Reappraisal of electrical cure of atrioventricular nodal reentrant tachycardia — lessons from a modified catheter ablation technique

h~ternationul Journal of Cardiology. 37 (1991) 5 I-60 ‘(” 1992 Elsevier Science Publishers B.V. All rights reserved

CARD10

51 0167-5273/92/$05.00

01.523

Reappraisal of electrical cure of atrioventricular nodal reentrant tachycardia - lessons from a modified catheter ablation technique Shih-Ann Chen, Wing-Ping Tsang, Hon-I Yeh, Teh-Ching Wang, Chih-Ping Hsia, Chih-Tai Ting, Chi-Woo Kong, Shih-Pu Wang, Benjamin N. Chiang and Mau-Song Chang Dilirion of Cardiology, Depurtment of Medicine. National Yang-Ming Medical Colle,ye. Tbiprt and Veteruns Gencwl Hospital- Taipei. Tuiwan. ROC (Received

11 November

1991: revision

accepted

9 May 1992)

Chen S-A, Tsang W-P, Yeh H-I, Wang T-C, Hsia C-P, Ting C-T, Kong C-W, Wang S-P, Chiang BN, Chang M-S. Reappraisal of electrical cure of atrioventricular nodal reentrant tachycardia - lessons from a modified catheter ablation technique. Int J Cardiol 1992;37:51-60. A modified catheter ablation technique was studied prospectively in 29 patients with atrioventricular (AV) nodal reentrant tachycardia. A His bundle electrode catheter was used for mapping and ablation. Cathodic electroshocks (loo-250 J) were delivered from the distal two electrodes (connected in common) of the His bundle catheter to the site selected for ablation. The optimal ablation site recorded the earliest retrograde atria1 depolarization, simultaneous or earlier than the QRS complex, with absence of a His bundle deflection during AV nodal reentrant tachycardia. One additional electrical shock was delivered if complete abolition of retrograde VA conduction persisted for more than 30 min and AV nodal reentrant tachycardia was not inducible during isoproterenol and/or atropine administration. With a cumulative energy of 323 + 27 J and a mean of 2.3 Ifr 0.5 shocks interruption or impairment of retrograde nodal conduction was achieved. Antegrade conduction, although modified, was preserved in 27 patients, with persistence of complete AV block in 2 patients. Two of the 27 patients still need antiarrhythmic agents to control tachycardia, the other 2.5 patients were free of tachycardia within a mean follow-up period of 13 f 2 months (range 7 to 20 months). Twenty-three patients received late follow-up electrophysiological studies (3-6 months after the ablation procedures), and the AV nodal function curves were classified into 4 types. The majority of the patients (15/23) had loss of retrograde conduction. Among the 8 patients with prolongation of retrograde conduction, 4 patients still had antegrade dual AV nodal property but all without inducible tachycardia. In conclusion, preferential interruption or impairment of retrograde conduction was the major, but not the sole, mechanism of electrical cure of AV nodal reentrant tachycardia. Key words: Atrioventricular Dual electrode configuration

nodal

reentrant

Correspondence to: Shih-Ann Chen, M.D., Division Taiwan. R.O.C. Tel. 886-Z-8757076. Fax 8X6-2-8735875.

tachycardia;

of Cardiology,

Catheter

Dept.

ablation;

of Medicine,

Veterans

General

Hospital.

Taipei,

52

Introduction Atrioventricular (AV) nodal reentrant tachycardia is one of the most common forms of supraventricular tachycardias. The components of pathways and precise reentrant circuits used are often unknown. Some authors favored the use of an AV node to atrium connection as the retrograde limb of the usual type of AV nodal reentrant tachycardia and suggested the critical involvement of perinodal fibers in the reentrant circuit [l-4]. Both cryodestruction and surgical dissection around the AV node were effective in abolishing AV nodal reentrant tachycardia [5-71.

