Simultaneous epicardial and endocardial substrate mapping and radiofrequency catheter ablation as first-line treatment for ventricular tachycardia and frequent ICD shocks in chronic chagasic cardiomyopathy

Background and Aims  

Slow conduction scarred areas are related with ventricular tachycardia (VT) arrhythmogenesis in nonischemic cardiomyopathy. The purpose of this study was to characterize the substrate in both epicardial and endocardial surfaces of the left ventricle and to evaluate the effectiveness of substrate mapping and ablation for VT in Chagas cardiomyopathy.     

动态基质标测在致心律失常右室心肌病患者室性心动过速射频消融中的应用

目的　探讨应用非接触球囊导管标测系统行动态基质标测,指导对致心律失常右室心肌病(ARVC)患者室性心动过速(室速)消融的价值。方法　应用非接触球囊导管标测系统在窦律下对 3例ARVC室速患者行动态基质标测,在确定室速的最早激动点、出口部位和传导顺序后,寻找与室速相关的峡部并行线性消融。结果　3例患者存在 3种不同形态的基质,分别位于右室流出道、右室前壁和右室前侧壁。共诱发 5种室速,平均心动周期为(348±65)ms,其中 3种室速起源于基质或基质边缘, 2种室速的起源远离基质; 1种室速经基质传导。5种室速全部消融成功。平均随访 20个月,无心动过速发作。结论　应用非接触球囊导管标测系统确定异常电生理基质有助于理解ARVC室速的发生机制和制定消融策略,行室速相关峡部的线性消融可有效治疗室速。     

Localization of the isthmus in reentrant circuits by analysis of electrograms derived from clinical noncontact mapping during sinus rhythm and ventricular tachycardia

INTRODUCTION: New methods for electrogram analysis accurately estimated reentrant circuit isthmus location and shape in a canine model. It was hypothesized that these methods also would locate reentrant circuits causing clinical ventricular tachycardia (VT). METHODS AND RESULTS: Intracardiac electrogram recordings, obtained with a noncontact mapping system, were analyzed retrospectively from 14 patients with reentrant VT who had undergone successful radiofrequency ablation for prevention of VT initiation. Unipolar electrograms from 256 uniformly distributed endocardial sites were reconstructed by mathematical transformation. Twenty-seven tachycardias were mapped; 15 (in 11 patients) had a complete endocardial reentrant circuit with a figure-of-eight conduction pattern. During sinus rhythm, the location and axis of the slowest and most uniform conduction in the region of latest endocardial activation (the primary axis), the limits of which were defined as boundaries with >15 ms difference in electrogram duration between contiguous recordings, identified the location and shape of the reentrant circuit isthmus with a mean sensitivity compared with activation mapping of 79.3% and a mean specificity of 97.6%. The midpoint of a theoretical "estimated best ablation line" drawn perpendicular to the primary axis of activation, spanning the estimated isthmus location was within 1.3 +/- 0.2 cm (mean distance +/- SD) of the actual ablation site that terminated tachycardia. Analysis of VT electrograms, based on time shifts in the far-field component of the local electrogram when cycle length changed (piecewise linear adaptive template matching [PLATM] method) in 5 of the cases, accurately estimated the time interval between activation at the recording site and the circuit isthmus slow conduction zone where the effective ablation lesion had been placed, which is proportional to the distance between the two locations (mean difference compared with activation mapping: +/-37.3 ms). CONCLUSION: In selected patients with VT who have a complete endocardial circuit, isthmus location and shape can be discerned by analysis of sinus rhythm or tachycardia electrograms, and an effective ablation site can be predicted without the need to construct activation maps of reentrant circuits.     

Electroanatomic mapping characteristics of ventricular tachycardia in patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia.

