Left Ventricular Endocardial Mapping Research Articles

Electrophysiological effects of adipose graft transposition procedure (AGTP) on the post-myocardial infarction scar: A multimodal characterization of arrhythmogenic substrate.

ObjectiveTo assess the arrhythmic safety profile of the adipose graft transposition procedure (AGTP) and its electrophysiological effects on post-myocardial infarction (MI) scar.BackgroundMyocardial repair is a promising treatment for patients with MI. The AGTP is a cardiac reparative therapy that reduces infarct size and improves cardiac function. The impact of AGTP on arrhythmogenesis has not been addressed.MethodsMI was induced in 20 swine. Contrast-enhanced magnetic resonance (ce-MRI), electrophysiological study (EPS), and left-ventricular endocardial high-density mapping were performed 15 days post-MI. Animals were randomized 1:1 to AGTP or sham-surgery group and monitored with ECG-Holter. Repeat EPS, endocardial mapping, and ce-MRI were performed 30 days post-intervention. Myocardial SERCA2, Connexin-43 (Cx43), Ryanodine receptor-2 (RyR2), and cardiac troponin-I (cTnI) gene and protein expression were evaluated.ResultsThe AGTP group showed a significant reduction of the total infarct scar, border zone and dense scar mass by ce-MRI (p = 0.04), and a decreased total scar and border zone area in bipolar voltage mapping (p < 0.001). AGTP treatment significantly reduced the area of very-slow conduction velocity (<0.2 m/s) (p = 0.002), the number of deceleration zones (p = 0.029), and the area of fractionated electrograms (p = 0.005). No differences were detected in number of induced or spontaneous ventricular arrhythmias at EPS and Holter-monitoring. SERCA2, Cx43, and RyR2 gene expression were decreased in the infarct core of AGTP-treated animals (p = 0.021, p = 0.018, p = 0.051, respectively).ConclusionAGTP is a safe reparative therapy in terms of arrhythmic risk and provides additional protective effect against adverse electrophysiological remodeling in ischemic heart disease.

Cardiac reparative therapy with adipose graft transposition procedure reduces slow conduction areas in a chronic myocardial infarction swine model

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Insituto de Salud Carlos III BACKGROUND Cardiac regenerative therapy is a promising treatment for patients with ischemic heart disease, but there are some concerns on the potential increased risk of arrhythmic events following specific cell therapies. Adipose graft transposition procedure (AGTP) is a cardiac reparative therapy consisting in transposing a vascularized adipose flap from the autologous pericardium and placing it over the epicardial scar area and has demonstrated to reduce infarct size and improve the left ventricular ejection fraction in preclinical and human studies. Specific electrophysiological properties of the scar, (i.e. slow conduction velocity (CV)) have been identified as key features of ventricular tachycardia (VT) isthmuses. PURPOSE To assess the effect of the AGTP on VT inducibility and the electrophysiological properties of the post-MI scar with ultra-high density (UHD) mapping. METHODS A left circumflex artery (first marginal branch) MI was induced in 10 Landrace X Large White pigs by delivering 1-3 coils. Two weeks post-MI, all subjects underwent baseline left ventricular endocardial UHD mapping during right ventricular pacing with 64-electrode basket mapping catheter, as well as electrophysiological study (EPS) to test for VT inducibility. Following the mapping, subjects were allocated 1:1 to AGTP or sham group. UHD mapping and EPS were repeated 30 days post-treatment (6 weeks after MI). Voltage and activation maps were analyzed off-line with self-customized Paraview-based software. Voltage cut-offs of 1.5 and 0.5mV (bipolar) defined normal tissue, border zone (BZ) and dense scar, respectively, and 6.7mV for unipolar. Conduction velocity (CV) was determined for every pair of contiguous points and areas of similar CV were quantified for every 0.2m/s steps (for up to 4 m/s). RESULTS There were no differences between groups with regard of dense scar, BZ an low unipolar voltage areas. The AGTP group had a significant reduction of the size of slow CV (&amp;lt;0.2 m/s) areas, compared to the sham group in whom it increased (-4.1 ± 1.7 vs. +2.4 ± 1.6 mm2, p = 0.028)(Figure). There were no differences in the size of other ranges of CV. EPS did not induce VT in any subject at baseline, and only in 1 of the sham group at the follow-up EPS. CONCLUSIONS Cardiac reparative therapy with AGTP of post-MI scar reduced the size of slow conduction areas and could provide a protective effect against arrhythmic events in ischemic heart disease. Abstract Figure.

Influence of Intramyocardial Adipose Tissue on the Accuracy of Endocardial Contact Mapping of the Chronic Myocardial Infarction Substrate.