TABLE

1

Characteristics Case

Nonetheless, surgical ablation is expensive, and associated with not only the discomfort of a sternotomy, but also with risk and morbidity of open heart surgery. Although the operation mortality in some recent series has been zero, death is always a possible complication of cardiac surgery. In recent clinical reports, catheter-mediated direct current or radiofrequency current ablation of the AV junction without complete AV block may cure AV nodal reentrant tachycardia [g-lo]. Higher cumulative energies and a higher incidence of recurrent tachycardia were reported after direct-current ablation, a moderate success rate with proarrhythmic effects was reported af-

of 29 patients Age (yr)/ sex

who received

AV junction

ablation. Drug

Arrhythmia

(yr)

Duration

Frequency of attacks

(n)

Heart disease

1 2 3 4 5 6

23, 43, 70, 66, 74, 32,

M F M M M F

3 23 2 6 2 10

Weekly Weekly Monthly Weekly Weekly Weekly

7 6 2 3 6 3

MVP MVP HTN _ _ _

7 8

30, M 65, M

10 2

Weekly Daily

3 4

RHD _

9 10 11 12 13 14 15 16

59, 40, 62, 52. 68, 68. 58, 72.

M M M M M M M M

15 2 10 10 3 3 10 2

Weekly Monthly Weekly Monthly Monthly Monthly Monthly Monthly

4 2 2 3 5 4 2 2

CHD HTN

17 18

59, M 52, F

13 12

Weekly Daily

4 4

_

19 20 21

72, M 64, M 40, M

10 2 2

Weekly Monthly Weekly

3 2 3

HTN _ _

22 23 24 25

55, 57, 49, 28,

M F F F

10 3 2 8

Monthly Weekly Weekly Weekly

3 3 3 4

_ _ _

26 27 28 29

61, 65, 23, 70,

M F F M

5 10 2 20

Monthly Weekly Weekly Weekly

3 3 2 3

LSVC _ _ _

CHD = coronary heart disease; HTN = hypertension; MVP = mitral rheumatic heart disease; LSVC = left-sided superior vena cava.

valve

prolapse;

- = no associated

_ _ _ _ _

heart

disease:

RHD =

ter radiofrequency current ablation [&lo]. Furthermore, the mechanisms of electrical cure of tachycardia have been unclear. A dual electrode configuration (distal pair of electrodes connected in common) has the advantage of delivering direct current energy over a larger area, and thereby might decrease the cumulative energy, with a higher success rate [ll]. Double electrodes as the cathode could increase the electrode surface and might decrease the amount of air bubble formation, arching. and barotrauma, thus decrease the complications [12]. In our laboratory, we used a modified method consisting of (1) delivering direct current with a dual electrode configuration, (2) delivering lower energy to decrease complications, (31 one additional electrical shock after initial elimination of retrograde AV nodal conduction to minimize the possibility of later recurrence of AV nodal reentrant tachycardia. The purpose of this study was to investigate the efficacy and safety of this modified catheter-mediated ablation technique, and to elucidate the mechanisms of cure of AV nodal reentrant tachycardia. Materials

and Methods

Patient characteristics

Twenty-nine patients with documented AV nodal reentrant tachycardia underwent cathetermediated ablation. There were 21 males and 8 females, with mean age of 54 yr (ranging from 23 to 74 yrl. Echocardiography and nuclear ventriculography for ventricular function were routinely performed in all the patients. Eight of them had associated cardiovascular diseases. They were refractory or intolerant to multiple antiarrhythmic drugs (mean, 3.4 + 0.2 drugs; range 2-7 drugs). Each patient gave informed consent for the ablation after the nature of ablation, its possible benefits and risks had been fully explained. Their clinical data are summarized in Table 1. Baseline

electrophysiological

study

Before catheter ablation, each patient underwent an electrophysiological study while in the fasting, unsedated state, at least five half-lives

after discontinuation of antiarrhythmic drugs. A tripolar catheter (0.5 cm interelectrode space, USCI) was introduced from right femoral vein and placed in right atrium against the septal leaflet of the tricuspid valve to record His bundle electrogram. One quadripolar electrode catheter (0.5 cm interelectrode space, USCI) was introduced from right internal jugular vein and placed in the coronary sinus to record left atria1 electrogram. Two quadripolar electrode catheters (1 cm interelectrode space, USC11 were introduced from the right or left femoral vein and placed in high right atrium and right ventricle, respectively, for programmed electrical stimulation and recording. Intracardiac electrograms were displayed simultaneously with electrocardiographic leads 1, II and V, on a multichannel oscilloscopic recorder (Electronics for Medicine, VR-12) and were recorded on paper at a speed of 100 mm/s. The filter was set as from 30 to 500 Hz. A programmed digital stimulator (Bloom and Associates) was used to deliver electrical impulses of 2.0 ms duration at approximately twice diastolic threshold. Programmed electrical stimulations consisting of atria1 and ventricular incremental pacing and extrastimulation were first performed to ascertain antegrade and retrograde AV conduction patterns and inducibility of AV nodal reentrant tachycardia, atria1 arrhythmias or ventricular arrhythmias. AV nodal reentrant tachycardia was documented using standard criteria [13,14]. Mapping of retrograde elective site for ablation

