Ventricular Tachycardia Substrate Research Articles

Ventricular Tachycardia in Coronary Artery Disease

The diagnosis, definition, localization, and management of postinfarct ventricular tachycardia (VT) in the patient with coronary artery disease depends critically on the surface 12-lead ECG. A systematic analysis of both the sinus rhythm and tachycardia ECGs provides much information that is critical for further decision making. The 12-lead ECG is used to exclude the other differential diagnostic possibilities, outline the substrate for postinfarct VT, define the likely region of VT exit from the scar border, as well as allow for detailed intracardiac analysis using entrainment and pace mapping during catheter ablation procedures.

Select Articles Published on the Topic of Arrhythmia and Electrophysiogy in 2013

Select Articles Published on the Topic of Arrhythmia and Electrophysiogy in 2013

Sinus rhythm detection of conducting channels and ventricular tachycardia isthmus in arrhythmogenic right ventricular cardiomyopathy

The identification of conducting channels (CCs) based on its relative high voltage or the presence of electrograms with delayed components has been proposed for substrate-guided scar-related ventricular tachycardia (VT) ablation. The relationship of these channels with the VT isthmuses remains unclear. To assess the link between CCs identified during sinus rhythm (SR) and VT isthmuses in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC). Twenty-two consecutive patients with ARVC undergoing substrate-guided VT ablation (scar dechanneling technique) were analyzed. High-density endocardial and epicardial electroanatomic maps were obtained during SR. Standard bipolar cutoff values (0.5-1.5 and <0.5 mV) were used to define border zone and dense scar. The CCs were identified by voltage threshold adjustment (voltage channels) or by tagging the electrograms with delayed components that are sequentially activated (late potential channels). A total of 87 CCs were identified; 65 (74.7%) of them on the epicardial surface. Twenty-four (27.6%) CCs were voltage channels, and compared with late potential CCs, these had a higher bipolar voltage (0.96 [0.48-1.29] mV vs 0.39 [0.26-0.50] mV; P < .001] and required more radiofrequency applications (5 [4-7] vs 3 [2-5]; P = .048]. Eighteen (90%) of 20 identified VT isthmuses were located on the epicardium. Only 8 (40%) VT isthmuses were related to a voltage CC. The remaining 12 (60%) VT isthmuses were linked to a late potential CC. Late potential CCs more frequently act as the VT substrate in ARVC and therefore should also be considered to guide SR substrate-guided ablation.

Characterization of Trans-septal Activation During Septal Pacing

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 (&lt;8.3 mV) and delayed enhancement on cardiac MRI with/without abnormal bipolar voltage (&lt;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 &gt;40 ms (sensitivity 60%, specificity 100%; P &lt;0.001) and EGM duration &gt;95 ms during pacing (sensitivity 22%, specificity 91%; P &lt;0.001) identified septal scar (13/26 pts). Conclusions— In patients with nonischemic cardiomyopathy, VT and septal scar, delayed transmural conduction time (&gt;40 ms) and fractionated, late, split, and wide (&gt;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.

