paradoxical use demand pacemaker treatment of due...

Paradoxical Use of a Demand Pacemakerin Treatment of Supraventricular TachycardiaDue to the Wolff-Parkinson-White Syndrome

Observation on Termination of Reciprocal Rhythm

By GERALD F. RYAN, M.D., ROBERT M. EASLEY, JR., M.D.

LAWRENCE I. ZAROFF, M.D., AND SIDNEY GOLDSTEIN, M.D.

SUMMARYThis paper describes a new technique for terminating attacks of supraventricular

tachycardia in a patient with Wolff-Parkinson-White syndrome by using a demandpacemaker. The circuitry of this demand pacemaker generator is designed so thata magnet held near the generator converts the unit from demand to fixed mode ata pre-set discharge rate of 72/ min. During an attack of tachyeardia, a magnet held near

the generator pocket activates a fixed rate discharge and produces competitive pacing.Retrograde atrial depolarization occurs with resultant reversion to sinus rhythm.

Additional Indexing Words:Retrograde atrial depolarizationLactate production

Ventricular premature beat Sinus rhythm

DESPITE the rather precise descriptionof both the anatomic'-4 and electrical

pathways5-13 of the impulses causing thetachycardia in the Wolff-Parkinson-White(WPW) syndrome, treatment in some casesremains perplexing and difficult. Although inmost patients the arrhythmias are well toler-ated,14 in others they result in severe symp-toms'5 and occasionally in sudden death.16"17Quinidine and procainamide in combinationwith digitalis'8 and propranololl'0 have beenrecommended as the treatment of choice toabolish and prevent tachycardias. Direct cur-rent cardioversion has also been used in thetreatment of supraventricular tachycardia(SVT).20 22 Recently direct surgical interrup-tion of the A-V bundle with implantation of a

From the Cardiology Section, Rochester GeneralHospital, and the Department of Medicine, Universityof Rochester School of Medicine and Dentistry,Rochester, New York. Dr. Easley was the recipientof support from the John Sable Heart Fund.

Circulation, Volume XXXVIII, Decemnber 1968

pacemaker has been reported as a treatmentfor refractory SVT.23 24

Attacks of SVT in the WPW syndrome canbe both initiated and terminated by appropri-ately timed pacemaker-induced atrial or ven-tricular premature beats.5' 6 The purpose ofthis paper is to report a new technique for thetreatment of SVT in a patient with the WPWsyndrome who experienced frequent and de-bilitating attacks of SVT. This was accom-plished by using a permanent demand pace-maker to produce a ventricular prematurebeat and retrograde atrial depolarization.

Report of CaseM.L., a 52-year-old white married female with

known WPW syndrome, has experienced recur-rent attacks of SVT of increasing severity andfrequency for the past 15 years. These attacks areassociated with weakness, diaphoresis, lighthead-edness, and anterior chest pressure and pain withextension into her left arm. In the last year, shehas had approximately 20 emergency room visitsand 11 hospital admissions.

Attempts to prevent these attacks with pro-cainamide (4.0 g daily), diphenylhydantoin (400

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RYAN ET AL.

mg daily), quinidine (1.6 g daily), digoxin (0.5mg daily), and propranolol (240 mg daily) wereall unsuccessful. During the attacks, intravenousinjection of lidocaine, edrophonium hydrochlor-ide, propranolol, phenylephrine hydrochloride,and metaraminol were all used on numerous oc-casions with variable results. The attacks usuallylasted 12 to 18 hours and occasionally revertedspontaneously after failure of various therapeuticmaneuvers.

The patient has been known to have diabetesmellitus for many years and has been takingacetohexamide (250 mg daily) for the last 5years. She has also been moderately hyperten-sive with blood pressures averaging 180/90mm Hg.

