Endocardial Exit Research Articles

Epicardial–Endocardial Reentry in Ischemic Cardiomyopathy

In ischemic cardiomyopathy, endocardial reentry has traditionally been the mechanistic paradigm for understanding ventricular tachycardia (VT). However, recognition is growing that epicardial myocardium is a critical component for VT substrate, even in patients with ischemic cardiomyopathy. In this report, we present a novel case of a three-dimensional VT reentry involving epicardial components and an endocardial exit.

Endo-Epicardial Mapping of InVivo Human Sinoatrial Node Activity.

The aim of the current study was to examine electrophysiological characteristics of sinoatrial node (SAN) activity from an endo-epicardial perspective. Electrophysiological properties of the invivo human SAN and its exit pathways remain poorly understood. Twenty patients (75% male; median age 66 years [59 to 73 years]) with structural heart disease underwent simultaneous endo-epicardial mapping (256 unipolar electrodes, interelectrode distance 2mm). Conduction times, endo-epicardial delays (EEDs), and R/S ratio were examined in the surrounding 10mm of SAN activation. Areas of conduction block were defined as conduction delays≥12ms and endo-epicardial asynchrony as EED≥15 m. Three distinct activation patterns were observed in a total of 28 SAN-focal activation patterns (SAN-FAPs) (4 patients exhibited >1 different exit site), including SAN activation patterns with: 1) solely an endocardial exit site (n=10 [36%]); 2) solely an epicardial exit site (n=13 [46%]); and 3) simultaneously activated endo-epicardial exit sites (n=5 [18%]). Median (interquartile range) EED at the origin of the SAN-FAP was 10ms (6 to 14 ms) and the prevalence of endo-epicardial asynchrony in the surroundings of the SAN-FAP was 5% (2% to 18%). Electrograms at the origin of the SAN-FAPs exhibited significantly larger R-peaks in the mid right atrium (RA) compared with the superior RA (mid R/S ratio 0.15 [0.067 to 0.34] vs. superior R/S ratio 0.045 [0.026 to 0.062]; p=0.004). Conduction velocity within a distance of 10mm from the SAN-FAP was 125cm/s (80 to 250 cm/s). All 6 SAN-FAPs at the mid RA were observed in patients with a history of atrial fibrillation. Variations in activation patterns of the SAN observed in this study highlight the complex 3-dimensional SAN geometry and indicate the presence of interindividual differences in SAN exit pathways. Solely in patients with a history of atrial fibrillation, SAN activity occurred more caudally, which indicates changes in preferential SAN exitpathways.

Exit sites on the epicardium rarely subtend critical diastolic path of ischemic VT on the endocardium: Implications for noninvasive ablation.

Noninvasive electrocardiographic mapping of ventricular tachycardia (VT) and ablation using stereotactic radiotherapy was recently reported. This strategy does not directly evaluate the critical diastolic components and assumes that the epicardial exit site of VT subtends closely over the endocardial mid-diastolic isthmus. To determine if the epicardial exit site of VT spatially corresponds to the critical diastolic components of ischemic scar-related VT. Intraoperative simultaneous endocardial and epicardial mapping were performed during VT using a 112-bipole endocardial balloon and 112-bipole epicardial sock array. In eight patients, nine VTs having entire diastolic circuit mapped were included in the study. The diastolic path and VT-exit sites (epicardial and endocardial) were determined. The diastolic path was mapped in the endocardium for all nine VTs (median length, 50; interquartile range [IQR], 28 mm). The tachycardia cycle length ranged from 210-500 ms. The VT-exit site was early in the endocardium for six VTs and on the epicardium for three VTs. The mid-diastolic isthmus and endocardial exit site of the six endocardial VTs were spatially distant from their epicardial exit site by a median distance of 32 and 27 mm, respectively. For the three VTs with an early epicardial exit, the isthmus and endocardial exit sites were distant from the epicardial exit site by a median distance of 34 and 38 mm, respectively. The epicardial exit site and the mid-diastolic isthmus sites were spatially distant and discrepant. Surface electrocardiography (ECG)-derived strategy in identifying epicardial exit site to select noninvasive ablation targets is prone to identify epicardial exit sites and may not identify critical targets in ischemic scar VT.

Localization of ventricular activation origin using patient-specific geometry: Preliminary results.