Recent studies have demonstrated that intramyocardial adipose tissue (IMAT) may contribute to ventricular electrophysiological remodeling in patients with chronic myocardial infarction. Using an ovine model of myocardial infarction, we aimed to determine the influence of IMAT on scar tissue identification during endocardial contact mapping and optimal voltage-based mapping criteria for defining IMAT dense regions. In 7 sheep, left ventricular endocardial and transmural mapping was performed 84 weeks (15-111 weeks) post-myocardial infarction. Spearman rank correlation coefficient was used to assess the relationship between endocardial contact electrogram amplitude and histological composition of myocardium. Receiver operator characteristic curves were used to derive optimal electrogram thresholds for IMAT delineation during endocardial mapping and to describe the use of endocardial mapping for delineation of IMAT dense regions within scar. Endocardial electrogram amplitude correlated significantly with IMAT (unipolar r=-0.48±0.12, P<0.001; bipolar r=-0.45±0.22, P=0.04) but not collagen (unipolar r=-0.36±0.24, P=0.13; bipolar r=-0.43±0.31, P=0.16). IMAT dense regions of myocardium reliably identified using endocardial mapping with thresholds of <3.7 and <0.6 mV, respectively, for unipolar, bipolar, and combined modalities (single modality area under the curve=0.80, P<0.001; combined modality area under the curve=0.84, P<0.001). Unipolar mapping using optimal thresholding remained significantly reliable (area under the curve=0.76, P<0.001) during mapping of IMAT, confined to putative scar border zones (bipolar amplitude, 0.5-1.5 mV). These novel findings enhance our understanding of the confounding influence of IMAT on endocardial scar mapping. Combined bipolar and unipolar voltage mapping using optimal thresholds may be useful for delineating IMAT dense regions of myocardium, in postinfarct cardiomyopathy.

Development of Time- and Voltage-Domain Mapping (V-T-Mapping) to Localize Ventricular Tachycardia Channels During Sinus Rhythm.

In ventricular scar, impulse spread is slow because it traverses split and zigzag channels of surviving muscle. We aimed to evaluate scar electrograms to determine their local delay (activation time) and inequality in voltage splitting (entropy), and their relationship to channels. We reasoned that unlike innocuous channels, which are often short with multiple side branches, ventricular tachycardia (VT) supporting channels have very slow impulse spread and possess low entropy because of their longer protected length and relative lack of side-branching. Patients with ischemic cardiomyopathy and multiple VT were studied. In initial mapping stage (16 patients and 58 VTs), left ventricular endocardial mapping was performed in sinus rhythm. Detailed pace mapping was used to identify VT channels and confirmed, when feasible, by entrainment. Scar electrograms were analyzed in time and voltage domains to determine mean activation time, dispersion in activation time, and entropy. Predictive performances of these properties to detect VT channels were tested. In the application stage (7 patients and 20 VTs), these properties were prospectively tested to guide catheter ablation. A mean number of 763±203 sampling points were taken. From 1770 pace maps, 47 channels corresponded to VTs. A combination of scar electrograms with the latest mean activation time and minimum entropy, in a high activation dispersion region, accurately recognized regions containing VT channels (κ=0.89, sensitivity=86%, specificity=100%, positive predictive value=93%, and negative predictive value=100%). Finally, focused ablation within 5-mm rim of the prospective channel regions eliminated 18 of 20 inducible VTs. Activation time and entropy mapping in the scar accurately identify VT channels during sinus rhythm. The method integrates principles of reentry formation to recognize VT channels without pace mapping or mapping during VT.

Evaluation of a novel high-resolution mapping system for catheter ablation of ventricular arrhythmias

The mapping of ventricular arrhythmias in humans using a minibasket 64-electrode catheter paired with a novel automatic mapping system (Rhythmia) has not been evaluated. The purpose of this study was to evaluate the safety and efficacy of mapping ventricular arrhythmias and clinical outcomes after ablation using this system. Electroanatomic maps for ventricular arrhythmias were obtained during 20 consecutive procedures in 19 patients (12 with ventricular tachycardia [VT] and 2 with ventricular ectopy [VE]). High-density maps were acquired using automatic beat acceptance and automatic system annotation of electrograms. Forty-seven electroanatomic maps (including 3 right ventricular and 9 epicardial maps) were obtained. Left ventricular endocardial mapping by transseptal (n = 13) and/or transaortic (n = 11) access was safe with no complications related to the minibasket catheter. VT substrate maps (n = 14; median 10,184 points) consistently demonstrated late potentials with high resolution. VT activation maps (n = 25; median 6401 points) obtained by automatic annotation included 7 complete maps (covering ≥90% of the tachycardia cycle length) in 5 patients in whom the entire VT circuit was accurately visualized. VE timing maps (n = 8) successfully localized the origin of VEs in all, with all accepted beats consistent with clinical VEs. Over a median follow-up of 10 months, no arrhythmia recurrence was noted in 75% after VT ablation and 86% after VE ablation. In this first human experience for ventricular arrhythmias using this system, ultra-high-density maps were created rapidly and safely, with a reliable automatic annotation of VT and consistent recording of abnormal electrograms. Medium-term outcomes after ablation were encouraging. Further larger studies are needed to validate these findings.

