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Adenosine-Sensitive Ventricular TachycardiaClinical Characteristics and Response to Catheter Ablation
David J. Wilber, MD; Jeffrey Baerman, MD; Brian Olshansky, MD;John Kall, MD; and Douglas Kopp, MD
Background. Sustained ventricular tachycardia in the absence of structural heart disease may havediverse mechanisms. Termination of the tachycardia by adenosine suggests triggered automaticity as theetiology in many of these patients. We examined the clinical characteristics, electrophysiologicalresponses, and results of catheter ablation in this patient subgroup.Methods and Results. Intravenous adenosine terminated sustained ventricular tachycardia in seven of 14
consecutive patients without evidence of structural heart disease. In each of these patients, the tachycardiahad a left bundle branch block, inferior-axis QRS configuration and occurred predominantly duringstress or exertion. A morphologically similar sustained tachycardia was induced in six of seven patientsduring programmed ventricular stimulation, although day-to-day reproducibility was poor. Signal-averaged ECGs were normal in all patients. Imaging with '"I-metaiodobenzylguanidine did not revealfocal abnormalities in any of five patients. A discrete site of origin was identified in the free wall of thepulmonary infundibulum in all patients. Limited application of direct current shocks (two patients) or
radiofrequency energy (five patients) resulted in long-term abolition of spontaneous and inducibleventricular tachycardia in all patients.
Conclusions. Adenosine-sensitive ventricular tachycardia appears to arise from relatively discrete sitespredominantly located in the free wall of the pulmonary infundibulum. The localized nature of thistachycardia renders it amenable to long-term cure by catheter ablation techniques. (Circulation1993;87:126-134)KEY WoRDS * pace mapping * activity, triggered
V entricular tachycardia in patients without struc-tural heart disease is an uncommon clinicalentity.' In a large proportion of such patients,
the tachycardia has a uniform left bundle branch block,inferior-axis QRS configuration, suggesting an origin inthe right ventricular outflow tract.2-13 However, theselatter patients do not constitute a homogeneous group.Clinical presentations range from incessant runs ofmonomorphic nonsustained ventricular tachycardia toinfrequent episodes of sustained ventricular tachycar-dia. Exercise may either suppress or facilitate tachycar-dia initiation. Attempts to classify tachycardia mecha-nism by the response to programmed stimulation andpharmacological manipulation (verapamil, isoprotere-nol) suggest diverse potential etiologies including reen-try, triggered activity, and catecholamine-mediatedautomaticity.4,6-8Lerman et a17 recently described a group of patients
with exercise-induced sustained ventricular tachycardiawith a left bundle branch block, inferior-axis QRSconfiguration in whom adenosine reliably terminatedthe tachycardia. The response to adenosine and toautonomic maneuvers that antagonize catecholamine-associated increases in cAMP provided strong evidence
From the Section of Cardiology, Loyola University MedicalCenter, Maywood, Ill.Address for reprints: David J. Wilber, MD, Section of Cardiol-
ogy, Loyola University Medical Center, 2160 South First Avenue,Maywood, IL 50153.
Received March 2, 1992; revision accepted September 22, 1992.
for cAMP-mediated triggered automaticity as the mech-anism of tachycardia. These observations also suggestedthat adenosine may be used as a diagnostic tool toidentify a unique subset of patients with idiopathicventricular tachycardia.The purpose of this report is to further characterize
the clinical presentation and electrophysiological re-sponses of patients with adenosine-sensitive, catechola-mine-mediated ventricular tachycardia. Detailed map-ping and pacing studies demonstrated that thesetachycardias arise from discrete foci in the free wall ofthe pulmonary infundibulum. Catheter ablation at thesesites resulted in long-term abolition of spontaneousventricular tachycardia.
MethodsPatient Selection
In 14 patients presenting with spontaneous sustainedventricular tachycardia without evidence of structuralheart disease, intravenous adenosine was administeredduring the tachycardia to assess effects on termination(see below). Adenosine failed to terminate ventriculartachycardia in seven patients. The remaining sevenpatients, all with adenosine-sensitive left bundle branchblock, inferior-axis ventricular tachycardia, comprisethe study group. In these patients, ambulatory monitor-ing, formal exercise testing, and signal-averaged ECGs(method of Simpson14) were performed before electro-physiological evaluation.
