Macroreentrant Ventricular Tachycardia Research Articles

A non-invasive gateway to identifying potential substrates for macro-reentrant ventricular tachycardia in tetralogy of Fallot.

A non-invasive gateway to identifying potential substrates for macro-reentrant ventricular tachycardia in tetralogy of Fallot.

Rationale and Design of the Multicenter Catheter Ablation of Ventricular Tachycardia Before Transcatheter Pulmonary Valve Replacement in Repaired Tetralogy of Fallot Study

Patients with repaired tetralogy of Fallot are at elevated risk for ventricular arrhythmia and sudden cardiac death. Over the past decade, the pathogenesis and natural history of ventricular tachycardia has become increasingly understood, and catheter ablation has emerged as an effective treatment modality. Concurrently, there has been great progress in the development of a versatile array of transcatheter valves that can be placed in the native right ventricular outflow tract for the treatment of long-standing pulmonary regurgitation. Although such valve platforms may eliminate the need for repeat cardiac operations, they may also impede catheter access to the myocardial substrates responsible for sustained macro-reentrant ventricular tachycardia. This manuscript provides the rationale and design of a recently devised multicenter study that will examine the clinical outcomes of a uniform, preemptive strategy to eliminate ventricular tachycardia substrates before transcatheter pulmonary valve implantation in patients with tetralogy of Fallot.

Successful termination of ventricular tachycardia with intrinsic anti-tachycardia pacing

Intrinsic anti-tachycardia pacing (iATP) is a novel automated ATP algorithm that employs post-pacing interval (PPI) to design the next ATP sequence based on an analysis of the prior failed ATP sequence. A patient with hypertrophic cardiomyopathy received an implantable cardioverter-defibrillator (ICD) (Cobalt™ XT DR, Medtronic, Minneapolis, MN, USA) following an episode of syncope due to macro-reentrant ventricular tachycardia (VT) (right bundle branch block configuration, cycle length [CL] 280 ms). The VF zone was set to VTCL <300 ms and iATP therapy was prescribed before and during capacitor charging. The iATP was initiated when VT recurred 3 months later. The first attempt with an assumption of 150 ms propagation time from the pacing site to the VT circuit (9 pulses) could not reset the VT, leaving a PPI of 650 ms. A subsequent attempt involving 20 pulses with an assumption of 250 ms propagation time terminated the VT. Failure to reach the circuit is a major cause of unsuccessful ATP. In this regard, iATP is expected to have theoretical advantages over empirical and traditional ATP therapies. To the best of our knowledge, this is the first intracardiac electrogram illustrating how automated precision ATP terminates VT in a clinical setting.

Close-coupled pacing to identify the “functional” substrate of ventricular tachycardia: Long-term outcomes of the paced electrogram feature analysis technique

The conduction delay and block that compose the critical isthmus of macroreentrant ventricular tachycardia (VT) is partly "functional" in that they only occur at faster cycle lengths. Close-coupled pacing stresses the myocardium's conduction capacity and may reveal late potentials (LPs) and fractionation. Interest has emerged in targeting this functional substrate. The purpose of this study was to assess the feasibility and efficacy of a functional substrate VT ablation strategy. Patients with scar-related VT undergoing their first ablation were recruited. A closely coupled extrastimulus (ventricular effective refractory period + 30 ms) was delivered at the right ventricular apex while mapping with a high-density catheter. Sites of functional impaired conduction exhibited increased electrogram duration due to LPs/fractionation. The time to last deflection was annotated on an electroanatomic map, readily identifying ablation targets. A total of 40 patients were recruited (34 [85%] ischemic). Median procedure duration was 330 minutes (interquartile range [IQR] 300-369), and ablation time was 49.4 minutes (IQR 33.8-48.3). Median functional substrate area was 41.9 cm2 (IQR 22.1-73.9). It was similarly distributed across bipolar voltage zones. Noninducibility was achieved in 34 of 40 patients (85%). Median follow-up was 711 days (IQR 255.5-972.8), during which 35 of 39 patients (89.7%) did not have VT recurrence, and 3 of 39 (7.5%) died. Antiarrhythmic drugs were continued in 53.8% (21/39). Functional substrate ablation resulted in high rates of noninducibility and freedom from VT. Mapping times were increased considerably. Our findings add to the encouraging trend reported by related techniques. Randomized multicenter trials are warranted to assess this next phase of VT ablation.

