Demonstration of the Reentrant Circuit of Verapamil-SensitiveIdiopathic Left Ventricular Tachycardia: Direct Evidence for

Macroreentry as the Underlying MechanismMITSUNORI MARUYAMA, M.D., TAKESHI TADERA, M.D.,

SHINJIRO MIYAMOTO, M.D., and TAKESHI INO, M.D.

From the Department of Internal Medicine, Tama-Nagayama Hospital, Nippon Medical School, Tokyo, Japan

Reentrant Circuit of Idiopathic LV Tachycardia. The exact reentrant circuit of verapamil-sensitive idiopathic left ventricular tachycardia (ILVT) remains unclear. This case report demonstratesthe reentrant circuit of ILVT. A 20-pole electrode catheter was placed along the left posterior fascicleduring electrophysiologic study. ILVT was reproducibly induced by programmed ventricular stimulation.During the tachycardia, sequential diastolic potentials bridging the entire diastolic period were observedin the recordings from the electrodes positioned from left ventricular mid-septum to inferoapical septum.The slow conduction zone appeared to be composed of a false tendon in this patient. Entrainment of theILVT from the right ventricular out� ow tract at a different pacing cycle length revealed that a dominantconduction delay occurred at the proximal site of the slow conduction zone. Entrainment studies fromseveral sites on the left ventricular septum con� rmed that these sites where sequential electrical activitywas recorded were included within the reentrant circuit. However, the left posterior fascicle itself seemedto be a bystander. This report provides the direct evidence of macroreentry as the underlying mechanismof this ILVT, adjacent to the left posterior fascicle. (J Cardiovasc Electrophysiol, Vol. 12, pp. 968-972,August 2001)

idiopathic left ventricular tachycardia, reentrant circuit, macroreentry, false tendon, left posterior fascicle

Introduction

Idiopathic left ventricular tachycardia (ILVT) withoutappreciable structural heart disease is a distinct clinicalentity characterized by a QRS morphology with right bun-dle branch block and left-axis deviation, and is responsive toverapamil. Reentry is believed to be the mechanism ofILVT, based on the results of electrophysiologic and en-trainment studies.1 ,2 However, the exact reentrant circuitremains to be determined, and there is still some debate asto whether macroreentry or microreentry is the underlyingmechanism of ILVT.3 -8 Only one report is available withevidence favoring microreentry.5 In that report, continuouselectrical activity throughout the entire cardiac cycle wasrecorded at a localized area during the tachycardia.5 On theother hand, several studies showed that successful radiofre-quency ablation of ILVT could be achieved at a site distantfrom the tachycardia exit site, suggesting that the reentrantcircuit was of considerable size.6 ,7 ,9 -12 The main reason whymicroreentry is proposed as the responsible mechanism ofILVT is that attempts to record intervening electrical activ-ity bridging the entire diastolic period failed, even though itwas reported that a few diastolic potentials were recordedduring tachycardia.

This case report demonstrates the reentrant circuit ofverapamil-sensitive ILVT using a 20-pole electrode cathe-ter. We discuss the location of the slow conduction zone and

relationship between the reentrant circuit and left posteriorfascicle.

Case ReportA 39-year-old man had noted episodes of palpitations since

he was 17 years old. During an episode, the ECG showedventricular tachycardia (VT) with a right bundle branch blockmorphology and left-axis deviation ( 2 75°) at a rate of 214beats/min. Class I antiarrhythmic drugs failed to terminate theVT, but intravenous injection of verapamil restored sinusrhythm. Coronary arteriography was normal. He was referredto our institution for catheter ablation. The ECG during sinusrhythm revealed no abnormal � ndings. Results of physicalexamination, chest roentgenography, blood examination, andthallium myocardial perfusion scintigraphy were normal. Atreadmill exercise test was performed, but neither induciblearrhythmia nor ischemic changes were observed. Transtho-racic echocardiography was normal except for the presence ofa false tendon extending from the left ventricular inferoapicalseptum to the mid-septum (Fig. 1A). The length and width ofthe false tendon were 35 and 3 mm, respectively. The signal-averaged ECG was negative for a late potential.

