Document Detail

Radiofrequency catheter ablation of idiopathic right ventricular outflow tract arrhythmias.
Jump to Full Text
MedLine Citation:
PMID:  23329871     Owner:  NLM     Status:  PubMed-not-MEDLINE    
Abstract/OtherAbstract:
Idiopathic ventricular arrhythmias (VA) consist of various subtypes of VA that occur in the absence of clinically apparent structural heart disease. Affected patients account for approximately 10% of all patients referred for evaluation of ventricular tachycardia (VT). Arrhythmias arising from the outflow tract (OT) are the most common subtype of idiopathic VA and more than 70-80% of idiopathic VTs or premature ventricular contractions (PVCs) originate from the right ventricular (RV) OT. Idiopathic OT arrhythmias are thought to be caused by adenosine-sensitive, cyclic adenosine monophosphate (cAMP) mediated triggered activity and, in general, manifest at a relatively early age. Usually they present as salvos of paroxysmal ventricular ectopic beats and are rarely life-threatening. When highly symptomatic and refractory to antiarrhythmic therapy or causative for ventricular dysfunction, ablation is a recommended treatment with a high success rate and a low risk of complications.
Authors:
Naiara Calvo; Monique Jongbloed; Katja Zeppenfeld
Publication Detail:
Type:  Journal Article     Date:  2013-01-01
Journal Detail:
Title:  Indian pacing and electrophysiology journal     Volume:  13     ISSN:  0972-6292     ISO Abbreviation:  Indian Pacing Electrophysiol J     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2013-01-18     Completed Date:  2013-01-21     Revised Date:  2013-05-30    
Medline Journal Info:
Nlm Unique ID:  101157207     Medline TA:  Indian Pacing Electrophysiol J     Country:  India    
Other Details:
Languages:  eng     Pagination:  14-33     Citation Subset:  -    
Affiliation:
Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Full Text
Journal Information
Journal ID (nlm-ta): Indian Pacing Electrophysiol J
Journal ID (iso-abbrev): Indian Pacing Electrophysiol J
Journal ID (publisher-id): Indian Pacing Electrophysiol J
ISSN: 0972-6292
Publisher: Indian Heart Rhythm Society
Article Information
Download PDF
Copyright: © 2013 Calvo et al.
open-access:
collection publication date: Season: Jan-Feb Year: 2013
Electronic publication date: Day: 01 Month: 1 Year: 2013
Volume: 13 Issue: 1
First Page: 14 Last Page: 33
PubMed Id: 23329871
ID: 3540113
Publisher Id: ipej130014-00

Radiofrequency Catheter Ablation of Idiopathic Right Ventricular Outflow Tract Arrhythmias
Naiara Calvo, MD1
Monique Jongbloed, MD, PhD12
Katja Zeppenfeld, MD, PhD1
1Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands
2Department of Anatomy and Embryology, Leiden University Medical Center, Leiden, The Netherlands
Correspondence: Address for correspondence: Dr. Zeppenfeld, Leiden University Medical Center, Department of Cardiology, Albinusdreef 2, 2333 ZA Leiden, The Netherlands.K.Zeppenfeld@lumc.nl

Introduction

Idiopathic ventricular arrhythmias (VA) consist of various subtypes of VA that occur in the absence of clinically apparent structural heart disease. Affected patients account for approximately 10% of all patients referred for evaluation of ventricular tachycardia (VT) [1]. Arrhythmias arising from the outflow tract (OT) are the most common subtype of idiopathic VA and more than 70-80% of idiopathic VTs or premature ventricular contractions (PVCs) originate from the right ventricular (RV) OT [2]. Idiopathic OT arrhythmias are thought to be caused by adenosine-sensitive, cyclic adenosine monophosphate (cAMP) mediated triggered activity and, in general, manifest at a relatively early age. Usually they present as salvos of paroxysmal ventricular ectopic beats and are rarely life-threatening. When highly symptomatic and refractory to antiarrhythmic therapy or causative for ventricular dysfunction, ablation is a recommended treatment with a high success rate and a low risk of complications.

The aim of this review is to provide insights into the development and anatomy of the RVOT as related to arrhythmias and to describe the clinical characteristics and the current methods to localize and ablate these arrhythmias.


Embryological development of the outflow tracts

Initially, the outlet portion of the heart is a single myocardial tube that connects to the aortic sac and the connecting pharyngeal arch arteries. Septation of the outlet portion structures takes place at three levels: 1. the level of the myocardial OT, 2. the level of the semilunar valves and 3. the level of the aortic sac that will divided into an aorta and a pulmonary trunk [3,4]. During development a significant lengthening of the right ventricular outflow tract occurs, whereas the left ventricular outflow tract (LVOT) remains relatively short, reflecting the right/left asymmetry. This is further substantiated by the fact that the putative left ventricle is one of the first compartments to be recognized in the embryonic heart, whereas the right ventricle is added to the heart during later developmental stages [5], including a marked lengthening of the sub-pulmonary myocardium characterized by a specific gene expression pattern [6].

