograms (AEGs) may result from detecting inaccurate time points at phase inversion (π to −π) in the instantaneous phase waveform converted from AEG. The purpose of this study was to evaluate the accuracy of phase analysis to detect atrial activations recorded from the high-density mapping of AF in patients with persistent and long-standing persistent (LSP) AF. Methods and Results: During open heart surgery, we recorded activation from both atria simultaneously using 512 electrodes in 7 patients with persistent and LSP AF. The phase analysis was compared to manual measurements during 4 s of data. For the accuracy of activation sequence maps, a successful recording site was defined as having ≤4 mismatched activation times during the 4 s. In all AF episodes, the accuracy of the phase analysis was only 82% of the total number of activation times due to either activation time differences (14.7%), under-sensing (2.7%), or over-sensing (0.6%). Only 67.9% of the total recording sites met the requirement of a successful recording site by phase analysis. In unsuccessful recording sites, AEG characteristics were relatively irregular cycle length (CL), complex AEG, and double potential AEG. Conclusion: The phase analysis was less accurate in recording sites with a relatively irregular CL, complex AEG, or double potential AEG. As a result, phase analysis may lead to the misinterpretation of atrial activation patterns during AF. A visual review of the original AEG is needed to confirm the detected AF sources of phase analysis before performing targeted ablation.

Clinical impact of high density mapping in atypical atrial flutters ablation: outlining critical circuits in complex atrial tachycardias

Abstract Introduction Mapping and ablation of atypical atrial flutter (AFL) continue to be a challenge for clinical electrophysiologists. The advent of high-density (HD) mapping has allowed the generation of electro-anatomic maps with a very high resolution level. Purpose In this single center retrospective analysis, we evaluated the clinical impact of the ultra HD activation sequence mapping compared with the standard low density (LD) ablation catheter mapping technique in the treatment of AFLs. Methods We performed a 7 years-single center retrospective analysis of patients undergoing radiofrequency ablations (RFA) for right and left atypical AFL. We evaluated procedural and clinical outcomes of patients approached with a Low Density (LD) electro-anatomical (EAM) strategy compared with patients mapped with new automatic multipolar HD Mapping (HD Group). Results Seventy-five patients were included. Patients were almost male (60%), relatively old (65±8 years), with a moderate CHA2DS2Vasc score (2.3±1.3), a preserved ejection fraction (58±6) and moderate atrial dilatation (44±7 mm). Baseline clinical characteristics were comparable between groups (p=NS). Among 88 AFLs, 10 (11%) were located in the right and 78 (89%) in the left atrium, including 22 (28%) roof dependent and 37 (47%) mitral dependent (p=NS). Regarding procedural outcomes, Sinus rhythm restoration during ablation was more frequently observed in the HD Group (79% vs 56%, p=0.037), even if no differences in mapping time, procedural time and radiological dose were observed (p=NS). Freedom from AFL/atrial fibrillation (AF) at 1-year was lower in the HD Group (83% vs 45%, p=0.009) with an increased trend for AF recurrences during long term follow-up (17% vs 23% at 1 and 3-years respectively, p=0.059). At the multivariate analysis, HD map (OR 0,17; 95% CI 0,04–0,66) and younger age (OR 1,09; 95% CI 1,01–1,19) were identified as independent predictors of ablation success at 1 year. Conclusions Acute procedural success of ablation of atypical atrial flutter is higher in case of HD mapping strategy. Patient age and HD strategy resulted independent predictors of overall atrial arrhythmias recurrences. During follow-up, AFL recurrences are rare beyond 12 months, differently from AF which continues to show increasing trends. Funding Acknowledgement Type of funding sources: None. Procedural outcomesAtypical atrial flutter HD map