49-05: Defining arrhythmogenic ventricular scar using time- and voltage-domain mapping (V-T-mapping): a new approach to ventricular tachycardia channel localization during sinus rhythm

Aims: In ventricular scar, the impulse spread is slow as it traverses multiple split and zigzag channels of surviving muscle. We aimed to evaluate electrograms in the scar to determine their local delay in relation to the onset of ventricular activation (activation time) and inequality in voltage splitting (entropy), and their relationship to channels. We reasoned that unlike innocuous bystander channels, which are often short with multiple side branches, ventricular tachycardia (VT) supporting channels have very slow impulse spread and possess low entropy due to their longer protected length and relative lack of side branching. Methods: Patients with ischemic cardiomyopathy and multiple inducible VT were studied. In the initial mapping stage (16 patients, 58 VTs), left ventricular endocardial mapping was performed in sinus rhythm. Detailed pace mapping was used to identify VT channels, and confirmed, when feasible, by entrainment. The scar electrograms were analyzed in time- and voltage-domains to determine mean activation time, dispersion in activation time and entropy. The predictive performances of these properties to detect VT channels were tested. In the application stage (7 patients, 20 VTs), these properties were prospectively tested to guide catheter ablation. Results: A mean of 763 ± 203 sampling points per-patient were taken, 451 ± 145 points in dense scar. From 1770 pace maps, 174 channels were identified, and 47 corresponded to inducible VTs. A combination of scar electrograms with the latest mean activation time and minimum entropy, in a high activation dispersion region, accurately recognized regions containing VT channels (kappa = 0.89, sensitivity = 86%, specificity = 100%, positive predictive value = 93%, and negative predictive value = 100%). Finally, focused ablation within the prospective channel regions eliminated 18/20 inducible VTs. Conclusion: Activation time and entropy mapping in the scar accurately identifies VT channels during sinus rhythm. This can expedite recognition of VT channels without pace mapping or mapping during VT and minimize extensive ablation.

Transcoronary ethanol ablation for incessant ventricular tachycardia: a salvage technique when faced with left ventricular thrombus.

A 77-year-old man with a history of bypass surgery following an anterior myocardial infarction was admitted with a VT storm (Fig. 1A). Coronary angiography revealed occlusion of the left anterior descending (LAD) artery with a patent vein graft to the distal vessel, backfilling the mid-anterior septum. Left ventriculography demonstrated poor left ventricular (LV) systolic function and a calcified apical aneurysm with thrombus (confirmed by contrast echocardiography). LV endocardial mapping was therefore abandoned. Epicardial mapping identified no target. After further shocks and failed medical therapy, endocardial mapping revealed an exit site at the right ventricular septum adjacent to a scar zone and the thrombus within the LV aneurysm (Fig. 2A). The red asterisk marks the site of the best pacemap (Fig. 1B) where the tip of the catheter is on the right side of the interventricular septum. Angiography was performed with the LAD graft (white arrowhead) and the distal LAD (black arrowhead) patent (Fig. 2B). The shaded area denotes the superimposed territory of a mid-LAD septal branch on angiography (Fig. 2A and ​andB).B). An interventional wire was retrogradely advanced into the septal branch of the LAD (black asterisk) that subtended the territory of VT origin (shaded region). A balloon occluded (black arrowhead) the retrograde limb of the LAD with contrast injection confirming the position (white dotted line) (Panel C, Fig. 2). After injection of a single 2mL aliquot of ethanol (dehydrated alcohol, Martindale) over 3 min, final angiographic assessment confirmed occlusion of the retrograde limb of the LAD (Panel D, Fig. 2). Clinical VT was rendered non-inducible. Follow-up at 15 months confirmed no further VT. Transcoronary ethanol ablation represents a viable salvage technique when faced with LV thrombus. Fig. 1 Twelve-lead ECG of ventricular tachycardia (Panel A) and at the site of pacemap match (Panel B) Fig. 2 Fluoroscopic images of best pacemap (red asterisk) at VT exit site on RV side of interventricular septum (Panel A); patent LAD graft (white arrowhead) and distal LAD (black arrowhead) with interventional wire retrogradely inserted into septal branch of ...

