Characteristics of slow conduction zone demonstrated during entrainment of idiopathic ventricular tachycardia of left ventricular origin

Characteristics of Slow Demonstrated During Idiopathic Ventricular Left Ventricular

Conduction Entrainment Tachycardia Origin

Zone of of

Ken Okumura, MD, Hiroshige Yamabe, MD, Takeshi Tsuchiya, MD, Toshifumi Tabuchi, MD, Atsushi Iwasa, MD, and Hirofumi Yasue, MD Idiopathic ventricular tachycardia (VT) with the right bundle bmnch block pattern and left-axis deviation has been shown to be due to reentry, but the property of the slow conduction zone within the reentry circuit is little understood. In 7 patients (mean VT cycle length (Cl]: 361 * 49 ms), mpid pacing from the right ventricular outflow tract was performed during VT while recording electrograms at the earfy activation site in the left ventricle and at the right ventricular apex; also, conduction times from the pacing site to these recording sits (St-A and St-B intervals, respectivefy) were measured. Both constant fusion (except for the last paced beat) and progressive fusion were seen in all patients, indicating VT entrainment. The left ventricular site was captured orthodromically with an St-A interval of 394 f 57 ms at the pacin CL of 35 1 f 47 ms during entrainment, while the rig a t ventricular apex was captured directfy with an St-B interval of 63 f 19 ms. The St-A interval was gradually prolonged with the shortening

of the pacing Cl, whereas the St-B interval remained unchanged. VT was interrupted in all patients at the cing CL of 279 f 39 ms. The effects of intravenous p”idocaine (1 mg/kg) and verapamil (1 mg) were examined in 5 and 7 patients, respectively. Neither drug terminated VT but the VTCL was increased to 369 f 57 ms after lidocaine (p 4.05) and to 413 f 69 ms after verapamil ( 4.05) (p ~0.05 vs after lidocaine). The St-A intewa Pwas significantfy increased after lidocaine (p eO.05) and after vempamil (p cO.O5), while the StB interval remained unchanged. A significant correkrtion between changes in St-A interval and VT-CL after Vera mil was noted (p
erapamil-sensitive idiopathic ventricular tachycarV dia (VT) with the QRS morphology of right bundle branch block and left-axis deviation in relatively

and without any underlying heart disease were studied. The electrocardiogram during VT showed a right bundle branch block pattern and left-axis deviation in all patients. Intravenous verapamil (5 to 10 mg) was effective in terminating VT in all patients. A bolus of 100 mg of lidocaine terminated VT in 1 of the 7 patients. AI1 drugs were stopped 23 days before the study. All patients gave informed written consent. Electrophysiokgic str& With use of standard techniques, 2 quadripolar electrode catheters (Josephson, USCI, Billerica, Massachusetts) were placed at the right ventricular apex and outflow tract and were used for recording electrograms and pacing. A 7Fr, deflectable quadripolar electrode catheter (Cordis Webster, Baldwin Park, California) was inserted in the left ventricle to perform endocardial catheter mapping during VT by recording an electrogram from the distal electrode pair. All electrograms were filtered with a bandpass between 50 and 1,000 Hz and recorded with 3 electrocardiographic leads (I, II, and V,) using a polygraph (RMC-2000, Nihon Kohden, Tokyo, Japan). Ventricular pacing was performed with an output of twice the diastolic threshold strength using a programmable stimulator.

young patients has been shown to constitute a clinical entity.‘-’ Reentry with an excitable gap has gained acceptance as the most likely mechanism of this VT because it can be induced and terminated with programmed stimulation,2+7 an inverse relation between the coupling interval of the extrastimulus and the first VT return cycle is observed,” and entrainment criteria are demonstrated.6*7 During entrainment of this VT, we have shown that slow conduction is present within the reentry circuit,7 but its electrophysiologic characteristics are little understood. In this study, we examined how the slow conduction zone shown during entrainment of this VT responds to overdrive pacing and to sodium and calcium channel blocking agents in an attempt to clarify the basal mechanism for slow conduction within the reentry circuit. METHODS Study patients: Seven patients (5 men and 2 women, mean age 23 years, range 14 to 29) with recurrent VT From the Divisiol of Cardiology, Kumcmoto University School of Medicice. Kumomoto,Japan. Manuscript received August 7, 1995; revised aaruscript received Ocober 1 1, 1995, and accepted October 12. Address for reprints: Ke7 Okurxro, MD, Division of Cardiology, Kumomoto University Schoo of Medicine, Han/o 1 -l-l, Kumamoto, 860 Japan.