B-PO05-015 HIGH ACTIVATION FREQUENCIES DO NOT INDICATE FIXED DISCHARGING SOURCES DURING PERSISTENT ATRIAL FIBRILLATION

Activation frequencies during AF may indicate fixed sources driving the tachyarrhythmia. However, which types of activation patterns give rise to these high-frequency sites are unclear. Identifying patterns of activation at high-frequency sites may be crucial to further improve ablation target identification. Our aim was to 1) identify high-frequency sites using known experimental methodologies and characterize the activation patterns that occur at these activation sites and 2) assess local activation frequencies at focal activation sites. Epicardial high-density mapping (interelectrode distance: 2mm) of the atria including Bachmann’s bundle was performed during 10 seconds of spontaneous, persistent AF in 15 patients prior to surgical correction of aortic valve disease. Activation sequence mapping was performed to identify different types of activation patterns - early focal activity, freely passing wavefronts and conduction block. For each mapping site, the fractionation index (FI) was defined as the mean interval between all negative deflections in the unipolar electrograms. The dominant frequencies (DF) were determined within a range of 3.3-20Hz using fast Fourier transform. Relation between sites of highest activation frequencies (DFmax and FImax) and the prevalence of different patterns of activation were assessed. DFmax were located in the left atrium in most patients (77%), the FImax was primarily located at Bachmann’s bundle or the pulmonary vein area (each 38%). 3% of local activations were explained by early focal activation at sites of FImax [range:0-5%] and DFmax [range:0-9%]. Remaining activations were caused by passing waves (FImax: 65[31-99]%, DFmax: 36[9-100]%) or wave discontinuity at the site (FImax: 29[1-64]%, DFmax: 62[0-95]%). There was no strong correlation between DF or FI and the prevalence of different activation patterns (spearman’s rho <0.5 for all comparisons). Sites with focal activation were found across the entire spectrum of activation frequencies and did not occur more often at sites with fast compared to slower activation frequencies. High activation frequencies as determined by the maximum FI or DF are not related to fixed focal sources driving persistent AF.

New Insights Into Understanding Rotor Versus Focal Activation in Patients With Persistent Atrial Fibrillation.

This study was to test the hypotheses that: 1) when using phase analysis, repetitive Wannabe re-entry produces a phase singularity point (i.e., a rotor); and 2) the location of the stable rotor is close to the focal source. Recent contact mapping studies in patients with persistent atrial fibrillation (AF) demonstrated that phase analysis produced a different mechanistic result than classical activation sequence analysis. Our studies in patients with persistent AF showed that focal sources sometimes produced repetitive Wannabe re-entry, that is, incomplete re-entry. During open heart surgery, we recorded activation from both atria simultaneously using 510 to 512 electrodes in 12 patients with persistent AF. We performed activation sequence mapping and phase analyses on 4s of mapped data. For each detected stable rotor (>2 full rotations [720°] recurring at the same site), the corresponding activation patterns were examined from the activation sequence maps. During AF, phase singularity points (rotors) were identified in both atria in all patients. However, stable phase singularity points were only present in 6 of 12 patients. The range of stable phase singularity points per patient was 0 to 6 (total 14). Stable phase singularity points were produced due to repetitive Wannabe re-entry generated from a focal source or by passive activation. A conduction block sometimes created a stable phase singularity point (n=2). The average distance between a focal source and a stable rotor was 0.9 ± 0.3cm. Repetitive Wannabe re-entry generated stable rotors adjacent to a focal source. No true re-entry occurred.

Successful radiofrequency ablation of para-left bundle branch premature ventricular contractions: Aimingat the breakout point to spare the conduction system

Background: The origin of the arrhythmia and its breakout point may be located apart. This has been described for arrhythmias originating within the His-Purkinje system. Case presentation: We report a case of a 70-year-old man with right bundle branch block and left anterior fascicular block with idiopathic nonsustained ventricular tachycardia originating in the septal left ventricular outflow close to the proximal left bundle branch. Ablation was successfully and safely performed away from the origin of the arrhythmia near the left anterior fascicle, at the breakout point. Arrhythmias from the conduction system may have different preferential exits and meticulous activation sequence mapping is the preferable strategy to select the ablation site.