BACKGROUND: Ventricular tachycardia (VT) in arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVD) has been previously explored using entrainment mapping techniques but little is know about VT mechanisms and the characteristics of their circuits using an electroanatomical mapping system. METHODS AND RESULTS: Three-dimensional electroanatomical mapping was performed in 11 patients with well tolerated sustained VT and ARVD. Sinus rhythm mapping of the right ventricle was performed in eight patients showing areas of low bipolar electrogram voltage (<1.2 mV). In total 12 tachycardias (mean cycle length 382+/-62 ms) were induced and mapped. Complete maps demonstrated a reentry mechanism in eight VTs and a focal activation pattern in four VTs. The reentrant circuits were localized around the tricuspid annulus (five VTs), around the right ventricular outflow tract (one VT) and on the RV free lateral wall (two VTs). The critical isthmus of each peritricuspid circuit was bounded by the tricuspid annulus with a low voltage area close to it. The isthmus of tachycardia originating from the right ventricular outflow tract (RVOT) was delineated by the tricuspid annulus with a low voltage area localized on the posterior wall of the RVOT. Each right ventricular free wall circuit showed an isthmus delineated by two parallel lines of block. Focal tachycardias originated on the right ventricular free wall. Linear radiofrequency ablation performed across the critical isthmus was successful in seven of eight reentrant tachycardias. The focal VTs were successfully ablated in 50% of cases. During a follow-up of 9-50 months VT recurred in four of eight initially successfully ablated VTs. CONCLUSIONS: Peritricuspid ventricular reentry is a frequent mechanism of VT in patients with ARVD which can be identified by detailed 3D electroanatomical mapping. This novel form of mapping is valuable in identifying VT mechanisms and in guiding RF ablation in patients with ARVD.     

Anatomic characterization of endocardial substrate for hemodynamically stable reentrant ventricular tachycardia: Identification of endocardial conducting channels

BACKGROUND: Detailed anatomic characterization of endocardial substrate of ventricular tachycardia (VT) is limited. OBJECTIVES: The purpose of this study was to determine the endocardial dimensions and local electrogram voltage characteristics of the reentrant circuit. VT-related conducting channels corresponding to zones of slow conduction may be identified. METHODS: Electroanatomic mapping was performed in 26 patients with uniform VT. Entrainment mapping was performed in 53 VTs, of which 19 entrance, 37 isthmus, 48 exit, and 32 outer loop sites were identified. The color display of voltage maps was adjusted to identify conducting channels associated with VT circuits. A conducting channel was defined as a path of multiple orthodromically activated sites within the VT circuit that demonstrated an electrogram amplitude higher than that of surrounding areas as evidenced by voltage color differences. RESULTS: Forty-seven (84%) of 56 entrance or isthmus sites were located within dense scar (<0.5 mV). Nearly all exits (92%) were located in abnormal endocardium (<1.5 mV), with more than half (54%) located in the border zone (0.5-1.5 mV). VT-related conducting channels was identified in 18 of 32 VTs with detailed mapping (average length 32 +/- 22 mm). The voltage threshold in the conducting channels ranges from 0.1 to 0.7 mV (mean 0.33 +/- 0.15 mV). CONCLUSION: (1) Most entrance and isthmus sites of hemodynamically stable VT are located in dense scar, whereas exits are located in the border zone. (2) VT-related conducting channels may be identified by careful voltage threshold adjustment. These findings have important implications regarding strategies for substrate-based VT ablation.     

