patterns of atrial activation during pacing with kent · retrograde atrial activation patterns...

British Heart JYournal, 1979, 42, 192-200

Patterns of atrial activation during right ventricularpacing in patients with concealed left-sidedKent pathwaysD. E. WARD, A. J. CAMM, AND R. A. J. SPURRELL

From the Cardiology Department, St. Bartholomew's Hospital, London

suMMARY A 'concealed' accessory pathway was suspected in 12 patients because of eccentric left atrialactivation during tachycardia. Retrograde conduction during ventricular pacing may occur over theatrioventricular node, the accessory pathway, or both. There were 4 patterns of ventriculoatrialconduction in response to ventricular extrastimuli (V2) at various coupling intervals: (1) exclusiveaccessory pathway conduction throughout the cardiac cycle in 2 patients; (2) exclusive accessory

pathway conduction at long coupling intervals and exclusive atrioventricular node conduction at shortcoupling intervals in 2 patients; (3) variably fused accessory pathway/atrioventricular node conductionat long coupling intervals but exclusive accessory pathway conduction at short coupling intervals in4 patients; (4) fused accessory pathway/atrioventricular node conduction at long coupling intervals butexclusive atrioventricular node conduction at short coupling intervals in 4 patients.

With increased prematurity of V2 the ventricle to right atrial interval prolonged conspicuously in11 of 12 patients whereas the ventricle to left atrial interval remained constant until the refractoryperiod of the accessory pathway in all but 2 instances where intraventricular delay occurred. This studyemphasises the importance of left atrial recordings in these patients.

It is now well recognised that concealed ventriculo-atrial anomalous pathways provide the anatomicalsubstrate for a large proportion of paroxysmal re-entrant tachycardias (Slama et al., 1973; Spurrellet al., 1974; Rowland et al., 1977). These pathwaysare designated 'concealed' because they do notconduct anterogradely and therefore there are noelectrocardiographic signs of ventricular pre-excitation. They do, however, produce atrial pre-excitation in response to ventricular stimulation.The degree of atrial pre-excitation via a concealedaccessory pathway is dependent upon tissuerefractoriness and conduction times from the pointof ventricular stimulation to the atrial recording site.Constancy of the ventriculoatrial conduction timehas been used as a criterion for conduction in ananomalous ventriculoatrial pathway, but evidence inpatients with overt Wolff-Parkinson-White syn-drome (Tonkin et al., 1975; Sung et al., 1977a)suggests that this criterion taken by itself may resultin underdiagnosis of concealed ventriculoatrialpathways.

Received for publication 19 December 1978

This study was designed to investigate retrogradeconduction patterns in patients with concealedventriculoatrial pathways.

Patients and methods

The 12 patients were admitted for investigation ofrecurrent paroxysmal tachycardias. Clinical detailsare summarised in Table 1. In all patients physicalexamination, chest radiography, and routine haema-tological investigations were normal. In 5 patientsthe PR interval was short and in 7 patients it wasnormal. The QRS complex during sinus rhythmwas normal in all patients.

All patients were studied in the post-absorptive,non-sedated state and medications were dis-continued at least 72 hours before study. Under-local anaesthetic, 4 bipolar USCI electrode catheterswith 1 cm interelectrode distance were introducedvia the femoral vein and positioned in the rightventricular apex, against the septal leaflet of thetricuspid valve and in the high right atrium (2catheters). A quadripolar USCI catheter with 1 cminterelectrode distances, was inserted via the left

192

on October 6, 2020 by guest. P

rotected by copyright.http://heart.bm

j.com/

Br H

eart J: first published as 10.1136/hrt.42.2.192 on 1 August 1979. D

ownloaded from

http://heart.bmj.com/

Atrial activation in concealed WPW

Table 1

Case Age, ECG Documentedno. sex symptoms PR (s) QRS arrhythmias

1 48, M Palpitation 0-20 N SVT2 40, F Palpitation and

dizziness 0-11 N SVT, AF3 21, F Palpitation 0-12 N SVT4 50, M Palpitation 0-18 N SVT, AF5 41, M Palpitation 0-12 N SVT6 47, F Palpitation 0-20 N SVT7 39, M Palpitation 019 N SVT8 54, F Palpitation 0-21 N SVT9 40, F Palpitation 0-20 N SVT10 47, M Palpitation 0-12 N SVT11 63, M Palpitation 0 11 N SVT, AF12 15, F Palpitation 0-16 N SVT

