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VIEWPOINT Electrocardiographic recognition and ablation of outflow tract ventricular tachycardia Rupa Bala, MD, Francis E. Marchlinski, MD From the Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania. Outflow tract tachycardias comprise a subgroup of idio- pathic ventricular tachycardias (VTs) that occur in the ab- sence of structural heart disease. The arrhythmia mechanism appears to be calcium-dependent triggered activity, and no discrete anatomic abnormalities have been identified. In our experience, most of these outflow tract tachycardias origi- nate from a fairly narrow anatomic zone. These arrhythmias originate in an arc-like fashion from the right ventricular (RV) inflow region to the anteroseptal aspect of the right ventricular outflow tract (RVOT) under the pulmonic valve. The arc then extends leftward to include the cusp region of the aortic valve and the anterior left ventricle (LV) in front of the aortic valve, both endocardially and epicardially, and then further extends toward the aorto–mitral continuity and superior mitral annulus. Most outflow tract tachycardias originate in perivalvular tissue, which may be anatomically predisposed to fiber disruption that enhances arrhythmogen- esis. In addition, the proximity of the outflow tract to the epicardial fat pads containing the ganglionated plexuses and the unique response to exercise and hormonal changes sug- gest that the autonomic nervous system also plays a role in this arrhythmogenesis. Because outflow tract tachycardias tend to occur in the absence of structural heart disease and are focal in origin, the 12-lead ECG recorded during VT is a precise localizing tool. In this review, we highlight the ECG features of outflow tract tachycardias that aid in lo- calization and describe our approach to mapping and abla- tion. Important anatomic considerations The RVOT region is defined superiorly by the pulmonic valve and inferiorly by the RV inflow tract and the top of the tricuspid valve. The lateral aspect of the RVOT region is the RV free wall, and the medial aspect is formed by the interventricular septum at its base of the RVOT and RV musculature opposite the root of the aorta at the region just inferior to the pulmonic valve. From the coronal view above the pulmonic valve, the RVOT region is seen wrapping around the root of the aorta and extending leftward. The top of the RVOT may be convex or crescent shaped, with the posteroseptal region directed rightward and the anteroseptal region directed leftward. Occasionally, an extreme convex- ity of the superior septal RVOT region creates a leftward direction for the most posterior and anterior aspects of the septal RVOT and results in a net negative QRS complex in lead I from either site. The anteroseptal aspect of the RVOT actually is located in close proximity to the LV epicardium, adjacent to the anterior interventricular vein and in proxim- ity to the left anterior descending coronary artery. The aortic valve cusps sit squarely within the crescent-shaped septal region of the RVOT and are inferior to the pulmonic valve. The posteroseptal aspect of the RVOT is adjacent to the region of the right coronary cusp, and the anterior septal surface is adjacent to the anterior margin of the right coro- nary cusp or the medial aspect of the left coronary cusp. In young patients, the aortic valve is parallel to the pulmonic valve and perpendicular to the mitral valve. In older pa- tients, the aortic valve may have a more vertical tilt and parallel the mitral valve. In addition, the location, rotation, and horizontal position of the heart in the chest cavity influence surface ECG characteristics. These anatomic considerations are critical in analyzing 12-lead ECG patterns and localizing the site of origin of outflow tract tachycardias. 1 RVOT tachycardias RVOT tachycardias have a left bundle branch block mor- phology with a precordial QRS transition that begins no earlier than lead V 3 and more typically occurs in lead V 4 . The frontal plane axis, precordial QRS transition, QRS width, and complexity of the QRS in the inferior leads can pinpoint the origin of VT in RVOT. Tachycardias originat- ing from the top of the tricuspid valve in the inflow area of the RVOT, which is lower and to the right in the outflow tract, will have a positive QRS deflection in lead aVL, QRS amplitude in lead II lead III, and typically a very positive QRS complex in lead I. A study from our institution further divided the septal and free wall areas into distinct anatomic sites, and pace mapping was performed at each site. The 12-lead ECG QRS KEYWORDS Electrocardiographic recognition; Right ventricular outflow tract tachycardia; Left ventricular outflow tract tachycardia; Epicardial tachycardia (Heart Rhythm 2007;4:366 –370) Address reprint requests and correspondence: Dr. Francis E. March- linski, Cardiac Electrophysiology, 9 Founders Pavilion, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, Pennsylva- nia 19104. E-mail address: [email protected]. 1547-5271/$ -see front matter © 2007 Heart Rhythm Society. All rights reserved. doi:10.1016/j.hrthm.2006.11.012

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lectrocardiographic recognition and ablation of outflow tractentricular tachycardiaupa Bala, MD, Francis E. Marchlinski, MD

rom the Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.