Novel Mapping Strategies for Ventricular Tachycardia Ablation

Despite advances in antiarrhythmic and device therapy, ventricular tachycardia (VT) continues to be a major cause of increased morbidity and mortality. During scar-mediated monomorphic ventricular tachycardia ablation, the search for critical isthmus sites continues to be the primary goal during successful ablative procedures. However, given the overwhelming hemodynamic instability of most ventricular arrhythmias (>?70%), VT ablation is increasingly performed during sinus rhythm. This technique requires either a greater reliance on isthmus surrogates, or more extensive ablation techniques and is a more probabilistic approach to substrate modification. We believe that a better understanding of scar physiology and activation during sinus rhythm has important implications for clinical workflow and mechanistic improvements with current ablation strategies. With advancements in high-density mapping and multi-electrode catheter technology, mapping of VT substrates is performed with higher resolution, with improved visualization of local abnormal ventricular activities (LAVA), and with a more nuanced functional understanding of late potentials. As a prerequisite, our practice for VT ablation starts with a high-density structural map to identify voltage abnormalities as well as an isochronal functional map of sinus rhythm activation to identify region of discontinuous wavefront propagation. As the era of increased automation has emerged, there continues to be vast array of customizable features, and we have adopted the use of multiple wavefront mapping to further elucidate possible arrhythmogenic substrate. Our emerging understanding of how scar propagation patterns relate to areas of abnormal signals and critical isthmuses may greatly improve the ability to identify surrogates during sinus rhythm and help localize the most arrhythmogenic regions within a given scar. In the hemodynamically unstable patients, we routinely integrate isochronal late activation mapping (ILAM) to identify areas of slow conduction to initiate our targeted ablation and substrate modification. Multi-electrode delineation of the entire reentrant VT circuit has value in understanding the size of the circuit, rotational nature, and transmural extent of human reentry. Correlative studies between the activation of the complete VT circuit and sinus rhythm are likely to provide important mechanistic insights on where fixed and/or functional block occurs within a complex scar substrate.     

Ventricular tachycardia ablation in patients with coronary heart disease: beyond the reentry circuit.

INTRODUCTION: Patients with coronary heart disease and left ventricular dysfunction are at increased risk for the development of ventricular tachycardia (VT) related to areas of myocardial fibrosis. Although the mechanism and the circuit of this arrhythmia are well understood, little is known about the triggers that precipitate VT episodes. Purkinje fiber potentials may be responsible for idiopathic VT, and recent studies have related them to polymorphic VT and ventricular fibrillation. METHODS: Between January 2002 and December 2003, we performed ablation in 10 patients with coronary heart disease, left ventricular systolic dysfunction and VT refractory to pharmacological therapy. All patients had implantable cardioverter-defibrillators. Electroanatomical activation and voltage mapping (CARTO) and electrophysiological criteria (premature activation during VT, pace mapping, and presence of diastolic potentials) were used to define scar regions, slow conduction areas and the reentry circuit isthmuses. RESULTS: Spike potentials were recorded in the scars of three patients. These potentials were almost fused with the ventricular electrogram during sinus rhythm, and were more premature during VT, probably reflecting local activation of Purkinje fibers. During ablation, we were able to dissociate the spike from the ventricular electrogram, thus terminating the VT. In the cases with conduction recovery, ventricular; ectopic beats recurred, preceded by a spike and degenerating into short runs of VT. The ablation strategy was not modified since persistence of the VT required the isthmus. CONCLUSION: The results suggest that residual Purkinje fibers may be present in scar regions and that the activity of these fibers may trigger VT in pre-established circuits.     

Characterization of the infarct substrate and ventricular tachycardia circuits with noncontact unipolar mapping in a porcine model of myocardial infarction

BACKGROUND: Conventional mapping of ventricular tachycardia (VT) after myocardial infarction is limited in patients with hemodynamically untolerated or noninducible VT. OBJECTIVES: The purpose of this study was to develop a unique strategy using noncontact unipolar mapping to define infarct substrate and VT circuits. METHODS: Dynamic substrate mapping (DSM) was performed in seven pigs with healed anterior myocardial infarction. This technique defined substrate as the intersection of low-voltage areas identified in sinus rhythm and during pacing around the infarct. Pacing was also performed within the substrate to determine exit sites. RESULTS: Anteroapical transmural scar was identified in all animals. A mean of three pacing sites was used for substrate definition. The mean area (+/- SD) was 18.4 +/- 8.8 cm2 by DSM and 15.4 +/- 6.9 cm2 by pathology (P >.5). A mean of 4.5 sites was paced within substrate. Ten of 18 paced wavefronts exited substrate adjacent to the pacing area, seven exited at distant areas, and one had two exits. VT was induced in five animals (1.6 morphologies per animal). Except for one VT, circuit exit sites were identified at substrate borders on the endocardium. VT exit sites were at (n = 6) or near (n = 3) a pacing exit site. Electrogram voltages differed significantly between substrate, border, and nonsubstrate areas in infarcted animals and in comparison with control animals. No substrate was identified in two control animals. CONCLUSION: DSM is a reliable method for infarct substrate localization in this model. Pacing within substrate can predict VT exit sites and may prove useful for ablation of unmappable VT after myocardial infarction.     