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a-blockers; V, verapamil; Q, quinidine; M, mexiletine; F, flecainide; PA, procainamide; N, norpace; AM, amiodarone;PP, propafenone; EM, ethmozine; PVCs, premature ventricular complexes; NSVT, nonsustained ventriculartachycardia.
*Parentheses indicate number of nonsustained tachycardia beats.
Electrophysiological TestingStudies were performed in the postabsorptive state in
the absence of antiarrhythmic drug therapy after in-formed consent had been obtained. Quadripolar cathe-ters were inserted percutaneously and advanced underfluoroscopic guidance to the high right atrium, rightventricular apex, and the atrioventricular junction. Bi-polar electrograms were filtered at 30-500 Hz anddisplayed simultaneously with six surface ECG leads ona multichannel oscilloscope (Siemens-Elema, Inc.Solna, Sweden). Data were stored on magnetic tape(Teac XR-510, Montebello, Calif.) and printed on anink-jet recorder (Siemens-Elema Mingograf) for imme-diate review. Electrical stimulation was performed witha programmable stimulator and an isolated constantcurrent source (Bloom Associates, Ltd., Narbeth, Pa.)using rectangular pulses of 2-msec duration at twicediastolic threshold. Decremental burst atrial pacing andthe introduction of single atrial extrastimuli at decre-mental intervals during multiple paced atrial cyclelengths were performed in all patients. Ventricularstimulation, which included the introduction of single,double, and triple extrastimuli during multiple pacedcycle lengths at two right ventricular sites, was per-formed as previously described.'5 Burst ventricular pac-ing at cycle lengths of 200-400 msec was alsoperformed.
If sustained ventricular tachycardia could not beinduced during baseline stimulation, the stimulationprotocol was repeated during isoproterenol infusion(2-8 g/min). Intravenous adenosine (6-18 mg) wasinjected via a central vein during sustained ventriculartachycardia to assess the effect on termination. Duringsustained tachycardia, autonomic maneuvers, includingboth right and left carotid sinus massage and theValsalva maneuver, were also performed.
Mapping and Catheter AblationAfter completion of electrophysiological studies, ac-
tivation sequence mapping of the right ventricle wasperformed during sustained or nonsustained ventriculartachycardia. Electrograms from the distal bipolar pair of
the mapping catheter (2-mm bipolar separation) werefiltered between 30 and 500 Hz, and activation timeswere recorded relative to the onset of the surface QRS.Positioning of the catheter tip was confirmed in multipleprojections and recorded on film. Since all tachycardiashad a left bundle branch block, inferior-axis morphol-ogy, mapping efforts were concentrated in the region ofthe right ventricular outflow tract. Pace mapping wasperformed during sinus rhythm at a rate similar to theinduced tachycardia or during ventricular tachycardia ata rate slightly faster than the tachycardia rate. The QRSmorphology in each of 12 leads was compared with themorphology during ventricular tachycardia. Optimalpace maps were defined as those with the closestpossible match between QRS morphologies in each ofthe 12 leads.
After identification of the putative site of tachycardiaorigin, ablation was performed using either direct cur-rent shocks or application of radiofrequency energy.For patients undergoing direct current shocks, the distaltip of a 7F quadripolar catheter (USCI, Billerica, Mass.)was connected to the cathodal output of a standarddefibrillator. A 16-cm2 cutaneous patch electrode (R-2Corporation, Morton Grove, Ill.) positioned on the backwas used as the anode. During direct current shocks, allpatients were anesthetized with intravenous midazolam.Radiofrequency energy applications were made using aprogrammable lesion generator with 300-kHz outputwith continuous monitoring of voltage and impedance(Radionics Inc., Burlington, Mass.). The cathodal out-put was delivered to the distal 4-mm tip electrode of asteerable quadripolar catheter (Mansfield, Boston Sci-entific Corp., Watertown, Mass.). The anode was acutaneous patch.
