Scar Border Research Articles

Connexin43 Gene Transfer Reduces Ventricular Tachycardia Susceptibility After Myocardial Infarction

The aim of this study was to evaluate the links between connexin43 (Cx43) expression, myocardial conduction velocity, and ventricular tachycardia in a model of healed myocardial infarction. Post-infarction ventricular arrhythmias frequently cause sudden death. Impaired myocardial conduction has previously been linked to ventricular arrhythmias. Altered connexin expression is a potential source of conduction slowing identified in healed scar border tissues. The functional effect of increasing border-zone Cx43 has not been previously evaluated. Twenty-five Yorkshire pigs underwent anterior infarction by transient left anterior descending coronary artery occlusion, followed by weekly testing for arrhythmia inducibility. Twenty animals with reproducibly inducible sustained monomorphic ventricular tachycardia were randomized 2:1:1 to receive AdCx43, Adβgal, or no gene transfer. One week later, animals underwent follow-up electrophysiologic study and tissue assessment for several functional and molecular measures. Animals receiving AdCx43 had less electrogram fractionation and faster conduction velocity in the anterior-septal border zone. Only 40% of AdCx43 animals remained inducible for ventricular tachycardia, while 100% of controls were inducible after gene transfer. AdCx43 animals had 2-fold higher Cx43 protein levels in the anterior-septal infarct border, with similar percents of phosphorylated and intercalated disk-localized Cx43 compared with controls. These data mechanistically link Cx43 expression to slow conduction and arrhythmia susceptibility in the healed scar border zone. Targeted manipulation of Cx43 levels improved conduction velocity and reduced ventricular tachycardia susceptibility. Cx43 gene transfer represents a novel treatment strategy for post-infarction arrhythmias.

Layered Activation of Epicardial Scar in Arrhythmogenic Right Ventricular Dysplasia

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 cm 2 ) than the endocardium (57±44 cm 2 ; 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.

Integration of 3-Dimensional Scar Models from SPECT to Guide Ventricular Tachycardia Ablation

The integration of myocardial scar models in 3-dimensional (3D) mapping systems may provide a novel way of helping to guide ventricular tachycardia (VT) ablations. This study assessed the value of (201)Tl SPECT perfusion imaging to define ventricular myocardial scar areas and to characterize electrophysiology voltage-derived myocardial substrate categories of scar, border zone (BZ), and normal myocardium regions. Scar and BZ regions have been implicated in the genesis of ventricular arrhythmias. Ten patients scheduled for VT ablation underwent (201)Tl SPECT before the ablation procedure. 3D left ventricular (LV) scar models were created from the SPECT images. These scar models were registered with the LV voltage maps and analyzed with a 17-segment cardiac model. Scar location and scar burden were compared between the SPECT scar models and voltage maps. In addition, (201)Tl SPECT uptake was quantified using a 68-segment cardiac model and compared among voltage-defined scar, BZ, and normal segments. 3D models of LV myocardium and scar were successfully created from (201)Tl SPECT images and integrated in a clinical mapping system. The surface registration error with the electrophysiology voltage map was 4.4 ± 1.0 mm. The 3D scar location from SPECT matched in 72% of the segments with the voltage map findings. All successful ablation sites were located within the SPECT-defined scar or within 1 cm of its border, with 73% of the successful ablation sites within 1 cm of the scar border. Voltage measurements in SPECT-defined scar and normal areas were 1.2 ± 1.7 and 3.4 ± 2.8 mV, respectively (P < 0.001). The fractional SPECT scar burden area (18.8% ± 5.2%) agreed better with the abnormal (scar plus BZ) voltage area (20.8% ± 15.7%) than with the scar voltage area (5.8% ± 5.8%). Mean normalized (201)Tl uptake was 55% ± 21% in the voltage-defined scar, 63% ± 20% in BZ, and 79% ± 17% in normal myocardial segments (P < 0.05 for scar or BZ vs. normal). 3D SPECT surface models of LV scar were accurately integrated into a clinical mapping system and predicted endocardial voltage-defined scar. These preliminary data support the possible use of widely available (201)Tl SPECT to facilitate substrate-guided VT ablations.

