case...preexcitation and tachyeardias in wolff-parkinson-white syndrome, type b a case report byjohn...

Preexcitation and Tachyeardiasin Wolff-Parkinson-White Syndrome, Type B

A Case Report

By JOHN W. LISTER, M.D., FRANCIS X. WORTHINGTON, JR., M.D.,

THOMAS 0. GENTSCH, M.D., JOHN A. SWENSON, M.D.,DAVID A. NATHAN, M.D., AND ARTHUR J. GoSSELIN, M.D.

SUMMARYElectrophysiologic events in a 52-year-old man with Wolff-Parkinson-White (W-P-W)

syndrome, type B, recurrent supraventricular tachyeardias, and coronary artery diseasewere studied during cardiac catheterization and at open-heart surgery.

During cardiac catheterization reciprocal tachyeardias were repeatedly initiated bypremature atrial beats and terminated by rapid right atrial pacing. Our results confirmthat the tachycardia usually seen in the W-P-W syndrome is reciprocal tachycardiaswith orthograde conduction to the ventricles through the normal atrioventricular con-

duction system and retrograde conduction to the atria via the Kent bundle.The epicardial surface of the ventricles was "mapped" at surgery. The earliest site

of excitation was the posterior base of the left ventricle near the crux of the heart.Kent bundle conduction was temporarily ablated with lidocaine (Xylocaine) hydro-chloride.

This is the first case of W-P-W syndrome, type B, in which the anomalous A-Vbundle entered the left ventricle. Our results indicate that the analysis of the electro-cardiogram in localizing an abnormal A-V connection cannot be relied upon completely.

Additional Indexing Words:Kent bundle Atrial stimulation Epicardial "mapping"Ventricular activation sequence Reciprocating tachyeardias

T HE PATHOPHYSIOLOGY of the Wolff-Parkinson-White (W-P-W) syndrome

and associated tachyeardias is currently underintensive investigation. 1-4 Application of newtechnics of His bundle recordings,2 8 10 13"mapping" of ventricular activation times,3and surgical attempts at interruption of theKent bundle4 14 have contributed much to-ward clarifying the sequence of electrophysi-ologic events in the preexcitation syndromes.

From the Research Division and CardiopulmonaryLaboratory, Miami Heart Institute, Miami Beach,Florida.

Address for reprints: Dr. John W. Lister, MiamiHeart Institute, 4701 North Meridian Avenue, MiamiBeach, Florida 33140.

Received November 29, 1971; revision accepted forpublication January 21, 1972.

Presented below are electrophysiologic dataobtained from a patient with the W-P-W type-B syndrome. This information will help in thefurther elucidation of the mechanisms ofrecurrent supraventricular tachycardia and thevariability of ventricular preexcitation.

Case ReportA 50-year-old man with known W-P-W

syndrome was admitted to the hospital forevaluation of anginal pain. He had sustained amyocardial infarction 41% years previously. Afterrecovery, he was symptom-free for 3 years whenhe experienced his first anginal attack. Thisprogressed until pain occurred at rest, duringsleep, and with minimal exertion or anxiety.

For a prolonged period prior to his infarction,the patient had had frequent bouts of supraven-tricular tachycardia lasting from 5 min to 24hours. During the year preceding his admission

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for evaluation, this tachycardia had been associ-ated with severe angina and necessitated cardio-version on two occasions. Pharmacologic attemptsat its control were unsuccessful.

Examination of the precordium revealed theapical impulse in the fifth intercostal space at themidelavicular line. The first heart sound wasnormal. The aortic and pulmonic component ofthe second sound were also normal and splitphysiologically. An S4 was present at the apex.The remainder of the physical examination,including the chest X-ray, was unremarkable.The ECG findings fulfilled all the criteria for

the W-P-W type-B syndrome. The P-R intervalwas less than 0.12 sec, there was a prominentdelta wave, and the QRS interval was greaterthan 0.12 sec. As interpreted from the ECG, thedelta-wave vector was oriented to the left,superiorly and anteriorly (fig. 1).

Cardiac catheterization revealed hypokinesis ofthe anterior wall of the left ventricle and a leftventricular end-diastolic pressure of 18 mm Hg.