Catheter ablation of ventricular tachycardia (VT) may include induction of VT and localization of VT-exit site. Our aim was to assess localization performance of a novel statistical pace-mapping method and compare it with performance of an electrocardiographic inverse solution. Seven patients undergoing ablation of VT (4 with epicardial, 3 with endocardial exit) aided by electroanatomic mapping underwent intraprocedural 120-lead body-surface potential mapping (BSPM). Two approaches to localization of activation origin were tested: (1) A statistical method, based on multiple linear regression (MLR), which required only the conventional 12-lead ECG for a sufficient number of pacing sites with known origin together with patient-specific geometry of the endocardial/epicardial surface obtained by electroanatomic mapping; and (2) a classical deterministic inverse solution for recovering heart-surface potentials, which required BSPM and patient-specific geometry of the heart and torso obtained via computed tomography (CT). For the MLR method, at least 10-15 pacing sites with known coordinates, together with their corresponding 12-lead ECGs, were required to derive reliable patient-specific regression equations, which then enabled accurate localization of ventricular activation with unknown origin. For 4 patients who underwent epicardial mapping, the median of localization error for the MLR was significantly lower than that for the inverse solution (10.6vs. 27.3mm, P=0.034); a similar result held for 3 patients who underwent endocardial mapping (7.7vs. 17.1mm, P=0.017). The pooled localization error for all epicardial and endocardial sites was also significantly smaller for the MLR compared with the inverse solution (P=0.005). The novel pace-mapping approach to localizing the origin of ventricular activation offers an easily implementable supplement and/or alternative to the preprocedure inverse solution; its simplicity makes it suitable for real-time applications during clinical catheter-ablation procedures.

Endocardial ablation of postinfarction ventricular tachycardia with nonendocardial exit sites

Most infarct-related ventricular tachycardias (VTs) have an exit site that can be targeted by endocardial ablation. However, some VT reentry circuits have an exit site that is intramural or epicardial. Even these circuits may have an endocardial component that can be endocardially ablated. To assess the prevalence of postinfarction VTs with a nonendocardial exit site that can be successfully eliminated by endocardial ablation. Twenty-eight consecutive patients with postinfarction VT (27 men, age 69 ± 8 years, ejection fraction 0.25% ± 0.15%) were referred for VT ablation. A total of 213 VTs were inducible (cycle length 378 ± 100 ms). Pace mapping was performed throughout the scar, and critical sites were identified for 137 VTs (64.5%). Critical sites identified by entrainment mapping and/or pace mapping were divided into exit and nonexit sites depending on the stimulus-QRS/VT cycle length ratio (S-QRS/VT CL ≤ 0.3 vs>0.3). Endocardial exit sites (S-QRS/VTCL ≤ 0.3) were identified for 100 of 137 VTs. Only critical nonexit sites were identified for 37 of 137 (27%) VTs. Nonexit sites were confined to a smaller area within the endocardium (1.81 ± 1.7 cm(2)) and were located within dense scar (0.28 ± 0.24 mV) further away from the border zone (2.05 ± 2.79 cm) than did the VT exit sites. Exit sites had a larger area of matching pace maps (3.86 ± 1.9 cm(2); P<.01) and were at a closer distance to the border zone (0.93 ± 1.06 cm; P<.01). A total of 133 of 137 VTs were ablated. The success rate was similar for VTs in which exit sites were targeted (n = 90 of 100) and VTs in which only nonexit sites were targeted (n = 36 of 37) (P = .83). In about one-third of postinfarction VTs for which critical sites were identified, the exit site was not endocardial. Critical nonexit sites that are effective for ablation are often within dense scar at a distance from the border zone and can be missed if only the border zone is targeted.

Can noncontact mapping distinguish between endo- and epicardial foci?