During development and after looping of the primitive heart tube, several so-called "transitional zones" can be recognized, that are related to elements of the putative cardiac conduction system (Figure 1A,B), which show slow conducting properties as opposed to the remainder of the embryonic heart [7]. One of these transitional zones is found at the level of the myocardial OT. Several markers related to the developing cardiac conduction system have been described in these zones [8], including the Hyperpolarization-activated cyclic nucleotide-gated channel 4 (HCN4), that is responsible for the (If) or funny current in the sino-atrial node [9]. The expression of HCN4 among other markers, including CCS-lacZ and MinK-lacZ [10,11], in particular areas of the developing heart may explain the occurrence of arrhythmias at specific predilection sites in the adult heart, including the RVOT. The developing cardiac conduction system thus covers a much broader area than the definitive adult cardiac conduction system, and although the definitive cause of idiopathic RVOT VA or ectopy has not been resolved to date, either a re-expression of an embryonic phenotype, or embryonic remnants of tissue may provide an explanation the arrhythmogenic potential of this area.


Anatomy of the outflow tracts

During OT development the great arteries achieve their definitive relationship, with the aorta situated in a central position, right posterior of the pulmonary trunk. The RVOT thus courses anterior to the LVOT, from a rightward inferior to a leftward superior direction (Figure 1C). Both the LVOT and RVOT have their own morphological characteristics. The RVOT is characterized by the presence of a muscular sub-pulmonary infundibulum that forms a circular muscular tube below the pulmonary valve. Due to the length of this sub-pulmonary myocardium, the pulmonary valve has a more superior position as compared to the aortic valve. The pulmonary annulus is thus positioned superior and to the left of the aortic annulus and the pulmonary trunk continues leftward and divides in a right and left pulmonary artery, the right of which will course below the aortic arch [12].

The posterior wall of the sub-pulmonary infundibulum is situated between the tricuspid valve and the pulmonary valve. The proximal medial wall of the RVOT is formed by the anterior part of the interventricular septum and is separated from the inflow part by the trabecula septomarginalis that contains the right bundle branch (Figure 1C) [13]. Of importance, there is no continuity between the distal medial and posterior wall of the RVOT and the aorta. The term "septal" RVOT is therefore misleading (Figure 1D, arrow)

On the left side there is fibrous continuity between the aortic valve and the mitral valve (Figure 1E). The sub-aortic region is formed by the fibrous tissue of the aortic leaflet of the mitral valve, the membranous part of the ventricular septum, as well as by the muscular ventricular septum, and the anterior left ventricular wall. The fibrous tissues of the tricuspid valve, mitral valve and aortic valve are all part of the fibrous heart skeleton, whereas the pulmonary valve is positioned more anterosuperiorly and is usually not in fibrous continuity with the other valves. The bundle of His, in the normal heart the only myocardial bundle passing the annulus fibrosus, and thereafter runs in the lower edge of the membranous part of the ventricular septum, is situated on top of the muscular part of the ventricular septum, where is branches into a left and right bundle branch.


Clinical characteristics

Patients usually present in their second to fifth decade [14] with symptomatic palpitations. Presyncope and light-headedness may be observed, but true syncope is infrequent (<10%). Although the arrhythmia may be sustained, it is usually characterized by repetitive bursts of nonsustained VT or frequent PVCs. Arrhythmias can often be provoked by exercise, caffeine and emotional stress. In women, who are more frequently affected, RVOT VA are commonly reported during the premenstrual and perimenopausal period and during pregnancy, suggesting hormonal flux as a trigger for RVOT arrhythmias [14,15]. However, in a significant number of patients, exercise suppresses the arrhythmia and VA arises during the recovery phase or during rest [16] (Figure 2).

In general, tachycardia from the OT shows a benign course. However, it has been reported that frequent PVCs and VTs can cause left ventricular (LV) dysfunction that can be reversed by suppression of VA with antiarrhythmic agents or radiofrequency catheter ablation [17,18].

It is important to distinguish idiopathic RVOT VA from VA caused by structural heart diseases, such as arrhythmogenic right ventricular dysplasia (ARVD), in which the RVOT may be one of the origins of potential life threatening VA [19]. A careful analysis of the 12-lead surface ECG, a detailed medical and family history,exercise testing and cardiac imaging may be warranted to establish the diagnosis.

Idiopathic RVOT VA typically occurs in patients with no structural heart disease. However, several MRI studies have reported subtle areas of focal thinning and segmental contraction abnormalities, as well as focal fatty infiltration [20-23]. In contrast, other studies showed no evidence of structural heart disease on MRI [24,25]. Therefore, to date, there is not conclusive evidence for structural abnormalities associated with truly "idiopathic" RVOT VA.