Compartmentalized Structure of the Moderator Band Provides a Unique Substrate for Macroreentrant Ventricular Tachycardia

Background Papillary muscles are an important source of ventricular tachycardia (VT). Yet little is known about the role of the right ventricular (RV) endocavity structure, the moderator band (MB). The aim of this study was to determine the characteristics of the MB that may predispose to arrhythmia substrates. Methods Ventricular wedge preparations with intact MBs were studied from humans (n=2) and sheep (n=15; 40-50 kg). RV endocardium was optically mapped, and electrical recordings were measured along the MB and septum. S1S2 pacing of the RV free wall, MB, or combined S1-RV S2-MB sites were assessed. Human (n=2) and sheep (n=4) MB tissue constituents were assessed histologically. Results The MB structure was remarkably organized as 2 excitable, yet uncoupled compartments of myocardium and Purkinje. In humans, action potential duration heterogeneity between MB and RV myocardium was found (324.6±12.0 versus 364.0±8.4 ms; P<0.0001). S1S2-MB pacing induced unidirectional propagation via MB myocardium, permitting sustained macroreentrant VT. In sheep, the incidence of VT for RV, MB, and S1-RV S2-MB pacing was 1.3%, 5.1%, and 10.3%. Severing the MB led to VT termination, confirming a primary arrhythmic role. Inducible preparations had shorter action potential duration in the MB than RV (259.3±45.2 versus 300.7±38.5 ms; P<0.05), whereas noninducible preparations showed no difference (312.0±30.3 versus 310.0±24.6 ms, respectively). Conclusions The MB presents anatomic and electrical compartmentalization between myocardium and Purkinje fibers, providing a substrate for macroreentry. The vulnerability to sustain VT via this mechanism is dependent on MB structure and action potential duration gradients between the RV free wall and MB.

49 * Tachyarrhythmias in adults with previous rastelli repair: mechanistic insights from single center expereince

Introduction: Late arrhythmias are common in adults undergoing Rastelli repair with a right ventricle (RV) to pulmonary artery (PA) conduit. The mechanism of arrhythmias has not been described. We sought to describe the prevalence, clinical predictors and mechanisms of supraventricular (SVT) and ventricular tachycardia (VT) in this population. Methods: We retrospectively reviewed charts for adults (age >18 years) with discordant ventriculo-arterial connection (d-TGA (and double outlet RV), VSD and pulmonary stenosis (PS) that underwent Rastelli operations who were seen in our clinic. Twenty-nine patients (pts) [median age 28 (IQR 15) yrs, 59% male] were included. Results: Over median post-operative follow-up of 22 (IQR 9) yrs, 10 pts had arrhythmia (SVT=7, VT=1, both= 2). The median age at arrhythmia onset was 28 (IQR 11) yrs. Pts with arrhythmias were older than those without [36 (14) vs 24 (12) yrs, p=0.005] with greater time since surgery [26 (9) vs 19 (7) yrs, p=0.01]. The number of surgical interventions post-Rastelli [2 (2) vs 2 (1)], the LV and RV systolic function at last follow-up, the right ventricular size and systolic pressure, and the severity of pulmonary regurgitation grade were similar between pts with and without arrhythmias. The median follow-up time from arrhythmia onset was 4.5 (IQR 11) yrs. The majority of pts with SVT (7/9) were managed with medications. Two pts with SVT had catheter ablation. Both pts had multiple intra-atrial reentrant tachyarrhythmia (IART) (cavo-tricuspid isthmus dependent and incisional IART); more than one procedure was required to eliminate all IART. Two pts with VT were drug refractory and had ablation. One pt had a macro-reentrant VT around the RV-PA conduit (Figure 1A); the VT terminated during ablation with no recurrence after 9 years. The second pt underwent ablation twice with a focal/micro-reentrant VT- source from scar at the base of RV-PA conduit (Figure 1B) with no recurrence 8 months after the 2nd procedure. Conclusions: Tachyarrhythmias were seen in ≥ 1/3 of adults with Rastelli repair. The prevalence of arrhythmias increased with age. The mechanisms of SVT included CTI-dependent and incisional RA scar IART. The mechanisms of VT were macro-reentrant and focal, both originating around RV-PA conduit junction.

