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enalase is a molecular marker for peripheral and central neuroendocrine ceils. Nature 197X$276:834-6. Glancey DL, Roberts WC. The heart in malignant melanoma: a study of 70 autopsy cases. Am J Cardiol 1968;21:555-71. Berge T, Sievers J.-Myocardial metaatases: a pathological and electrocardiographic studv. Br Heart J 1967:30:383-90. Waller BF, Gotidiener Js, Virmani R, et ai. The “charcoal heart”: melanoma of the car. Chest 1980,77:671-6. Hanley PC, Shub C, Seward JB, et al. Intracavitary cardiac melanoma diagnosed by endomyocardial left ventricular biopsy. Chest 1983;84:195-8. Amparo EG, Higgins CB, Farmer D, Gordon G, McNamara M. Gated MRI of cardiac and paracardiac masses: initial experience. Am J Roentgen01 1984;143:1151-6.

Localization of slow conduction in a ventricular tachycardia circuit: Implications for catheter ablation

William G. Stevenson, M.D., James Weiss, M.D., Isaac Wiener, M.D., Daniel Wohlgelernter, M.D., and Lawrence Yeatman, M.D. Los Angeles, Calif.

Reentry is the likely mechanism of ventricular tachycar- dia arising from an area of healed myocardial infarction’s2 For reentry to occur, unidirectional conduction block and an area of slow conduction must be present in the tachycardia circuit.2 Reports of entrainment of ventricular tachycardia have suggested that an area of slow conduc- tion is present during ventricular tachycardia in hu- mans.2-5 Canine studies6 have suggested that damaging the area of slow conduction is likely to be successful in controlling reentrant ventricular tachycardia. This report describes a patient with ventricular tachycardia in whom an area of slow conduction participating in the tachycar- dia circuit was identified by programmed electrical stimu- lation at that site.

A 54-year-old man was referred to UCLA for manage- ment of recurrent sustained ventricular tachycardia that had developed 4 years after an anterior myocardial infarc- tion. Ventricular tachycardia had occurred during therapy with procainamide, quinidine, tocainide, mexiletine, amiodarone, and combinations of these agents. At the time of study he had been on amiodarone for 7 months (most recent dose 600 mg/day). Contrast ventriculography demonstrated a left ventricular ejection fraction of 20% with akinesis of the anterior wall. Following informed consent, left ventricular mapping and endocardial cathe- ter ablation were performed according to the protocol approved by the UCLA Human Subjects Protection Com- mittee. A No. 5 French quadripolar catheter was posi-

From The Division of Cardiology, UCLA School of Medicine and Center for the Health Sciences.

Reprint requests: William G. Stevenson, M.D., Division of Cardiology, UCLA, CHS 47-123, Los Angeles, CA 90024.

Brief Communications 1253

tioned in the right ventricular apex and a No. 6 French quadripolar catheter with a 1 cm interelectrode distance (USCI, Billerica, Mass.) was inserted into the right femo- ral artery and advanced into the left ventricle. Surface ECG leads and intracardiac electrograms were recorded at paper speeds of 100 to 150 mm/set on an Electronics for Medicine VR-12 chart recorder (Electronics for Medicine/ Honeywell Inc., Pleasantville, N.Y.). Full standard 12- lead ECGs were recorded on a separate three-channel recorder (Marquette Electronics Inc., Milwaukee, Wise.). Programmed electrical stimulation was performed by the use of stimuli with a 2 msec pulse width and amplitude of twice the late diastolic threshold in the right ventricle or an amplitude of 10 mA in the left ventricle (Bloom Associates Ltd., Reading, Pa.).

Sustained monomorphic ventricular tachycardia with a cycle length of 420 msec and right bundle branch block superior axis QRS morphology identical to the patient’s spontaneous tachycardia was initiated by single ventricu- lar extrastimuli delivered during pacing from the right ventricular apex (Fig. 1). During tachycardia, continuous electrical activity was recorded at a site on the inferior aspect of the apical left ventricular septum (site l-2). As shown in Fig. 1, initiation of tachycardia by a premature stimulus was associated with a sudden increase in the interval between the initial portion of the ECG at site l-2 and the late fractionated portion of the electrogram.