Reconsidering the multiple wavelet hypothesis of atrial fibrillation

Moe and Abildskov proposed the multiple wavelet hypothesis of atrial fibrillation (AF) on the basis of observations in the canine vagal nerve stimulation (VNS) AF model. Data from mapping studies in an invitro canine AF model by Allessie etal (Allessie MA, Lammers WJEP, Bonke FIM, Hollen SJ. Experimental evaluation of Moe's multiple wavelet hypothesis of atrial fibrillation. In: Zipes DP, Jalife J, eds. Cardiac Electrophysiology and Arrhythmias. Orlando, FL: Grune & Stratton; 1985:265-275.) were used to evaluate the Moe/Abildskov hypothesis, which revealed that a critical number of wavelets sustained AF. The purpose of this study was to reassess VNS mapping data using the same methods used by Allessie to evaluate Moe's multiple wavelet hypothesis. Using the canine VNS AF model in 6 dogs, 510 unipolar atrial electrograms were recorded simultaneously from both atria. Activation sequence maps were produced from sustained AF during VNS in each dog. Per Allessie, consecutive 10 ms activation windows were analyzed over a period of 300 ms. Repetitive activation analysis was applied to Moe's canine VNS AF model. The number of wavefronts in each AF episode was 0-8 in Allessie's studies measured by sequential atrial mapping and 0-10 in our biatrial simultaneous mapping studies. In both studies, an electrically silent period was observed in each atrium and was reactivated by wavefronts emanating from focal sources. Allessie postulated that an electrically silent atrium was reactivated by a wavefront propagating from the other atrium. However, in our biatrial simultaneous mapping studies, each electrically silent atrium was reactivated by a distinct focal source. Data from both studies showed a similar number of wavefronts, similar AF activation patterns, and periods of electrical atrial silence reactivated by focal sources. Also, in our studies, independent focal sources initiated wavefronts reactivating the atria, thereby explaining the mechanism maintaining AF.

Entrainment Mapping.

Mapping during ventricular tachycardia (VT) aims to elucidate mechanism, describe myocardial propagation, and identify the origin and critical regions of VT that can be targeted for ablation, most commonly with radiofrequency ablation. Most VTs in structural heart disease are due to macro-reentry in and around scar. A combination of mapping techniques, including mapping to identify the arrhythmia substrate, activation sequence mapping, pace-mapping, and entrainment mapping, may be used to identify putative ablation targets. This review describes the principles of entrainment mapping as it pertains to catheter ablation of scar-related VT.

Noninvasive epicardial and endocardial electrocardiographic imaging of scar-related ventricular tachycardia

BackgroundThe majority of life-threatening ventricular tachycardias (VTs) are sustained by heterogeneous scar substrates with narrow strands of surviving tissue. An effective treatment for scar-related VT is to modify the underlying scar substrate by catheter ablation. If activation sequence and entrainment mapping can be performed during sustained VT, the exit and isthmus of the circuit can often be identified. However, with invasive catheter mapping, only monomorphic VT that is hemodynamically stable can be mapped in this manner. For the majority of patients with poorly tolerated VTs or multiple VTs, a close inspection of the re-entry circuit is not possible. A noninvasive approach to fast mapping of unstable VTs can potentially allow an improved identification of critical ablation sites. MethodsFor patients who underwent catheter ablation of scar-related VT, CT scan was obtained prior to the ablation procedure and 120-lead body-surface electrocardiograms (ECGs) were acquired during induced VTs. These data were used for noninvasive ECG imaging to computationally reconstruct electrical potentials on the epicardium and on the endocardium of both ventricles. Activation time and phase maps of the VT circuit were extracted from the reconstructed electrograms. They were analyzed with respect to scar substrate obtained from catheter mapping, as well as VT exits confirmed through ablation sites that successfully terminated the VT. ResultsThe reconstructed re-entry circuits correctly revealed both epicardial and endocardial origins of activation, consistent with locations of exit sites confirmed from the ablation procedure. The temporal dynamics of the re-entry circuits, particularly the slowing of conduction as indicated by the crowding and zig-zag conducting of the activation isochrones, collocated well with scar substrate obtained by catheter voltage maps. Furthermore, the results indicated that some re-entry circuits involve both the epicardial and endocardial layers, and can only be properly interpreted by mapping both layers simultaneously. ConclusionsThis study investigated the potential of ECG-imaging for beat-to-beat mapping of unstable reentrant circuits. It shows that simultaneous epicardial and endocardial mapping may improve the delineation of the 3D spatial construct of a re-entry circuit and its exit. It also shows that the use of phase mapping can reveal regions of slow conduction that collocate well with suspected heterogeneous regions within and around the scar.