High density mapping of ventricular scar- a comparison of ventricular tachycardia supporting channels with channels that do not support VT

Introduction: Surviving myocytes within scar may form channels that become critical component of a ventricular tachycardia (VT) reentrant circuit. There is little data on the physiognomies of channels that comprise VT circuits and those which are non-VT channels. Methods: Twenty-two patients with ischemic cardiomyopathy (LVEF 32±8%) and multiple inducible VT (n=73) were evaluated. Left ventricular endocardial mapping was done with high-density PentaRay™ catheter connected to the Ensite Velocity™ system. Pacing was done from bipoles showing low voltage (≤1.5V) with late potentials and/ or fractionation. A channel was defined as series of matching pace-maps with stimulus (S) to QRS time ≥40ms. Sites were determined to be part of VT channel if there were matching pace-maps to the induced VT morphology. This was confirmed with entrainment mapping when possible. The anatomical and electrophysiologic properties of these channels were evaluated. Results: A mean of 760±205 voltage points were taken, with 431±137 within dense scar (≤0.5mV). Overall 2507 pace maps (114±62 per patient) were performed. Of the 238 channels identified, 57 channels corresponded to an inducible VT. Channels that were part of a VT circuit were of greater length (mean 52±31 vs 36±26mm), had longer S-QRS (73±60 vs 62±25ms), longer conduction time (108±90 vs 35±25ms) and slower conduction velocity (CV) (0.7±0.5 vs 1.3±1.1m/s) than non-VT channels (p 80ms was 5.3 times higher in a VT channel relative to an unshared non-VT channel (95% CI 2.6 to 10.6, p<0.01). VT channels were more commonly located within dense scar (95% vs 81% non-VT channels, p=0.04). Of all the fractionated (mean 130±105) late (mean 10±5) and very late (mean 4±3) potentials located in scar, only 22%, 30% and 35% respectively were recorded within VT channels. Compared to elsewhere within the scar, in the region of VT channels fractionated potentials were longer in duration (104±26ms vs 95±26ms, p<0.001), and very late potentials were poorly coupled (309±159ms vs 240±119ms, p=0.04) to the intrinsic QRS. Following ablation targeting channels, the clinical VT was abolished in 95% of patients, and no VT could be induced in 64%. Conclusion: High density mapping shows substantial differences among channels in ventricular scar. Channels supporting VT are more commonly located in dense scar, longer than non-VT channels, and have slower CV. Only a minority of scar related potentials participate in the VT supporting channels. These findings have pertinent implications for substrate based ablation strategies.

Standard model - a deductive strategy from multiple deflection mapping in sinus rhythm for field localization of ventricular tachycardia supporting channels in ischemic cardiomyopathy

Purpose: Current substrate based ablation strategies for ventricular tachycardia (VT) advocate targeting all excitable abnormal ventricular electrograms within the scar. However only a fraction of these electrograms populate the VT supporting channels. We hypothesized that the electrogram properties in the standard model can identify information content specific to the location of VT supporting channels and lead intent and focused substrate ablation. Methods: Study was conducted in three stages. Firstly, patients with ischemic cardiomyopathy (ICM; n=16) and multiple inducible VT (n=58) undergoing catheter ablation were evaluated. Left ventricular endocardial mapping was performed with high-density PentaRay™ catheter and NavX™ system. VT channel was defined as series of matching pacemaps with stimulus to QRS interval ≥40ms. Entrainment mapping confirmed pace map findings whenever feasible. In the blinded second stage, the standard model was applied to all SR maps. The timing of local activation was determined as mean of activation times of all electrogram peak deflections, and dispersion was quantified by their standard deviation. Shannon entropy (ShEn) was calculated as an index of electrogram amplitude distribution. A VT channel region was identified in the model by assemblage of node of latest mean activation and proximate low ShEn in a zone of high dispersion with adjoining interface of low dispersion. Channel locations built on this model were compared with VT channels developed in the first stage. Finally, for the test of concept, performance of this model was examined prospectively in 3 additional ICM patients to lead catheter ablation. Results: Mean 763±203 sampling points were taken, 451±145 points in dense scar (≤0.5mV). From 1770 pacemaps, 174 channels were identified, 47 corresponded to inducible VTs. Of all the fractionated (mean 114±85), late (mean10±5) and very-late (mean 3±3) potentials, only 18%, 23% and 35%, respectively were recorded in the VT channels. Channels built on the model had high agreement with VT channels [κ =0.89, 95% CI 0.84 to 0.94] with high sensitivity (86%, 95% CI 76 to 93), specificity (100%, 95% CI 99.8 to 100), positive (93%, 95% CI 84 to 98) and negative (100%, 95% CI 99 to 100) predictive value for localizing an inducible VT channel. Finally, focused ablation in 3 patients within the postulated channel regions eliminated 6/8 inducible VTs. Conclusion: The standard model can hasten identification of VT channels compared to other frequently employed electrogram characteristics. This will reduce the difficulties in the current substrate based ablation strategies.

