cardiac arrhythmias (part 4) - circulationcirc.ahajournals.org/content/47/4/872.full.pdfsymposium...

SYMPOSIUM

Cardiac Arrhythmias(Part 4)

Wolff-Parkinson-White Syndrome

A Review

By ONKAR S. NARULA, M.D.

SUMMARYRecent developments in the field of electrophysiology and surgical therapy in selected cases of

Wolff-Parkinson-White syndrome (W-P-W) su port the concept of anomalous A-V pathways.Impulse transmission usually occurs simultaneously through both the normal and anomalous path-ways resulting in a fusion QRS complex. Atrial tachycardia is usually due to reentry through thenormal and anomalous A-V pathways. However, reentry may occur independently in the A-Vnode alone exclusive of the anomalous pathway. Anomalous connections, despite varyinganatomic locations, may result in similar electro 2ardiographic manifestations characteristic of W-P-W. His bundle recordings together with electrophysiologic studies may be clinically useful(1) to differentiate various types of anomalous connections, (2) for possible determination of thereentry circuit, (3) to predict the maximum ventricular rate possible during supraventriculartachycardia by evaluating the refractory period of the A-V pathways, or (4) to compare theefficacy of different drugs in a given patient. Surgical interruption of the anomalous pathwayin selected cases with W-P-W (type B) is feasible but is most commonly not necessary. The in-dications for medical and surgical management of symptomatic cases with W-P-W are reviewed.

Additional Indexing Words:A-V pathways Atrial tachycardia

RECENT developments in the field of electro-physiology and the success with a surgical

approach in a few selected cases have regeneratedinterest in the subject of Wolff-Parkinson-White(W-P-W) syndrome. It is an electrocardiographicphenomenon in which an impulse originating in theatrium activates a portion or the whole of theventricular muscle prematurely in an anomalousfashion compared to transmission via the normalatrioventricular (A-V) conduction system. Wilsoninitially described the ECG findings which were

subsequently considered typical of W-P-W pattern.'These were first labeled as a distinctive clinical

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Supraventricular tachycardia

entity seen in healthy young adults and associatedwith paroxysmal attacks of tachycardia by W-P-W.2The electrocardiographic pattern of W-P-W may bepresent with or without the attacks of tachycardia,and only when associated with the latter is it calledthe W-P-W syndrome. Although difficult to evalu-ate, the reported incidence of the W-P-W patternranges from 0.1 to 3.1 per 1000 population.3 Most ofthe patients are relatively asymptomatic; diagnosisis usually made after a routine electrocardiogram.Forty to 80% of the cases with W-P-W patternexperience paroxysms of tachycardia which are

usually short and inconsequential.3 However, insome patients frequent and prolonged episodes oftachycardia may be completely disabling or lifethreatening, and sudden death may occur.4, 5 It isthe occurrence of the latter that changes this

Circulation, Volume XLVII, April 1973

From the Division of Cardiology, Department ofMedicine, Mount Sinai Medical Center, Miami Beach,Florida, and the University of Miami School of Medicine,Coral Cables, Florida.

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W-P-W SYNDROME

syndrome from an electrophysiologic curiosity toone of potential hazard.

Electrocardiogram and ClassificationThe three characteristic electrocardiographic fea-

tures are: (1) a delta wave; (2) a shortened P-Rinterval; and (3) a widened QRS complex.The delta wave is a thick and slurred deflection

deforming the initial portion of the QRS complexand usually ranges between 0.03 and 0.06 sec induration and rarely exceeds 5 mm in amplitude. Itis usually upright when associated with a dominant-ly upright QRS complex, and vice versa. There is awide spectrum to the spatial orientation of the deltavector, i.e. in the frontal plane from +1200 to -75°.In a majority of the cases it is directed to the lefteither superiorly or inferiorly.3 Depending on thedirection of the delta-wave vector, the Q wave ofthe QRS complex may be obliterated or enhanced.In the latter event the fallaciously wide and deep Qwave may mimic myocardial infarction.The P-R interval is abbreviated due to the delta

wave and the widening of the QRS complex. The P-R interval during W-P-W pattern is _ 0.12 sec(usually= 0.10 sec, range 0.04-0.20). It is shorterthan that observed in the absence of the W-P-Wpattern and, accordingly, it need not always beshort (. 0.12 sec) and may even be prolonged tomore than 0.20 sec. It is the presence of a deltawave and the demonstration of a comparativelylonger P-R interval in the absence of the W-P-Wpattern which are of diagnostic significance. The P-J interval, defined as the interval between thebeginning of the P wave and junction of the QRScomplex with the S-T segment, remains constantduring normal and W-P-W patterns.The QRS complex in W-P-W beats is widened

due to the addition of the delta wave to its initialportion. The remaining segment of the QRScomplex may or may not show any change. Theremay be a concomitant shift in axis, usually to theleft. The QRS duration is usually 0.10-0.12 sec, butmay range up to 0.20 sec. The changes in the shapeof the QRS complex are associated with secondaryS-T-segment and T-wave changes. The widenedbizarre QRS complexes in W-P-W beats mayresemble a bundle-branch block (BBB) pattern.The ECG may simulate left bundle-branch block intype B and right bundle-branch block, rightventricular hypertrophy, or true posterior wallinfarction in cases with type A W-P-W syndrome.However, occasionally a true BBB may occur inconjunction with W-P-W.Circulation, Volume XLVII, April 1973

The W-P-W syndrome has been divided into twotypes (A and B) on the basis of the direction of thedominant QRS deflection in lead Vi.6 In type A thedelta wave and the remainder of the QRS complexare primarily upright in lead V, which shows R, RS,Rs, RSr', and Rsr' patterns. A negative delta wave isseen in lead I. In type B the delta wave and the QRScomplex are usually negative in lead V,, whichshows QS or rS patterns. Lead I shows a positivedelta wave.

In addition, there are cases with intermediateforms which cannot be clearly classified in either ofthe above two types. Recently, a third group, AB,has been suggested for the cases with intermediateforms.7

Anatomic ConsiderationsConsiderable controversy has centered around

the anatomic basis of the W-P-W syndrome. One ofthe postulates is that, besides the normal A-Vconduction system, there are several other lateralconnections (bundles of Kent) around the A-Vrings which bridge the gap between the atria andventricles (fig. 1).8 Anatomic studies have demon-strated bundles of Kent in some and not other caseswith known W-P-W syndrome.5 9-11 In four caseswith type B W-P-W (discussed below), efforts toablate bundles of Kent by a through-and-throughsurgical incision along the right lateral border havebeen successful in abolishing anomalous ventricularexcitation. It would thus appear, as also pointed outby Lev, that bundles of Kent are in some wayrelated to the W-P-W syndrome but are notindispensable for its production. There may also be

K

-- ....*-'**--w-e...KI " '

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Figure 1Diagrammatic representation of the various possible anom-alous A-V pathways in W-P-W syndrome. K = Kent fibers;J = James fibers; M = Mahaim fibers; AVN = A-V node;BH = bundle of His.

