Epicardial Conduction Speed, Electrogram Abnormality, and Computed Tomography Attenuation Associations in Arrhythmogenic Right Ventricular Cardiomyopathy.

OBJECTIVES: This study sought to evaluate the association between contrast-enhanced multidetector computed tomography (CE-MDCT) attenuation and local epicardial conduction speed (ECS) and electrographic abnormalities in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) and ventricular tachycardia (VT). BACKGROUND: CE-MDCT is a widely available and fast imaging technology with high spatial resolution that is less prone to defibrillator generator-related safety issues and image artifacts. However, the association between hypoattenuation on MDCT and VT substrates in ARVC remains unknown. METHODS: Patients with ARVC who underwent CE-MDCT followed by endocardial (n = 30) and epicardial (n = 21) electroanatomical mapping (EAM) and VT ablation were prospectively enrolled. Right ventricular (RV) mid-myocardial attenuation was calculated from 3-dimensional MDCT images and registered to EAM. Local ECS was calculated by averaging the ECS between each point and 5 adjacent points with concordant wave front direction. RESULTS: A total of 17,311 epicardial and 5,204 endocardial points were included. In multivariable regression analysis clustered by patient, RV myocardial attenuation was associated with epicardial bipolar voltage amplitude (2.5% decrease in amplitude per 10 HU decrease in attenuation; p < 0.001), with endocardial unipolar voltage amplitude (0.9% decrease in amplitude per 10 HU decrease in attenuation; p < 0.001), and with ECS (0.4% decrease in ECS per 10 HU decrease in attenuation; p = 0.001). CONCLUSIONS: CE-MDCT attenuation distribution is associated with regional ECS and electrographic amplitude in ARVC. Regions with low attenuation likely reflect fibro-fatty involvement in the RV and may serve as important VT substrates in patients with ARVC who are undergoing VT ablation.

Utility of ripple mapping for identification of slow conduction channels during ventricular tachycardia ablation in the setting of arrhythmogenic right ventricular cardiomyopathy.

BACKGROUND: Ripple mapping displays every deflection of a bipolar electrogram and enables the visualization of conduction channels (RMCC) within postinfarction ventricular scar to guide ventricular tachycardia (VT) ablation. The utility of RMCC identification for facilitation of VT ablation in the setting of arrhythmogenic right ventricular cardiomyopathy (ARVC) has not been described. OBJECTIVE: We sought to (a) identify the slow conduction channels in the endocardial/epicardial scar by ripple mapping and (b) retrospectively analyze whether the elimination of RMCC is associated with improved VT-free survival, in ARVC patients. METHODS: High-density right ventricular endocardial and epicardial electrograms were collected using the CARTO 3 system in sinus rhythm or ventricular pacing and reviewed for RMCC. Low-voltage zones and abnormal myocardium in the epicardium were identified by using standardized late-gadolinium-enhanced (LGE) magnetic resonance imaging (MRI) signal intensity (SI) z-scores. RESULTS: A cohort of 20 ARVC patients that had undergone simultaneous high-density right ventricular endocardial and epicardial electrogram mapping was identified (age 44 ± 13 years). Epicardial scar, defined as bipolar voltage less than 1.0 mV, occupied 47.6% (interquartile range [IQR], 30.9-63.7) of the total epicardial surface area and was larger than endocardial scar, defined as bipolar voltage less than 1.5 mV, which occupied 11.2% (IQR, 4.2 ± 17.8) of the endocardium (P < 0.01). A median 1.5 RMCC, defined as continuous corridors of sequential late activation within scar, were identified per patient (IQR, 1-3), most of which were epicardial. The median ratio of RMCC ablated was 1 (IQR, 0.6-1). During a median follow-up of 44 months (IQR, 11-49), the ratio of RMCC ablated was associated with freedom from recurrent VT (hazard ratio, 0.01; P = 0.049). Among nine patients with adequate MRI, 73% of RMCC were localized in LGE regions, 24% were adjacent to an area with LGE, and 3% were in regions without LGE. CONCLUSION: Slow conduction channels within endocardial or epicardial ARVC scar were delineated clearly by ripple mapping and corresponded to critical isthmus sites during entrainment. Complete elimination of RMCC was associated with freedom from VT.

Importance of the Interventricular Septum as Part of the Ventricular Tachycardia Substrate in Nonischemic Cardiomyopathy.