Pursuing the “Holy Grail”

Over the past decade, several large, randomized trials have allowed us to better define the appropriate population for primary prevention implantable cardioverter-defibrillator (ICD) placement, saving thousands of lives every year. MADIT II (Multicenter Automatic Defibrillator Implantation Trial II) and SCD-HeFT (Sudden Cardiac Death in Heart Failure Trial) have demonstrated a survival benefit of 31% and 23% over 20 and 45.5 months follow-up, respectively.1,2 However, our selection criteria that are mostly based on the left ventricular ejection fraction (LVEF) are of limited specificity. Long-term follow-up data show that only 35% of patients ever receive an appropriate shock for ventricular tachycardia (VT) and ventricular fibrillation (VF) during a 3-year follow-up.3 Article see p 178 In this issue of Circulation: Cardiovascular Imaging , Wu et al4 report their intriguing results in 235 patients who underwent ICD implantation for primary prevention according to the SCD-HeFT/MADIT II criteria. Ischemia was the most prevalent etiology (58%) of the cardiomyopathy, and all patients underwent cardiac magnetic resonance (CMR) as well as baseline blood draws at the time of implantation. At least 90% of patients were receiving β-blocker and angiotensin-converting enzyme inhibitor/angiotensin receptor blocker therapy. During the median follow-up period of 3.6 years, 19% of patients experienced the primary end point of appropriate ICD shock for VT/VF or cardiac death. The full-width half-maximum method previously published by the group was used to separate delayed enhancement on MRI into dense scar (scar core) or heterogeneous scar (gray zone). Indeed, the investigators found that the gray zone mass was significantly higher in patients who experienced the primary end point, whereas LVEF was only of borderline significance. In a multivariate analysis comparing patients according to tertiles of gray zone, the middle or highest tertile had a hazard ratio of 3.9 (95% CI, 1.2–12.4) and 4.6 (95% …

Calcium-Mediated Arrhythmia Substrates Associated with Oxidative Stress during Myocardial Infarction

Following myocardial infarction (MI), ventricular arrhythmias commonly originate from the MI border zone (BZ) but the cause for this is not clear. Increased oxidative stress is a hallmark of MI and an important mechanism of intracellular calcium dysregulation. We hypothesize that following MI, increased oxidative stress in the infarct BZ creates a substrate for calcium-mediated arrhythmias. Methods: Male Lewis rats (n=12) underwent ligation of the left-anterior descending artery. At 4 weeks, hearts were isolated and high-resolution optical mapping of intracellular calcium (Indo-1AM) and reactive oxygen species (ROS, dichlorofluorescein diacetate) were performed. Blebbistatin (7μM) was used to eliminate motion artifact. Calcium transient alternans (CaT_Alt) and multicellular-spontaneous calcium release (mSCR) were induced by rapid pacing (200–670 bpm) before and after the CaMKII blocker KN-93. Sites within 2mm of the anatomical scar border where designated as BZ. All other sites in the mapping field outside the BZ and scar were considered remote. Results: CaT_Alt and mSCR activity were significantly greater in the MI BZ (15±3%, 20±2%) as compared to remote sites (3.3±2%, p<0.01; 9.0±2%, p<0.001), respectively. Additionally, ROS density was increased by 283±53% (p<0.001) in the BZ compared to remote regions, which was confirmed offline by tissue sample analysis. Interestingly, treatment with KN-93 significantly decreased CaT_Alt in the BZ by 50±10% (p<0.05) but did not decrease mSCR activity. Conclusions: These results demonstrate that increased ROS in the infarct BZ is associated with a significant increase in calcium-mediated arrhythmia substrates (CaT_Alt and mSCR). In addition, CaMKII activation may be a mechanism of CaT_Alt but not spontaneous calcium release in the BZ, suggesting multiple calcium regulatory targets of oxidative stress associated with MI.

