Entrainment Mapping Research Articles

Mapping and ablation of left atrial tachycardias occurring after atrial fibrillation ablation

Regular left atrial tachycardias are a frequent complication of atrial fibrillation ablation procedures. The arrhythmia mechanism appears to be due to focal pulmonary vein reentry in patients who undergo only electrically guided pulmonary vein isolation. The most common site of origin is the septal and inferior aspect of the right pulmonary veins. Attention to avoiding gaps when ablating along this region will minimize the occurrence of these tachycardias. In patients who also undergo linear left atrial ablation lesions and in patients with significant left atrial disease, macroreentry around the mitral annulus or ipsilateral pulmonary veins is frequently observed. Confirming electrical block across any prophylactic linear lesions (mitral isthmus line, left atrial roof line) likely is important for preventing gap-related proarrhythmic tachycardias. When tachycardias do occur, temporizing with ventricular rate control and cardioversion is initially indicated, as approximately one third of these atrial tachycardias may resolve with time. For tachycardias persisting after ablation, detailed three-dimensional activation and entrainment mapping can facilitate localization of the atrial tachycardia and guide the approach to eliminating the arrhythmias. This review provides a systematic approach to the evaluation, diagnosis, localization, and elimination of left atrial tachycardias occurring after atrial fibrillation ablation.

Critical Slow Conduction Zone Located between the Tricuspid Annulus and a Myocardial Infarct Scar in a Patient with Multiple Ventricular Tachycardia Late after Myocardial Infarction

A patient underwent an electrophysiological study (EPS) and catheter ablation (CA) for ventricular tachycardia (VT) that developed 11 years after myocardial infarction. Entrainment mapping (EM) of the left ventricle did not identify the origin of the VT during induction. Electro-anatomical mapping revealed a low voltage area from the anterior to the inferior left ventricular wall. Another EPS was performed for right ventricular mapping. A basket catheter was placed in the right ventricle to evaluate impulse propagation and we attempted to identify the VT circuit with EM during the same VT (complete left bundle branch block configuration, inferior axis) as the previous EPS. Eight different VT appeared, three of which were sustained during CA. The reentry circuit exit was identified on the tricuspid annulus (TA) at the 9:00 site and radiofrequency (RF) ablation was performed, but the axis transformed from the inferior to the superior and another VT appeared. Despite RF ablation to the VT circuit exit at the 5:00 site, another sustained VT appeared. Finally, it was terminated by ablation to a critical slow conduction zone (SCZ) located near the 7:00 site one year later. Electro-anatomical voltage mapping detected a critical isthmus between TA and right ventricle infarct scar. Here, we describe a rare SCZ proximal to the TA in a patient with VT late after myocardial infarction.

Stepwise approach to substrate modification of ventricular tachycardia after myocardial infarction

Recently, substrate mapping (SM) has been described to facilitate catheter ablation of stable and unstable ventricular tachycardia (VT) after myocardial infarction. However, SM is time consuming with potential disadvantages of multiple ablation lines such as impairment of ventricular function or proarrhythmia. The aim of the present study was to delineate a stepwise approach to SM to shorten procedure time and limit the possibility of complications. SM was performed in 14 infarct survivors referred for VT ablation using an electroanatomical mapping system (CARTO) to define infarct regions. A new stepwise approach for SM was designed as follows. The initial ablation site was identified by pace- and entrainment mapping in case of stable VT and by pace mapping only in case of unstable VT. Based on the CARTO voltage mapping, linear ablation was done from this site to the center of the scar and perpendicular to the boundary of the scar or to the mitral annulus. Additional lines were performed only when VT remained inducible. A maximum of 3 ablation lines were created during one procedure. A total of 57 VTs (21 stable, 36 unstable) were induced during the procedures. VT was no longer inducible after the first linear ablation in 2 patients, after the second linear ablation in 6 patients and after the third linear ablation in 3 patients. Either VT or ventricular fibrillation was still inducible at the end of the procedure in 3 patients. Procedure time averaged (291 +/- 85) minutes, fluoroscopy time (10 +/- 7) minutes. VT recurred in 3 patients. Following a second procedure in 2 patients, there were no further VT recurrences. Overall, there was a significant reduction in VT episodes 3 months after [median: 0, interquartile ranges (IQR): 0 - 1] compared with 3 months before ablation (median: 25, IQR: 16 - 105, P < 0.01). This stepwise approach to SM is effective in facilitating ablation of stable and unstable VT. It reduces procedure and fluoroscopy time, and may help to improve the risk-benefit ratio of VT ablation.