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Entrainment from the right ventricukrr

oulflow

tract:

After VT was induced by ventricular extrastimulation or burst pacing, endocardial mapping was performed during VT and the early activation site relative to the QRS complex was determined. While recording the electrogram at this left ventricular site and right ventricular CONDUCTION

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apex, ventricular pacing was done at a rate 5 beats/min faster than the VT rate for approximately 5 seconds from the right ventricular outflow tract. In this particular VT, pacing from the right ventricular outflow tract is associated with entrainment criteria, but pacing from the right ventricular apex or left ventricle is not.’ When ventricular pacing did not interrupt VT, the pacing protocol was repeated by increasing the pacing rate 5 to 10 beats/min until VT was interrupted. During pacing from the right ventricular outflow tract, the time intervals from the stimulus artifact to the electrograms at the early activation site and right ventricular apex were measured and defined as St-A and St-B intervals, respectively. Similar ventricular pacing was also done during sinus rhythm. Effects of liiaine

and verapamil

during

study, when the VT rate and the conduction times returned to the respective baseline values before lidoCaine, a small dose of verapamil (I mg) was injected and the entrainment study was repeated In the remaining 2 patients, only the etfect of verapamil was examined. Statistical analysis: All data are shown as mean f 1 SD. The effects of the drugs on the cycle length (CL) of VT and conduction times were analyzed with a 2-tailed paired t test and wcrc compared with each other with an unpaired t test. The correlations between changes in StA interval and VT-CL after the drugs were administered were examined with linear regression analysis. A p value co.05 was considered significant.

RESULTS

entrainment

After VT was induced again, the entrainment study with the pacing rate 5 to 10 beats/min faster than the VT rate was performed again and St-A and St-B intervals were measured again. In 5 of the 7 patients, lidocaine (I mgkg) was irrjectcd for 1 minute and the cntminment study was performed. Approximately 15 minutes after the hdocaine

VT (mean rate 169 k 23 beats/min) was repeatedly induced in all patients. Endocardial mapping during VT identified the early activation site, with an activation time of -20 a 6 ms relative the QRS complex in the left ventricular inferior wall or posterior interventricular septum in all patients.

170 bpm

180 bpm

500 msec

FKXJRE 1. Tracings of an dectrocardiimphic bad V, and intracardiac d&mgrams recorded at the right ventricular outfbw tract (RVOT), right ventricular apex (RVA), and ea activation site in the left ventricle (LV) during ventricubr tachycardia (W). A, ventricular pacing at rates of 170, 180, 190, and r5 00 heats/ min (bpm) was perfwmed from the right ventricular outflow tract during VT, which resulted in VT entrainment. An activation time at the left ventricular site relative ta the onset of the QRS complex was -20 ms. 8, ventricular pacing at a rate of 180 beats/min was performed from the same site during sinus rhythm. See text for discussion. All numbers are in milliseconds; numbers in circles show conduction times. S = stimulus artifact.

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of ventricular tachycardia and changes in times during entrainment: During pacing from the right ventricular outflow tract, constant fusion (except Entrainment