Rarely, ectopy from the RVOT can trigger ventricular fibrillation and/or polymorphic VT (Figure 3) [26-28]. A shorter coupling interval (CI) to the preceding QRS complex, and a shorter cycle length (CL) during monomorphic VT, if present, have been found to predict the occurrence of VF or polymorphic VT [29]. In contrast, a more recent study [30] demonstrated that the prematurity index (PI) (defined as the ratio of the CI of the first VT beat or isolated PVC to the preceding R-R interval of the sinus cycle just before the VT or isolated PVC), but no the CI, was the only independent predictor for polymorphic VT; a PI value of <0.73 predicted occurrence of polymorphic VT with a sensitivity of 91% and a specificity of 44%.


Arrhythmia mechanism

The majority of idiopathic OT arrhythmias are thought to be due to calcium-dependent triggered activity mediated through cAMP resulting in delayed afterdepolarizations [31,32]. Rapid burst pacing, isoproterenol infusion, and rarely aminophylline, calcium infusion, or atropine may facilitate arrhythmia induction [33]. These interventions lead to increased intracellular cAMP, which, via activation of the protein kinase A, increases the slow inward Ca2+ current and the calcium release from the sarcoplasmic reticulum through phosphorylation of the ryanodine receptor. Calcium released from the SR can activate the electrogenic Na+/Ca2+ exchanger, resulting in a transient inward current and delayed afterdepolarization [34,35].


Localization of the site of origin

RVOT VAs often arise from the distal medial ("septal") and anterior surface [2,16,36-40]. However, a free wall focus has also been reported in 20-30% of patients undergoing radiofrequency (RF) ablation of RVOT VA [41].

The majority of "septal" and free wall VA originates from the distal RVOT. Yamashina et al. [42] have evaluated the distribution of successful ablation sites within the RVOT using a three-dimensional electroanatomical mapping system and demonstrated that 88.7% of successful ablation sites were located in the transitional-voltage zone beneath the pulmonary valve, with a mean vertical length of 8.1 mm. However, RVOT VAs arising from the pulmonary artery or near the bundle of His have also been described [43-46].


The role of the 12-lead electrocardiogram

Ventricular arrhythmias originating from the RVOT typically demonstrate left bundle branch block morphology with an inferiorly directed frontal QRS axis. On the basis of pace-mapping, several electrocardiographic algorithms have been proposed to guide catheter ablation of ventricular arrhythmias originating from the RVOT [2,47-49]. A QS complex in frontal lead I suggests an anterior site, while an R or qR complex indicates a more posterior site of origin (Figure 4) [50-52].

The precordial lead transition (defined as the first precordial lead with R≥S) moves leftward as the origin moves diagonally from the distal-posterior "septal" aspect of the RVOT to the proximal-anterior region. In OT VA with a precordial R/S transition in lead V3, a V2 transition ratio <0.6 and a precordial transition of the VA QRS later than the transition of the sinus rhythm (SR) QRS reliably predicted an RVOT origin (53) (Table 1) (Figure 5).

A wider QRS complex and notching of the R-wave in the inferior leads have been associated with free wall RVOT VA. In contrast, a "septal" origin leads to a simultaneous right- and left sided activation causing a relatively narrow QRS complex. An isoelectric or positive QRS complex in lead aVL is typically recorded if the site of origin is located in the proximal RVOT while a distal site of origin produces a negative QRS complex [50].

More recently, Zhang et al. [54] have developed a new ECG algorithm based on the location of successful ablation sites as identified by detailed 3D mapping using a non-contact-electroanatomical mapping system (Ensite system, Ensite array, St Jude Medical, St. Paul, MN). According to their observations, a transitional zone of ≥V4, a R wave duration index of less than 0.5, or a R/S amplitude index of less than 0.3 in the precordial leads V1 and V2 was highly predictive for an RVOT origin (Table 1). Although the precise localization of the site of origin based on ECG criteria is limited by the close anatomic relation of the LVOT, an inferior QRS axis and a very early precordial transition zone (RS ratio ≥1 in leads V1 or V2) is usually consistent with a LVOT origin (basal septum or aortic commissures) or with an origin from the LV epicardium [37,48].


Mapping strategy

Ablation based on activation mapping and/or pace-mapping is considered the favored technique for eliminating idiopathic VT/PVC arising from the RVOT. Systematic point-by-point activation mapping is the initial preferred technique in the presence of sustained tachycardia or frequent PVCs [31,55-57]. The use of a three-dimensional electroanatomical (EAM) systems can assist in relating the anatomy to the mapping data [49,55,57-63] and may facilitate mapping and ablation (Figure 6D). New imaging tools to guide mapping, such as rotational angiography have been recently described [64]. In a small study, performed in 8 patients, the anatomical details provided by three-dimensional rotational angiography were found to be qualitatively superior to the 3D electroanatomical reconstruction using the CARTO system (Biosense Webster, DiamondBar, CA, USA) with comparable procedural characteristics including fluoroscopic exposure [64].