OBJECTIVES: This study sought to characterize septal substrate in patients with nonischemic left ventricular cardiomyopathy (NILVCM) undergoing ventricular tachycardia (VT) ablation. BACKGROUND: The interventricular septum is an important site of VT substrate in NILVCM. METHODS: The authors studied 95 patients with NILVCM and VT. Electroanatomic mapping using standard bipolar (<1.5 mV) and unipolar (<8.3 mV) low-voltage criteria identified septal scar location and size. Analysis of unipolar voltage was performed and scars quantified using graded unipolar cutoffs from 4 to 8.3 mV were correlated with delayed gadolinium-enhanced cardiac magnetic resonance (DE-CMR), performed in 57 patients. RESULTS: Detailed LV endocardial mapping (mean 262 ± 138 points) showed septal bipolar and unipolar voltage abnormalities (VAs) in 44 (46%) and 79 (83%) patients, most commonly with basal anteroseptal involvement. Of the 59 patients in whom the septum was targeted, bipolar and unipolar septal VAs were seen in 36 (61%) and 54 (92%). Of the 35 with CMR-defined septal scar, bipolar and unipolar septal VAs were seen in 18 (51%) and 31 (89%). In 12 patients without CMR septal scar, 6 (50%) had isolated unipolar septal VAs on electroanatomic mapping, a subset of whom the septum was targeted for ablation (44%). In the graded unipolar analysis, the optimal cutoff associated with magnetic resonance imaging septal scar was 4.8 mV (sensitivity 75%, specificity 70%; area under the curve: 0.75; 95% confidence interval: 0.60 to 0.90). CONCLUSIONS: Septal substrate by unipolar or bipolar voltage mapping in patients with NILVCM and VT is common. A unipolar voltage cutoff of 4.8 mV provides the best correlation with DE-CMR. A subset of patients with septal VT had normal DE-CMR or endocardial bipolar voltage with abnormal unipolar voltage.

Characterization of the Electroanatomic Substrate in Cardiac Sarcoidosis: Correlation With Imaging Findings of Scar and Inflammation.

OBJECTIVES: This study sought to characterize the electroanatomic (EAM) substrate in patients with cardiac sarcoidosis (CS) and ventricular tachycardia and its relationship to imaging findings of inflammation and fibrosis. BACKGROUND: CS is characterized by coexistence of active inflammation and replacement fibrosis. METHODS: A total of 42 patients with CS based on established criteria and ventricular tachycardia underwent high-density EAM mapping. Abnormal electrograms (EGM) were collected and independently classified as multicomponent fractionated, isolated, late, and split according to standard criteria and regardless of the peak-to-peak bipolar/unipolar voltage. A total of 29 patients (69%) underwent pre-procedural cardiac magnetic resonance (CMR) and positron emission tomography (PET)/computed tomography (CT). The distribution of EAM substrate was correlated with regions of late gadolinium enhancement (LGE) on CMR and increased 18F-fluorodeoxyglucose uptake on PET/CT. RESULTS: Of 21,451 bipolar and unipolar EGM, 4,073 (19%) were classified as abnormal with a predominant distribution in the basal perivalvular segments and interventricular septum. Using the standard bipolar (<1.5 mV) and unipolar (<8.3 mV for left ventricle <5.5 mV for the right) voltage cutoff values, 40% and 22% of the abnormal EGM were located outside the EAM low-voltage areas, respectively. LGE was present in 26 of 29 patients (90%), whereas abnormal 18F-fluorodeoxyglucose uptake in 14 of 29 patients (48%) with imaging. Segments with abnormal EGM had more LGE-evident scar transmurality [median: 24% (interquartile range [IQR]: 4% to 40%) vs. median: 5% (IQR: 0% to 15%); p < 0.001] and lower metabolic activity (median: 20 g glucose [IQR: 14 g to 30 g] vs. median: 29 g glucose [IQR: 18 g to 39 g]; p < 0.001). Overall, the agreement between the presence of abnormal EGM was higher with the presence of LGE (κ = 0.51; p < 0.001) than with the presence of active inflammation (κ = -0.12; p = 0.003). CONCLUSIONS: In patients with CS and ventricular tachycardia, pre-procedural imaging with CMR and PET/CT can be useful in detecting EAM abnormalities that are potential targets for substrate ablation. Abnormal EGM were more likely located in segments with more scar transmurality (LGE) at CMR and a lower degree of inflammation on PET.

