Catheter Ablation of Mahaim Fibers With Nodal ... - Circulation

Catheter ablation of Mahaim fibers with preservation of atrioventricular nodal 

conduction. 

M Haissaguerre, J F Warin, P Le Metayer, L Maraud, L De Roy, P Montserrat and J P 

Massiere 

Circulation. 1990;82:418-427 

doi: 10.1161/01.CIR.82.2.418 

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418 

Catheter Ablation of Mahaim Fibers With 

Preservation of Atrioventricular 

Nodal Conduction 

Michel Haissaguerre, MD, Jean-Frangois Warin, MD, Philippe Le Metayer, MD, 

Luc Maraud, MD, Luc De Roy, MD, Paul Montserrat, MD, and Jean-Paul Massiere, MD 

Three patients with refractory preexcited tachycardia implicating Mahaim fibers underwent 

attempted catheter ablation of the accessory pathway. In the absence of demonstrable 

retrograde conduction in Mahaim fibers, we located the accessory pathway ventricular 

insertion site using the criteria of concordance between paced and spontaneous QRS morphologies 

during pace-mapping and earliest onset of local electrogram relative to surface preexcited 

QRS. At this site, a QS-like pattern of unfiltered unipolar electrograms with steep downstroke 

was recorded. The optimal site appeared radiologically at the right ventricular anterior wall or 

the adjacent septum, 2-4 cm from the tricuspid anulus. Three to six 160-J shocks were 

delivered at this site using an anterior chest wall plate as anode. After fulguration, conduction 

through the Mahaim tract was absent. A right bundle branch block persisted in two patients. 

All patients remained free of preexcited tachycardia during 12-16 months of follow-up. 

Postablation electrophysiological assessment showed no preexcitation in any patient. No 

reciprocating tachycardia was inducible, even during isoproterenol infusion. Atrioventricular 

nodal conduction parameters were unchanged from baseline study. Catheter ablation of 

Mahaim fibers is an effective alternative method for the treatment of tachycardias that include 

the accessory pathway in the circuit. (Circulation 1990;82:418-427) 

P atients with Mahaim fibers are prone to paroxysmal 

reciprocating tachycardias.1-23 These 

anomalous conduction pathways can either 

participate in the reentrant circuit or serve a bystander 

role.6,8,10,12,14-16,21 Recently, specific surgical 

interruption of Mahaim fibers has been reported by 

several authors24-27 for disabling and drug-refractory 

tachycardias. Because of their presumed intimate 

relation with the atrioventricular node, these fibers 

have been thought to be unapproachable by ablative 

techniques due to the risk of complete atrioventricular 

block. However, His bundle ablation has been 

performed in some patients12,28-30; although anterograde 

conduction continued over the accessory pathway 

in certain patients,12,28,29 a permanent pacemaker 

was often implanted. In this report, we 

describe three patients whose Mahaim fibers were 

successfully ablated by endocardial DC shocks 

applied at the ventricular insertion of the pathway. 

From the Service de Cardiologie et Medecine Interne (M.H., 

J.-F.W., P.L.M., L.M., P.M., J.-P.M.), Hopital Saint-Andre, Bordeaux, 

France, and Cliniques Universitaires (L.D.R.), UCL, 

Mont-Godinne, Belgium. 

Address for correspondence: Michel Haissaguerre, MD, Hopital 

Saint-Andre, 1, rue Jean Burguet, 33075 Bordeaux, France. 

Received May 16, 1989; revision accepted April 3, 1990. 

Moreover, this study provides some anatomical and 

electrophysiological insights into Mahaim fibers. 

Methods 

Patient Characteristics 

Three patients (52, 25, and 31 years old) were 

referred for treatment of disabling paroxysmal wide 

QRS tachycardias with left bundle branch block 

morphology and superior axis (Figure 1). Patient 1 

also had episodes of atrial tachycardia with narrow 

QRS complexes. Patient 3 had two episodes of atrial 

fibrillation with minimal preexcited RR interval of 

260 msec. A fourth patient with Mahaim fibers was 

referred during the same period; after catheter ablation 

of a left posterior accessory pathway serving as 

retrograde limb of the reentrant circuit, no tachycardia 

remained inducible. Thus, no ablation of the 

Mahaim tract was attempted. 

