Radiofrequency Ablation Strategies for Intramural Ventricular Arrhythmias.

Catheter ablation is an established treatment strategy for ventricular arrhythmias. However, the presence of intramural substrate poses challenges with mapping and delivery of radiofrequency energy, limiting overall success of catheter ablation. Advances over the past decade have improved our understanding of intramural substrate and paved the way for innovative treatment approaches. Modifications in catheter ablation techniques and development of novel ablation technologies have led to improved clinical outcomes for patients with ventricular arrhythmias. In this review, we explore mapping techniques to identify intramural substrate and describe available radiofrequency energy delivery techniques that can improve overall success rates of catheter ablation.

Coronary Venous Mapping and Catheter Ablation for Ventricular Arrhythmias.

Catheter ablation is an effective treatment method for ventricular arrhythmias (VAs). These arrhythmias can often be mapped and targeted with ablation from the left and right ventricular endocardium. However, in some situations the VA site of origin or substrate may be intramural or epicardial in nature. In these cases, the coronary venous system (CVS) provides an effective vantage point for mapping and ablation. This review highlights situations in which CVS mapping may be helpful and discusses techniques for CVS mapping and ablation.

Electrical Substrate Ablation for Refractory Ventricular Fibrillation: Results of the AVATAR Study.

[Figure: see text].

Cardiopulmonary support in patients undergoing catheter ablation of poorly tolerated ventricular arrhythmias and electrical storm.

INTRODUCTION: Catheter ablation is an important treatment option for sustained ventricular arrhythmias (VA) that are refractory to pharmacological treatment; however, patients with fast VA or electrical storm (ES) are at risk for cardiogenic shock. We report our experience using cardiopulmonary support with extracorporeal membrane oxygenation (ECMO) during catheter ablation of VA. METHODS: Nineteen patients (mean age, 62 ± 10 years; 84% male) were referred to our center for CA of ES between January 2017 and April 2018. ES was defined as the occurrence of ≥3 ventricular tachycardia or ventricular fibrillation episodes requiring electrical cardioversion or defibrillation in a 24-hour period. ECMO support was implemented for all patients. RESULTS: CA of ES was completed in all patients. Activation mapping was performed for all VTs and substrate modification was performed by targeting sites identified by late/fragmented abnormal potentials. VTs were not inducible after ablation in 16 of 19 patients (84%). With regard to procedural complications, two patients underwent percutaneous angioplasty with stenting for a femoral artery dissection and one patient was treated for a dislodged ECMO arterial cannula and subsequent hemorrhagic shock. After a median follow-up of 10 months, three patients died from refractory heart failure and one patient died as a result of ES. Overall, the procedural success rate was 68% and the Kaplan-Meier mortality rate was 21%. CONCLUSIONS: ECMO support may be used for ablation procedures in patients with ES.

Epicardial Substrate as a Target for Radiofrequency Ablation in an Experimental Model of Early Repolarization Syndrome.

BACKGROUND: Early repolarization syndrome (ERS) is an inherited cardiac arrhythmia syndrome associated with sudden cardiac death. Approaches to therapy are currently very limited. This study probes the mechanisms underlying the electrocardiographic and arrhythmic manifestation of experimental models of ERS and of the ameliorative effect of radiofrequency ablation. METHODS: Action potentials, bipolar electrograms, and transmural pseudo-ECGs were simultaneously recorded from coronary-perfused canine left ventricular wedge preparations (n=11). The Ito agonist NS5806 (7-10 µmol/L), calcium channel blocker verapamil (3 µmol/L), and acetylcholine (1-3 µmol/L) were used to pharmacologically mimic the effects of genetic defects associated with ERS. RESULTS: The provocative agents induced prominent J waves in the ECG secondary to accentuation of the action potential notch in epicardium but not endocardium. Bipolar recordings displayed low-voltage fractionated potentials in epicardium because of temporal and spatial variability in appearance of the action potential dome. Concealed phase 2 reentry developed when action potential dome was lost at some epicardial sites but not others, appearing in the bipolar electrogram as discrete high-frequency spikes. Successful propagation of the phase 2 reentrant beat precipitated ventricular tachycardia/ventricular fibrillation. Radiofrequency ablation of the epicardium destroyed the cells displaying abnormal repolarization and thus suppressed the J waves and the development of ventricular tachycardia/ventricular fibrillation in 6/6 preparations. CONCLUSIONS: Our findings suggest that low-voltage fractionated electrical activity and high-frequency late potentials recorded from the epicardial surface of the left ventricle can identify regions of abnormal repolarization responsible for ventricular tachycardia/ventricular fibrillation in ERS and that radiofrequency ablation of these regions in left ventricular epicardium can suppress ventricular tachycardia/ventricular fibrillation by destroying regions of ER.