Successful Ablation of an Epicardial Ventricular Tachycardia Using a Surgical Ablation Tool

A 62-year-old woman with ischemic cardiomyopathy (left ventricular ejection fraction, 15%) underwent HeartMate II (Thoratec, Inc, Pleasanton, CA) left ventricular assist device (LVAD) placement in January 2011 for cardiogenic shock. After implantation, the patient's hemodynamic status improved, but she had multiple episodes of ventricular tachycardia (VT) leading to implantable cardioverter-defibrillator therapies. The episodes led to marked reduction in LVAD flows and presyncope. Amiodarone, mexilitine, and quinidine therapy did not change the VT burden. The patient underwent endocardial catheter ablation in March 2011 at an outside institution. During this procedure, the basal lateral LV was noted to have low voltage consistent with scar, yet pace maps obtained in this region did not match the clinical VT. Despite extensive ablation of late potentials and scar border zones, the clinical VT remained inducible. In April 2011, the patient underwent epicardial mapping and ablation of VT at our institution. Because the patient had previous cardiac surgery and the 12-lead ECG of the clinical VT suggested a basal anterolateral exit, epicardial access was obtained by limited anterior thoracotomy in the cardiac catheterization laboratory, as described previously.1 Based on the clinical VT morphology and preprocedure CT, the fourth intercostal space was chosen for the incision (Figure 1A). Figure 1. CT scan, voltage map, and ECG. A , Preprocedure CT imaging demonstrating the left ventricular assist device inflow cannula site as well as …

Abstract 8208: Scar Border and Transmural Core Defined by Magentic Resonance Imaging Contribute to T wave Alternans in Patients with Cardiomyopathy: Implications for Identifying Arrhythmogenic Substrate

BACKGROUND Structural barriers can lead to discordant action potential (AP) alternans in animal studies by slowing conduction and increasing AP gradients. We hypothesized that border zone and midwall scar will promote T wave alternans (TWA) in patients with cardiomyopathy by potentially slowing conduction and uncoupling transmural APs, respectively. METHODS AND RESULTS We prospectively studied 40 patients (53±14 yrs, LVEF 40±17%) with ischemic (n=12), dilated (n=12), or hypertrophic cardiomyopathy (n=16). Scar core and border zone were quantified as a percent of LV mass by applying signal-intensity thresholding to late gadolinium enhanced cardiac magnetic resonance images. The transmural distribution of core was determined from the short-axis LV slices and classified as endocardial, epicardial, midwall and full thickness core. TWA was evaluated during incremental atrioventricular pacing at 100, 110 and 120 bpm. TWA was quantified from ECG recordings using the spectral method and classified as positive if Valt &gt;1.9 µV and k &gt;3. +TWA was detected in 27 (68%) patients. The percentages of border zone, epicardial core and midwall core were greater in +TWA vs. - TWA. Maximum TWA magnitude correlated with the relative size of border zone (r=0.52, P&lt;0.001), epicardial core (r=0.54, P&lt;0.001) and midwall core (r=0.40, P=0.01). The heart rate onset for TWA (Valt &gt;0 µV, k &gt;3) was significantly lower in those patients with greater border zone and epicardial core. Multivariate analysis revealed border zone to be the only independent predictor of +TWA (Odds Ratio 1.22/10%, P=0.003). CONCLUSIONS In cardiomyopathy patients, scar border zone, epicardial core and midwall core contribute to +TWA. These structural barriers in the presence of +TWA may together provide a potent substrate for lethal ventricular arrhythmias.

Robotic catheter ablation of left ventricular tachycardia: initial experience

Catheter ablation of ventricular tachycardia (VT) can be technically challenging due to difficulty with catheter positioning in the left ventricle (LV) and achieving stable contact. The Hansen Sensei Robotic system (HRS) has been used in atrial fibrillation but its utility in VT is unclear. The purpose of this study was to test the technical feasibility of robotic catheter ablation of LV ventricular tachycardia (VT) using the HRS. Twenty-three patients underwent LV VT mapping and ablation with the HRS via a transseptal, transmitral valve approach. Nineteen patients underwent substrate mapping and ablation (18 had ischemic cardiomyopathy, 1 had an apical variant of hypertrophic cardiomyopathy). Four patients had focal VT requiring LV VT mapping and ablation. Procedural endpoints included substrate modification by endocardial scar border ablation and elimination of late potentials, or elimination of inducible focal VT. Mapping and ablation were entirely robotic without requiring manual catheter manipulation in all patients and reaching all LV regions with stable contact. Fluoroscopy time of the LV procedure was 22.2 ± 11.2 minutes. Radiofrequency time was 33 ± 21 minutes. Total procedural times were 231 ± 76 minutes. Complications included a left groin hematoma (opposite to the HRS sheath), 1 pericardial effusion without tamponade that was drained successfully, and transient right ventricular failure in a patient with previous left ventricular assist device. At 13.4 ± 6.7 months of follow-up (range 1-19 months), recurrence of VT occurred in 3 of 23 patients. Our initial experience suggests that the HRS allows successful mapping and ablation of LV VT.