Intramyocardial Adiposity After Myocardial Infarction

Background— Collagen has been attributed as the principal structural substrate of ventricular tachycardia (VT) after myocardial infarction (MI), even though adiposity of myocardium after MI is well recognized histologically. We investigated the effects of intramyocardial adiposity compared with collagen on electrophysiological properties, connexin43 expression, and VT induction after MI. Methods and Results— Simultaneous left ventricular plunge-needle, noncontact mapping was performed in sheep without MI (MI−; n=5), with MI and inducible VT (MI+VT+; n=7), and with MI and no inducible VT (MI+VT−; n=8). Histological intramyocardial quantity of adipose and collagen and degree of discontinuity were coregistered with electrophysiological parameters (MI+; 290 specimens). Additional assessment of connexin43 expression was performed. Left ventricular scar contained a body mass–independent abundance of adipocytes (adipose:collagen=0.8). Increased adipose density and discontinuity contributed to a greater inverse correlation ( r ) with conduction velocity ( r for adipose=0.39, r for discontinuity=0.45, r for collagen=0.26) and electrogram amplitude ( r for adipose=0.73, r for contiguity=0.77, r for collagen=0.68) compared with collagen. Collagen density was similar between the MI+ groups ( P &gt;0.29). However, the MI+VT+ group demonstrated a significant (all P ≤0.01) increase in adipose (8%) and discontinuity (qualitative) and decrease in conduction velocity (13%) and electrogram amplitude (21%) at MI borders compared with the MI+VT− group. In scar, myocytes adjacent to fibrofatty interfaces demonstrated increased connexin43 lateralization. A gradient increase in adipose was observed at sites that supported preferential presystolic VT activation and exhibited attenuation of excitation wavelength ( P &lt;0.001). Conclusions— Intramyocardial adiposity, in association with myocardial discontinuity within left ventricular scar borders, is a significant factor associated with altered electrophysiological properties, aberrant connexin43 expression, and increased propensity for VT after MI.

Circulation : Clinical Summaries

<i>Circulation</i> : Clinical Summaries

Characterization of Respiratory and Cardiac Motion from Electro-Anatomical Mapping Data for Improved Fusion of MRI to Left Ventricular Electrograms

Accurate fusion of late gadolinium enhancement magnetic resonance imaging (MRI) and electro-anatomical voltage mapping (EAM) is required to evaluate the potential of MRI to identify the substrate of ventricular tachycardia. However, both datasets are not acquired at the same cardiac phase and EAM data is corrupted with respiratory motion limiting the accuracy of current rigid fusion techniques. Knowledge of cardiac and respiratory motion during EAM is thus required to enhance the fusion process. In this study, we propose a novel approach to characterize both cardiac and respiratory motion from EAM data using the temporal evolution of the 3D catheter location recorded from clinical EAM systems. Cardiac and respiratory motion components are extracted from the recorded catheter location using multi-band filters. Filters are calibrated for each EAM point using estimates of heart rate and respiratory rate. The method was first evaluated in numerical simulations using 3D models of cardiac and respiratory motions of the heart generated from real time MRI data acquired in 5 healthy subjects. An accuracy of 0.6–0.7 mm was found for both cardiac and respiratory motion estimates in numerical simulations. Cardiac and respiratory motions were then characterized in 27 patients who underwent LV mapping for treatment of ventricular tachycardia. Mean maximum amplitude of cardiac and respiratory motion was 10.2±2.7 mm (min = 5.5, max = 16.9) and 8.8±2.3 mm (min = 4.3, max = 14.8), respectively. 3D Cardiac and respiratory motions could be estimated from the recorded catheter location and the method does not rely on additional imaging modality such as X-ray fluoroscopy and can be used in conventional electrophysiology laboratory setting.

Assessment of Ventricular Tachycardia Scar Substrate by Intracardiac Echocardiography

Intracardiac echocardiography (ICE) is increasingly used to guide complex ablation procedures. This study aimed to assess the scar substrate of ventricular tachycardia (VT) by ICE in patients undergoing VT ablation. In 22 patients undergoing VT ablation (10 ischemic, 12 nonischemic), the Biosense CARTOSOUND module (Biosense Webster, Diamond Bar, CA, USA) was used for three-dimensional reconstruction of the ventricles. The characteristics and appearance with ICE imaging of voltage-defined scar zones (bipolar voltage <0.5 mV), border zones (0.5-1.5 mV), and normal myocardium (>1.5 mV) on electroanatomic maps were evaluated. The standard image analysis software Image J (National Institutes of Health, Bethesda, MD, USA) was used to analyze signal intensity (mean pixel signal intensity unit [SIU]) and heterogeneity (standard deviation of signal intensity in analyzed area) on ICE images. A total of 83 myocardial areas were analyzed from two-dimensional ICE images (15 scars, 31 border zones, and 37 normal). Voltage-defined scar zones had increased signal intensities compared to border zones (149 SIU vs 104 SIU, P < 0.0001) and normal myocardium (88 SIU, P < 0.0001). Border zones were more likely to have heterogeneous densities compared to normal myocardium (standard deviation of signal intensity 20 SIU vs 12 SIU, P < 0.0001). In receiver-operator characteristic analyses, signal intensity ≥ 137 SIU differentiated scar from nonscar zones (area under curve 0.91, P < 0.0001). Software-based color enhancement of areas with signal intensity ≥ 137 SIU allowed identification of the VT substrate in all 15 patients with voltage-defined scar zones. ICE provides important information about the VT anatomical substrate and may have potential to identify areas of scarred myocardium.