AV nodal

pathway

and

The orifice of the coronary sinus, visualized after injection of contrast medium via coronary sinus catheter, and the site with maximal His potential were marked on the fluoroscopic screen (right anterior oblique, left anterior oblique, and anteroposterior projections) for future reference. Careful mapping of retrograde atria1 activation during tachycardia was performed at the perinodal atria1 site and around the orifice of the coronary sinus with the distal two electrodes of the tripolar His bundle catheter under multiplanar fluoroscopy. Retrograde atria1 activation was

54

initially recorded in the His-bundle region, and might be superimposed on the ventricular electrogram during tachycardia. To distinguish the retrograde atria1 component from ventricular activation, paced ventricular extrastimuli were delivered during tachycardia at 10 ms decrements. The recording site which had the earliest retrograde atria1 activation concomitant with complete absence of His activation was the site elective for ablation (Fig. 1). Ablation

procedure

(Fig. 2)

Arterial pressure was monitored through a short intraarterial catheter. A short-acting anesA

67, M,VGH283692-2

P cs ---Jv--~y.--~--+ recording of surface leads II, VI and Fig. 1 Simultaneous Intracardiac recordings from high right atrium (HRA), tripolar His catheter (HBE), and proximal portion of the coronary sinus (PCS) from patient 14. A. During atrioventricular nodal reentrant tachycardia, the atrial deflection is inscribed within the ventricular electrogram, thus obscuring the determination of earliest atrial depolarization. A paced ventricular stimulus was introduced during AV nodal reentrant tachycardia. The paced ventricular complex is dissociated from tachycardia. thus allowing for determination of the earliest atrial defection. B. The intracardiac electrogram from the site elective for ablation. His bundle potential is absent and the atrial deflection recorded on His catheter is synchronous with the onset of QRS complex on surface electrocardiogram.

150 I.: controt IO

20

30

' 1w

. 2w

* 3w

LW

.'.' 2M

3M

TIME

Fig. 2. Prolongation of PR interval was seen immediately after the ablation procedures. PR interval shortened progressively during the following days and remained fixed about one month after ablation. D = days; W = weeks; M = months; * p < 0.05 vs control.

thetic agent (0.5-l mg/kg methohexital sodium, intravenous) was given prior to delivering each cathodal shock. The cathodal shock was delivered from the distal two electrodes (connected in common) of the mapping catheter to the selected site during AV nodal reentrant tachycardia. The mapping catheter was checked for insulation before it was used to deliver the cathodal shock. The delivered energy was 200-250 J/shock in the initial 7 patients. It was decreased to a lower energy (loo-150 J/shock) in the remaining 22 patients. The anode was a large skin electrode (81 cm’, NIKOMED) positioned over the left scapular area. If the first shock was successful in eliminating retrograde ventriculoatrial conduction, isoproterenol and/or atropine was administered to ascertain the’abolition of VA conduction 30 min later. If AV nodal reentrant tachycardia was not inducible or VA conduction was absent after isoproterenol and/or atropine admiiiistration, one additional shock with the same or lower stored energy was delivered to the same site to minimize the possibility that retrograde VA conduction through the AV node might resume later. If the first shock was not successful in eliminating VA conduction or AV nodal reentrant tachycardia was still inducible, mapping procedures were repeated to find the elective site for ablation. Additional direct current energy was not delivered if antegrade secondary degree AV block or

complete AV block lasted for more than 30 rnin, even after isoproterenol and/or atropine administration. Postablation

monitoring

and evaluation

A 6F hexapolar catheter was left in right ventricular apex at the end of the ablation procedure for temporary ventricular pacing during the occurrencc of complete AV block, if any, and reevaluation of the retrograde VA conduction. All patients were monitored in a coronary care unit for 24 h after the ablation procedures, then underwent continuous electrocardiographic monitoring for 3 more days. Serial creatine-kinase and creatine-kinase MB fraction levels were measured. In each patient, a two-dimensional and Doppler echocardiogram was obtained immediately and 1 week after the procedure. A transesophageal echocardiogram was performed 1-2 days after the procedure. A technetium pyrophosphate scintigram and a pulmonary ventilation perfusion scintigram were obtained 2-4 days after the catheter ablation procedure, A nuclear ventriculogram was performed 1 week after the