New Unipolar Electrogram Criteria to Identify Irreversibility of Nonischemic Left Ventricular Cardiomyopathy

This study sought to assess the value of left ventricular (LV) endocardial unipolar electroanatomical mapping (EAM) in identifying irreversibility of LV systolic dysfunction in patients with left ventricular nonischemic cardiomyopathy (LVCM). Identifying irreversibility of LVCM would be helpful but cannot be reliably accomplished by bipolar EAM or cardiac magnetic resonance identification of macroscopic scar. Detailed endocardial LV EAM was performed in 3 groups: 1) 24 patients with irreversible LVCM (I-LVCM) but with no or minimal macroscopic scar (<15% LV surface) evidenced on bipolar voltage EAM and/or cardiac magnetic resonance; 2) 14 patients with reversible ventricular premature depolarization-mediated LVCM (R-LVCM); and 3) 17 patients with structurally normal hearts. LV endocardial unipolar electrogram amplitude and area of unipolar amplitude abnormality were defined after excluding macroscopic scar. Unipolar amplitude differed in the 3 groups: median of 7.6 (interquartile range [IQR]: 5.5 to 9.7) mV in I-LVCM group, 13.2 (IQR: 10.4 to 16.2) mV in R-LVCM group, and 16.3 (IQR: 13.6 to 19.8) mV in structurally normal hearts group (p < 0.001). Areas of unipolar abnormality represented a large proportion of total LV surface in I-LVCM, 64.7% (IQR: 47.5% to 75.9%) compared with R-LVCM, 5.2% (IQR: 0.0% to 19.1%) and structurally normal hearts, 0.1% (IQR: 0.0% to 0.9%), groups (p < 0.001). A unipolar abnormality area cutoff of 32% of total LV surface was 96% sensitive and 100% specific in identifying irreversible cardiomyopathy among patients with LV dysfunction (I-LVCM and R-LVCM), p < 0.001. Detailed unipolar voltage mapping can identify irreversible myocardial dysfunction consistent with fibrosis, even in the absence of bipolar EAM or cardiac magnetic resonance abnormalities, and may serve as valuable prognostic tool in patients presenting with LVCM to facilitate clinical decision making.

Relationship of bipolar and unipolar electrogram voltage to scar transmurality and composition derived by magnetic resonance imaging in patients with nonischemic cardiomyopathy undergoing VT ablation

Bipolar voltage mapping has a role in defining endocardial-based scar in postinfarct patients undergoing ventricular tachycardia catheter ablation. The utility of bipolar and unipolar voltages in characterizing scar has not been evaluated in patients with nonischemic cardiomyopathy. To relate left ventricular (LV) endocardial bipolar and unipolar voltages in these patients to scar transmurality (endocardial vs nonendocardial) and composition (homogeneous core vs heterogeneous gray). Ten consecutive cardiomyopathy patients undergoing endocardial LV tachycardia ablation were included (age 48 ± 14 years; left ventricular ejection fraction 43% ± 15%). Preablation late gadolinium-enhanced magnetic resonance imaging was used to quantify core and gray scar by using signal-intensity thresholding. Electroanatomic LV endocardial mapping provided bipolar and unipolar voltages. Electroanatomic maps and late gadolinium-enhanced magnetic resonance imaging were rigidly registered in order to relate voltage to scar (registration error 3.6 ± 2.9 mm). Bipolar voltage was lower in endocardial core than in no scar (P <.001). Unipolar voltage was lower in endocardial core and nonendocardial core than in no scar (P <.001). Endocardial and nonendocardial gray scar had an effect similar to that of core in reducing bipolar and unipolar voltages (P <.001). The mass of healthy myocardium and endocardial core scar independently predicted bipolar and unipolar voltages using general estimating equation modeling. With receiver operating characteristic curve analysis, bipolar voltage >1.9 mV and unipolar voltage <6.7 mV had a high negative predictive value (91%) for detecting nonendocardial scar from either endocardial scar or no scar. In patients with nonischemic cardiomyopathy, LV endocardial bipolar voltage is dependent on endocardial core and gray scar, while the unipolar voltage is influenced by core and gray scar across the LV wall as defined by late gadolinium-enhanced magnetic resonance imaging.

The main trunk of the left bundle branch is not part of the re-entry circuit of verapamil-sensitive idiopathic left ventricular tachycardia

We report the case of a 19-year-old man with verapamil-sensitive idiopathic left ventricular tachycardia (ILVT), who had paroxysmal palpitations for 3 years. Programmed right atrial and ventricular stimulation easily induced ventricular tachycardia (VT) with QRS duration of 125ms, right bundle branch block pattern, and right inferior axis, which are characteristics of ILVT. Left ventricular endocardial mapping accidentally produced a complete left bundle branch block and provoked prolongation of the QRS duration of VT, which was 143ms. However, no changes occurred in the cycle length, inducibility, or maintenance of VT. The VT was eliminated successfully by catheter ablation at the pre-Purkinje potential (PP) recording site. These findings suggest that the main trunk of the left bundle branch is not a critical component of the re-entry circuit of ILVT.