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Outflow tract tachycardias comprise a subgroup of idio-athic ventricular tachycardias (VTs) that occur in the ab-ence of structural heart disease. The arrhythmia mechanismppears to be calcium-dependent triggered activity, and noiscrete anatomic abnormalities have been identified. In ourxperience, most of these outflow tract tachycardias origi-ate from a fairly narrow anatomic zone. These arrhythmiasriginate in an arc-like fashion from the right ventricularRV) inflow region to the anteroseptal aspect of the rightentricular outflow tract (RVOT) under the pulmonic valve.he arc then extends leftward to include the cusp region of

he aortic valve and the anterior left ventricle (LV) in frontf the aortic valve, both endocardially and epicardially, andhen further extends toward the aorto–mitral continuity anduperior mitral annulus. Most outflow tract tachycardiasriginate in perivalvular tissue, which may be anatomicallyredisposed to fiber disruption that enhances arrhythmogen-sis. In addition, the proximity of the outflow tract to thepicardial fat pads containing the ganglionated plexuses andhe unique response to exercise and hormonal changes sug-est that the autonomic nervous system also plays a role inhis arrhythmogenesis. Because outflow tract tachycardiasend to occur in the absence of structural heart disease andre focal in origin, the 12-lead ECG recorded during VT isprecise localizing tool. In this review, we highlight theCG features of outflow tract tachycardias that aid in lo-alization and describe our approach to mapping and abla-ion.

mportant anatomic considerationshe RVOT region is defined superiorly by the pulmonicalve and inferiorly by the RV inflow tract and the top of thericuspid valve. The lateral aspect of the RVOT region ishe RV free wall, and the medial aspect is formed by thenterventricular septum at its base of the RVOT and RVusculature opposite the root of the aorta at the region just

EYWORDS Electrocardiographic recognition; Right ventricular outflowract tachycardia; Left ventricular outflow tract tachycardia; Epicardialachycardia (Heart Rhythm 2007;4:366–370)

ddress reprint requests and correspondence: Dr. Francis E. March-inski, Cardiac Electrophysiology, 9 Founders Pavilion, Hospital of theniversity of Pennsylvania, 3400 Spruce Street, Philadelphia, Pennsylva-

mia 19104. E-mail address: [email protected].

547-5271/$ -see front matter © 2007 Heart Rhythm Society. All rights reserved

nferior to the pulmonic valve. From the coronal view abovehe pulmonic valve, the RVOT region is seen wrappinground the root of the aorta and extending leftward. The topf the RVOT may be convex or crescent shaped, with theosteroseptal region directed rightward and the anteroseptalegion directed leftward. Occasionally, an extreme convex-ty of the superior septal RVOT region creates a leftwardirection for the most posterior and anterior aspects of theeptal RVOT and results in a net negative QRS complex inead I from either site. The anteroseptal aspect of the RVOTctually is located in close proximity to the LV epicardium,djacent to the anterior interventricular vein and in proxim-ty to the left anterior descending coronary artery. The aorticalve cusps sit squarely within the crescent-shaped septalegion of the RVOT and are inferior to the pulmonic valve.he posteroseptal aspect of the RVOT is adjacent to the

egion of the right coronary cusp, and the anterior septalurface is adjacent to the anterior margin of the right coro-ary cusp or the medial aspect of the left coronary cusp. Inoung patients, the aortic valve is parallel to the pulmonicalve and perpendicular to the mitral valve. In older pa-ients, the aortic valve may have a more vertical tilt andarallel the mitral valve. In addition, the location, rotation,nd horizontal position of the heart in the chest cavity influenceurface ECG characteristics. These anatomic considerationsre critical in analyzing 12-lead ECG patterns and localizinghe site of origin of outflow tract tachycardias.1