Efficacy of Endocardial Ablation of Drug-Resistant Ventricular Fibrillation in Brugada Syndrome: Long-Term Outcome.

Background Both endocardial trigger elimination and epicardial substrate modification are effective in treating ventricular fibrillation (VF) in Brugada syndrome. However, the primary approach and the characteristics of patients who respond to endocardial ablation remain unknown. Methods Among 123 symptomatic Brugada syndrome patients (VF, 63%; syncope, 37%), ablation was performed in 21 VF/electrical storm patients, the majority of whom were resistant to antiarrhythmic drugs. Results Careful endocardial mapping revealed that 81% of the patients had no specific findings, whereas 19% of the patients, who experienced the most frequent VF episodes with notching of the QRS in lead V1, had delayed low-voltage fractionated endocardial electrograms. Ablation of VF triggers followed by endocardial substrate modification was performed in the right ventricular outflow tract in 85% of the cases and in the right ventricle in 15%. VF triggers could not be completely eliminated in 1 patient and VF became noninducible in 14 (88%) patients among 16 patients who underwent VF induction with normalization of Brugada-type ECG in 3. During follow-up (56.14±36.95 months), VF recurrence was observed in 7 patients. Importantly, all patients who had nothing of QRS in lead V1 did not respond to endocardial ablation despite presence of VF-triggering ectopic beats during ablation. Conclusions With careful documentation of VF-triggering ectopic beats and detailed endocardial mapping, endocardial VF trigger elimination followed by endocardial substrate modification has an excellent long-term outcome, whereas presence of QRS notching in lead V1 was associated with high VF recurrence suggesting epicardial substrate ablation as effective initial approach.

Heterogeneous distribution of substrates between the endocardium and epicardium promotes ventricular fibrillation in arrhythmogenic right ventricular dysplasia/cardiomyopathy.

Aims: Whether the distribution of scar in arrhythmogenic right ventricular cardiomyopathy (ARVC) plays a role in predicting different types of ventricular arrhythmias is unknown. This study aimed to investigate the prognostic value of scar distribution in patients with ARVC. Methods and results: We studied 80 consecutive ARVC patients (46 men, mean age 47 ± 15 years) who underwent an electrophysiological study with ablation. Thirty-four patients receive both endocardial and epicardial mapping. Abnormal endocardial substrates and epicardial substrates were characterized. Three groups were defined according to the epicardial and endocardial scar gradient (<10%: transmural, 10-20%: intermediate, >20%: horizontal, as groups 1, 2, and 3, respectively). Sinus rhythm electrograms underwent a Hilbert-Huang spectral analysis and were displayed as 3D Simultaneous Amplitude Frequency Electrogram Transformation (SAFE-T) maps, which represented the arrhythmogenic potentials. The baseline characteristics were similar between the three groups. Group 3 patients had a higher incidence of fatal ventricular arrhythmias requiring defibrillation and cardiac arrest during the initial presentation despite having fewer premature ventricular complexes. A larger area of arrhythmogenic potentials in the epicardium was observed in patients with horizontal scar. The epicardial-endocardial scar gradient was independently associated with the occurrence of fatal ventricular arrhythmias after a multivariate adjustment. The total, ventricular tachycardia, and VF recurrent rates were higher in Group 3 during 38 ± 21 months of follow-up. Conclusion: For ARVC, the epicardial substrate that extended in the horizontal plane rather than transmurally provided the arrhythmogenic substrate for a fatal ventricular arrhythmia circuit.