I IAVR

There was a 90% occlusion of the left anteriordescending coronary altery and an 80% occlusionof the obtuse marginal branch of the circumflexcoronary artery.

Saphenous vein aortocoronary artery bypasssurgery was performed with separate vein bypassgraft to the distal circumflex and left anteriordescending arteries. Since surgery the patient hashad no further anginal episodes.

Investigative MethodsHis Bundle Recordings and Arrhythmia Studies

at Cardiac Catheterization. During cardiac cath-eterization, shortly after coronary angiography,three bipolar electrode catheters with electrodes 1cm apart were positioned in the right heart: (1)to record the low right atria (LRA) and Hisbundle (BH) bipolar electrograms; (2) to recordthe high right atrial (HRA) bipolar electrogram;and (3) to stimulate the atria electrically. Thecatheter through which the LRA and BH

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C.R. 5/1/71; 511 E 71

Figure 1

A 12-lead ECG typical of the W-P-W syndrome, type B. The P-R interval is less than 0.12sec; the QRS duration is greater than 0.12 sec; the mean electrical axis of the delta wave isdepicted to the left, superiorly and anteriorly; while the mean QRS vector is directed to theleft superiorly and posteriorly. Paper speed 50 mm/sec. Time lines 1 sec. Abbreviations forall figures: HRA = right atrial electrogram; LRA - low right atrial electrogram; BH - bundleof His electrogram; A-A - intraatrial conduction time; A-H - conduction time from LRAto BH (approximate A-V nodal conduction time); H-V = interval from BH activation to onsetof ventricular activation; and V = ventricles.

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W-P-W SYNDROME, TYPE B

electrograms were obtained was positioned adja-cent to the septal leaflet of the tricuspid valve.The HRA electrogram was obtained through acatheter placed in the right atrium near the entryof the superior vena cava. The catheter used foratrial stimulation was also situated high in theright atrium. Recording catheters were connectedto a distribution box which was in turn attachedto a multichannel oscilloscopic photographicrecorder. Tracings were obtained at a paperspeed of 50 or 100 mm/sec. The atrial-stimulationcatheter was connected to a paired pulsegenerator (Medtronic model 5837). For theplacing of premature beats, a specially designedinstrument was employed, designed and built by

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the Biomedical Engineering Department of theMiami Heart Institute. The methods used forrecording the BH electrograms have been de-scribed elsewhere. 1. 15

Epicardial "Mapping" at Surgery. Prior tocoronary artery bypass surgery, fixed close bipolarplaque electrodes with five silver contacts 2-5 mmapart were sutured to the epicardial surface of thesinus node and on the high lateral posteriorepicardial surface of the right ventricle. An L-shaped bipolar roving electrode was used torecord electrograms from 10 predetermined pointson the ventricular epicardium. One cc of 1%lidocaine (Xylocaine) hydrochloride (10 mg)was injected into the ventricular myocardium at

IDA 144W L kx- nWLJLUwJBHR A1- w- r i 9

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Figure 2

Premature A-V junctional beats. Simultaneous recordings of bipolar high right atrial (HRA),low right atrial (LRA), and bundle of His (BH) electrograms and lead 1 ECG. The first,second, fifth, sixth, and seventh beats are typical W-P-W beats (fusion beats) and exhibit deltawaves. The third and fourth beats are premature A-V junctional beats which arise above theBH recording site and are solely conducted to the ventricles through the normal A-V conductionstystem. In the beats which exhibit ventricular preexcitation the BH is activated simultaneouslywith the delta wave, and the A-H time is normal. In the premature A-V junctional beats, theH-V time is normal, and the interval between the preceding sinus beat and BH deflectionis too short to permit normal A-V conduction. Therefore, these are dissociated beats.The sinus rhythm is undisturbed throughout the record. Faper speed 50 mm/sec. Time lines1 sec.