She was admitted to the Rochester GeneralHospital in March 1968, with an attack of un-usual severity that failed to respond to any ofthese methods of treatment. Shortly after admis-sion, the attack terminated spontaneously. Physi-cal examination was unremarkable except forblood pressure of 170/90 mm Hg. The cardiacexamination revealed a prominent left ventricularimpulse. No murmurs or gallop sounds wereaudible. Roentgenograms of the chest showedmoderate left ventricular hypertrophy.An electrocardiogram taken during rest dem-

onstrated a pattern consistent with those of typeA WPW syndrome. Cardiac catheterization andselective coronary angiography were performedto evaluate her anginal symptoms. Transmyocar-dial lactate studies were performed by simul-taneous sampling of the coronary sinus andbrachial artery blood at rest and after 20 min ofatrial pacing at 105 beats/min. These demon-strated lactate production during atrial pacing atwhich time the patient experienced recurrence

of her anginal pain (fig. 1). Selective coronary

angiography and left ventriculography revealednormal coronary vessels with good ventricularcontractions.

Following discharge from the hospital, multipleepisodes of tachycardia continued to recur andbecame more severe. On May 8, 1968, an epi-sode of unusual severity associated with a systolicpressure of 80 mm Hg occurred and could notbe reverted by any of the drugs used previously.To generate a ventricular premature contractionand record the electrical events, two no. 5 bipolarpacing catheters (U. S. Catheter and InstrumentCorporation) were passed percutaneously by way

of the femoral veins through two large boreneedles. One catheter was placed in the right ven-

tricle for stimulation and one in the right atriumfor intracardiac electrocardiographic recording.A ventricular premature contraction mechanicallyproduced with the catheter in the right ventricle

caused the attack to revert promptly to sinusrhythm.

Fifteen days later after having had numerousattacks of short duration at home, the patiententered the emergency room with another severeepisode of SVT again accompanied by diaphore-sis, hypotension, and severe chest pain. Onceagain, two transvenous bipolar pacemaker cath-eters were passed by the same technique one tothe right atrium and one to the right ventricle. Acontinuous pacemaker stimulus of 5 ma was de-livered at a rate of 75/min via the right ventricu-lar endocardial catheter using a Medtronic no.5800 external pacemaker generator. Competitiveventricular pacing was induced with retrogradeA-V conduction and reversion of the SVT tosinus rhythm (figs. 2 and 3).

Because of the severity of these attacks andthe difficulty experienced in reverting them withstandard techniques, a permanent endocardialelectrode catheter, of demand type, was insertedinto the right ventricular apex. Pacing thresholdwas 1.3 ma. This particular demand pacemaker(American Optical Company) has as part of itscircuitry, the capability to be changed from de-mand to fixed rate pacing by the external applica-tion of a magnet over the generator. With thepatient in sinus rhythm at a rate exceeding thepre-set rate of the demand pacemaker or duringthe SVT, the demand pacemaker is nonfunction-ing. During an attack of SVT application of themagnet diagonally over the generator will switchthe unit to fixed rate discharge.

Since the implantation of the pacemaker, SVThas recurred on numerous occasions. Applica-tion of a magnet over the generator pocket, how-ever, has produced competitive pacing withfixed rate discharge and has restored sinus rhythm.

LACTATE and HEMODYNAMIC RESPONSE to PACING

+20-

(extracted)

+10-

% LACTATE

(A-VY O

(MV)

10- HR Cl S I

(produced) - Rest 58 2.1 36---Paced 105 2.0 19

-20,

CORONARY SINUS Distal Mid ProximalLOCATION

Figure 1

See case report for discussion.Circulation, Volume XXXVIII, December 1968

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PARADOXICAL USE OF DEMAND PACEMAKER

AEC:G 240

mmH

::::A EC:: ::;

f:0:0::000.i:?SP::::::

900:::

f:X:::

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i:f-F Ca:;

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Figure 2Simultaneous lead I, intra-atrial electrocardiogram (IAECG), and brachial artery pressurerecording illustrate reversion of supraventricular tachyeardia induced by the sixth pacemakerstimulus (S). R-R' time of this beat is 280 msec with an R'-P' time of 170 msec. The first pace-maker stimulus with an R-R' time of 320 msec does not terminate the tachycardia.

G

I

A 1 380 1 280 1

A-V le 100 170-*V I 380 280 -II

Figure 3Intra-atrial electrocardiogram (IAECG) and standard ECG lead I with pacemaker stimulus (S)inducing a VPB (R') at 280 msec from the previous QRS that caused early retrograde activationof the atria (R'-P' time of 170 msec). In this case the antegrade pathway following P1 wasrefractory and the tachycardia terminated.