candu&n

for the last paced beat) and progressive fusion with the increment of the pacing rate (i.e., VT entrainment) were demonstrated in all patients.8.9 Figure IA shows an example of entrainment. The morfrhology of the clcctrogram at the early activation site in the left ventricle remained unchanged during entrainment at 170 and 180 beats/min, indicating orthodromic capture of this site. Morphology at the right ventricular apex, however, changed to the one observed during pacing done during sinus rhythm (Figure lB), indicating direct capture. When the pacing rate was further increased to 200 beats/min, the morphology of the elcctrogram of the former site also changed to the one during pacing during sinus rhythm, indicating a change from orthodromic to antidromic capture (fourth entrainment critcrion).‘c During entrainment at 190 beats/min, the elcctrogram morphology at the early activation site differed from that during VT and pacing during sinus rhythm. This may be due to local fusion of orthodromic and antidromic wavefronts at the recording site. The St-A interval was 395 ms during pacing at 170 beats/min, 410 ms at 180 bcats/min, and 100 ms at 200 beats/min, whereas the St-B interval was 70 ms at all pacing rates. A similar observation was made in all 7 patients: The early activation site in the left ventricle was captured orthodromically at relatively lowcr pacing rates and antidromically at higher rates. The right ventricular apex was always captured directly during entrainment. The minimal pacing rate at which the early activation site was captured antidromically was 192 + 23 beats/min, which was 23 k 8 beats/min faster than the VT rate. When the pacing rate was further increased to 218 f 25 bcats/min, VT was interrupted in all patients.

Baseline I

,--yf--

The changes in St-A and St-B intervals with the increase in the pacing rate are shown in Figure 2. StA and St-B intervals are shown as percentages of VTCI,, and the pacing rate as percentages of the VT rate. As the pacing rate was increased, the St-A interval was gradually prolonged during orthodromic capture in all 120

St-A

1

7 100

110

120

Pacing

100

rate (%VT

110

120

rate)

I FIGURE 2. Changes in St-A and St-B intervals with the increase in the pacin rate. The intervals are shown as the percen of the cycle 0 ength of ventricular tachycardia (VT) on the 2r inote and the pacing rate as the percentage of the VT rate an he abscissa. As the pacing rate was increased, the St-A interval was mdually probm during orthodromic capture and then sudknly shortened P uring antidromic capture, while St-B interval remained unchanged. See text for discussion.

Verapamil

Lidocaine y--

St-B

-

,,

500

msec

FIGURE 3. An example of the effects of lidocaine and verapamil on the conduction times measured during entrainment. Ebctrocardiographic leads I, II, and V, are shown along with the electrograms recorded from the electrodes at the right ventricubr outfbw tract (RVOT) and right ventrtcular apex (RVA) and from the proximal (LVp) and distal (LVd) pairs of the electrodes at the early activation site in the left ventricle. St-A and St-B intervals were 475 and 60 ms at baseline, 490 and 60 ms after liiocairie, and 560 and 60 ms after verapamil, respectively. All numbers are in milliseconds; numbers in the circles show conductian times. S = stimulus artifact. AR9t IYiHMIAS

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patients and then suddenly shortened during antidromic capture. The maximal St-A interval was 405 f 57 ms, and the St-A interval during antidromic capture was 88 f 19 ms. The St-B interval was 63 + 19 ms and remained unchanged. Effects af lidacaine and vempamil an canduch times during entrainment: Figure 3 shows an example of the

effects of lidocaine and verapamil. At baseline, the pacing rate was 140 beats/min, and the St-A and St-B intervals were 475 and 60 ms, respectively. After lidocaine (1 mg/kg), the St-A interval was slightly increased to 490 ms, while the St-B interval remained unchanged. After verapamil(1 mg), although the pacing rate was decreased to 130 beats&n because of a decrease in VT rate, the St-A interval was prolonged to 560 ms. The effects of lidocaine (n = 5) and verapamil (n = 7) on VT-CL and St-A interval are shown in Figures 4 and 5, respectively. Neither drug at the doses given during the entrainment study terminated VT in any patients. After lidocaine, VTCL was increased from 353 + 56 to 369 f 57 ms (p =

0.0371), and the St-A interval from 378 + 62 to 393 + 61 ms (p = 0.0362) (Figure 4A). After verapamil, VT-CL was increased from 361 f 49 to 413 f 69 ms (p = 0.0068), and the St-A interval from 391 f 55 to 444 f 84 ms (p = 0.0115) (Figure 5A). The changes after verapamil were both significantly greater than those after lidocaine (both, p 4.05). Neither drug affected St-B interval. The relations between the changes in St-A interval and VT-CL after lidocaine (Figure 4B) and verapamil (Figure 5B) were examined. There was a significant correlation between the changes induced by verapamil (r2 = 0.99, p = 0.0001). Although there was a tendency toward a correlation between the changes after lidocaine, no statistical significance was seen (r* = 0.53, p = 0.1629).