Simultaneous Biatrial High-Density (510–512 Electrodes) Epicardial Mapping of Persistent and Long-Standing Persistent Atrial Fibrillation in Patients

Background— The mechanism(s) of persistent and long-standing persistent (LSP) atrial fibrillation (AF) is/are poorly understood. We performed high-density, simultaneous, biatrial, epicardial mapping of persistent and LSP AF in patients undergoing open heart surgery (1) to test the hypothesis that persistent and LSP AF are due to ≥1 drivers, either focal or reentrant, and (2) to characterize associated atrial activation. Methods and Results— Twelve patients with persistent and LSP AF (1 month to 9 years duration) were studied at open heart surgery. During AF, electrograms were recorded from both atria simultaneously for 1 to 5 minutes from 510 to 512 epicardial electrodes with ECG lead II. Thirty-two consecutive seconds of activation sequence maps were produced per patient. During AF, multiple foci (QS unipolar atrial electrograms) of different cycle lengths (mean, 175±18 ms) were present in both atria in 11 of 12 patients. Foci (2–4 per patient, duration 5–32 s) were either sustained or intermittent, were predominantly found in the lateral left atrial free wall, and likely acted as drivers. Random and nonrandom breakthrough activation sites (initial r or R in unipolar atrial electrograms) were also found. In 1 of 12 patients, only breakthrough sites were found. All wave fronts emanated from foci and breakthrough sites, and largely either collided or merged with each other at variable sites. Repetitive focal QS activation occasionally generated repetitive wannabe reentrant activation in 5 of 12 patients. No actual reentry was found. Conclusions— During persistent and LSP AF in 12 patients, wave fronts emanating from foci and breakthrough sites maintained AF. No reentry was demonstrated.

Confirmation of Novel Noninvasive High-Density Electrocardiographic Mapping With Electrophysiology Study

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 &gt;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.

Electromechanical wave imaging for noninvasive mapping of the 3D electrical activation sequence in canines and humans in vivo

Cardiovascular diseases rank as America's primary killer, claiming the lives of over 41% of more than 2.4 million Americans. One of the main reasons for this high death toll is the severe lack of effective imaging techniques for screening, early detection and localization of an abnormality detected on the electrocardiogram (ECG). The two most widely used imaging techniques in the clinic are CT angiography and echocardiography with limitations in speed of application and reliability, respectively. It has been established that the mechanical and electrical properties of the myocardium change dramatically as a result of ischemia, infarction or arrhythmia; both at their onset and after survival. Despite these findings, no imaging technique currently exists that is routinely used in the clinic and can provide reliable, non-invasive, quantitative mapping of the regional, mechanical, and electrical function of the myocardium. Electromechanical Wave Imaging (EWI) is an ultrasound-based technique that utilizes the electromechanical coupling and its associated resulting strain to infer to the underlying electrical function of the myocardium. The methodology of EWI is first described and its fundamental performance is presented. Subsequent in vivo canine and human applications are provided that demonstrate the applicability of Electromechanical Wave Imaging in differentiating between sinus rhythm and induced pacing schemes as well as mapping arrhythmias. Preliminary validation with catheter mapping is also provided and transthoracic electromechanical mapping in all four chambers of the human heart is also presented demonstrating the potential of this novel methodology to noninvasively infer to both the normal and pathological electrical conduction of the heart.

