Cory M. Tschabrunn

High-Resolution Mapping of Scar-Related Atrial Arrhythmias Using Smaller Electrodes with Closer Interelectrode Spacing

Background—The resolution of mapping is influenced by electrode size and interelectrode spacing. Smaller electrodes with closer interelectrode spacing may improve mapping resolution, particularly in scar. The aims of this study were to establish normal electrogram criteria in the atria for both 3.5-mm electrode tip linear catheters (Thermocool) and 1-mm multielectrode-mapping catheters (Pentaray) and to compare their mapping resolution in scar-related atrial arrhythmias. Methods and Results—Normal voltage amplitude cutoffs for both catheters were validated in 10 patients with structurally normal atria. In 20 additional patients with scar-related atrial arrhythmias, similar sequential mapping with both catheters was performed. Normal bipolar voltage amplitude was similar between 3.5- and 1-mm electrode catheters with a fifth percentile of 0.48 and 0.52 mV, respectively (P=0.65). In patients with scar-related atrial arrhythmias, the total area of bipolar voltage <0.5 mV measured using 1-mm electrode catheters was smaller than that measured using 3.5-mm catheter (14.7 versus 20.4 cm2; P=0.02). The mean bipolar voltage amplitude in this area of low voltage was significantly higher with 1-mm electrode catheters (0.28 and 0.17 mV; P=0.01). Importantly, 54.4% of all low voltage data points recorded with 1-mm electrode catheter had distinct electrograms that allowed annotation of local activation time compared with only 21.4% with 3.5-mm electrode tip catheters (P=0.01). Overdrive pacing with capture of the tachycardia from within the area of low voltage was more frequent with 1-mm electrode catheters (66.7 versus 33.4; P=0.01). Conclusions—Mapping with small closely spaced electrode catheters can improve mapping resolution within areas of low voltage.

Ablation of ventricular arrhythmias arising near the anterior epicardial veins from the left sinus of Valsalva region: ECG features, anatomic distance, and outcome.

BACKGROUND Left ventricular outflow tract tachycardia/premature depolarizations (VT/VPDs) arising near the anterior epicardial veins may be difficult to eliminate through the coronary venous system. OBJECTIVE To describe the characteristics of an alternative successful ablation strategy targeting the left sinus of Valsalva (LSV) and/or the adjacent left ventricular (LV) endocardium. METHODS Of 276 patients undergoing mapping/ablation for outflow tract VT/VPDs, 16 consecutive patients (8 men; mean age 52 ± 17 years) had an ablation attempt from the LSV and/or the adjacent LV endocardium for VT/VPDs mapped marginally closer to the distal great cardiac vein (GCV) or anterior interventricular vein (AIV). RESULTS Successful ablation was achieved in 9 of the 16 patients (56%) targeting the LSV (5 patients), adjacent LV endocardium (2 patients), or both (2 patients). The R-wave amplitude ratio in lead III/II and the Q-wave amplitude ratio in aVL/aVR were smaller in the successful group (1.05 ± 0.13 vs 1.34 ± 0.37 and 1.24 ± 0.42 vs 2.15 ± 1.05, respectively; P = .043 for both). The anatomical distance from the earliest GCV/AIV site to the closest point in the LSV region was shorter for the successful group (11.0 ± 6.5 mm vs 20.4 ± 12.1 mm; P = .048). A Q-wave ratio of <1.45 in aVL/aVR and an anatomical distance of <13.5 mm had sensitivity and specificity of 89%, 75% and 78%, 64%, respectively, for the identification of successful ablation. CONCLUSIONS VT/VPDs originating near the GCV/AIV can be ablated from the LSV/adjacent LV endocardium. A Q-wave ratio of <1.45 in aVL/aVR and a close anatomical distance of <13.5 mm help identify appropriate candidates.

Assessing Epicardial Substrate Using Intracardiac Echocardiography During VT Ablation

Background— 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. Methods and Results— 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 cm2; minimum-maximum, 2.1–31.7 cm2) in 9 patients (5 posterolateral LV, 4 perivalvular LV). Detailed epicardial mapping revealed areas of low voltage (39 cm2; minimum-maximum, 18.5–96.3 cm2) 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. Conclusions— 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.

