Transcript

European Heart Journal (1996) 17 (Supplement Q, 10-20

The value of the ECG in the diagnosis ofsupraventricular tachycardias

H. J. J. Wellens

Academic Hospital, Maastricht, The Netherlands

By combining the 12 lead ECG with information from (Eur Heart J 1996; 17 (Suppl C): 10-20)intracardiac activation studies, it has become possible tocorrectly diagnose the type of supraventricular tachycardia Key Words: Supraventricular tachycardia, electrocardio-on the 12 lead ECG. In this article the typical ECG features gram.allowing that diagnosis are discussed and illustrated.

Introduction ablation of the tachycardia substrate, or interruptionof the tachycardia pathway and a better understanding

Information from programmed electrical stimulation o f h o w a n d w h e r e a n t i a r r h y t h m i c drugs exert theirof the heart combined with excitation mapping has ^e&aal effects. Last but not least, in the past twoled to a much better understanding of the site of the d e c a d e s w e h a v e ^ m a j o r a d v a n c e s i n o u r a b i I i t y

ongin and the mechanism of supraventncular tachy- t 0 comctiy i n t e r p r e t the 12-lead electrocardiogramcardias1 -*. It has also resulted in the development of ( E C G ) o f s u p r a v e n t r i c u i a r tachycardias™. This hasnew treatment modalities, such as surgical or electncal m a d e t h e E C G a r e H a b l e a n d inexpensive tool with

which to diagnose the site of origin and frequently theCorrespondence: Dr H. J. J. Weliens, Academic Hospital mechanism of a supraventricular arrhythmia, thusMaastricht, Department of Cardiology, PO Box 5800, 6202 AZ providing the first Step in guiding our therapeuticMaastricht, The Netherlands. approach.

Table 1 Classification of supraventricular tachycardia according to their site oforigin and mechanism

Re-entry DAD AbnAuto

Atrial tachycardiaParoxysmal + +Incessant +

Atrial flutter +Atrial fibrillation + (mult circ)AV nodal tachycardia

Common form (slow-fast) +Uncommon form (fast-slow) +

AV junctional accelerated rhythmDigitalis induced ?Post cardiac surgery +Infectious +Ischaemic +

AV junctional circus movement tachycardiaParoxysmal

V-A conduction over arapidly conducting AP +

Non-paroxysmalV-A conduction over a

slowly conducting AP +

Abn = abnormal; AP=accessory pathway; Auto = automaticity; AV=atrioventricular; DAD =delayed after depolarization; mult circ=multiple circuits; V-A = ventriculo-atrial.

0195-668X/96/0COO10 +11 S18.00/0 (£} 1996 The European Society of Cardiology

Dow

nloaded from https://academ

ic.oup.com/eurheartj/article/17/suppl_C

/10/484700 by guest on 04 February 2022

The ECG in supraventricular tachycardias 11

JwA/JWFigure 1 Schematic drawing of the three mechanisms ofatrial tachycardia. As indicated, atrial tachycardia in-cludes sinus node re-entrant tachycardia which is basedupon re-entry between the sinus node and adjacent atrialtissue (1). Atrial tachycardia can be caused by abnormalautomaticity (usually leading to incessant tachycardia)reentry (2) and triggered activity (both resulting inparoxysmal tachycardia (3).

Classification of a supraventriculartachycardias

Arrhythmias can be classified according to their site oforigin, their mechanism and their electrocardiographicfeatures. Table 1 lists the different types of supraven-tricular tachycardias according to site of origin andmechanism. Since emphasis in this article will be on theelectrocardiographic features, the investigation of thetachycardia mechanism will not be discussed in detail.