Radiofrequency catheter ablation of paediatric idiopathic left ventricular tachycardia by P potential mapping under sinus rhythm

ObjectiveTo investigate the feasibility and effectiveness of P potential mapping in radiofrequency catheter ablation (RFCA) of paediatric idiopathic left ventricular tachycardia (ILVT) in difficult to be induced or uninducible case...

Imaging the electromechanical activity of the heart in vivo.

Cardiac conduction abnormalities remain a major cause of death and disability worldwide. However, as of today, there is no standard clinical imaging modality that can noninvasively provide maps of the electrical activation. In this paper, electromechanical wave imaging (EWI), a novel ultrasound-based imaging method, is shown to be capable of mapping the electromechanics of all four cardiac chambers at high temporal and spatial resolutions and a precision previously unobtainable in a full cardiac view in both animals and humans. The transient deformations resulting from the electrical activation of the myocardium were mapped in 2D and combined in 3D biplane ventricular views. EWI maps were acquired during five distinct conduction configurations and were found to be closely correlated to the electrical activation sequences. EWI in humans was shown to be feasible and capable of depicting the normal electromechanical activation sequence of both atria and ventricles. This validation of EWI as a direct, noninvasive, and highly translational approach underlines its potential to serve as a unique imaging tool for the early detection, diagnosis, and treatment monitoring of arrhythmias through ultrasound-based mapping of the transmural electromechanical activation sequence reliably at the point of care, and in real time.

Three Dimensional Electroanatomical Mapping of Lower Loop Reentry in Patients with Intracardiac Operation

Introduction: The aim of this study was to clarify the characteristics of lower loop reentry (LLR. in patients who underwent cardiac surgery.Methods: Of 194 patients from 2000 to 2007 with negative flutter waves in the inferior leads (II, III, and aVf), 4 patients had LLR and reentrant circuits identified by a 3D activation sequence mapping system. We studied the characteristics of the surface electrocardiogram (ECG. patterns of those LLRs.Results: All 4 patients had a history of an intracardiac operation. The 3D activation sequence mapping system during the LLR exhibited a clockwise (CW. wavefront around the inferior vena cava (IVC. from the caudal view. During the LLR, the right atrium (RA. free wall was activated in a caudal‐cranial sequence and a collision of two activation wavefronts from the lower RA and upper RA occurred at the RA free wall.Conclusions: The 3D activation mapping during the AT revealed an activation wavefront propagating around the IVC and the diagnosis of LLR. Detailed 3D electroanatomical mapping and pacing study are needed to identify the reentrant circuit of LLR in patients with previous intracardiac surgery.

Three-Dimensional Mapping of Cardiac Arrhythmias

Catheter mapping and ablation are increasingly performed for complex arrhythmias that require a complete understanding of mapping techniques to identify the arrhythmia substrate. In this session of Teaching Rounds, we begin a 3-part series that focuses on key issues related to 3-dimensional electroanatomic mapping. The general principles, rationale, and working of the various mapping systems have been explained well in the existing literature.1–4 In brief, these systems use an electromagnetic or impedance-based catheter location method that allows creation of a 3D anatomic shell of the cardiac chamber of interest. During mapping, the electrogram obtained at a given site is stored and the activation time catalogued as compared with some selected electric signal preference. The accrued points in the map are assigned to an isochronal color scale based on their respective activation times. In addition to the activation map, maps that display the voltage of the recorded electrograms can be created. For successful interpretation of these maps, a variety of considerations must be understood and meticulously managed. Good catheter contact, correct interpretation of the colors in the map, appropriate choice of reference electrogram, complete mapping of the correct chamber of interest, and strategies to address catheter tip migration with respiration or change in cardiac rhythm and annotation of complex intracardiac signals are all examples of such requisites for success.5–8 During activation sequence mapping, data points are acquired as the catheter moves across the chamber of interest and the timing of these electrograms are compared with a predetermined reference. As this process continues, a color scheme begins to emerge. With present systems, regions of red color indicate sites of “early activation” and activation becomes progressive later proceeding through the colors of the rainbow to yellow-green, and finally the blue and purple hues that define the sites …