Blockade of A2B adenosine receptor reduces left ventricular dysfunction and ventricular arrhythmias 1 week after myocardial infarction in the rat model

Remodeling occurs after myocardial infarction (MI), leading to fibrosis, dysfunction, and ventricular tachycardias (VTs). Adenosine via the A2B adenosine receptor (A2BAdoR) has been implicated in promoting fibrosis. To determine the effects of GS-6201, a potent antagonist of the A2BAdoR, on arrhythmogenic and functional cardiac remodeling after MI. Rats underwent ischemia-reperfusion MI and were randomized into 4 groups: control (treated with vehicle), angiotensin-converting enzyme inhibitor (treated with enalapril 1 day after MI), GS-6201-1d (treated with GS-6201 1 day after MI), GS-6201-1w (treated with GS-6201 administered 1 week after MI) . Echocardiography was performed at baseline and 1 and 5 weeks after MI. Optical mapping, VT inducibility, and histologic analysis were conducted at follow-up. Treatment with the angiotensin-converting enzyme inhibitor improved ejection fraction (57.8% ± 2.5% vs 43.3% ± 1.7% in control; P < .01), but had no effect on VT inducibility. Treatment with GS-6201 improved ejection fraction (55.6% ± 2.6% vs 43.3% ± 1.7% in control; P < .01) and decreased VT inducibility (9.1% vs 68.4% in control; P < .05). Conduction velocities were significantly higher at border and infarct zones in hearts of rats treated with GS-6201 than in those of other groups. The conduction heterogeneity index was also significantly lower in hearts of rats treated with GS-6201. Histologic analysis showed that while both GS-6201 and enalapril decreased fibrosis in the noninfarct zone, only GS-6201 reduced the heterogeneity of fibrosis at the border, which is consistent with its effect on VT reduction. Treatment with an A2BAdoR antagonist at 1 week results in the improvement in cardiac function and decreased substrate for VT. The inhibition of fibrogenesis by A2BAdoR antagonists may be a new target for the prevention of adverse remodeling after MI.

Robotically assisted ventricular tachycardia substrate modification ablation with the novel Lynx™ integrated sheath and RF ablation catheter : case report - online article

Catheter ablation of ventricular tachycardia (VT) is demanding and time consuming. Robotically controlled catheter ablation reduces operator fatigue and exposure to X-rays, and provides greater precision and stability of the catheter. A new flexible, integrated robotic sheath and ablation catheter has recently been introduced (Lynx(TM)) and used in atrial ablation procedures. We describe the first VT substrate modification ablation in the world with the Lynx(TM) robotic radio frequency ablation catheter.