Atrial tachycardia

Typically, during atrial tachycardia the P wave precedesthe QRS complex on the ECG (Fig. 1). The polarity ofthe P wave, the P-R interval and the ratio between Pwaves and QRS complexes depend on the site of originin the atrium, the rate of abnormal impulse formation,and atrioventricular (AV) nodal transmission character-istics. As indicated in Table 1, there are different formsof atrial tachycardia. The paroxysmal form is the mostcommon type, characterized by sudden onset and ces-sation of the arrhythmia151. An example is shown in Fig.2. The behaviour of this arrhythmia during programmedelectrical stimulation of the heart and its response todifferent antiarrhythmic drugs suggests that paroxysmalatrial tachycardia is either based upon re-entry (80% ofcases) or on triggered activity (20%). Triggered activityis an arrythmogenic mechanism resulting from delayedafter depolarization161.

A relatively rare but serious arrhythmia isincessant (or permanent) atrial tachycardia (Fig. 3).In patients suffering from this rhythm disturbance,the arrhythmia is present for more than 50% of theday. As pointed out elsewhere'51, the rate of atrialimpulse formation, which is probably caused by ab-normal automaticity, frequently increases during exer-cise. The persistent nature of the tachycardia and theinability to control the ventricular rate by failing toprevent the rate increase of the arrhythmia and 1 to 1AV conduction, may result in dilated (tachycardiainduced) cardiomyopathy171. Recognition that thearrhythmia is the cause rather than the consequenceof the cardiomyopathy is important. Destruction orisolation of the atrial area that led to abnormalimpulse formation should cure the arrhythmia andimprove pump function.

"ilL 800 L.ms - .

Figure 2 Example of a paroxysmal atrial tachycardia. Note the onset of thearrhythmia after three conducted sinus beats with a P wave that precedes the QRScomplex but has a different configuration from the sinus P waves.

Eur Heart J, Vol. 17, Suppl C 1996

Dow

nloaded from https://academ

ic.oup.com/eurheartj/article/17/suppl_C

/10/484700 by guest on 04 February 2022

12 H. J. J. Wellens

L "*-

; ; t ; i : 4 i I • | ' - i f - ^ - - ••• i I • ' i i - i < ; : < i - i — - — — —

- w. rv. ^« ~w T ^w» ^-r ^r- ^ r ^ ^ ^™v * fi ^ ^1 s t 79326

5 Example of an incessant atrial tachycardia. This patient, initiallyshowing 2:1 and later 1:1 AV conduction, has been continuously in tachycardia for12 years and presented with a picture of a dilated cardiomyopathy.

400 ms

Figure 4 Carotid sinus massage reveals that atrial flutter is the underlying rhythmat the atrial level.

Atrial flutter

Observations both in the tissue bath and in patients[6~l2]

suggest that re-entry is the basis for atrial flutter. Theclassical sawtooth pattern of atrial activity is the ECGhallmark of the arrhythmia. Carotid sinus massage-inducedAV block facilitates recognition of the arrhythmia (Fig. 4).

Atrial fibrillationTypically, the ECG shows rapid, irregular atrial activity,with, in the case of normal atrioventricular conduction arapid, irregular rhythm.

Experimental work in animals and mappingstudies during surgery suggest that multiple re-entrantwavelets are the basis for atrial fibrillation'13'141.

It is important to be aware of two types ofparoxysmal atrial fibrillation that can occur in patients

without apparent heart disease. Coumel et al.ll5], haveindicated the so-called vagally induced and thecatecholamine-sensitive types. Characteristically, theformer arrhythmia is found in middle-aged men andbegins at night, during rest, or after a meal.Catecholamine-sensitive atrial fibrillation is less com-monly encountered in clinical practice. The arrhythmiais most often observed in young women. It is related tostress and exercise, and can be provoked by caffeine andalcohol. Holter recordings show the occurrence of thearrhythmia in the daytime, usually in the morning, andpreceded by an increase in sinus rate.