N, normal; SVT, supraventricular tachycardia; AF, atrialfibrillation.

basilic vein and positioned in the coronary sinus.Electrograms from the intracardiac catheters wererecorded on a 16-channel Elema Mingografrecorder at a paper speed of 100 mm/s togetherwith surface electrocardiographic leads I, aVF, VI,and V6. Intracardiac signals were filtered between

50 and 700 Hz. Stimulation was performed using aDevices 4270 isolated stimulator with pulse widthsof 1-5 to 2 ms at a voltage approximately twice thediastolic threshold.

In all patients anterograde and retrogradeconduction studies were performed using the extra-stimulus technique (Durrer et al., 1967). Retrogradeconduction was studied during right ventricularapical pacing. The ventriculoatrial conduction timeswere measured from the onset of ventricularactivation to the earliest clearly distinguishableatrial electrogram in the right atrium (V-RA) andcoronary sinus (V-LA). The earliest point of atrialactivation during sustained tachycardia was takenas indicating the approximate location of theaccessory pathway. This point was determined bycoronary sinus withdrawal mapping. The atrialactivation sequence during tachycardia was con-sidered to represent atrial depolarisation by exclusiveconduction in the accessory pathway (Fig. 1).Rapid atrial pacing at right and left atrial sites

was performed in all patients. In 7 patients atrialfibrillation was induced electively. Anterograde

Exclusive V- A conduction via accessory pathway

HRAE -, ,1. _ J. _ A

PCSE --_ ____-

DCSE --r~Si 505 SI 2d0 2 A'

HBE ->-- - W ; i

RVAE

AVF

vi/

V6 -f i

Ventricular premcature beat

360 A'

A'

Al = 'Al-_ [,

Tachycardia

Fig. 1 Comparison of atrial activation sequence after a ventricular premature beat (leftpanel) and during tachycardia (right panel) in case 3 (group 3). A ventricular prematurestimulus (S2) at 260 ms coupling interval after a regular paced sequence (S1-S1) results inretrograde atrial activation (A') identical to that seen during re-entrant tachycardia.HRAE, high right atrial electrogram; PSCE, proximal coronary sinus electrogram;DCSE, distal coronary sinus electrogram; HBE, His bundle electrogram; RVAE, rightventricular apex electrogram (not recorded during ventricular pacing).I, AVF, Vl, V6 = surface electrocardiographic leads.

193



j.com/

Br H


ownloaded from


D. E. Ward, A. J7. Camm, and R. A. J. Spurrell

conduction in the accessory pathway was excludedby the lack of pre-excitation in response to atrialstimulation near the accessory pathway (Boineauet al., 1973; Denes et al., 1977) and in 7 patients bythe absence of pre-excitation during atrial fibrilla-tion. Retrograde conduction curves were obtainedby plotting the values of V-LA and V-RA and thecorresponding intervals between successive atrialelectrograms in response to the premature stimulusV2 against the coupling interval V1-V2 of the extra-stimulus.

Results

The results are summarised in Table 2.In all 12 patients re-entrant atrioventricular

tachycardia was initiated by a single atrial prematurestimulus. In 5 patients a right ventricular apicalstimulus was also effective in initiating tachycardia.Earliest atrial activation during tachycardia was inthe coronary sinus recording in all 12 patients:proximal coronary sinus in 7 patients and distalcoronary sinus in 5 patients. The low right atrialelectrogram could be clearly seen during tachycardiain all 12 patients and followed the earliest atrialelectrogram in the coronary sinus region.

Retrograde atrial activation patterns during rightventricular pacing and programmed extrastimula-tion were of 4 different types (Table 2).