Entrainment mapping for rapid distinction of left and right atrial tachycardias

Distinguishing left from right atrial tachycardia is a critical step for guiding ablation. The purpose of this study was to develop and validate a simple algorithm predicting the location of macroreentrant atrial tachycardia (AT) circuits from limited entrainment mapping in right atrium (RA) and coronary sinus (CS). In 180 patients with organized reentrant AT, entrainment was performed at the high RA, proximal CS, and distal CS. The difference between the postpacing interval (PPI) and tachycardia cycle length (TCL) was calculated at each site. The location of the AT reentrant circuit was determined by mapping and ablation. An algorithm predicting AT regions was developed from 104 ATs in the first 90 patients (group I) and prospectively evaluated in a validation cohort of 106 ATs in the second 90 patients (group II). In group I, PPI-TCL difference <50 or >50 ms at the high RA distinguished RA from LA reentrant circuits. For RA tachycardias, PPI-TCL difference at the proximal CS distinguished common flutter from lateral RA circuits. For LA circuits, PPI-TCL difference at the proximal and distal CS distinguished perimitral reentry from reentry involving the right pulmonary veins and septum. In group II, an algorithm based on PPI-TCL difference >50 or <50 ms at the high RA, proximal CS, or distal CS had sensitivity of 94%, specificity of 88%, and predictive accuracy of 93% for predicting the successful ablation region. Limited entrainment from sites accessible from the RA can expeditiously suggest the AT location to guide more detailed mapping and potentially avoid unnecessary transseptal punctures in some patients.

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

Detailed anatomic characterization of endocardial substrate of ventricular tachycardia (VT) is limited. 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. 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. 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). (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.

Substrate-based endocardial ablation of postinfarction ventricular tachycardia

c d t u t The last decade has brought about substantial changes in he conceptualization and approach to ablation of ischemic entricular tachycardia (VT). Activation mapping in conunction with the response to pacing maneuvers during VT entrainment mapping) have been increasingly suppleented and/or replaced by substrate-based approaches for electing target sites for ablation. The latter methodology educes or eliminates the need for mapping during proonged periods of tachycardia and extends the potential enefits of ablation to the large majority of VTs that are emodynamically unstable. This brief review outlines the urrent state and future development of substrate-based enocardial VT ablation.

Narrow, Slow‐Conducting Isthmus Dependent Left Atrial Reentry Developing After Ablation for Atrial Fibrillation: ECG Characterization and Elimination by Focal RF Ablation

The complete circuit of reentrant left atrial tachycardias (LATs) occurring after ablation for atrial fibrillation (AF) has not been well described. Identifying discrete isthmuses critical to these LATs may simplify their elimination by catheter ablation. Fifteen patients (all male, 56 +/- 8 years) with 15 reentrant LATs following AF ablation underwent activation and entrainment mapping. Eleven patients (11 LATs) had a single localized site with low amplitude (0.16 +/- 0.05 mV), fractionated long duration (131 +/- 23 msec) electrograms coinciding with an isoelectric interval of 106 +/- 24 msec between flutter waves on all 12 ECG leads. Three-dimensional mapping and entrainment revealed this site to be a narrow markedly slowly conducting isthmus adjacent to ablated left (n = 8) or right (n = 3) pulmonary vein (PV) ostia, and critical to nine small diameter (15 +/- 3 mm) and two large diameter (49 +/- 2 mm) circuits. One radiofrequency (RF) application on this isthmus eliminated LAT in all 11 patients. Four patients (four LATs) with large circuits around the mitral annulus and/or PV ostia lacked isoelectric ECG intervals and slow-conducting isthmuses and required multiple RF applications across anatomically wide, rapidly conducting isthmuses. Focally ablatable narrow isthmuses of slow conduction are critical for the majority of reentrant LAT occurring after ablation for AF. The role and presence of these isthmuses can be anticipated by observing significant isoelectric intervals between flutter waves on all 12-surface ECG leads. Their distinctive electrophysiological characteristics allow their identification and elimination by simple RF ablation.