A simple and definite proof of complete cavotricuspid isthmus block

Complete bidirectional block of the cavotricuspid isthmus (CTI) after radiofrequency ablation of typical atrial flutter is an established endpoint. Methods to determine completeness of block are subject to debate, 3‐6 since the ultimate electrophysiological proof does not seem to exist. Additionally, because of increasing economic constraints, the number of usable catheters and poles may become limited. The criterion for clockwise (CW) CTI block based on the anterior right atrium (RA) activation sequence during septal CTI pacing has been proposed to overcome the limitations of other criteria. 7 Pastor et al. elegantly and meticulously evaluate the clinical significance of this method, validating it as a powerful predictor of a freedom of recurrence after more than 3 years. Several issues are to be raised. First, in this retrospective series, three types of ablation catheters have been used which may partially affect the conclusion that can be drawn from this study: a solid 4 mm-tip catheter, a solid 8 mm-tip catheter, and an openirrigation 4 mm-tip catheter. It seems that the solid 4 mm-tip catheter was the least effective and accounted for the majority of recurrences. Secondly, the importance of obtaining non-ambiguous evidence of complete bidirectional CTI block is stressed again. Atrial flutter recurrence rate was only 3% in the presence of bidirectional block vs. 22% in the case of unidirectional block and 67% in the absence of block (P , 0.001 vs. bidirectional block). This is not a new observation but interestingly and, in our opinion, of major importance, CW CTI block, as demonstrated by completely descending anterior RA activation sequence during septal CTI pacing, was simultaneously proven by differential pacing in only 64% of these cases. The limited sensitivity of septal differential pacing was attributed to the unclear local CTI electrogram interpretation (due to the low voltage and fragmented potentials) and was observed in 36% of cases, which is similar to our experience. 5 Moreover, CTI anfractuous anatomy 8,9 makes detailed assessment of the ablation line difficult. We still think that accurate activation mapping of the anterior RA activation sequence during septal CTI pacing is of prime importance to clearly identify complete CTI block. The usefulness of a multipolar catheter is stressed out once more in this paper, with its distal poles placed along the antero-inferior RA wall but in the most immediate vicinity of the ablation line. Many cases of localized slow (yet persistent) conduction are then easily ruled out.

Guidance for catheter ablation of ventricular arrhythmia

Efficient pumping of the heart requires simultaneous contraction of all cardiac muscle cells. The necessary coordination is obtained by transmission of ‘‘action potentials:’’ periodic changes in transmembrane voltage which, in muscle cells, trigger the calcium influx needed for contraction. In cardiac muscle, they also cause an electric current flow to neighboring cells through intercellular connections. This current causes an action potential in each neighbor, leading to rapid activation of the whole heart. Normally the initial activation comes from a specialized region called the sinus node, at a regular pace adapted to the needs of the body. Ventricular tachycardia (VT) is a potentially fatal disturbance of this mechanism, characterized by a very fast heart rate and an abnormal activation pattern. VT can be caused by an ‘‘ectopic focus,’’ a small area of tissue that starts activating itself and its neighbors on its own account. A far more common cause, however, are scars due to infarction, cardiomyopathy, or surgery. These can embed a maze of small surviving muscle fibers through which activation may proceed during a substantial part of a heartbeat before it reaches the healthy myocardium again. The activation may then round the scar and re-enter the narrow pathway (see Fig. 1). Continuous reentry in this fashion results in re-entrant VT. Treatment options for VT include pharmacological suppression, implantation of a cardioverter-defibrillator (ICD), surgical resection of the arrhythmogenic area, and catheter ablation. None of these methods is perfect. Pharmacological treatment often fails [7]. An ICD can reliably terminate VT but does not prevent it from recurring; frequent ICD shocks can cause significant morbidity [7]. Surgical treatment is limited by its invasiveness and relatively high morbidity and mortality. Catheter ablation is only minimally invasive and, if successful, can provide a definitive cure. It is presently considered as a first-choice treatment for focal VT in patients with structurally normal hearts, and as a secondary treatment in patients who are experiencing too many ICD discharges. Procedures to find a suitable ablation site include ‘‘pace mapping’’ and ‘‘activation sequence mapping.’’ In pace mapping, the heart is stimulated from the catheter tip, resulting in an electrocardiogram (ECG) that mimics the ECG that would be obtained if the VT originated at the catheter tip location. Comparison with an ECG recorded during VT provides an estimate of the origin relative to the catheter tip. After displacing the catheter and stimulating again, a new ECG is made. This procedure is repeated until the two ECGs match, and allows for the localization of the ‘‘exit site,’’ where the abnormal activation reaches the healthy myocardium. Patients with more than one VT circuit can have several exit sites. In activation sequence mapping, the VT is induced, and the activation pattern is assessed by recording signals at many locations with one or two catheters. The goal is to find the earliest activated site. This is a time-consuming procedure, during which the patient has to be kept in VT. To gain time, the exit site found by pace mapping can be used as a starting point [3]. M. Potse (&) Research Center, Sacre-Coeur hospital, Montreal, QC, Canada e-mail: mark@potse.nl

