Wolff-Parkinson-White syndrome

Fundamentals of clinical cardiology

Wolff-Parkinson-White

syndrome

Koo- Young Chung, M.D.* Thomas J. Walsh, M.D., F.A.C.C.** Edward Make, F.A.C.C., F.A.C.P.*** St. Louis, MO.

T

he Wolff-Parkinson-White (WPW) syndrome was first recognized as a clinical entity by Wolff, Parkinson and White’ in 1930. The electrocardiographic findings that were later considered to be characteristic of this syndrome were described initially by Wilson2 in 1915, and by Wedd3 in 1921. This syndrome can be diagnosed only by the electrocardiogram or vectorcardiogram, since, in the last analysis, the diagnosis rests on the finding of a short P-R interval and prolonged QRS interval due to a delta-wave in the electrocardiogram ; the latter corresponds to the conduction delay and abnormal inscription of the initial portion of the QRSsl? loop in the vectorcardiogram. Patients with this syndrome are predisposed to recurrent episodes of paroxysmal ectopic tachycardias.1B4-12 The purpose of this paper is to review the previous literature concerning the WPW syndrome, with particular emphasis placed on the occurrence of specific types of ectopic tachycardia in this syndrome and the related electrocardiographic and vectorcardiographic findings. Forty cases of the WPW syndrome collected from the Heart Station and Cardiovascular Laboratories of Barnes Hospital will also be discussed. From

General

consideration

WPW syndrome has been known as a benign syndrome, and there are no subjective manifestations or hemodynamic disturbances resulting from ventricular pre-excitation itself.r3 However, paroxysmal tachycardia, which tends to be associated with this condition, may come at any time (during rest, exercise, or emotional difficulty, or as a manifestation of allergy’“) and may begin at birth or during infancy, childhood, or adult life.6 Sixty to 70 per cent of the cases of WPW syndrome have been found in healthy individuals without organic heart disease.4,7,8J5J6The incidence of the WPW syndrome is difficult to evaluate because ventricular pre-excitation itself does not produce symptoms unless paroxysmal ectopic rapid heart action develops. Consequently, electrocardiograms are not usually taken in the majority of asymptomatic individuals with WPW syndrome. Frequently, ventricular pre-excitation is found incidentally in electrocardiograms taken for other reasons in later decades. The incidence of the WPW syndrome has been estimated to be 1.5 per 1,000 patients by Hejtmancik and Herrmann,15 and 0.16 per cent in 67,375 subjects by Averill”; there were only 6 cases among

the Department of Medicine, Washington University School of Medicine, and the Heart Station and the Cardi+ vascular Laboratory, Barnes Hospital, St. Louis. MO. Received for publication June 25. 1964. *Fellow. National Institutes of Health. Present address: Meharry Medical College, Nashville, Tan., 37208. **Assistant Professor of Clinical Medicine. ***Associate Professor of Clinical Medicine.

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5,000 patients, as reported by Manning,18 and only 2 cases in 1,000 patients studied by Packard and associates.1g An incidence of 0.056 per cent was found by 0hnell,20 and the WPW syndrome was observed in 80 of 50,000 cases reviewed by Katz and Pick.’ The syndrome occurs more frequently in men than in women, with an incidence of between 54 and 70 per cent in males in the various series which have been published.10J6~20 A relatively high incidence of thyrotoxicosis in the WPW syndrome has been reported by different observers 12*21-24and Master and associates23 repdrted that the WPW syndrome disappeared after thyroidectomy was performed to control hyperthyroidism. Lepeschkin22 found thyrotoxicosis in 6 per cent of the patients with the WPW syndrome, and stated that the WPW syndrome became manifest as a result of adrenergic preponderance due to hyperthyroidism. Theory and mechanism: of WPW syndrome and associated tachycardias

There are different theories in regard to the mechanism of the WPW syndrome and the occurrence of various arrhythmias in this syndrome. It is generally agreed that premature activation of a portion of the ventricular myocardium is responsible for the short P-R interval, the early onset of the QRS deflection with initial slurring (delta-wave), and the resultant widening of the ventricular complex characteristic of this condition. In Group A, the premature activation probably occurs in the left ventricle, and in Group B, the premature excitation occurs in the right ventricle.13*2!5The most acceptable theory at the present time is that involving conduction over an accessory pathway.5-9J3s26-30 Holzmann and Scherf30 and Wolferth and Wood2r postulated the bundle-of-Kent theory and demonstrated an anomalous A-V muscular bundle (in patients who had this condition) similar to that described by Kent3’ in 1893. This theory was further supported by the experimental reproduction of the entire syndrome6J3c32 and was also proved anatomically by autopsy findings in patients with the WPW syndrome.6J3~20~32J3 Pick13 stated

