Right Ventricular Outflow Tract Region Research Articles

Novel strategy of remote magnetic navigation-guided ablation for ventricular arrhythmias from right ventricle outflow tract

The optimized strategy to further increase the success rate of ablation for ventricular arrhythmias (VAs) from the right ventricular outflow tract (RVOT) is challenging. Recent studies have shown that the pulmonary sinus cusp (PSC) region may be the origin of certain RVOT VAs. We evaluated the efficacy of preferential ablation below the pulmonary valve (PV) and alternated radiofrequency delivery in the PSC using remote magnetic navigation (RMN). Sixty-five (65) consecutive patients experiencing VAs with RVOT-like appearance were included in this study. Mapping and ablation were preferentially performed below the PV. Ablation in the PSC would only be attempted when intensified ablation below the PV could not eliminate VAs. Finally, if ablation in the RVOT region failed, the aortic sinus cusp (ASC) would be mapped. Sixty-one (61) of 65 (93.8%) patients achieved procedural success. Except 7 cases of which the VAs were ablated in the ASC, the rest 54 VAs were thought to be originate from the RVOT region. Fifty (50) of 54 VAs were successfully ablated below the PV, and in the presence of a local special signal in the bipolar electrogram a more aggressive ablation was required. Subsequent ablation in the PSC with assistance of the RMN system achieved success in the remaining 4 patients. No complications occurred in this study. Our strategy of using RMN-guided ablation below the PV for VAs of RVOT origin was proved to be effective. PSC mapping and ablation using a magnetic catheter may provide the optimal strategy for treating these types of arrhythmias.

Catheter ablation in highly symptomatic Brugada patients: a Dutch case series.

In the past few years, promising results were described in targeting the arrhythmogenic substrate of the epicardial right ventricular outflow tract (RVOT) region in patients with Brugada syndrome (BrS). In this report, we describe our experience with endo- and epicardial substrate mapping and ablation in a series of highly symptomatic BrS patients. This case series consists of seven patients with clinical BrS diagnosis who underwent catheter ablation in two Dutch hospitals (Isala hospital Zwolle; and Amsterdam University Medical Centre, location AMC, Amsterdam) and Hamad Heart Hospital in Qatar between 2013 and 2017. All patients had an ICD and recurrent ventricular arrhythmia (VA) episodes. All patients underwent endo-and epicardial mapping of the RVOT region. Elimination of all abnormal potentials and disappearance of BrS ECG pattern during the ablation procedure was the aimed endpoint. The study group consisted of seven patients with mean age 45.6 ± 16.9years. Five patients had SCN5A mutations. One patient was excluded from analysis, since ablation could not be performed due to a very large low-voltage area and was later diagnosed with arrhythmogenic right ventricular cardiomyopathy, associated with an SCN5A mutation. One patient underwent both endo- and epicardial ablation to eliminate VA. During a mean follow-up of 3.6 ± 1.5years, 5/6 patients remained VA free with two patients continuing quinidine. In patients with BrS and drug-refractory VA, ablation of the arrhythmogenic substrate in the RVOT region was associated with excellent long-term VA-free survival. The majority of these highly symptomatic BrS patients had an SCN5A mutation and also low-voltage areas epicardially.

Evaluation of the Mandibular Incisive Canal by Panoramic Radiography and Cone-Beam Computed Tomography

Background: Radiofrequency ablation (RFA) in Brugada syndrome (BrS) has been performed both endocardially and epicardially. The substrate in BrS is thus unclear. Objectives: To investigate the functional endocardial substrate and its correlation with clinical, electrophysiological and ECG findings in order to guide an endocardial ablation. Methods: Thirteen patients (38.7±12.3 years old) with spontaneous type 1 ECG BrS pattern, inducible VF with programmed ventricular stimulation (PVS) and syncope without prodromes were enrolled. Before to endocardial mapping the patients underwent flecainide testing with the purpose of measuring the greatest ST-segment elevation for to be correlated with the size and location of substrate in the electro-anatomic map. Patients underwent endocardial bipolar and electro-anatomic mapping with the purpose of identify areas of abnormal electrograms (EGMs) as target for RFA and determine the location and size of the substrate. Results: When the greatest ST-segment elevation was in the 3rd intercostal space (ICS), the substrate was located upper in the longitudinal plane of the right ventricular outflow tract (RVOT) and a greatest ST-segment elevation in 4th ICS correspond with a location of substrate in lower region of longitudinal plane of RVOT. A QRS complex widening on its initial and final part, with prolonged transmural and regional depolarization time of RVOT corresponded to the substrate locateded in the anterior-lateral region of RVOT. A QRS complex widening rightwards and only prolonged transmural depolarization time corresponded with a substrate located in the anterior, anterior-septal or septal region of RVOT. RFA of endocardial substrate suppressed the inducibility and ECG BrS pattern during 34.7±15.5 months. After RFA, flecainide testing confirmed elimination of the ECG BrS pattern. Endocardial biopsy showed a correlation between functional and ultrastructural alterations in two patients.