DiscussionSupraventricular tachycardias in the WPW

syndrome represent a serious threat to life be-cause of their hemodynamic consequencesand are frequently refractory to pharmacolog-Circulation, Volume XXXVIII, December 1968

ical therapy. Kimball and Burch1b reviewedthe literature to 1947 and found eight deaths,and Okel17 in a more recent review found a to-tal of 22 cases of sudden death due to theWPW syndrome. As pointed out by Saunders

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and Ord,15 cerebral insufficiency, faintness,and extreme weakness can occur with thetachycardia. Although Ferrer and associates25found no change in blood pressure in one pa-tient and minimal change in another, theblood pressure change associated with ter-mination of an attack of SVT in our patient isillustrated in figure 2. Prompt remission ofchest pain and dyspnea has always occurredwith termination of an attack.The development of hypotension and an-

gina in our patient emphasized the danger ofprolonged attacks of SVT. Although anginahas been reported to occur in the presence ofnormal coronary arteries by Likoff and co-workers,26 lactate production is thought to oc-cur only when significant coronary disease ispresent.27 The production of lactate duringartificial pacing at accelerated rates is a goodindex of anaerobic metabolism of the heart.The development of lactate production withangina in our patient with normal coronaryarteries suggests that during SVT coronaryblood flow is decreased in relation to increasedmyocardial oxygen requirements.Anti-arrhythmic drugs may be ineffective

in the treatment and prevention of SVT as-sociated with WPW.8, 18 Burchell and asso-ciates24 reported a case of WPW syndromeand recurrent tachycardias in which surgicalinterruption of the Kent bundle was attempt-ed, but following surgery episodes of tachy-cardias continued to recur. The surgicalproduction of complete heart block in thetreatment of SVT with23 and without WPWsyndrome28 has been successfully carried outusing cardiopulmonary bypass by interruptionof the conduction bundle just below the atrio-ventricular node followed by the implantationof a synchronous pacemaker. We had contem-plated such a procedure in the patient pre-sented, but after the successful demonstrationin our laboratory of the feasibility of ter-minating the attacks of tachycardia by themethod described, we decided that implanta-tion of a permanent transvenous pacemakersystem was preferable, because of the muchlower morbidity associated with transvenouspacemaker insertion.

Since the original description of the Wolff-Parkinson-White syndrome in 1930,29 ana-tomic1-4 and electrophysiological studies5-13have led to the description of the anomalouspathways causing accelerated conductionfrom the atria to the ventricles through thebundle of Kent or bypass fibers of James andMahaim either separately or in combination.The genesis of tachyeardias in the WPW syn-drome is still not clearly defined, but theyare thought to occur when a supraventricularimpulse is conducted antegrade over the nor-mal pathway and re-enters in a retrograde di-rection via the accessory pathway causingatrial depolarization. The atrial impulse isthen discharged in an antegrade directionand finding the anomalous pathway refrac-tory (unidirectional block) is conductedagain via the normal pathway with some de-gree of A-V block, thus establishing a recipro-cal rhythm.30-34Moe and associates35 were able to show in

the dog that an appropriately timed atrial im-pulse could initiate a paroxysm of A-V nodaltachycardia and also that a more criticallytimed impulse would terminate an attack byinterrupting the reciprocal rhythm within theA-V node.Massumi and associates,5 utilizing paired

atrial stimuli in much the same manner asMoe and associates, were able on numerousoccasions to terminate a reciprocating tachy-cardia in a 10-year-old girl recovering fromrheumatic carditis. Their work confirmed theapplication of this technique to patients.Durrer and associates6 initiated and ter-

minated attacks of SVT in four patients withWPW syndrome and agreed with the hypoth-esis that the basic mechanism for the genesisof the tachycardia was retrograde activationof the atrium through the accelerated bypasspathway. Their studies demonstrated thatduring SVT premature atrial depolarization,either by direct atrial stimulation or ventricu-lar stimulation with retrograde atrial depolari-zation, terminated the SVT by interruptingthe re-entry pathway. A pacemaker stimulus,applied to the right ventricle during the