If spontaneous PVCs or VT are absent, programmed stimulation and burst pacing should be performed, and often, catecholamine infusion is required to facilitate induction. Occasionally, epinephrine or phenylephrine may be more effective than isoproterenol. In some patients arrhythmia may manifest after isopreterenol infusion is discontinued [65].

All antiarrhythmic medications should be discontinued for at least five half-lives before the procedure. Deep sedation may also result in non-induciblity of RVOT tachycardia and should be avoided.


Activation mapping

During activation mapping the earliest bipolar activity and recording of a local unipolar QS pattern are used to identify the site of origin. Earliest local ventricular activation recorded from the mapping catheter should precede the onset of the surface QRS complex by 10 to 60 ms [56,65]. An unipolar QS pattern with rapid intrinsic deflection demonstrates a high sensitivity for successful ablation sites, but may also be recorded at unsuccessful sites up to 11 mm from the site of origin [66-68]. A newly proposed approach from our centre combines local bipolar activation time with the recording of reversed polarity. The presence of reversed polarity was evaluated from the bipolar electrograms recorded from the distal (M1-M2) and mid (M2-M3) electrode pairs of the mapping catheter and was defined as a rapid simultaneous deflection in opposite direction of the initial part of the bipolar electrograms occurring before the onset of the VA QRS (Figure 7) [66]. This novel approach resulted in a high negative predictive value as well as in a high positive predictive value for identifying a successful ablation site. Conventional mapping based on bipolar activity and an unipolar QS configuration had a comparable negative predictive value but a poor positive predictive value.

If mapping in the RVOT is not successful, the pulmonary artery should be explored. The local bipolar recording at the successful ablation site may demonstrate high frequency, low-voltage signals preceding the main local ventricular activation. Discrete potentials can be recorded from the pulmonary artery preceding the QRS complex during ventricular tachycardia and following the QRS complex in sinus rhythm [45].


Pace mapping

Pace mapping is useful in the absence of frequent PVCs or if tachycardia is not reproducible inducible. It should be performed at the VT cycle length or at a cycle length similar to the coupling interval of ventricular ectopy. Pacing at faster cycle lengths or shorter coupling intervals may lead to rate-dependent changes in QRS morphology [69,70]. The ideal pace-map is an identical QRS pattern in all 12 surface ECG leads (12/12 match) between the clinical arrhythmia and the paced QRS morphology (Figure 8) [57,71]. Pacing should be performed at stimulus strengths only slightly higher than the diastolic threshold to avoid capture over a large area which is likely to reduce accuracy. In the absence of a good pace map, the catheter should be carefully repositioned within the area of interest.

However, it is important to consider that the spatial resolution of pace-mapping was found to be inferior to that of activation mapping [56]. A good pace-map could be obtained at sites with a mean distance of 7.3±5mm from the effective ablation site. In addition, in 18% of the patients the pace-map at the successful ablation site was poor. The latter was explained by a site of origin located deep to the endocardium with conduction through preferential fibers connecting the site of origin to the endocardium.


Indications and contraindications for an ablative approach

According to the current guidelines [1], catheter ablation is recommended in patients with severely symptomatic ventricular ectopy/tachycardia or if antiarrhythmic drug therapy remains ineffective, is poorly tolerated or not desired. In addition, catheter ablation is indicated for recurrent sustained polymorphic VT and VF that is refractory to antiarrhythmic therapy when there is a suspected trigger that can be targeted for ablation. Finally, catheter ablation is recommended for patients with frequent PVCs, nonsustained VTs, or VT that is presumed to cause ventricular dysfunction. Contraindications to catheter ablation are asymptomatic ventricular ectopy or infrequent nonsustained tachycardia or if OT tachycardia is due to reversible causes [1].


Catheter choice and energy settings

Ablation within the RVOT may be performed using a conventional solid tip or an irrigated tip catheter. If an irrigated tip catheter is used, power should be carefully titrated (up to 35W) with a maximum temperature of 45ºC. Termination is expected to occur within 10 seconds of radiofrequency current energy delivery; otherwise mapping should be continued. Acceleration of the tachycardia during ablation, followed by gradual slowing or abrupt termination may be observed [31]. Similarly, application of radiofrequency (RF) current during sinus rhythm at sites of the origin of the VA may also lead to induction of repetitive responses or VA with similar morphology as seen during spontaneous RVOT VA. The changing patterns of repetitive ventricular response (slowing and/or disappearance) have been shown to be consistent with successful RF ablation [72].