Catheter ablation of ventricular fibrillation: Importance of left ventricular outflow tract and papillary muscle triggers

BACKGROUND Monomorphic ventricular premature depolarizations (VPDs) have been found to initiate ventricular fibrillation (VF) or polymorphic ventricular tachycardia (PMVT) in patients with and without structural heart disease. OBJECTIVE The purpose of this study was to describe and characterize sites of origin of VPDs triggering VF and PMVT. METHODS The distribution of mapping-confirmed VPDs, electrophysiology laboratory findings, and results of radiofrequency catheter ablation were analyzed. RESULTS Among 1132 consecutive patients who underwent ablation for ventricular arrhythmias, 30 patients (2.7%) with documented VF/PMVT initiation were identified. In 21 patients, VF/PMVT occurred in the setting of cardiomyopathy; in 9 patients, VF/PMVT was idiopathic. The origin of VPD trigger was from the Purkinje network in 9, papillary muscles in 8, left ventricular outflow tract in 9, and other low-voltage areas unrelated to Purkinje activity in 4. Each distinct anatomic area of origin was associated with VF/PMVT triggers in patients with and without heart disease. Acute VPD elimination was achieved in 26 patients (87%), with a decrease in VPDs in another 3 patients (97%). During median follow-up of 418 days (interquartile range [IQR] 144-866), 5 patients developed a VF/PMVT recurrence after a median of 34 days (IQR 1-259). Rare recurrence was noted in patients with and without structural disease and from each distinct anatomic origin. The total burden of VF/PMVT episodes/shocks was reduced from a median of 9 (IQR 2.5-22.5) in the 3 months before ablation to 0 (IQR 0-0, total range 0-2) during follow-up (P <.0001). CONCLUSION Catheter ablation of VPD-triggered VF/PMVT is highly successful. Left ventricular outflow tract and papillary muscles are common and are previously unrecognized sites of origin of these triggers in patients with and without structural heart disease.

Long-Term Outcome With Catheter Ablation of Ventricular Tachycardia in Patients With Arrhythmogenic Right Ventricular Cardiomyopathy

Background—Catheter ablation of ventricular tachycardia (VT) in arrhythmogenic right ventricular cardiomyopathy improves short-term VT-free survival. We sought to determine the long-term outcomes of VT control and need for antiarrhythmic drug therapy after endocardial (ENDO) and adjuvant epicardial (EPI) substrate modification in patients with arrhythmogenic right ventricular cardiomyopathy. Methods and Results—We examined 62 consecutive patients with Task Force criteria for arrhythmogenic right ventricular cardiomyopathy referred for VT ablation with a minimum follow-up of 1 year. Catheter ablation was guided by activation/entrainment mapping for tolerated VT and pacemapping/targeting of abnormal substrate for unmappable VT. Adjuvant EPI ablation was performed when recurrent VT or persistent inducibility after ENDO-only ablation. Endocardial plus adjuvant EPI ablation was performed in 39 (63%) patients, including 13 who crossed over to ENDO–EPI after VT recurrence during follow-up, after ENDO-only ablation. Before ablation, 54 of 62 patients failed a mean of 2.4 antiarrhythmic drugs, including amiodarone in 29 (47%) patients. During follow-up of 56±44 months after the last ablation, VT-free survival was 71% with only a single VT episode in additional 9 patients (15%). At last follow-up, 39 (64%) patients were only on &bgr;-blockers or no treatment, 21 were on class 1 or 3 antiarrhythmic drugs (11 for atrial arrhythmias), and 2 were on amiodarone as a bridge to heart transplantation. Conclusions—The long-term outcome after ENDO and adjuvant EPI substrate ablation of VT in arrhythmogenic right ventricular cardiomyopathy is good. Most patients have complete VT control without amiodarone therapy and limited need for antiarrhythmic drugs.