Noncontact mapping has been demonstrated to facilitate RF ablation of ventricular arrhythmias, but the reproducibility in the localization of endocardial exit sites during focal ventricular tachycardia ("VT") originating from defined myocardial layers has not been systematically studied. Furthermore, it remains unclear whether noncontact mapping can distinguish between endo- and epicardial foci. In six dogs, constant pacing was applied through octopolar needle electrodes in the left ventricle to mimic VT of subendocardial, midmyocardial (mid1; mid2) or subepicardial origin. Using noncontact mapping, the site of origin was determined for each of 50 consecutive beats of all "VTs" and the variation between respective exit sites was measured. Exit sites were reconstructed for 50 consecutive beats of each "VT" and the time span between site of origin and exit site was measured as a parameter of intramural conduction. While subendocardial and midmyocardial (mid1, mid2) foci were pinpointed with a variation of <or=2 mm, a variation of 4 mm was encountered for subepicardial foci. A gradual increase in intramural conduction was evident from endocardial towards epicardial foci, with significant differences between subendocardial (4.8 +/- 0.9 ms), midmyocardial (mid1 = 11.1 +/- 4.6 ms; mid2 = 11.8 +/- 3.5 ms) and subepicardial (16.8 +/- 3.6 ms) foci (P < 0.005). Systematic differences in the morphology of virtual waveforms depending on the site of origin could not be detected. Except for subepicardial foci, noncontact mapping localized focal activity in the LV with high reproducibility. In contrast to morphological parameters, the determination of intramural conduction provides a fair estimate of the depth of foci and is proposed as a novel parameter to identify a subepicardial origin.

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 …

Catheter Ablation of Multiple Ventricular Tachycardias After Myocardial Infarction Guided by Combined Contact and Noncontact Mapping

Insights gained from noncontact mapping of ventricular tachycardia (VT) have not been systematically applied to contact maps. This study sought to unify both techniques for an individualized approach to the patient with multiple ischemic VTs irrespective of cycle length. For 12 consecutive patients with chronic myocardial infarction and recurrent VT, bipolar contact maps were acquired during sinus or paced rhythm. Additional noncontact maps were obtained during 48 induced VTs (cycle length 192 to 579 ms). Endocardial exit sites were superimposed on contact maps and verified by pace-mapping. Radiofrequency lesions were extended for critical borders defined by multiple neighboring exits and followed the isovoltage contour line of contact maps. Nine critical borders were identified in 8 patients and constituted the substrate for 31 VTs. The voltage at exit sites was 0.8 mV (range 0.1 to 2.3). Noncontact maps revealed 23+/-18% of isthmus conduction. Thirty-seven (77%) of all and 83% of clinically documented VTs were rendered noninducible irrespective of cycle length by application of 27 radiofrequency lesions (range 18 to 56). Spontaneous transitions between distinct VTs along critical borders were demonstrated in 4 patients. Pace-mapping reproduced the QRS morphology of 81% of VTs and was associated with successful ablation (P<0.01). Noninducibility of any sustained VT was reached for 8 (67%) patients. During 15 months (range 5 to 28) of follow-up, 8 patients remained without recurrence, and VT episodes were reduced in the other 4 patients (P<0.01). VT cycle length was not predictive for acute or long-term success. The combined approach of contact and noncontact mapping effectively defines critical borders as the substrate of multiple VTs without limitation for unstable VTs.

Catheter ablation of haemodynamically unstable or non-sustained ventricular tachycardia

Background — Ventricular tachycardia (VT) may be haemodynamically unstable or non-sustained, interfering with detailed activation mapping. Non-contact mapping permits beat-by-beat analysis of VT, projected upon a 3-dimensional reconstructed geometry of the cardiac chamber.Objective —The aim of the present study is to determine the utility of non-contact endocardial mapping to guide ablation of haemodynamically unstable VT or non-sustained VT.Methods and results — Eighteen VTs in 17 patients were induced (cycle length 336±58ms) and mapped. Three patients were mapped during premature ventricular complexes (PVCs) because sustained VT could not be induced. Analysis of the archived non-contact activation maps was performed to identify the exit point and/or the diastolic pathway of the VT reentry circuit.The endocardial exit points (10±16ms before QRS) were defined in 17/18 VTs (94%). A diastolic pathway was identified in 5/6 ischaemic VTs.The earliest activation sites were identified in all 3patients with PVCs. Radiofrequency current was applied around the exit point or to create a line of block across the diastolic pathway. Catheter ablation was performed in 17/18 VTs, including 3patients mapped using only PVCs. Ablation was successful in 16/18 VTs (89%) and in 15/17patients (82%). Catheter ablation was not performed in one patient (peri-hisian VT) and was unsuccessful in one patient (mapped during PVCs).Conclusions — Non-contact endocardial mapping is useful to guide radiofrequency catheter ablation of untolerated or non-sustained VTs.