Catheter Ablation for Ventricular Tachycardia

Sustained ventricular tachycardia (VT) is an important cause of morbidity and sudden death in patients with heart disease.1 Implantable cardioverter-defibrillators (ICDs) terminate VT episodes, reducing the risk of sudden death. Recurrent VT develops in 40% to 60% of patients who receive an ICD after an episode of spontaneous sustained VT. A first episode of VT occurs in ≈20% of patients within 3 to 5 years after ICD implantation for primary prevention of sudden death in high-risk groups.2–4 ICD shocks reduce quality of life and are associated with an increased risk of death.2–4 Antiarrhythmic drug therapy with amiodarone or sotalol reduces VT episodes but with disappointing incidence of side effects and efficacy.2 Catheter ablation is useful for reducing VT episodes and can be life-saving when VT is incessant.1,5,6 Idiopathic VTs occur in patients without structural heart disease and rarely cause sudden death. Electrophysiological study with catheter ablation is often warranted to confirm the diagnosis, to provide further evidence for the absence of ventricular scar or other disease, and often to cure the arrhythmia. Ablation is also an option for symptomatic nonsustained VT and frequent ventricular ectopy in these patients.1 The appearance of the VT on ECG often suggests its likely cause and associated heart disease (Figure 1). Monomorphic VT has the same QRS complex from beat to beat, indicating repetitive ventricular activation from a structural substrate or focus that can be targeted for ablation. Most are due to reentry through regions of ventricular scar.7 Figure 1. ECG types of VT and most common causes are shown with characteristic ECG features of selected VTs. LBBB indicates left bundle-branch block; LVOT, LV outflow tract; RBBB, right bundle-branch block; L, left; and R, right. Polymorphic VTs have a changing ventricular activation sequence that can be due to …

Patient-specific surgical strategy for atrial fibrillation: Promises and challenges

The same approach was used in the development of the Cox maze procedure. 9 Activation sequence mapping data were recorded in animal models of AF and in humans. The complexity of the data and the time needed to analyze the data limited the usefulness of map-directed treatment of AF. The data from humans exhibited changing patterns of activation in which reentrant circuits were present but were not stable. 10 The animal data, obtained in studies in which more extensive mapping could be performed, showed reentrant circuits that were anchored to the thoracic veins (pulmonary veins [PVs], superior and inferior venae cavae) and valve annuli. Although there was no definitive anatomic substrate to target, the human mapping data did provide useful information. Large regions of the atria activated synchronously during AF, suggesting that the random reentrant patterns predicted by Moe’s multiple wavelet hypothesis was not the underlying mechanism in these patients. Based on these studies, a salvage procedure was developed that was anatomically based and could be used if intraoperative mapping