Electrocardiographic left ventricular scar burden predicts clinical outcomes following infarct-related ventricular tachycardia ablation

Conducting channels within scars form the substrate for infarct-related ventricular tachycardia (VT) and are targeted during catheter ablation. Whether the amount of left ventricular scar (LVS) affects outcomes after VT ablation is not known. To test the hypothesis that increased LVS is associated with worsened clinical outcomes and reduced survival after VT ablation. Patients with coronary artery disease and intrinsic AV nodal conduction undergoing infarct-related VT ablation were studied. A validated 32-point scoring system was used to measure LVS from 12-lead ECGs. Primary endpoint was all-cause mortality or transplantation. Secondary endpoint was a composite of death, transplantation, or readmission due to VT recurrence within 1 year of discharge. Of 356 patients undergoing 466 infarct-related VT ablations screened, 192 (84% male, age 66 ± 11 years, 52% prior coronary artery bypass graft, ejection fraction 28% ± 11%) who underwent 245 procedures for VT (2.4 ± 1.5 VTs per patient, 31% with VT storm, refractory to 2.7 ± 1.2 antiarrhythmic drugs) between 1999 and 2009 were included. During mapping, all patients had low-voltage areas. Mean LVS was 21.4% ± 15.0%. Over 3.4 ± 3.1 years, 78 patients (41%) reached the primary endpoint (73 deaths, 5 transplants). In the first year after discharge, the secondary endpoint was reached in 56 subjects (29%). In a multivariate model, larger LVS (hazard ratio [HR] 1.03 for every 3% increase in LVS, P < .01), renal dysfunction (HR 2.66, P <.01), and increased age (HR 1.05 per year, P < .01) predicted mortality, whereas noninducibility of any VT was protective. (HR 0.36, P < .01) Larger LVS and renal dysfunction were associated with worsened 1-year outcomes, whereas noninducibility was protective. LVS burden derived from 12-lead ECGs is a significant and independent predictor of mortality and clinical outcomes in subjects with infarct-related VT.

Postinfarction Ventricular Tachycardia Substrate Characterization: A Comparison Between Late Enhancement Magnetic Resonance Imaging and Voltage Mapping Using an MR-Guided Electrophysiology System

Catheter ablation of ventricular tachycardia (VT) is preceded by characterization of the myocardial substrate via electroanatomical voltage mapping (EAVM). The purpose of this study was to characterize the relationship between chronic myocardial fibrotic scar detected by multicontrast late enhancement (MCLE) MRI and by EAVM obtained using an MR-guided electrophysiology system, with a final aim to better understand how these measures may improve identification of potentially arrhythmogenic substrates. Real-time MR-guided EAVM was performed in six chronically infarcted animals in a 1.5T MR system. The MCLE images were analyzed to identify the location and extent of the fibrotic infarct. Voltage maps of the left ventricle (LV) were created with an average of 231 ± 35 points per LV. Correlation analysis was conducted between bipolar voltage and three MR parameters (infarct transmurality, tissue categorization into healthy and scar classes, and normalized relaxation rate R1). In general, tissue regions classified as scar by normalized R1 values were well correlated with locations with low bipolar voltage values. Moreover, our results demonstrate that MRI information (transmurality, tissue classification, and relaxation rate) can accurately predict areas of myocardial fibrosis identified with bipolar voltage mapping, as demonstrated by ROC analysis. MCLE can help overcome limitations of bipolar voltage mapping including long durations and lower spatial discrimination and may help identify the sites within scars, which are commonly believed to trigger arrhythmic events in postinfarction patients.

ASSA13-02-21 Variations of Left Ventricular Conduction System and Markers of Successful Ablation in Patients with Verapamil–Sensitive Idiopathic Left Ventricular Tachycardia