Electrophysiologic Study and Radiofrequency AblationElectrophysiologic study was performed with the patient in

the fasting state, free of antiarrhythmic drugs, and under lightsedation with oral diazepam. In addition to the electrode cath-eters for conventional electrophysiologic study to record theintracardiac bipolar electrograms from the right atrial ap-pendage, His-bundle region, coronary sinus, and right ventric-ular apex (RVA) or out� ow tract (RVOT), a 7-French 20-poleelectrode catheter (1-3-1 mm interelectrode spacing; Cordis-Webster, Baldwin Park, CA, USA) was positioned at the leftventricular septum to record 10 bipolar electrogramsalong theputative left posterior fascicle (Fig. 1B). During sinus rhythm,sequential high-frequency potentials were observed betweenthe His-bundle electrogram and the distal left ventricular elec-

Address for correspondence: Mitsunori Maruyama, M.D., Department ofInternal Medicine, Tama-Nagayama Hospital, Nippon Medical School,1-7-1 Nagayama, Tama-shi, Tokyo 206-8512, Japan. Fax: 81-42-372-7379; E-mail: maru@nms.ac.jp

Manuscript received 31 December 2000; Accepted for publication 7 May2001.

968

trograms, indicating that they were left posterior fascicularelectrograms (Fig. 1C). The atrial-His and His-ventricular in-tervals were 80 and 48 msec, respectively. Of note, low-fre-quency delayed potentials were observed and seemed to consistof ascending and descending impulses. Atrial rapid pacingrevealed second-degree atrio-Hisian block at rates > 110 beats/min and no tachycardia was inducible. During ventricularpacing from the RVA, delayed potentials with the same mor-phology and activation sequence as those observed in sinusrhythm also were recognized after the ventricular electro-grams, despite the high-frequency potentials becoming buriedin the ventricular electrograms (Fig. 2A). When the couplinginterval of the ventricular extrastimuli from the RVA (S1-S2)was shortened up to 250 msec at a basic cycle length of 400msec, the delayed impulse ascending from the apical septumwas blocked and the descending impulse from the mid-septumwas able to propagate distally. The descending impulse wasblocked at the apical septum, probably because the distal siteremained refractory. Subsequently, as S1-S2 was furthershortened, decremental conduction occurred, especially at theproximal site. When S1-S2 reached 210 msec, the descendingimpulse reentered the ventricular myocardium, resulting ininitiation of a VT exhibiting AV dissociation with an identicalQRS morphology to the clinical VT (Fig. 2B). During the VT,sequential diastolic potentials (DPs) bridging the entire dia-stolic period were recorded over the catheter length of 33 mm.The DPs tended to have a lower frequency in the earlierdiastolic period and had a small amplitude of 0.93 6 0.17 mV.In addition to this low-frequency diastolic electrical activity,high-frequency presystolic potentials (PPs) were recorded im-mediately preceding the ventricular electrograms (Fig. 2C).The sequence of the PPs was in the distal-to-proximal direc-tion, and they were followed by a retrograde His-bundle po-tential, suggesting that the PP represented retrograde activa-

tion of the left posterior fascicle. Interestingly, the cycle lengthof the PPs � uctuated spontaneously despite the observationthat the cycle length of the VT and DPs remained constant(Fig. 3A).

VT could not be entrained by overdrive atrial pacing be-cause of limited AV nodal conduction. Rapid pacing from theRVOT during the VT at a cycle length of 260 msec resulted inconstant fusion beats, except for the last entrained beat. Adifferent degree of constant fusion was noted with shorteningof the pacing cycle length to 245 msec (e.g., progressive fusion).When the pacing cycle length was shortened from 260 to 245msec, the DPs remained orthodromically captured, and themorphology and activation time of the distal ventricular elec-trograms changed. Shortening of the pacing cycle lengthcaused prolongation of the conduction time between the prox-imal DPs, suggesting that the area had a decremental conduc-tion property (Fig. 3B).