A case of a human ventricular fibrillation rotor localized to ablation sites for scar-mediated monomorphic ventricular tachycardia

Ventricular tachycardia (VT) and ventricular fibrillation (VF) are the most common causes of sudden cardiac death. Currently, knowledge of the reentrant mechanism of monomorphic VT circuits in relation to complex scar anatomy allows for various mapping techniques including electroanatomic and entrainment mapping to accomplish catheter ablation of VT.1, 2 Clinically, it may be observed that ablation to eliminate recurrent macro-reentrant VT may also eliminate recurrent VF, as defined for instance by electrograms from implanted cardioverter-defibrillators (ICD).3, 4 However, whether this represents elimination of the VT trigger for VF, or directly of the substrate for VF, is unclear since the mechanism of VF in relation to scar is not known. Recent work targeting localized rotors in atrial fibrillation ablation has shown promise,5 but its implications for VF are unknown. We report here a case where VT termination and a VF rotor occurred at spatially coincidental sites in a patient with ischemic cardiomyopathy, suggesting that VF rotors may localize to the same anatomic substrate that promotes VT.

Correspondence Between Simple 3-D MRI-Based Computer Models and In-Vivo EP Measurements in Swine With Chronic Infarctions

The aim of this paper was to compare several in-vivo electrophysiological (EP) characteristics measured in a swine model of chronic infarct, with those predicted by simple 3-D MRI-based computer models built from ex-vivo scans (voxel size <1 mm(3)). Specifically, we recorded electroanatomical voltage maps (EAVM) in six animals, and ECG waves during induction of arrhythmia in two of these cases. The infarct heterogeneities (dense scar and border zone) as well as fiber directions were estimated using diffusion weighted DW-MRI. We found a good correspondence (r = 0.9) between scar areas delineated on the EAVM and MRI maps. For theoretical predictions, we used a simple two-variable macroscopic model and computed the propagation of action potential after application of a train of stimuli, with location and timing replicating the stimulation protocol used in the in-vivo EP study. Simulation results are exemplified for two hearts: one with noninducible ventricular tachycardia (VT), and another with a macroreentrant VT (for the latter, the average predicted VT cycle length was 273 ms, compared to a recorded VT of 250 ms).

Successful Catheter Ablation of Focal Automatic Left Ventricular Tachycardia Presented with Tachycardia-Mediated Cardiomyopathy

Non-reentrant focal tachycardias occur spontaneously, facilitated by catecholamine infusion, but they cannot be initiated or terminated with programmed stimulation. These tachycardias exhibit early activation before the QRS, however, do not typically show the mid-diastolic potential that is crucial for reentrant tachycardia maintenance. Electrophysiological studies are useful for distinguishing focal from macro-reentrant ventricular tachycardia. We report herein a case of patient without a history of structural heart disease who presented with a focal Purkinje ventricular tachycardia and heart failure. The focal Purkinje ventricular tachycardia was eliminated by radiofrequency catheter ablation. All of the patien's symptoms were improved after ablation.

Radiofrequency Catheter Ablation of Ventricular Tachyarrhythmia Under Navigation Using EnSite Array

EnSite array (EA) provides virtual activation of ventricular tachycardia (VT) and premature ventricular contraction (PVC) on a beat-to-beat basis. Fifty-five consecutive patients (age 52+/-16 years) with 79 VTs/PVCs undergoing EA-guided radiofrequency catheter ablation (RFA) were studied, of whom 7 patients had organic heart diseases. A virtual activation map showed that 66 VTs/PVCs originated from the right ventricle (RV), including the RV outflow tract in 57, lateral wall of RV in 4, His bundle region in 3 and tricuspid annulus in 2. Ten VTs/PVCs originated from the left ventricle (LV), including the LV endocardium in 7 and aortic sinus cusp in 3. The origins of 3 PVCs, one each in 3 patients, were not identified. Six of 38 VTs were sustained and the remaining 32 VTs were non-sustained. RFA eliminated all but 3 focal PVCs, and all macroreentrant VTs at a critical conducting pathway, which was identified by the combined use of contact voltage and virtual activation maps. There were 11+/-9 applications, and the radiofrequency energy and fluoroscopy time were 11,354+/-13,360 J and 30+/-21 min, respectively. All patients with acute success were free of any symptoms during a follow up of 21+/-11 months. EA-guided RFA is safe and effective for VT/PVC, irrespective of its origin, mechanism, sustainability, hemodynamic condition, and underlying heart disease.