Microstructural substrate in RVOT for Brugada syndrome

Brugada syndrome is linked to ventricular fibrillation (VF), a precursor to sudden cardiac death. This patient population suffers from electrical abnormalities originating from the right ventricular outflow tract (RVOT). The mechanisms underlying such arrhythmic activity remain unclear, but clinical electrophysiological observations have indicated conduction abnormalities in the RVOT. To mimic sub-clinical epicardial microstructural defects in the RVOT to provide a substrate for conduction delay as a possible mechanism of BrS. Dual coronary-perfused left and right ventricular wedge preparations were studied in 20 pigs (35–45 kg). Patchy microlesions were created through an array of ablation needles in either the RVOT, right ventricle (RV) or both (DOUBLE ablation) and compared to a control group in the absence of ablation. Paced and arrhythmic activity were assessed by optical mapping of the epicardial surface in the presence and absence of the sodium channel blocker, flecainide. At baseline, the action potential duration (APD80) is shorter in the RVOT region compared to the RV free wall (209.8 ms ± 26.91 vs. 212.6 ± 37.19, P = 0.026). APD80 of the RVOT is prolonged by ablation (228.1 ms ± 23.02 for RVOT ablation and 231.2 ms ± 27.18 for double ablation vs 202.5 ms ± 45.37 for RV ablation and 209.8 ms ± 26.91 for control, P < 0.0001). Arrhythmia complexity was greatest in the RVOT ablation group compared to control (dominant frequency 8.016 Hz ± 1.286 vs. 5.834 Hz ± 1.726, P = 0.0191). Rotors were preferentially clustered to the ablation area in the RVOT ablation group compared to control. Microstructural defects in the RVOT provides the substrate for sustained ventricular arrhythmias.

Pulmonary sinus cusp mapping and ablation: A new concept and approach for idiopathic right ventricular outflow tract arrhythmias

Right ventricular outflow tract (RVOT) ventricular arrhythmias (VAs) may originate from the pulmonary sinus cusps (PSCs) far more frequently than previously recognized. The purpose of this study was to assess whether mapping and ablation in PSCs might be an appropriate first-choice treatment in unselected patients with idiopathic RVOT VAs. Ninety consecutive patients with VAs of RVOT-type origin were prospectively enrolled at our institution between August 2015 and September 2016. Pulmonary valve (PV) and PSCs were precisely localized by pulmonary arteriography. Activation and pace-mapping were performed in the PSCs and RVOT region below the PV, and ablation was preferentially performed in PSCs. In 81 patients (90%), earliest activation of VAs was found in PSCs, and ablation resulted in elimination of VAs without any additional ablation in the RVOT region underneath the PV. The best pace-map was obtained at successful ablation sites in PSCs in 96.3% of patients. In the remaining 9 patients, final successful ablation sites were in the aortic coronary cusps in 5 and at the lowest and most posterior part of the RVOT in 4. During mean follow-up of 15.2 ± 9.5 months, single procedural success rate was 96.7%. In this single-center, prospective study, a strategy based on PSC mapping and ablation eliminated 90% (81/90) of unselected idiopathic RVOT-type VAs with favorable mid-term effectiveness.

Acute Cardiac Tamponade after Left Sided Premature Ventricular Contraction Ablation