TABLE

2

Change

of AV nodal

function

ablation procedures. Follow-up electrophysiological studies were performed 1 week and 3-6 months after the ablation procedure. Furthermore. ventricular programmed extrastimulation from two right ventricular sites with 2 extrastimuli was performed during control and isoproterenol infusion to assess the possible arrhythmogenie effect of ablation. After hospital discharge, all patients were followed up closely. Long-term efficacy was assessed clinically based on the resting surface electrocardiogram, 24-h Holter recording and clinical symptoms. Statistical

analysis

All data were expressed as mean i SE. Differences among the electrophysiological data obtained before, early and late after transcatheter shocks to the AV node were examined with analysis of variance (ANOVA). Student’s t-test, corrected for multiple comparisons, was used to analyze the difference in means when appropriate. A probability of less than 0.05 was considered as statistically significant.

after ablation. B

I

2D

1w

3-h M

Antegradc AVB-N (n) 1 2 3 Duality (n) AH (ms) AVWB (ms) AVNERP (ms)

29 0 0 0 29 78 i 3 325 * 9 266 i_ 7

0 2.5 I 3 16 220 + 8 580 + 15 460 * 10

0 26 1 2

0 27 0 2 I6 t34* 9 442 + 23 361 * 26

0 ‘7 0 7 16 128k 8 420 & 29 345 + 3’

Retrograde VAB (?I) VAWB (ms) VAERP (ms)

0 335 * 9 259 + 8

15 380 i 37 284 * 28

15 452 + 60 330 + 44

AH = conduction time from third-degree of atrioventricular paced cycle length 500 or 600 Wenckebach block: D = day; conduction effective refractory paced cycle length just before

29

atrium (A) to the His bundle (H); B = before ablation: AVB-N, 1. 2, 3 = none, first. secondary. conduction block; AVNERP = atrioventricular node effective refractory period (obtained at atrial ms); AVWB = shortest atrial paced cycle length just before the occurrence of atrioventricular node I = immediately after ablation; M = months; n = number of patients; VAERP = ventriculoatrial period (obtained at ventricular paced cycle length 500 or 600 ms): VAWB = shortest ventricular the occurrence of ventriculoatrial Wenckebach block: W = week.

Electrophysiological

Results Preablation

electrophysiological

characteristics

The results of baseline electrophysiologic studies were shown in Table 2. All patients had antegrade dual AV nodal pathways and the earliest retrograde conduction was on the proximal AV nodal area, without shift of retrograde atria1 activation to the area near coronary sinus orifice. Results of ablation

After delivering 2.3 k 0.5 shocks with mean cumulative energy 323 + 47 J per patient, AV nodal reentrant tachycardia was noninducible in all the patients. Patient 3 had spontaneous occurrence of AV nodal reentrant tachycardia on the third day after ablation, and received a successful second ablation one week later. Patient 23 had recurrence of tachycardia on the fifth day after the first ablation session and received a secondary ablation session. Unfortunately, tachycardia still occurred but it could be under control after taking procainamide (500 mg, every 6 h) and verapamil (80 mg, every 8 h). Patient 18 had recurrence of reentrant tachycardia 3 weeks after the ablation procedure. The tachycardia cycle length was longer than before ablation procedure (500 ms vs 310 ms> and it could be suppressed by oral nadolol (80 mg, daily), which was not effective before receiving ablation. Patients 12 and 26 had persistent complete AV block and received permanent pacemaker implantation. The other 25 patients did not receive antiarrhythmic agent after the ablation procedure and had no occurrence of AV nodal reentrant tachycardia during a mean follow-up period of 13 +_2 months (range 7 to 20). TABLE

3

Possible

mechanisms

I 11 III IV

of electrical

Retrograde Retrograde Retrograde Retrograde

VA VA VA VA

Antegrade dual AVN = antegrade n = number of oatients.