On the basis of contiguous activation during the VT overthe left ventricular septum, we performed an entrainmentstudy from several sites of the left ventricular septum. Whenthe VT was entrained from the left ventricular proximal elec-trode pair (LV7), the interval from the stimulus to the onset ofthe QRS complex was 240 msec. This was almost the same asthe interval from the ventricular electrogramat the pacing siteto the onset of the QRS complex, which was 236 msec duringthe VT (Fig. 4A). When entrainment was achieved from thedistal electrode pair (LV1), the stimulus to QRS interval was16 msec and again was almost equal to the local electrogram toQRS interval of 14 msec measured during the VT (Fig. 4B).Moreover, both of the postpacing intervals (PPI) measured atthese two different sites were almost the same as the VT cyclelength. These � ndings suggested that these two representativesites (i.e., LV7 and LV1) were located close to the entrance andexit of the slow conduction zone in the reentrant circuit. The

Figure 1. (A) Transthoracic echocardiography, apical view. The false tendon straddling from the left ventricular mid-septum to the inferoapical septum,parallel to the interventricular septum, is indicated by the white arrowheads. (B) Fluoroscopic images of the 20-pole electrode catheter placed along theleft ventricular septum as well as conventional electrode catheters used for electrophysiologic study. The right anterior oblique projection (RAO, upperpanel) and left anterior oblique projection (LAO, lower panel) are shown. Note that the course of the 20-pole electrode catheter almost coincides with thatof the false tendon. (C) Surface leads I, aVF, and V1, and intracardiac bipolar electrograms recorded during sinus rhythm from the right atrial appendage(RAA), His-bundle electrogram (HBE), left ventricular septal electrograms (LV1 to LV10), and right ventricular apex (RVA). The number of the septalelectrogram corresponds to the same number location indicated in Figure 1B. Sequential high-frequency potentials, considered to be the left posteriorfascicular electrograms, were recorded (arrowheads). Fragmentation in the distal part of the fascicular electrograms is noted. Low-frequency delayedpotentials are seen, and the arrows indicate the activation sequence of these potentials. AV 5 aortic valve; CS 5 coronary sinus; LA 5 left atrium; LV 5left ventricle; RA 5 right atrium; RV 5 right ventricle.

Maruyama et al. Reentrant Circuit of Idiopathic LV Tachycardia 969

distance between the entrance and the exit was estimated asapproximately 3 cm. When we attempted to entrain the VTfrom the mid-portion of the LV catheter (LV5), two modes ofentrainment were observed. One was selective capture of theDP during entrainment and is shown in Figure 4C. The appliedstimulus entrained the VT and exhibited a QRS complex andintracardiac electrograms identical to those observed duringthe VT. The stimulus to QRS interval was 116 msec, and thisinterval again was identical to the DP to QRS interval mea-sured during the VT. The PPI measured by means of theinterval between the last stimulus to the � rst DP coincided withthe VT cycle length. These � ndings suggested that the stimulussuccessfully and selectively captured the slow conduction zoneinsulated from the surrounding myocardium and that this sitewas on the reentrant circuit. The other mode of entrainmentwas selective capture of the local ventricular electrogram,which was achieved more easily than selective capture of theDP (Fig. 4D). During this mode of entrainment, the DP was notcaptured locally but was advanced orthodromically (whitearrowheads in Fig. 4D). The interval from the stimulus to theonset of the QRS complex was 250 msec and was almost thesame as the interval from the local ventricular electrogram tothe onset of the QRS complex during the VT. The PPI mea-sured during this mode of entrainment was almost identical tothe VT cycle length, suggesting that the captured ventricularmyocardium also was located within the reentrant circuit.

The 20-pole electrode catheter was removed and a 7-Frenchablation catheter (Marinr; Medtronic, Minneapolis, MN, USA)was inserted. First, we attempted to obtain a mid-DP, but itwas dif� cult to record such a potential. The ablation catheterwas slightly withdrawn and a low-frequency early DP preced-ing the onset of the QRS complex by 174 msec during the VTwas recorded. Based on the � ndings from the 20-pole electrodecatheter recordings, this site corresponded to near the en-trance site, and temperature-controlled (60°) radiofrequency

energy was applied at this site during the VT. The VT termi-nated 4.2 seconds after initiating the energy application andwas no longer inducible. No clinical recurrence of the tachy-cardia was documented during a 1-year follow-up period with-out any drug treatment.