Recently, the efficacy, safety, and feasibility of new techniques for RVOT VA ablation, such as remote-controlled magnetic navigation system, have been reported. This technique may have advantages with respect to reduction in the operator's and patient's radiation exposure and a lower incidence of catheter-induced PVCs [73].


Complications

Complications are rare and they are usually related to damage of structures in close anatomical proximity to the site of ablation. The distance from the leftward posterior aspect of the RVOT to the left main coronary artery is 4.1±1.9 mm (Figure 6A,B) [74]. Therefore, ablation along the posterior RVOT may result in damage to the left main coronary artery. Other risks include cardiac perforation resulting in tamponade, complications related to vascular access or damage to the His bundle with consecutive heart block.


Procedural outcome following catheter ablation of OT tachycardias

The acute success rate for ablation of RVOT tachycardia ranges from 75 to 100% with a low recurrence rate of 5% (Table 2). Wen et al. [80] described a poor pace-map score of <10/12, reliance on pace-map only in patients with no sufficient ventricular tachycardia for identification of ablation sites, and a later local activation time at ablation site as predictors of recurrence. Flemming et al.[82] found that the best discriminator of outcome was the QRS duration in lead V2 with a likelihood of successful ablation with an endocardial approach in the right ventricular outflow tract of 95% when VT/bigeminy QRS duration was ≥ 160 ms compared with only 54% if the QRS duration in V2 was <160 ms in duration. However, in a previous study [79], an unsuccessful outcome was associated with a delta wave-like onset of the QRS complex during ventricular tachycardia, suggesting that a slow onset of the QRS complex may indicate an intramural or epicardial origin of the ventricular tachycardia. Other factors predictive of unsuccessful ablation were more than one induced VT morphology and a match between the clinical VT and pace-map in less than 11 of 12 leads.


Conclusions

Idiopathic VA occurs in individuals with no structural disease and predominantly originate from the RVOT. These arrhythmias have a focal origin with triggered activity due to delayed after-depolarizations as the main underlying mechanism. The typical QRS morphology during idiopathic focal RVOT VT shows LBBB configuration with an inferior (right or left) axis.

Precise localization for ablation is ideally guided by activation mapping, although pace mapping, or a combination of both methods may be applied in case of infrequent arrhythmia. RF catheter ablation of RVOT-VT is a safe treatment option with an acute success > 90% and a low risk of complications, and could be considered first-line therapy in selected patients.


Acknowledgements

The authors thank Margot M. Bartelings and Adriana C. Gittenberger de Groot for their comments while preparing the Anatomy & Embryology part of the manuscript.