LONG-TERM RESULTS OF SUBSTRATE-BASED VENTRICULAR TACHYCARDIA ABLATION IN PATIENTS WITH PREVIOUS MYOCARDIAL INFARCTION. IDENTIFICATION OF ANATOMICAL AND ELECTROPHYSIOLOGICAL SUCCESS PREDICTORS

Methods: We analyzed 60 patients (age 67±9, LVEF: 30±11%) with chronic myocardial infarction who underwent substrate based VT ablation (SBVTA). Electroanatomic maps were obtained to measure the scar (≤1,5 mV) and dense scar ((≤ ,5 mV ) and to delimit the scar borders. The targets of SBVTA were all E-IDC and CC of the scar tissue. Results: Ablation targeted E-IDC and CC in 95% and 75% of patients, in 5 % the ablation targeted multicomponent electrogram from the scar border where pace-mapping reproduced VT morphology. The ablation area was 14±10 cm 2, no major life-threatening complications/incessant VT were observed after the procedure. During a median follow-up of 35 months 57% of patients remained free of VT recurrences. Patients with an above-median dense scar extension (25 cm 2 ) were at higher risk for VT recurrence compared with those with a below-median (65% versus 24%, p<0.0001, median follow-up 31 vs. 39 months, p: 0.1). Multivariable analysis showed that scar extension was the only predictors of VT recurrence (p<0.004). Conclusion: In patients with a prior MI SBVTA is safe and effective, the extent of dense scar provides incremental prognostic value post MI smvt recurrence

MRI-Guided Ventricular Tachycardia Ablation

Background— Substrate-guided ablation of ventricular tachycardia (VT) in patients with implanted cardioverter-defibrillators (ICDs) relies on voltage mapping to define the scar and border zone. An integrated 3D scar reconstruction from late gadolinium enhancement (LGE) MRI could facilitate VT ablations. Methods and Results— Twenty-two patients with ICD underwent contrast-enhanced cardiac MRI with a specific absorption rate of &lt;2.0 W/kg before VT ablation. Device interrogation demonstrated unchanged ICD parameters immediately before, after, or at 68±21 days follow-up ( P &gt;0.05). ICD imaging artifacts were most prominent in the anterior wall and allowed full and partial assessment of LGE in 9±4 and 12±3 of 17 segments, respectively. In 14 patients with LGE, a 3D scar model was reconstructed and successfully registered with the clinical mapping system (accuracy, 3.9±1.8 mm). Using receiver operating characteristic curves, bipolar and unipolar voltages of 1.49 and 4.46 mV correlated best with endocardial MRI scar. Scar visualization allowed the elimination of falsely low voltage recordings (suboptimal catheter contact) in 4.1±1.9% of &lt;1.5-mV mapping points. Display of scar border zone allowed identification of excellent pace mapping sites, with only limited voltage mapping in 64% of patients. Viable endocardium of &gt;2 mm resulted in &gt;1.5-mV voltage recordings despite up to 63% transmural midmyocardial scar successfully ablated with MRI guidance. All successful ablation sites demonstrated LGE (transmurality, 68±26%) and were located within 10 mm of transition zones to 0% to 25% scar in 71%. Conclusions— Contrast-enhanced cardiac MRI can be safely performed in selected patients with ICDs and allows the integration of detailed 3D scar maps into clinical mapping systems, providing supplementary anatomic guidance to facilitate substrate-guided VT ablations.