Tachycardia recurred daily in patient 1 and every 

1-3 months in the other patients. Ineffective drugs 

included quinidine, 8-blocking drugs, flecainide, and 

amiodarone, either singly or in multiple combinations. 

Physical examination, surface electrocardiogram, 

and echocardiogram were normal in patients 1 

and 2. In patient 3, the QRS complexes were perma- 

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Haissaguerre et al Catheter Ablation of Mahaim Fibers 419 

R 

A B c 

V.~W 

4I 

6 7 , F \ 

-4 

FIGURE 1. Electrocardiograms during reciprocating tachycardia 

in patients 1(A), 2 (B), and 3 before first ablation 

attempt (C). 

nently preexcited, and an echocardiogram revealed a 

dilated cardiomyopathy. Clinical characteristics are 

summarized in Table 1. 

Baseline Electrophysiological Study 

The patients were studied after all cardioactive 

medications had been discontinued for 5 days. Amiodarone 

was discontinued more than 6 months 

before the study in two patients and was prescribed 

to patient 1 at the time of referral. 

Three or four 6F USCI, Billerica, Mass., multipolar 

electrode catheters were introduced through a 

femoral or subclavian vein and positioned within the 

right atrium, right ventricle, and coronary sinus and 

across the tricuspid valve for recording the His 

bundle and right bundle branch electrograms. In 

addition to the intracardiac recordings (filtered 

between 30 to 500 Hz), surface leads I, II, III, and V1 

were recorded on an Electronics for Medicine VR12 

recorder at a paper speed of 100 mm/sec. Programmed 

electrical stimulation was performed from 

the right atrium and right ventricular apex with a 

Savita stimulator, VPA Medical, Paris, with a pulse 

duration of 1 msec at twice-diastolic threshold. 

Presence and participation of Mahaim connections 

as components of the tachycardia circuit were 

defined according to criteria suggested by Gallagher 

et al.10 With incremental atrial pacing and progressive 

prematurity of atrial extrastimuli, the QRS 

became increasingly preexcited as the H deflection 

merged into the QRS complex and the AV interval 

concurrently lengthened. The QRS complexes 

assumed a left bundle branch morphology identical 

to the configuration during tachycardia. During right 

ventricular pacing, the earliest atrial activation was 

recorded at the His bundle lead. Baseline accessory 

pathway conduction properties and refractory periods 

are listed in Table 2. Spontaneous tachycardia 

was reproducible by a premature atrial or ventricular 

stimulus (Table 2) or by rapid atrial or ventricular 

pacing in all patients. In patient 1, tachycardia induction 

was concomitant with a sudden prolongation of 

the AH interval, which lengthened from 180 to 250 

msec for an atrial coupling interval decreasing from 

360 to 350 msec. In this patient, atrial tachycardia 

with narrow QRS complexes (cycle length, 430-500 

msec) could also be induced. In all patients, the 

sequence of retrograde atrial activation was the same 

during tachycardia as it was during ventricular pacing. 

Tachycardia induction and preexcitation were 

also associated with a reversal in the relation 

between His and right bundle electrograms (Figure 

2); the His-to-right-bundle electrogram interval 

shifted from +10 to -5 or -10 msec, and the right 

bundle electrogram occurred within the first 30 msec 

of QRS complex onset. It is noteworthy that a 

catheter-induced right bundle branch block in 

patient 2 did not prevent tachycardia reinduction but 

instead lengthened retrograde conduction (Table 2 

and Figure 3); furthermore, patient 3 had underlying 

right bundle branch block as evidenced by atrial 

extrastimuli performed during the refractory period 

of Mahaim fibers and by spontaneous escape rhythm 

arising in the His bundle. This patient had the most 

TABLE 1. Clinical Characteristics and Drugs Used in Each Patient 

Age Age at first ECG during 

Patient (yr)/sex Cardiac diagnosis Sinus rhythm tachycardia (yr) tachycardia Previous ineffective drugs 

1 52 /F ... Narrow QRS 10 (160 beats/mim) Verapamil, quinidine, 

LBBB 

sotalol, flecainide, and 

amiodarone 

2 25 /F ... Narrow QRS 14 (200 beats/min) Verapamil, quinidine, 

LBBB 

flecainide, amiodarone, 

amiodarone, and flecainide 

3 31/M Dilated Preexcitation 17 (180 beats/mim) Quinidine, sotalol, 

cardiomyopathy LBBB propafenone, flecainide, 

and amiodarone 

ECG, electrocardiogram; LBBB, left bundle branch block morphology. 