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other bypasses, i.e. James fibers and Mahaimfibers.10-1The existence in normal hearts of "bypass" tracts,

which enter the inferior margin of the A-V node,has been demonstrated by James (fig. 1) .12 Thesetracts are an obvious route by which an impulse cancircumvent the A-V node and may explain thesyndrome of a short P-R interval with a normalQRS complex. Mahaim and his associates havedemonstrated that short but direct connecting fibersare frequently present between the His bundle orthe proximal portion of the bundle branches andthe ventricular septum. Occasionally these Mahaimfibers may be present between the A-V node andthe ventricular septum.'0-13

Electrophysiologic ConsiderationsIn addition to the standard ECC, His bundle

electrogram, atrial stimulation, and His bundle

NSR

BE . ,,(BH)

A-A 850 msecA-H 60 msec

A L-1A1aVF

v1v

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stimulation are of use in further defining theelectrophysiologic behavior of anomalous andnormal A-V pathways in a given patient.

His Bundle RecordingsHis bundle (BH) recordings enable the division

of the P-R interval into three component conduc-tion intervals, i.e. intraatrial (P-A), A-V nodal (A-H), and His-Purkinje system (H-V or H-Q). Thenormal range for these intervals is P-A= 25-45 msec,A-H =50-120 msec, H-V = 35-45 msec, and variesslightly with different laboratories. In cases with W-P-W, BH recordings can be used to analyzewhether the P-R interval is shortened due to anabbreviated A-H and/or H-V interval. Severalreports, in addition to our findings, indicate that theBH electrogram may be recorded at a short intervalpreceding (H-V = 10-30 msec) or simultaneous withthe onset of the QRS complex (H-V =0 msec) orwithin the QRS complex (fig. 2). The reason

A v_

BH

1

A V C

A-A 600 msecA-H 80 msecPl-R 135 msec

/0-I1ill

A Pacing A !r

BH~h H

Ii~~~~~~~~~~~~~i

A-A 540 msecl A AAA046 msec .A-A mc

PI-R 135 msecP

Gar., M. #96613 9/17/71 Oh

Figure 2His bundle (BH) recordings in a case with W-P-W (type A) during normal sinus rhythm (NSR) show thatthe BH deflection just precedes the onset of the QRS complex (A, first two beats). Atrial (A) pacing atprogressively increasing rates shows lengthening of A-H irterval from 60 to 105 msec. (B). The BH deflectionmoves into the QRS complex which consequently becomes more aberrant because of increasing or exclusiveconduction through the anomalous pathway. Pacing impulse (PI) to QRS interval (PI-R) remains constantthroughout but PI-J interval lengthens. On this and subsequent figures time lines = 1 sec.

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for this variability in the relationship between theBH deflection and the onset of the QRS complexlies in the fact that each atrial impulse ispropagated concurrently through both the path-ways, i.e. the anomalous and the normal A-Vpathway (A-V node and His-Purkinje system). Therelative conduction time through the two pathwaysgoverns the relationship between the BH electro-gram and the onset of the QRS or V complex.Dependent on a shorter or longer conduction timethrough the normal A-V pathway as compared tothat of the anamolous pathway, the BH electrogrammay be recorded preceding the onset of the QRScomplex or within the QRS complex, respectively.The various possible patterns of BH recordings that

may be seen with different types of the anomalousconnections are illustrated in figure 3 and table 1.

Atrial Stimulation

In most of the cases with W-P-W, the QRScomplex widens with premature atrial beats(PABs). A progressive increase in prematurity ofthe PABs usually results in a progressive increase inaberration and duration of the QRS complex but aconstant P-R interval. Due to the normal physiolog-ic properties of the A-V node, an increase inprematurity of the PABs results in prolongation ofthe conduction time through the normal A-Vpathway (A-V node) and an increasing delay inBH depolarization. However, initial ventriculardepolarization through the anomalous pathway is

A NormalNSR

BH

AHmHV

L-2-Ag

AP

BHHV

pi

1-2-

D Mahaim Tract ConductionNSR 1

AP

B Bundle of Kent ConductionNSR A

C James Tract ConductionNSR A

APBH

L-2

E James and Kent FibresNSR

BHAHL

1-2

AP

F James and Mahaim FibresNSR A

APBH

L-2-ON 1257

Figure 3

Pattern of BH recordings in various types of anomalous connections during NSR and atrial pacing (AP).(A) In a normal case the A-H lengthens but H-V remains constant on AP. (B) During NSR the BH eitherslightly precedes or occurs simultaneous with or within the QRS. On AP the BH moves into the QRS dueto a lengthening of A-H time (a normal response); QRS complex becomes more aberrant. (C) The A-H isvery short during NSR and lengthens slightly on AP. The normal QRS complex and the H-V interval areunchanged with AP. (D) The H-V time is short. The A-H is normal and lengthens with AP. The shape ofthe QRS and the H-V time are unchanged with AP. (E) The QRS complex may be normal during NSR. OnAP a delta wave may be seen and the A-H lengthens slightly with resultant movement of the BH toward orwithin the QRS. (F) This is similar to C except for the presence of the delta wave.


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Table 1

Patterns of BH Recordinigs during NSR and AP in Cases with W-P-WV due to Various AnomalousConnections

Normal A-V Anomalous Connectionspathway Kent James Mahaim James, Kent James, Mahaim

/ QRS Normal A Normal A Normal or A AP-R Normal Short Short Short or Short Short

NSR normalA-H Normal Normal Short Normal Short Short

/ H-V Normal Short or Usually Short Normal, short, Shortminu.s normal or minus

| QRS Constant Usually Constant Constant Usually widens ConstantI widensP-R Prolonigs Constant Slightly Prolongs Slightly prolongs Slightly

AP prolongs oIr cuonstant prolongsA-H Prolongs Prolongs Slightly Prolongs Slightly prolongs Slightly

Constant ~{inus prolongs prolongsH-V Constant Minus Constant Constant Short or minus Constant

BH QRS Normal Normal Normal A Normal Apacing PI-R, H-V = H-V* -H-V = H-V = H-V* H-V

Abbreviations: NSR = normal sinus rhythm; AP = atrial pacing; BH = His bundle; A - delta wave;minus = BH follows the onset of the QRS complex; PI-R = pacing impulse to the QRS interval.*H-V in non-W-P-W beats.

not delayed because of its constant conduction timewhich in contrast to the A-V nodal conduction timeis independent of prematurity or number ofimpulses. Therefore, the BH deflection shiftstoward and finally appears within or after the QRScomplex. Consequent to the delayed impulse arrivalat the BH and bundle branches, a proportionatelydecreasing amount of ventricular muscle is excitedthrough the normal A-V pathway and increasingamounts through the anomalous pathway andresults in a more aberrant QRS complex (fig. 4A,B).