Three-Dimensional Contrast-Enhanced Multidetector CT for Anatomic, Dynamic, and Perfusion Characterization of Abnormal Myocardium To Guide Ventricular Tachycardia Ablations

Background— Advances in contrast-enhanced multidetector CT enable detailed characterization of the left ventricular myocardium. Myocardial scar and border zone (BZ), as the target of ventricular tachycardia ablations, displays abnormal anatomic, dynamic, and perfusion characteristics during first-pass CT. This study assessed how contrast-enhanced CT can predict voltage-defined scar and BZ and integrate its scar reconstructions into clinical mapping systems to guide ventricular tachycardia ablations. Methods and Results— Eleven patients with ischemic cardiomyopathy underwent contrast-enhanced CT before ventricular tachycardia ablation. Segmental anatomic (end-systolic and end-diastolic wall thickness), dynamic (wall thickening, wall motion), and perfusion (hypoenhancement) characteristics were evaluated. Receiver operating characteristic curves assessed the ability of CT to determine voltage-defined scar and BZ segments. Three-dimensional epi- and endocardial surfaces and scar borders were reconstructed, coregistered, and compared to voltages using a 17-segment model. Abnormal anatomic, dynamic, and perfusion data correlated well with abnormal (&lt;1.5 mV) endocardial voltages ( r =0.77). Three-dimensional reconstruction integrated into the clinical mapping system (registration accuracy, 3.31±0.52 mm) allowed prediction of homogenous abnormal voltage (&lt;1.5 mV) in 81.7% of analyzed segments and correctly displayed transmural extent and intramural scar location. CT hypoperfusion correlated best with scar and BZ areas and encompassed curative ablations in 82% cases. Conclusions— Anatomic, dynamic, and perfusion imaging using contrast-enhanced CT allows characterization of left ventricular anatomy and 3D scar and BZ substrate. Integration of reconstructed 3D data sets into clinical mapping systems supplements information of voltage mapping and may enable new image approaches for substrate-guided ventricular tachycardia ablation.

Catheter Ablation for Electrical Storm as Polymorphic Ventricular Tachycardia in a Case with Ischemic Cardiomyopathy after Coronary Artery Bypass Graft

We report a case involving a patient with ischemic cardiomyopathy who developed polymorphic ventricular tachycardia (PVT) and ventricular fibrillation storm after coronary artery bypass graft. Because PVT was initiated by various right bundle branch type premature ventricular contractions (PVCs), we assessed the relatively monomorphic ventricular tachycardia (MVT) during PVT. Electroanatomical mapping revealed that the earliest ventricular activation of the MVT was located in the scar border zone at the posterior septum of the left ventricle. Stable potentials which preceded the MVT were observed. Catheter ablation for the preceding potential suppressed the maintenance of the PVT, although triggered PVCs appeared frequently. Catheter ablation was effective as a bailout therapy in a patient with PVT‐induced cardiomyopathy after cardiac operation.

Image Integration Using Intracardiac Ultrasound and 3D Reconstruction for Scar Mapping and Ablation of Ventricular Tachycardia

Ablation of ventricular tachycardia (VT) reduces implantable cardioverter defibrillator shocks. Intracardiac ultrasound (ICE) can visualize and quantify the function of all left ventricular wall segments. We thus hypothesized that ICE could identify scar tissue and provide a guide to facilitate substrate-guided VT ablation. Eighteen patients underwent VT ablation with real time ICE mapping from the right atrium and ventricle with online 3D-image reconstruction of scar segments. The left ventricle was also scar mapped by traditional electroanatomic mapping (CARTO) for comparison. Images from these 2 scar mapping techniques were compared to each other as well as to a preprocedure transthoracic echocardiogram. The average age was 65 +/- 12 years and 12 (67%) were male (15 [83%] had ischemic cardiomyopathy). Two patients (12%) had recurrence of their clinical VT (1 remained on an antiarrhythmic medication, the other had a repeat ablation) over a follow-up of 127 +/- 33 days. No periprocedural or long-term adverse events occurred. A total of 248 wall segments were analyzed. All 3 modalities were concordant in scar identification in 193 (78%) segments. The ICE segments correlated with the electroanatomic map in 213 (86%) segments versus 198 (80%), which correlated with transthoracic echocardiography and electroanatomic mapping (P = 0.046). Specifically, the ICE wall motion scores were closer to the electroanatomic mapping in the basal segments and showed a higher accuracy in ischemic heart disease. These data demonstrate that real time ICE images provide accurate chamber geometries and scar boundaries of the left ventricle. These scar borders were more accurate than transthoracic echocardiography and illustrate the feasibility of ICE for substrate-based ablation for VT.