GROUP 1In this group of 2 patients, the ventriculoatrialintervals remained constant at all coupling intervals(V1-V2) of ventricular extrastimuli (V2). In 1patient there was a small but equal increase in theV-LA and V-RA conduction times at very shortcoupling intervals. The relation between the rightand left atrial electrograms did not change. Inboth patients tachycardia was initiated by a

Table 2

Mode of Pattern ofCase Site of AP initiation of atrial activation Group.no. tachycardia (VPBs)

1 Distal CS APB F -AVN 42 Distal CS APB, VPB F --AP 33 Proximal CS APB F --AP 34 Proximal CS APB AP-÷AVN 25 Distal CS APB F -+AVN 46 Proximal CS APB AP-+AVN 27 Proximal CS APB, VPB AP-* 18 Proximal CS APB, VPB F --AP 39 Distal CS APB F -+AVN 4

10 Proximal CS APB F --AVN 411 Proximal CS APB, VPB AP-- 112 Distal CS APB F -AP 3

AP, accessory pathway; CS, coronary sinus; AVN, AV nodal;F, fusion; APB, programmed atrial premature beat;VPB, prugrammed ventricular premature beat.

600Al -A2

400(ms)

200

0400

V2-A

200

600Al-A2

400-(ms)

200-

ER GPILRA .PCS o

TZ

0Re(eI e

600Al-A2

400-(ms)

200'

200 460 600 0V1-V2 (ms) 400

V2-A.. ...---- 200-0000000 0 0 0 0 0

0LV GPIII

TZ .

... 00

0oHRA o

DCS o

200 400 600400 Vl - V2 (ims)V2-A200- ~000Oo 000 066

6006 Al-A2

400-(ms)

200-

0

400-

V2-A-200 -

ES GPIII 0

o~

06

asHRA .PCS °

260 400 600O.Vl-V2(ms)

°06 5

000 00 00 0 0

JR GPIV

00

.0

6

HRA @DCS o

200 400 60CV1- V2 (ims)

ooo6ee *QQQ

Fig. 2 Retrograde conduction curves from patientsrepresenting each of the 4 groups. For discussion see text.LRA, low right atrial electrogram; HRA, high rightatrial electrogram; PCS, proximal coronary sinuselectrogram; DCS, distal coronary sinus electrogram;TZ, tachycardia zone.

programmed atrial or ventricular premature beat.The atrial activation sequence during tachycardiawas identical to that observed during programmedventricular extrastimulation. The retrograde con-duction curve from one of these patients is shownin Fig. 2a.

GROUP 2In 2 patients, the V-LA and V-RA conductionintervals remained more or less constant at longcoupling intervals of V2. At shorter couplingintervals there was a sudden increase in the V-LAand V-RA intervals. At all values of V1-V2 shorterthan that which resulted in the sudden increase inthe ventriculoatrial intervals, there was a progressivesmooth increase in the ventriculoatrial conductiontimes without a further change in the relation ofthe atrial electrograms (Fig. 2b). In this group,

194



j.com/

Br H


ownloaded from



tachycardia could not be initiated by a ventricularpremature stimulus but was reliably initiated by asingle atrial premature stimulus. In 1 of thesepatients the atrial activation sequence duringtachycardia was identical to that observed withpremature beats in the range of coupling intervalswhich resulted in constant ventriculoatrial intervals.In the other patient (case 4), the recordings weredifficult to interpret partly because the low rightatrial electrogram was not clearly seen. Theserecordings are shown in Fig. 3 and the resultspresented graphically in Fig. 4.