Finally, with a further increase in prematurity ofthe PABs, the refractory period (RP) of theanomalous pathway is reached, and the inducedimpulse is either conducted through the normal A-Vpathway with a longer P-R interval and a normal or

an aberrant QRS complex (different from that seen

during W-P-W beats), or completely blockedbecause both the normal and the anomalouspathways are refractory (fig. 4C). This electrophys-iologic parameter provides a clinically usefulmeans to assess the refractory period of theanomalous and normal A-V pathways and thus en-

ables prediction of the maximum ventricular rate

possible during supraventricular tachyeardias. TheRP of the anomalous pathway as evaluated by thePABs in our series (eight cases) ranged from 295to 600 msec, and in another (six cases) studyranged from 300 to 250 msec.'8

In a recent study (cases with W-P-W type A), itwas postulated that the spatial dimensions of thecircus movement are rather small and that theanomalous A-V connection in patients with type Ais situated not far from the A-V junction. This wasbased on the observation that only left atrial andneither right atrial nor ventricular premature beatscould influence the time relations of the tachyear-dia.19 However, in a W-P-W type A case studied byus, properly timed right atrial stimulation (fig. 5A)could initiate tachycardia and also shorten one cycleof the tachycardia with a shift of the followingcycles to an earlier time (fig. 5B). Our observationsindicate that the above statement by Wellens et al.may not be applicable to all the type A cases.

In all but one of the reported studies it has beenobserved that with a progressive increase in atrialrate by atrial pacing (AP), the QRS complexprogressively becomes wider and more aberrant.The P-J interval lengthens but the P-R intervalremains constant (fig. 2 ).14, 17, 20 During slow atrialrates the impulse is usually transmitted simultane-ously through both the normal and anomalouspathways. However, at high atrial rates increasingA-V nodal conduction delays, through the normalA-V pathway as opposed to a constant conductiontime through the anomalous pathway, permitimpulse transmission exclusively through the latterresulting in a widened QRS complex.


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W-P-W SYNDROME

BE(BH)

AB-1E

(BBHE)