Assessing Epicardial Substrate Using Intracardiac Echocardiography During VT Ablation

Intracardiac echocardiography (ICE) has played a limited role in defining the substrate for ventricular tachycardia (VT). The purpose of this study was to assess whether ICE could identify abnormal epicardial substrate in patients with nonischemic cardiomyopathy (NICM) and VT. We studied 18 patients with NICM and recurrent VT who had abnormal echogenicity identified on ICE imaging. Detailed left ventricular (LV) endocardial and epicardial electroanatomic mapping was performed in all patients. Low-voltage areas (<1.0 mV) in the epicardium were analyzed. ICE imaging in the NICM group was compared to a control group of 30 patients with structurally normal hearts who underwent ICE imaging for other ablation procedures. In 18 patients (age, 53±13 years; 17 men) with NICM (ejection fraction, 37±13%), increased echogenicity was identified in the lateral LV by ICE imaging. LV endocardial electroanatomic mapping identified normal voltage in 9 patients and at least 1 confluent low-voltage area (6.6 cm(2); minimum-maximum, 2.1-31.7 cm(2)) in 9 patients (5 posterolateral LV, 4 perivalvular LV). Detailed epicardial mapping revealed areas of low voltage (39 cm(2); minimum-maximum, 18.5-96.3 cm(2)) and abnormal, fractionated electrograms in all 18 patients (15 posterolateral LV, 3 lateral LV). In all patients, the epicardial scar identified by electroanatomic mapping correlated with the echogenic area identified on ICE imaging. ICE imaging identified no areas of increased echogenicity in the control group. ICE imaging identified increased echogenicity in the lateral wall of the LV that correlated to abnormal epicardial substrate. These findings suggest that ICE imaging may be useful to identify epicardial substrate in NICM.

Abstract 4089: Unique Epicardial Substrate in Non-Ischemic CM: Echo Signature, Electrogram Correlates and Outcome with Substrate Based Ablation

We present a unique series of patients (pts) with non-ischemic cardiomyopathy (NICM) and unmappable ventricular tachycardia (VT) who demonstrated predominantly normal left ventricular (LV) endocardial (ENDO) voltage and abnormal epicardial (EPI) substrate defined by intracardiac echo (ICE) and fractionated electrograms (EGMS). This substrate served as an appropriate ablation target for VT. All patients underwent ICE imaging and detailed ENDO and EPI voltage mapping to further characterize the substrate and define the EGM correlates. 5 pts with NICM had increased echogenicity in the lateral epicardium by ICE imaging. Detailed LV ENDO mapping (199 ± 94.5 points) identified no voltage abnormalities in 4 pts. In one pt, a 16.2cm2 low voltage area in the LV ENDO was present and adjacent to the EPI abnormality. In all pts, detailed EPI mapping (477 ± 158 points) revealed a distinct area (20.6 ± 3.6 cm2) of low voltage (&lt;1.0mV) that correlated with the echogenic area. These areas displayed low amplitude EGMS that were wide (&gt;80msec), split, and late (beyond QRS). (Figure 1 ). After excluding coronary branch vessels and the course of the phrenic nerve, all pts underwent substrate based ablation based on pace-mapping and targeting of abnormal EGMS to eliminate the targeted VT. No VT has recurred during mean follow-up of 20mo (range 1–30 mo). Unique EPI substrate in NICM, defined by echo imaging and confirmed by EGM correlates, can be successfully targeted for RF ablation to provide effective VT control.

Combined epicardial and endocardial electroanatomic mapping in a porcine model of healed myocardial infarction.

Substrate mapping of post-myocardial infarction ventricular tachycardia involves electroanatomic delineation of scarred tissue on the basis of electrogram characteristics during sinus rhythm. A percutaneous transthoracic technique was recently described that allows catheter mapping of the epicardial surface of the heart. This study sought to determine whether the epicardial extent of a myocardial infarct could be defined during sinus rhythm. In a porcine model of healed anterior wall myocardial infarction (n=13 animals), detailed in vivo left ventricular endocardial and ventricular epicardial electroanatomic mapping was performed. Catheter access to the pericardial space was achieved by subxyphoid puncture under fluoroscopic guidance. Bipolar electrogram amplitude and duration characteristics of normal tissue were established on the basis of in vivo epicardial mapping data in 8 additional normal animals. With the use of these criteria, radiofrequency lesions (4 to 11 per animal) were placed along the endocardial and epicardial scar borders as defined by the electroanatomic map. The area of epicardial scar defined by abnormal bipolar voltage correlated well with the dimensions measured on pathological examination. The size and location also correlated well with the scar dimensions defined by electrogram duration criteria. Late potentials were noted in the border zones of both surfaces of the scar. During pathological examination, the radiofrequency lesions were situated at the borders of the epicardial scar. A 3-dimensional construct of the infarcted myocardium can be rendered by combined epicardial and endocardial electroanatomic mapping. This experimental protocol is propaedeutic to future clinical studies incorporating endocardial and epicardial substrate mapping into catheter ablation strategies to treat post-myocardial infarction ventricular tachycardia.