Segmental Conduction Block in a Low-Voltage Area Suppressed Macro-Reentrant Ventricular Tachycardia after Surgical Repair of Tetralogy of Fallot

Macro-reentrant ventricular tachycardia (VT) developed in a 20-year-old man, 17 years after surgical repair of tetralogy of Fallot. Activation mapping of the VT revealed its counterclockwise propagation around the right ventricle, and through a critical pathway between a transannular patch and the tricuspid annulus. This critical pathway was 6 cm long and contained myocardium with a normal amplitude, while the area of low voltage was limited adjacent to the transannular patch. A linear lesion was created by radiofrequency energy delivered only to the low voltage area. After ablation, the activation wavefront through the low voltage area was blocked, and VT became non-inducible.

Multiple macroreentrant ventricular tachycardias exhibiting centrifugal endocardial activations from the scar border zone after myocardial infarction

A 53-year-old man with a ventricular tachycardia (VT) electrical storm during the chronic phase of an extensive anteroseptal myocardial infarction underwent electrophysiologic testing and catheter ablation. An electroanatomical map during 7 induced macroreentrant VTs demonstrated multiple centrifugal endocardial activations from sites that were located at the circumferential border zone of a large scar area. Interestingly, during the radiofrequency catheter ablation of 4 of the VTs, the elimination of the substrate of the previous VTs converted one VT to another probably because those VTs might have shared a central common pathway of the macroreentrant circuit with different exits.

Macroreentrant ventricular tachycardia mimicking focal ventricular tachycardia in a case with arrhythmogenic right ventricular cardiomyopathy

A 67-year-old man with ventricular tachycardia (VT) due to arrhythmogenic right ventricular cardiomyopathy (ARVC) underwent electrophysiologic testing. Electroanatomic mapping during the VT seemed to reveal a focal mechanism from near the tricuspid annulus (TA). Several radiofrequency applications delivered at the presumed focus resulted in termination but re-induction of the VT. Additional electroanatomic mapping underneath the TA led to the diagnosis of macroreentrant VT. Several RF applications targeting isolated and late potentials observed there during sinus rhythm eliminated the VT. In ARVC cases, detailed mapping underneath the TA should be performed to reveal the VT mechanism, resulting in suppressing VT recurrences.

Ventricular Tachycardia With Participation of the Left Bundle‐Purkinje System in Patients With Structural Heart Disease: Identification of Slow Conduction During Sinus Rhythm

Idiopathic left ventricular tachycardia (VT) originating from the left posterior fascicle can be eliminated by ablation at sites with abnormal diastolic potentials (DPs) during sinus rhythm. We investigated whether such DPs can also be recorded in patients with structural heart disease and VT involving the left bundle-Purkinje system. Eight patients (mean age 67 +/- 11 years) with nonischemic cardiomyopathy (n = 5) or prior myocardial infarction (n = 3) presented with VT involving the left bundle-Purkinje system (cycle length 376 +/- 45 ms). Three types of VT were observed: macroreentrant VT with participation of both left bundle fascicles in three patients, fascicular VT involving the left posterior fascicle in two patients, and scar-related VT with Purkinje fibers as part of the reentrant circuit in three patients. In all patients, abnormal isolated DPs of low amplitude with a QRS-earliest DP interval of 374 +/- 86 ms were found during sinus rhythm in the mid- or inferior left ventricular septum in areas with Purkinje potentials. The abnormal DPs during sinus rhythm coincided or were in proximity to DPs during the VT in six patients. VT ablation targeting the sites with the earliest abnormal DPs during sinus eliminated the VT in 7 of 8 patients with freedom from VT recurrence in six patients during the follow-up of 11 +/- 5 months. Isolated DPs during sinus rhythm were found in proximity to the posterior Purkinje network in patients with VT involving the left bundle-Purkinje system associated with heart disease and can be used to guide successful catheter ablation.