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that anatomic demonstration of an A-V bypass was accomplished in over half of the cases examined. A muscular communication in the right A-V orifice was proposed by Kent,31r34*36 and later by Wolff and associates,‘J3 and a communication between the A-V node and ventricular musculature was observed by Segers and associatesa and Scherf and Schonbrunner.36 6hnellz0 noted a muscular connection between the left atrium and left ventricle which was thought to be congenital,6*gJ3and possibly hereditary,13~20~37-39 since this syndrome was found in infants,7J3,25,40-42 occasionally in premature infants9 and sometimes was associated with other cardiac malformations.13~20~z8~33~43-50 This syndrome has also been observed in several members of one family.13*20~25~37-39 Rosenbaumr3 pointed out that there may be more than a single anomalous pathway in the WPW syndrome. In support of this possibility, we have also noted several different kinds of QRS complexes with anomalous A-V conduction and different QRSsl? loop configurations in the same patient. 51Pick13stated that an anomalous bypass of the A-V node must be present in WPW syndrome, since otherwise one could not explain either the occurrence of predominantly supraventricular tachycardias nor the persistence of pre-excitation complexes during atria1 fibrillation. With regard to the mechanism proposed as the explanation of the rapid ectopic tachycardias which occur in the WPW syndrome, the re-entry phenomenon has been postulated by different authors.5*7-9 In paroxysmal atria1 tachycardia and A-V nodal tachycardia, a paroxysm of rapid heart action may be precipitated by passage of the ectopic atria1 or A-V nodal impulse downward through the A-V node and its subsequent return to the atria or A-V node via the accessory pathway, thus constituting a form of re-entry.s The paroxysmal tachycardia will persist if the re-entry phenomenon is repetitive. Consistent with this explanation is the fact that, in general, the last ventricular beat preceding the onset of an atria1 or nodal tachycardia or atria1 fibrillation, and also the ventricular complexes during the period of tachycardia, particularly in paroxysmal atria1 tachycardia, are

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usually not of the pre-excitation type.” In paroxysmal atria1 fibrillation or flutter, the above-mentioned re-entry phenomenon alone is not a satisfactory explanation of the mechanism, since impossibly high ventricular rates would have to be assumed. However, some investigators*,g have postulated that the mechanism initating the parosysm may be re-entry, but that the impulse is returned to the atria very early. If it arrives during the partial refractory or “vulnerable” period of the atria, the re-entry impulse may cause onset of atria1 fibrillation or flutter. During these arrhythmias, a rapid, almost constant, stream of atria1 impulses passes down either the accessory bundle or the A-V node and bundle branch system, depending upon which is less refractory at time of onset of the tachycardia. Normally conducted or pre-excitation QRS complexes may be seen in atria1 fibrillation, flutter, or paroxysmal atria1 tachycardia in the WPW syndrome, since the impulse may be conducted through either normal or accessory pathways. The impulse in atria1 fibrillation may arrive at the A-V node at a rate faster than the normal A-V pathway is capable of conducting, since more rapid ventricular rates in atria1 fibrillation or flutter in the WPW syndrome show, in general, anomalous QRS complexes with delta-waves5 although this phenomenon is not always present. From the foregoing observations, one is justified in assuming that both conduction systetns are capable of transmitting impulses. Another factor that favors the accessory-pathway theory is that Pick observed ectopic beats arising from the bypass fibers.y,13 Prinzmeta113 has proposed the theory of accelerated A-V conduction and has stated that the WPW syndrome could be acquired. The evidence in support of his concept is incomplete and inconclusive.8’r3 For that matter, it is not logical to expect more rapid A-V conduction in diseased specialized conducting tissue than in the normal, when in reality the reverse occurs clinically, as is often observed in the case of rheumatic myocarditis or acute myocardial infarction. The theory of an ectopic focus in the right septal mass was proposed by Sodi-Pallares,13 and extrasystoles resembling pre-escitation beats were pro-

duced experimentally bye him. However, Pick was critical of the afore-mentioned experimental study because he believed that the rhythm and beats produced represented an artificial A-V dissociation, although an irritable ectopic center of impulse formation may be adequate to esplain the occurrence of the ectopic tachycardias.6 Material