Usefulness of a Limited Linear Ablation of Post-Myocardial Infarction Ventricular Tachycardia Using a Standardized Approach Based on Sinus Rhythm Mapping

The ablation of ventricular tachycardia (VT) can be achieved using anatomically guided approaches using differentiated mapping and ablation techniques. The aim of this study was to evaluate the efficacy of limited linear ablation in the VT exit region identified during sinus rhythm mapping alone. One hundred fifteen consecutive patients presenting for ablation of post-myocardial infarction VT were included. After induction of the target VT during invasive electrophysiology, left ventricular substrate mapping during sinus rhythm to identify scar and border zone on the basis of endocardial bipolar voltage was performed. The exit site of the target VT was regionalized by a simplified vector pace mapping approach and targeted using limited linear ablation within the scar border zone. Seventy-seven percent of all inducible VT was successfully ablated. In 71 patients (62%), no sustained VT was inducible at the end of ablation procedure (complete success). During a median follow-up period of 16 + or - 10 months, 89 patients (77%) had no documented sustained ventricular arrhythmia. Seven patients (2%) had recurrences of the initially ablated VT, and 16 (14%) had new-onset VT. Patients with complete success had a significantly lower number of ventricular arrhythmia reoccurrences than patients with incomplete ablation success (11% vs 37%, p = 0.002). In conclusion, postinfarct VT was effectively ablated in 97% of patients without mapping during ongoing VT using a simplified regional linear ablation approach targeting the scar border zone. Freedom from any ventricular arrhythmia was achieved in 77% of patients during midterm follow-up.

Bipolar Ablation of the Interventricular Septum is More Efficient at Creating a Transmural Line than Sequential Unipolar Ablation

Post infarct ventricular tachycardia (VT) often involves the interventricular septum (IVS) and requires transmural septal ablation. The purpose of this study was to compare the efficacy of bipolar ablation (BIA) versus sequential unipolar ablation (SUA) in creating a transmural ablation line along the IVS scar border. Both ablation strategies were compared in a phantom agar model first and then in 10 post infarct sheep. In the phantom agar model BIA lesions were larger, transmural, and less dependent on catheter alignment and contact compared with SUA. Noncontact mapping was used in the animals to identify the septal scar border and create a 30-mm ablation line. In five animals BIA (50 W) was performed between two irrigated catheters on either side of the IVS, and in five control animals SUA (50 W) was performed, first on the left ventricle (LV) septal scar border and then on the opposing right ventricle (RV) septal surface. Electrical block along ablation lines was confirmed with noncontact mapping. BIA required significantly less ablations (12 + or - 1 vs 29 + or - 7, P = 0.001), ablation time (22 + or - 3 vs 48 + or - 6 minutes, P < 0.001), and energy (58 + or - 7 vs 124 + or - 21 kJ, P < 0.001). At pathological examination all ablation lines in both groups were transmural at the IVS border. BIA endocardial ablation lines (LV + RV) were significantly longer than SUA lines (76 + or - 10 vs 49 + or - 11 mm, P = 0.003). BIA of the IVS is highly effective at creating a transmural ablation line, requiring less ablation and creating longer lesions than SUA. BIA ablation may have a role for post infarct VT involving the IVS.