Outcome of ventricular tachycardia catheter ablation in ischemic heart disease patients using a high-density mapping substrate-based approach: A prospective cohort study

Introduction and objectiveRadiofrequency catheter ablation (RCA) for ventricular tachycardia (VT) in patients with ischemic heart disease (IHD) is associated with a reduced risk of VT storm and implantable cardioverter defibrillator (ICD) shocks. We aim to report the outcome after a single RCA procedure for VT in patients with IHD using a high-density substrate-based approach.MethodsWe conducted a prospective, observational, single-center and single-arm study involving patients with IHD, referred for RCA procedure for VT using high-density mapping catheters. Substrate mapping was performed in all patients. Procedural endpoints were VT non-inducibility and local abnormal ventricular activities (LAVAs) elimination. The primary end point was survival free from appropriate ICD shocks and secondary end points included VT storm and all-cause mortality.ResultsSixty-four consecutive patients were included (68±9 years, 95% male, mean ejection fraction 33±11%, 39% VT storms, and 69% appropriate ICD shocks). LAVAs were identified in all patients and VT inducibility was found in 83%. LAVA elimination and non-inducibility were achieved in 93.8% and 60%, respectively. After a mean follow-up of 25±18 months, 90% and 85% of patients are free from appropriate ICD shocks at one and two years, respectively. The proportion of patients experiencing VT storm decreased from 39% to 1.6%. Overall survival was 89% and 84% at one and two years, respectively.ConclusionsRCA of VT in IHD using a high-density mapping substrate-based approach resulted in a steady freedom of ICD shocks and VT storm.     

Impact of substrate-based ablation for ventricular tachycardia in patients with frequent appropriate implantable cardioverter-defibrillator therapy and dilated cardiomyopathy: Long-term experience with high-density mapping

IntroductionRecurrent ventricular tachycardia (VT) episodes have a negative impact on the clinical outcome of implantable cardioverter-defibrillator (ICD) patients. Modification of the arrhythmogenic substrate has been used as a promising approach for treating recurrent VTs. However, there are limited data on long-term follow-up.AimTo analyze long-term results of VT substrate-based ablation using high-density mapping in patients with severe left ventricular (LV) dysfunction and recurrent appropriate ICD therapy.MethodsWe analyzed 20 patients (15 men, 55% with non-ischemic cardiomyopathy, age 58±15 years, LV ejection fraction 32±5%) and repeated appropriate shocks or arrhythmic storm (>2 shocks/24 h) despite antiarrhythmic drug therapy and optimal heart failure medication. All patients underwent ventricular programmed stimulation (600 ms/S3) to document VT. A sinus rhythm (SR) voltage map was created with a three-dimensional electroanatomic mapping system (CARTO, Biosense Webster, CA) using a PentaRay® high-density mapping catheter (Biosense Webster, CA) to delineate areas of scarred myocardium (ventricular bipolar voltage ≤0.5 mV – dense scar; 0.5-1.5 mV – border zone; ≥1.5 mV – healthy tissue) and to provide high-resolution electrophysiological mapping. Substrate modification included elimination of local abnormal ventricular activities (LAVAs) during SR (fractionated, split, low-amplitude/long-lasting, late potentials, pre-systolic), and linear ablation to obtain scar homogenization and dechanneling. Pace-mapping techniques were used when capture was possible. The LV approach was retrograde in nine cases, transseptal in five and epi-endocardial in four. In two patients ablation was performed inside the right ventricle.ResultsLAVAs and scar areas were modified in all patients. Mean procedure duration was 149 min (105-220 min), with radiofrequency ranging from 18 to 70 min (mean 33 min) and mean fluoroscopy time of 15 min. Non-inducibility was achieved in 75% of cases (in four patients with hemodynamic deterioration and an LV assist device, VT inducibility was not performed). There were two cases of pericardial tamponade, drained successfully. During a follow-up of 50±24 months, 65% had no VT recurrences. Among the seven patients with recurrences, three underwent redo ablation and four, with fewer VT episodes, received appropriate ICD therapy. There were five hospital readmissions due to heart failure decompensation, one patient died in the first week after unsuccessful ablation of a VT storm and three died (stroke and pneumonia) >1 year after ablation.ConclusionCatheter ablation based on substrate modification is feasible and safe in patients with frequent VTs and severe LV dysfunction. This approach may be of clinical relevance, with potential long-term benefits in reducing VT burden.     