L-1B aVF

V,

BE -(BH)

~~~~~H.

CL-1OVF

Imm., I., #83366 4/22/70

;BH A

-18N h,}

A-A 1045 msec 505A-H 60 msoc

K- - -.l

Figure 4His bundle recordings in a case with W-P-W (type B) show the effect of increase in prematurity of induced(PI) PABs. Initially the QRS complex becomes more aberrant (A and B) with a constant PI-R interval. Afurther increase in prematurity (A-A = 465 nsec) shows abolition of W-P-W pattern, a lengthening of PI-Rinterval, and a conduction with a right bundle-branch block (RBBB) pattern with a normal H-V time (45msec) (C). This indicates the refractory period of the anomalous pathway.

Similar to the response seen with PABs, a furtherincrease in AP rate may result in narrow QRScomplexes (or aberrant with a different shape)because the anomalous pathway usually becomesrefractory earlier than the A-V node. With thenarrowing of the QRS complex the P-R intervalbecomes longer as the rapid impulses are nowexclusively transmitted through the normal A-Vpathway. Of course at higher rates even the normalA-V pathway may become refractory and result incomplete block of some of the impulses. As withPABs, AP may: (1) initiate or terminate SVT; and(2) be clinically useful in determination of the RPof the anomalous pathway.

His Bundle StimulationThe catheter technic described previously has

been used for BH stimulation in our cases of W-P-W.21 This resulted in normalization of the QRSCirculation, Volume XLVII, April 1973

complex in all (eight cases) with pacing impulse tothe QRS (PI-R) interval similar to the H-V timerecorded in the absence of W-P-W and longer thanthe pseudoshort H-V time during W-P-W pattern,One of our cases with W-P-W type B andunderlying right bundle-branch block (RBBB) is ofinterest. The QRS complex, which was almostnormal (right-sided preexcitation abolishing theRBBB) during NSR despite anomalous conduction,exhibited RBBB during BH stimulation with thedisappearance of W-P-W pattern (figs. 4C and 6).These observations suggest that in our cases: (1)the anomalous pathway was not located within orin the vicinity of the BH as proposed by others;22(2) the W-P-W pattern was not due to longitudinaldissociation within the BH as suggested by James23;and (3) the W-P-W pattern was not due to Mahaimfibers.

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A

B

C 450 45 415 30 3(i

Gar., M. #96613 9/17/71

Figure 5

Significance of properly timed atrial stimulation in the initiation and termination of reentrant atrial tachy-cardia. (A) A premature atrial beat at a coupling interval (A-A) of 340 mmec results in reentrant atrialtachycardia mimicking ventricular tachycardia. BE (RA) =bipolar electrogram recorded from high rightatrium. (B and C) AP at a cycle length of 300 mee was successful in terminating the tachycardia onlywhen the last atrial paced beat was completely blocked in antegrade fashion (C) thus breaking the reentrantcircuit, but failed when the last paced impulse was conducted to the ventricles permitting retrograde con-duction and perpetuation of reentry circuit as in (B).

ON 1240 8

Genesis of W-P-W Syndrome(Nature of the Anomalous Complex)Various hypotheses have been proposed to

explain the genesis of the W-P-W beats.(1) The typical QRS complex of the W-P-W

syndrome has been generally regarded as a fusioncomplex.24 The sinus or atrial impulse is conducted

down both the normal and anomalous pathways tothe ventricles. The impulse is transmitted fasterthrough the anomalous pathway than through thenormal A-V pathway. This results in premature orpreexcitation of a portion of the ventricle and ashort P-R interval. The delta wave is due to thedepolarization of the ventricle around the insertion


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BE

Ai-i~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

A L-1

aVF r

V,

v v i ~ v.

A ~~ ~~~~45H-VA5SmictL, H~B

vlBH ..

-v -o -0

45 j

BE(RA)

BH Pacing

A

BaVF

V, K

(Cycle length =

Ai-545 msec)

A AA

Pil, A- 1- - 1

PI-R 45 msecP1-A 160 msec

N_~N4

' AA PI- A

---0.___vs________A_ _____ =- '----bwwQ. m -woW o e -e 101 -m h

45160

1'- 1'4580

_ .~K~Imm., 1., #83366 4/22/70

Figure 6

His bundle (BH) stimulation in a case with W-P-W (type B) and an underlying right bundle-branch block(RBBB). (The same case as in fig. 4). (A) During supraventricular tachycardia A-V conduction is seen

through both the pathways, i.e. anomalous (first two beats) and normal A-V pathway (last five beats). TheH-V time in the beats conducted through the normal A-V pathway = 45 msec. (B) His bundle (BH) stimula-tion resulted in QRS complexes similar to the non-W-P-W beats (A) with exclusive conduction through thenormal A-V pathway showing right bundle-branch block pattern. The PI-R (45 msec) is similar to the H-Vtime in the non-W-P-W beats (A).

of the anomalous pathway from which site furtherimpulse transmission occurs slowly through theordinary myocardium. The simultaneous slowerimpulse conduction through the normal A-Vpathway, after its exit from the A-V node, is rapidlytransmitted to the rgmainder of the ventriclesthrough the efficient network of the His-Purkinjesystem. The normal portion of the QRS complex isproduced by the latter mode of ventricularexcitation. The evidence supporting the above viewis provided by: (a) studies mapping the sequence

of epicardial excitation;4' 7 25 (b) cases with suc-

cessful surgical ablation of the anomalous pathwaywith normalization of the sequence of ventricularexcitation;7' 17,26 and (c) studies utilizing thecatheter technic for recording BH electrograms (inboth types A and B) have demonstrated a BHdeflection preceding, simultaneous with, or withinthe QRS complex (figs. 2 and 4) .14-17

Cifculation, Volume XLVII, April 1973

(2) In contrast to the overwhelming evidence infavor of the fusion mechanism in W-P-W beats, Lauand his co-workers have made a challengingstatement, "thus we conclude that W-P-W complex

is not a fusion beat as postulated by others," andproposed that the anomalous and normal compo-

nents of the W-P-W are due to complete bypass ofthe A-V node or exclusive Kent conduction.20 Intheir patients the P-R, P-S (P-J) intervals, and theQRS complex remained relatively constant with an

increase in atrial rate by AP. The reasons for thisdiscrepancy in findings as compared to a large mass

of evidence to the contrary provided by severalrecent reports14-17 may be explained on thefollowing basis: (a) the cases studied by Lau et al.are a minority group in a wide spectrum of differentmechanisms of W-P-W; or (b) even during controlstates at slower rates, i.e. NSR, the impulse was

being exclusively conducted through the anomalouspathway with a maximum of aberration of the QRS

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V-T-- ------IT -- -11 If' 1 ,l,---I----- --- y----T

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complex as the conduction time through theanomalous pathways was much shorter than that ofthe normal A-V pathway. Hence, a further increasein rate by AP could not prolong the QRS complex.It is obvious that the views of Lau et al. cannot becategorically applied to the majority of patientswith W-P-W syndrome.