GROUP 3In 4 patients various degrees of atrial fusion (V-LAand V-RA not changing concordantly) were seenin response to longer coupling intervals of V2. Asthe coupling interval of V2 was reduced, the V-RA

HRE -, if;_ , * . , _ ,.--~~~ ~~~~~~

PCSE l rr-

DCSErHBE-'!\,9A t , ; '~~~~~t,,

S1 610 81 430 82

HRA1-HRA2430 V2-HRA185PCS1-PCS2 -430 V2-PCS- 145

AVF --v/

V6 ~/2 ~~,__

HRAE - - ~-r ^

PCSE A- A-

DCSE - ---Sr -_________i

HBE !ii' 610 81' 2602

HRAl-HRA2-420 V2-HRA=345PCSI-PCS2 -420 V2-PCS-305

AVF

Vi

V6

interval increased gradually but the V-LA intervalremained constant. Further decreases in the V1-V2interval resulted in an attenuation of the increasein V-RA time which gradually plateaued, forminga curve parallel to the V-LA curve (Fig. 2c). TheV-LA interval remained constant throughout in 2patients, with a small increase in V-LA and V-RAintervals at very short coupling intervals in 1patient. In case 3 this basic pattern was modified(Fig. 5). At coupling intervals greater than 360 ms(Fig. 5 and 6) low right atrial activation wasprogressively delayed as V1-V2 was decreased. At360 ms, there was a sudden increase in the V-RAinterval which remained constant with couplingintervals, V1-V2 between 360 and 320 ms. TheV-LA interval remained unchanged. At V1-V2 of300 ms the V-RA interval shortened again andincreased as V2 become more premature. Coupling

§1 610 81 300 S2'

HRA1-HRA2=340 V2-HRAu225PCS1-PCS2 =300 V2-PCS-145

-, ,\ _

Fig. 3 Programmed ventricularpremature stimuli (S2) at couplingintervals (S1-S2) of 430 ms (upperleft), 300 ms (upper right), and 260 ms(lower left) in case 4. For discussionsee text.A', retrograde atrial electrogram;H, His potential.

,- ------ f

I>F I/ /I\,f/ --

195



j.com/

Br H


ownloaded from


D. E. Ward, A. J. Camm, and R. A. J. Spurrell

sudden increase produced a progressive concordant° increase in V-LA and V-RA intervals (Fig. 2d).

<E) Tachycardia could be initiated by atrial extra-stimuli but ventricular premature beats wereineffective. The atrial activation sequence duringtachycardia was different from that observed inresponse to a ventricular extrastimulus at anycoupling interval.

Discussion

200-

0

400

V2 -A:

200

200Vl -V2

000

(V2 -H )

0.

000

Fig. 4 Retrograde conduction curve

For clarity H1-H2 intervals are omittinterval is plotted on the lower part adiscussion see text.

intervals of V2 shorter than 260in any further increase in the V-R

In all 4 patients in this groupcardia could be initiated by a singbeat but a single ventriculareffective in only 3 patients. Tbsequence during tachycardia wa

observed at coupling intervals ofin parallel V-RA and V-LA cur

GROUP 4In the 4 patients in this groupalso observed at longer couplinAs V1-V2 was decreased the V-RH.increased while the V-LA interstant. At a shorter coupling intsudden increase in the V-LA iV1-V2 shorter than that whici

Four distinct patterns of retrograde conductionwere observed in this series of patients. Thesebasic patterns are determined by the relativecontribution to atrial activation over the normal andaccessory pathways.

(1) Patients in group 1 showed constancy of theventriculoatrial intervals at all coupling intervals of

400 600 V2 as a result of predominant conduction in the(ims) accessory pathway (Fig. 2a) (Narula, 1974; Wellens

and Durrer, 1974). The small but equal increasein V-RA and V-LA intervals in 1 patient wasattributed to intraventricular delay.

(2) Conduction over the accessory pathway pre-dominated at longer coupling intervals of V2 inpatients in group 2. When the V1-V2 interval was

reduced to within the retrograde effective refractoryo o o o o o period of the accessory pathway the sudden increase

in V-RA and V-LA intervals and altered atrialactivation sequence reflects continued conductionin the normal pathway (Fig. 2b).