Efficacy of an Anatomical Approach in Radiofrequency Catheter Ablation of Idiopathic Ventricular Arrhythmias Originating From the Left Ventricular Outflow Tract.

BACKGROUND: When anatomic obstacles preclude radiofrequency catheter ablation of idiopathic ventricular arrhythmias (VAs) originating from the left ventricular outflow tract (LVOT), an alternative approach from the anatomically opposite side (endocardial versus epicardial or above versus below the aortic valve) may be considered (anatomic ablation). The purpose of this study was to investigate the efficacy of an anatomic ablation in idiopathic LVOT VAs. METHODS AND RESULTS: We studied 229 consecutive patients with idiopathic LVOT VAs. Radiofrequency ablation from the first suitable site was successful in 190 patients, and in the remaining 39 patients, it was unsuccessful or had to be abandoned because of anatomic obstacles. In 22 of these 39 patients, an anatomic ablation was successful, and the VA origins were located in the intramural LVOT in 17 patients, basal left ventricular summit in 4, and LVOT septum near the His bundle in 1. The anatomic ablation was highly successful for idiopathic VAs originating from the intramural LVOT (>75%) and lateral LVOT, whereas it was unlikely to be successful for idiopathic VAs originating from the basal left ventricular summit (25%) and sepal LVOT. CONCLUSIONS: When a standard catheter ablation targeting the best electrophysiological measure of idiopathic LVOT VAs was unsuccessful or had to be abandoned because of anatomic obstacles, an anatomic ablation was moderately successful. These idiopathic LVOT VAs with a successful anatomic ablation commonly arose from the intramural LVOT among the left coronary cusp, aortomitral continuity, and epicardium, occasionally the basal left ventricular summit, and rarely the LVOT septum near the His bundle.

Irrigated Needle Ablation Creates Larger and More Transmural Ventricular Lesions Compared With Standard Unipolar Ablation in an Ovine Model.

BACKGROUND: Ventricular tachycardia recurrence can occur after ventricular tachycardia ablation because of incomplete and nontransmural ventricular lesion formation. We sought to compare the lesions made by a novel irrigated needle catheter to conventional radiofrequency lesions. METHODS AND RESULTS: Thirteen female sheep (4.6±0.7 years, 54±8 kg) were studied. In 7 sheep, 60-s radiofrequency applications were performed using an irrigated needle catheter. In 6 sheep, conventional lesions were made using a 4-mm irrigated catheter. 1.5T in vivo and high-density magnetic resonance imaging (9.4T) were performed on explanted hearts from animals receiving needle radiofrequency. Conventional lesion volume was calculated as (1/6)×π×(A×B(2)+C×D(2)/2). Needle lesion volume was measured as Σ(π×r(2))/2 with a slice thickness of 1 mm. The dimensions of all lesions were also measured on gross pathology. Additional histological analysis of the needle lesions was performed. One hundred twenty endocardial left ventricular ablation lesions (conventional, n=60; needle, n=60) were created. At necropsy, more lesions were found using needle versus conventional radiofrequency (90% versus 75%; P<0.05). Comparing needle versus conventional radiofrequency: lesion volume was larger (1030±362 versus 488±384 mm(3); P<0.001), lesion depth was increased (9.9±2.7 versus 5±2.4 mm; P<0.001), and more transmural lesions were created (62.5% versus 17%; P<0.01). Pericardial contrast injection was observed in 4 apical attempts using needle radiofrequency, however, with no adverse effects. Steam pops occurred in 3 attempts using conventional radiofrequency. CONCLUSIONS: Irrigated needle ablation is associated with more frequent, larger, deeper, and more often transmural lesions compared with conventional irrigated ablation. This technology might be of value to treat intramural or epicardial ventricular tachycardia substrates resistant to conventional ablation.