420 Circulation Vol 82, No 2, August 1990 

TABLE 2. 

Baseline Electrophysiological Evaluation 

Retrograde conduction via 

normal AV conducting system 

(msec) 

Anterograde conduction via Mahaim 

fibers (msec) 

Tachycardia 

(msec) 

Patient 

WCL 

VA HA' 

VA' 

time ERP 

WCL 

AV 

AV 

increment ERP HV H-RB 

Tachycardia 

initiation 

Cycle 

length A'V VA' VH HA' 

1 300 40 105-155


1 

I 

i;N1za 1-~~~'- 1t 

'Wlm.: _. 

WITH 

11 

1300 

I VH 25 \ fL P4 

2VHZ5 

HrSe II 

.. 

1 

11 

RBBB 

1- 

1 

,.. 

.200mr.1 P 

:1 

stH 55 1 

JA4. 

IIESr2 x- 

FIGURE 3. Intracardiac recordings during reciprocating 

tachycardia in patient 2, with (right panel) or 

without (left panel) right bundle branch block during 

sinus rhythm. H, His bundle potential; RA, lateral right 

atrium; RV, right ventricle; MCS and PCS, middle and 

proximal coronary sinus; V, onset of ventricular activity 

(vertical line from top to bottom); A', atrial activity at 

His bundle region. This atrial electrogram is clearly seen 

in tight panel but is partially concealed on left panel 

(withdrawal of recording catheter allows differentiation 

of atrial component of electrogram). Tachycardia has a 

cycle length increasing from 270 to 300 msec with 

production of right bundle branch block; this change is 

linked to a prolongation of VI interval from 25 to 

55 msec. 

VH interval in patient 3 was probably not linked to 

atrioventricular nodal reentry, with Mahaim fibers 

intervening in a bystander role. 

Catheter Ablation Protocol 

After a discussion of the options available, the 

patients provided informed consent for catheter electrical 

ablation. 

In the absence of demonstrable retrograde conduction 

in the Mahaim fibers, all efforts were made to 

locate the ventricular insertion site of the accessory 

pathway. Concordance of two parameters was 

required to identify the optimal preablation sitepace-mapping 

reproducing spontaneous tachycardia 

morphology (or maximal preexcitation during atrial 

pacing) in the 12 electrocardiographic leads (best 

pace-mapping was chosen by comparing slightly different 

patterns obtained through adjacent bipoles of a 

multipolar electrode catheter) and the earliest ventricular 

electrogram (relative to QRS complex onset) 

during maximal preexcitation. This mapping was performed 

with two electrode catheters (bipolar or multipolar) 

previously tested for fulguration.31 When an 

early ventricular potential was detected at one site, the 

other catheter was moved around this point to record 

possible earlier potential and so on until a site not 

surrounded by an earlier activated zone was found. 

Activation times were measured from the main rapid 

deflection to the earliest onset of preexcited QRS. 

At the preablation site, unipolar electrogram morphology 

was recorded to analyze its characteristics 

(see "Results"). 

Before fulguration, the position of the preablation 

site in the right ventricle relative to His bundle 

location was documented by radiographs performed 

in the anterior, left anterior oblique (600), right 

anterior oblique (300), and left profile views. Then, a 

pigtail catheter was introduced, and contrast material 

was injected into the right ventricle to outline the 

tricuspid anulus. By using the known interelectrode 

distance of the catheters, the location of the preablation 

site was defined. 

The selected electrode was connected to the 

cathodal output of a defibrillator (Robert et Carriere, 

Paris). The anode was a 66-cm2 plate placed on 

the anterior chest wall. The patients were then 

anesthetized with sodium thiopental, and three successive 

160-J discharges synchronized to the QRS 

were delivered at the selected site -two through the 

distal electrode and one through the immediately 

more proximal electrode. 

Atrial and ventricular stimulations were repeated 

after fulguration to assess short-term effects on atrioventricular 

conduction. A 6F multipolar electrode 

catheter was left in place at the end of the procedure 

to reevaluate anterograde and retrograde conduction. 

Creatine kinase and creatine kinase-MB fraction 

levels were measured 6 hours after fulguration. 