The role of Purkinje and pre-Purkinje potentials in the reentrant circuit of verapamil-sensitive idiopathic LV tachycardia.

Although the mechanism of verapamil-sensitive idiopathic left ventricular tachycardia (ILVT) is usually reentry, the actual reentrant circuit is not clearly understood. This study examined the relationship between the Purkinje potential (PP) and a dull potential preceding PP (pre-PP) during ILVT to elucidate the roles of these potentials in the reentrant circuit of ILVT. Electrophysiological studies and radiofrequency catheter ablation were performed in ten patients (7 men, 3 women, mean age 29 years) who had an ILVT with a right bundle branch block configuration and left-axis deviation. Left ventricular endocardial mapping using an octapolar catheter and entrainment and resetting studies during VT was performed by pacing from the right ventricular outflow tract (RVOT) and each site of the left ventricular mapping catheter. PP and pre-PP were recorded simultaneously during VT in all patients. The earliest PP during VT was recorded at the inferoposterior septum, and PP was activated bidirectionally toward the proximal (basal) and distal (apical) sites along the left posterior fascicle. In contrast, pre-PP was recorded at sites slightly proximal to the earliest PP recording site, and was activated toward the earliest PP site. Pacing from RVOT confirmed manifest entrainment, and the stimulus to pre-PP interval was prolonged with a shorter pacing cycle length. Concealed entrainment was demonstrated by capture of the PPs of the left ventricular mapping catheter in six patients, and the postpacing interval at each PP site was equal to the tachycardia cycle length. The pre-PP was orthodromically activated from the proximal to the distal site during pacing. More rapid pacing also produced delay in activation from PP to pre-PP, indicating slow conduction in ILVT. Catheter ablation was performed at the pre-PP recording site during VT, and was successful in all patients. The reentrant circuit of ILVT could be constructed based on the pre-PP, PP, and slow conduction between the PP and pre-PP. Catheter ablation of ILVT was successful at the pre-PP recording site.

Biosense Left Ventricular Electromechanical Mapping

Biosense is a new technology for left ventricular endocardial mapping and catheter-based intramyocardial therapeutics. The system reconstructs electromechanical maps of the left ventricle without using x-ray fluoroscopy. The 3-dimensional electromechanical maps generated by the system are utilized to precisely identify viable target zones based on integration of endocardial electrical and mechanical signals for online diagnosis of myocardial viability in the catheterization laboratory. It may be used for guidance of radiofrequency ablation and may potentially be used to apply intramyocardial therapy by its integration with a laser fiber for transmyocardial laser revascularization procedures.

Significance of late diastolic potential preceding Purkinje potential in verapamil-sensitive idiopathic left ventricular tachycardia.

Verapamil-sensitive idiopathic left ventricular tachycardia (VT) is due to reentry with an excitable gap. A late diastolic potential (LDP) is recorded during endocardial mapping of this VT, but its relation to the reentry circuit and significance in radiofrequency (RF) ablation remain to be elucidated. Sixteen consecutive patients with this specific VT were studied (12 men and 4 women; mean age, 32 years). In all patients, sustained VT was induced and during left ventricular endocardial mapping, LDP preceding Purkinje potential (PP) was recorded at the basal (11 patients), middle (3 patients), or apical septum (2 patients). The area with LDP recording was confined to a small region (0.5 to 1.0 cm2) in each patient and was included in the area where PP was recorded (2 to 3 cm2). The relative activation times of LDP, PP, and local ventricular potential (V) at the LDP recording site to the onset of QRS complex were -50.4+/-18.9, -15.2+/-9.6, and 3.0+/-13.3 ms, respectively. The earliest ventricular activation site during VT was identified at the posteroapical septum and was more apical in the septum than the region with LDP in every patient. In 9 patients, VT entrainment was done by pacing from the right ventricular outflow tract while recording LDP. During entrainment, LDP was orthodromically captured, and as the pacing rate was increased, the LDP-to-PP interval was prolonged, whereas stimulus-to-LDP and PP-to-V interval were constant. In 3 patients, the pressure applied to the catheter tip at the LDP region resulted in conduction block between LDP and PP and in VT termination. RF energy application at the LDP recording site successfully eliminated VT. LDP was suggested to represent the excitation at the entrance to the specialized area with a conduction delay in response to the increase in the rate within the critical slow conduction zone participating in the reentry circuit of this VT. LDP can be a useful marker for successful RF ablation for this VT.