DISCUSSION

This study showed that with use of tachycardia entrainment, the mechanism of this idiopathic VT is reentry with a slow conduction zone; this zone shows a decremental conduction property such as that recognized in the atrioventricular node with an increase in the pacing rate. This conA duction property is similar to that B bnsed demonstrated during entrainment of 600 VT-CL St-A VT associated with healed myocardial infarction.“-13 Considering the fact that vcrapamil is highly effective in terminating this VT,6 we believe that tissue with electrophysiologic property similar to the atrioventricular node may be involved in the slow conduction zone. A recent report described that this VT entity does not represent a homogeneous group because some patients had I exercise-induced VT and required isoBaseline Lidocaii Baseline Lidacaine A St-A (msec) proterenol infusion for VT induction.14 These findings do not necessarily rule out reentry with a slow conduction zone as the mechanism, and mid-diasFIGURE 4. A, effects a4 liiocaine on IIE cycle length d ventricular tuchycardia (Wtolic potentials suggesting direct reCl.) and St-A interval measured during entrainment. Cbsed circles and vertical bars cording at the slow conduction zone indicate mean f SD. 6, relation between cha es (A) in St-A interval and cycle Iengh af ventricular tachycardia. See text for 3 ~scussian. were demonstrated in this recent report. In the previous VT entrainment studies in patients with underlying A B heart disease, localized conduction bseo~ block within the slow conduction VT-CL St-A -1 zone, associated with VT interruption (third entrainment criterion),sv9 was 120 Y-0.88x+3.17 seen in 4 of 10 episodes” and in 13 of 100 r2-o.9B 20 episodes. I5 In the idiopathic VT in w I-.~1 this study, however, localized conduc60 tion block was never observed even Y) though the pacing rate was critically 20 increased.. This is one of the characteristics of this VT, and the slow con0m 0 20 40 60 a0 loo 120140 duction zone was readily activated rctA St-A (msec) Baseline Vempamil Baseline Verapamil rogradely by the antidromic wavefront from the pacing impulse with the increment of the pacing rate. Although FIGURE 5. A, effects af vempamil an the cycb length of ventricukr tachycardia localized conduction block was not (VT-CL) and St-A interval measured during entrainment. Closed circles and vedictd seen, it must have occurred in the slow bars indicate mean f SD. fl, rebtian between changes (A) in St-A interval and cycle length af ventricular tachycardia. ke text far discussion. conduction zone during pacing at a

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critically high rate, since all of the VT was interrupted by the pacing. This study showed that a small dose of verapamil slowed the VT rate and a significant correlation was found between the changes in St-A interval and VT-CL after verapamil. Because the St-B interval remained unchanged, verapamil slowed the VT rate by selectively suppressing the slow conduction zone. This is similar to the finding that procainamide preferentially suppresses conduction through the slow conduction zone of VT associated with myocardial infxction.‘“~” This study also showed that lidocaine slightly, but significantly, suppressed conduction through the slow conduction zone. Because the St-B interval remained unchanged after lidoCaine, the effect of lidocaine also was confined to the slow conduction zone. The present dose of lidocaine is unlikely to affect conduction within the normal myocardium unless the pacing rate is sufficiently high, but it might suppress conduction through the myocardial cells with partially depolarized membrane potential.‘8T’9 Thus, it is indicated that the main cellular mechanism for slow conduction of this VT is calcium channel-dependent conduction, and depressed sodium channel-dependent conduction is partially involved in it. Lidocaine was effective in terminating the present form of VT in selected patients.h The degree of contribution of depressed sodium channel-dependent conduction to slow conduction seems to vary from patient to patient with this particular VT.

I. %ipea DP, Foster PK. Troup PJ. Pedersm l)ll. Alrial induction of ventricular tachycanha. Reentry wrsus triggered aulomaticity. Am J (brdiol 1979;44: l-8. 2. Belhas.sen B. Rotmensch HH, Laniado S. Responu of recurrent sustamed ventricular tachycardia to verapamil. Hr Heon J lYXl;46:679~XZ. 3. Mason JW. Swcrdlow CD. Mitchell I.H. Efficacy of rcrapamil in chronic. recurrent ventricular tachycardia. Am J Curdiol 1983;51:1611-1617.