ResultsPatient CharacteristicsThe clinical characteristics of the study population
are summarized in Table 1. All patients had a history ofsustained exertional or stress-related palpitations. Atleast one spontaneous episode of sustained monomor-phic ventricular tachycardia with a left bundle branch
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extrastimuli; PVCs, premature ventricular complexes; NSVT, nonsustained ventricular tachycardia; SMVT, sustainedmonomorphic ventricular tachycardia; NT, not tested.*Number of nonsustained tachycardia beats.
block, inferior-axis QRS configuration was documentedelectrocardiographically in each patient. Five patientshad syncope or near syncope. In the absence of sus-tained ventricular tachycardia, spontaneous ventricularpremature complexes with a similar QRS configurationwere present in all patients and usually increased duringperiods of stress or exercise. Ambulatory monitoringdemonstrated fewer than 200 ventricular prematurecomplexes per 24-hour period in five patients. Only onepatient had repetitive paroxysms of monomorphic non-sustained ventricular tachycardia during ambulatorymonitoring. In this patient (No. 3), ventricular prema-ture complexes comprised 43% of recorded beats.Coronary arteriography and left ventriculography
were normal in all patients. Two-dimensional echocar-diographic assessment of right ventricular size andfunction was normal in all patients. Myocardial biopsywas performed in three patients and was normal ineach. The signal-averaged ECG did not meet any crite-rion for late potentials (total filtered QRS >120 msec,root mean-squared amplitude of the terminal 40 msec<25 V, duration of low amplitude signals >39 msec14)in any patient.
Electrophysiological TestingThe results of preablation electrophysiological testing
are summarized in Table 2. In the absence of isopro-terenol, sustained ventricular tachycardia was initiatedreproducibly in only one patient. During isoproterenolinfusion, sustained ventricular tachycardia was inducedin an additional five patients. In one patient (No. 5),only nonsustained ventricular tachycardia could be in-duced. All induced tachycardias had a left bundlebranch block, inferior-axis QRS configuration.The relation between the coupling interval of the last
paced beat and the return cycle of the first tachycardiabeat was examined in four patients. There was noconsistent relation between these two variables in anypatient. Single and double extrastimuli were introducedduring sustained ventricular tachycardia at progressivelyshorter coupling intervals in four patients. Resettingwas not observed in any patient. In all patients with
induced sustained ventricular tachycardia, burst ventric-ular pacing terminated the tachycardia.
Electrophysiological testing was performed in theabsence of antiarrhythmic drug therapy on multipledays in four patients. In these patients, the induction ofsustained ventricular tachycardia was variable. In pa-tient 4, sustained ventricular tachycardia could not beinduced by any technique on two consecutive days.However, sustained ventricular tachycardia was inducedduring programmed ventricular stimulation on the pre-ablation study 4 months later. In patients 2 and 7,sustained ventricular tachycardia could be induced onlyat the second of two studies 1 and 3 months apart,respectively. Patient 3 underwent three studies. Sus-tained ventricular tachycardia was not induced initiallybut was reproducibly induced on two different days 6months later.
Response to Adenosine and Autonomic ManeuversAdenosine (6-12 mg) was administered during sus-
tained ventricular tachycardia in all seven patients. Ineach patient, the tachycardia had persisted for at least 3minutes before injection and was terminated within 15seconds of injection. At least two successful termina-tions of induced sustained ventricular tachycardia weredocumented in six patients. In one patient (No. 5) inwhom sustained ventricular tachycardia could not beinduced during electrophysiological testing, adenosinehad terminated a previous episode of spontaneoussustained ventricular tachycardia. Autonomic maneu-vers were performed in three patients (No. 2, No. 3, andNo. 6). Carotid sinus massage reproducibly terminatedsustained ventricular tachycardia in all three patients.The Valsalva maneuver reproducibly terminated sus-tained ventricular tachycardia in two patients.