effects of ablation

Early follow-up electrophysiological studies were performed one week after ablation in 27 patients and late electrophysiological studies were performed 3 to 6 months (mean 4 i 1) after ablation in 23 patients (Table 2). AV nodal reentrant tachycardia, atria1 reentrant beats and ventricular tachycardia were not inducible in all the patients before and after isoproterenol and/or atropine administration. According to the late electrophysiological results, the changes of antegrade and retrograde AV nodal function were classified into four types (Table 3). Fifteen patients had retrograde VA block, 12 of them still had dual AV nodal pathway properties and the other three did not have duality (Fig. 3). Eight patients had prolongation of retrograde VA conduction, four of them still had dual AV nodal pathway properties (Fig. 41, and the other four did not have duality. A single slow-fast form echo was inducible in the 4 patients who had antegrade AV nodal duality with retrograde conduction prolongation. Complications

Accidental AV block, proarrhythmias, and myocardial injury (CK-MB) are shown in Table 4. Discussion Major findings

This study shows that when careful mapping obtains both the earliest appearance of the atria1 electrogram and the absence of Hisian deflection during tachycardia, a direct current shock delivered from the distal two electrodes to this site is

cure of AVNRT. Anterograde Anterograde Anterograde Anterograde

(blocked) (blocked) (prolonged) (prolonged) dual

AV nodal

pathway

property:

dual dual dual dual

AVN AVN AVN AVN

Retrograde

(modified) (absent) (modified) (absent) VA = retrograde

n = 12 n=3 tl=4 n=4 ventriculoatrial

conduction;

effective in the treatment of AV nodal reentrant tachycardia. Twenty-five patients were free of tachycardia without any antiarrhythmic agents, and only 2 patients had persistence of complete AV block after the procedures. Mechanisms

of electrical

cure of tachycardia

The exact site of the AV nodal reentrant tachycardia is still controversial. Some experimental [15,16] and clinical data [17,18] support the concept that the circuit is all intranodal. Iinuma et al. Ll9.201 using an isolated rabbit heart

I f

350

I l

’ 250

1

d

3oc,

350

I AlA

. . . . . . 0.

500

l*.

I 450

qrn

q

t

2

.

.

.

.

.

.

.

mm

.mm

.

.

n

..

.

400

;

t 350 . 300

I

3cI)

350

500

550

B

3ooh C7

.

.

.

l.

0 Pre-

’ 250

1 300

I

I

350

400 V1V2

550

Abl

q Post-Abi

l *o

t 1

I

. . . .

350

Pre-Abl

q Post-Abl i / l-%c

400 450 AIAZ (msec)

I 450

1 500

L 550

(msec)

Fig. 4. Atrioventricular nodal function curve before (black circles) and after (open squares) ablation. Retrograde conduction time was prolonged and antegrade AV nodal dual pathway property was present after ablation. VlV? = coupling interval of ventricular extrastimulus.

500-

$

, 550

0de*

E

I

I 5co

. 0

x

1

450 4co (msec)

B 550

;‘

Abi

300) f&Y

A

Pre-

0 Post-Abl

t

450-

: 5

400

-

350

-

f

AI A2 Cmsec)

Fig. 3. AV nodal function curve before (black circles) and after (open squares) ablation in two patients. The two patients had retrograde conduction block after ablation. AV nodal dual pathway property was present in the upper panel, but it was absent in the lower panel. The drive cycle length was 600 ms. AlA = coupling interval of atrial extrastimulus: HlH2 = coupling interval of His potential.

preparation, provided evidence for incorporation of atria1 tissue in an arrhythmia similar to AV nodal reentrant tachycardia and showed that discontinuous curves characteristic of dual AV node pathways could be reproduced when the perinodal region was the site of one of the pathways. The mechanisms of cure of AV nodal reentrant tachycardia in this study varied. Among the 27 patients who received an early follow-up electrophysiological study, 19 patients had loss of retrograde conduction and 8 patients had resumption of retrograde conduction through AV

58 TABLE

4

Postablation

complications.

Complete AV block t n) Transient AT (n) Echocardiography New valvular insufficiency (n) Thrombus (n) New wall motion impairment (11) Pulmonary V-P scanning Pulmonary embolism (n) TC-99 heart scanning positive uptake (n) Peak CK-MB (IU/I) Nuclear ejection fraction (5%) RV. LV(B/A) (%)

2 2 0 0 0 0 0 loi3 49* 1.53*2/ 4x+3,51 +4

A = after ablation, AT = atrial tachycardia; B = before ablation: LV = left ventricle: n = number of patients; RV = right ventricle; V-P = ventilation-perfusion.