Bipolar left ventricular stimulation was performed at site l-2 from the distal pair of electrodes on the left ventricular catheter and a bipolar electrogram was record- ed from the proximal electrode pair. The 12-lead ECG recorded during pacing at this site demonstrated excellent concordance with the QRS morphology of the spontane- ous ventricular tachycardia (Fig. 2). In addition, the duration from the stimulus artifact to the onset of ventric- ular depolarization in all surface ECG leads was greater than 120 msec, suggesting that the pacing site was within an area of slow conduction even in the absence of ventric- ular tachycardia. More rapid ventricular pacing at site l-2 initiated a second morphology of ventricular tachycardia, which displayed a right bundle branch block configuration and right axis deviation. As shown in Fig. 3, during left ventricular pacing at a cycle length of 400 msec the interval between the stimulus artefact and left ventricular electrogram, recorded from the electrode pair 1 cm proxi- mal to the pacing electrodes, increased slightly from 170 to 180 msec on the first two beats shown. Following the third stimulus, the stimulus-to-electrogram interval increased markedly to 300 msec, the morphology of the left ventric- ular electrogram changed, and sustained ventricular tachycardia was initiated. The change in morphology of the left ventricular electrogram is consistent with activa- tion of that site from a different direction as a result of marked slowing or block of conduction in the pathway that had activated it in the previous beat, as shown schematically in Fig. 4. Fractionated electrical activity was recorded from the distal electrode pair at site l-2 during the second morphology of ventricular tachycardia (not shown).

As shown in panel A of Fig. 5, overdrive pacing at a

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Fig. 1. Initiation of sustained ventricular tachycardia of the same morphology as the spontaneous tachycardia. From the top of each panel are 50 msec time lines, surface electrocardiogram leads I, AVF, and V,, and bipoiar intracardiac recordings from the right ventricular apex (RVA), distal electrode pair of the left ventricular catheter positioned at site l-2 on the inferior apical septum (dLV,.&, and the proximal electrode pair of the left ventricular catheter (pZV,.J. In A a single ventricular stimulus (S,) with a coupling interval (S,-S,) of 340 msec captures the ventricle. Fractionated activity is present in the left ventricular recording. In B an extrastimulus 20 msec earlier than in A results in a sudden increase in the interval from the initial part of the left ventricular electrogram to the later low amplitude fractionated portion, and sustained ventricular tachycardia is initiated. Organized continuous electrical activity is present at dLV,.,.

cycle length of 400 msec from left ventricular site l-2 continuously reset the tachycardia to the pacing rate (entrainment) but without altering the tachycardia QRS morphology. The interval between the stimulus artefact and the eleetrogram recorded at the proximal electrodes of the left ventricular catheter 1 cm distant from the pacing site was 340 msec. Following termination of pacing, the first post pacing beat followed the preceding electrogram by an interval equal to the pacing cycle length of 400 msec, as measured from the surface ECG or right ventricular

apex. Thus the first post pacing beat was advanced by the last stimulus and was therefore entrained.? As shown in panel B, left ventricular pacing at a slightly faster cycle length of 385 msec terminated and then reinitiated tachy- cardia. The third stimulus was not followed by a QRS complex. The fourth stimulus conducted with a shorter stimulus-to-left ventricular electrogram interval of 180 msec and a different QRS and electrogram morphology. Thus, local conduction block terminated tachycardia and was followed by activation of the site distal to the area of

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slow conduction from a different direction, with a shorter stimulus-to-electrogram interval, satisfying another crite- rion for entrainment.7s8 Single stimuli delivered to site l-2 also reset the tachycardia without altering the morphology of the QRS complex and electrograms distant from the pacing site. Following general anesthesia, two 200 J (stored energy) shocks were delivered at left ventricular site l-2 between the distal eletrode of the catheter and a cutaneous electrode patch (R-2 Corp., Morton Grove, Ill.). Ten minutes after the shocks, only nonsustained polymor- phic ventricular arrhythmias were initiated by up to three extrastimuli delivered during right and left ventricular stimulation. Amiodarone was discontinued. Ten days lat- er, programmed stimulation performed from the right ventricular apex initiated sustained monomorphic ven- tricular tachycardia similar in morphology to the previ- ously occurring spontaneous ventricular tachycardia. Left ventricular stimulation was not performed. Amiodarone was reinstituted. The patient has had no spontaneous occurrences of ventricular tachycardia over the following 12 months.