Characteristics of Cavotricuspid Isthmus–Dependent Atrial Flutter After Left Atrial Ablation of Atrial Fibrillation

Patients who have previously undergone ablation of atrial fibrillation may experience cavotricuspid isthmus (CTI)-dependent atrial flutter during follow-up. The effects of left atrial (LA) ablation on the characteristics of CTI-dependent flutter have not been described. Fifteen patients underwent ablation of CTI-dependent flutter late after LA ablation of AF. The ECG, biatrial activation patterns, and LA voltage maps during flutter were analyzed. Thirty age- and gender-matched patients who underwent ablation of CTI-dependent flutter without prior LA ablation served as control subjects. Among the patients with prior LA ablation, mapping revealed counterclockwise activation around the tricuspid annulus in 12 of 15 patients (80%) and clockwise activation in 3 of 15 patients (20%). The flutter waves in the inferior leads were upright in 9 of the 15 patients (60%) with prior LA ablation and in none of the control subjects (P<0.001). The upright flutter waves in the inferior leads in patients with counterclockwise flutter corresponded to craniocaudal activation of the right atrial free wall. LA activation contributed little to the genesis of the flutter waves in these patients because of a significant reduction in bipolar LA voltage (0.44+/-0.20 versus 1.54+/-0.19 mV in patients with biphasic/negative flutter waves; P<0.001). CTI-dependent flutter that occurs after LA ablation of atrial fibrillation often has atypical ECG characteristics because of altered LA activation. In patients presenting with atrial flutter after LA ablation, entrainment mapping should be performed at the CTI even if the ECG is uncharacteristic of CTI-dependent flutter.

Ablation of Incisional Reentrant Tachycardia Caused by Lung Transplantation

A 58 year old female underwent orthotopic left lung transplantation for emphysema. She enjoyed rapid recovery from her surgical procedure but developed almost daily episodes of symptomatic palpitations, persisting 32 months following transplant. Electrocardiogram demonstrated atypical atrial flutter, and she reported to the electrophysiology (EP) laboratory for mapping and catheter ablation. At EP study, she was found to have left atrial flutter, cycle length 230 ms, with variable atrioventricular conduction. Entrainment and activation mapping were both consistent with left atrial origin. Transseptal mapping demonstrated high frequency fractionated diastolic atrial electrograms recorded from the site of posterior anastamosis between the grafted pulmonary vein and the left atrium. Post pacing intervals recorded from this site were identical to the tachycardia cycle length. A single radiofrequency lesion terminated the tachycardia, rendering the patient noninducible. She has remained free of symptoms for over six months post ablation. This is the first published report of incisional reentrant atrial tachycardia involving a lung transplant. Standard entrainment mapping and radiofrequency ablation techniques proved satisfactory in curing the arrhythmia.

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

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. 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. 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.

Reentry Within the Cavotricuspid Isthmus: An Isthmus Dependent Circuit

We describe a new cavotricuspid isthmus (CTI) circuit. This study includes 8 patients referred for atrial flutter (AFL) ablation whose tachycardia circuit was confined to the septal CTI and the os of the coronary sinus (CS(OS)) region. Entrainment mapping was performed within the CTI, CS(OS), and other right atrial annular sites (tricuspid annulus (TA)). Electroanatomic mapping was available in 2 patients. Sustained AFL occurred in all patients with mean tachycardia cycle length (TCL) of 318 +/- 54 (276 - 420) ms. During tachycardia, fractionated or double potentials were recorded at either the septal CTI and/or the region of CS(OS) in all, and concealed entrainment with post-pacing interval (PPI)--TCL < or = 25 ms occurred in this area; but manifest entrainment with PPI > TCL was demonstrated from the anteroinferior CTI and other annular sites in 7/8 patients. In one, tachycardia continued with conduction block at the anteroinferior CTI during ablation. Up to three different right atrial activation patterns (identical TCL) were observed. The tachycardia showed a counterclockwise (CCW) pattern in 6, a clockwise pattern in 2, and simultaneous activation of both low lateral right atrium and septum in 5. Electroanatomic mapping was available in 2, showing an early area arising from the septal CTI in 1, and a CCW activation sequence along the TA in another. Radiofrequency application to the septal CTI terminated tachycardia in 4, and tachycardia no longer inducible in all. We describe a tachycardia circuit confined to the septal CTI/CS(OS) region, and hypothesize that this circuit involves slow conduction within the CTI and around the CS(OS), which acts as a central obstacle.