(3) Conduction over both the normal andof case 4 (group 2). accessory pathways resulting in atrial fusion at

ef thegraph. For long coupling intervals of V2 was observed inpatients in group 3 (Fig. 2c). Conduction in theaccessory pathway results in a constant V-LAinterval throughout, while delayed conduction inthe normal pathway results in a gradual increase of

ms did not result the V-RA interval.LA interval (Fig. 5). While this delay exceeds the conduction timeI, re-entrant tachy- from the accessory pathway to the right atrium (at,le atrial premature the site of recording) the V-RA interval parallels theextrastimulus was V-LA interval. In 2 patients the beginning of theLe atrial activation V-RA 'plateau' is coincident with the upper limitIs identical to that of the tachycardia zone suggesting that block ratherV2 which resulted than delay in the normal pathway allowed capture

ves. of the right atrium as a result of spread of activationfrom the accessory pathway.

(4) Atrial fusion was observed at all couplingatrial fusion was intervals of V2 until block in the accessory pathway

Ig intervals of V2. in patients in group 4 (Fig. 2d and Fig. 7). The

v interval gradually gradual increase in the V-RA interval as V1-V2 was

val remained con- increased indicates atrial activation as a result of

terval, there was a conduction over the normal pathway. In contrast,interval. Values of the V-LA interval remains constant until block

h resulted in the occurs in the accessory pathway. Continued conduc-

600 -

A1-A2

(ms)400-

EG GPIII

HRA SPCs o

60.00

196



j.com/

Br H


ownloaded from



HRAE .

PCSEV'A'

DCSE IFX(jS

HBE -K.'. ' __WX VIA'

V'LLRA'.11, LRA'1-LRA'2. 460(RVAE) V2'PCS'.125, PCS'l-PCS'2- 430

AVF 7\ /VI

V6

HRAE

PCSE -----r--

DCSE - - o51, 505 Si 300 S2

HBE -Yr-W

(RVAE) V2-RA'-130 1'RA2 320 ___V2-PCS'- 125, PCS'1-PCS'2. 300

AVF a hI

vI~~~~~~~

I., VA'

Si 505 Si 360 S2VAI - A2--RA' j,RAlAR1- 43 __

Sl CS1151X! PS1 lPCi 23602 ^

I ~~~VA'

_AK,'Ah < Al

V2-LRA'- 190, LRA'1-LRA'2. 340V2-PCS'- 125, PCS'1-PCS'2- 260

I, ^ - ' j- --

'-/ 'N A

V6

Retrograde conduction intervals

Fig. 5 Programmed ventricular premature stimuli (SO) at coupling intervals of 430 ms (upper left),360 ms (upper right), 300 ms (lower left), and 260 ms (lower right) in case 3. For discussion see text.

tion in the normal pathway results in a sudden jumpin the V-LA interval associated with a change inatrial activation sequence (Tonkin et al., 1975).Exclusive accessory pathway conduction, therefore,never occurred in this group. Two patients, one

from each of group 2 and group 3 showed conduc-tion patterns which appeared to represent a

modification of the basic conduction pattern of thegroup. In case 4 the slight increase in the V-RAinterval between coupling intervals of V2 ofbetween 430 and 300 ms was attributed to intra-atrial delay. The absence of any severe changes inatrial activation sequence throughout the curve

(Fig. 3) is not unexpected because the accessorypathway was sited near the atrioventricular node in

this patient and conduction in either the normal oraccessory pathways may result in similar retrogradeactivation sequences (Gallagher et al., 1977).However, because the low right atrial electrogramwas not clear, the complete atrial activation sequenceis not known.

Case 3 had a variation of the basic pattern ofgroup 3 (Fig. 5 and 6). It is postulated that thesudden delay in the right atrial electrogram,sustained over a small range of coupling intervals,is a result of failure of ventriculoatrial conductionin the normal pathway, allowing capture of the rightatrium by continued conduction in the accessorypathway. This interpretation is supported by theobservation that the V-RA intervals in this zone

197



j.com/

Br H


ownloaded from



600.Al -A2

(mis)

400 -

200-

0

400

V2-A'

JC. GPIII

LRA .