Ventricular arrhythmias associated with left ventricular noncompaction: Electrophysiologic characteristics, mapping, and ablation.

BACKGROUND: Left ventricular noncompaction (LVNC) is a primary cardiomyopathy that can present with recurrent ventricular arrhythmias (VAs). Data on the benefit of catheter ablation of VAs in LVNC are lacking. OBJECTIVE: The purpose of this study was to describe the electrophysiologic features and outcomes of catheter ablation of VAs in LVNC. METHODS: The cohort consisted of 9 patients (age 42 ± 15 years) with diagnosis of LVNC based on established criteria and VA (ventricular tachycardia [VT] in 3 and frequent premature ventricular contractions (PVCs) in 6) despite treatment with a mean of 2 ± 1 antiarrhythmic drugs. Ablation sites were identified using a combination of entrainment, activation, late/fractionated potential ablation, and pace-mapping. RESULTS: A total of 8 patients (89%) had left ventricular (LV) systolic dysfunction (mean ejection fraction 40% ± 13%). Patients who presented with VT had evidence of abnormal electroanatomic substrate involving the mid- to apical segments of the LV, which matched the noncompacted myocardial segments identified by preprocedural magnetic resonance imaging or echocardiography. In patients presenting with frequent PVCs, the site of origin was identified at the papillary muscles (50%) and/or basal septal regions (67%). After median follow-up of 4 years (range 1-11) and a mean of 1.8 ± 1.1 procedures, VAs recurred in 1 patient (11%). Significant improvement in LV function occurred in 4 of 8 cases (50%). No patients died or underwent heart transplantation. CONCLUSION: The VA substrate in patients with LVNC and VT typically involves the mid-apical LV segments, whereas focal PVCs often arise from LV basal-septal regions and/or papillary muscles. Catheter ablation is safe and effective in achieving good VA control over long-term follow-up in most patients.

Multimodality Imaging for Guiding EP Ablation Procedures.

Recent advances in 3-dimensional electroanatomical mapping have been met by continuous improvements in the field of cardiac imaging and image integration during ablation procedures. Echocardiography, computed tomography, cardiac magnetic resonance, and nuclear imaging provide information about cardiac anatomy and ultrastructure of the heart that may be crucial for a successful ablation procedure. Techniques and value of pre-procedural, intraprocedural, and post-procedural imaging and image integration are discussed in this review article. Pre-procedural imaging provides key anatomic information that can be complemented by intraprocedural imaging to minimize procedural complications. Furthermore, the presence and extent of structural heart disease can be assessed pre-procedurally and can be displayed intraprocedurally to limit and focus the mapping and ablation procedure to the area of interest. Pre-procedural imaging combined with imaging obtained during the ablation procedure further enhances procedural safety, reduces exposure to ionizing radiation from fluoroscopy, reduces procedure time, and may improve outcomes.

Characterization of trans-septal activation during septal pacing: criteria for identification of intramural ventricular tachycardia substrate in nonischemic cardiomyopathy.

BACKGROUND: Identification of intramural basal-septal ventricular tachycardia (VT) substrate is challenging in nonischemic cardiomyopathy. We sought to (1) characterize normal/abnormal trans-septal right ventricular (RV) to left ventricular activation; (2) assess the effect of opposite RV pacing on left ventricular septal bipolar electrograms (EGMs); and (3) establish criteria for the identification of intramural septal VT substrate. METHODS AND RESULTS: Endocardial activation mapping and local EGM assessment of the left interventricular septum was performed during RV basal septal pacing in 40 patients undergoing VT ablation with no evidence of septal scar (group 1, n=14) and with septal scar (group 2, n=26) defined by low septal unipolar voltage (<8.3 mV) and delayed enhancement on cardiac MRI with/without abnormal bipolar voltage (<1.5 mV) in sinus rhythm. Left ventricular trans-septal activation time was prolonged in Group 2 compared with Group 1 (55.3±33.0 versus 25.7±8.8 ms; P=0.003). In 6 group 2 patients, left ventricular septal breakthrough was displaced to the scar border. During RV pacing, group 2 had fractionated (8.8%), late (2.8%), and split (5.7%) EGMs not seen in group 1. Trans-septal activation >40 ms (sensitivity 60%, specificity 100%; P<0.001) and EGM duration >95 ms during pacing (sensitivity 22%, specificity 91%; P<0.001) identified septal scar (13/26 pts). CONCLUSIONS: In patients with nonischemic cardiomyopathy, VT and septal scar, delayed transmural conduction time (>40 ms) and fractionated, late, split, and wide (>95 ms) bipolar EGMs during RV basal pacing identify intramural VT substrate. In select cases, the basal septum appears compartmentalized as the stimulated wavefront is rerouted to the scar border.