and

method

The study seriesconsists of vectorcardiograms recorded from 40 patients whose electrocardiograms were considered to be diagnostic according to the criteria currently accepted by the authors, which are as follows: (1) short P-R interval of 0.12 second or lessin most of the cases; (2) QRS interval between 0.09 and 0.16 second; (3) initial slurring (delta-wave) of the QRS deflection occurring on its ascending limb if the major deflection is upward, or on its descending limb if the major deflection is downward ; (4) secondary S-T segment and T-wave changes in the majority of cases; (5) a predisposition to paroxysmal ectopic tachycardia. In addition, the configuration of the QRS deflection in the precordial leads divides the Wolff -Parkinson-White syndrome into two groups,13,26 as follows: In Group A, the premature component and the remainder of the QRS complex are primarily upright in both left and right precordial leads. In general, Lead V, shows R,RS,Rs, RSr’, and Rsr’ patterns, and Lead Vg shows Rs or R deflections. In Group B, the left precordial leads show tall R waves with delta-waves in all cases, and Leads Vr and Vs show delta-waves and QRS complexes which are usually resultantly negative. Thus, these leads show rS or QS patterns. The vectorcardiograms were displayed on the Sanborn Viso-Scope in the three standard planes, as follows: (1) horizontal, (2) right sagittal, and (3) frontal. They were recorded with the corrected lead system described by Frank.52 The method of Helm and FowlerS3 was used to determine the vectorcardiographic QRSsI?TsE angle. The orientation of the vectorcardiogram was expressed in terms of a reference frame divided into -30 degree segments in a counterclockwise

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Table I. Electrocardiographic and vectorcardiographic analysis of patients with Wolff-ParkinsonWhite syndrome Group’A

/

Group B

I

P-R

interval

(sec.)

0.08 0.09 O.ll0.13

or less - 0.10 0.12 or more

QRS

interval

(sec.)

0.10 0.11 0.13

or less - 0.12 or more

11 8 5

0.02 0.03 0.05 0 07

or less - 0.04 - 0.06 or more

3 11 7 3

Delta-wave

interval

Conduction

delay

Direction

Inscription

by ECG

by VCG

of delta-wave

of QRSsl?

(sec.)

0.02 or less 0.03 - 0.04 0.05 - 0.06 Entire efferent

(sec.)

(initial

3 5 6 2

vector)

Ant. Ant. Ant. Ant. Post. Post.

Sup. Inf. Sup. Inf. Sup. Inf.

Left Left Right Right Left Left

H

loop

angle

(degree)

0 31 61 91 121 1.51

3 0 7 6 -

12 6 2 4

7 6 1 2 0 0

c/cc cc cc/c QRSsf?-Ts#?

2 5 3 6

limb

C

Spatial

2 12 7 3

30 60 90 120 150 180

s 7 5 3 1 3 6 3 0 3 1

F

H

S

F

8 3 2 3

1 2 17 4

15 4 2 3

4 2 17 1

1 3 2 3 9 6

C: Clockwise.C/CC: Clockwisein e&rent limb and counterclockwisein afferentlimb. CC: Counterclockwise. CC/C: Counterclockwise in efferentlimb and clockwisein afferentlimb. H: Horizontal. S: Sagittal. F: Frontal.

direction and +30 degree segments in a clockwise direction from 0 to 180 degrees. Thus, 0 degree in the reference frame is situated to the left (the observer’s right) in the frontal and horizontal planes, and anteriorly in the right sagittal plane; +90 degrees is located inferiorly in the frontal and sagittal planes and anteriorly in the horizontal plane. The hospital charts of all 40 patients in this series were reviewed. Twenty nine of the subjects were males, and 11 were females. The ages of these patients varied between 4 and 79 years.

Results

Table I summarizes the electrocardiographic and vectorcardiographic findings of the 40 patients whose electrocardiograms were considered to be compatible with the diagnosis of ventricular preexcitation. Sixteen electrocardiograms and vectorcardiograms exhibited the Group A ventricular pre-excitation pattern, and 24 showed the Group B variety. Electrocardiographicfindings. P-R INTERVAL. The P-R intervals in the 40 electrocardiograms varied between 0.06 and 0.14 second, with those of Group B