PCS o G* .00

* @@.00

200 400V1- V2 (ms)

G

2000~occcMJ00Q 9000

Fig. 6 Retrograde conduction curve from case 3(group 3). For discussion see text. G, gap in retrogradeHis Purkinje/atrioventricular nodal conduction.

are similar to those seen at short coupling intervalsof V2 when accessory pathway conduction pre-dominates. In effect, there is a gap in ventriculo-atrial conduction in the normal pathway (Akhtaret al., 1974) but this gap is concealed by continuedconduction in the accessory pathway. A similar casehas been described by Wellens (1977).

Svenson et al. (1975) studied patterns ofventriculoatrial conduction in patients with overtWolff-Parkinson-White syndrome and found fusionpatterns only in patients with lateral bypass tracts.In the 5 patients in our series with accessory path-ways in the region of the distal coronary sinus,atrial fusion was demonstrated at long couplingintervals of V2, with exclusive accessory pathwayconduction at short coupling intervals in 2 patientsand exclusive atrioventricular nodal conduction atshort coupling intervals in 3 patients. In contrastto the observation of Svenson et al. (1975) we

showed atrial fusion patterns in 3 of the 7 patientswith proximally located bypass tracts, 2 of whomshowed exclusive bypass tract conduction only at

short coupling intervals of V2. Of the other 4patients with proximally located pathways, 2 dis-closed predominant accessory pathway conductionthroughout (group 1) and 2 had the pattern typicalof group 2.Of the 5 patients with short PR intervals, 4

patients had atrial fusion patterns at long couplingintervals of V2 and 1 patient showed exclusiveaccessory pathway conduction throughout. Retro-grade conduction in an atrionodal pathway mayresult in earliest atrial activation in the region ofthe proximal coronary sinus (Camm et al., 1978).In 2 patients this possibility was excluded by thefinding of earliest atrial activity in the distal coronarysinus electrogram. In the 3 other patients withproximally situated bypass tracts a ventricular pre-mature stimulus delivered at the time of the Hisbundle potential resulted in exact atrial capture.This observation excludes retrograde conduction inan atrionodal pathway (Ward et al., 1978) andconfirms ventriculoatrial conduction in a directventriculoatrial connection (Coumel and Attuel,1974; Zipes et al., 1974; Neuss et al., 1975; Sellerset al., 1976).

Tachycardia could not be initiated by a ventricu-lar premature beat in any patient in whom therewas evidence of normal pathway ventriculoatrialconduction at all coupling intervals of V2 (group 2and group 4). It is suggested that re-entry towardsthe ventricles over the atrioventricular node-Hispathway was prevented by continued retrogradeconduction in this pathway. Ventricular prematurebeats were effective in initiating tachycardia in 2 ofthe 4 patients who showed exclusive accessorypathway conduction only at short coupling intervals(group 3). In these patients, the upper limit of the

a Intra-atrial conduction timesq N a \ b AV nodal conduction time anda ,->-8 _0 retractoriness

bcTX~\t- c Accessory pathway refractoriness>\Ac \ and conduction time

4lk ) d Intraventriculcr conduction times

\

Fig. 7 Determinants of retrograde conduction patternsduring right ventricular extrastimulation in patients withaccessory bypass tracts. The pattern of atrial activation isdetermined by the relative conduction times from thesite of stimulation to the site of recording in both thenormal and abnormal pathways and the state ofrefractoriness in these pathways.

198



j.com/

Br H


ownloaded from


Atrial activation in concealed WPW 1

tachycardia zone coincided with the upper limit ofthe V-RA interval plateau. The inability ofventricular premature beats to initiate tachycardiain the other 2 patients in group 3 may be related toconcealed retrograde invasion of the normal path-way at short coupling intervals (Wellens, 1977).These observations are similar to those made bySung et al. (1977a) in patients with overt type AWolff-Parkinson-White syndrome.