Verapamil-sensitive left anterior fascicular ventricular tachycardia: results of radiofrequency ablation in six patients.

Verapamil-sensitive left ventricular tachycardia (VT) with a right bundle branch block (RBBB) configuration and left-axis deviation has been demonstrated to arise from the left posterior fascicle, and can be cured by catheter ablation guided by Purkinje potentials. Verapamil-sensitive VT with an RBBB configuration and right-axis deviation is rare, and may originate in the left anterior fascicle. Six patients (five men and one woman, mean age 54+/-15 years) with a history of sustained VT with an RBBB configuration and right-axis deviation underwent electrophysiologic study and radiofrequency (RF) ablation. VT was slowed and terminated by intravenous administration of verapamil in all six patients. Left ventricular endocardial mapping during VT identified the earliest ventricular activation in the anterolateral wall of the left ventricle in all patients. RF current delivered to this site suppressed the VT in three patients (ablation at the VT exit). The fused Purkinje potential was recorded at that site, and preceded the QRS complex by 35, 30, and 20 msec, with pace mapping showing an optimal match between the paced rhythm and the clinical VT. In the remaining three patients, RF catheter ablation at the site of the earliest ventricular activation was unsuccessful. In these three patients, Purkinje potential was recorded in the diastolic phase during VT at the mid-anterior left ventricular septum. The Purkinje potential preceded the QRS during VT by 66, 56, and 63 msec, and catheter ablation at these sites was successful (ablation at the zone of slow conduction). During 19 to 46 months of follow-up (mean 32+/-9 months), one patient in the group of ablation at the VT exit had sustained VT with a left bundle branch block configuration and an inferior axis, and one patient in the group of ablation at the zone of slow conduction experienced typical idiopathic VT with an RBBB configuration and left-axis deviation. Verapamil-sensitive VT with an RBBB configuration and right-axis deviation originates close to the anterior fascicle. RF catheter ablation can be performed successfully from the VT exit site or the zone of slow conduction where the Purkinje potential was recorded in the diastolic phase.

Mapping of septal ventricular tachycardia: Clinical and experimental correlations

In patients with chronic myocardial infarction, ventricular tachycardia originating in the interventricular septum may account for a significant number of arrhythmia recurrences after direct ablative operations. We used total computer-assisted cardiac mapping (epicardial sock, left and right ventricular endocardial balloon electrode arrays) to assess whether tachycardia originating in deep or right-sided layers of the interventricular septum is associated with a specific pattern of epicardial activation sequence. We performed these studies during operations in 18 patients and during experiments in 12 dogs in which a septal myocardial infarction was produced by ligating the anterior septal coronary artery. Intraseptal needle electrodes were plunged into the septum of all animal preparations to generate pace-mapping data and to obtain intraseptal recordings (six preparations) during reentrant ventricular tachycardia induced by programmed stimulation. In addition, pace-mapping data of infarcted canine heart preparations were compared with those of nine healthy heart preparations. In the clinical study, 31 ventricular tachycardias with a septal site of origin were analyzed. Twenty tachycardias displayed an epicardial breakthrough in the area of the interventricular groove, whereas 11 had an epicardial breakthrough in the right ventricular free wall. Biventricular endocardial mapping revealed that left septal endocardial activation preceded right septal activation in the former and that right septal activation occurred earlier in the latter. In the experimental study, 14 ventricular tachycardias (cycle length 146 ± 34 msec) were induced by programmed stimulation in 11 infarcted heart preparations. Eight tachycardias displaying an epicardial breakthrough on the right ventricle were found to originate in the right ventricular septal subendocardial layers, whereas six tachycardias in which the epicardial breakthrough occurred on the anterior interventricular groove originated in the left ventricular septal subendocardial layers. The epicardial breakthrough preceded the left ventricular endocardial breakthrough in six tachycardias (85.7%) originating in intermediate or right ventricular septal layers, but in only one of five tachycardias originating in the left ventricular septal layers. In the pace-mapping study, the epicardial breakthrough shifted progressively from the right ventricular free wall toward the interventricular groove area in response to pacing from the right, intermediate, and left ventricular thirds of the basal septum. This relationship was similar for infarcted and noninfarcted hearts, although transseptal conduction time was prolonged in infarcted hearts (45 ± 10 msec vs 33 ± 7 msec, p < 0.01). Therefore the information integrated from the localization of the epicardial breakthrough and the relative timing between the epicardial and the left ventricular endocardial breakthroughs can be used to estimate the depth of the site of origin of septal ventricular tachycardias. This study confirms that a three-dimensional view of the substratum of ventricular tachycardia can be derived from simultaneous epicardial and left ventricular endocardial mapping and can provide a superior basis for therapeutic interventions. (J T HORAC C ARDIOVASC S URG 1996;112:914-25)