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4. Lin FC. Finly CD, Rahimtoola SH. Wu D. Idiopathic paroxysmal ventricular tachycardia with a QRS pattern of right bundle branch block and left axis dcviation. A unque clinical entity with specific properties. Am J Cardiol 1983;52: 95.-100. 5. Klein GJ, Millman PJ, Yee R. Recurrent ventricular tachycardia responsive to verapamil. PACE 1984;7:938-948. 6. Ohe ‘I‘, Shimomura K. Aihara N. Kamakura S. Matsuhisa M. Sate 1. Nakagawa H, Shimizu A. Idiopathic sustained left ventricular tachycardia. Clinical and clcctmphysiologic characteristics. Circularion 1988;77:56&568. 7. Okumura K. Matsuyama K. Miyagl H, Tsucbiya T , Yasue H. l%mainmcn~ of idinpathic ventricular tachycardia of left ventricular origin with evidence for reentry with an area of slow conduction and effect of wrap&l. Am J Curdiol 1988:62:727-732. 8. Waldo AL, Plumb VJ. Arciniegas JG, MacLean WAH. Coopcr ‘1% Priest MB, James TN. Transient entrainment and interruption of the atrioventricular bypass type of paroxysmal atrial tachycardia. A model for understanding and identifying reentrant arrhythmias. Circularion 1983:67:73-83. 9. Okumura K, Ilentborn KW, Epstein AE, Plumb VJ, Waldo AL. Further ohsermt~onc on transient entrainment. Importance of pacing site and properties of the components of the reentry circuit. Cirnlorion 198.5;72: 129~1307. 10. Henthom RW. Okumura K. Olshansky B, Plumb VJ, Hess PG. Waldo AL. A fourth criterion for transient entrainment. The electrogram equivalent of progressive fusion. Circrdorion 1988;77:1003-1012. 1 I. Okumura K. Olshansky B. Henthom RW, Epstein AE:.. Plumb VJ. Waldo AL. Demonstration of the presence of slow conduction during sustained venuicular tacbycardia in man. Use of transient entrainment of the tachycardia. Circularion 1987;75:369-378. 12. Kay GN. Epstein AE, Plumb VJ. Region of slow conduction in sustained kentricular tachycardia. Direct endocardial recordings and functional cbarecteriration in humans. JAW CON Cardiol 1988;11:109-116. 13. Morady F. Frank R. Kou W. Tonet JL. Nelson SD. Kounde S, De Buitleir M. Fontaine G. Identification and catheter ablation of a ame of slow conduction in the reentrant circuit of ventricular tachycardia in humans. J Am Co// Cardiol 1988: 1 I : 77%782. 14. Konkamp H, Chen X, Hindricks G. Willems S, Haverkamp W. Wichter T , Breithardt G. Borggrefe M. Idiopathic left ventricular tachycardia. New insights into rlectrophysiological charactcricticc and radiofrquency catbeler ablation. PACE 1995:18:1285-1297. 15. Aiwwa Y, Niwano S. Chmushi M. Tamam M. Kusano Y. Miyajima T . Kit‘vawa H, Shibata A. Incidence and mechanism of interruption of reentrant ventricular txhycxdia with rapid ventricular pacing. Circu[arion 1992;85:58%.595, 16. Kay GN, Epstein AE. Plumh VJ. Preferential effecn of procainamide on the reentrant circuit of vcnuicular tachycardia. J Am Co11 Curdiol lYXY:l4:382-3Y0. 17. Okumura K. Honda T , Nishigami K. Hayasaki K. Facilitation of localixd conduction block with procainamide during entrainment of sustained ventricular tachycardia. Am Ileorv J 1989;l 18:63(M32. 18. Chen C. Genes LS, Katzung BG. Effect of lidocaine on steady-state charactenstics and recovery kinetics of (dV/dt),,, in guinea pig ventricular myocardium. Circ KPS 197.5;37:20-29. 19. Lxxara R. Hope RR. El-Sherif N. Scherlag BJ. Effects of lidocaine on hypoxic and ischemic cardiac cells. Am J Curdiol 1978;41:872-879.

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