Discussion

The mechanism of ILVT has been thought to be reentryin the previous studies; however, whether ILVT results frommacroreentry or microreentry remains controversial.1 -1 2 Wedemonstrated sequential electrical activity throughout theentire cardiac cycle during VT over the region extendingfrom the left ventricular mid-septum to inferoapical septumusing a 20-pole electrode catheter. Several representativesites where sequential electrical activity was recorded werecon� rmed to be involved in the reentrant circuit by means ofan entrainment technique in which a PPI identical to thetachycardia cycle length was reported to imply that theelectrogram recording site was within the reentrant circuit.13

Thus, our results provide direct evidence of macroreentry asthe mechanism for the ILVT in our case.

The PPs recorded in this case were considered to repre-sent activation of the left posterior fascicle, because theretrograde His-bundle electrogram followed the PPs and thefrequency of the PPs resembled that of left posterior fascic-ular potentials observed during sinus rhythm and ventricularextrastimuli from the RVA (Fig. 2). On the other hand, theorigin of the DP, which had a lower frequency, is a morecontroversial issue. Because both PP and DP were recordedsimultaneously from a single catheter, the structures thatproduce these potentialswere considered to run parallel, andclose, to each other in this region. One possible explanation

Figure 2. (A,B) Induction of ventricular tachycardia by ventricular extrastimulation from the right ventricular apex. (A) During the basic drive (S1),low-frequency delayed potentials identical to those recorded during sinus rhythm are observed following the ventricular electrograms. At a couplinginterval of 250 msec (S2), the ascending impulse is blocked, which allows the descending impulse to be conducted to the apical septum, but it is blockedin the distal limb of the slow conduction zone. Retrograde conduction of the left posterior fascicle (arrowheads) followed by retrograde activation of theHis bundle (Retro H) is seen. (B) When the coupling interval is decreased to 210 msec, proximal conduction delay makes the delayed descending impulsepossible to reenter the ventricular myocardium, resulting in initiating ventricular tachycardia. Note that sequential diastolic potentials covering the entirediastolic period are recorded during the tachycardia (white arrowheads). (C) Septal electrograms recorded during the tachycardia, especially focused onthe presystolic period. To easily recognize low-amplitude electrical activity in this period, the gain of the amplitude of LV1 to LV4 is decreased in orderto avoid overlap among the electrograms. Note that retrograde activation of the left posterior fascicle is seen just before the ventricular electrograms(arrowheads). Abbreviations as in Figure 1C.

970 Journal of Cardiovascular Electrophysiology Vol. 12, No. 8, August 2001

is that the DP represents activation of the false tendon,which runs from the inferoapical septum to the mid-septumof the left ventricle. Gallagher et al.1 4 described a patientwith ILVT cured by intraoperative laser photocoagulationof a false tendon in the posteroinferior region of the leftventricle. Suwa et al.1 5 described a patient with ILVT curedby surgical resection of a false tendon and cryoablation inthe posteroinferior left ventricular insertion site. Thakur etal.1 6 reported that the presence of a false tendon was aconsistent � nding in patients with ILVT, but it was found inonly 5% of the control group. Further, they observed aproximity of the successful ablation site to the false tendonin one patient by using transesophageal echocardiographyperformed simultaneously. In our case, the course of the20-pole electrode catheter mostly coincided with that of a

false tendon documented by echocardiography (Figs. 1Aand 1B), although it was not performed simultaneously. Analternative explanation could include longitudinal dissocia-tion of the left posterior fascicle or a diseased Purkinjepotential as the mechanism of the DP. Longitudinal disso-ciation of the left posterior fascicle theoretically is possiblebut has not yet been proven. In the present study, weobserved two patterns of entrainment during pacing fromthe mid-portion of the reentrant circuit, resulting in eitherthe DP or ventricular myocardial potential capture. How-ever, neither could not be captured simultaneously despitethe use of a relatively high pacing output of 4.0 V. These� ndings may suggest that the changes in the mode ofcapture were caused by a subtle shift in catheter position.Although we cannot totally discard the possibility of adiseased Purkinje � ber insulated from the surrounding myo-cardium, our � ndings and previous data might favor thehypothesis that the DP re� ects activation of the false tendon