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Figure 3

(A) Initiation of a reciprocal tachycardia by a paced premature atrial beat. The first and secondbeats are typical W-P-W beats. They exhibit a short P-R interval, and the His bundle is simul-

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the point of earliest ventricular activation. Thesinus node electrogram became the referencepoint in determining the ventricular activationtimes. The leads from the electrodes wereconnected to a distribution box which was, as

before, attached to a multichannel oscilloscopicphotographic recorder. Electrograms used to plotepicardial activation times were obtained at a

paper speed of 200 mm/sec while rhythm stripswere recorded at 50 mm/sec. The detailed stepsfor recording epicardial electrograms have beenpreviously described.'6' 17

ResultsArrhythmia Studies at Cardiac Catheteriza-

tion. During normal sinus rhythm, preexcita-tion of the ventricles was constantly present.The intracardiac electrograms and ECGsduring sinus rhythm were typical of the W-P-W syndrome (figs. 1-3; see also fig. 5). Thesequence of atrial activation and the A-H timewere normal. The His bundle deflectionoccurred simultaneously with the delta wave

on the ECG, and the temporal relationshipbetween the BH and ventricular deflections on

the LRA and BH electrogram were shorterthan normal (35-55 msec ) 8 (figs. 2, 3).Occasionally, A-V junctional beats originatingproximal to the BH recording site occurredspontaneously (fig. 2). These beats invariablyexhibited a narrowed QRS complex (normalventricular activation) and normal H-V times.

The typical reciprocal supraventricular tachy-cardia (RSVT) was repeatedly initiated by a

properly timed premature atrial beat (PAB)and terminated by atrial pacing (x 8) (fig.3A). The PABs which initiated the RSVTwere placed 285-305 msec after the previoussinus beat and exhibited a markedly pro-

longed A-H time. They were blocked at theanomolous atrioventricular pathway and en-

tered the ventricles via the normal atrioven-tricular conduction system (AVCS). In every

instance ventricular activation during theRSVT occurred via the normal AVCS, andthere was 1:1 ventriculoatrial conduction(retrograde atrial activation) which was

transmitted through the anomolous atrioven-tricular connection. The RSVT was terminatedby atrial pacing at the slightly greater ratethan the intrinsic rate of the RSVT. In eachinstance it required the apparent completepacemaker capture of two atrial beats toterminate the RSVT. An example of termina-tion of the tachycardia is depicted in fig. 3B.

Epicardial "Mapping" at Surgery. Thispatient's 12-lead ECG is typical of the W-P-Wtype-B syndrome (fig. 1). The early sequence

of ventricular activation during normal sinusrhythm and ventricular preexcitation is shownin figure 4. The duration of the delta wave on

the ECG is 70 msec. The first point on the

taneously activated with the delta wave of the QRS. The paced premature atrial beat isinitiated 290 msec after the preceding sinus beat. This premature beat is solely conductedthrough the normal A-V conduction system with a prolonged A-H time, and initiates areciprocal tachycardia. During the tachycardia, the QRS configuration and H-V time normalizebecause orthograde conduction to the ventricles occurs completely through the normal A-Vconduction pathway. Retrograde conduction from ventricles to atria occurs through theaccessory pathway. LRA precedes HRA activation documenting that atrial activation wasretrograde. Paper speed 50 mm/sec. Time lines 1 sec.

(B) Termination of reciprocal tachycardia by rapid atrial pacing. Atrial pacing was initiatedat 197 beats/min. The rate of tachycardia is 188 beats/min. The first four pacemaker impulsescaptured the HRA but not the LRA, and intraatrial dissociation is present. From the fifthpacemaker impulse on, there appears to be complete capture of the atrium by the pacemaker.The fifth and sixth paced beats are blocked in the A-V node. The first of these beats "peeled"back the refractory period of the reentry pathway and permitted the second blocked beat topenetrate and interrupt the reentry pathway for antigrade ventricular conduction. The sevenththrough tenth atrial paced beats exhibit grossly aberrant ventricular activation. In these beatsA-V conduction occurs solely through the anomalous A-V bundle. After the tenth paced beat,atrial pacing is discontinued, and sinus rhythm with typical ventricular preexcitation ensues.Note that during normal sinus rhythm the HRA is activated prior to the LRA, while duringthe tachycardia the LRA is activated prior to the HRA. Paper speed 50 mm/sec. Time lines1 sec.