An approach to help differentiate postinfarct scar from borderzone tissue using Ripple Mapping during ventricular tachycardia ablation

Background

Ventricular scar is traditionally highlighted on a bipolar voltage (BiVolt) map in areas of myocardium <0.50 mV. We describe an alternative approach using Ripple Mapping (RM) superimposed onto a BiVolt map to differentiate postinfarct scar from conducting borderzone (BZ) during ventricular tachycardia (VT) ablation.

Methods

Fifteen consecutive patients (left ventricular ejection fraction 30 ± 7%) underwent endocardial left ventricle pentaray mapping (median 5148 points) and ablation targeting areas of late Ripple activation. BiVolt maps were studied offline at initial voltage of 0.50–0.50 mV to binarize the color display (red and purple). RMs were superimposed, and the BiVolt limits were sequentially reduced until only areas devoid of Ripple bars appeared red, defined as RM-scar. The surrounding area supporting conducting Ripple wavefronts in tissue <0.50 mV defined the RM-BZ.

Results

RM-scar was significantly smaller than the traditional 0.50 mV cutoff (median 4% vs. 12% shell area, p < .001). 65 ± 16% of tissue <0.50 mV supported Ripple activation within the RM-BZ. The mean BiVolt threshold that differentiated RM-scar from BZ tissue was 0.22 ± 0.07 mV, though this ranged widely (from 0.12 to 0.35 mV). In this study, septal infarcts (7/15) were associated with more rapid VTs (282 vs. 347 ms, p = .001), and had a greater proportion of RM-BZ to RM-scar (median ratio 3.2 vs. 1.2, p = .013) with faster RM-BZ conduction speed (0.72 vs. 0.34 m/s, p = .001). Conversely, scars that supported hemodynamically stable sustained VT (6/15) were slower (367 ± 38 ms), had a smaller proportion of RM-BZ to RM-scar (median ratio 1.2 vs. 3.2, p = .059), and slower RM-BZ conduction speed (0.36 vs. 0.63 m/s, p = .036). RM guided ablation collocated within 66 ± 20% of RM-BZ, most concentrated around the RM-scar perimeter, with significant VT reduction (median 4.0 episodes preablation vs. 0 post, p < .001) at 11 ± 6 months follow-up.

Conclusion

Postinfarct scars appear significantly smaller than traditional 0.50 mV cut-offs suggest, with voltage thresholds unique to each patient.     

New Endpoint for Ablation of Ventricular Tachycardia: Change in QRS Morphology with Pacing at Protected Isthmus as Index of Isthmus Block

New Endpoint for Ablation of Ventricular Tachycardia. Introduction: Endpoints confirming block in the critical isthmus in sinus rhythm and with pace mapping have not been established. Methods and Results: A 44‐year‐old man with a history of Tetralogy of Fallot presented with recurrent ventricular tachycardia (VT). Entrainment mapping was consistent with a macroreentrant circuit rotating in a clockwise fashion under the pulmonic valve. After termination of the VT in a critical isthmus located on the conal free wall, a pace map proximal to the site of successful ablation was consistent with a change in QRS morphology. This change in QRS morphology suggested critical isthmus block and successful ablation, which was confirmed by noninducibility with programmed stimulation. Conclusion: Evidence of conduction block can be used as an additional endpoint for successful ablation of VT. (J Cardiovasc Electrophysiol, Vol. 21, pp. 320–324, March 2010)     

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. Introduction: 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). Methods: 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. Results: Applying DSM, the critical diastolic pathway of the VT was identified in all 7 patients that corresponded to the regions targeted for ablation. Conclusion: 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)     

Electrophysiologic features of protected channels in late postinfarction patients with and without spontaneous ventricular tachycardia

Purpose

Protected channels of surviving myocytes in late postinfarction ventricular scar predispose to ventricular tachycardia (VT). However, only a few patients develop VT spontaneously. We studied differences in electric remodeling and protected channels in late postinfarction patients with and without spontaneous VT.