Atrioventricular nodal tachycardia

Programmed stimulation of the heart resulting in repro-ducible initiation and termination of paroxysmal AV

Eur Heart J, Vol. 17, Suppl C 1996

Dow

nloaded from https://academ

ic.oup.com/eurheartj/article/17/suppl_C

/10/484700 by guest on 04 February 2022

The ECG in supraventricular tachycardias 13

Figure 5 Schematic drawing of the mechanism of thecommon form of AV nodal reentrant tachycardia. Antero-grade conduction in the reentry circuit goes over a slowpathway, retrograde conduction over a fast pathway. Thefast pathway may lie within the AV node (left panel) ormay be partly outside the AV node (right panel).

Ill

Figure 7 The three types of supraventricular tachy-cardia resulting in a negative P wave in front of theQRS complex in lead II of the electrocardiogram.Statistically the most probable occurrence is a circusmovement tachycardia with atrioventricular conductionover the atrioventricular node and ventriculo-atrial con-duction over a slowly conducting accessory pathway(1). The other two possibilities are an atrioventricularnodal tachycardia of the unusual (fast-slow) form (2)or a low atrial tachycardia in the vicinity of the AVnode (3).

TrffTTTTT

800 ms

Figure 6 Example of the common form of AV nodaltachycardia. Note the pseudo S wave in leads II and IIIand the pseudo incomplete right bundle branch blockpattern in lead V,, caused by the P wave during tachy-cardia.

JJLFigure 8 Schematic representation of a circus movementtachycardia using a 'concealed' fast-conducting (left panel)or slow-conducting (right panel) accessory AV pathway.The corresponding ECGs during tachycardia with theircharacteristic R-P/P-R ratio are shown in Fig. 9.

Eur Heart J, Vol. 17, Suppl C 1996

Dow

nloaded from https://academ

ic.oup.com/eurheartj/article/17/suppl_C

/10/484700 by guest on 04 February 2022

14 H. J. J. Wellens

Figure 9 Two types of circus movement tachycardia. Cir-cus movement tachycardia due to a rapid (A) and slow (B)conducting accessory pathway (AP). The rapidly conduct-ing AP (A) is associated with a short R-P, the slow conduct-ing AP (B) with a long R-P. In (A) and (B), the P waves arerelatively narrow, inverted in the inferior leads, and isoelec-tric in lead I, suggesting a septal or paraseptal location.

nodal tachycardia suggests that re-entry is the under-lying mechanism. This is supported by finding 'dual' AVnodal conduction in many patients'151. The common

type of paroxysmal AV nodal tachycardia typicallyshows simultaneous activation of the atrium and theventricle during the arrhythmia'171. Anterograde conduc-tion in the AV node during tachycardia is considered tooccur over a slowly conducting pathway and retrogradeconduction over a rapidly conducting pathway (Fig. 5).On the ECG during tachycardia, this results in the Pwave being either completely hidden in the QRS com-plex or distorting the terminal portion of the QRScomplex151. This pattern is graphically represented inFig. 5, and an ECG of the arrhythmia is shown in Fig. 6.The common type of AV nodal tachycardia occurs twiceas often in women as men.

The uncommon type of paroxysmal AV nodaltachycardia is characterized by a P wave following theQRS complex, the mechanism being anterograde AVnodal conduction over a rapid pathway and retrogradeconduction over a slow pathway. The R-P interval islong, and the P wave becomes located in front of thesubsequent QRS complex. This is a rare, seldom sus-tained, arrhythmia, and has to be differentiated from alow atrial tachycardia or a circus movement tachycardiausing a slowly conducting accessory pathway forventriculo-atrial conduction (Fig. 7).

Circus movement tachycardia

Epicardial mapping1'81 and electrophysiological in-vestigations'1'181 have shown that accessory connectionsbetween the atrium and ventricle frequently participatein tachycardia circuits. However, intracardiac stimu-lation techniques and recordings are required to demon-strate the location and participation of these extraconnections.

An interesting subgroup of patients with supra-ventricular tachycardia are those with a so-called'concealed' accessory pathway*20'2'1. These connectionsconduct the impulse in a ventriculoatrial direction only.