VOT tachycardiasVOT tachycardias have a left bundle branch block mor-hology with a precordial QRS transition that begins noarlier than lead V3 and more typically occurs in lead V4.he frontal plane axis, precordial QRS transition, QRSidth, and complexity of the QRS in the inferior leads caninpoint the origin of VT in RVOT. Tachycardias originat-ng from the top of the tricuspid valve in the inflow area ofhe RVOT, which is lower and to the right in the outflowract, will have a positive QRS deflection in lead aVL, QRSmplitude in lead II � lead III, and typically a very positiveRS complex in lead I.A study from our institution further divided the septal

nd free wall areas into distinct anatomic sites, and pace

apping was performed at each site. The 12-lead ECG QRS

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367Bala and Marchlinski ECG Recognition and Ablation of Outflow Tract VT

omplex from the pace maps and from spontaneous VT thatas successfully localized and ablated were analyzed.2 The

eptal and free-wall sites just under the pulmonic valve wereesignated as site 1 (posterior/right), site 2 (mid), and site 3anterior/left) to maintain simplicity with respect to theomenclature used to describe the anatomic location. TheRS complex changes most notably in lead I when moving

rom site 3—anterior and leftward (negative QRS inead I)—to site 1—posterior and rightward (positive QRS inead I). In contrast to the corresponding septal sites, theree-wall sites demonstrated a later QRS transition, widerRS duration and notching, and decreased amplitude in the

nferior leads and lateral precordial leads.The most common site of origin for RVOT tachycardias

s the left septal side of the outflow tract just underneath theulmonic valve. These tachycardias produce a characteristic2-lead ECG appearance with large positive QRS com-lexes in leads II, III, and aVF and large negative com-lexes in leads aVR and aVL. The QRS morphology in leadtypically is multiphasic and has a net QRS vector of zero

igure 1 Right ventricular outflow tract (RVOT) tachycardia from thelectroanatomic map (A) and fluoroscopic image (B), one can see how thend can generate a negative QRS complex in lead I during ventricular tachyachycardia (bottom). The gross anatomic specimen (C) depicts the septalnd free-wall sites just under the pulmonic valve are designated as site 1 (puring mapping.

r only modestly positive. Frequently, the VT may originate t

t the leftward edge of the septal aspect of the outflow tractust under the pulmonic valve. This extreme “leftward”spect of the RVOT actually produces a negative QRSomplex in lead I, consistent with how far this aspect of theVOT wraps around the aortic root and is located to the leftf the apical septum (Figure 1).

Of note, placement of the limb leads on the chest willnfluence the lead I QRS vector, particularly when VTriginates from the right posterior septal RVOT location.ace maps from this region are positive when the leads arelaced on the shoulders and negative when the leads arelaced on the chest. This change is likely due to a narrowingf the overall vector of lead I when “limb” leads are placedn the chest, as commonly done with exercise testing. Rec-gnition of the influence of limb lead and precordial leadlacement can prevent inaccurate VT localization based onCG interpretation.

VOT tachycardiaseft bundle morphology VT from the aortic cusp region and

tal side of the outflow tract just underneath the pulmonic valve. From thewraps around the aortic root, is located to the left of the apical septum,

The pace map from this leftward and anterior site is identical to the clinicalof the RVOT underneath the pulmonic valve. In our laboratory, the septalr/right), site 2 (mid), and site 3 (anterior/left) to simplify the nomenclature

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arlier than from the RVOT region. The R wave is positivey lead V2 or V3 with VT from the right coronary cusp andy lead V1 or V2 from the left coronary cusp. Ouyang et al3

oted a broad R-wave duration in lead V1 or V2 in the cuspegion vs the RVOT and thus reported an R-wave durationndex �50% and R/S ratio �30% in lead V1 or V2 in theireries of seven patients when VT originated from the aorticinuses. Of note, the noncoronary cusp is notable for atrialapture during pace mapping as it abuts the interatrial sep-um and may be the source of atrial arrhythmias.