(3) Scherf and James hypothesized that all thefeatures of the W-P-W syndrome can be explainedby their postulation of a "synchronized sino-ventricular conduction system" and longitudinaldissociation within the His bundle.'3 Despite itsattractiveness at first glance, it is believed that theabove hypothesis is not valid for the followingreasons: (a) The epicardial mapping studies intype B W-P-W indicate that the area of the earliestventricular excitation is located at the A-V marginof the right lateral border well away from the A-Vnode, and subsequent to surgical interruption thesequence of epicardial excitation was reversed andnormalized.7 17 26 (b) In the majority of cases witha W-P-W a change in atrial stimulation site does notshow any alteration in the shape of the QRScomplex. Furthermore, with an increase in atrialrate, despite a constant stimulation site, the QRScomplexes usually become progressively more bi-zarre (widening of P-J interval with a fixed P-Rinterval) (fig. 2). The findings in a single patient(type B) in whom, with increasing prematurity ofthe PABs the W-P-W pattern disappeared initiallywith the appearance of right bundle-branch block(with a long P-R interval) and eventually completeblock distal to the His bundle deflection wasmanifested, cannot be explained by the Jameshypothesis (fig. 4). (c) If longitudinal dissociationwithin the BH plays a role, then the activity of earlywavefronts in the BH responsible for preexcitationshould be recordable. Several studies from differentlaboratories have not recorded such a deflection. Asingle BH deflection has been recorded slightlypreceding, simultaneous with, or after the onset ofthe delta wave.14-17 Furthermore, BH stimulation inall of our cases (type A and B) resulted in abolitionof W-P-W pattern; the PI-R was longer than thepseudoshort H-V time during W-P-W pattern. (d)His bundle stimulation in several hundred caseswithout W-P-W has not shown evidence of longi-tudinal dissociation within the BH in even one caseto date. (Narula OS: Unpublished data.) Findingsin another experimental study, using selective stim-ulation of a portion of the BH, are in agreementwith our observations in man.27

Mechanism of TachyeardiasSupraventricularOf the various supraventricular tachycardias,

atrial tachycardia is the most common. The possiblemechanisms are discussed below.

It is commonly believed that the paroxysmalatrial tachycardias in patients with W-P-W are dueto a reciprocal mechanism.4 , 14,15, 28 Elegantelectrophysiologic studies support this hypothesisboth by initiation and termination of the tachycar-dia by a properly timed isolated premature stimulus(fig. 5) 28 Further evidence in favor of thereciprocal mechanism is provided, despite a limitednumber of patients, by the successful surgicalresults characterized by disappearance of parox-ysms of tachycardia after the ablation of theanomalous pathway or the A-V junction.'7' 26. 29), 30The initiation of this type of reciprocal mechanismdepends on the properly timed premature atrialexcitation caused by either premature atrial beats orpremature ventricular beats with retrograde con-duction to the atrium. The circus movement may bemanifested in either of these two fashions: (a) In amajority of the cases the supraventricular impulsetravels in antegrade direction through the A-V nodeand His bundle to the ventricular myocardium andreturns to the atrium through the anomalouspathway. Depending upon the time of arrival ofthis retrogradely conducted impulse, it may excitethe atria and/or the A-V junction (A-V node andHis bundle) and once again be conducted to theventricles. In this manner a self-perpetuating circusmovement may be established. (b) Infrequently,antegrade impulse conduction occurs through theanomalous pathway and retrograde transmissionthrough the normal A-V pathway, i.e. His bundleand A-V node. Figure 5 is probably an example ofthis type although an alternative explanationproposing A-V-nodal reciprocation can be offered.During SVT, in the majority of cases, the impulsetransmission in antegrade direction occurs throughthe A-V node instead of the anomalous pathwaybecause the latter usually has a longer refractoryperiod as opposed to the former. Thus theanomalous pathway is usually refractory to the verypremature atrial beats capable of initiating circusmovement.A second possibility is the occurrence of an atrial

echo initiating a self-sustained reentry mechanismin the A-V junction, entirely independent andexclusive of the anomalous pathway and unrelatedto W-P-W. It is the belief of the present author thatthis may be a more frequent than hitherto


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considered mechanism of SVT in cases with W-P-Wfor the following reasons: (a) The cases withunsuccessful surgical attempts to produce A-V blockby incision in the region of the A-V junction butwith abolition of paroxysms of SVT and persistentW-P-W are suggestive evidence to indicate thatfibers (other than anomalous pathway) in andaround the A-V node are responsible for reentryand were excised.1 (b) Recent reports have alsosuggested that in isolated cases A-V nodal reentrywas the mechanism responsible for the SVTbecause atrial or ventricular premature beats werefollowed by a compensatory pause during tachy-cardias.'5 28 (C) In cases with W-P-W and SVTresistant to medical therapy, it is believed that, inmost of these, anomalous pathways (bundle ofKent) are responsible for the preexcitation or W-P-W pattern, but possibly independent reentrycircuits in and around the A-V node (probably withthe participation of bypass tracts other than theKent bundle) are responsible for SVT. This conceptmay be explained on the basis of anatomic studiesby James, showing the "bypass" tracts of the A-Vnode.12 The supraventricular impulse partiallybypasses the A-V node and enters its lower part.When properly timed this impulse establishes areentry circuit involving the upper portion of the A-V node independent and exclusive of the anomalouspathway. Each impulse during SVT is transmittedonly through a part of the A-V node, and thisexplains the inefficacy of drugs to decrease thenumber of conducted impulses. The proposedhypothesis may explain why all patients with W-P-W do not develop SVT and why all are not resistantto drug therapy because "bypass" tracts, althoughpresent even in normal hearts, are not alwaysfunctional.

It is suggested that the latter view may beevaluated as follows. In cases with W-P-W and SVTthe number of impulses that can be conductedantegradely throurh the anomalous pathway onlyshould be determined by AP. If the number of theseconducted impulses is less than the heart rate seenduring spontaneous SVT, then the reentry circuitduring SVT in all probability was not completedthrough the anomalous pathway. Secondly, A-Vnodal reentry is more likely to be the mechanismwhen a properly timed premature stimulus initiat-ing SVT is conducted with a marked prolongationof the A-H interval or A-V nodal delay. A third lesslikely possible mechanism for atrial tachycardia isthat an atrial impulse arriving at the atrioventricu-lar nodal centers early in diastole may precipitateCirculation, Volume XLVII, April 1973

rapid firing at this area initiating a junctionaltachycardia.32

Ventricular TachycardiaA true ventricular tachycardia (VT) can occur in

patients with W-P-W. However, wide aberrant QRScomplexes with rapid ventricular rate may mimicthe ECG manifestations of ventricular tachycardia.This may result from a large number of impulsesconducted exclusively through the anomalous path-way, through the normal A-V pathway with rate-dependent aberration in the distal His-Purkinjesystem (HPS), and in patients with underlyingpermanent bundle-branch block. The increase inatrial rate may be due to atrial fibrillation, atrialflutter, or reentrant tachycardia. In the latter casethe circuit movement may be completed eitherthrough the A-V node alone, or via the anomalous-to-normal A-V pathway and back to the atrium (orvice versa). Documentation of cases mimicking VTwith antegrade conduction through the anomalouspathway and retrograde conduction through thenormal A-V pathways is rare.28 Figure 5 shows SVTwith exclusive antegrade conduction through theanomalous pathway simulating ventricular tachy-cardia.

ManagementThe ECG pattern of preexcitation without