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tachycardia 260 to 290 msec after the pre-ceding QRS, wduld induce a ventricular pre-mature contraction that terminated the tachy-cardia. In contrast, a stimulus applied laterin the cardiac cycle would induce a ventricu-lar premature beat (VPB) but would not al-ter the SVT, the pause between the VPB andthe next ventricular complex being fully com-pensatory.The interruption of the SVT by premature

atrial and ventricular depolarization appearsto occur by different mechanisms. Prematureatrial stimulation as demonstrated by Durrerand associates rendered the atria refractory toretrograde depolarization by the impulsefrom the accelerated pathway. Prematureventricular stimulation generates early retro-

IAECG A

grade activation of the atria with identicalconduction (R-P) time as the ectopic rhythm.Then when the impulse from this atrial de-polarization travels in the antegrade directionthrough the normal A-V conduction system,the junctional tissue is refractory and the re-ciprocal rhythm is blocked. Thus, if the ven-tricular premature beat does not occur earlyenough, its resultant atrial antegrade trans-mission is able to penetrate the junctional tis-sue with a longer conduction time becauseof a partial refractory state. We were able todemonstrate in our patient that a stimulus ap-plied at 280 msec after the QRS induced aVPB that caused early retrograde activationof the atria and stopped the tachyeardia (fig.3). A stimulus occurring later than 290 msec

Figure 4

IAECG and standard ECG lead I with pacemaker stimulus (S) inducing a VPB with R-R'interval of 300 msec. The P-R time is 210 msec and the R-P time is 170 msec. Following theVPB, retrograde atrial depolarization (P') occurs via the Kent bundle at the usual R-P time of170 msec. The antegrade conduction following P' finds the A-V junctional pathway partiallyrefractory; and it does penetrate the A-V junction but with a longer P-R time. (P'-R duration =290 msec.)

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induced a VPB that would not break thetachycardia (fig. 4). This retrograde beatchanged the P-P interval of the SVT by ini-tiating the P-R delay in the next beat due toconcealed antegrade conduction of the previ-ous atrial beat. The point in the cycle atwhich retrograde activation of the atria takesplace is, therefore, of critical importance ininterrupting the tachycardia. From our stud-ies, it appears that the R-R interval requiredto break the tachycardia was between 260and 290 msec with the R-P time of SVT andVPB being the same (170 msec).The danger of eliciting repetitive ventric-

ular discharge by our method of treatment re-quires critical evaluation of the problem ofrepetitive beats induced by an artificial pace-maker stimulus. In multiple episodes of ini-tiating and terminating SVT in four patientswith WPW syndrome, Durrer and associates6failed to induce ventricular tachycardia orfibrillation. A number of factors may influencethe development of repetitive beats in the nor-mal heart, and these same factors can be ex-pected to apply to the patient with WPWsyndrome. These include an impulse durationof over 5 msec,36 myocardial ischemia, andexcess sympathomimetic activity.37 The pro-duction of lactate indicative of anaerobicmyocardial metabolism and therefore, isch-emia, suggests that one of these factors is pres-ent in our patient. It is felt, nevertheless, thatthe morbidity and risk of mortality in an at-tack of SVT jusified this method of treatmentin our patient. To date since the pacemakerwas implanted, all of our reversion episodeshave been electrocardiographically monitoredand have not been associated with a singlerepetitive beat. Propranolol has been contin-ued because of its possible beneficial effect inreducing the likelihood of repetitive beats,and also because the attacks of SVT havebeen less frequent since the inception of pro-pranolol therapy.

This method of terminating SVT in theWPW syndrome seems established as a safeand effective method when the basic atria]rhythm during an episode of SVT is coupledwith the reciprocal rhythm within the A-V

node. However, when atrial fibrillation occursin conjunction with an episode of SVT, ter-mination of the SVT by the method describedmay not be possible. Further investigation ofpatients in whom atrial fibrillation or flutteroccurs in conjunction with the pre-excitationsyndrome is necessary before this method oftreatment can be extended to include all typesof SVT in the WPW syndrome.

AcknowledgmentWe are grateful to Dr. Conrad E. Good for per-

mitting us to study his patient.

References1. LEV, M., LEFFLER, W., LANGENDORF, R., AND

PICK, A.: Anatomic findings in a case of ven-tricular pre-excitation (W-P-W) terminationin complete atrioventricular block. Circula-tion 34: 718, 1966.