Catheter ablation of arrhythmic storm triggered by monomorphic ectopic beats in patients with coronary artery disease

Frequent episodes of polymorphic ventricular tachycardias/ventricular fibrillation (VT/VF) in patients with coronary artery disease can be triggered by monomorphic ventricular premature beats (VPBs) and thus, amenable to catheter ablation. The goal of this study was to review single-center experience in catheter ablation of electrical storm caused by focally triggered polymorphic VT/VF. Catheter ablation of electrical storm due to focally triggered polymorphic VT/VF was performed in nine patients (mean age, 62+/-7 years; two females). All patients had previous myocardial infarction (interval of 3 days to 171 months). Mean left ventricular ejection fraction was 27+/-6 percent. All patients presented with repeated runs of polymorphic VT/VF triggered by monomorphic VPBs. Based on mapping data, the ectopic beats originated from scar border zone on interventricular septum (n=5), inferior wall (n=3), and lateral wall (n=1). Catheter ablation was performed to abolish the triggering ectopy and to modify the arrhythmogenic substrate by linear lesions within the infarct border zone. The ablation procedure was acutely successful in eight out of nine patients. During the follow-up of 13+/-7 months, two patients died due to progressive heart failure. One patient had late recurrence of electrical storm due to ectopic beats of different morphology and was successfully reablated. Electrical storm due to focally triggered polymorphic VT/VF may occur either in subacute phase of myocardial infarction or substantially later after index event. Catheter ablation of ectopic beats triggering these arrhythmias can successfully abolish electrical storm and become a life-saving procedure.

Contact versus Noncontact Mapping for Ablation of Ventricular Tachycardia in Patients with Previous Myocardial Infarction

The aim of this study was to compare contact versus noncontact mapping for radiofrequency (RF) ablation of any sustained post-myocardial infarction (MI) ventricular tachycardia (VT). Forty patients with tolerated VT post-MI were randomized to RF ablation with contact (group 1) or noncontact (group 2) mapping systems. In both groups ablation of tolerated VT was guided by VT activation map confirmed by concealed entrainment. When untolerated VTs were induced, ablation was performed in group 1 according to pace mapping starting from the scar border zone and in group 2 according to the VT activation map confirmed by pace mapping. No differences were seen between the groups in terms of acute success rate of clinical VT ablation (95% vs 100%, respectively; P = ns) and in the noninducibility of any VT at the end of the procedure (55% vs 85%, respectively; P = 0.08). Moreover, untolerated VTs were eliminated in 30% of group 1 versus 83.3% of group 2 patients (P < 0.05). The mean total procedural and fluoroscopy times were 236.4 +/- 42.7 and 29.0 +/- 7.8 minutes in group 1 and 144.5 +/- 50.8 and 23.4 +/- 5.8 minutes in group 2 (P < 0.001 and < 0.05, respectively). At a mean follow-up of 15.2 +/- 6.7 months no differences were seen in VT recurrences between groups, but noninducibility at the end of the procedure was predictive of freedom from recurrences (P < 0.001). Both systems are useful for ablation of tolerated VT. Noncontact mapping is more effective for ablation of untolerated VT and allows the reduction of procedural and fluoroscopy times. Noninducibility at the end of the procedure seems predictive of freedom from recurrences during follow-up.

Simultaneous Biventricular Noncontact Mapping and Ablation of Septal Ventricular Tachycardia in a Chronic Ovine Infarct Model

We assessed a novel simultaneous biventricular mapping and ablation approach for septal ventricular tachycardia (VT) in a chronic ovine infarct model. In 8 sheep with inducible VT, mapping and ablation were performed 9+/-3 months after percutaneously induced myocardial infarction, with left ventricular ejection fraction 23+/-8%. Scar was identified by EnSite Dynamic Substrate Mapping plus CARTO voltage mapping. Thirty VT episodes (cycle length, 235+/-42 ms) were mapped with simultaneous analyses using EnSite arrays deployed in both the left ventricle and the right ventricle. Short ablation lines were created perpendicular to the breakout pathway along the scar border in the ventricle with earliest activity. If septal VT was still inducible, this line was extended before ablation in the second chamber. The end point of noninducibility of VT was achieved in all animals. The mean difference in delay in noncontact breakout timing between the ventricles was shorter for VT with (n=18) than without (n=12) septal breakout (32+/-7.8 ms, P<0.001). In 5 of 6 animals, after ablation in one ventricle, septal VT was still inducible with a common breakout site in the second ventricle. After septal ablation in the second ventricle, VT was no longer inducible. In the 6 animals in which septal VT had been ablated, transmural septal ablation was identified at the scar border, with overlapping left ventricular and right ventricular ablation lesions present in 5 of 6 (septal thickness 8 to 17 mm) and left ventricular endocardial ablation being transmural in 1 of 6 (6 mm). Biventricular scar and VT activation mapping correctly localizes septal VT pathways, directing ablation from one or both septal endocardial aspects. Creation of a transmural septal lesion at the scar border interrupting VT exit points is highly effective at ablating septal VT.