Continuous electrocardiographic monitoring was 

performed for 3 days, and a 24-hour ambulatory 

electrocardiographic recording was obtained during 

the 24 hours after fulguration. Exercise testing and 

electrophysiological study were performed between 

days 4 and 6. No antiarrhythmic drug was prescribed 

after discharge. 

A follow-up electrophysiological study was repeated 

2-5 months after fulguration in all patients. 

Results 

Ablation Procedure 

The preablation site had the following characteristics 

(Table 3). First, pace-mapping was achieved in the 

three patients with no resulting significant difference 

between paced and preexcited QRS complexes (Figure 

4). Second, the earliest recorded peak ventricular 

electrogram occurred 0-5 msec before the onset of 

surface electrocardiographic QRS. A small, rapid 


422 Circulation Vol 82 No 2, August 1990 

TABLE 3. Data on Preablation Site and Delivered Energy 

Bipolar 

Unipolar 

electrograms electrograms Delivered Creatine 

Patient 

Pacemapping 

VR 

Small 

potential Pattern 

Amplitude 

(mV) 

Slope of downstroke 

(mV/10 msec) 

energy (J) 

(160 J) 

kinase-MB 

level (IU/l) 

1 Concordant -5 - QS 11 (d) 2.6 3 x 71 

10 (p) 

2 Concordant 0 + 3x 176 

3 Concordant 0 + QS 8.5 (d) 3.4 3x 84 

7 (p) 

Concordant 0 + QS 10 (d) 3.3 3 x 120 

8 (p) 

d and p, distal and immediately more proximal electrode of electrode catheter. VR, interval from peak ventricular 

electrogram (V) to onset of QRS complex (R). 

deflection possibly arising in the specialized conducting 

system preceded the main potential in two patients 

(Figures 5 and 6). This rapid deflection disappeared 

when the mapping catheter was moved a short distance 

away from the preablation site; no atrial activity 

was present at the preablation site. Third, unfiltered 

unipolar electrograms showed a high, steep uniphasic 

QS-like pattern through the two electrodes of a bipolar 

catheter in patient 1 and through the two most 

distal electrodes of a quadripolar catheter in patient 3. 

This morphology changed when the electrode was 

moved slightly, the patterns becoming QS-like with a 

smooth slope or rS-like. In patient 2, no unipolar 

recording mode could be used due to the disappearance 

of tachycardia and preexcitation during mapping. 

This phenomenon was presumed to be attributable to 

a catheter-induced block in Mahaim fibers. 

Multiple radiographic views and right ventricular 

angiography revealed that the preablation site was at 

the right ventricular anterior wall (Figure 7) or the 

adjacent anterior septum, 2-4 cm from the tricuspid 

valve. Between this site and the anulus, new attempts 

to record an earlier ventricular electrogram during 

preexcitation were unsuccessful. 

Three 160-J shocks were delivered in each patient-ttwo 

through the distal electrode and one 

through the adjacent electrode. No atrioventricular 

block, ventricular arrhythmia, or hemodynamic instability 

occurred after the shocks. A right bundle branch 

block was present since the first shock. No tachycardia 

or preexcitation was inducible after fulguration. 

Short-term Results 

Preexcitation remained absent in patients 1 and 2 

as demonstrated by repeated atrial pacing. In patient 

3, it reappeared 3 hours after shocks with a left 

deviated axis of QRS complexes and a QS pattern in 

lead V2 (Figure 6). In the latter patient, a second 

ablation session was performed the next day; maximal 

preexcitation was notably different from initial 

morphology, and tachycardia remained inducible 

(Figure 4). The criteria for the optimal lead position 

(Table 3) were met at a site located 1.5 cm more 

apically inferior and toward the septum than the site 

of the previous attempt. No earlier ventricular potential 

could be recorded between this distant point and 

the tricuspid anulus. Three 160-J shocks (two distal 

and one proximal) were delivered at this site and led 

to the disappearance of preexcitation. This patient 

complained of chest pain on waking, but echocardiograms 

on days 1 and 5 revealed no trace of pericardial 

effusion or other anomaly. 

Echocardiographic studies were normal in the 

other two patients. The mean value of creatine 

kinase-MB fraction (Table 3) was 112 IU/l (normal 

values, 0-16 IU/I). 