References
Aliot EM,et al. EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias: developed in a partnership with the European Heart Rhythm Association (EHRA), a Registered Branch of the European Society of Cardiology (ESC), and the Heart Rhythm Society (HRS); in collaboration with the American College of Cardiology (ACC) and the American Heart Association (AHA) Europace Year: 20091177119443434
Movsowitz C,et al. Idiopathic right ventricular outflow tract tachycardia: narrowing the anatomic location for successful ablationAm Heart JYear: 19961319308615312
Gittenberger-de Groot AC,et al. Basics of cardiac development for the understanding of congenital heart malformationsPediatr ResYear: 20055716915611355
Bartelings MM,et al. Morphogenetic considerations on congenital malformations of the outflow tract. Part 1: Common arterial trunk and tetralogy of FallotInt J CardiolYear: 1991322131917172
Cai CL,et al. Isl1 identifies a cardiac progenitor population that proliferates prior to differentiation and contributes a majority of cells to the heartDev CellYear: 2003587714667410
Parisot P,et al. Tbx1, subpulmonary myocardium and conotruncal congenital heart defectsBirth Defects Res A Clin Mol TeratolYear: 20119147721591244
de Jong F,et al. Persisting zones of slow impulse conduction in developing chicken heartsCirc ResYear: 1992712401628384
Jongbloed MR,et al. Development of the cardiac conduction system and the possible relation to predilection sites of arrhythmogenesisScientific World JournalYear: 2008823918379704
Vicente-Steijn R,et al. Funny current channel HCN4 delineates the developing cardiac conduction system in chicken heartHeart RhythmYear: 20118125421421080
Jongbloed MR,et al. Embryonic conduction tissue: a spatial correlation with adult arrhythmogenic areas J Cardiovasc Electrophysiol Year: 20041534915030427
Kondo RP,et al. Development of the cardiac conduction system as delineated by minK-lacZJ Cardiovasc ElectrophysiolYear: 20031438312741710
Asirvatham SJ,et al. Correlative anatomy for the invasive electrophysiologist: outflow tract and supravalvar arrhythmiaJ Cardiovasc ElectrophysiolYear: 20092095519490263
Bartelings MM,et al. The outflow tract of the heart--embryologic and morphologic correlationsInt J CardiolYear: 1989222892651326
Nakagawa M,et al. Gender differences in various types of idiopathic ventricular tachycardia J Cardiovasc Electrophysiol Year: 20021363312139282
Marchlinski FE,et al. Sex-specific triggers for right ventricular outflow tract tachycardia Am Heart J Year: 2000139100910827381
Buxton AE,et al. Right ventricular tachycardia: clinical and electrophysiologic characteristics Circulation Year: 1983689176137291
Yarlagadda RK,et al. Reversal of cardiomyopathy in patients with repetitive monomorphic ventricular ectopy originating from the right ventricular outflow tractCirculationYear: 2005112109216103234
Grimm W,et al. Reversal of tachycardia induced cardiomyopathy following ablation of repetitive monomorphic right ventricular outflow tract tachycardiaPacing Clin ElectrophysiolYear: 20012416611270695
Corrado D,et al. Three-dimensional electroanatomical voltage mapping and histologic evaluation of myocardial substrate in right ventricular outflow tract tachycardia J Am Coll Cardiol Year: 20085173118279737
Markowitz SM,et al. Adenosine-sensitive ventricular tachycardia: right ventricular abnormalities delineated by magnetic resonance imagingCirculationYear: 19971911929286949
Carlson MD,et al. Right ventricular outflow tract ventricular tachycardia: detection of previously unrecognized anatomic abnormalities using cine magnetic resonance imaging J Am Coll Cardiol Year: 1994247208077544
White RD,et al. Right ventricular arrhythmia in the absence of arrhythmogenic dysplasia: MR imaging of myocardial abnormalities Radiology Year: 19982077439609899
Globits S,et al. Significance of morphological abnormalities detected by MRI in patients undergoing successful ablation of right ventricular outflow tract tachycardiaCirculationYear: 19979626339355904
Tandri H,et al. Findings on magnetic resonance imaging of idiopathic right ventricular outflow tachycardia Am J Cardiol Year: 200494144115566923
Grimm W,et al. Magnetic resonance imaging and signal-averaged electrocardiography in patients with repetitive monomorphic ventricular tachycardia and otherwise normal electrocardiogram Pacing Clin Electrophysiol Year: 19972018269249838
Haissaguerre M,et al. Mapping and ablation of idiopathic ventricular fibrillation Circulation Year: 200210696212186801
Viskin S,et al. The "short-coupled" variant of right ventricular outflow ventricular tachycardia: a not-so-benign form of benign ventricular tachycardia J Cardiovasc Electrophysiol Year: 20051691216101636
Noda T,et al. Malignant entity of idiopathic ventricular fibrillation and polymorphic ventricular tachycardia initiated by premature extrasystoles originating from right ventricular outflow tract J Am Coll Cardiol Year: 200546128816198845
Shimizu W,et al. Arrhythmias originating from the right ventricular outflow tract: how to distinguish "malignant" from "benign"?Heart RhythmYear: 20096150719695964
Igarashi M,et al. Electrocardiographic Determinants of the Polymorphic QRS Morphology in Idiopathic Right Ventricular Outflow Tract TachycardiaJ Cardiovasc ElectrophysiolYear: 2011 Epub ahead of print.
Wilber DJ,et al. Adenosine sensitive ventricular tachycardia: clinical characteristics and response to catheter ablationCirculationYear: 1993871268418999