Long-term results after ablation of infarct-related ventricular tachycardia

The purpose of this study was to assess the long-term effects of ablation of infarct-related ventricular tachycardia (VT) and the subsequent requirement for implantable cardioverter-defibrillator (ICD) therapy. The long-term consequences after initially successful catheter ablation of infarct-related VT remain unclear. Forty patients who presented with infarct-related VT were studied using noncontact mapping to guide ablation. One hundred forty VTs were mapped using the noncontact mapping system, including 36 (25.7%) clinical VTs. An endocardial exit site was determined in 100% of VT circuits, diastolic endocardial activity in 77 VTs (55%), and complete circuits in 24 VTs (17.1%). Eighty-one VTs (57.9%) were targeted for ablation, of which 67 (82.7% of targeted) were successfully ablated, including 27 clinical VTs (75% of clinical). Documented recurrence of an ablated VT occurred in 7.5% of patients over 36.3 +/- 21.0 months of follow-up. Episodes of new or recurrent, nontargeted VT or ventricular fibrillation (VF) occurred in 37.5% and VT recurrence without documentation of cycle length in 5%. In patients with ICDs, mean shock frequency was reduced from 6.8 +/- 7.3 per month in the year prior to ablation to 0.05 +/- 0.12 per month after ablation, over 24.7 +/- 18.9 months of follow-up (P < .0001). In patients with infarct-related VT, noncontact mapping-guided VT ablation is associated with a high procedural success rate, and VT recurrence necessitating ICD therapy delivery is significantly reduced. However, only 42.5% of patients remain free from VT/VF 3 years after ablation. Catheter ablation for infarct-related VT is indicated as an adjunctive therapy in patients with symptomatic VT but cannot substitute for ICDs and antiarrhythmic drugs.

Noncontact mapping of ventricular tachycardia in a closed-chest animal model of chronic myocardial infarction.

Treatment of ventricular tachyarrhythmias in the setting of chronic myocardial infarction requires accurate characterization of the arrhythmia substrate. New mapping technologies have been developed that facilitate identification and ablation of critical areas even in rapid, hemodynamically unstable ventricular tachycardia. A noncontact mapping system was used to analyze induced ventricular tachycardia in a closed-chest sheep model of chronic myocardial infarction. Twelve sheep were studied 96 +/- 10 days after experimental myocardial infarction. During programmed stimulation, 15 different ventricular tachycardias were induced in nine animals. Induced ventricular tachycardia had a mean cycle length of 190 +/- 30 ms. In 12 ventricular tachycardias, earliest endocardial activity was recorded from virtual electrodes, preceding the surface QRS onset by 30 +/- 7 ms. Noncontact mapping identified diastolic activity in ten ventricular tachycardias. Diastolic potentials were recorded over a variable zone, spanning more than 30 mm. Timing of diastolic potentials varied from early to late diastole and could be traced back to the endocardial exit site. Entrainment with overdrive pacing was attempted in nine ventricular tachycardias, with concealed entrainment observed in seven. Abnormal endocardium in the area of chronic myocardial infarction identified by unipolar peak voltage mapping was confirmed by magnetic resonance imaging. These data suggest that induced ventricular tachycardia in the late phase of myocardial infarction in the sheep model is due to macroreentry involving the infarct borderzone. The combination of this animal model with noncontact mapping technology will allow testing of new strategies to cure and prevent ventricular tachycardia in the setting of chronic myocardial infarction.

Non-contact mapping to guide catheter ablation of untolerated ventricular tachycardia

Aims The role of a novel non-contact mapping system (ESI 3000, Endocardial Solutions) to guide radiofrequency catheter ablation of untolerated ventricular tachycardia was investigated in 17 patients; 11 with prior myocardial infarction, three with arrhythmogenic right ventricular dysplasia, and three with idiopathic dilated cardiomyopathy. Methods Twenty-seven monomorphic ventricular tachycardias were induced (mean cycle 320±60ms, range 230–450ms), mapped for 15–20s, and terminated by overdrive pacing or DC shock. Off-line analysis of isopotential activation mapping was performed to identify the diastolic pathway and/or the exit point of the ventricular tachycardia reentry circuit. Radiofrequency current was applied to create a line of block across the diastolic pathway or around the exit point. Results All 27 ventricular tachycardias were mapped with the non-contact system. The endocardial exit point (−7±15ms before QRS onset) was defined in 21/21 postinfarction ventricular tachycardias, in 3/3 arrhythmogenic right ventricular dysplasia and in 1/3 idiopathic dilated cardiomyopathy ventricular tachycardias, respectively. The diastolic pathway (earliest endocardial diastolic activity: −65±49ms before QRS onset) was identified in 17/21 postinfarction ventricular tachycardias, in 1/3 arrhythmogenic right ventricular dysplasia and in 1/3 idiopathic dilated cardiomyopathy ventricular tachycardias, respectively. Catheter ablation was performed in 25/27 ventricular tachycardias (93%) in 15/17 patients (88%): 16/25 ventricular tachycardias (64%) were successfully ablated in 10/17 patients (59%). Catheter ablation was not performed in two patients or proved unsuccessful in five patients. At a follow-up of 15±5 months, there was no recurrence of documented ventricular tachycardia in all 10 patients with successful catheter ablation; in two of them a previously non-documented ventricular tachycardia occurred. A high recurrence of ventricular tachycardia was observed in patients with a failed procedure (5/7: 71%). No major complication or death occurred. Conclusions Non-contact mapping can be effectively used to map and guide radiofrequency catheter ablation of untolerated ventricular tachycardias. Given the favourable acute and clinical long-term results, this approach proves to be more effective in patients with postinfarction ventricular tachycardias, in comparison to patients with arrhythmogenic right ventricular dysplasia and idiopathic dilated cardiomyopathy.