Arrhythmias in Adult Patients With Congenital Heart Disease

By the time patients with congenital heart disease (CHD) reach adolescence and early adulthood, rhythm status has often become an active issue, if not the central issue, in their cardiac management. For some, arrhythmias are intrinsic to the structural malformation itself, as is the case with Wolff-Parkinson-White syndrome in the setting of Ebstein’s anomaly, or atrioventricular (AV) block in the setting of “congenitally corrected” transposition of the great arteries (L-TGA). For most other CHD patients, arrhythmias represent an acquired condition related to the unique myocardial substrate created by surgical scars in conjunction with cyanosis and abnormal pressure/volume loads of long duration. This review will attempt to address the major rhythm difficulties faced by adults with CHD, concentrating on electrophysiological features that distinguish CHD from more conventional forms of adult heart disease. A listing of specific arrhythmias and commonly associated congenital defects is provided in Table 1 to serve as an outline for the discussion. View this table: TABLE 1. Specific Arrhythmias and Associated Defects in Adults With Congenital Heart Disease As of 2001, there were estimated to be 800 000 adults with CHD living in the United States,1 a number that has grown steadily as more survivors of childhood surgery reach maturity. Of these, roughly 45% are considered to have mild forms of CHD (eg, atrial septal defect, valvar pulmonary stenosis), 40% are classified as having moderate disease (eg, tetralogy of Fallot, Ebstein’s anomaly), and 15% are considered to have complex disease (eg, single ventricle, transposition of the great arteries). Although arrhythmias can develop within any of the 3 subgroups, the incidence is highest for patients in the moderate and severe categories. Tetralogy of Fallot is an instructive example of moderate CHD with a large arrhythmia burden. As many as one third of patients with repaired tetralogy develop symptomatic atrial tachycardias by …

Catheter Ablation of Recipient Right Ventricular Tachycardia after Heterotopic Heart Transplantation

Ventricular tachycardia after heart transplantation. A case is reported of ventricular tachycardia (VT) in a 62-year-old male after heterotopic heart transplantation, who occasionally had attacks of palpitation. Surface electrocardiogram suggested VT arising from the recipient heart. Intracardiac electrograms and entrainment mapping confirmed macroreentrant VT located in the recipient right ventricle. Radiofrequency ablation using an electroanatomical mapping system (CARTO, Biosense Webster, Diamond Bar, CA, USA) successfully eliminated VT.

Mechanisms underlying ventricular arrhythmias in idiopathic dilated cardiomyopathy: implications for management.

Ventricular arrhythmias (VA) have been associated with mortality in idiopathic dilated cardiomyopathy (IDCM). All 3 main mechanisms of arrhythmogenesis - reentry, trigger activity, and automatism - have been implicated. Arrhythmogenic substrates in IDCM favor these mechanisms and are often potentiated by electrolyte imbalance secondary to diuretic treatment, by antiarrhythmic drugs, or by bradycardia, leading to polymorphic ventricular tachycardia (VT). Myocardial macroreentry is the mechanism most frequently responsible for monomorphic VT in IDCM; however, focal activation and His-Purkinje macroreentry are often responsible and, especially in the latter case, are frequently unrecognized. Clinical suspicion and final recognition by electrophysiologic testing have important therapeutic consequences, because both focal activation and His-Purkinje macroreentry can be treated effectively by catheter ablation. On the other hand, the frequent recurrences of myocardial macroreentrant VT after ablation require this therapy to be used in combination with drugs or an implantable cardioverter defibrillator (ICD). beta-Adrenoceptor antagonists (beta-blockers) have a beneficial effect for primary prevention of VA in IDCM. Type III antiarrhythmics have a neutral effect on mortality and type I antiarrhythmics should be avoided. Treatment of nonsustained VT in IDCM is controversial because it often presents without symptoms and is linked more to overall mortality than to arrhythmic mortality. Empiric treatment with amiodarone or electrophysiologically guided sotalol are preferred to the use of other drugs for secondary prevention of sustained VA. ICDs should be implanted in patients who have been resuscitated from cardiac arrest due to VA, or in those with poorly tolerated VT and severe left ventricular dysfunction. Empiric treatment with amiodarone or electrophysiologically guided class III antiarrhythmics may also be alternatives for patients with IDCM and no severe left ventricular dysfunction, especially if VT is well tolerated.