Objective The substrates of verapamil-sensitive idiopathic left ventricular tachycardia (ILVT) had been shown involving a slow conduction zone (SCZ) and posterior Purkinje network. However, the variation of these was not understood. The purpose was to investigate the variation of the left ventricular conduction system (LVCS) and markers of successful ablation. Methods Electroanatomical mapping was performed during sinus rhythm in 20 patients with ILVT and 20 control subjects with paroxysmal supraventricular tachycardia. LVCS and SCZ were tagged and the anatomic aspects of them were investigated. Results According to the distribution of Purkinje potential, LVCS was distinguished into 3 types: 1: left bundle branch was divided into two discrete fascicles without interconnections; 2: was divided into three separate fascicles; 3: fanlike structure distribution over septum broadly. The length of left bundle branch and its fascicles in ILVT patients were slight longer than those of controls (P > 0.05). SCZ was located at inferoposterior septum in 17 patients with ILVT and 4 controls. The size of SCZ in the ILVT group was remarkably greater (P = 0.007) than those of the control group. Two SCZs were located at posterior and mid-septal in 2 patients, and inferior apical septum in 1 patient. At the crossover junction area with diastolic potential and Purkinje potential, with the size of 1.5 ± 0.4cm 2 , concealed entertainment and/or ablation were obtained successfully in all patients with patients. Conclusions The anatomy of LVCS and SCZ is variable in human subjects in particular those with ILVT. These variabilities suggest that the electrophysiological mechanism of ILVT is complex. While exact mechanism of reentry of ILVT was not confirmed because of the lack of the activation electroanatomic mapping, the crossover junction area with Purkinje potential and diastolic potential might be a marker of radiofrequency ablation of ILVT.

Specific organized substrates of ventricular fibrillation: Comparison of 320-slice CT heart images in non-ischemic ventricular fibrillation subjects with non-ischemic sustained and non-sustained ventricular tachycardia subjects

If specific organized substrates of ventricular-fibrillation (VF) are identified, they may provide important-information for prevention of sudden-cardiac-death. To identify specific organized substrates of VF, we compared 320-slice CT heart images in non-ischemic VF subjects with non-ischemic sustained and non-sustained ventricular-tachycardia (VT) subjects. Retrospective analysis of a total of 103 subjects who had VF (17 subjects; age, 59 ± 16 years), sustained VT (20 subjects; 62 ± 19 years), or non-sustained VT (66 subjects; 60 ± 15 years) underwent 320-slice CT (Aquilion one). After excluding 26 ischemic subjects with >50% stenosis in any coronary arteries on CT, myocardial infarction, or coronary vasospastic angina, a total of 77 non-ischemic subjects (12 VF subjects; age, 58 ± 18 years), (13 sustained VT subjects; 55 ± 20 years) or (52 non-sustained VT subjects; 58 ± 15 years) were analyzed. On CT, myocardial abnormal-late-enhancement was significantly more frequent in the VF group (75%, all myocardial abnormal-late-enhancement in left-ventricle) than in the sustained VT group (31%) and the non-sustained VT group (35%) (both P<0.01). Myocardial fatty change was significantly more frequent in the sustained VT group (54%) than in the VF group (17%) and the non-sustained VT group (12%) (both P<0.01). Final diagnoses of the non-ischemic VF and sustained groups included four subjects in each case with normal cardiac structure on transthoracic echocardiogram; the former included two subjects who had abnormal-late-enhancement on CT without specific ECG findings. Myocardial abnormal-late-enhancement and fatty change on CT may be substrates of VF or sustained VT in non-ischemic subjects. 320-slice CT can evaluate both coronary arteries and myocardium.

Towards cardiac and respiratory motion characterization from electrophysiology data for improved real time MR-integration

Background Electro-anatomical voltage mapping (EAM) is an invasive technique used for the identification of ventricular tachycardia (VT) substrate and subsequent guidance of VT ablation [1]. The mapping of VT substrate is very timeconsuming procedure, requires highly skilled electrophysiologist, is associated with patient risk and is an invasive procedure. Late gadolinium enhancement (LGE) MRI allows non-invasive evaluation of 3D structure of scar. Therefore, LGE has the potential to identify the VT substrate and can now be integrated in the current clinical platform for guidance of VT ablation as a roadmap. However, fusion of the two imaging modality is very challenging due to respiratory and cardiac motion during the mapping which results in large errors in data fusion. Our aim in this study is to develop a novel algorithm to detect the respiratory and cardiac-induced motion of the mapping catheter during the VT ablation to facilitate integration of LGE MRI to EAM data. Methods