Exercise testing led to a mean maximal heart rate 

of 165 min-1 without significant change in ST or T 

waves or arrhythmia. 

Electrophysiological study confirmed the disappearance 

of preexcitation and reciprocating tachycardia. 

Despite the right bundle branch block, anterograde 

and retrograde atrioventricular nodal conduction values 

were unchanged from baseline values. In patient 

1, atrial tachycardia with the same cycle length 

remained inducible with one atrial extrastimulus. 

Long-term Follow-up 

Patients were discharged without antiarrhythmic 

drugs. No recurrence of preexcited tachycardia 

occurred during follow-up periods of 16, 14, and 12 

months, respectively. Two months after discharge, 

patient 1 complained of palpitations that were associated 

with unsustained episodes of atrial tachycardia; 

she is now asymptomatic with quinidine. Patient 

3 complained of marked pains in the subclavian 

region where a catheter had been left in place; he 

then presented in chest pain with pleural effusion. 

Pulmonary scintigraphy showed perfusion defects. 

Despite normal phlebography of upper and lower 

limbs, the diagnosis was pulmonary embolism complicating 

a subclavian vein thrombosis. 

Electrocardiograms showed persistence of right 

bundle branch block in patients 2 and 3 and its 

disappearance in patient 1. 

Electrophysiological study performed 2-5 months 

after fulguration (after discontinuation of drug therapy 

in patient 1) demonstrated the absence of an- 


AOF 

4 

PM 

AXA' 

RA ST PM SVT 

;r m TlIII imX1,.l.l...l;lI., 

YV 4V 

6~~~ 

FIGURE 4. Two examples of concordant pace-maps (PMs) 

in patient 3. Upper panel occurred during first ablation 

attempt, and lower panel occurred during second session. 

Note differences in QRS complexes between two right atrial 

stimulations (RA ST), particularly in leads II, aVR, V,, V2, 

and V6. A 12-lead electrocardiogram of tachycardia (SVT) is 

shown during the second ablation attempt; it is also slightly 

differentfrom the morphology of clinical tachycardia shown in 

Figure 1G. QRS complexes of PMs are very similar to preexcited 

QRS complexes resulting from atrial stimulation. Arrows 

indicate stimulation artifacts. In lower panel, first QRS complex 

shown during RA ST is spontaneous and clearly preceded 

by a P wave. 

terograde and retrograde Mahaim fiber conduction. 

Reciprocating tachycardia was not inducible in any 

patient, even during isoproterenol infusion. Despite 


right bundle branch block, the proximal right bundle 

branch electrogram could be recorded in all patients. 

Retrograde right bundle branch potential was 

recorded in patient 1 during ventricular pacing, thus 

indicating its activation after the His bundle potential. 

Therefore, despite the disappearance of right 

bundle branch block on electrocardiography in this 

patient, retrograde conduction in this branch 

remained altered. No significant alteration of atrioventricular 

nodal conduction was apparent (Table 4). 

The mean atrioventricular nodal AH and infranodal 

(HV) conduction times were 100 and 48 msec, 

respectively. The mean minimum paced atrial cycle 

length associated with 1:1 conduction was 324 msec. 

During ventricular pacing, 1: 1 retrograde conduction 

was present at a paced cycle length of 243 msec with 

a ventriculoatrial conduction time increasing from 

137 to 175 msec; these times were slightly longer 

(+25, +20, and + 15 msec, respectively) than before 

ablation. The mean atrioventricular nodal effective 

refractory period was equal to or less than the atrial 

functional refractory period in patients 1 and 2 and 

was 320 msec in patient 3. Duality (Table 4) was 

noted in patient 1. In patients 2 and 3, single echo 

beats considered atrioventricular nodal reentry were 

inducible (HA' intervals, 35 and 40 msec, respectively). 

No sudden jump (>40 msec) in A2H2 interval was 

observed before the appearance of echo beats. In 

patient 2, echo beats followed A2H2 interval of 190 

msec obtained with an atrial premature stimulus 

(A1A2) of 240 or 230 msec. In patient 3, echo beats 

followed A2H2 interval ranging from 230 to 340 msec 

obtained with an atrial premature stimulus ranging 

from 410 to 320 msec. No more prolonged reentrant 

arrhythmia could be obtained, even during isoproterenol 

infusion. 