Noncontact mapping to guide ablation of right ventricular outflow tract tachycardia

ObjectivesThe aim of this study was to determine whether noncontact mapping is feasible in the right ventricle and assess its utility in guiding ablation of difficult-to-treat right ventricular outflow tract (RVOT) ventricular tachycardia (VT). BackgroundIn patients without inducible arrhythmia, RVOT VT may be difficult to ablate. Noncontact mapping permits ablation guided by a single tachycardia complex, which may facilitate ablation of difficult cases. However, the mapping system may be geometry-dependent, and it has not been validated in the unique geometry of the RVOT. MethodsTen patients with left bundle inferior axis VT, no history of myocardial infarction and normal left ventricular function underwent noncontact guided ablation; seven had failed previous ablation and three had received a defibrillator. All noncontact maps were analyzed by a blinded reviewer to determine whether the arrhythmia focus was epicardial and to predict on the basis of the map whether arrhythmia would recur. ResultsThe procedure was acutely successful in 9 of 10 patients. During a mean follow-up of 11 months, 7 of 9 patients remained arrhythmia-free. Both patients in whom the blinded reviewer predicted failure had arrhythmia recurrence: one due to epicardial origin with multiple endocardial exit sites and one due to discordance between site of lesion placement and earliest activation on noncontact map. ConclusionsMechanisms of ablation failure in RVOT VT include absence of sustained arrhythmia, difficulty with substrate localization and epicardial origin of arrhythmia. In this study, noncontact mapping was safely and effectively used to guide ablation of patients with difficult-to-treat RVOT VT.

Non-contact mapping to guide catheter ablation of untolerated ventricular tachycardia

The role of a novel non-contact mapping system (ESI 3000, Endocardial Solutions) to guide radiofrequency catheter ablation of untolerated ventricular tachycardia was investigated in 17 patients; 11 with prior myocardial infarction, three with arrhythmogenic right ventricular dysplasia, and three with idiopathic dilated cardiomyopathy. Twenty-seven monomorphic ventricular tachycardias were induced (mean cycle 320+/-60 ms, range 230-450 ms), mapped for 15-20 s, and terminated by overdrive pacing or DC shock. Off-line analysis of isopotential activation mapping was performed to identify the diastolic pathway and/or the exit point of the ventricular tachycardia reentry circuit. Radiofrequency current was applied to create a line of block across the diastolic pathway or around the exit point. All 27 ventricular tachycardias were mapped with the non-contact system. The endocardial exit point (-7+/-15 ms before QRS onset) was defined in 21/21 postinfarction ventricular tachycardias, in 3/3 arrhythmogenic right ventricular dysplasia and in 1/3 idiopathic dilated cardiomyopathy ventricular tachycardias, respectively. The diastolic pathway (earliest endocardial diastolic activity: -65+/-49 ms before QRS onset) was identified in 17/21 postinfarction ventricular tachycardias, in 1/3 arrhythmogenic right ventricular dysplasia and in 1/3 idiopathic dilated cardiomyopathy ventricular tachycardias, respectively. Catheter ablation was performed in 25/27 ventricular tachycardias (93%) in 15/17 patients (88%): 16/25 ventricular tachycardias (64%) were successfully ablated in 10/17 patients (59%). Catheter ablation was not performed in two patients or proved unsuccessful in five patients. At a follow-up of 15+/-5 months, there was no recurrence of documented ventricular tachycardia in all 10 patients with successful catheter ablation; in two of them a previously non-documented ventricular tachycardia occurred. A high recurrence of ventricular tachycardia was observed in patients with a failed procedure (5/7: 71%). No major complication or death occurred. Non-contact mapping can be effectively used to map and guide radiofrequency catheter ablation of untolerated ventricular tachycardias. Given the favourable acute and clinical long-term results, this approach proves to be more effective in patients with postinfarction ventricular tachycardias, in comparison to patients with arrhythmogenic right ventricular dysplasia and idiopathic dilated cardiomyopathy.