Idiopathic right ventricular arrhythmias not arising from the outflow tract: Prevalence, electrocardiographic characteristics, and outcome of catheter ablation

BACKGROUND Most idiopathic right ventricular (RV) ventricular tachycardias (VTs) originate from the outflow tract. Data on VT from the lower body of the RV are limited. OBJECTIVE The purpose of this study was to describe a large experience with idiopathic VT detailing the prevalence and characteristics of VT arising from the body of the RV. METHODS The distribution of mapping confirmed VTs within the RV body, ECG characteristics, and results of radiofrequency (RF) ablation were analyzed. RESULTS Among 278 patients who underwent ablation for idiopathic VT or ventricular premature depolarizations (VPDs) arising from the RV, 29 (10%) had VT/VPDs from the lower RV body. Fourteen (48%) patients had VT/VPDs within 2 cm of the tricuspid valve annulus (TVA), 8 (28%) from the basal and 7 (24%) from the apical RV segments. Among the VT/VPDs from the TVA, 8 (57%) originated from the free wall and 6 (43%) from the septum. All but one RV basal or apical VT/VPDs originated from the free wall. All VT/VPDs had a left bundle branch block pattern. VT/VPDs from the free wall had longer QRS duration (P = .0032) and deeper S wave in lead V(2) (P = .042) and V(3) (P = .046) than those from the septum. Apical VT/VPDs more often had precordial R wave transition ≥V(6) (P = .0001) and smaller R wave in lead II (P = .024) and S wave in lead aVR (P = .001) compared to VT/VPDs from basal RV or TVA. RF catheter ablation eliminated VT/VPDs in 96% of patients. No complications were observed. During median follow-up of 27 months (range 4-131 months), 81% of patients had elimination of all symptomatic VT/VPDs. Nineteen percent had rare symptoms (8% without medications, 11% on beta-blocker). CONCLUSION Idiopathic VT/VPDs from the body of RV comprise an important subgroup of idiopathic RV VTs. Although most VTs originate from the RV free wall and nearly 50% from the TVA region, septal and more apical VTs are common. ECG characteristics distinguish free-wall versus septal and more apical origin of VTs, and RF catheter ablation provides good long-term arrhythmia control.

Layered activation of epicardial scar in arrhythmogenic right ventricular dysplasia: possible substrate for confined epicardial circuits.

Background— Ventricular tachycardia ablation in arrhythmogenic right ventricular dysplasia (ARVD) is more successful when including epicardial ablation. Scarring may cause independent, layered epicardial activation and promote epicardially confined ventricular tachycardia circuits. We aimed to characterize transmural right ventricular activation in ARVD patients and to compare this with reference patients without structural heart disease. Methods and Results— Eighteen ARVD patients underwent detailed endocardial and epicardial sinus rhythm electroanatomic mapping. Bipolar activation was annotated at the sharpest intrinsic deflection including late potentials and compared with 6 patients with normal hearts. Total scar area was larger on the epicardium (97±78 cm2) than the endocardium (57±44 cm2; P =0.04), with significantly more isolated potentials. Total epicardial activation time was longer than endocardial (172±54 versus 99±27 ms; P <0.01), and both were longer than in reference patients. Earliest endocardial site was the right ventricular anteroseptum in 17 of 18 ARVD patients versus 5 of 6 controls ( P =0.446), and latest endocardial site was in the outflow tract in 13 of 18 ARVD patients versus 4 of 6 controls and tricuspid annulus in 5 of 18 ARVD patients versus 2 of 6 controls ( P =1.00). In reference patients, epicardial activation directly opposite endocardial sites occurred in 5.2±1.9 ms, suggesting direct transmural activation. In contrast, ARVD patients had major activation delay to the epicardium with laminar central scar activation from the scar border, not by direct transmural spread from the endocardium. Conclusions— Transmural right ventricular activation is modified by ARVD scarring with a delayed epicardial activation sequence suggestive of independent rather than direct transmural activation. This may predispose ventricular tachycardia circuits contained entirely within the epicardium in ARVD and explains observations on the need for direct epicardial ablation to eliminate ventricular tachycardia.Background— Ventricular tachycardia ablation in arrhythmogenic right ventricular dysplasia (ARVD) is more successful when including epicardial ablation. Scarring may cause independent, layered epicardial activation and promote epicardially confined ventricular tachycardia circuits. We aimed to characterize transmural right ventricular activation in ARVD patients and to compare this with reference patients without structural heart disease. Methods and Results— Eighteen ARVD patients underwent detailed endocardial and epicardial sinus rhythm electroanatomic mapping. Bipolar activation was annotated at the sharpest intrinsic deflection including late potentials and compared with 6 patients with normal hearts. Total scar area was larger on the epicardium (97±78 cm2) than the endocardium (57±44 cm2; P=0.04), with significantly more isolated potentials. Total epicardial activation time was longer than endocardial (172±54 versus 99±27 ms; P<0.01), and both were longer than in reference patients. Earliest endocardial site was the right ventricular anteroseptum in 17 of 18 ARVD patients versus 5 of 6 controls (P=0.446), and latest endocardial site was in the outflow tract in 13 of 18 ARVD patients versus 4 of 6 controls and tricuspid annulus in 5 of 18 ARVD patients versus 2 of 6 controls (P=1.00). In reference patients, epicardial activation directly opposite endocardial sites occurred in 5.2±1.9 ms, suggesting direct transmural activation. In contrast, ARVD patients had major activation delay to the epicardium with laminar central scar activation from the scar border, not by direct transmural spread from the endocardium. Conclusions— Transmural right ventricular activation is modified by ARVD scarring with a delayed epicardial activation sequence suggestive of independent rather than direct transmural activation. This may predispose ventricular tachycardia circuits contained entirely within the epicardium in ARVD and explains observations on the need for direct epicardial ablation to eliminate ventricular tachycardia.