Traditional mapping techniques have emphasized the timing of the local electrogram in relation to the onset of the surface ECG QRS complex? However, the onset of the QRS may be difficult to identify during rapid tachycardias or when the QRS duration has been prolonged by antiar- rhythmic medications. It is also possible to record diastol- ic activity and even continuous electrical activity from “dead-end” pathways of slow conduction that are not involved in the tachycardia circuit.l~‘o Therefore, addition- al methods for demonstrating that the electrode catheter is in close proximity to the reentry circuit are desirable. This report describes three observations that may be useful in identifying areas of slow conduction that partic- ipate in ventricular reentry circuits: (1) Pacing from the site during ventricular tachycardia entrains the tachycar- dia without changing the tachycardia QRS morphology. (2) Initiation of tachycardia is associated with a sudden increase in the interval between the stimulus artefact and the adjacent local ventricular electrogram. (3) Slow con- duction is present at the site in the absence of ventricular tachycardia, as indicated by the marked delay between the stimulus artifact and the onset of the QRS complex in the 12-lead ECG during pacing at that site. The latter was demonstrated with a standard 12-lead ECG to avoid the error that would be introduced if the initial portion of the QRS complex were isoelectric in some leads.

Entrainment of a tachycardia by overdrive pacing has been defined as continuous resetting of the reentry circuit by the stimulated wavefront of depolarization.7*8 Previous reporW5 have demonstrated entrainment of ventricular tachycardia during pacing from the atrium and ventricu- lar sites remote from the tachycardia origin, and have stressed the importance of the site of pacing as a determi- nant of the ability to demonstrate entrainment. In these reports the stimulated wavefront of ventricular depolar- ization collides with the wavefront emerging from the tachycardia focus, producing fusion QRS complexes while

VT1

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Brief Conmunications 1255

LV l-2 Pace Map .,._ :.. .i ..-- $ ..-- i-

; .j i_--_

1. .i i...; : j--j.- i- -1

- ,. ..,.._, .:

Fig. 2. Six ECG leads of the spontaneous ventricular tachycardia are shown on the left side of the figure and the corresponding ECG leads during left ventricular pac- ing at site l-2 at 100 bpm are shown on the right. There is excellent concordance between the spontaneous tachycar- dia and the paced QRS morphology.

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T I I I I - -

R” “-y-- : II”. -~v?r-d~7r

St s. 4th s 400 s 400 s V--J

Fig. 3. Initiation of the second morphology of ventricular tachycardia by pacing from left ventricular site l-2. From the top are l-second time lines, surface ECG leads I, AVF, and VI, the bipolar electrogram from the right ventricular apex (RVA), stimulus marker channel (St), and the bipolar electrogram from the proximal electrode pair of the left ventricular catheter (pLVJ. See text for discussion.

irtfarct

Fig. 4. Schematic representation of the proposed mechanism of tachycardia initiation by left ventricular pacing. The irregular solid lirie represents th& infarct boider with the center of the infarct to the right of the line. The pacing site is at the distal dlectrode pair of the left ventricular catheter (d) and the recordmg site is at the proximal electrodes (p). Slow conduction is indicated by the dashed lines and normal conduction velocity by heavier continuous lines. Diagram A represents pacing at site d at sloiv rates or during the first two beats in Fig. 3. The impulse conducts slowly from site d and exits the abnormal area near site p, depolarizing the remainder of the ventricle. Rapid depolarization of the ventricle along the border of the infarct invades another potential point of exit from the arc of slow conduction, colliding with and extinguishing the slpw impulse. Diagram B represents the third beat in Fig. 3. The prematurity of the stimulated impulse originating from site d produces ti arc of functional conduction block between sites d and p, indicated by the irregular heavy line. The impulse proceeds superiorly dong the arc of block and exits the site of slow conduction at a site above that in panel A and also conducts around the arc of block towards site p. In diagram C, the impulse continues &round the arc of conduction block past site d and produces the first nonpaced beat of ventricular tachycardia.

entering the circuit and continously resetting the tachy- cardia.6 In contrast to the findings of previous reports, we were able to continuously ieset (entrairi) the tachycardia without changing the tachycardia QRS morphology. There was no evidence of fusion between the paced and tachyc’ardia QRS complexes (Fig. 3): A change in QRS moiphology may be difficult to detect if pacing were performed at the site of exit of the reentrant impulse from its origin, since the patied QRS morphology at that site would be similar to the tachkcardia QRS morphology. This was not the case in our patient, since the paced QRS morphology in the absence of ventricular tachycardia was

much different from the QRS morphology of the tachycar- dia that was entrained (Fig. 3). Also, there was no evidence of ftiion in the eridocardial electrograms. These findings cti be explained by pacing from within the reentry circuit itself, since fusion will be absent unless the local electio- gram is recorded from the portion of the circuit where the antedroinic and orthodromic wavefronts are colliding.8 The extremely long delay (340 msec) between delivery of the stimulus at the distal electrode pair and activation at the proximal pair only 1 cm away is consistent with this interpretation.