Pace mapping of postinfarction scar to detect ventricular tachycardia exit sites and zones of slow conduction.

The exit site and central common pathway of slow conduction are preferred sites to guide radiofrequency ablation of postinfarction ventricular tachycardia (VT). Both require inducibility of VT. In addition, their low amplitude hampers direct recording of potentials generated by activation in pathways of slow conduction. We hypothesized that pace mapping during sinus rhythm would help to detect the VT exit site and potentials generated by activation in pathways of slow activation. In 13 patients suffering from VT late after anterior (n = 10) or inferior (n = 3) myocardial infarction, stimulation was performed in scarred endocardium at 23.5 (range 13 to 36) sites per patient during arrhythmia surgery. Multielectrode recordings (64 sites) during stimulation at a fixed cycle length of 500 msec were obtained. Endocardial breakthrough sites distant (>2 cm) from the pacing site were found at 4.3 (range 3 to 19) pacing sites per patient. Low-amplitude discrete potentials (LADPs) could be detected between the pacing site and the breakthrough site in 2.3 (range 0 to 13) of 4.3 stimulation sequences. In these patients, 19 VTs were induced and the exit site determined. In 6 patients, the distant pacing breakthrough site was identical to the VT exit site; in 7 patients, no similar exit sites were found. LADPs during VT were found at a median 2.0 (range 0 to 14) sites per patient. Pace mapping of the postinfarction endocardial scar during sinus rhythm revealed 50% of the endocardial exit sites of VT and the same number of LADPs observed during VT.

Reentrant pathway during ventricular echoes is confined to the atrioventricular node : high-resolution mapping and dissection of the triangle of koch in isolated, perfused canine hearts.

Background-During ventricular echoes, reentrant excitation is supposed to involve 2 functionally distinct pathways in the atrioventricular (AV) nodal area. The exact pathway of reentrant excitation is unknown. The objectives of this study were to analyze electrical activity in the AV nodal area after ventricular stimulation and during ventricular echoes and to assess the role of perinodal atrial tissue in AV nodal reentry. Methods and Results-In 16 isolated, blood-perfused canine hearts, multiterminal electrodes were used to map electrical activity in Koch's triangle after ventricular stimulation and during ventricular echoes. The subendocardial cell layers were chemically destroyed in 3 hearts. Incisions in the posterior approach to the compact node were made in 6 hearts. The apex of the triangle of Koch was surgically dissociated from the perinodal atrial tissue in 5 hearts. Retrograde atrial activation occurred via 2 distinct endocardial exit sites. Ventricular echoes could be induced in all hearts irrespective of the atrial activation pattern. Simultaneous retrograde activation of both exit sites often preceded reciprocation. Ventricular echoes were demonstrable after chemical destruction of the endocardium and after surgical dissociation of the perinodal atrial tissue from the AV node. Conclusions-Our data show that the reentrant pathway during ventricular echoes is confined to the AV node. The tissue that connects the node to the endocardial exit sites has to be excluded from the reentrant circuit responsible for single echoes.

Current Role and Future Perspectives for Radiofrequency Catheter Ablation of Postmyocardial Infarction Ventricular Tachycardia