Left coronary cusp VT and VT originating from thendocardium or epicardium just in front of the left coronaryusp is often associated with a W- or M-shaped pattern inead V1 and thus is difficult to classify as a true left or rightundle branch block pattern. Similar to RVOT tachycardias,T from the left coronary cusp and usually the right coro-ary cusp has a tall QRS in the inferior leads if the valveemains parallel to the pulmonic valve. The basis for this tallRS morphology in the inferior leads probably is the fact

hat the muscular septum is located below both valve planesnd is activated in a similar fashion from both the right and

igure 2 ECG patterns associated with selected outflow tract locations.f the right ventricular outflow tract (RVOT), anteroseptal aspect of the RVnd superior mitral annulus are shown. As one moves from right to left froract, it is clear that the precordial transition becomes earlier, with an eveignature W shape in lead V of the left coronary cusp VT and the qR in lea

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alve; NC � noncoronary cusp; PV � pulmonic valve.

eft septal perivalvular structures. As mentioned previously,ging may draw the aortic valve down in a vertical tilt inelation to the pulmonic valve; thus, right coronary cuspachycardias can exhibit a QRS complex in lead II � leadII and a biphasic (positive/negative) complex in lead aVL.n this situation, the left coronary cusp remains superior andxhibits a positive QRS in the frontal plane axis. Changes inhe QRS complex in lead I are important in the aortic cuspegion. The left coronary cusp tends to have a QS or rSomplex in lead I, whereas the right coronary cusp hasreater R-wave amplitude in lead I based on how posteriornd rightward the right coronary cusp is positioned. Inoung patients with a vertical heart, the QRS complex inead I may be negative in and around both the left coronaryusp and right coronary cusp regions. In patients with aorizontal heart, the area surrounding the aortic valve wille directed rightward relative to the LV apex/lateral wall,nd a positive QRS complex in lead I can be seen. Becausef the paucity of muscle fibers, pace mapping in the aorticusp region can be challenging and often requires goodontact, stability, high current strength, and placement into

-lead ECG pace maps or ventricular tachycardia (VT) from the free wallpical RVOT VT origin), left coronary cusp, aorto-mitral (A-M) continuity,VOT free wall to the anteroseptum and across the left ventricular outflowonophasic R wave in lead V1 from the superior mitral annulus. Note theom the aorto-mitral continuity pace map. AV � aortic valve; MV � mitral

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369Bala and Marchlinski ECG Recognition and Ablation of Outflow Tract VT

he base of the sinus. In our experience, pace maps and, ascorollary, VT across a single cusp occasionally vary whenne moves right to left for the right coronary cusp andnterior to posterior for the left coronary cusp.

Moving leftward to the aorto–mitral continuity on thendocardium, a qR complex typically is seen in lead V1 andn Rs/rs complex is noted in lead I. With VT originatingurther leftward across the anterior mitral annulus, the Rave in lead I diminishes and a broad, positive R wave is

een in lead V1 (Figure 2).4

VT from LV epicardial sites of origin, anterior to theortic valve, is frequently similar to patterns from the leftoronary cusp. In a study by Daniels et al,5 these tachycar-ias were seen to cluster at perivascular sites at the LVpicardium, with the majority at the junction of the greatardiac vein/anterior interventricular vein and proximal an-erior interventricular vein. The majority were notable for aeft bundle morphology in lead V1, and all had slurring inhe initial portion of the QRS indexed by the maximumeflection index (onset of R or r wave to nadir of S duration

igure 3 Representation of epicardial ventricular tachycardia (VT) fromhe anterobasal LV. Arrows indicate the typical QS complex in lead I and

2. A delayed or slurred pattern of initial QRS activation is noted. Red arroottom: Superimposed three-dimensional electroanatomic map of the LV enterobasal epicardium identified by the red color (large black arrow). M

roximity to the left anterior descending coronary artery and the catheter tip posi

n any precordial lead/total QRS duration �55%). In ourxperience, LV epicardial VT in this region commonly haveQS morphology in lead I and may show a characteristicRS transition pattern break, with the QRS in lead V2 being

ess positive or having a smaller R wave than in both lead

1 and V3. This pattern break is noted for VT with a leftundle branch block or slightly more leftward positionedT with a right bundle branch block QRS morphology