Discussion 

Results from this study suggest that transcatheter 

shocks applied to the ventricular insertion of Mahaim 

fibers are effective and safe. The only complication 

was the creation of a permanent right bundle branch 

block in two of the three patients, but in one of these 

two patients, anomalous conduction in right bundle 

branch was present before the procedure. Therefore, 

this technique appears to be an attractive alternative 

to other therapeutic options offered to patients with 

disabling and drug refractory tachycardias associated 

with Mahaim fibers. It can be applied to patients with 

or without retrograde conduction. Indeed, specific 

surgical interruption of Mahaim fibers has been 

reported in some patients.24,27 However, catheter 

ablation obviates the mortality and morbidity of open 

heart surgery. Furthermore, surgical25 or catheter 

ablation28,30 of the atrioventricular conducting system 

has been used successfully with antegrade conduction 

continuing over the anomalous pathway. In most 

of these patients, a permanent pacemaker was 

inserted as a precautionary measure because the 

reliability and durability of accessory pathway conduction 

is unknown. Despite the induced right bun- 



PM 

ME 1 1 ~~~~~i1 

1% / 

V3 

SIT 

t,X~Hi 

FIGURE 5. Bipolar and unipolar recordings 

in patient 1 (left) and bipolar recordings 

inpatient 2 (right) at preablation site 

during reciprocating tachycardia. Main 

bipolar potential occurs 5 msec before 

QRS onset in patient 1: It is synchronous 

with occurrence of right bundle potential 

shown in Figure 3. It is also synchronous 

with QRS onset in patient 2 and preceded 

by a small potential (arrow). Unfiltered 

unipolar electrograms show steep negative 

deflection with a uniphasic QS-like 

pattem. 

cited tachycardias, but these pathways have also been 

mentioned as having bystander roles during atrioventricular 

nodal reentry tachycardia.6A8,10,1214-"16,21 

Thus, accurate identification of the tachycardia circuit 

is crucial to avoid ablating "innocent" pathways. 

In our patients, several criteria10 converged to demonstrate 

the participation of the Mahaim fibers in the 

mechanism of reciprocating tachycardia. Constancy 

of VA' interval during initiation of preexcited tachycardia, 

influence of ventricular premature beats, and 

effects of right bundle branch block on tachycardia 

suggest the participation of the right ventricle in the 

dle branch block in two patients, we did not feel that 

our patients needed a permanent pacing system 

because of the absence of atrioventricular block after 

shocks and because other parameters of anterograde 

conduction were unchanged. 

In our patients, typical features of a Mahaim 

tract10 were present, that is, progressively premature 

atrial depolarizations resulted in progressive prolongation 

of atrioventricular nodal conduction, with 

progressive fusion of the His potential within the 

QRS complex. In most reported cases, it has been 

concluded that Mahaim fibers participate in preexg 

{ i-'- -h '-\l W ti / 

3 

FIGURE 6. Bipolar and unipolar recordings at preablation 

site in patient 3 at first session (left) and at second 

session (right). Note that the preexcited QRS complex 

notably differs in lead V2 between the two sessions. Bipolar 

recordings are vety similar to each other and to the pattems 

ofpatient 2. Peak potential is synchronous with QRS onset 

and is preceded by a small deflection (arrow); no bipolar 

atial activity is present. Unipolar wave forms are high and 

QS-like through distal (D) and immediately proximal (P) 

electrodes of ablation catheter. 

1 

H2v 

H 

.i ... - :1 

lOOms 



1cm 

FIGURE 7. Radiographic position of catheters at preablation 

site (right anterior oblique 300 in upper panel and left profile 

in lower panel) in patient 2. A quadripolar electrode catheter 

introduced via a subclavian vein is on right ventricular inferior 

wall. A bipolar catheter is at His bundle region (small arrow). 