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showing shorter P-R intervals than those of Group A. The majority of the 40 cases had intervals between 0.09 and 0.12 second. The P-R intervals were 0.13 second or more in 5 of our cases, the longest interval being 0.20 second without any demonstrable disease. Similar cases have been reported both in healthy4~g~54 and diseased hearts.44s55The P-R intervals were 0.12 second or less in 3.5 cases (87.5 per cent) of our series, which is somewhat similar to the findings in Wolff’s study.6 QRS INTERVAL. The QRS intervals of the 40 electrocardiograms varied between 0.08 and 0.16 second on the whole. The QRS intervals in the Group B tracings generally were shorter than those in the Group A electrocardiograms; 11 of the 24 Group B casesrevealed QRS intervals of 0.10 second or less. The QRS intervals were 0.10 second or less in 13 cases (32.5 per cent) of our series, which is similar to what Grant and associates2greported. It was interesting to note that about half of the Group B cases showed normal QRS intervals with deltawaves, whereas the majority of Group A electrocardiograms showed prolonged QRS intervals with delta-waves. All electrocardiograms DELTA-WA4VE. showed some degree of slurring of the initial portion of the QRS complexes, with delta-wave durations varying between 0.02 and 0.08 second. The usual value of the pre-excitation interval was between 0.03 and 0.06 second. QRS COMPLEX CONFIGURATION. In Group A, the majority of electrocardiograms showed R, Rs, or RS patterns in Lead VI, and Rs or R complexes in Lead VS. In Group B, the majority of records showed a QS or rS pattern in Leads Vi, and an R wave in Lead V6 in all cases. Vectorcardiographic findings. The WPW syndrome has been studied vectorcardiographically by a number of different authors.8~2g~44~56-63 The over-all results of our vectorcardiographic study are presented in Table I and Fig. 1. The vectorcardiograms of the 40 patients comprising the study series were divided into Groups A and R, according to the characteristics of the QRSsl? 10op.l~,?~There were 16 patients with Group -4 vectorcardiograms, and 24 patients with Group B vectorcar-

diagrams. It should be noted that the values for range in orientation of the mean vectors are intended to be read in a clockwise direction in the appropriate reference frame. INITIAL CONDUCTION DELTA VECTOR* OF THE

DELAY QRS&

AND LOOP.

THE

The initial conduction delay was much more marked in Group ,L\ than in Group B. Six of the 16 Group A cases showed conduction delay involving the entire efferent limb. The initial conduction delay was less than 0.03 second in half of Group B, whereas such a finding was made in only 2 cases of Group ,4. It is interesting to note that there was a discrepancy in the duration of the conduction delay betlveen the electrocardiographic and vectorcardiographic findings, as shown in Table I. The delta vector* was directed anteriorly, either superiorly or inferiorly, and to the left in the majority of cases (26 patients) in both groups. Less than one half of the Group B vectorcardiograms had deltawaves directed posteriorly and to the left and either superiorly or inferiorly. PLANAR

QRS

LOOPS.

1. Horizontal QRS loop: The maximal mean instantaneous QRS vector was oriented between +18 and +90 degrees (average +47 degrees) in Group A, and between -55 and +38 degrees (average - 8 degrees) in Group B. 2. Right sagittal QRS loop: The maximal mean instantaneous QRS vector varied widely, ranging between - 125 and +75 degrees (average +4 degrees) in Group A, and between + 15 and - 15 degrees (average +175 degrees) in Group B. 3. Frontal QRS loop: The maximal mean instantaneous QRS vector ranged between - 120 and +72 degrees (average +5 degrees) in the Group A cases, and between -45 and +40 degrees (average +5 degrees) in Group B cases. The average orientation of the maximal QRS vector in the horizontal plane was quite different in both groups, but the average orientation of the maximal QRS vector in the frontal plane in the two groups was the same. INSCRIPTION

OF THE QRS&

1. Horizontal *Tk

delta vectrlr initial segment

1.001'.

plane: The QRSsl? loop

was measured as the terminal vector of the QRS loop showing conduction

of the

delay.

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GROUP A (16 Cotasl

t-37* ttc4izonlol

Right Sagittol

Frontal

GROUP B (24 Cases1

l

ORS loop maximal

0

Fig. 1. Distribution vectors in Groups

FfOllkll

Right Sogittot

Horizontal

1 twp

moximd

vector vector

4 ---b

Av. 0% Av. T

of individual average orientations B of the Wolff-Parkinson-White

A and

in the horizontal projection was inscribed counterclockwise either in its entirety or in the efferent limb in the majority of cases in both groups (13 of 16 cases in Group A, and 21 of 24 cases in Group B) (See Table I). 2. Right sagittal plane: The majority of cases showed clockwise inscription of either the entire loop or of the efferent limb in both groups (12 of 16 cases in Group A, and 19 of 24 cases in Group B). 3. Frontal plane: The QRSsl? loop in the frontal projection was inscribed clockwise in Group A (8 of 16 cases) and counterclockwise in Group B (17 of 24 cases). The QRSsl? loop showed a figure-ofeight inscription in at least two planes (clockwise in the efferent limb and counterclockwise in the afferent limb, or vice versa) in about one half of Group A cases, but in only one fourth of Group B cases.

loop maximal vector loop maximet vcctol

of the maximal syndrome.