Mapping and ablating ventricular premature contractions that trigger ventricular fibrillation: trigger elimination and substrate modification.

Ventricular fibrillation (VF) is a malignant arrhythmia, usually initiated by a ventricular premature contraction (VPC) during the vulnerable period of cardiac repolarization. Ablation therapy for VF has been described and increasingly reported. Targets for VF triggers are VPC preceded Purkinje potentials or the right ventricular outflow tract (RVOT) in structurally normal hearts, and VPC triggers preceded by Purkinje potentials in ischemic cardiomyopathy. The most important issue before the ablation session is the recording of the 12-lead electrocardiogram (ECG) of the triggering event, which can prove invaluable in regionalizing the origin of the triggering VPC for more detailed mapping. In cases where the VPC is not spontaneous or inducible, ablation may be performed by pacemapping. During the session, mapping should be focused on the earliest activation and determining the earliest potential is the key to a successful ablation. However, a modification of the Purkinje network might be applied when the earliest site cannot be determined or is located close to the His-bundle. Furthermore, the electrical isolation of the pulmonary artery (PA) can suppress RVOT type polymorphic ventricular tachycardia in some patients with rapid triggers from the PA. Suppression of VF can be achieved by not only the elimination of triggering VPCs, but also by substrate modification of possible reentry circuits in the Purkinje network, or between the PA and RVOT. Further studies are needed to evaluate the precise mechanisms of this arrhythmia.

Ablation of ventricular arrhythmias.

Ventricular arrhythmias (VAs) commonly occur in patients with structural heart disease and may present as ventricular premature depolarizations (VPDs), monomorphic ventricular tachycardia (VT), or polymorphic VT/ventricular fibrillation. Idiopathic VAs can also occur in patients with normal hearts. This review explores the etiology, clinical presentation, and management strategies for different types of VAs. Medical and invasive treatment strategies are discussed, and different approaches to catheter ablation are outlined. While ablation of VPDs and idiopathic VT provides a cure for the majority of patients, investigation is ongoing to define the optimal ablation strategy for patients with scar-related VT.

Mapping and ablation of ventricular fibrillation-how and for whom?

The involvement of the Purkinje system in a subset of patients with idiopathic ventricular fibrillation or polymorphic VT/VF related to structural heart disease was first demonstrated in the pioneering work of Michel Haissaguerre and co-workers (Circulation 106:962-967, 2002 and Lancet 359:677-678, 2002). It is very important to identify these patients with recurrent episodes of ventricular fibrillation and/or ICD shocks with regard to the presence of triggering premature ventricular contractions (PVC), which may be amenable to mapping and catheter ablation by screening Holter and ICD recordings. The practical problem, which is frequently encountered, is the absence of these PVCs when the patients are brought to the EP lab. However, catheter ablation is an important adjunctive tool to antiarrhythmic drug treatment, beta blocker therapy, and general anesthesia in this setting. Local electrogram criteria related to this phenomenon have been identified guiding mapping and ablation (e.g., low amplitude, high-frequency Purkinje potentials preceding a closely coupled ventricular signal (Fig. 1a)). The favorable long-term follow-up after catheter ablation has been demonstrated in the setting of right and left ventricular Purkinje-related PVCs leading to polymorphic VT/VF (Leenhardt et al., Circulation 89:206-215, 1994) and also following myocardial infarction (Baensch et al., Circulation 108:3011-3016, 2003) and right ventricular outflow tract-associated VF (Noda et al., Journal of the American College of Cardiology 46:1288-1294, 2005). Most recently, epicardial ablation strategies leading to suppression of polymorphic VT/VF episodes related to the Brugada syndrome have been described irrespective to the presence of premature ventricular beats (Nademanee et al., Circulation 123:1270-1279, 2011).