Table 2 Findings on carotid sinus massage in different types of tachycardia

Tachycardia

Sinus tachycardiaAtrial tachycardia

Paroxysmal form

Incessant form

Atrial flutter

Atrial fibrillation

AV nodal tachycardia

Circus movementtachycardia (using overtor concealed accessory pathway)

a.b.a.b.a.b.c.a.b.a.b.a.b.

Effect of carotid sinus massage

Gradual and temporary slowing in heart rate.

Cessation of tachycardiaNo effectTemporary slowing because of increase in AV blockNo effectTemporary slowing because of increase in AV blockTransformation into atrial fibrillationNo effectTemporary slowing because of increase in AV blockNo effectCessation of tachycardiaNo effectCessation of tachycardiaNo effect

Eur Heart J, Vol. 17, Suppl C 1996

Dow

nloaded from https://academ

ic.oup.com/eurheartj/article/17/suppl_C

/10/484700 by guest on 04 February 2022

The ECG in supraventricular tachycardias 15

(A)

932080 400 ms

Figure 10 Example of electrical alternans of the QRS com-plex during a circus movement tachycardia using a 'concealed'accessory AV pathway. Note that QRS alternation is seen inmany leads.

Figure 11 Presence of a slower heart rate during supraventricular tachycar-dia, in a case of right bundle branch block. As explained in Fig. 10, thisindicates a circus movement tachycardia using an accessory atrioventricularpathway on the same side as the blocked bundle branch. In this exampletherefore, the accessory pathway is between the right atrium and the rightventricle.

Eur Heart J, Vol. 17, Suppl C 1996

Dow

nloaded from https://academ

ic.oup.com/eurheartj/article/17/suppl_C

/10/484700 by guest on 04 February 2022

16 H. J. J. Wellens

They are often present in patients referred for evaluationof a supraventricular tachycardia. Two groups ofpatients have concealed accessory pathways (Figs 8 and9), and the smaller group is formed by those with aslowly conducting accessory pathway. In the latter type,atrial activation typically follows the QRS complex withan R-P interval longer than the P-R interval. This typeof supraventricular tachycardia must be differentiatedfrom low atrial tachycardia and the uncommon type ofAV nodal tachycardia (Fig. 7).

Circus movement tachycardia via an accessoryatrioventricular pathway is twice as common in men asin women. Concealed accessory pathways are about halfas common as overt anterogradely conducting accessorypathways (ventricular pre-excitation). Age at onset offirst tachycardia attack in patients with accessory path-ways is a mean of 10 years younger than patients withAV nodal tachycardia'221.

Additional ECG findings

Carotid sinus massage

Carotid sinus massage-induced changes in the ECGduring tachycardia can be helpful in differentiatingbetween the different types of supraventricular tachy-cardia (Table 2).

Electrical alternans of the QRS complex

Alternating changes in the QRS complex during narrowQRS tachycardia are highly suggestive of a circus move-ment tachycardia using an accessory pathway for ven-triculoatrial conduction1231. It is important to stress thatQRS alternations as a clue to circus movement tachy-cardia can only be used when present more than 5 s afterthe start of the tachycardia. Changes in QRS configur-ation are common at the start of a supraventriculartachycardia because the sudden acceleration in ventricu-lar rate leads to different degrees of changes in refrac-toriness and conduction velocity in the conductionsystem during the first beats of the tachycardia. Inpatients with circus movement tachycardia and a narrowQRS, the incidence of electrical alternans increases withincreasing heart rates during tachycardia'231. An exampleof electrical alternans is given in Fig. 10.

ace. pathway

His bundle

RBB

AVnode

LBB

280

vrrrcrrrnr280

Figure 12 Increase in the length of the reentry circuitwhen bundle branch block develops during circus move-ment tachycardia using an accessory pathway on thesame side as the bundle branch block. In {A) there is aright-sided accessory pathway. In (B) the tachycardiacircuit is confined to the AV node. When right bundlebranch block (RBB) develops in the patient with aright-sided accessory pathway, the circuit becomeslonger and the tachycardia rate slows (compare V,before and after right bundle branch block on the left).In contrast (shown in (B)), nothing happens with thetachycardia rate when bundle branch block developsduring AV nodal re-entrant tachycardia (measurementsare in ms).

presence of a circus movement tachycardia. This uses anaccessory AV pathway for ventriculoatrial conduction,inserting into the free wall of the ventricle on the sameside as the blocked bundle branch.