In the absence of accessory ventriculoatrialconnections, atrial activation during ventricularpacing begins close to the atrioventricular node andspreads to more distant points (Amat-y-Leon et al.,1976; Gallagher et al., 1977). The relative timing ofatrial activation at different sites is determined byintra-atrial conduction times to the sites of record-ing. When two or more ventriculoatrial pathwaysare present the atrial activation patterns dependson the relative contribution to atrial depolarisationby each conduction pathway. The presence of twoor more concealed ventriculoatrial accessory path-ways may make interpretation difficult especially ifthese pathways have similar characteristics andlocation. Several determinants may interact toproduce any given activation pattern (Fig. 7).Though we have seen 4 basic patterns of ventriculo-atrial conduction in patients with concealedaccessory pathways, other varieties may occur. Forexample, atrial fusion at all coupling intervals of V2was reported by Sung et al. (1977a) in 3 of 29patients with type A Wolff-Parkinson-White syn-drome. The presence of intra-atrial or intra-ventricular delay or gaps in ventriculoatrialconduction in the normal pathway (Akhtar et al.,1974) or accessory pathway may result in variationsof basic patterns. In addition, the basic pattern maybe modified by changes in the ventricular drivingrate.

Retrograde atrial activation patterns may beimportant in the diagnosis and location of concealedaccessory pathways especially in those patients inwhom it may not be possible to initiate tachycardiaat electrophysiological study. It is clear thatconstancy of the ventriculoatrial interval is, by itself,an inadequate criterion for the diagnosis of concealedventriculoatrial pathways. If the V-RA interval isconsidered, a progressive increase was shown in 8patients (group 3 and group 4) and a suddenincrease in 2 patients one of whom had intra-atrial delay. In the absence of left atrial recordingsthese V-RA patterns may have been reasonablyattributed to conduction in the normal pathwayalone. For this reason, it is important that atrialactivity should be recorded from sites closelyadjacent to both normal and accessory pathways.

Recently it has been re-emphasised that concealed

accessory pathways may in fact be the anatomicalsubstrate for tachycardias previously diagnosed asdepending on intranodal re-entry (Barold andCoumel, 1977; Sung et al., 1977b; Pritchett et al.,1978). The distinction between these mechanismsis clearly of therapeutic importance particularly ifsurgical intervention is considered.

References

Akhtar, M., Damato, A. N., Caracta, A. R., Batsford, W. P.,and Lau, S. H. (1974). The gap phenomenon duringretrograde conduction in man. Circulation, 49, 811-817.

Amat-y-Leon, F., Dhingra, R. C., Wu, D., Denes, P.,Wyndham, C., and Rosen, K. M. (1976). Catheter mappingof retrograde atrial activation. Observations during ventri-cular pacing and A-V nodal re-entrant paroxysmaltachycardia. British Heart Journal, 38, 355-362.

Barold, S. S., and Coumel, P. (1977). Mechanisms of atrio-ventricular junctional tachycardia. Role of re-entry andconcealed accessory pathways. American J'ournal ofCardiology, 39, 97-105.

Boineau, J. R., Moore, E. N., Spear, J. F., and Sealy, W. C.(1973). Basis of static and dynamic electrocardiographicvariations in Wolff-Parkinson-White syndrome. AmericanJrournal of Cardiology, 32, 32-45.

Camm, A. J., Ward, D. E., and Spurrell, R. A. J. (1978).Gaps in anterograde conduction in patients with the shortPR interval, normal QRS complex syndrome. British HeartJ7ournal, 40, 1119-1126.

Coumel, P., and Attuel, P. (1974). Reciprocating tachycardiain overt and latent pre-excitation. Influence of functionalbundle branch block on the rate of the tachycardia.European Journal of Cardiology, 1, 423-436.

Denes, P., Wyndham, C. R., Amat-y-Leon, F., Wu, D.,Dhingra, R. C., Miller, R. H., and Rosen, K. M. (1977).Atrial pacing at mutliple sites in the Wolff-Parkinson-Whitesyndrome. British Heart Journal, 39, 506-514.

Durrer, D., Schoo, L., Schuilenburg, R. M., and Wellens,H. J. J. (1967). The role of premature beats in the initiationand termination of supraventricular tachycardias in theWPW syndrome. Circulation, 36, 644-662.

Gallagher, J. J., Pritchett, E. L. C., Benditt, D. G., Tonkin,A., Campbell, R. W. F., Dugan, F., Bashore, T., Tower, A.,and Wallace, A. G. (1977). New catheter techniques foranalysis of sequence of retrograde atrial activation in man.European Journal of Cardiology, 6, 1-14.