Mapping and AblationMapping during sustained or nonsustained ventricu-
lar tachycardia revealed endocardial activation beforethe onset of the surface QRS in the right ventricularoutflow tract in all patients, although presystolic activa-tion was recorded over a relatively large area. Activation
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Wilber et al Adenosine-Sensitive Ventricular Tachycardia
TABLE 3. Catheter Ablation Data
SMVT CL Frontal EAT AblationPatient (msec) axis (msec) site Technique
1 270 +115 -20 A DC (200 J, 1 application)2 220 +75 -10 C RF (50 Wx30 seconds, 4 applications)3 390 +90 -20 B RF failed, DC (200 J, 1 application)4 290* +90 -30 B RF (40 Wx30 seconds, 6 applications)5 270* +75 -10 C RF (40 Wx30 seconds, 6 applications)6 350 +90 -20 B RF (50 Wx30 seconds, 7 applications)7 380 +75 -10 C RF (50 Wx30 seconds, 4 applications)
SMVT, sustained monomorphic ventricular tachycardia; CL, cycle length; EAT, earliest activation time; DC, directcurrent shock; RF, radiofrequency energy; A, site near septal attachment of the free wall; B, site on mid free wall ofthe outflow tract; C, free wall site posterolaterally (closer to tricuspid valve).*CL of nonsustained ventricular tachycardia at preablation testing.
at the site of successful ablation preceded the onset ofthe surface QRS by 10-30 msec (Table 3). Low-ampli-tude or fractionated electrograms were not observed.The optimal pace map in each patient demonstrated
a close concordance of QRS configuration in each of the12 leads (Figure 1). In each patient, the site of theoptimal pace map was discrete and generally reproduc-ible only within a few millimeters. Presystolic activationwas frequently recorded at sites with poor pace mapmatches. For this reason, the optimal pace map wasused as the primary guide for selection of the ablationsite.
VT PACING
11 ^
R vWw
L -,w
VT PACING
V1 g
V2g1
V4 A A MAJ,
V5
V6
kM
FIGURE 1. QRS configuration in each of 12 surface ECGleads during ventricular tachycardia (VT) (left panel) andventricular pacing from the optimal pace map site (rightpanel) in patient 2. Horizontal bar indicates 1 second. See text
for details.
Optimal pace maps and the subsequent sites ofsuccessful ablation were all located on the anterior freewall of the pulmonary infundibulum (Figure 2 andTable 3), ranging from sites near the septal attachmentanteromedially to sites closer to the tricuspid valveposterolaterally. The frontal-plane QRS axis was anexcellent predictor of the site of the optimal pace map.A predominantly negative QRS in lead I was associatedwith a site near the septal attachment of the free wall(site A). An isoelectric QRS in lead I was associatedwith a site on the mid free wall of the outflow tract (siteB). A third distinct morphology had a predominantlypositive QRS configuration in lead I and was associatedwith a free wall site posterolaterally (site C), closer tothe tricuspid valve (Figure 3).
Direct current shock was the initial energy modalityin the first patient only. Radiofrequency energy was theinitial treatment in the remaining six patients. Applica-tion of radiofrequency energy during the tachycardiawas associated with brief acceleration followed by irreg-ular slowing for several seconds before termination(Figure 4). The goal of radiofrequency application wasthe elimination of all spontaneous ventricular ectopyand inducible tachycardia (sustained or nonsustained)during isoproterenol infusion. If spontaneous ectopy orinducible ventricular tachycardia persisted, minor repo-sitioning of the catheter within a few millimeters wasperformed, and another application was given. In onepatient with unsuccessful radiofrequency ablation, asingle direct current shock applied to the same site wassuccessful. In the remaining five patients, spontaneousand inducible ventricular arrhythmias were eliminatedwith two to five radiofrequency applications.
Follow-upThere were no immediate adverse sequelae in any
patient. The initial patient, who received a single directcurrent shock, had several runs of polymorphic nonsus-tained ventricular tachycardia (three to seven beats)within the first 24 hours after ablation. No treatmentwas given, and these arrhythmias resolved spontane-ously. Two-dimensional echocardiograms were per-formed 1-4 weeks after ablation in four patients (pa-tients 1-4), and no abnormalities were observed.