High-Resolution Mapping of Postinfarction Reentrant Ventricular Tachycardia: Electrophysiological Characterization of the Circuit.

Background: In vivo description of ventricular tachycardia (VT) circuits is limited by insufficient spatiotemporal resolution. We used a novel high-resolution mapping technology to characterize the electrophysiological properties of the postinfarction reentrant VT circuit. Methods: In 15 swine, myocardial infarction was induced by left anterior descending artery balloon occlusion. Animals were studied 6 to 8 weeks after myocardial infarction. Activation mapping of VTs was performed by using the Rhythmia mapping system. Activation time was based on a combination of bipolar and unipolar electrograms. The response to overdrive pacing from different zones of the circuit was examined. Results: A total of 56 monomorphic VTs were induced (3.8±2.1 per animal). Among these, 21 (37.5%) were hemodynamically stable and allowed mapping of the circuit. Isthmuses were 16.4±7.2 mm long and 7.4±2.8 mm wide. Conduction velocities were slowest at the inward curvature into the isthmus entrance (0.28±0.2 m/s), slightly faster at the outward curvature exit (0.40±0.3 m/s) and nearly normal at the central isthmus (0.62±0.2 m/s). In 3 animals, 2 VT morphologies with opposite axes sharing the same isthmus were mapped. Conduction velocities within the shared isthmus were dependent on the activation vector, consistently slower at the proximal curvature. Overdrive pacing from isthmus sites determined by activation mapping was consistent with entrainment criteria for isthmus. However, dimensions of the isthmus defined by entrainment exceeded dimensions of the isthmus measured by activation mapping by 32±18%. Conclusions: In postinfarction reentrant VT, conduction velocities are slowest at the proximal and distal curvatures. Entrainment mapping overestimates the true size of the isthmus. High-resolution activation mapping of VT may better guide ablation therapy. # Clinical Perspective {#article-title-25}Background: In vivo description of ventricular tachycardia (VT) circuits is limited by insufficient spatiotemporal resolution. We used a novel high-resolution mapping technology to characterize the electrophysiological properties of the postinfarction reentrant VT circuit. Methods: In 15 swine, myocardial infarction was induced by left anterior descending artery balloon occlusion. Animals were studied 6 to 8 weeks after myocardial infarction. Activation mapping of VTs was performed by using the Rhythmia mapping system. Activation time was based on a combination of bipolar and unipolar electrograms. The response to overdrive pacing from different zones of the circuit was examined. Results: A total of 56 monomorphic VTs were induced (3.8±2.1 per animal). Among these, 21 (37.5%) were hemodynamically stable and allowed mapping of the circuit. Isthmuses were 16.4±7.2 mm long and 7.4±2.8 mm wide. Conduction velocities were slowest at the inward curvature into the isthmus entrance (0.28±0.2 m/s), slightly faster at the outward curvature exit (0.40±0.3 m/s) and nearly normal at the central isthmus (0.62±0.2 m/s). In 3 animals, 2 VT morphologies with opposite axes sharing the same isthmus were mapped. Conduction velocities within the shared isthmus were dependent on the activation vector, consistently slower at the proximal curvature. Overdrive pacing from isthmus sites determined by activation mapping was consistent with entrainment criteria for isthmus. However, dimensions of the isthmus defined by entrainment exceeded dimensions of the isthmus measured by activation mapping by 32±18%. Conclusions: In postinfarction reentrant VT, conduction velocities are slowest at the proximal and distal curvatures. Entrainment mapping overestimates the true size of the isthmus. High-resolution activation mapping of VT may better guide ablation therapy.