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C.R,4/23/71Figure 4

Epicardial "map" of activation obtained at cardiac surgery. The anomalous A-V bundle entersthe left ventricle approximately 1 cm to the left of the posterior descending coronary artery.The area encompassed by the broken line approximates the area of the ventricular preexcitation.The first point activated on the ventricular epicardial surface was excited 113 msec after thesinoatrial node and was simultaneous with the onset of the delta wave on the ECG. From thispoint it appears that activation spread slowly across the posterior base of both ventricles. Theslow spread of activation during the delta wave of the ECG suggests muscle conduction. Onecc of 1% lidocaine (Xylocaine) hydrochloride was injected into the myocardium and almostimmediately abolished ventricular preexcitation (see fig. 5). SAN = sinoatrial node; FE - fixed

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epicardial surface of the ventricles to beactivated was situated at the posterior base ofthe left ventricle, approximately 1 cm to theleft of the posterior descending coronary

artery and just below the A-V groove. Thisarea was activated 113 msec after depolariza-tion of the sinoatrial node and was simulta-neous with the onset of the delta wave on theECG. Although the impulse entered the leftventricle through the anomalous A-V path-way, the spread of activation was such thatthe posterior basal portions of both ventriclesshowed early activation. In figure 4, theepicardial area activated during the deltawave of the ECG was assumed to be the area

of ventricular preexcitation. To further docu-ment the site of entry of the anomalous A-Vpathway into the left ventricle, 1 cc of 1%Xylocaine hydrochloride (10 mg) was inject-ed into the left ventricular myocardium at thepoint of earliest activation (fig. 4). Thisprocedure almost immediately eliminated ven-

tricular preexcitation, and inverted therhythm. Three minutes after lidocaine admin-istration, there was an A-V junctional rhythmwith an apparently normal QRS and 1:1retrograde atrial activation (fig 5A and B).Five minutes later, normal sinus rhythm withexclusive conduction through the normalAVCS ensued (fig. 5C). Approximately 232hours later normal sinus rhythm with ventricu-lar preexcitation recurred. No attempt was

made to transect the anomalous A-V conduc-tion pathway because of its precarious ana-

tomic location in the immediate vicinity of thecrux of the heart and the normal AVCS.

DiscussionAs early as 1926, de Boerl8 proposed that

tachyeardias in patients with anomalous A-Vconnections may be caused by a circusmovement. If antegrade conduction is onlypossible in the normal AVCS because oftemporary refractoriness of the Kent bundle,

normal excitation of the ventricles will occur

with activation of their basal part at a timewhen the Kent bundle is no longer refractory.This will be followed by retrograde activationof the atria via the Kent bundle.

Clinical evidence in favor of retrogradeconduction through an accessory pathwayduring RSVT was first presented by Wolf19and Harnischfeger.20 The first experimentaldata to support the above hypothesis derivedfrom the work of Butterworth and Poindex-ter.21 These investigators produced tachy-cardias in the feline heart by retrograde atrialstimulation with an amplified QRS signal. Inrecent years electrical stimulation of theheart,2 19 His bundle recordings,3 4 and the"mapping" of the sequence of epicardialactivation,4 6 14 have been used to study indetail the preexcitation syndrome. All theobservations made with these newer technics,as well as our findings, support the earlierconcepts that in the W-P-W syndrome thetachyeardias are reciprocal supraventricularrhythms, usually with orthograde ventricularactivation through the normal AVCS and withretrograde conduction to the atria via theaccessory pathway.

Massumi10 reported a case in which simul-taneous block occurred in the normal AVCS(bilateral bundle-branch block) and in theKent bundle. He proposed that in his patientthe AVCS and the Kent bundle were in closeproximity to each other. In our patient, theclose anatomic location of the normal AVCSand the anomalous A-V connection have beendocumented by direct observations (epicardi-al "mapping" and blocking of the Kent bundlewith lidocaine hydrochloride). In our case, inthe absence of tachycardia, there appeared tobe a complete functional separation of theKent bundle and normal AVCS. Duringpreexcitation, fusion beats with normal con-

duction across the A-V node were present.

reference electrode; RE = roving electrode; AUE atrial unipolar electrogram recorded fromSAN electrode; ECG llead 1 ECG; and A through J = electrograms recorded from cor-responding points shown on map. The SAN ECG was used for the reference point (0 point) indetermining the activation time of the ventricular epicardium. Records were obtained at 200mm/sec.