Characteristics of intramural scar in patients with nonischemic cardiomyopathy and relation to intramural ventricular arrhythmias.

BACKGROUND: Ventricular arrhythmias have been described to originate from intramural locations. Intramural scar can be assessed by delayed-enhanced MRI, but MRIs cannot be performed on every patient. The objective of this study was to assess the value of voltage mapping to detect MRI-defined intramural scar and to correlate the scar with ventricular arrhythmias. METHODS AND RESULTS: In 15 consecutive patients (3 women; age 55±16 years; ejection fraction, 49±13%) with structural heart disease, intramural scar was detected by delayed-enhanced MRI. All patients underwent endocardial unipolar and bipolar voltage mapping guided by the registered intramural scar. Scar volume by MRI was 11.7±8 cm3 with a scar thickness of 4.6±0.7 mm and a preserved endocardial/epicardial rim of 3.3±1.6 and 4.8±2.6 mm, respectively. Endocardial bipolar voltage was 1.6±1.73 mV at the scar, 2.12±2.15 mV in a 1 cm perimeter around the scar, and 2.83±3.39 mV in remote myocardium without scar. The corresponding unipolar voltage was 4.94±3.25, 6.59±3.81, and 8.32±3.39 mV, respectively (P<0.0001). Using receiver-operator characteristic curves, a unipolar cut-off value of 6.78 mV (area under the curve, 0.78) and a bipolar cut-off value of 1.55 mV (area under the curve, 0.69) best separated endocardial measurements overlying scar as compared with areas not overlying a scar. At least 1 intramural ventricular arrhythmia was eliminated in all but 2 patients in this series. CONCLUSIONS: Intramural scar can be detected by unipolar and bipolar voltage, unipolar voltage being more useful. Mapping and ablation of intramural arrhythmias originating from an intramural focus can be accomplished.

Delayed-enhanced MR scar imaging and intraprocedural registration into an electroanatomical mapping system in post-infarction patients.

Post-infarction arrhythmias are most often confined to scar tissue. Scar can be detected by delayed-enhanced cardiac magnetic resonance. The purpose of this study was to assess the feasibility of pre-procedural scar identification and intraprocedural real-time image registration with an electroanatomical map in 23 patients with previous infarction and ventricular arrhythmias (VAs). Registration accuracy and cardiac magnetic resonance/electroanatomical map correlations were assessed, and critical areas for VA were correlated with the presence of scar. With a positional registration error of 3.8 ± 0.8 mm, 86% of low-voltage points of the electroanatomical map projected onto the registered scar. The delayed-enhanced cardiac magnetic resonance-defined scar correlated with the area of low voltage (R = 0.82, p < 0.001). All sites critical to VAs projected on the registered scar. Selective identification and extraction of delayed-enhanced cardiac magnetic resonance defined scar followed by registration into a real-time mapping system are feasible and help to identify and display the arrhythmogenic substrate in post-infarction patients with VAs.

Septal involvement in patients with post-infarction ventricular tachycardia: implications for mapping and radiofrequency ablation.

OBJECTIVES: The purpose of this study was to assess the prevalence of the re-entry circuit within the interventricular septum in post-infarction patients referred for ventricular tachycardia (VT) ablation. BACKGROUND: Post-infarction ventricular tachycardia can involve the endocardial myocardium, the intramural myocardium, the epicardium, or the His Purkinje system. METHODS: Among 74 consecutive patients with recurrent post-infarction VT, 33 patients (45%) were identified in whom the critical part of the VT involved the interventricular septum. A total of 206 VTs were induced in these 33 patients. In 46 of the 206 VTs, a critical component was identified in the interventricular septum. The critical isthmus of the re-entry circuit was identified by entrainment mapping, activation mapping, or pace-mapping. RESULTS: In 32 of 46 VTs (70%), the critical component of the re-entry circuit was confined to the endocardium. In 9 of 46 VTs (20%), the critical component involved the Purkinje system, and in 5 of 46 VTs (11%), an intramural area was critical. Entrainment and/or pace-mapping helped to identify critical areas of endocardial VTs as well as VTs involving the Purkinje fibers, but neither of these mapping techniques localized intramural VTs. Electrocardiographic characteristics were specific for each of the septal locations. All VTs mapped to the interventricular septum were acutely successfully ablated. VTs recurred in 9 of 33 patients with septal VTs during a mean follow-up period of 40 ± 20 months. CONCLUSIONS: Post-infarction VT involving the interventricular septum can involve the endocardial muscle, Purkinje fibers, or intramural muscle fibers. Electrocardiographic characteristics differ depending on the type of tissue involved.