Slowing in heart rate duringtachycardia when bundle branch block

develops

Figures 11 and 12 illustrate the importance of carefullymeasuring the rate of a tachycardia when bundle branchblock develops and disappears during supraventriculartachycardia'2'1. As shown in Fig. 12, slowing in tachy-cardia rate during bundle branch block indicates the

Mode of initiation

Initiation of a supraventricular tachycardia by a singleatrial premature beat during sinus rhythm after markedprolongation of the P-R interval suggests the presence ofdual AV nodal pathways'161 and AV nodal reentranttachycardia as the mechanism of the arrhythmia (Fig. 13).In contrast, initiation of a supraventricular tachycardiaduring sinus rhythm without prolongation of the P-Rinterval suggests a circus movement tachycardia using an

Eur Heart J, Vol. 17, Suppl C 1996

Dow

nloaded from https://academ

ic.oup.com/eurheartj/article/17/suppl_C

/10/484700 by guest on 04 February 2022

The ECG in supraventricular tachycardias 17

400 ms

Figure 13 Clinical example of initiation of the common form of AV nodaltachycardia. After two sinus beats conducted to the ventricle, an atrial prematurebeat is conducted to the ventricle with marked P-R prolongation, indicatingconduction over the slow AV nodal pathway. This is followed by perpetuation ofre-entry in the AV node and AV nodal tachycardia. Six precordial leads wererecorded simultaneously.

II

Figure 14 Initiation of a supraventricular tachycardia during sinus rhythm. Notethat an acceleration in rate during sinus rhythm is followed by a tachycardia with anarrow QRS complex. The R-P interval exceeds the P-R interval during tachycardiawith negative P waves in leads II, II, V s and V6. These findings indicate the presenceof a circus movement tachycardia using a slowly conducting accessory pathway forventriculo-atrial conduction.

accessory AV pathway for ventriculoatrial conduction Mode Of termination(Fig. 14). Initiation of a supraventricular tachycardia by asingle ventricular premature beat argues in favour of a As explained in Fig. 16, it is extremely unlikely that ancircus movement tachycardia, incorporating an accessory AV nodal tachycardia will be terminated by a singleatrioventricular pathway (Fig. 15). ventricular premature beat, whereas this is common in a

Eur Heart J, Vol. 17, Suppl C 19%

Dow

nloaded from https://academ

ic.oup.com/eurheartj/article/17/suppl_C

/10/484700 by guest on 04 February 2022

18 H. J. J. Wellens

AVnode AVnode

ace. pathway

VPB VPB

Figure 15 During sinus rhythm, a circus movement tachycardia using anaccessory AV pathway can easily be initiated by a single ventricular prema-ture beat (VPB) because the VPB finds the distal conduction system refrac-tory and is retrogradely conducted to the atrium over the accessory pathway.In contrast, because of refractoriness of the distal conduction system, a VPBcannot gain access to tbe AV node to initiate AV nodal reentry.

(B)

AV nodeAVnode

ace. pathway

VPB VPB

Figure 16 Different ways for a ventricular premature beat (VPB) to gainaccess to the tachycardia circuit (and to terminate tachycardia) in AV nodaltachycardia and in circus movement tachycardia using an accessory path-way for ventriculo-atrial conduction. As shown in panel (B), the VPB in AVnodal tachycardia will be blocked distal to the reentry circuit, whereas, asshown in panel (A), the VPB easily invades the reentry circuit during circusmovement tachycardia.

circus movement tachycardia using an accessory AVpathway for ventriculo-atrial conduction.