Role of Left Ventricular Scar and Purkinje‐Like Potentials During Mapping and Ablation of Ventricular Fibrillation in Dilated Cardiomyopathy

Purkinje-like potentials (PLPs) have been described as important contributors to initiation of ventricular fibrillation (VF) in patients with normal hearts, ischemic cardiomyopathy, and early after-myocardial infarction. Of the 11 consecutive patients with VF storm, nonischemic cardiomyopathy (68 +/- 22 years, left ventricular ejection fraction 28 +/- 8%) who were given antiarrhythmic drugs and/or heart failure management, five had recurrent VF and underwent electrophysiology study (EPS) and catheter ablation. At EPS, frequent monomorphic premature ventricular contractions (PVC) and/or ventricular tachycardia did not occur. With isoproterenol, VF was induced in three patients, and sustained monomorphic PVCs were induced in one patient. Three-dimensional electroanatomical mapping using CARTO (Biosense-Webster Inc., Diamond Bar, CA) revealed posterior wall scar in four of the five patients. PLP in sinus rhythm were recorded around the scar border in these four patients, and radiofrequency ablation targeting PLP was successfully performed at these sites. The patient without PLP did not undergo ablation. During follow-up (12 +/- 5 months), only the patient without PLP had four VF recurrences requiring implantable cardioverter-defibrillator (ICD) shocks. In patients with VF and dilated cardiomyopathy, left ventricular posterior wall scar in the vicinity of the mitral annulus seems to be a common finding. Targeting PLP along the scar border zone for ablation seems to efficiently prevent VF recurrence in these patients.

Abstract 4090: Substrate Modification Using Electroanatomically-guided Linear Ablation During Sinus Rhythm To Treat Post-infarction Ventricular Tachycardia

Catheter ablation of ventricular tachycardia (VT) in the setting of ischemic cardiomyopathy can be performed to modify the underlying substrate. We evaluated the efficacy of a linear VT ablation procedure based on sinus rhythm (SR) substrate maps to treat ischemic VT in consecutive patients. Methods: In 110 consecutive patients with ischemic VT (56% not tolerated) catheter ablation was attempted. During SR left ventricular scar mapping was performed identifying scar tissue (bipolar voltages 1.5mV). Regionalization of VT-exit regions was performed based on pace-mapping within the scar border zone. Ablation was directed towards the identified exit region performing linear ablation along the scar border. ICD-holter interrogation was performed during follow-up. Results: A mean of 2.7±1.6 different VTs were inducible per patient (total 286). In 97% (107) of all patients (74% of all inducible VTs ablated: 213/286) the clinical VT was successfully ablated. In 68 patients (62%) no sustained monomorphic VT (complete success) was inducible at the end of the ablation procedure whereas in 39 patients (35%) VTs (partial success) were still inducible. Over a median follow-up of 12 months (6 –39) 88 (80%) patients were free from any ventricular arrhythmia. 19 successfully ablated patients had recurrences in between 6 to 36 months post intervention but the number of episodes treated by the ICD was significantly reduced (16±4 within 3 months (3±2) (p=0.02). No difference in patients with tolerated compared to non-tolerated VTs were detected (recurrences in 7/48 (15%) tolerated and 15/62 (24%) non-tolerated; p=0.13). There was a significant difference in freedom from any VT in patients with complete (88%) versus partial success (72%) (p=0.04). Conclusions: Substrate modification targeting only the scar-border zone including the VT exit site based on SR-maps is highly effective in suppressing the occurrence of a clinical VT in patients with remote myocardial infarction (97%). Based on the electro-anatomical findings complete freedom from any ventricular arrhythmia over a median of 1 year can be achieved in 80% of all patients. No difference in regard to freedom from any ventricular arrhythmia can be documented in patients with tolerated and non-tolerated VTs.