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 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. 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.

Endocardial unipolar voltage mapping to detect epicardial ventricular tachycardia substrate in patients with nonischemic left ventricular cardiomyopathy.

BACKGROUND: Patients with nonischemic left ventricular cardiomyopathy (LVCM) and ventricular tachycardia (Vt) have complex 3-dimensional substrate with variable involvement of the endocardium (ENDO) and epicardium (EPI). The purpose of this study was to determine whether ENDO unipolar (UNI) mapping with a larger electric field of view could identify EPI low bipolar (BIP) voltage regions in patients with LVCM undergoing Vt ablation. METHODS AND RESULTS: The reference value for normal ENDO unipolar voltage was determined from 6 patients without structural heart disease. Consecutive patients undergoing Vt ablation over an 8-year period with detailed (>100 points) LV ENDO and EPI mapping and normal LV ENDO BIP voltage were identified. From this cohort, we compared patients with structurally normal hearts and normal EPI BIP voltage (EPI-, group 1) with patients with LVCM and low LV EPI BIP voltage regions present (EPI+, group 2). Confluent regions of ENDO UNI and EPI BIP low voltage (>2 cm(2)) were measured. The normal signal amplitude was >8.27 mV for LV ENDO UNI electrograms. Detailed LV ENDO-EPI maps in 5 EPI- patients were compared with 11 EPI+ patients. Confluent ENDO UNI low-voltage regions were seen in 9 of 11 (82%) of the EPI+ (group 2) patients compared with none of 5 EPI- (group 1) patients (P<0.001). In all 9 patients with ENDO UNI low voltage, the ENDO UNI low-voltage regions were directly opposite to an area of EPI BIP low voltage (61% ENDO UNI-EPI BIP low-voltage area overlap). CONCLUSIONS: EPI arrhythmia substrate can be reliably identified in most patients with LVCM using ENDO UNI voltage mapping in the absence of ENDO BIP abnormalities.

Effect of left atrial circumferential ablation for atrial fibrillation on left atrial transport function.

BACKGROUND: The effects of left atrial (LA) circumferential ablation on LA function in patients with atrial fibrillation (AF) have not been well described. OBJECTIVES: The purpose of this study was to determine the effect of LA circumferential ablation on LA function. METHODS: Gated, multiphase, dynamic contrast-enhanced computed tomographic (CT) scans of the chest with three-dimensional reconstructions of the heart were used to calculate the LA ejection fraction (EF) in 36 patients with paroxysmal (n = 27) or chronic (n = 9) AF (mean age 55 +/- 11 years) and in 10 control subjects with no history of AF. Because CT scans had to be acquired during sinus rhythm, a CT scan was available both before and after (mean 5 +/- 1 months) LA circumferential ablation (LACA) in only 10 patients. A single CT scan was acquired in 8 patients before and in 18 patients after LACA ablation. Radiofrequency catheter ablation was performed using an 8-mm-tip catheter to encircle the pulmonary veins, with additional lines along the mitral isthmus and the roof. RESULTS: In patients with paroxysmal AF, LA EF was lower after than before LACA (21% +/- 8% vs 32 +/- 13%, P = .003). LA EF after LA catheter ablation was similar among patients with paroxysmal AF and those with chronic AF (21% +/- 8% vs 23 +/- 13%, P = .7). However, LA EF after LA catheter ablation was lower in all patients with AF than in control subjects (21% +/- 10% vs 47% +/- 5%, P < .001). CONCLUSION: During medium-term follow-up, restoration of sinus rhythm by LACA results in partial return of LA function in patients with chronic AF. However, in patients with paroxysmal AF, LA catheter ablation results in decreased LA function. Whether the impairment in LA function is severe enough to predispose to LA thrombi despite elimination of AF remains to be determined.