Suppression of ventricular fibrillation by electrical modification of the Purkinje system in hypertrophic cardiomyopathy.

A 56-year-old man in hypertrophic cardiomyopathy had an electrical storm caused by ventricular fibrillation (VF). Mapping during the initiation of the VF triggered by a premature ventricular contraction (PVC1), with right bundle branch block (RBBB)-like morphology and superior axis, demonstrated a prominent Purkinje-muscle junction (PMJ) delay at the distal portion of the left posterior fascicle. Delivery of radiofrequency (RF) energy to this area abolished the VF triggered by the PVC1. However, VF emerged by triggering another PVC (PVC2) with RBBB-like morphology and inferior axis. Similarly, the initiation of VF was associated with the PMJ delay at the peripheral left anterior fascicle, where RF delivery completely suppressed the VF. The PMJ delay and subsequent Purkinje-muscle reentry-like activity could be essential for the initiation of the Purkinje-related VF.

An organized approach to the localization, mapping, and ablation of outflow tract ventricular arrhythmias.

The outflow tract (OT) regions of the right and left ventricles, common sites of origin for idiopathic ventricular arrhythmias (VA), have complex three-dimensional anatomical relationships. The understanding of in situ or "attitudinal" relationships not only informs the electrocardiographic interpretation of VA site of origin, but also facilitates their catheter-based mapping and ablation strategies. By viewing each patient as his or her own "control," the expected changes in ECG morphology (i.e., frontal plane QRS axis and precordial transition) between adjacent intracardiac structures (e.g., RVOT and aortic root) can be reliably predicted. Successful mapping of OT VAs involve a combination of activation and pacemapping guided by fluoroscopy, electroanatomical mapping, and intracardiac echocardiography. The purpose of this manuscript is to provide a simple, reliable strategy for catheter based mapping and ablation of OT VAs. We also discuss 2 specific challenges in OT VA mapping: (1) differentiating posterior RVOT from right coronary cusp VA origin; and (2) mapping VAs originating from the LV summit.

Renal sympathetic denervation as an adjunct to catheter ablation for the treatment of ventricular electrical storm in the setting of acute myocardial infarction.

We present a case of ventricular storm (VS) in a patient with acute ST-elevation myocardial infarction (STEMI). After initial successful thrombus extraction and percutaneous coronary intervention (PCI) of the proximal left anterior descending (LAD) coronary artery, a 63-year-old male patient showed recurrent monomorphic ventricular tachycardia (VT) and fibrillation (VF) episodes refractory to antiarrhythmic drug therapy. After initial successful VT ablation, fast VT and VF episodes remained an evident problem despite maximum antiarrhythmic drug therapy. Due to an increasing instability, renal sympathetic denervation (RDN) was performed. ICD interrogation and 24-hour Holter monitoring excluded recurrent episodes of VT or VF at a 6-month follow-up (FU) after discharge. This case highlights that RDN was effective and safely performed in a hemodynamically unstable patient with VS after STEMI and adjunct catheter ablation. RDN may open a new avenue for an adjunctive interventional bailout treatment of such highly challenging patients.

Rotors and the dynamics of cardiac fibrillation.

The objective of this article is to present a broad review of the role of cardiac electric rotors and their accompanying spiral waves in the mechanism of cardiac fibrillation. At the outset, we present a brief historical overview regarding reentry and then discuss the basic concepts and terminologies pertaining to rotors and their initiation. Thereafter, the intrinsic properties of rotors and spiral waves, including phase singularities, wavefront curvature, and dominant frequency maps, are discussed. The implications of rotor dynamics for the spatiotemporal organization of fibrillation, independent of the species being studied, are described next. The knowledge gained regarding the role of cardiac structure in the initiation or maintenance of rotors and the ionic bases of spiral waves in the past 2 decades, as well as the significance for drug therapy, is reviewed subsequently. We conclude by examining recent evidence suggesting that rotors are critical in sustaining both atrial and ventricular fibrillation in the human heart and its implications for treatment with radiofrequency ablation.