2. WOOD, F. C., WOLFERTH, C. C., AND GECKELER,G. D.: Histologic demonstration of accessorymuscular connections between auricle and ven-tricle in a case of short P-R interval andprolonged QRS complex. Amer Heart J 25:454, 1943.

3. LEv, M.: The pre-excitation syndrome: Ana-tomic considerations of anomalous A-V path-ways. In Mechanisms and Therapy of CardiacArrhythmias, edited by L. S. Driefus and W.S. Koff. New York, Grune & Stratton, Inc.,1966, p. 665.

4. JAMES, T. N.: Identification of the supraventricu-lar arrhythmias: The specialized conducting tis-sue of the atria. In Mechanisms and Therapy ofCardiac Arrhythmias, edited by L. S. Driefusand W. S. Koff. New York, Grune & Strat-ton, Inc., 1966, p. 97.

5. MASSUmI, R. A., KISTIN, A. D., AND TAWAKKOL,A. A.: Termination of reciprocating tachycardiaby atrial stimulation. Circulation 36: 637,1967.

6. DURRER, D., ScHoo, L., SCHUILENBURG, R. M.,AND WELLENS, H. J.: Role of premature beatsin the initiation and termination of supraven-tricular tachyeardia in the WPW syndrome.Circulation 36: 644, 1967.

7. FERRER, M. I.: New concepts relating to the pre-excitation syndrome. JAMA 201: 1038, 1967.

8. CHUNG, K. Y., WALSH, T. J., AND MASSIE, E.:Wolff-Parkinson-White syndrome. Amer HeartJ 69: 116, 1965.

9. SCHAMROTH, L.: Reversed reciprocating parox-ysmal tachyeardia and its relationship to theWolff-Parkinson-White syndrome. Amer HeartJ 59: 506, 1960.


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10. SCHAMROTH, L., AND KRIKLER, D. M.: Locationof the pre-excitation areas in the W-P-W syn-drome. Amer J Cardiol 19: 889, 1967.

11. LAU, S. H., STEIN, E., KosowsKY, B. D., HAFT,J. I., LISTER, J. W., AND DAMATO, A. N.: Atrialpacing and atrioventricular conduction in anom-alous atrioventricular excitation (Wolff-Par-kinson-White syndrome). Amer J Cardiol.19: 354, 1967.

12. MCHENRY, P. L., KNOEBEL, S. B., FISCH, C.:WPW syndrome with supernormal conductionthrough the anomalous bypass. Circulation 34:734, 1966.

13. HECHT, H. H., et. al.: Anomalous atrioventricularexcitation: Panel Discussion. Ann NY AcadSci 65: 826, 1956.

14. BERKMAN, N. L., AND LAMB, L. E.: The Wolff-Parkinson-White electrocardiogram: Follow-upstudy of five to twenty-eight years. New Eng JMed 278: 492, 1968.

15. SAUNDERS, D. W., JR., AND ORD, J. W.: Hemo-dynamic effects of paroxysmal supraventriculartachycardia in patients with Wolff-Parkinson-White syndrome. Amer J Cardiol 9: 223, 1962.

16. KIMBALL, J. L., AND BURCH, G.: Prognosis of theWolff-Parkinson-White syndrome. Ann InternMed 27: 239, 1947.

17. OKEL, B. B.: The Wolff-Parkinson-White syn-drome. Amer Heart J 75: 673, 1968.

18. GOLDBERGER, E., BELLET, S., HEJTMANCIK, M. R.,AND WHITE, P. D.: Treatment of arrhythmias,particularly paroxysmal tachycardia associatedwith the Wolff-Parkinson-White syndrome.Amer J Cardiol 17: 104, 1966.

19. HARRIS, A.: Long term treatment of paroxysmalcardiac arrhythmias with propranolol. Amer JCardiol 18: 431, 1966.

20. KNOEBEL, S. B., KING, H., AND FIsCH, C.: Termi-nation of supraventricular tachycardia compli-cating the Wolff-Parkinson-White syndromewith external countershock. Circulation 28: 111,1963.