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XYLOCAINEJ

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Figure 5

(A) Termination of ventricular preexcitation by administration of Xylocaine hydrochloride.After the second beat, 1 cc of 1% Xylocaine hydrochloride was injected into the myocardiumat the point of earliest ventricular activation (see fig. 4). The subsequent four beats show aprogressive diminution in the magnitude of the delta wave of the QRS. From the fifth beaton, there is an A-V junctional rhythm during which all the beats exhibit A-V dissociationexcept the last, which shows retrograde atrial activation. In each beat, except the last, theSAN is activated prior to the LA. In the last beat, the SAN and LA are activated simultaneouslydocumenting that there has been a sudden change in atrial activation (retrograde atrialexcitation). Paper speed 50 mm/sec. Time lines 1 sec. (B) At 3 min after Xylocaine hydro-chloride administration. There is an A-V junctional rhythm with 1:1 retrograde atrial activation.The retrograde atrial excitation is documented by the simultaneous activation of the LA and

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Occasionally, when the QRS normalized, thebeats arose in the A-V junction above the Hisbundle recording site and were conducted tothe ventricles solely through the normal AVCS(fig. 2). However, our observations indicatethat during RSVT the reentry pathway was

short. In figure 3B, the first beat whichappeared to capture the entire atrium "peeled"back the refractory period so that the nextbeat could penetrate to a deeper level andinterrupt the reentry pathway of the tachy-cardia. This suggests that either the atrium isexcluded from the reentrant pathway or only a

small portion of the atrium is involved.In previous reports of the W-P-W, type-B

syndrome,4 14 studied at open-heart surgery,

the anomalous A-V conduction pathway en-

tered the lateral margin of the right ventricle.Although the delta wave in our subject hadthe same electrocardiographic spatial orienta-tion as the case studied by Burchell,4 the entryof the anomalous A-V connection into theventricles was not at the lateral margin of theright ventricle but at the basal posteriormedial area of the left ventricle (fig. 4). Levand his associates' carefully studied a case ofW-P-W type-B syndrome at postmortem inwhich no atrioventricular bridges were found.They explained their patient's ECG by thefinding of atrial septal muscle fibers bypassingthe A-V node and the existance of numerous

Maheim fibers extending between the A-Vnode and the posterior portion of the ventricu-lar septum. In our case, the incongruity of theECG findings of W-P-W type-B syndrome andthe anomalous A-V connection entering theleft ventricle near the crux of the heart may

best be explained by the vector resulting fromthe slow spread of depolarization (muscleconduction) during the period of the deltawave and/or Maheim fibers entering the rightside of the ventricular septum or rightventricular endocardium. These Maheim fibersif present, could not be detected by our

method of ventricular "mapping" because we

only explored the epicardial surface of theheart. Since publication of the successfultreatment of RSVT in patients with preexcita-tion syndrome by transection of anomalousA-V bundles14 or of the normal AVCS,6 thedetermination of the exact location of theanomalous A-V connecting pathway has as-

sumed clinical importance. The analysis of theECG in localizing the abnormal A-V connec-

tion cannot be relied upon completely. This isthe first reported case of the W-P-W type-Bsyndrome in which the deviant A-V connec-

tion did not enter the right ventricle.

Acknowledgments

We wish to acknowledge Dr. Minor Duggan for hiseditorial assistance in the preparation of themanuscript and Mrs. Klara Soos for her skilled typinghelp.