Abstract Introduction: Premature ventricular complex (PVC) is the most common cardiac arrhythmia, which in some circumstances can lead to syncope, arrhythmia-induced cardiomyopathy and sudden death. In idiopathic PVCs, the first choice of treatment is radio-frequency ablation. Identification of the substrate location makes it possible to determine the ablation site, leading to an increased success rate. Complications are related mainly to the ablation technique, peri-procedural anticoagulation therapy, and the access site. Pericardial tamponade is a rare complication. A case in which the ablation procedure of idiopathic PVCs, complicated by cardiac tamponade, is presented in this paper. Case presentation: A 56-year-old female presented with symptomatic premature ventricular contractions. She had frequent palpitations, dyspnea, and exercise intolerance for ten years. Holter-monitoring demonstrated a total burden of 30,549 PVCs with monomorphic morphology, and with both bigeminal and trigeminal patterns. Surface ECG suggested a left-sided, left aortic cusp localization of the PVC, with a possible epicardial origin. Three-dimensional mapping was performed including the RVOT (right ventricular outflow tract) region, aorta, and coronary sinus. The ablation clinical status suggested a cardiac tamponade, which was confirmed by echocardiography. Radioscopy-controlled pericardial puncture was performed with the extraction of 300 ml of blood. Following this maneuver, the general status of the patient improved. During follow-up checks after twenty-four hours, Holter-monitoring recorded 5000 PVCs with a significant improvement in the clinical status of the patient. Discussions: Pericardial tamponade after radio-frequency ablation is a rare complication. The risk of tamponade in a right chamber perforation is more dangerous in patients on anticoagulation therapy or with pulmonary hypertension. In order to prevent this side effect complication of the interventional procedures, certain safety maneuvers should be followed, including the use of irrigated-type catheters, or when possible, contact force catheters, ensuring invasive arterial blood pressure monitoring during intervention, and after heparin administration and the determination of ACT every twenty minutes. Transthoracic echocardiograph examination and pericardial puncture set should be readily available in the electrophysiology laboratory.

ST-Segment Elevation and Fractionated Electrograms in Brugada Syndrome Patients Arise From the Same Structurally Abnormal Subepicardial RVOT Area but Have a Different Mechanism.

Brugada syndrome (BrS) is characterized by a typical ECG pattern. We aimed to determine the pathophysiologic basis of the ST-segment in the BrS-ECG with data from various epicardial and endocardial right ventricular activation mapping procedures in 6 BrS patients and in 5 non-BrS controls. In 7 patients (2 BrS and 5 controls) with atrial fibrillation, an epicardial 8×6 electrode grid (interelectrode distance 1 mm) was placed epicardially on the right ventricular outflow tract (RVOT) before video-assisted thoracoscopic surgical pulmonary vein isolation. In 2 other BrS patients, endocardial, epicardial RV (CARTO), and body surface mapping was performed. In 2 additional BrS patients, we performed decremental preexcitation of the RVOT before endocardial RV mapping. During video-assisted thoracoscopic surgical pulmonary vein isolation and CARTO mapping, BrS patients (n=4) showed greater activation delay and more fractionated electrograms in the RVOT region than controls. Ajmaline administration increased the region with fractionated electrograms, as well as ST-segment elevation. Preexcitation of the RVOT (n=2) resulted in ECGs that supported the current-to-load mismatch hypothesis for ST-segment elevation. Body surface mapping showed that the area with ST-segment elevation anatomically correlated with the area of fractionated electrograms and activation delay at the RVOT epicardium. ST-segment elevation and epicardial fractionation/conduction delay in BrS patients are most likely related to the same structural subepicardial abnormalities, but the mechanism is different. ST-segment elevation may be caused by current-to-load mismatch, whereas fractionated electrograms and conduction delay are expected to be caused by discontinuous conduction in the same area with abnormal myocardium.

Atypical Variants of Right Ventricular Outflow Arrhythmias

Right ventricular outflow tract (RVOT) arrhythmias are a common form of ventricular tachycardia (VT) in patients with structurally normal heart. The underlying mechanism is due to triggered activity. Mapping and ablation is relatively straightforward targeting the earliest point of activation. Previously reported causes of difficult ablation in the RVOT region include under recognized right ventricular cardiomyopathy/sarcoidosis, presence of endocavitary structures, close proximity to the coronary vasculature, and origin from non-RVOT structures. We identified all patients undergoing PVCs/sustained RVOT VT ablation from January 2013 to December 2013. This included 33 patients. Of these, we identified procedures that were considered difficult despite a single morphology arrhythmia being targeted and no underlying cardiomyopathy present. Difficulty was specifically considered when ablation at the earliest site of activation was not successful and eventual successful ablation was at a distance of greater than 15 mm from the early activation site. We identified 3 patients (n = 3, 100% male) with evidence of reentrant arrhythmia based on slow conduction zones necessary for the tachycardia/arrhythmia, mid diastolic signals during VT or preceding bigeminal PVCs, pace mapping from the site abnormal signals reproducing the arrhythmia morphology but with prominent conduction delay, the entire cycle length of the tachycardia or coupling interval for the PVCs being mapping, or based on reset characteristics. In patients with atypical forms of RVOT VT, careful mapping and ablation of the myocardial sleeves near the pulmonic valve can eliminate the arrhythmia.