Lerman BB,et al. Adenosine sensitive ventricular tachycardia: evidence suggesting cyclic AMP-mediated triggered activity Circulation Year: 1986742703015453
Lerman BB,et al. Adenosine sensitive ventricular tachycardia: evidence suggesting cyclic AMP-mediated triggered activityCirculationYear: 1986741986
Lermann BB. Mechanism of outflow tract tachycardiaHeart RhythmYear: 2007497317599688
Farzaneh Far A,et al. Idiopathic ventricular outflow tract tachycardia Heart Year: 20059113615657214
Pietras RJ,et al. Chronic recurrent right ventricular tachycardia in patients without ischemic heart disease: clinical, hemodynamic, and angiographic findings Am Heart JYear: 19831053576829398
Schafers M,et al. Cardiac sympathetic innervation in patients with idiopathic right ventricular outflow tract tachycardiaJ Am Coll CardiolYear: 1998321819669268
Marchlinski FE,et al. Sex-specific triggers for right ventricular outflow tract tachycardia Am Heart JYear: 2000139100910827381
Klein LS,et al. Radiofrequency catheter ablation of ventricular tachycardia in patients without structural heart diseaseCirculationYear: 19928516661572025
Calkins H,et al. Relation between efficacy of radiofrequency catheter ablation and site of origin of idiopathic ventricular tachycardiaAm J CardiolYear: 19937127
Wilber DJ,et al. Catecholamine sensitive right ventricular outflow tract tachycardia: Intraoperative mapping and ablation of a free-wall focusPacing Clin ElectrophysiolYear: 19891218512481280
Yamashina Y,et al. Distribution of successful ablation sites of idiopathic right ventricular outflow tract tachycardiaPacing Clin ElectrophysiolYear: 20093272719545334
Tada H,et al. Idiopathic ventricular arrhythmias arising from the pulmonary artery: prevalence, characteristics, and topography of the arrhythmia origin Heart Rhythm Year: 2008541918313601
Sekiguchi Y,et al. Electrocardiographic and electrophysiologic characteristics of ventricular tachycardia originating within the pulmonary artery J Am Coll Cardiol Year: 20054588715766825
Timmermans C,et al. Idiopathic left bundle-branch block-shaped ventricular tachycardia may originate above the pulmonary valve Circulation Year: 2003108196014530199
Yamauchi Y,et al. Electrocardiographic characteristics of repetitive monomorphic right ventricular tachycardia originating near the His-bundle J Cardiovasc Electrophysiol Year: 200516104116191113
Dixit S,et al. Electrocardiographic patterns of superior right ventricular outflow tract tachycardias distinguishing septal and free-wall wits of origin J Cardiovasc Electrophysiol Year: 200314112625602
Ito S,et al. Development and validation of an ECG algorithm for identifying the optimal ablation site for idiopathic ventricular outflow tract tachycardia J Cardiovasc Electrophysiol Year: 200314128014678101
Joshi S,et al. Ablation of idiopathic right ventricular outflow tract tachycardia: current perspectivesJ Cardiovasc ElectrophysiolYear: 200516Suppl 1S5216138887
Kamakura S,et al. Localization of optimal ablation site of idiopathic ventricular tachycardia from and left ventricular outflow tract by body surface ECG CirculationYear: 19989815259769306
Jadonath RL,et al. Utility of the 12-lead electrocardiogram in localizing the origin of right ventricular outflow tract tachycardia Am Heart JYear: 199513011077484743
Shima T,et al. The relation between the pacing sites in the right ventricular outflow tract and QRS morphology in the 12-lead ECG Jpn Circ J Year: 1998623999652313
Betensky BP,et al. The V(2) transition ratio: a new electrocardiographic criterion for distinguishing left from right ventricular outflow tract tachycardia origin J Am Coll Cardiol Year: 201157225521616286
Zhang F,et al. Electrocardiographic algorithm to identify the optimal target ablation site for idiopathic right ventricular outflow tract ventricular premature contraction Europace Year: 200911121419706640
Azegami K,et al. Spatial resolution of pacemapping and activation mapping in patients with idiopathic right ventricular outflow tract tachycardia J Cardiovasc Electrophysiol Year: 20051682316101622
Bogun F,et al. Spatial resolution of pace mapping of idiopathic ventricular tachycardia/ectopy originating in the right ventricular outflow tract Heart Rhythm Year: 2008533918313589
Miller JM,et al. Catheter mapping and ablation of right ventricular outflow tract ventricular tachycardia J Cardiovasc Electrophysiol Year: 20061780016836686
Tanner H,et al. Outflow tract tachycardia with R/S transition in lead V3: six different anatomic approaches for successful ablation J Am Coll Cardiol Year: 20054541815680722
Friedman PA,et al. Non-contact mapping to guide ablation of right ventricular outflow tract tachycardia J Am Coll Cardiol Year: 200239180812039496
Ribbing M,et al. Endocardial mapping of right ventricular outflow tract tachycardia using noncontact activation mapping J Cardiovasc Electrophysiol Year: 20031460212875421
Aiba T,et al. Clinical usefulness of a multielectrode basket catheter for idiopathic ventricular tachycardia originating from right ventricular outflow tract J Cardiovasc Electrophysiol Year: 20011251111386509
Greil GF,et al. Radiofrequency ablation of right ventricular outflow tract tachycardia using a magnetic resonance 3D model for interactive catheter guidance Clin Res Cardiol Year: 20069561016998745