node with long VA conduction time. Twenty-three patients received late electrophysiologic study, 15 patients had retrograde VA block, 8 patients had prolongation of retrograde VA conduction. Although the dual AV nodal pathway properties still existed in 4 of the 8 patients with VA prolongation, the AV nodal reentrant tachycardia was not inducible. Poor conduction property in the retrograde limb resulting in retrograde block might be the mechanism. Nevertheless in the other four patients without duality, the mechanism of noninducibility of AV nodal reentrant tachycardia might be due to loss of antegrade dual AV nodal properties and/or retrograde block in the poor conduction limb. We suggest that preferential interruption or impairment of retrograde ventriculoatrial conduction was the major, but not the sole, mechanism of electrical cure of AV nodal reentrant tachycardia. Nonspecific modification of antegrade fast and slow pathway conduction properties, and the atria1 fibers critical for maintenance of the tachycardia, may, in part, play a role. Comparison to other reports of catheter-mediated ablation on AV nodal reentrant tachycardia

duction. The His bundle potential was absent or with an amplitude of less than 0.1 mV on the electrograms of the ablation sites and the ablation sites were approached from the subclavian vein (34 patients) or the femoral vein (8 patients). Tachycardia was eliminated in 70% of patients, and 10% required permanent pacemaker. Twelve patients (30%) needed more than one session (2 or 3 sessions) to cure AV nodal reentrant tachycardia. The cumulative energy and numbers of delivering energy were 518 _t 60 J, 3.0 f 0.4, respectively. Epstein et al. [9] delivered direct current energy on the perinodal area spreading from the coronary sinus ostium to the His bundle. Tachycardia was eliminated in 67% of patients, and none required permanent pacing. Three patients (33%) needed more than one session (2 or 3 sessions) to cure AV nodal reentrant tachycardia. Lee et al. [lo] delivered radiofrequency current on the perinodal region to eliminate AV nodal reentrant tachycardia in 39 patients. Thirty-two patients (82%) were free of tachycardia and did not have high-degree AV block. Three patients (8%) developed complete AV block, 5 patients failed. During the follow-up electrophysiological study, 3 of 19 patients had atypical AV nodal reentrant tachycardia inducible, possibly due to proarrhythmic effects of ablation. In our study, a modified method consisted of (1) the ablation sites approached from the femoral vein by using the tripolar His catheter, (2) the His bundle potential absent on the electrograms of the ablation sites, (31 the distal pair of electrodes (connected in common) was used to deliver energy, (4) one additional direct current shock was delivered after initial elimination of retrograde AV nodal conduction. A lower cumulative energy (323 & 27 J), smaller numbers of discharges (2.3 f 0.51, a higher success rate (86%) and a lower incidence of repeated sessions (2 patients with 2 sessions, 7%), reflect the possible advantages of this modified technique. Limitations

Recently, Haissaguerre et al. [8] reported catheter ablation of retrograde conduction in 42 patients after careful mapping of retrograde con-

The main of antegrade

risk of the procedure is impairment conduction. The 7% incidence of

inadvertent AV block is comparable with that reported by Haissaguerre et al. [8] for direct current and Lee et al. [lo] for radiofrequency current ablation on AV nodal reentrant tachycardia. Preliminary surgical reports describe a low incidence (O-2%) of postoperative AV block. This apparent advantage of operative ablation must be considered in the context of the increased expense and morbidity of open heart surgery. Roman et al. Il.51 delivered radiofrequency energy to the posterior septum and provided a new insight into the preferential modification of the slow pathway with a low risk of AV block. More decrease in delivered energy probably offers the hope of reducing the incidence of AV block. The absence of hypotension, wall motion impairment, valvular regurgitation, thrombus formation, and the absence of new arrhythmias during the longterm follow-up in the present study might be due to less cumulative energy.

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basis of reciprocal

of a dual A-V

system in the isolated

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14 Brugada

Acknowledgements

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Guillem

Our experiences suggest this modified catheter-mediated ablation technique for AV nodal reentrant tachycardia could achieve a high success rate and a low incidence of recurrence, even when delivered energy is decreased to 100-150 J/shock. If subsequent studies confirm these preliminary results, then this modified procedure may be offered to patients with symptomatic AV nodal reentrant tachycardia refractory or intolerable to antiarrhythmic drugs. However, the potential risk of direct-current shock must be considered, and it may just be regarded as an alternative to surgical ablation in patients who fail to respond to radiofrequency ablation.

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