Figure 3).Successful ablation of outflow tract tachycardias begins

ith a careful analysis of the 12-lead ECG pattern of theT, coupled with recognition of the common sites of VTrigin. A detailed electroanatomic map can help delineatehe anatomic features of the outflow tract (Figures 1 and 3).ace mapping is performed in regions of interest based onnalysis of the 12-lead ECG during VT, with attention to anxact match for all 12 ECG leads. Activation mapping withnipolar and bipolar recordings is used to corroborate theace map finding when recurrent ventricular premature de-olarizations (VPDs) or VT is observed. Intracardiac echo-

terobasal left ventricle (LV). Left: ECG pattern of the epicardial VT fromacteristic pattern break from leads V1–V3, with relative negativity in leadtifies the epicardial electrogram recording 40 ms before the QRS. Middle,dium (ENDO) and epicardium (EPI) shows the earliest activation from thetop: Fluoroscopic image shows the successful site of VT elimination in

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tion corresponding to the exact 12/12 pace map match (right).

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370 Heart Rhythm, Vol 4, No 3, March 2007

ardiography can be used to assess catheter tip position inhe aortic cusp region to confirm anatomic location androximity to coronary anatomy. Prior to ablation in theortic cusp region and in the LV endocardium/epicardium inront of the aortic valve, angiography usually is performedo assess proximity to the coronary circulation. The areanterior to the aortic valve and next to the proximal anteriornterventricular vein is adjacent to the left main/left anteriorescending coronary artery bifurcation, and caution must bexercised when ablating in this area (Figure 3). Standard-mm-tip radiofrequency ablation is almost uniformly ef-ective if care is paid to precisely localizing the focal originf the VT for both RVOT and LVOT VTs.

onclusionCG recognition of outflow tract tachycardia location al-

ows one to distinguish right from left and epicardial fromndocardial VTs. Careful attention to frontal plane axis,recordial QRS transition, QRS width, and complexity ofhe QRS in the inferior leads can further pinpoint the origin

f VT. This analysis is helpful for planning the ablation

rocedure, counseling patients with regard to risks andnticipated outcomes, and facilitating a nearly uniform suc-essful ablation strategy.

eferences. Marchlinski FE, Lin D, Dixit S, Jacobson J, Sauer W, McKernan M, Ren JF.

Ventricular tachycardia from the aortic cusps: localization and ablation. In:Raviele A, editor. Cardiac Arrhythmias 2003: Proceedings of the 8th Interna-tional Workshop on Cardiac Arrhythmias, Venice, October 5–8, 2003. Springer-Verlag Italia, pp. 357–371.

. Dixit S, Gerstenfeld EP, Callans DJ, Marchlinski FE. Electrocardiographicpatterns of superior right ventricular outflow tract tachycardias: distinguishingseptal and free wall sites of origin. J Cardiovasc Electrophysiol 2003;13:1–7.

. Ouyang F, Fotuhi P, Ho SY, Hebe J, Volkmer M, Goya M, Burns M, Antz M,Ernst S, Cappato R, Kuck KH. Repetitive monomorphic ventricular tachycardiaoriginating from the aortic sinus cusp: electrocardiographic characterization forguiding catheter ablation. J Am Coll Cardiol 2002;39:500–508.

. Dixit S, Gerstenfeld EP, Lin D, Callans DJ, Hsia HH, Nayak HM, Zado E,Marchlinski FE. Identification of distinct electrocardiographic patterns from thebasal left ventricle: distinguishing medial and lateral sites of origin in patientswith idiopathic ventricular tachycardia. Heart Rhythm 2005;2:485–491.

. Daniels DV, Lu Y-Y, Morton JB, Santucci PA, Akar JG, Green A, Wilber DJ.Idiopathic epicardial left ventricular tachycardia originating remote from thesinus of Valsalva: electrophysiological characteristics, catheter ablation, and

identification from the 12-lead electrocardiogram. Circulation 2006;113:1659–1666.