All patients were discharged on no antiarrhythmicmedications. Follow-up electrophysiological testing, in-cluding stimulation during isoproterenol infusion, wasperformed at 1-4 weeks in all patients. Nonsustained or
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FIGURE 2. Representation of the heart in an angulated left anterior oblique projection. The right ventricle is opened with theendocardial surface of the free wall depicted on the segment to the right. A, B, and C indicate the ablation sites corresponding tothe respective QRS configurations indicated in Table 3.
sustained ventricular tachycardia could not be induced inany patient. Ambulatory monitoring and formal tread-mill testing performed during a similar time frame re-vealed at most rare premature ventricular complexes(often with a different QRS configuration) in all patients.During a mean follow-up of 16 months (range, 5-33
months), no patient had recurrent ventricular tachycar-dia or sustained palpitations. Transtelephonic eventmonitors were used in all patients to investigate com-plaints of palpitations or "cardiac awareness." In allinstances, only isolated premature ventricular com-plexes were documented.
Five patients underwent radionuclide scanning withthe guanethidine analogue 13I-metaiodobenzylguani-dine (MIBG) 1-4 months after ablation to assess theintegrity of cardiac adrenergic innervation.16 Focal ab-normalities were absent in all patients. In four patients,cardiac uptake of the tracer was dense and homogenousthroughout, including the region of the pulmonaryinfundibulum. In one patient, cardiac uptake of thetracer was minimal throughout the heart despite normaluptake in other organs, suggesting diffusely rapid turn-over of cardiac neurotransmitters.16 These observationssuggest that the mechanism of successful ablation wasdirect tissue injury rather than focal denervation orlocal catecholamine depletion.
Patients With Ventricular TachycardiaUnresponsive to Adenosine
Patients without structural heart disease in whomadenosine did not terminate ventricular tachycardia
were a heterogeneous group (Table 4). The tachycar-dias had a left bundle branch block, inferior-axis QRSconfiguration in two patients, and activation/pace map-ping identified a site of origin on the septum of the rightventricular outflow tract. Five patients had right bundlebranch block, superior-axis tachycardias. Mapping infour of these patients revealed a site of origin in the leftventricular inferior apical septum. Two of these patientshad exercise-induced ventricular tachycardia and re-quired isoproterenol for induction of the tachycardiaduring programmed stimulation. Verapamil suppressedinducible and spontaneous tachycardias in one of theselatter patients.
DiscussionMajor Findings
This study demonstrates that adenosine reproduciblyterminates ventricular tachycardia in a large proportionof patients with structurally normal hearts, particularlythose who present with a left bundle branch block,inferior-axis QRS configuration. These patients shareseveral common features. Patients typically have stress-related or exertion-related sustained ventricular tachy-cardia; repetitive paroxysms of monomorphic nonsus-tained tachycardia are rare. The provocation of sustainedtachycardia during standard exercise testing and pro-grammed ventricular stimulation is not always reproduc-ible. With the exception of adenosine sensitivity, thesecharacteristics may also be observed in other patientswith idiopathic ventricular tachycardia. However, in each
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Wilber et al Adenosine-Sensitive Ventricular Tachycardia
FIGURE 3. Radiograph in the rightantet ior oblique projection illustrat-ing the positioning of catheters forablation in patient 2. Catheters arepositioned in the right ventricular in-flow tract (bottom right), the rightatrium (middle left), and at the op-timal pace mapping site on the freewall of the pulmonary infundibulum(top middle).
adenosine-responsive patient, the tachycardia had a leftbundle branch block, inferior-axis QRS configurationand arose from a discrete site in the free wall of thepulmonary infundibulum. Focal ablation at this siteresulted in long-term abolition of ventricular tachycardia.
Electrophysiological MechanismsThe use of adenosine to identify a common tachycar-
dia mechanism in patients with idiopathic ventricular
tachycardia is of particular importance, given the unre-liability of other diagnostic maneuvers or clinical find-ings. The only known effect of adenosine in ventricularmyocardium is the antagonism of catecholamine-stimu-lated elevations in cAMP.'7 The efficacy of adenosine interminating ventricular tachycardia strongly supportstriggered activity as the responsible mechanism in thesepatients. The response to carotid sinus massage and theValsalva maneuver in the study patients and those
FIGURE 4. Onset of radiofrequency application during sustained ventricular tachycardia (indicated by bold line above the rightventricular outflow tract [RVOT1 electrogram). There is an initial acceleration of the tachycardia followed by progressive slowingand irregularity. After 14 seconds, ventricular tachycardia terminates and does not recur. Bold vertical line is equal to 200 msec.