The practical approach

When analysing the 12 lead ECG of a supra ventriculartachycardia a stepped approach is used (Fig. 17).

The steps include the relationship between atrial andventricular events during supraventricular tachycardia;presence or absence of electrical alternans, and thelocation and configuration of the P wave. If that analysisdoes not allow a definite diagnosis, an electrophysiologi-cal study is indicated, especially when the tachycardiais symptomatic, leads to myocardial dysfunction orbecause of its frequent occurrence is annoying andsocially incapacitating for the patient.

Eur Heart J, Vol. 17, Suppl C 1996

Dow

nloaded from https://academ

ic.oup.com/eurheartj/article/17/suppl_C

/10/484700 by guest on 04 February 2022

The ECG in supraventricular tachycardias 19

(1) 2nd degree AV block?(spontaneous or after CSM)I 1

No Yes

Atrial rate

>250.minI

Atr flutter

"1

Atr T AVNT with2:1 block

(2) QRS alternation?

(3)

P R > R-PI

CMT with fast AP

No

P wave location?"I

P inRI

AVNT

Yes

CMT with AP

P R < R-P

Atrial T CMT with slow AP

(4a) P axis (frontal plane)

Inferior-Superior

Atrial T AVNT CMT with AP-Slow-Fast (septal)

Other,—-' ——

Atrial T CMT with fast AP(Right or left)

(4b) P axis (horizontal plane)

Right -•Left Left Right

Atrial T CMT with slow APAtrial T

Figure 17 Four steps to be taken when analysing the 12-lead ECG ofa regular supraventricular tachycardia. As shown, information should beobtained on the relationship between atrial and ventricular events duringsupraventricular tachycardia (spontaneously and after carotid sinusmassage (CSM)) followed by a search for electrical alternans of theQRS complex. Thereafter the location of the P wave in relation tothe QRS complex and the polarity of the P wave in the frontaland horizontal plane should be studied. Atr=atrial; T=tachycardia;AVN=atrioventricular nodal; CMT=circus movement tachycardia;AP=accessory pathway.

References

[1] Wellens HJJ. Electrical stimulation of the heart in the studyand treatment of tachycardias. Baltimore: University ParkPress, 1971.

[2] Josephson ME, Wellens HJJ. Differential diagnosis of supra-ventricular tachycardia. In: Scheinman MM, ed. CardiologyClinics. Philadelphia: W. B. Saunders, 1990: 411-42.

[3] Zipes DP. Cardiac electrophysiology. Promises and contri-butions. J Am Coll Cardiol 1989; 13: 1329-52.

[4] Wellens HJJ, Conover MB. The ECG in emergency decisionmaking. Philadelphia: W. B. Saunders, 1992: 73-103.

[5] Wellens HJJ. Differential diagnosis of narrow QRS tachycar-dia. In: Fisch C, Surawicz S, eds. Cardiac electrophysiologyand arrhythmias. New York: Elsevier, 1991: 164-75.

[6] Rosen MR. The links between basic and clinical cardiacelectrophysiology. Circulation 1988; 77: 251-63.

[7] Wellens HJJ, Rodriguez LM, Smeets JLRM, Cheriex EC,Pieters F, Den Dulk K. Tachycardiomyopathy in patientswith supraventricular tachycardia with emphasis on atrial

Eur Heart J, Vol. 17, Suppl C 1996

Dow

nloaded from https://academ

ic.oup.com/eurheartj/article/17/suppl_C

/10/484700 by guest on 04 February 2022

20 H. J. J. Wellens

fibrillation. In: Olsson SB, Allessie MA, Campbell RWF, eds.Atrial fibrillation. Armonk: Futura Publishing, 1994: 333—42.