Identification and ablation of macroreentrant ventricular tachycardia with the CARTO electroanatomical mapping system.

Monomorphic ventricular tachycardias associated with regions of scar are most commonly due to reentry. Catheter based techniques have recently been described for mapping of reentry circuits. Fluoroscopic methods have obvious limitations when attempting to map large ventricular reentry circuit and localize target-sites of radiofrequency ablation. Three-dimensional right ventricular endocardial mapping was performed in a 38-year-old patient with ventricular tachycardia 28 years after surgical correction of tetralogy of Fallot by using the CARTO electroanatomical system. The map of electrogram voltage showed low amplitude electrograms over the anterior wall of the right ventricle extending into the right ventricular outflow tract, consistent with the location of the ventriculotomy scar. Recording of local activation time was combined with entrainment mapping to define the macroreentrant circuit during ventricular tachycardia. Since the activation propagated through a broad path around the right ventriculotomy scar, ablation was performed by creating a line of block, which was facilitated by tagging of the lesion sites on the endocardial activation map. Large ventricular reentry circuits can be identified and interrupted by creation of a line of block to interrupt a broad path. A practical approach to mapping combining analysis of electrogram voltage, activation sequence, and entrainment is presented.

Long-term results of radiofrequency catheter ablation in non-ischemic sustained ventricular tachycardia with underlying heart disease. Nonuniform arrhythmogenic substrate and mode of ablation.

This study examined 12 VTs in 8 patients who underwent radiofrequency (RF) catheter ablation for ventricular tachycardia (VT) associated with non-ischemic underlying heart diseases, and who were followed-up for more than 24 months after ablation. The site of VT origin was determined to be within a narrow site (within 1.0 x 1.0 cm) in 5 VTs (4 patients), but VT originated from a wide origin (more than 1.0 x 1.0 cm) in the other 5 VTs (3 patients). The remaining patient had two macroreentrant VTs revolving around an anatomical obstacle in both the clockwise and counterclockwise directions. Two of 5 VTs originating from a narrow site were successfully ablated by 2-3 RF applications. In VT associated with a wide origin, two perpendicular linear RF lesions with 6.0 +/- 1.8 RF applications were required to ablate the VT. Eight of the 12 VTs (66.7%) were finally ablated by RF current (30-50 watts), and they did not recur during the follow-up period of 31.2 +/- 6.5 months. An excellent long-term outcome is expected, even in VT associated with non-ischemic underlying heart disease, if VT is successfully treated by RF ablation.

Reentrant and focal mechanisms underlying ventricular tachycardia in the human heart.

To determine the mechanisms of ventricular tachycardia (VT) in humans, three-dimensional intraoperative mapping of up to 156 intramural sites was performed in 13 patients with healed myocardial infarction and refractory VT. Mapping was of sufficient density to define the mechanism of 10 VTs in eight patients. In five of 10 cases, sustained VT was initiated in the subendocardium or epicardium by intramural reentry with marked conduction delay as well as functional and anatomic block most prominent in the subendocardium and midmyocardium. The initiating beats of reentrant VT induced by programmed electrical stimulation arose in the endocardium or midmyocardium by progressive slowing of conduction leading to unidirectional block. Multiple simultaneous reentrant circuits can be present. In contrast, five of the 10 sustained VTs were initiated by a focal mechanism as defined by the absence of electrical activity between the termination of one beat and the initiation of the next despite the presence of multiple intervening intramural electrode recording sites. Comparisons of the mapping data with results of histopathological analysis of tissue demonstrated that the location of infarction as well as that of adjacent fibrotic muscle determined sites of both fixed and functional conduction block during macroreentrant VT and that slowing of conduction occurred in a direction transverse rather than longitudinal to fiber orientation. Both intramural reentry and a focal mechanism underlie sustained VT in patients with healed myocardial infarction.