Methods

Patients with ischemic cardiomyopathy (ICM) with recurrent sustained monomorphic VT (n?=?22) were compared with stable ICM patients without spontaneous VT (control group; n?=?5). Left ventricular mapping was performed with a 20-pole catheter. Detailed pace mapping was used to identify channels of protected conduction, and confirmed, when feasible, by entrainment. Anatomical and electrophysiological properties of VT channels and non-VT channels in VT patients and channels in controls were evaluated.

Results

Seventy-three (median 3) VTs were inducible in VT patients compared to two (median 0) in controls. The VT channels in VT patients (n?=?57, 3?±?1 per patient) were lengthier (mean?±?SEM 53?±?5 vs. 33?±?4 vs. 24?±?8 mm), had longer S-QRS (73?±?4 vs. 63?±?3 vs. 44?±?8 ms), longer conduction time (103?±?13 vs. 33?±?4 vs. 24?±?8 ms), and slower conduction velocity (CV) (0.85?±?0.21 vs. 1.39?±?0.20 vs. 1.31?±?0.41 m/s) than non-VT channels in VT patients (n?=?183, 8?±?6 per patient) (p?≤?0.01) and channels in controls (n?=?46, 9?±?8 per patient) (p?≤?0.01). Additionally, non-VT channels in VT patients had longer S-QRS (p?=?0.02); however, they were similar in length, conduction time, and CV compared to channels in controls.

Conclusions

Channels supporting VT are lengthier, with longer conduction times and slower CV compared to channels in patients without spontaneous VT. These observations may explain why some ICM patients have spontaneous VT and others do not.

     

Identification of the slow conduction zone in a macroreentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia using electroanatomic mapping

Identification of the Slow Conduction Zone in a Macroreentry. Background: Although idiopathic left ventricular tachycardia (ILVT) has been shown to possess a slow conduction zone (SCZ), the details of the electrophysiological and anatomic aspects are still not well understood. Objective: We hypothesized that the SCZ can be identified using a 3‐dimensional electroanatomic (EA) mapping system. Methods : Ten patients with ILVT were mapped using a 3‐dimensional electroanatomic (EA) mapping system. After a 3‐dimensional endocardial geometry of the left ventricular was created, the conduction system with left Purkinje potential (PP) and the SCZ with diastolic potential (DP) in LV were mapped during sinus rhythm (SR) and ventricular tachycardia (VT) and were tagged as special landmarks in the geometry. The electrophysiological and anatomic aspects of it were investigated. Results: EA mapping during SR and VT was successfully performed in 7 patients, during VT in 3 patients. The SCZ with DPs located at the inferoposterior septum was found in 7 patients during SR and all patients during VT. The length of the SCZ was 25.2 ± 2.3 mm with conduction velocity 0.08 ± 0.01 m/s. No differences in these parameters were found between patients during SR and VT (P > 0.05). An area with PP was found within the posterior septum. A crossover junction area with DP and PP was found in 7 patients during SR and VT. This area with DP and PP during SR coincided or were in proximity to such area during VT and radiofrequency ablation targeting the site within the area abolished VT in all patients. Conclusion: The ILVT substrate within the junction area of the SCZ and the posterior fascicular can be identified and can be used to guide the ablation of ILVT. (J Cardiovasc Electrophysiol, Vol. 23, pp. 840‐845, August 2012)     

Optical mapping of the functional reentrant circuit of ventricular tachycardia in acute myocardial infarction.