Initiation of ventricular tachycardia following an

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Fig. 5. Entrainment of ventricular tachycardia. Recordings and abbreviations are the same as in Fig. 3. In A left ventricular pacing entrains ventricular tachycardia without changing the tachycardia QRS morphology. In B pacing at a faster rate terminates and reinitiates tachycardia. See text for discussion.

increase in the interval between the pacing stimulus and local electrogram and accompanied by a change in mor- phology of the local electrogram (Figs. 3 and 4) suggests that an area of functional conduction block, necessary for reentry, developed close to the pacing site during tachy- cardia initiation. This finding is similar to the demonstra- tion of a local area of conduction block that resolves with termination of tachycardia, which is another criteria for the demonstration of entrainment7** Thus, it appears that an area of functional conduction block that was present only during the tachycardia prevented the pacing impulse from conducting more rapidly to the rest of the ventricle (as indicated by the absence of a fusion QRS complex), but did not prevent it from entering the reentry circuit. Thus, the pacing site must have been very close to or within the reentry circuit.

The QRS morphology during pacing at the left ventric- ular site in the absence of ventricular tachycardia was similar to the morphology of the ventricular tachycardia that occurred spontaneously and that was initiated by right ventricular pacing, but was much different from the QRS morphology of the tachycardia initiated by left ventricular pacing, in which entrainment was demonstrat- ed. Left ventricular pacing was not performed during the first tachycardia that was initiated by right ventricular pacing. Fractionated electrical activity was recorded at the

same left ventricular site for both morphologies of tachy- cardia. Immediately following endocardial shocks at this site, neither morphology of ventricular tachycardia was inducible. We speculate that the same area of slow conduction was used by both tachycardias and the differ- ent QRS morphologies may have been due to different exit points into the surrounding myocardium.” The exit point from the tachycardia focus appeared to be determined by the site of stimulation used to initiate the tachycardia. This has also been observed in a canine model of inducible ventricular tachycardia.12

Although monomorphic ventricular tachycardia could not be initiated shortly after the endocardial shocks, it could again be initiated by programmed stimulation 10 days later. We speculate that some degree of reversible damage produced by the shocks resolved prior to the follow-up study and the amount of permanent damage was insufficient to ablate the area of slow conduction. The size of the area of damage produced by shocks of this magnitude as well as the amount of tissue that must be damaged to abolish a critical portion of a ventricular reentry circuit remain to be determined. We cannot exclude the possibility that the catheter was still too far from the reentry circuit for the shocks to be effective or that a larger area of damage at the site of flow conduction would have been required to prevent inducible tachycar-

1258 Brief Communications

dia. Further investigation is warranted to determine if the localization of areas of slow conduction by programmed stimulation will be useful in selecting sites for endocardial ablation techniques.

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El-Sherif N, Mehra R, Gough WB, Zeiler RH. Reentrant ventricular arrhythmias in the late myocardial infarction period. Interruption of reentrant circuits by cryothermal techniques. Circulation 1983;68:644. Waldo AL, Plumb VJ, Areiniegos JC, MacLean WAH, Coo- per JB, Priest MF, James TN. Transient entrainment and interruption of the atrioventricular bypass pathway type of paroxysmal atria1 tachycardia. Circulation 1983;67:73. Brugada P, Wellens HJJ. Entrainment as an electrophysio- log& phenomenon. J Am Co11 Cardiol 1984;3:451. Horowitz LN. Josenhson ME. Harken AHG. Euicardial and endocardial activation during sustained ventricular tachycar- dia in man. Circulation 1980;61:1227. Brugada P, Abdollah H, Wellens SHJJ. Continous electrical activity during sustained monomorphic ventricular tachycar- dia. Am J Cardiol 1985;55:402. Miller JM, Kienzle MG, Harken AH, Josephson ME. Mor- phologically distinct sustained ventricular tachycardias in coronary artery disease: significance and surgical results. J Am Co11 Cardiol 1984;4:1073. Gough WB, Restivo M, Kowtha V, Assadi MA, El-Sherif N. The dependence of reentry on the site of stimulation in the ischemic canine ventricle [Abstract]. J Am Co11 Cardiol 1986;7:166.