The most common substrate for ventricular tachycardia (VT) is a postmyocardial infarction (MI) scar. Radiofrequency catheter ablation (RFCA) in post-MI VT faces clinical, electrophysiologic, anatomic, and methodologic difficulties not found in many other human tachycardias. The pathophysiologic understanding of post-MI VT is incomplete; this influences the process of selecting RFCA target sites, which is time consuming, demands catheter stability, and has low sensitivity and predictive value for VT interruption by RF current. Improving and simplifying the methodology of RFCA in post-MI VT is badly needed. We review the pathophysiology of post-MI VT from the data reported on endocardial, epicardial, and intramural ventricular mapping obtained either intraoperatively or in a Langendorff perfused set-up in hearts from transplanted patients. From these studies we conclude that (1) some post-MI VT cases are not amenable to RFCA (reentry around the scar, VT having a subepicardial or deep intramural substrate, or a wide, extensive, subendocardial intrascar area of slow conduction); and (2) searching for the endocardial exit is advantageous for selecting the RFCA targets. We also comment on a new self-reference mapping catheter that allows the recording of high gain, noise-free, unfiltered and filtered unipolar signals as well as unipolar pacing. Among the unresolved issues in these patients is the meaning of fast nonclinical VT induced after successful RFCA of the clinical VT, which may explain why a substantial number of these patients still receive an implantable cardioverter-defibrillator. (Am J Cardiol 1996;78(suppl 5A):76–88)

Fulguration of Ventricular Tachycardia Using High Cumulative Energy: Results in Thirty‐one Patients with a Mean Follow‐Up of Twenty‐seven Months

Catheter electrical ablation of ventricular tachycardia (VT) was attempted in 31 patients (57 +/- 15 years) who had refractory recurrent VT. Fifteen patients had coronary artery disease, seven had arrhythmogenic right ventricular dysplasia, four had cardiomyopathy and five had no structural heart disease. Ten patients were NYHA class III-IV. Ten patients experienced cardiac arrest or syncope during VT. Twenty-two patients had only one documented morphologic type of spontaneous VT. Whereas nine patients had more than one: the VT was incessant or daily in 17 patients. One to 16 shocks (mean 5.6) of 160 to 240 joules each (1162 +/- 1060 joules) were delivered to the endocardial exit site of VT--as identified by endocardial activation mapping (29 patients) and pacemapping (31 patients)--during one (22 patients) or more than one session (nine patients). Cumulative delivered energy was 840 +/- 558 joules for right ventricular VT (11 patients) and 1362 +/- 1240 joules for left ventricular VT (20 patients). Reversible side effects occurring immediately after shocks included: nonclinical VT (two patients), ventricular fibrillation (two patients), AV block (three patients). Mean CK-MB fraction 6 hours after shocks was 91 +/- 46 IU/1. An electrophysiology study performed 7 to 10 days later demonstrated that the original clinical VT was inducible in seven patients, nonclinical monomorphic VT was inducible in eight patients and no VT was inducible in 13 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Catheter ablation of ventricular tachycardia with intracardiac shocks: results in 33 patients.

Catheter electrical ablation of ventricular tachycardia (VT) was attempted in 33 patients who had recurrent unimorphic VT refractory to 3.7 +/- 1.2 (mean +/- SD) antiarrhythmic drugs. Their mean age was 56 +/- 14 years. Twenty-two patients had coronary artery disease, six had other types of heart disease, and five had no structural heart disease. The mean left ventricular ejection fraction was 0.34 +/- 0.17. Thirty patients had only one documented morphologic type of spontaneous VT, whereas three patients had more than one. One to four shocks of 100 to 300 J each were delivered to the endocardial exit site of VT, as identified by endocardial activation mapping and pace-mapping. In each patient endocardial activation at the exit site of VT preceded the onset of the QRS complex (mean activation time -50 +/- 30 msec). Pace-mapping was possible in 26 patients, and in all but two patients the QRS complexes during VT and during pacing at the exit site of VT were very similar in at least 10 of 12 electrocardiographic leads. In 29 patients, shocks were delivered between an endocardial electrode (cathode) and a patch electrode on the chest wall (anode). Seven patients (including three who first received shocks using an external anode) whose VT originated in the septum received transseptal shocks between two electrodes positioned on either side of the septum. The procedure was successful in 15 patients (45%), who had no recurrence of VT either on no antiarrhythmic therapy or on the same regimen that was ineffective before ablation, over a follow-up period of 15.5 +/- 10 months (range 5 to 35). The ablation attempt was unsuccessful in 18 patients (55%). There were no significant differences in clinical and electrophysiologic variables between patients with and without a successful outcome. Seven nonfatal complications occurred in six patients: sustained nonclinical VT immediately after the shock, ventricular fibrillation on days 5 and 6 after ablation, neurologic deficits (n = 2), atrioventricular block (n = 2), and brachial artery thrombosis. In conclusion, catheter electrical ablation of VT has modest efficacy and is relatively safe in a selected group of patients who have predominantly one configuration of unimorphic VT.