Figure 4. Entrainment of the ventricular tachycardia from a point near theentrance of the slow conduction zone (A), near the exit site of the slowconduction zone (B), and the mid-portion of the reentrant circuit (C,D).Selective capture of the diastolic potential is depicted in panel C; selectivecapture of the myocardial potential is depicted in D. The white arrowheadindicates the diastolic potential that is captured orthodromically duringselective local capture of the myocardial potential. All numbers are givenin milliseconds. DP-QRS 5 interval from the diastolic potential to onset ofthe QRS complex; PCL 5 pacing cycle length; PPI 5 postpacing intervalmeasured at the pacing lead; S-QRS 5 interval from the stimulus to onsetof the QRS complex; V-QRS 5 interval from the local myocardial potentialto onset of the QRS complex; VTCL 5 ventricular tachycardia cyclelength. See the text for details.

Figure 3. (A) Dissociation of left posterior fascicular electrograms fromthe ventricular tachycardia. Spontaneous variation in the cycle length ofthe fascicular electrograms (arrowhead, PP-PP) followed by His-bundleelectrograms (arrow, H-H) is observed despite a constant cycle length ofthe VT and DP (white arrowhead, DP-DP). (B) Entrainment of the ven-tricular tachycardia from the right ventricular out� ow tract (RVOT) at adifferent cycle length of 260 msec (left) and 245 msec (right). Both panelsshow the last entrained beat. Constant fusion and progressive fusionduring entrainment are noted on the surface electrograms. The intervalfrom the stimulus to diastolic potential (S-DP) is measured, and the italicnumber represents the interelectrode conduction time. Note that conduc-tion delays with shortening of the pacing cycle length (PCL) occur pre-dominantly at the proximal site of the slow conduction zone. All numbersare in given in milliseconds. Abbreviations as in Figure 1C.

Maruyama et al. Reentrant Circuit of Idiopathic LV Tachycardia 971

that is close to, but anatomically apart from, the septalmyocardium. In human histologic study, the false tendon ofadults was composed of muscle and connective tissue invarious proportions, and some false tendons contained Pur-kinje � bers.1 7 Most of the connective tissue was observed inthe area of the false tendon’s proximal attachment to theinterventricular septum. This � nding might be noteworthy,because the proximal region near the entrance of the slowconduction zone had a prominent decremental property inthis patient.

Early retrograde His-bundle activation, in addition to thecharacteristic QRS morphology, suggested that ILVT orig-inates from the posterior fascicle of the left bundlebranch.3 ,1 8 ,19 However, in our patient, the left posteriorfascicle did not appear to be involved in the reentrantcircuit, that is, it appeared to be a bystander. It was sug-gested from the � ndings that spontaneous variation in thecycle length of left posterior fascicular activation occurreddespite a constant VT cycle length.

The results of the present study allow us to speculate onthe reentrant circuit of this patient as follows. First, theentrance and exit of the slow conduction zone in the reen-trant circuit are believed to be located at the posterior aspectof the left interventricular septum and are approximately 3cm apart. Second, the descending limb is believed to becomposed of a false tendon that runs close and parallel tothe interventricular septum, and it has markedly slow anddecremental conduction property, especially at its proximalportion. Last of all, the ascending limb is not believed to bea left posterior fascicle but rather composed of the leftinterventricular myocardium.

In conclusion, this case report demonstrates the reentrantcircuit of verapamil-sensitive ILVT. One reason why anearly DP has never been described might be that a low-frequency potential, such as that recorded in our study, maynot have been regarded as a signi� cant potential. The eti-ology of the low-frequency event might not be merely afar-� eld potential, because successful ablation was achievedrapidly after a radiofrequency application at the site wheresuch a potential was recorded. Further studies are needed tocon� rm that our results hold true for the majority of patientswith verapamil-sensitive ILVT.

Acknowledgment: We thank Mr. John Martin for linguistic assistance withthis manuscript.

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