Electrogram Characteristics in Postinfarction Ventricular Tachycardia: Effect of Infarct Age

The purpose of this study was to correlate infarct age with characteristics of the endocardial electrograms (EGM) obtained in patients undergoing mapping procedures for postinfarction ventricular tachycardia (VT). Experimental studies have demonstrated that infarct age influences EGM duration in the subepicardial left ventricle (LV). The relationship between infarct age and endocardial EGM characteristics has not been investigated in patients with postinfarction VT. In a consecutive series of 23 patients with a history of remote infarction (range 1 to 31 years) and VT, endocardial LV mapping was performed with an electroanatomical mapping system (CARTO, Biosense Webster Inc., Diamond Bar, California) during sinus rhythm. Electrogram morphology and width were analyzed and correlated with infarct age. Isthmus sites of the VT re-entry circuits were identified by entrainment mapping and related to the results of substrate mapping. There was a significant correlation between infarct age and width of the bipolar endocardial EGM during baseline rhythm in the peri-infarct zone (r = 0.84; p < 0.0001). Increasing infarct age was associated with progressive activation delays in the scar and with isolated potentials separated by an isoelectric interval, the duration of which also correlated with infarct age (r = 0.77; p < 0.001). Among all endocardial sites, the VT isthmus sites displayed the most delay and broadest EGMs during sinus rhythm. The presence of broad, fractionated EGMs and isolated potentials indicates a healed myocardial infarction; the older the infarction, the broader the EGM width. Remodeling over time alters the electrophysiologic properties of the peri-infarct tissue.

Novel voltage characteristics of cavotricuspid isthmus and mitral isthmus: Implication for catheter ablation of right and left atrial flutter

(25 impulses with stepwise reduction of pacing cycle length from 300 down to 200ms). EP testing was performed in the standard fashion using a 20-pole Halo catheter in the right atrium and 2 quadri-polar catheters positioned into the coronary sinus and various locations in the right atrium. AFL was characterized as CTI-dependent or CTI-independent based on activation and entrainment mapping. Results: 41 out of 42 pts with persistent AFL had CTI-dependent AFL, while only 2 of 16 pts with paroxysmal AFL (p 0.0001) had CTIdependent AFL. 37 out of 40 pts who presented to the EP lab in AFL had CTI-dependent AFL, but only 2 of 16 who presented to the EP lab in another rhythm had inducible CTI-dependent AFL (p 0.0001). Other induced rhythms included CTI-independent AFL (n 4) and atrial fibrillation (n 6) in these pts. Isthmus dependence of AFL was not predicted by history of atrial fibrillation, structural heart disease, hypertension, or previous cardiac surgery. There was no significant difference in age between pts with CTI-dependent and CTI-independent AFL (63 12 and 60 13 years). Conclusion: The presence of persistent rather than paroxysmal AFL and presentation to the EP lab in AFL are strong predictors of cavotricuspid isthmus dependent AFL. Paroxysmal AFL is rarely CTI-dependent. These findings have important implications for referral of patients for catheter ablation of AFL.

Entrainment mapping for rapid distinction of left versus right atrial arrhythmias

Entrainment mapping for rapid distinction of left versus right atrial arrhythmias