Is the left ventricle the preferred pacing site in all children with atrioventricular block?

This editorial refers to ‘Preserved cardiac synchrony and function with single-site left ventricular epicardial pacing during mid-term follow-up in paediatric patients’ by M. Tomaske et al., on page 1168 Cardiac pacing for the treatment of bradycardia has been applied in children of all age groups for many years. In the paediatric population, the most common indications for cardiac pacing are auto-immune-mediated congenital atrioventricular block (CAVB) and acquired CAVB after congenital heart surgery. Traditionally, the right ventricular (RV) apex has been used for transvenous ventricular pacing leads because it is easily accessible and allows a stable position and low pacing thresholds. In young children, many centres prefer to place epicardial ventricular pacing leads, which are usually attached to either the RV apex or the RV free wall. Although thousands of children have profited from pacing the RV, there is increasing evidence that long-term RV apical pacing (RVP) eventually can result in LV failure. In animal studies, it has been demonstrated that chronic RVP leads to decreased LV function, dilatation, and asymmetric septal hypertrophy. 1 Clinical studies in adults have demonstrated that RVP is associated with increased mortality and morbidity related to heart failure. 2 Reports in children have also shown that long-term RVP causes LV mechanical dyssynchrony, which is associated with decreased LV function. 3,4 The deleterious effect of permanent RV pacing has become an important topic in cardiac pacing in the paediatric population, since this group requires pacemaker therapy over many decades. This young pacemaker population also includes a significant number of children with complex congenital heart disease at high risk for future heart failure. Literature data indicate that in children with normal cardiac anatomy, long-term RVP will lead to LV failure in 7%. 4 A very recent study by Gebauer et al. 5 reported even higher percentage (13%) of LV dilatation in a retrospective cohort of 82 patients after a mean pacing period of 7.4 years. In this study, children with epicardial RV free wall pacing had a higher risk of LV dilatation and LV dysfunction compared with those with RVP. 5 Furthermore, small case series has demonstrated that children with congenital CAVB who developed RV pacing-associated cardiomyopathy showed impressive improvement of LV function after cardiac resynchronization therapy (CRT). These findings indicate that mechanical dyssynchrony induced by RV pacing appeared to be the key factor in the development of heart failure in this group of congenital CAVB. Also, the CRT data in children and patients with congenital heart disease from three large studies have shown that 45‐70% of children undergoing CRT for heart failure had pacing-induced ventricular dyssynchrony. 6 So, if the RV apex appears inappropriate for long-term ventricular pacing, what then should we use as an alternative? In the RV, selective pacing sites at the high RV septum and RV outflow tract region may produce more synchronous contraction patterns and better haemodynamics. Therefore, RV septal pacing could decrease the long-term detrimental effects of RV pacing. Advanced tools and lead technology nowadays allow for pacing these specific RV sites, also in paediatric patients. However, to date, long-term clinical studies have been conflicting, and large randomized trials are now expected to demonstrate the significance of selective site RV pacing in the protection of LV function. 7 LV pacing appears to be less harmful than RVP as shown in acute haemodynamic studies in patients with normal LV function. 8 Animal studies as well as an acute haemodynamic study in children have suggested that the LV apex is the optimal pacing site in the LV. 9 Trials in adult patients have shown that single-site LV free wall pacing (LVP), comparable with biventricular pacing, has beneficial haemodynamic effects in patients with heart failure and left bundle branch block. 10 Also, a small study in children with LV dysfunction and RVP or intrinsic left bundle branch block has demonstrated improvement of LV function 1 month after single-site LVP. 11