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TABLE 4. Characteristics of Patients With Ventricular Tachycardia Not Responsive to Adenosine
Age SMVT Exercise Verapamil ProgrammedPatient (years)/sex morphology induced response stimulation Mapping1 38/M RBBB-sup Yes Yes SMVT (2 VES) LV IAS2 54/M RBBB-sup Yes No SMVT (2 VES) LV IAS3 14/F RBBB-sup No No SMVT (3 VES) LV IAS4 36/M RBBB-sup No No SMVT (3 VES) LV IAS5 14/M RBBB-sup No No SMVT (1 VES) NT6 42/M LBBB-inf No No SMVT (2 VES) RVOT septum7 72/M LBBB-inf No NT SMVT (3 VES)* RVOT septum
SMVT, sustained monomorphic ventricular tachycardia; RBBB, right bundle branch block; sup, superior axis; LBBB,left bundle branch block; inf, inferior axis; NT, not tested; VES, ventricular extrastimuli; LV, left ventricle; IAS, inferiorapical septum; RVOT, right ventricular outflow tract.*Two additional morphologies not seen clinically also induced.
characterized by Lerman et a17 are also consistent withthis mechanism.18
In contrast, the response to programmed stimulationhas important limitations in defining the mechanism ofventricular tachycardia18; both reentrant and triggeredventricular arrhythmias may be initiated by prematureextrastimuli and burst ventricular pacing.19 The induc-tion and termination of ventricular tachycardia by pro-grammed ventricular stimulation in the study patientsdoes suggest that normal or abnormal automaticity areunlikely mechanisms.'8
In previous reports of electrophysiological testing inpatients with catecholamine-associated, idiopathic, leftbundle branch block, inferior-axis sustained ventriculartachycardia, the induction of ventricular tachycardiaduring electrophysiological testing ranged from 0% to100%.2-10 Lerman and associates7 found that sustainedventricular tachycardia could be induced by pro-grammed ventricular stimulation in three of four pa-tients with adenosine-sensitive ventricular tachycardiaand by atrial pacing in the remaining patient. Sung andcoworkers8 found that atrial or ventricular pacing couldinduce ventricular tachycardia in four of four patientswith verapamil-sensitive, idiopathic, left bundle branchblock, inferior-axis ventricular tachycardia. In this study,the induction of sustained ventricular tachycardia re-quired the use of a relatively aggressive stimulationprotocol and repeated stimulation on different days.Thus, failure to induce ventricular tachycardia by pro-grammed stimulation at any single point in time doesnot exclude triggered automaticity as the underlyingmechanism of spontaneous tachycardia.
Neither verapamil sensitivity nor adrenergic respon-siveness are specific probes for tachycardia mechanisms.Catecholamines may facilitate arrhythmias caused byreentry, automaticity, or triggered activity,20 and,8-blockade occasionally may be effective in abolishingventricular tachycardias caused by any of these mecha-nisms.7,8,21 Although verapamil frequently suppressesventricular tachycardia presumed to be secondary totriggered automaticity,7,8 it has also been shown tosuppress arrhythmias consistent with reentry in bothischemic22 and normal hearts.23 One patient in this studyhad catecholamine-induced, verapamil-sensitive ventric-ular tachycardia that did not respond to adenosine.
Localization and Ablation TechniquesExperience with both direct surgical4'24 or percutane-
ous catheter ablation25,26 in patients with idiopathic
right ventricular tachycardia is limited. Reports of suc-cessful catheter ablation are limited to the use of directcurrent shocks. Stevenson et a125 described a patientwith catecholamine-mediated, left bundle branch block,inferior-axis ventricular tachycardia in whom three di-rect current shocks delivered to the right ventricularoutflow tract eliminated subsequent episodes of ventric-ular tachycardia and markedly reduced the frequency ofspontaneous premature complexes. Morady et a126 re-cently reported successful catheter ablation in eight of10 patients with idiopathic left bundle branch block,inferior-axis sustained ventricular tachycardia using di-rect current shocks applied to the right ventricularoutflow tract. None of these patients received adeno-sine, and specific localization of the ablation site withinthe outflow tract was not reported.