Comparison of intracardiac echocardiography and transesophageal echocardiography for imaging of the right and left atrial appendages.

BACKGROUND Transesophageal echocardiography (TEE) is the standard for diagnosis of atrial thrombi and is performed before ablation of atrial arrhythmias. Intracardiac echocardiography (ICE) is routinely used during these procedures and may provide an alternative imaging modality. OBJECTIVE The purpose of this study was to compare TEE and ICE for right atrial appendage (RAA) and left atrial appendage (LAA) anatomy and thrombus. METHODS This prospective blinded study enrolled 71 patients with atrial arrhythmias who presented for ablation. TEE and ICE were performed simultaneously to assess the RAA and LAA for thrombi, spontaneous echo contrast, and dimensions. ICE images were acquired sequentially from the right atrium, right ventricular outflow tract, and the pulmonary artery. RESULTS Imaging of the RAA and LAA was achieved in all 71 patients using ICE but in only in 69 patients using TEE because of inability to intubate the esophagus. A total of 4 thrombi were diagnosed (3 LAA, 1 RAA). All were detected by ICE but only 1 by TEE. Diagnostic imaging of the LAA was achieved in 71 patients (100%) with ICE and in 62 patients (87.3%) with TEE (P < .002). Spontaneous echo contrast was more commonly diagnosed with ICE (P < .01). There was strong correlation between TEE and ICE for length (r = 0.71), width (r = 0.94), and area (r = 0.88) of the LAA. Image quality with ICE was highest from the pulmonary artery and lowest from the right atrium. CONCLUSION ICE imaging is a viable alternative to TEE for visualization of the LAA and RAA during catheter ablation procedures.

High-Resolution Mapping of Ventricular Scar Comparison Between Single and Multielectrode Catheters

Background—Mapping resolution is influenced by electrode size and interelectrode spacing. The aims of this study were to establish normal electrogram criteria for 1-mm multielectrode-mapping catheters (Pentaray) in the ventricle and to compare its mapping resolution within scar to standard 3.5-mm catheters (Smart-Touch Thermocool). Methods and Results—Three healthy swine and 11 swine with healed myocardial infarction underwent sequential mapping of the left ventricle with both catheters. Bipolar voltage amplitude in healthy tissue was similar between 3.5- and 1-mm multielectrode catheters with a 5th percentile of 1.61 and 1.48 mV, respectively. In swine with healed infarction, the total area of low bipolar voltage amplitude (defined as <1.5 mV) was 22.5% smaller using 1-mm multielectrode catheters (21.7 versus 28.0 cm2; P=0.003). This was more evident in the area of dense scar (bipolar amplitude <0.5 mV) with a 47% smaller very low–voltage area identified using 1-mm electrode catheters (7.1 versus 15.2 cm2; P=0.003). In this region, 1-mm multielectrode catheters recorded higher voltage amplitude (0.72±0.81 mV versus 0.30±0.12 mV; P<0.001). Importantly, 27% of these dense scar electrograms showed distinct triphasic electrograms when mapped using a 1-mm multielectrode catheter compared with fractionated multicomponent electrogram recorded with the 3.5-mm electrode catheter. In 8 mapped reentrant ventricular tachycardias, the circuits included regions of preserved myocardial tissue channels identified with 1-mm multielectrode catheters but not 3.5-mm electrode catheters. Pacing threshold within the area of low voltage was lower with 1-mm electrode catheters (0.9±1.3 mV versus 3.8±3.7 mV; P=0.001). Conclusions—Mapping with small closely spaced electrode catheters can improve mapping resolution within areas of low voltage.