21. CASTELLANOS, A., JOHNSON, D., MAS, I., ANDLEMBERG, L.: Electrical conversion of paroxys-mal atrial fibrillation in the Wolff-Parkinson-White (pre-excitation) syndrome. Amer JCardiol 17: 91, 1966.

22. MEYER, A. D., AND GREENBERG, H. B.: Cardio-version of recurrent post-operative supraven-tricular tachycardia in the Wolff-Parkinson-White syndrome. Amer J Cardiol 18: 904,1966.

23. NICHOLS, H. T., ADAM, A., MORSE, D. P., BLAN-co, G., AND DREIFUS, L. S.: Surgical treatmentof Wolff-Parkinson-White syndrome. Circula-tion 35-36 (suppl. II): 11-199, 1967.

24. BURCHELL, H. B., FRYE, R. L., ANDERSON, M. W.,AND McGooN, D. C.: Atrioventricular andventriculoatrial excitation in Wolff-Parkinson-White syndrome: Temporary ablation at Sur-gery. Circulation 36: 663, 1967.

25. FERRER, M. I., HARVEY, R. M., WEINER, H. M.,CATHCART, R. I., AND COURNAND, A.: Hemo-dynamic studies in two cases of Wolff-Parkin-son-White syndrome with paroxysmal A-Vnodal tachycardia. Amer J Med 6: 725, 1949.

26. LIKOFF, W., KASPARIAN, H., SEGAL, B. L., No-VACK, P., AND LEHMAN, J. S.: Clinical correla-tion of coronary arteriography. Amer J Cardiol16: 159, 1965.

27. COHEN, L. S., ELLIOTT, W. C., KLEIN, M. D.,AND GORLIN, R.: Coronary heart disease: Clin-ical, cinearteriographic and metabolic con-siderations. Amer J Cardiol 17: 153, 1966.

28. GIANNELLI, S., AYRES, S. M., GOmPRECHT, R. F.,CONKLIN, E. F., AND KENNEDY, R. J.: Thera-peutic surgical division of the human conduc-tion system. JAMA 199: 155, 1967.

29. WOLFF, L., PARKINSON, J., AND WHITE, P. D.:Bundle branch block with short P-R interval inhealthy young people prone to paroxysmaltachycardia. Amer Heart J 5: 685, 1930.

30. WOLFF, L.: Anomalous atrioventricular excita-tion (Wolff-Parkinson-White syndrome) Circu-lation 19: 14, 1959.

31. PICK, A., AND KATZ, L. N.: Disturbances of im-pulse formation and conduction in the pre-excitation (W-P-W) syndrome: Their bearingon its mechanism. Amer J Med 19: 759, 1955.

32. HARNISCHFEGER, W. W.: Hereditary occurrenceof the pre-excitation (W-P-W syndrome) withre-entry mechanism and concealed conduction.Circulation 19: 28, 1959.

33. MOE, G. K., AND MENDEZ, C.: Physiologic basis ofreciprocal rhythm. Progr Cardiovasc Dis 8:461, 1966.

34. WATANABE, Y., AND DREIFUS, L. S.: Newer con-

cepts in the genesis of cardiac arrhythmias.Amer Heart J 76: 114, 1968.

35. MOE, G. K., COHEN, W., AND VICK, R. L.: Exper-imentally induced paroxysmal A-V nodal tachy-cardia in the dog. Amer Heart J 65: 87, 1963.

36. BROOKS, C. MCC., HOFFMAN, B. F., SUCKLING,E. E., AND ORIAS, O.: Excitability of theHeart. New York, Grune & Stratton, Inc. 1955,p. 131.

37. WIGGERS, C. J., WEGRIA, R., AND PINERA, B.:Effects of myocardial ischemia on the fibrilla-tion threshold: Mechanism of spontaneous ven-tricular fibrillation following coronary occlu-sion. Amer J Physiol 131: 309, 1940.


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SIDNEY GOLDSTEINGERALD F. RYAN, ROBERT M. EASLEY, JR., LAWRENCE I. ZAROFF and

Termination of Reciprocal RhythmTachycardia Due to the Wolff-Parkinson-White Syndrome: Observation on Paradoxical Use of a Demand Pacemaker in Treatment of Supraventricular

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