Previous mapping studies of catecholamine-associ-ated right ventricular outflow tract tachycardia indi-cated that such tachycardias arise predominantly fromthe intraventricular septum.3'4 In this study, all patientswith adenosine-responsive ventricular tachycardia hadeffective ablation with localized application of energy inthe free wall of the pulmonary infundibulum. In theformer studies, pace mapping and ablation were notused to corroborate information from activation se-quence mapping, and adenosine responsiveness was notassessed.Pace mapping provides a reliable, practical means to
identify appropriate ablation sites in patients with aden-osine-sensitive ventricular tachycardia. In contrast to itsunreliability in identifying appropriate ablation sites inreentrant ventricular tachycardia associated with myo-cardial infarction,27'28 pace mapping may more preciselyimitate activation patterns during ventricular tachycar-dia arising from a single anatomically discrete focus in astructurally normal heart.26 The optimal pace map inthe study patients invariably had a short stimulus toQRS interval, providing additional evidence that anarea of slow conduction did not participate in thegenesis of this arrhythmia.29
In this study, the only complication related to cathe-ter ablation was a new but self-limited nonsustainedventricular tachycardia early after direct current shock.Transient myocardial dysfunction and cardiac perfora-tion have also been described after the application ofdirect current shocks in the right ventricle.30'3' For thesereasons, radiofrequency energy remains the modality offirst choice. The cause of unsuccessful radiofrequency
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Wilber et al Adenosine-Sensitive Ventricular Tachycardia 133
ablation in one patient is uncertain because the subse-quent successful direct current shock was applied at thesame site. It is possible that inadequate electrodecontact precluded effective transmission of energy tothe endocardium.The apparent predilection of this tachycardia for
specific sites within the free wall of the pulmonaryinfundibulum is unexplained. Histological abnormalitiesat the site of tachycardia origin could not be identifiedin a previously reported patient undergoing direct sur-gical ablation.24 In addition, multiple or "latent" foci,which could increase the risk of late recurrences, werenot observed in any patient. A limited number of energyapplications within a very circumscribed area resultedin long-term abolition of all ventricular tachycardias. Ofinterest, there appear to be no regional inhomogeneitiesof sympathetic innervation in patients with adenosine-sensitive ventricular tachycardia, at least as reflected byMIBG scanning. The mechanism of successful ablationappears unrelated to sympathetic denervation.
LimitationsPatients with ventricular tachycardia and structurally
normal hearts, even those arising exclusively from theright ventricular outflow tract, are most likely a hetero-geneous group who may not share a common mecha-nism. We included only patients in whom sustainedtachycardias could be documented so that the responseto adenosine could be unequivocally demonstrated. It ispossible that many nonsustained ventricular tachycar-dias in patients without structural heart disease, includ-ing those with repetitive monomorphic ventriculartachycardia,12"13 also may be due to triggered automa-ticity. In this study, we did not observe adenosinesensitivity in idiopathic sustained ventricular tachycar-dias arising from other right or left ventricular sites.Further experience with the diagnostic use of adenosinemay modify this preliminary observation.
Clinical ImplicationsThe prognosis of patients with idiopathic right ven-
tricular tachycardia is reported to be excellent,432,33provided that occult right ventricular dysplasia or car-diomyopathy have been excluded.34 Pharmacologicaltherapy is often effective in these patientsl"4; however,recurrent disabling palpitations or intolerable side ef-fects during medical therapy are common. In patientswith adenosine-sensitive ventricular tachycardia, cathe-ter ablation, particularly with the use of radiofrequencyenergy, appears to provide a safe and highly effectivetherapeutic alternative.
AcknowledgmentsThe authors gratefully acknowledge the expert assistance of
Dr. Robert Henkin and Steven Karesh, who performed andinterpreted the MIBG scans, and the technical assistance ofSally Botkin in the performance of electrophysiological studiesand catheter ablation.
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