tachycardia requires no treatment. The patientsshould be warned of the possibility of developingrapid heart rates. Excessive use of coffee or alcoholand strenuous physical exercise are known toprecipitate attacks of tachycardia and should beavoided. It is the occurrence of tachycardia thatmakes W-P-W syndrome clinically significant.Paroxysms of tachycardia, especially of prolongedduration, may be disabling and have been reportedto result in congestive heart failure, chest pain,hypotension, syncope, and even death.4 5,17 Hence,treatment is discussed from the viewpoint ofmanagement during a bout of tachycardia and theprevention of tachyeardias.

Management during TachycardiaAtrial tachycardia is the most common. Its

treatment is directed toward interruption of thecircus movement at either of these two levels, i.e.the normal A-V pathway or the anomalouspathway. This may be achieved by:Vagotonic maneuvers, e.g., changes in posture,

eyeball pressure, carotid sinus massage, or Valsalvamaneuver. The reentry tachyeardias are quite

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responsive to vagotonia and terminate promptly.This increases the physiologic block at the A-V nodeand thus interrupts the circus movement at thislevel.Vagotonic drugs, e.g., prostigmine and digitalis,

may terminate the tachycardia in a similar fashion.Quinidine and procainamide are considered toincrease the block in the anomalous pathway.Propranolol may be more effective because of itsalleged effect on both the normal and anomalous A-V pathways.33 A calcium ion antagonist (Isoptin)may be of value in terminating attacks oftachyeardias. However, it has to be pointed out thatthe effect of these drugs on the conductingproperties of the anomalous pathway is unknown.In cases with atrial flutter and especially atrialfibrillation, vagotonic maneuvers and digitalisshould be avoided because the latter are known toshorten the refractory period (RP) of the atrialmuscle. If the anomalous pathway is made up ofmuscle fibers which are electrophysiologically simi-lar to that of the atrial muscle, then it is possiblethat vagotonia and digitalis, by shortening the RPof the anomalous pathway, in presence of atrialfibrillation, may increase the ventricular rate andeven produce ventricular fibrillation.7The reentry circuit may also be interrupted by

properly timed isolated atrial or ventricular prema-ture beats and atrial or ventricular pacing.28

In case of an emergency situation where time isof the utmost importance, or when the abovemaneuvers have been unsuccessful, a DC cardio-verter should be used for cardioversion.34

Prevention of Episodes of TachycardiaThis may be attempted as follows:

MedicalThe management with drugs, i.e. quinidine,

procainamide, digitalis, and propranolol, is the bestinitial approach. These may be used singly butmore successfully in various combinations, and thedosage level should be evaluated in each case. Ithas been discussed above that induced PABsand/or AP is a clinically useful means to determinethe RP of the anomalous and normal A-V pathways.This parameter may be used to study the effect ofdrugs. Since W-P-W syndrome is probably not theresult of one single mechanism, the drug effect mayvary in different patients, and for proper therapeu-tic selection the effect on RP should be determinedin individual cases. One of our cases with W-P-W(type A) during AP showed 1:1 conduction

through the anomalous pathway up to a cyclelength of 370 msec (162/mmin) (fig. 2). Whenrestudied following quinidine therapy (1.2 g/day)for 12 days, 1:1 conduction was seen only up to acycle length of 490 msec (122/min) (fig. 7). Theabolition of W-P-W at a cycle length of 450 msec(133/min) is indicative of a significant increase inRP of the anomalous pathways. In addition,reentrant atrial tachycardia which was readilyelicited by properly timed PABs could not beinitiated following quinidine therapy. Other studieshave recently demonstrated that 50 mg ajamalinei.v. abolished the delta wave and consequentlyincreased the P-R interval.15On the other hand, the commonly observed

normalization of the QRS complex, with vagolyticmaneuvers, e.g., exercise, atropine, and amylnitrate, is due to a different mechanism than thatobserved with drugs like quinidine. Atropine, byaccelerating impulse transmission through the A-Vnode, may equalize or shorten the conduction timethrough the normal A-V pathway as compared tothat of the anomalous pathway. This results inimpulse transmission exclusively through the nor-mal A-V pathway.

PacemakersThere are two indications for insertion of an

artificial pacemaker: (1) Patients treated with largedoses of propranolol for control of SVT maydevelop sinus bradyeardia and require a demandpacemaker to insure an adequate heart rate.14 33(2) Since atrial tachycardia is usually due to areciprocal mechanism, a properly timed atrial orventricular extrasystole may terminate atrial tachy-cardia in cases with W-P-W. Ryan et al. firstreported the successful use of a permanentimplanted demand right ventricular pacemaker in acase with type A W-P-W.35 In another case (typeA) the left atrium was selected as the site forpacemaker implantation.36 In each case the pace-maker was nonfunctioning unless activated by amagnet applied externally over the pacemakergenerator which initiates regular pacing in a fixedmode at a preset rate (70-100 beats/min). It wasreasoned that sooner or later one of these randomstimuli will fortuitously be properly timed toterminate the arrhythmia. The hazard of elicitingrepetitive (ventricular or atrial) discharge by thelatter method has to be entertained although notreported as yet.29' 35, 36 Despite pacemaker implan-tation, continuation of drug therapy may bebeneficial not only to minimize the frequency of


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NSR

BE(BH)

After Quinidine

AP (Cycle length 490 msec) AP (Cycle length = 450 msec

A-H 100 msec 110

H-V H-PI-R 135 msec R220 msec

#_ __

A Pacing (Cycle length 440 msec)

225 ". _85 ? 205

330M #9661 92/

Gar., M. #96613 9J29/71

.A

A-H 90 msec 120 200 220 -

PI-R 135 mseci

5 6

Figure 7After quinidine the refractory period (RP) of the anomalous pathway is prolonged and results in i:1conduction only up to a cycle length of 490 nsec (A, middle three beats), as opposed to a cycle length of370 msec during control state (fig. 2 B). At a cycle length of 450 msec the impulse is exclusively conductedthrough the normal A-V pathway with a prolongationof PI-R interval (from 135 to 220 msec) and probablya rate-dependent aberration of the QRS complex. The H-V time (55 msec) is slightly prolonged either dueto a rapid rate or secondary to quinidine effect on the His-Purkinfe system. At a cycle length of 440 msec

(B) Wenckebach type of 20 block in the A-V node is also manifested (second, sixth, and 11th A waves

completely blocked). The refractoriness of the anomalous pathway to the last three consecutive atrial (A)impulses (A and B) is indicative of the phenomenwon of repetitive concealed conduction in the anomalouspathway.

attacks but also to increase the refractory period ofthe anomalous pathway.

In selection of patients for therapy by pacemakerimplantation the following considerations should bemade: (1) the capability of predicting the absenceof atrial fibrillation or flutter because pacemakersare ineffective in terminating tachyeardias due tothe latter atrial arrhythmias, and because prematurestimuli are more likely to result in atrial fibrillationin patients prone to these arrhythmias: (2) demon-stration of the efficacy of this mode in individualcases with a temporary pacemaker; and (3)application of an alternate method may beconsidered, i.e. the use of rapid atrial stimulation(200-220 beats/min), especially in cases developingA-V block in both the pathways on atrial pacing ator below 200 beats/min.There are two theoretical advantages of this last

approach. Overdrive capture of the atrium, with


resultant complete block of some of the impulses,provides a method without the risk of numerous