Narula, 0. (1974). Retrograde pre-excitation. Comparison ofantegrade and retrograde conduction intervals in man.Circulation, 50, 1129-1143.

Neuss, H., Schlepper, M., and Thormann, J. (1975). Analysisof re-entry mechanisms in 3 patients with concealed Wolff-Parkinson-White syndrome. Circulation, 51, ,X5-81.

Pritchett, E. L. C., Gallagher, J. J., and Wallace, A. G. (1978).Re-entry within the atrioventricular node in man-a re-assessment. European Journal of Cardiology, 6, 437-447.

Rowland, E., Curry, P. V. L., Callowhill, E., and Krikler,D. M. (1977). Recognition and implications of concealedpre-excitation (abstract). British Heart Journal, 39, 932-933.

Sellers, T. D., jun, Gallagher, J. J., Cope, G. D., Tonkin, A.,and Wallace, A. (1976). Retrograde atrial pre-excitationfollowing premature ventricular beats during reciprocatingtachycardia in the Wolff-Parkinson-White syndrome.European Journal of Cardiology, 4, 283-294.

Slama, R., Coumel, P. L., and Bouvrain, Y. (1973). Lessyndromes de WPW de type A inapparents ou latents en

199



j.com/

Br H


ownloaded from



rhythm sinusal. Archives des Maladies du Coeur et desVaisseaux, 66, 639-653.

Spurrell, R. A. J., Krikler, D., and Sowton, E. (1974).Concealed bypasses of the atrioventricular node in patientswith paroxysmal supraventricular tachycardia revealed byintracardiac electrical stimulation and verapamil. AmericanJournal of Cardiology, 33, 590-595.

Sung, R. J., Castellanos, A., Mallon, S. M., Gelband, H.,Mendoza, I., and Myerburg, R. J. (1977a). Mode ofinitiation of reciprocating tachycardia during programmedventricular stimulation in the Wolff-Parkinson-Whitesyndrome. American Journal of Cardiology, 40, 24-31.

Sung, R. J., Gelband, H., Castellanos, A., Aranda, J., andMyerburg, R. J. (1977b). Clinical and electrophysiologicalobservations in patients with concealed accessory atrio-ventricular bypass tracts. American Journal of Cardiology,40, 839-847.

Svenson, R. H., Miller, H. C., Gallagher, J. J., and Wallace,A. (1975). Electrophysiological evaluation of the Wolff-Parkinson-White syndrome. Circulation, 52, 552-562.

Tonkin, A. M., Gallagher, J. J., Svenson, R. H., Wallace, A.,and Sealy, W. C. (1975). Anterograde block in accessorypathways with retrograde conduction in reciprocating

tachycardia. European Journal of Cardiology, 3, 143-152.Ward, D. E., Camm, A. J., and Spurrell, R. A. J. (1978).

Re-entrant tachycardia utilising two bypass tracts andexcluding the A-V node in the short PR interval, normalQRS complex syndrome. British Heart Journal, 40, 1127-1133.

Wellens, H. J. J. (1977). Modes of initiation of circus move-ment tachycardia in 139 patients with the Wolff-Parkinson-White syndrome studied by programmed electricalstimulation. In Re-entrant Arrhythmias, p. 153, ed H.Kulbertus. MTP Press, Lancaster.

Wellens, H. J. J., and Durrer, D. (1974). Patterns ofventriculo-atrial conduction in the Wolff-Parkinson-White syndrome.Circulation, 49, 22-31.

Zipes, D. P., DeJoseph, R. L., and Rothbaum, D. A. (1974).Unusual properties of accessory pathways. Circulation, 49,1200-1211.

Requests for reprints to Dr D E Ward, CardiacDepartment, St. Bartholomew's Hospital, LondonEClA 7BE.

200



j.com/

Br H


ownloaded from


patterns of atrial activation during pacing with kent · retrograde atrial activation patterns...

Documents