References

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2. DURRER D: Electrical aspects of human cardiacactivity; Clinical physiological approach toexcitation and stimulation. Cardiovasc Res 2:1, 1968

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

4. BURCHELL HB, FRYE RL, ANDERSON MW,McGooN DC: Atrioventricular and ventriculo-atrial excitation in Wolff-Parkinson-White syn-

drome (type B); Temporary ablation atsurgery. Circulation 36: 663, 1967

5. LOWN B, GANONG WF, LEVINE SA: Thesyndrome of short P-R interval, normal QRScomplex and paroxysmal rapid heart action.Circulation 5: 693, 1952

6. DREFUs LS, NICHOLs H, DRYDEN M, WATANABEY, TREUX R: Control of recurrent tachycardia ofWolff-Parkinson-White syndrome by surgicalligature of the A-V bundle. Circulation 38:1030, 1968

SAN. (C) At 8 min after Xylocaine hydrochloride administration. There is normal sinusrhythm with a normal P-R interval and normal ventricular excitation. These tracingsdemonstrate that Xylocaine only blocked the anomalous A-V conduction pathway, and at thepoint of entry into the ventricle the normal A-V conduction system and anomalous A-V con-nection are anatomically separate.


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7. LAU SH, STEIN E, KoSOWSKY BD, HAFT JI,LISTER JW, DAMATO AN: Atrial pacing andatrioventricular conduction in anomalous atrio-ventricular excitation (Wolff-Parkinson-Whitesyndrome). Amer J Cardiol 19: 354, 1967

8. CASTILLO C, CASTELLANOS A JR, AGHA AS,MYERBURG R: Significance of His bundlerecordings with short H-V intervals. Chest 60:142, 1971

9. DURRER D, SCHoO L, SCHUILENBURG RM,WELLENs HJJ: The role of premature beats inthe initiation and the termination of supraven-

tricular tachycardia in the Wolff-Parkinson-White syndrome. Circulation 36: 644, 1967

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11. DURRER D, SCHUILLENBuIRG RM, WELLENS HJJ:Pre-excitation revisited. Amer J Cardiol 25:690, 1970

12. WELLENS HJJ, SCHUILENBURG RM, DURRER D:Electrical stimulation of the heart in patientswith Wolff-Parkinson-White syndrome, type A.Circulation 43: 99, 1971

13. CASTILLO C, CASTELLANOS A JR: His bundlerecordings in patients with reciprocatingtachyeardias and Wolff-Parkinson-White syn-

drome. Circulation 42: 271, 197014. COBB FR, BLUMENSCHEIN SD, SEALY WC,

BOINEAU JP, WAGNER CS, WALLACE AG:

Successful surgical interruption of the bundleof Kent in patient with Wolff-Parkinson-Whitesyndrome. Circulation 38: 1018, 1968

15. SCHERLAG BJ, LAU SH, HELFANT RH, BERKOWITZWD, STEIN E, DAMATO AN: Cathetertechnique for recording His bundle activity inman. Circulation 39: 13, 1969

16. SEIDENSTEIN M, HOFMAN BF, STucKEY JH,VENEROSE RC, MICHAELS L: Activation of theepicardial surface of the left ventricle followingleft ventriculotomy and left bundle branchblock. Amer J Cardiol 10: 101, 1962

17. LISTER JW, KLOTZ DH, JOMAIN SL, STucyEY JH,HOFFMAN BF: Effect of pacemaker site on

cardiac output and ventricular activation indogs with complete heart block. Amer JCardiol 14: 494, 1964

18. DE BOER S: Die physiologische Crundlage undKlinik des unregelmassigen Herzschalges.Ergebn Inn Med Kinderheilk 29: 391, 1926

19. WOLFF L: Anomalous ventricular excitation(Wolff-Parkinson-White). Circulation 19: 14,1959

20. HARNISCHFEGER WW: Hereditary occurrence ofthe pre-excitation (Wolff-Parkinson-White)syndrome with re-entry mechanism and con-

cealed conduction. Circulation 19: 28, 195921. BUTTERWORTH JS, POINDEXTER CA: Short P-R

interval associated with a prolonged QRScomplex; Clinical and experimental study. ArchIntern Med (Chicago) 69: 437, 1942


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GOSSELINGENTSCH, JOHN A. SWENSON, DAVID A. NATHAN and ARTHUR J.

JOHN W. LISTER, FRANCIS X. WORTHINGTON, JR., THOMAS O.A Case Report

Preexcitation and Tachycardias in Wolff-Parkinson-White Syndrome, Type B:

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1972 American Heart Association, Inc. All rights reserved.

75231is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TXCirculation

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