random stimuli falling in the vulnerable phase ofthe atrium (fig. 5). In case of failure to terminatetachycardia, rapid atrial pacing may provide a

means of slowing the heart rate in the anomalousand normal A-V pathways because both of theseexhibit the phenomenon of repetitive concealedconduction (fig. 7).

SurgicalIn recent years surgical treatment in a few

selected cases consisted of a direct or indirect attackon the circus movement responsible for tachyear-dias by transecting the anomalous pathway or theA-V junction, respectively.4 7,17, 26, 29 31, 37

The bases for the direct approach were laid bythe work of Durrer and Roos. These investigators,in an effort to obtain direct proof of premature

L-1A

aVF

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B

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activation of a part of the ventricles and thelocation of this area, mapped the pattern ofepicardial excitation of the ventricles by unipolarrecordings during surgery for the repair of a largeatrial septal defect (secundum type) in a paticntwith associated type B W-P-W syndrome.5 Theearliest point of premature ventricular activationwas localized 10 msec after the end of the P wave(or simultan-eous with or after the BH depolariza-tion) at the right lateral border near the atrioven-tricular sulcus and a large distance away from theA-V node (fig. 8). In the normal heart, the earliestexcitation of the epicardial muscle occurs adjacentto the anterior descending coronary artery, whereasthe region near the lateral right A-V sulcus isexcited at about 90 msec after the BH activation.The above studies led to the era of surgicalmainagement w,vhich w;as uishered in by Burchell anidco-workers in 1967.4 Ini a 43-year-old man undergo-ing surgery foriatrial septal defect with associatedW-P-W type B and episodes of rapid heart action,the findinigs on unipolar epicardial mapping wereidentical to those of Durrer anid Roos. ? DurinIgsurgery, pressure with a finger and local injection ofprocaine in the area of the earliest excitationabolished tachycardia and the preexcitation of theventricle, respectively. In an effort to permanently

A ~~~~~~~~~~Prt

- ::||l-----:.A........

..........

interrupt the Kent bundle, a transverse cut, 1 em inlength, was made on the endocardial surface of theright atrium close and parallel to the A-V ring.Hoxvever, postoperatively W-P-W syndrome per-sisted. The authors admitted the undue timidness ofthe incision and proposed, for future attempts, acomplete separation of the atrial wall from theventricle by an incision (4-5 cm long) near thetricuspid ring in the area of the suspectedanomalous bundle.4The following year the first successful surgical

correction of W-P-W type B syndrome in a 32-year-old man vith intractable bouts of tachycardialeading to cardiomegaly and congestive heartfailure was reported by Cobb and co-workers.38 Thefindings on epicardial mapping were similar to thetxo cases discussed above with an area of earliestactivation confined to a width of 1.5 cm. A 5-6-cilong incision, 3 mm below the A-V groove in theright lateral margin, was successfully used tocompletely transect the communication between theatrium and the ventricle. The absence of W-P-Wdurinig the follow-up period of this case over 232years and two additional symptomatic cases withtype B successfully treated in a similar fashion with1 year and 9 month follow-ups, respectively, fromthe same institution, and another case reported by

B

ON 1259Figure 8

Se(Juen}1ce of epicardial excitation during W-P-W (type B) anid normal A-V conduction (postoperatively). Theepicardial excitation times are denoted in reference to the BH activation.

Cirt-lalion, Volume XLVII, April 1973

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Iwa et al., provide the suggestive evidence thatcertain selected patients may be relieved by thisapproach.'7, 26

However, the above surgical approach is not asattractive as it appears at first glance. The review ofsix reported surgical failures puts this approach intoproper perspective.4' 7 17 31 37 From the same institution in which the successful cases mentionedabove were operated, an unsuccessful result hasalso been reported in a case with atypical W-P-W(mostly consistent with type A).7,17 Burchell, apartfrom his own unsuccessful case (discussed above)has quoted another unsuccessful case personallycommunicated to him by Wellens and Durrer.4Cole and co-workers have reported unsuccessfulsurgical resection in two symptomatic patientsrefractory to medical management and in whom anarea of early ventricular activation was believed tohave been identified by mapping.3' In these twocases further attempts at resection of the area of theA-V node, although failing to produce A-V block,resulted in abolition of tachycardia in one andnormalization of the QRS in the other. The lattercase is of interest and indicates the presence of ananomalous pathway around the A-V node ratherthan in the area indicated by the mapping technic.Lindsay et al. have recently reported the sixthunsuccessful result in a patient with congestiveheart failure and mitral stenosis with repeatedepisodes of tachyarrhythmia and type B W-P-W.37In the latter case the mapping procedure hadrevealed a broad area of preexcitation in the A-Vgroove at the right lateral margin. A surgicalincision 4 cm in length and sparing only theendocardium was unsuccessful.An alternate procedure is the indirect surgical

approach which entails the interruption of thecircus movement at the level of the A-V bundle (A-V node or His bundle). The first case with type AW-P-W successfully managed by this mode wasreported by Dreifus et al.29 Medical therapy forbouts of tachycardia in this 55-year-old womanrequiring hospitalization on 17 occasions, was of noavail. Several sutures were placed along a wideregion of the A-V junction with a documentedtransient complete A-V block. Although A-Vtransmission subsequently resumed with the W-P-W pattern, indicating transmission through theanomalous pathway, complete elimination of theepisodes of tachycardia resulted. Edmonds and co-workers, in a 59-year-old man with chest pain andan old myocardial infarction and resistant tachycar-dia, were able surgically to produce complete A-VCirculation, Volume XLVII, April 1973

block by electrocoagulation of the region of the A-Vnode without cardiopulmonary bypass. This hassuccessfully prevented recurrence of tachyeardia.30Both of these cases were given pennanent implant-ed demand pacemakers so as to maintain anadequate ventricular rate in case the A-V transmis-sion fails through the anomalous pathway.

Indications and Criteria for Selectionfor Surgery

The role of surgery has, as yet, not beenaccurately defined, and it is to be emphasized thatthis is an experimental procedure and should beoffered in selected patients fulfilling the followingcriteria:

(1) Patients with severe associated organic heartor lung disease requiring surgical intervention andthoracotomy even without serious symptoms due toW-P-W syndrome.

(2) Patients with disabling, frequent, andprolonged episodes of tachycardia associated withventricular fibrillation, congestive heart failure,syncope, or severe angina, who have been resistantto medical management.

(3) Preoperative evaluation and demonstrationof type B W-P-W on standard ECG and vectorcar-diogram, or the following manifestations during Hisbundle recordings. (a) Normal H-V time in thenon-W-P-W beats. If the H-V time is prolonged, thepossibility of development of complete A-V blockpostoperatively and the need of a permanentdemand pacemaker implantation should be enter-tained. (b) Ventricular depolarization precedingthe BH potential in W-P-W beats to excludeMahaim fiber conduction. (c) An extremely shortrefractory period of the anomalous pathway indicat-ing conduction capabilities at rapid rates. (d)Absence of recordable early activity posteriorlyfrom the coronary sinus during the delta wave toexclude type A preexcitation.17 (e) Absence ofindependent and exclusive A-V nodal reentry circuit(without the participation of the anomalous path-way) during SVT. If the reentry circuit iscompleted through the A-V node alone, surgicalablation of the anomalous pathway should notabolish bouts of SVT.