Saleem MA,et al. New simplified technique for 3D mapping and ablation of right ventricular outflow tract tachycardia Pacing Clin Electrophysiol Year: 20052839715869671
Orlov MV,et al. First experience with rotational angiography of the right ventricle to guide ventricular tachycardia ablation Heart Rhythm Year: 2001820720920602
Lerman BB,et al. Zipes SP,et al.Ventricular tachycardia in patients with structurally normal heartsCardiac Electrophysiology: From Cell to BedsideYear: 1999PhiladelphiaSaunders640
van Huls van Taxis CF,et al. Reversed polarity of bipolar electrograms for predicting a successful ablation site in focal idiopathic right ventricular outflow tract arrhythmias Heart Rhythm Year: 2011866521215326
Man KC,et al. Accuracy of the unipolar electrogram for identification of the site of origin of ventricular activation J Cardiovasc Electrophysiol Year: 199789749300293
Soejima Y,et al. Ventricular unipolar potential in radiofrequency catheter ablation of idiopathic non-reentrant ventricular outflow tachycardia Jpn Heart J Year: 20044574915557716
Stevenson WG,et al. Recording techniques for clinical electrophysiology J Cardiovasc Electrophysiol Year: 200516101716174026
Goyal R,et al. Effect of coupling interval and pacing cycle length on morphology of paced ventricular complexes. Implications for pace mappingCirculationYear: 19969428438941111
Gerstenfeld EP,et al. Quantitative comparison of spontaneous and paced 12-lead electrocardiogram during right ventricular outflow tract ventricular tachycardia J Am Coll Cardiol Year: 200341204612798580
Chinushi M,et al. Repetitive ventricular response induced by radiofrequency ablation for idiopathic ventricular tachycardia originating from the outflowtract of the right ventriclePACEYear: 19986699584296
Konstantinidou M,et al. Catheter ablation of right ventricular outflow tract tachycardia: a simplified remote-controlled approachEuropaceYear: 20111369621307021
Vaseghi M,et al. Catheter ablation of right ventricular outflow tract tachycardia: value of defining coronary anatomy J Cardiovasc Electrophysiol Year: 20061763216836713
Coggins DL,et al. Radiofrequency catheter ablation as a cure for idiopathic ventricular tachycardia of both right and left ventricular origin J Am Coll Cardiol Year: 19942313338176091
Mandrola JM,et al. Radiofrequency catheter ablation of idiopathic ventricular tachycardia in 57 patients: Acute success and long term follow-up (abstract)J Am Coll CardiolYear: 199519A7798500
Gumbrielle TP,et al. Electrocardiographic features of septal location of right ventricular outflow tract tachycardia Am J Cardiol Year: 1997792139193030
Chinushi M,et al. Radiofrequency catheter ablation for idiopathic right ventricular tachycardia with special reference to morphological variation and long term outcomeHeartYear: 1997782559391287
Rodriguez LM,et al. Predictors for successful ablation of right- and left-sided idiopathic ventricular tachycardia Am J Cardiol Year: 1997793099036750
Wen MS,et al. Determinants of tachycardia recurrences after radiofrequency ablation of idiopathic ventricular tachycardiaAm J CardiolYear: 1998815009485145
Almendral J,et al. Farre J,et al.Radiofrequency catheter ablation of idiopathic right ventricular outflow tract tachycardiaTen Years of Radiofrequency Catheter AblationYear: 1998Armonk, NYFutura249
Flemming MA,et al. Predictors of successful ablation of tachycardia or bigeminy arising in the right ventricular outflow tract Am J CardiolYear: 199984126610569344
Lee SH,et al. Determinants of successful ablation of idiopathic ventricular tachycardias with left bundle branch block morphology from the right ventricular outflow tractPacing Clin ElectrophysiolYear: 200225134612380771
O'Donnell D,et al. Clinical and electrophysiological differences between patients with arrhythmogenic right ventricular dysplasia and right ventricular outflow tract tachycardiaEur Heart J Year: 20032480112727147
Vestal M,et al. Electrocardiographic predictors of failure and recurrence in patients with idiopathic right ventricular outflow tract tachycardia and ectopy who underwent radiofrequency catheter ablationJ ElectrocardiolYear: 20033632714661169
Takemoto M,et al. Radiofrequency catheter ablation of premature ventricular complexes from right ventricular outflow tract improves left ventricular dilation and clinical status in patients without structural heart diseaseJ Am Coll CardiolYear: 200545125915837259
Krittayaphong R,et al. Electrocardiographic predictors of long-term outcomes after radiofrequency ablation in patients with right ventricular outflow tract tachycardiaEuropaceYear: 2006860116772366
Kuhne M,et al. Radiofrequency ablation guided by mechanical termination of idiopathic ventricular arrhythmias originating in the right ventricular outflow tractJ Cardiovasc ElectrophysiolYear: 2010214219656248
Furushima H,et al. Relationship between electroanatomical voltage mapping characteristics and breakout site of ventricular activation in idiopathic ventricular tachyarrhythmia originating from the right ventricular outflow tract septumJ Interv Card ElectrophysiolYear: 20123313521993597

Article Categories:
  • Review Article

Keywords: ventricular arrhythmias, outflow tract, ICDs, premature ventricular contractions, ablation.

Previous Document:  Cardiac pacing and defibrillation in children and young adults.
Next Document:  Utility of the NavX® Electroanatomic Mapping System for Permanent Pacemaker Implantation in a Pregn...