Mechanism of focal atrial tachycardias occurring after pulmonary veins isolation

Introduction: A proarrhythmic consequence of pulmonary vein isolation (PVI) to treat atrial fibrillation can be a persistent left atrial tachycardia (LAT). We previously described that focal LATs can occur; however it is unclear whether the mechanism of these focal arrhythmias is reentry, triggered activity, or abnormal automaticity. We performed detailed pacing and pharmacologic maneuvers to determine the mechanism of focal LATs occurring after PVI. Methods: PVI was performed by segmental ostial ablation guided by a circular mapping catheter (Lasso). Patients whose recurrent arrhythmia was a LAT that persisted for more then 8 weeks returned for mapping and ablation. Results: Of 15 pts with persistent LAT, three (age 66 14, all male) had focal LAT (cycle length 268 21 ms) that remained stable in response to pacing. Electroanatomic maps demonstrated focal areas of early activation at the septal aspect of the right lower (2 pts) or right upper (1 pt) PV. Adenosine caused transient AV block but no change in tachycardia cycle length (TCL). Entrainment from multiple LA sites (N 23) outside the PVs demonstrated long post-pacing-intervals (PPI) (mean PPI-TCL 73 27 ms, range 46-127 ms). Entrainment from multiple poles around the Lasso catheter had a wide range of PPIs (PPI-TCL 22 18 ms, range -3 to 50 ms), suggesting both isthmus sites and sites outside the circuit. Septal Lasso sites and not lateral sites had PPI TCL. A single beat resetting curve in 2 pts demonstrated a mixed flat-increasing curve, consistent with reentry. In one pt, burst atrial pacing terminated and reinitiated the same tachycardia. Recordings at the critical isthmus demonstrated mid diastolic potentials or a long fractionated signal suggesting slow conduction. Ablation at the site of mid diastolic electrograms or best PPI (PPI-TCL 2 6 ms) resulted in LAT termination. Conclusions: Focal left atrial tachycardias may occur after segmental PVI, particularly at the septal aspect of the right pulmonary veins. Detailed entrainment mapping and resetting confirm that the mechanism of the stable tachycardias we studied is reentry. RF application at the critical isthmus results in tachycardia termination.

Catheter Ablation of Recipient Right Ventricular Tachycardia after Heterotopic Heart Transplantation

Ventricular tachycardia after heart transplantation. A case is reported of ventricular tachycardia (VT) in a 62-year-old male after heterotopic heart transplantation, who occasionally had attacks of palpitation. Surface electrocardiogram suggested VT arising from the recipient heart. Intracardiac electrograms and entrainment mapping confirmed macroreentrant VT located in the recipient right ventricle. Radiofrequency ablation using an electroanatomical mapping system (CARTO, Biosense Webster, Diamond Bar, CA, USA) successfully eliminated VT.

Ablation of atrial tachycardia after surgery for congenital and acquired heart disease using an electroanatomic mapping system: Which circuits to expect in which substrate?

The purpose of this study was to compare atrial tachycardia circuits after a range of cardiac operations. Knowledge of circuits occurring in a given postsurgical substrate should help to ablate these challenging tachycardias and develop potential preventive strategies. We analyzed tachycardia circuits in 83 consecutive patients (60 males; median age 47 years, range 9-73) after atrial incisions undergoing ablation of atrial tachycardias. A combined strategy of electroanatomic (CARTO) and entrainment mapping was used. Fifty-two patients (63%) underwent operation for congenital and 31 (37%) for acquired heart disease. Patients were divided into subgroups based on the intervention performed in the atria: right lateral atriotomy (39 patients), left atrial (11) and superior transseptal (10) approach to the mitral valve, biatrial heart transplantation (8), Mustard (8) and Fontan (4) procedure, and other interventions (3). Most of the 119 tachycardias mapped were isthmus-dependent atrial flutter (66) and incisional tachycardia (30). Isthmus-dependent atrial flutter was the most frequent arrhythmia in all subgroups except for Fontan patients, in whom incisional tachycardia was most frequent. The distribution of tachycardia circuits did not differ significantly among groups. The observed circuits did not differ among the postsurgical substrates. Isthmus-dependent atrial flutter should be the first circuit considered in patients after atrial incisions.