OBJECTIVES: We used optical mapping to characterize the reentrant circuit of ventricular tachycardia (VT) during acute myocardial infarction (MI) in isolated canine left ventricular preparations. BACKGROUND: The nature of the reentrant circuit that underlies VT during acute MI is not well understood. METHODS: Using optical mapping in isolated canine left ventricular preparations, we characterized the reentrant circuit of monomorphic VT (mean cycle length 245.3 +/- 15.6 ms, n = 7) induced by programmed stimulation during acute MI. RESULTS: Optical mapping during VT revealed a functional reentrant circuit consisting of four components: (1) a protected isthmus located between the infarction area and the functional line of block; (2) an entrance site located at one end of the isthmus; (3) an exit site located at the other end of the isthmus; and (4) an outer loop consisting of nonischemic normal tissue, connecting the exit and entrance sites. Rate-dependent slow conduction within the border zone was associated with significant changes (n = 6) in action potential amplitude (99.1 +/- 0.4 vs 71.4 +/- 0.6 mV, P < .01), maximal diastolic potential (-80.6 +/- 0.2 vs -65.4 +/- 0.6 mV, P < .05), action potential duration at 90% repolarization (APD(90); 188.4 +/- 1.0 vs 164.3 +/- 3.1 ms, P < .05), and dV/dt (302.4 +/- 7.9 vs 168.5 +/- 3.6 V/s, P < .05). Compared to preparations with no inducible VT (n = 7), formation of a functional line of block was the key mechanism for initiation of functional reentry in preparations with VT. When comparing preparations with sustained and nonsustained VT, preservation of slow conduction over the isthmus was the key component for maintenance of sustained VT. CONCLUSIONS: The reentrant circuit of monomorphic VT in the setting of acute MI involved both the infarction border zone and nonischemic normal tissue. The underlying mechanism is related to the presence of rate-dependent slow conduction and the development of a functional line of block in the border zone.     

Analysis of Posterior Mitral Annular Activation During Entrainment and Catheter Ablation of Mitral Isthmus Ventricular Tachycardia Using a Coronary Sinus Catheter

A detailed analysis of the ventricular activation along the posterior aspect of the mitral annulus was made using a multipolar catheter positioned in the coronary sinus in a patient with mitral isthmus ventricular tachycardia (VT) associated with a remote inferior myocardial infarction and prior cryosurgical ablation for the elimination of a different preexisting VT. A change in the timing and sequence of the ventricular activation along the isthmus could be observed during induction of the VT and entrainment pacing. A radiofrequency (RF) current application directed at the posterolateral region of the isthmus successfully eliminated this tachycardia. During the RF delivery, complete conduction block was confirmed by a sudden change in the activation sequence during sinus rhythm.     

Endomyocardial substrate of ventricular arrhythmias in patients with autoimmune rheumatic diseases

Introduction

Delayed enhancement-magnetic resonance imaging (DE-MRI) has demonstrated that nonischemic cardiomyopathy is mainly characterized by intramural or epicardial fibrosis whereas global endomyocardial fibrosis suggests cardiac involvement in autoimmune rheumatic diseases or amyloidosis. Conduction disorders and sudden cardiac death are important manifestations of autoimmune rheumatic diseases with cardiac involvement but the substrates of ventricular arrhythmias in autoimmune rheumatic diseases have not been fully elucidated.

Methods and Results

20 patients with autoimmune rheumatic diseases presenting with ventricular tachycardia (VT) (n = 11) or frequent ventricular extrasystoles (n = 9) underwent DE-MRI and/or endocardial electroanatomical mapping of the left ventricle (LV). Ten patients with autoimmune rheumatic diseases underwent VT ablation. Global endomyocardial fibrosis without myocardial thickening and unrelated to coronary territories was detected by DE-MRI or electroanatomical voltage mapping in 9 of 20 patients with autoimmune rheumatic diseases. In the other patients with autoimmune rheumatic diseases, limited regions of predominantly epicardial (n = 4) and intramyocardial (n = 5) fibrosis or only minimal fibrosis (n = 2) were found using DE-MRI. Endocardial low-amplitude diastolic potentials and pre-systolic Purkinje or fascicular potentials, mostly within fibrotic areas, were identified as the targets of successful VT ablation in 7 of 10 patients with autoimmune rheumatic diseases.