Endocardial mapping and catheter ablation for ventricular fibrillation prevention in Brugada syndrome.

UNLABELLED: Endocardial Mapping and Ablation of Brugada Syndrome. INTRODUCTION: Brugada syndrome (BS) is characterized by ST-segment elevation in the right precordial electrocardiogram (ECG) leads and episodes of ventricular fibrillation (VF). This study aimed to observe the feasibility of substrate modification by radiofrequency catheter ablation and its effects on VF storm. METHODS AND RESULTS: Ten BS patients (all men; median age 36.5 years) with VF storm (group I, n = 4) and no VF storm (group II, n = 6) were enrolled in the study between August 2007 and December 2008. All patients underwent electrophysiological study using noncontact mapping. The multielectrode array was placed in the right ventricular outflow tract (RVOT). The isopotential map was analyzed during sinus rhythm and the region that had electrical activity occurring during J point to +60 (J+60) milliseconds interval of the V1 or V2 of surface ECG was considered as the late activation zone (LAZ) and also the substrate for ablation. LAZ was found in RVOT with variable distribution in both groups. Endocardial catheter ablation of the LAZ modified Brugada ECG pattern in 3 of 4 patients (75%) and suppressed VF storm in all 4 patients in group I during long-term follow-up (12-30 months). One patient had complete right bundle branch block from the ablation procedure. CONCLUSIONS: LAZ on RVOT identified by noncontact mapping may serve as potential VF substrate in BS patients with VF episodes. Radiofrequency ablation on LAZ normalized ECG, suppressed VF storm, and reduced VF recurrence. The procedure is safe and may prevent VF occurrence.

Two distinct electrocardiographic forms of idiopathic ventricular arrhythmia originating in the vicinity of the His bundle.

AIM: The objective is to assess electrocardiographic characteristics predicting the precise location of ventricular arrhythmia (VA) origin within the right ventricle (RV) close to the His bundle (HB) region. METHODS AND RESULTS: Twenty-five patients (14 men, age 65 ± 14 years) underwent successful catheter ablation of para-Hisian VA. Ventricular arrhythmias were considered to arise in the vicinity of the HB region based on the criteria that mapping exhibited the earliest RV activation before QRS onset in the HB region. Surface 12-lead electrocardiogram during the para-Hisian VAs was analysed. Of the 25 patients, 8 originated from the RV antero-septum just above the HB region, and 17 arose from the RV mid-septum just below the HB region. There was no significant difference in precedence of the local ventricular electrogram of the HB region from the onset of surface QRS during VAs. Surface electrocardiographic findings were characterized according to R-wave amplitude in lead I (0.43 ± 0.18 vs. 0.67 ± 0.19 mV, P = 0.005), mean R-wave amplitude in inferior leads (1.12 ± 0.32 vs. 0.71 ± 0.24 mV, P = 0.002), R-wave amplitude ratio of leads III/II (0.77 ± 0.10 vs. 0.50 ± 0.23, P = 0.005), incidence of S-wave in lead III [1/8 (13%) vs. 16/17 (94%), P < 0.001], and QS morphology in lead V1 [3/8 (38%) vs. 17/17 (100%), P = 0.001]. CONCLUSIONS: Despite their adjacent locations, para-Hisian VAs could be classified into two subgroups with distinctive electrocardiographic characteristics according to origin either above or below the HB region. The present findings can be helpful for planning catheter ablation of para-Hisian VAs, and can reduce the risk of inadvertent atrioventricular block.