Value of Entrainment Mapping in Determining the Isthmus‐Dependent Nature of Atrial Flutter in the Presence of Amiodarone

Entrainment mapping is a useful procedure for localizing macroreentrant tachycardia circuits. In patients with isthmus-dependent atrial flutter, entrainment mapping from the isthmus during tachycardia results in postpacing intervals (PPI) close to the tachycardia cycle length (TCL). However, the influence of antiarrhythmic drugs on the method's value is not clearly established. The aim of our study was to assess the value of entrainment mapping in the presence of amiodarone in patients undergoing radiofrequency ablation (RFA) of isthmus-dependent atrial flutter. The study consisted of 83 patients with isthmus-dependent atrial flutter: 52 were taking amiodarone at the time of RFA (group 1) and 31 were in a drug-free state (group 2). Entrainment mapping was performed from the cavotricuspid isthmus, and PPI minus TCL was determined. The two groups had similar baseline clinical characteristics. In all patients, RFA of the isthmus resulted in termination of tachycardia, confirming the isthmus-dependent nature of the flutter. TCL was significantly longer in group 1 than in group 2 (263 +/- 31 msec vs 238 +/- 27 msec, P < 0.0002). PPI minus TCL at the isthmus was significantly longer in group 1 than in group 2 (17 +/- 17 msec vs 8 +/- 4 msec, P < 0.01). More patients in group 1 had PPI-TCL>20 msec compared to group 2 (37% vs 10%, P = 0.01). Amiodarone significantly alters the entrainment mapping response from the isthmus. In this setting, long return cycles exceeding the TCL by >20 msec do not exclude isthmus-dependent atrial flutter.

Endocardial and epicardial radiofrequency ablation of ventricular tachycardia associated with dilated cardiomyopathy: The importance of low-voltage scars

ObjectivesThe purpose of this study was to evaluate the occurrence, locations, and relationship of ventricular tachycardia (VT) to low-voltage areas in dilated cardiomyopathy (DCM). BackgroundThe substrate causing monomorphic VT after infarction is characterized by regions of low-voltage (<1.5 mV) scar on electroanatomic maps. The substrate causing VT associated with DCM is less well defined. MethodsA total of 28 patients were studied with endocardial (26 patients) and epicardial (8 patients) electroanatomic mapping. The VT circuits were defined by entrainment or pace mapping. ResultsVentricular tachycardia was due to focal VT in 5, bundle-branch re-entry in 2, and myocardial re-entry in 22 patients (both focal and re-entry VTs in 1 patient). All patients with myocardial re-entry had endocardial (20 of 20 patients) and/or epicardial (7 of 7 patients mapped) scar. Most (63%) endocardial scars were adjacent to a valve annulus. Of the 19 VT circuit isthmuses identified, 12 were associated with an endocardial scar and 7 with an epicardial scar. All myocardial re-entrant VTs were abolished in 12 of 22 patients, and inducible VT was modified in 4 patients. During follow-up of 334 ± 280 days, 54% of patients with myocardial re-entry were free of VT despite frequent episodes before ablation. ConclusionsThe VTs in DCM are most commonly the result of myocardial re-entry associated with scar. Scars are often adjacent to a valve annulus, deep in the endocardium, and can be greater in extent on the epicardium than on the endocardium. The use of epicardial mapping and radiofrequency is likely to improve success.

Recognition of far-field electrograms during entrainment mapping of ventricular tachycardia

ObjectivesThe goal of this study was to assess entrainment for distinguishing far-field potentials (FFP) due to depolarization of tissue at a distance from the mapping catheter from the local potential (LP) due to depolarization of tissue at the catheter electrode during mapping of ventricular tachycardia (VT). BackgroundElectrograms with multiple peaks commonly complicate mapping and identification of catheter ablation targets in infarcts. MethodsRetrospective analysis of catheter mapping data from eight patients with prior infarction was performed to evaluate multipotential electrograms at sites where pacing entrained VT. Potentials that were visible and not altered during pacing were defined as FFP. Potentials obscured by the pacing stimulus were designated possible LPs. The criteria for FFP were then assessed in a second cohort of five patients. ResultsAt 32 of 39 (82%) sites with multiple potentials, entrainment identified one of the potentials as an FFP. Radiofrequency ablation, assessed at 15 sites, reduced the amplitude of LPs by 62%, without significant effect on FFP amplitude. At 56% of sites with multiple potentials, measuring the postpacing interval to an FFP would lead to erroneous classification of the site location relative to the reentry circuit. In prospective evaluation, double potentials were identified at 77 sites in infarcts; entrainment demonstrated an FFP at 66 (86%) sites. ConclusionsFar-field potentials are common during mapping in infarcts. Many can be distinguished from local potentials by entrainment, improving the accuracy of mapping.