Conclusion

Global endomyocardial fibrosis can be a tool to diagnose severe cardiac involvement in autoimmune rheumatic diseases and may serve as the substrate of ventricular arrhythmias in a substantial part of patients.     

Simultaneous Endocardial and Epicardial Delineation of 3D Reentrant Ventricular Tachycardia

BackgroundMechanisms of scar-related ventricular tachycardia (VT) are largely based on computational and animal models that portray a 2-dimensional view.ObjectivesThe authors sought to delineate the human VT circuit with a 3-dimensional perspective from recordings obtained by simultaneous endocardial and epicardial mapping.MethodsHigh-resolution mapping was performed during 97 procedures in 89 patients with structural heart disease. Circuits were characterized by systematic isochronal analysis to estimate the dimensions of the isthmus and extent of the exit region recorded on both myocardial surfaces.ResultsA total of 151 VT morphologies were mapped, of which 83 underwent simultaneous endocardial and epicardial mapping; 17% of circuits activated in a 2-dimensional plane, restricted to 1 myocardial surface. Three-dimensional activation patterns with nonuniform transmural propagation were observed in 61% of circuits with only 4% showing transmurally uniform activation, and 18% exhibiting focal activation patterns consistent with mid-myocardial reentry. The dimensions of the central isthmus were 17 mm (12 to 28 mm) × 10 mm (9 to 19 mm) with 55% exhibiting a minimal dimension of <1.5 cm. QRS activation was transmural in 63% and located 43 mm (34 to 52 mm) from the central isthmus. On the basis of 6 proposed definitions for epicardial VT, the prevalence of an epicardial circuit ranged from 21% to 80% in ischemic cardiomyopathy and 28% to 77% in nonischemic cardiomyopathy.ConclusionsA 2D perspective oversimplifies the electrophysiological circuit responsible for reentrant human VT and simultaneous endocardial and epicardial mapping facilitates inferences about mid-myocardial activation. Intricate activation patterns are frequently observed on both myocardial surfaces, and the epicardium is functionally involved in the majority of circuits. Human reentry may exist within isthmus dimensions smaller than 1 cm, whereas QRS activation is often transmural and remote from the critical isthmus target. A 3-dimensional perspective of the VT circuit may enhance the precision of ablative therapy and may support a greater role for adjunctive strategies and technology to address arrhythmogenic tissue harbored in the mid-myocardium and subepicardium.     

Relationship of slow conduction detected by pace-mapping to ventricular tachycardia re-entry circuit sites after infarction

OBJECTIVES: This study sought to characterize the relationship of conduction delays detected by pace-mapping, evident as a stimulus to QRS interval (S-QRS) delay >or=40 ms, to ventricular tachycardia (VT) re-entry circuit isthmuses defined by entrainment and ablation. BACKGROUND: Areas of slow conduction and block in old infarcts cause re-entrant VT. METHODS: In 12 patients with VT after infarction, pace-mapping was performed at 890 sites. Stimulus to QRS intervals were measured and plotted in three-dimensional reconstructions of the left ventricle. Conduction delay was defined as >or=40 ms and marked delay as >80 ms. The locations of conduction delays were compared to the locations of 14 target areas, defined as the region within a radius of 2 cm of a re-entry circuit isthmus. RESULTS: Pacing captured at 829 sites; 465 (56%) had no S-QRS delay, 364 (44%) had a delay >or=40 ms, and 127 (15%) had a delay >80 ms. Sites with delays were clustered in 14 discrete regions, 13 of which overlapped target regions. Only 1 of the 14 target regions was not related to an area of S-QRS delay. Sites with marked delays >80 ms were more often in the target (52%) than sites with delays 40 to 80 ms (29%) (p < 0.0001). CONCLUSIONS: Identification of abnormal conduction during pace-mapping can be used to focus mapping during induced VT to a discrete region of the infarct. Further study is warranted to determine if targeting regions of conduction delay may allow ablation of VT during stable sinus rhythm without mapping during VT.