[8] Puech P, Latour M, Grolleau R. Le flutter et ses limites. ArchMai Coeur 1970; 63: 116-20.

[9] Wellens HJJ, Brugada P, Vanagt E, Ross DL, Bar FW. Newstudies with triggered automaticity. In: Cardiac arrhythmias.A decade of progress. Harrison DC, ed. Boston: G. K. Hall,1981: 601-10.

[10] Boineau JP, Mooney CR, Hudson RD, Hughes DG, ErchinRA Jr, Wylds AC. Observations on re-entrant excitationpathway and refractory period distributions in spontaneousand experimental atrial flutter in the dog. In: Kulbertus HE,ed. Re-entrant arrhythmias: mechanisms and treatment.Baltimore: University Park Press, 1977: 72-98.

[11] Waldo AL, Maclean WAH, Karp RB, Kouchoukos NT,James TN. Entrainment and interruption of atrial flutter withatrial pacing: studies in man following open heart surgery.Circulation 1977; 56: 737^(4.

[12] Allessie MA, Bonke FIM, Schopman FJG. Circus movementin rabbit atrial muscle as a mechanism of tachycardia III. The'leading circle' concept: a new model of circus movementin cardiac tissue without the involvement of an anatomicobstacle. Circ Res 1977; 41: 9-18.

[13] Allessie MA, Lammers WJEP, Bonke FIM, HoUen J. Exper-imental evaluation of Moe's multiple wavelet hypothesis ofatrial fibrillation. In: Zipes DP, Jalife J, eds. Cardiac Arrhyth-mias. New York: Grune & Stratton, 1985: 265-76.

[14] Falk RH, Podrid PJ. Atrial fibrillation. Mechanism andmanagement. New York: Raven Press, 1991.

[15] Coumel P, Attuel P, Leclercq JF. Arythmies auriculairesd'origine vagale ou catecholergique. Effects compares du

traitment beta-bloqueur et phenomenes d'echappement. ArchMai Coeur 1982; 75: 373.

[16] Denes P, Wu D, Dhingra RC, Chuguima R, Rosen KM.Demonstration of dual AV nodal pathways in patients withparoxysmal supraventricular tachycardia. Circulation 1973;48: 549-55.

[17] Wellens HJJ, Durrer D. The role of an accessory pathway inreciprocal tachycardia. Circulation 1975; 52: 58-72.

[18] Durrer D, Roos JP. Epicardial excitation of the ventricles ina patient with WolrT-Parkinson-White syndrome (type B).Circulation 1967; 35: 15-22.

[19] Durrer D, Schoo L, Schuilenburg RM, Wellens HJJ. Therole of premature beats in the initiation and termination ofsupraventricular tachycardia in the Wolff-Parkinson-Whitesyndrome. Circulation 1967; 36: 644-62.

[20] Coumel Ph, Attuel P. Reciprocating tachycardia in overt andlatent pre-excitation. Influence of functional bundle branchblock on the rate of tachycardia. Eur J Cardiol 1974; 1:423-36.

[21] Wellens HJJ, Brugada P, Farre J et al. Diagnosis and treat-ment of concealed accessory pathways in patients sufferingfrom paroxysmal AV junctional tachycardia. In: Frontiers ofcardiac electrophysiology. Rosenbaum MB, Elizari MV, eds.Martinus Nijhoff 1983: 773-97.

[22] -Rodriguez LM, De Chillou C, Schlapfer J et al. Age at onsetand gender of patients with different types of supraventriculartachycardias. Am J Cardiol 1992; 70: 1213-15.

[23] Green M, Heddle B, Dassen W et al. The value of QRSalteration in diagnosing the site of origin of narrow QRSsupraventricular tachycardia. Circulation 1983; 68: 368-73.

Eur Heart J, Vol. 17, Suppl C 1996

Dow

nloaded from https://academ

ic.oup.com/eurheartj/article/17/suppl_C

/10/484700 by guest on 04 February 2022


Recommended