The Left Ventricular Ostium

Received June 17, 2008; accepted September 4, 2008. Idiopathic ventricular arrhythmias (VAs) arising from the left ventricle (LV) are often accessible for catheter ablation from the aortic sinuses of Valsalva or adjacent to the mitral annulus (MA).1 The aortic and mitral valves are direct apposition and attach to an elliptical opening at the base of the LV known as the LV ostium.2 The VAs arising from this region are being increasingly recognized as targets for catheter ablation.3–7 This review describes the anatomic features of the LV ostium and the electrocardiographic, electrophysiological, and angiographic characteristics that are relevant to the mapping and ablation of these arrhythmias. The dominant central structure of the heart is the junction of the aorta with the LV. Fundamental for understanding idiopathic VAs arising near the aortic and mitral valves are 2 concepts: first, these arrhythmias arise from the LV ostium (Figure 1); and second, the LV ostium is covered by the aorto-ventricular membrane, a tough fibrous structure which is perforated by the aorta anteriorly and the mitral valve (MV) posteriorly (Figure 2). The anatomic concept of the LV ostium and its covering, the aorto-ventricular membrane, are based on the pioneering work of McAlpine.2 Figure 1. The left ventricular ostium (postero-cranial view). The left panel includes the aortic root with the right coronary sinus (R), left coronary sinus (L), and noncoronary sinus (N). In the right panel, the root of the aorta has been removed to demonstrate the elliptical ostium of the left ventricle (LV) with the junction of the right coronary cusp (RCC), left coronary cusp (LCC), and LV summit demonstrated. APM indicates anterior papillary muscle; LA, left atrium; LAFT, left anterior fibrous trigone; LFT, left fibrous trigone; L-RCC, the junction between the LCC and RCC; PPM, posterior papillary muscle; PSP, postero-superior …

Do Patients with Right Ventricular Outflow Tract Ventricular Arrhythmias Have a Normal Right Ventricular Wall Motion?

Background/Aim: Patients with ventricular ectopy from the right ventricular (RV) outflow tract (RVOT) are often referred for RV angiography to exclude disorders such as arrhythmogenic RV cardiomyopathy/dysplasia (ARVC/D). This is usually based on a qualitative assessment of the wall motion. We present a method to quantify the wall motion and to apply this method to compare patients with RVOT ectopy to normal subjects. Methods: RV angiograms were analyzed from 19 normal subjects and 11 subjects with RVOT ventricular arrhythmias (RVOT arrhythmia subjects) who had no other clinical or other evidence for ARVC/D. By a newly developed computer-based method, RV contours were first traced from multiple frames spanning the entire cardiac cycle. The fractional change in area between contours was then calculated as a serial function of time and location to determine both total contour area change and timing of contour movement. Contour area strain, defined as the differential change in area between nearby regions, was also computed. Results: The contour area change was greatest in the tricuspid valve region and least in the RVOT and midanterior regions. The onset of contraction was earliest in the RVOT region and latest in the apical, inferior, inferoapical, and subtricuspid valve regions. The contour strain was largest in superior tricuspid valve and inferior wall and near zero within the lateral tricuspid valve region. There were significant pairwise differences in contraction area, timing, and strain in the various regions. There were no significant differences between normal subjects and RVOT arrhythmia subjects. Conclusions: The RV wall motion is nonuniform in contour area change, strain, and timing of motion. Patients with RVOT ventricular ectopy demonstrate wall motion parameters similar to those of normal subjects. This technique should be applicable in analyzing RV wall motion in patients suspected of having ARVC/D.

Ablation of Nonsustained or Hemodynamically Unstable Ventricular Arrhythmia Originating From the Right Ventricular Outflow Tract Guided by Noncontact Mapping

Conventional activation or pacemapping is effective in guiding ablation of ventricular tachyarrhythmia originating from right ventricular outflow tract (RVOT). However, in selected patients with hemodynamically unstable or nonsustained tachycardia, noncontact mapping may be an effective alternative method to guide ablation in RVOT. Five patients with symptomatic hypotension during ventricular tachycardia (VT) or nonsustained tachyarrhythmia originating from the RVOT had radiofrequency ablation guided by noncontact mapping. All patients had a history of syncope and the tachyarrhythmias were refractory to antiarrhythmic therapy. Four patients had spontaneous sustained VT of a cycle length from 250 to 300 ms and one had symptomatic ventricular ectopic beats. Two patients were diagnosed to have arrhythmogenic right ventricular cardiomyopathy (ARVC). Sustained VT with hypotension was induced in two patients and nonsustained VT in three patients. Isopotential color maps were used to locate the earliest activation site of the tachyarrhythmia in RVOT. Three patients had tachyarrhythmia exit sites at the septal region and two at lateral region of RVOT. Low voltage area and diastolic activity were detected in the two patients with ARVC. Radiofrequency ablation guided by noncontact mapping was performed during sinus rhythm in all patients. The number of ablation attempts ranged from 1 to 14. After follow-up for 12 +/- 5.8 months, there was no recurrence of tachyarrhythmia and syncope in all five patients. Noncontact mapping is a safe and effective alternative method to guide ablation of hemodynamically unstable or nonsustained ventricular arrhythmia originating from RVOT.