Two adjacent catheters are on preablation site on right 

ventricular anterior wall, 4 cm from distal electrode of His 

bundle catheter. Concordant pace-map and earliest ventricular 

activity during preexcitation were obtained with bipolar 

catheter (1 cm interelectrode distance, large arrow) before 

observing the disappearance of preexcitation. Three 160-J 

shocks through this bipolar catheter resulted in accessory 

pathway ablation. 

tachycardia circuit. Furthermore, disappearance of 

tachycardias after ablation of the Mahaim tract and 

without alteration of the atrioventricular node is 

another strong argument for active participation of 

the nodoventricular pathway. Nevertheless, after 

ablation, two patients had atrioventricular nodal 

echo beats, and the third patient had duality of the 

atrioventricular node, as described in several other 

reports of patients with proved antidromic reciprocating 

tachycardia.2A9Jll1314,2022 It was not, however, 

possible to obtain more than one echo beat despite 

the use of isoprenaline; HA' intervals of these echo 

beats were lower than during tachycardia, providing 

another argument against atrioventricular nodal 

reentry being the mechanism of the tachycardia 

circuit. Moreover, no tachycardia was observed during 

a 12-16 month follow-up in any patient. We do 

not know if the occurrence of nodal echo beats is 

coincidental or relates to the occurrence of nodoventricular 

pathways. It is to be noted that a link 

between enhanced atrioventricular nodal retrograde 

conduction and the occurrence of nodal echo beats 

has been suggested.32,33 The "enhanced" retrograde 

conduction (more than 200 beats/min) observed in 

our patients might be an important (but not specific) 

condition for maintaining the reciprocating tachycardia; 

it was also frequently noted in other reports and 

in eight of Gallagher et al's 11 patients,12 in whom 

the shortest mean cycle length for 1:1 retrograde 

conduction was 280 msec. 

With the aid of right bundle branch recording,10,19,23 

the accessory pathway was demonstrated to 

have close anatomical continuity with the right bundle 

branch or immediately surrounding ventricular 

muscle. Indeed, the short VH interval and the reversal 

of the His and right bundle branch relation during 

tachycardia (or rapid atrial pacing) strongly suggest 

that the ventricular insertion site is linked to the 

middle or distal portion of the right bundle branch. 

Thus, the Mahaim fibers may be more properly 

termed "a nodofascicular tract."10,12,23 In two of our 

patients, preexistent or catheter-induced right bundle 

branch block did not prevent reentrant tachycardia 

but appeared to influence its characteristics. In 

patient 2, production of right bundle branch block 

lengthened the retrograde ventriculoatrial interval 

from 30 msec; patient 3 had the longest retrograde 

conduction time during tachycardia. In these two 

patients, such data might be linked to retrograde 

conduction over the left bundle branch due to the 

presence of a right bundle branch block. No additional 

effort was made to specify the exact anatomical 

nature of the circuit or, as suggested by Tchou et al,23 

to identify the proximal insertion of the Mahaim 

fibers (i.e., to discriminate between nodofascicular 

Mahaim fibers and atriofascicular connection). 

In our patients, retrograde conduction was not 

demonstrable in the Mahaim tract. Like in other 

reports, it is possible that retrograde conduction does 

not occur27 29 or that it is concealed by the conduction 

over the normal pathway. Thus, the electrophysiological 

technique used for identifying the optimal 

ablation site was directed at the ventricular pole of 

the accessory pathway. 

Local ventricular electrogram was recorded at, or 5 

msec before, QRS complex onset. The accuracy of this 

mapping was supported by pace-mapping and, in 

patient 2, by disappearance of preexcitation, probably 

induced by the mechanical action of the catheter. 

Moreover, unfiltered unipolar electrogram morphology 

supplied additional information corroborating the 

mapping; it simultaneously showed a high, steep 

deflection with uniphasic QS-like activity. This pattern 

is considered to indicate the immediate proximity of 

the excitation onset site.34 Indeed, Spach et a134 have 



TABLE 4. 

Follow-up Electrophysiological Study 

Months Anterograde conduction (msec) Retrograde conduction (msec) 

after WCL AV Nodal Pre- WCL VA VA H2A2 

Patient ablation AH HV AV ERP Duality echo beats excitation VA increment ERP interval 

1 5 100 45 315


Treatment of Tachycardias. Baltimore, Md, University Park 

Press, 1971, pp 97-109 

3. Tonkin AM, Dufan FA, Svenson Rh, Sealy WC, Wallace AG, 

Gallagher JJ: Coexistence of functional Kent and Mahaimtype 

tracts in the preexcitation syndrome: Demonstration by 

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KEY WORDS * accessory pathway * fulguration * Mahaim 

fibers * catheter ablation * tachycardias

Catheter Ablation of Mahaim Fibers With Nodal ... - Circulation

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