Cases with type B W-P-W are more amenable todirect surgical approach as opposed to type Abecause of the anterolateral location of thepreexcitation in the former. As yet no case ofsuccessful surgical interruption in type A has beenreported. The indirect surgical approach of inter-ruption of the normal A-V pathway may be

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attempted in situations where the anomalous tractis not easily accessible, i.e. on the left sideposteriorly, in the ventricular septum, or associatedwith the His bundle or where the direct interrup-tion of the anomalous pathway has been unsuccess-ful.

It is obvious from the foregoing discussion thatpatients with W-P-W syndrome do not comprise ahomogeneous group but are the result of differentmechanisms with varied electrophysiologic behav-ior. Each patient should be individually evaluatedfor management, and most of the patients shouldnot be considered for surgical treatment exceptthose who are virtually disabled.

References1. WILSON FN: A case in which the vagus influenced the

form of two ventricular complexes of the electrocar-diogram. Arch Intern Med (Chicago) 16: 1008,1915

2. WOLFF L, PARKINSON T. WHITE PD: Bundle branchblock with short P-R interval in healthy young peopleprone to paroxysmal tachycardia. Amer Heart J 5:685, 1930

3. CHUNG KY, WALSH Tj, MASSIE E: Wolff-Parkinson-White syndrome. Amer Heart J 69: 116, 1965

4. BURCHELL HB: Surgical approach to the treatment ofventricular pre-excitation. Advances Intern Med 16:43, 1970

5. WOOD FC, WOLFERTH CC, GECKELER GD: Histologicdemonstration of accessory muscular connectionsbetween auricle and ventricle in a case of short P-Rinterval and prolonged QRS complex. Amer Heart J25: 454, 1943

6. ROSENBAUM FF, HEcHr HH, WILSON FN, JOHNSTONFD: The potential variations of the thorax and theesophagus in anomalous atrioventricular excitation(Wolff-Parkinson-White syndrome). Amer Heart J29: 281, 1945

7. BOINEAU JP, MOORE EN: Evidence for propagation ofactivation across an accessory atrioventricular connec-tion in types A and B preexcitation. Circulation 41:375, 1970

8. KENT AFS: The right lateral auriculo-ventricularjunction of the heart. J Physiol 48: 22, 1914

9. OHNELE RF: Post-mortem examination and clinicalreport of a case of the short P-R interval and wideQRS wave syndrome (W-P-W). Cardiologia (Basel)4: 249, 1940

10. LEV H: The preexcitation syndrome: Anatomicconsiderations of anomalous A-V pathways. InMechanisms and Therapy of Cardiac Arrhythmias,edited by Dreifus LS, Likoff WS. New York, Grune &Stratton, 1966, p 665

11. LEv M, LEFFLER WB, LANGENDORF R, PICK A:Anatomic findings in a case of ventricular pre-excitation (WPW) terminating in complete atrioven-tricular block. Circulation 34: 718, 1966

12. JAMES TN: Morphology of the human atrioventricularnode with remarks pertinent to its electrophysiology.Amer Heart J 62: 756, 1961

13. MAHAIM I, CLERC A: Nouvelle forme anatomique debloc du coeur, a substituer au bloc dit d'aborisations(bloc bilateral manque). C R Soc Biol (Paris) 109:183, 1932

14. CASTELLANOS A, CHAPUNOFF E, CASTILLO C, MAYTIN0, LEMBERG L: His bundle electrograms in two casesof Wolff-Parkinson-White (preexcitation) syndrome.Circulation 41: 399, 1970

15. COUMEL PH, WAYNBERGER M, SLAMA R, BOUVRAIN Y:Interet de l'enregistrement des potentiels Hisiens aucours du syndrome de Wolff-Parkinson-White apropos de six observations. Acta Cardiol (Brux) 26:188, 1971

16. NARULA OS: Stimulation and recording of His bundlein cases with Wolff-Parkinson-White syndrome. Tobe published

17. WALLACE AG. BOINEAU JP, DAVMSON RM, SEALYWC: Wolff-Parkinson-White syndrome: A new look.Amer J Cardiol 28: 509, 1971

18. LAU SH. JOSEPHSON ME, GALLAGHER JJ, CARACTA AR,VARGHESE PJ, DAMATO AN: Refractoriness of theaccessory pathwav and mechanisms of re-entry in theWolff-Parkinson-White phenomenon. (Abstr) Amer JCardiol 29: 275, 1972

19. WELLENS HJJ, SCHUILENBuRO RM, DURRER D:Electrical stimulation of the heart in patients withWolff-Parkinson-White syndrome type A. Circulation43: 99. 1971

20. LAU SH, STEIN E, Kosowsic BD, HAFT JI, LISTERJW. DAMATO AN: Atrial pacing and atrioventricularconduction in anomalous atrioventricular excitation(Wolff-Parkinson-White syndrome) Amer J Cardiol19: 354. 1967

21. NARULA OS, SCHERLAG BJ, SAMET P: Pervenous pacingof the specialized conducting system in man: Hisbundle and A-V nodal stimulation. Circulation 41:77. 1970

22. SCHERF D, BORNEMANN C: Two cases of the pre-excitation syndrome. J Electrocardiol 2: 177. 1969

23. SHERF L, JAMES TN: A new electrocardiographicconcept: Synchronized sinoventricular conduction.Dis Chest 55: 127, 1969

24. HUNTEiR A. PAPP C, PARKINSON J: The syndrome ofshort P-R interval, apparent bundle branch block,and associated paroxysmal tachycardia. Brit Heart J2: 107, 1940

25. DURRER D, Roos JP: Epicardial excitation of theventricles in a patient with Wolff-Parkinson-Whitesvndrome (type B). Circulation 35: 15, 1967

26. IWA T. KAzuI T, SUGII S, WADA J: Wolff-Parkinson-White: Surgical treatment. Jap J Thorac Surg 23:513, 1970

27. LAZZARA R, KAHN N, YEH B: Conduction in caninebundle branches: Evidence for interconnectionsamong the fibers. Fed Proc 30: 553. 1971

28. DURRER D, SCHoo L, SCHUILENBURG RM, WELLENSHJJ: The role of premature beats in the initiation andtermination of supraventricular tachycardia in theWolff-Parkinson-White syndrome. Circulation 36:644, 1967


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29. DREIFUS LS, NICHOLS H, MORSE D, WATANABE Y,TRUEX R: Control of recurrent tachyeardia of Wolff-Parkinson-White syndrome by surgical ligature of theA-V bundle. Circulation 38: 1030, 1968

30. EDMONDS JH, ELLISON RG, CREw TL: Surgicallyinduced atrioventricular block as treatment forrecurrent atrial tachycardia in Wolff-Parkinson-Whitesyndrome. Circulation 39 (suppl I): I-105. 1969

31. CoLE JS, WiiLS RE, WINTERSCIIEm LC,REICHENBACH DD, BLACKMON JR: The Wolff-Parkinson-White syndrome: Problems in evaluationand surgical therapy. Circulation 42: 111, 1970

32. SCHERF D, COHEN J: The Atrioventricular Node andSelected Cardiac Arrhythmias. New York, Grune &Stratton, 1964, p 406

33. GmSON D, SOWTON E: The use of beta-adrenergicreceptor blocking drugs in dysrhythmias. ProgrCardiovasc Dis 12: 16, 1969

34. KNOEBEL SB, KING H, FISH C: Termination ofsupraventricular tachycardias complicating the Wolff-

Parkinson-White syndrome with external counter-shock. Circulation 28: 111, 1963

35. RYAN GP, EASLEY RM, ZAROFF LI, GOLDSTEIN S:Paradoxical use of a demand pacemaker in treatmentof supraventricular tachycardia due to the Wolff-Parkinson-White syndrome: Observation on termina-tion of reciprocal rhythm. Circulation 38: 1037,1968

36. PRESTON TA, KIRSH MM: Permanent pacing of the leftatrium for treatment of WPW tachycardia. Circula-tion 42: 1073, 1970

37. LINDSAY AE, NELSON RM, ABILDSKOV JA, WYATT R:Attempted surgical division of the pre-excitationpathway in the Wolff-Parkinson-White syndrome.Amer J Cardiol 28: 581, 1971

38. COBB FR, BLUMENSCHEIN SD, SEALY WC, BOINEAU JP,WAGNER GS, WALLACE AG: Successful surgicalinterruption of the bundle of Kent in a patient withWolff-Parkinson-White syndrome. Circulation 38:1018, 1968


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ONKAR S. NARULAWolff-Parkinson-White Syndrome: A Review

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1973 American Heart Association, Inc. All rights reserved.

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