Feasibility of real time integration of high-resolution scar images with invasive electrograms in electro-anatomical mapping system in patients undergoing ventricular tachycardia ablation

Background Ventricular tachycardia (VT) ablation is generally guided by invasive mapping of the left ventricle (LV) using electro-anatomical voltage mapping (EAM) to identify the VT substrate [1]. Late gadolinium enhancement (LGE) MRI allows excellent visualization of the scar. Heterogeneous area in LGE images has been shown to correlate with the VT substrate in animal models of VT. Retrospective studies in patients have also correlated the LGE signal enhancement to low voltage in EAM maps. However, current clinical EAM platform such as the Carto3 (Biosense Webster) does not allow integration of LGE images for facilitating the VT ablation. In this study, we described a workflow to integrate scar geometry extracted from highresolution 3D LGE images with EAM.

Simultaneous non-contact mapping fused with CMR derived grey zone to explore the relationship with ventricular tachycardia substrate in ischaemic cardiomyopathy

Background Cardiac magnetic resonance (CMR) imaging enables characterization of myocardial scar and the ‘grey zone’, an admixture of scar and healthy myocardium, which is an independent predictor of ventricular arrhythmia. We explored the relationship between the grey zone and ventricular tachycardia circuits (VT) in ischaemic cardiomyopathy. Methods Two patients with previous myocardial infarct underwent high-resolution late gadolinium enhanced CMR scar imaging (1.2x1.2x2.6mm) and a VT-stimulation study. The LV scar core was segmented using full-width-half-maximum method; and the grey zone was segmented with a cut-off signal intensity below that of the scar core and above 2 standard-deviation of the remote healthy myocardium. A multi-electrode array (MEA) was positioned in the LV cavity for simultaneous electroanatomical mapping during the study. The MEA shell was registered with the CMR-derived LV shell using anatomical landmark registration (Figure 1a,b) for comparison. Results Sustained monomorphic VT (SMVT) was induced in both patients. Scar core and grey zone regions correlated well with the low voltage area (≤ 30% maximum voltage) seen on the MEA (Figure 1a,c,d). The exit point during SMVT

The Substrate and Ablation of Ventricular Tachycardia in Patients With Nonischemic Cardiomyopathy

The term "nonischemic cardiomyopathy" (NICM) designates a myocardial disease characterized by mechanical and/or electrical dysfunction in the absence of significant coronary artery disease, valvular heart disease, hypertension, or congenital heart disease. Although sustained ventricular tachycardia (VT) occurs in only 5% of patients with NICM, it is an important cause of sudden cardiac death. In this review we summarize the current understanding of the anatomic and electrophysiologic substrates of VT in the different types of NICM. In addition, we discuss recent progress and experience with catheter ablation of VT in these patients.

Imaging-guided Ventricular Tachycardia Ablation.

Over the past decades important advances have been made in the field of ventricular tachycardia (VT) ablation, and as a result, VT ablation is now more widely being performed. The identification of ablation target sites still relies on electroanatomical substrate mapping, which is time-consuming, hampered by the intramural location of some scars and limited by epicardial fat. The potential of various imaging modalities to overcome these limitations have stimulated clinical electrophysiologists to perform studies on image integration during VT ablation. Imaging guidance has been used to identify, delineate and characterise the substrate for VT; to provide detailed anatomical information; to avoid ablation on coronary arteries; to delineate epicardial fat tissue; and to assess ablation lesions. In this review, reported applications and the potential advantages and limitations of different imaging modalities are discussed.

Improving the Resolution of Ventricular Tachycardia Substrate Mapping: Marrying (Ultra)Structure and Function

Improving the Resolution of Ventricular Tachycardia Substrate Mapping: Marrying (Ultra)Structure and Function