PLANAR

mean

QRS

and T

T LOOPS.

1. Horizontal T loop: The maximal mean T vector was discordant to the maximal mean QRS vector in most of the cases in both groups. It lay between - 145 and + 70 degrees (average - 37 degrees) in Group A cases, and between -30 and - 125 degrees (average +133 degrees) in Group B cases. 2. Right sagittal T loop: The maximal mean T vector had a wide range of orientation in both groups, just as was the case with the maximal vector of the right sagittal QRS loop. The average orientation of the maximal mean T vector was +106 degrees in Group A and +45 degrees in Group B cases. 3. Frontal T loop: The maximal mean T vector was discordant to the maximal mean QRS vector, as in the horizontal plane, and it lay between 0 and - 120 de-

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Fig. 2. Typical Group B WPW syndrome .shown vectorcardiographically and electrocardiographically. The QRSsfi loop is displaced posteriorly, inferiorly, and to the left. There is marked conduction delay in the entire efferent limb of the QRSsfi loop. The Tsi? loop is 180 degrees discordant to the QRSsE loop, and an ST vector is also present. The lower two lead strips show paroxysmal atria1 tachycardia (PAT) with a rate of 223 per minute. Sote that the QRS complex during the PAT exhibits no anomalous A-V conduction.

grees (average +87 degrees) in Group A and between +55 and - 140 degrees (average +133 degrees) in Group B. SPATIAL QRSS&-T& ANGLES. Group B vectorcardiograms presented wider spatial QRSsl?Tsl? angles than did the Group A vectorcardiograms. In the majority of Group B cases (20 of 24) the angles exceeded 60 degrees, whereas in more than one half of the Group A cases (9 of 16) the spatial QRSsI?Tsii angle was less than 60 degrees. We have been unable to attach any clinical significance to the finding of a narrow QRS&-T& angle in the Group A cases, or to a wider angle in the Group B cases. The vectorcardiographic findings in this study are somewhat different from those

encountered in our previous observations* or in the reports of other investigators,2gt44 probably because of the different lead systems utilized. Arrhythmias

It is a well-known fact that recurrent episodes of paroxysmal tachycardias1t4-‘” accompany the Wolff-Parkinson-White syndrome in a high percentage of cases. Wedd3 first called attention to the occurrence of paroxysmal tachycardia in this syndrome in 1921. The frequency of tachycardia varies between 40 and 80 per cent in the reports of many different authors.6-8,12,‘3,15,1~ Our study showed an incidence of 70 per cent (29 of the 40 cases), which agrees with that of W01ff.~J~ The type of tachy-

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cardia in the Wolff-Parkinson-White syndrome is a rapid regular supraventricular tachycardia in the majority of cases.5:7-g*12 In our study, 24 (82 per cent) of 29 patients had paroxysmal atria1 tachycardia (Figs. 2,3, and 4). The incidence and types of paroxysmal ectopic tachycardias are summarized in Table II.. There were additional patients with histories of unobserved episodes of rapid heart action, that may or may not have been ectopic tachycardia, but these were excluded from this series since we were interested only in documented or observed tachycardias. Atria1 fibrillation and atria1 flutter were rather u’ncommon in our experience8s5’ in cases of the Wolff-Parkinson-White syndrome, although these arrhythmias have been reported by others.1J-g~36,56~64 If atria1 fibrillation or flutter occurs, it is frequentl-y associated with rheumatic heart disease5~7~g~64 However, atria1 fibrillation with rapid ventricular response can occur in the WPW syndrome without any organic heart disease1s65; this was the case in one of the partients in our series. Atria1 flutter

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is encountered far more rarely in the WPW syndrome than is atria1 fibrillation.5v7-g*37 In our study, 4 patients (13.7 per cent) had atria1 fibrillation, and their electrocardiographic and vectorcardiographic patterns belonged in Group A (Fig. 5 and Table II). One of the 4 patients had rheumatic heart disease in addition to the WPW syndrome. There was no significant difference in the incidence of the tachyTable II. The occurrence of various arrhythmias in the Wolff-ParkinsonWhite syndrome I

Arrhythmia Paroxysmal atria1 tachycardia Atria1 fibrillation Atria1 flutter Ventricular premature contraction Nodal premature contraction Ventricular parasystole Atria1 parasystole

1 Group

A / Group

B

10 4 1

14 0 0

0

1

2 0 1

2 1 0

Fig. 3. The first portion of the upper strip of Lead II shows paroxysmal atria1 tachycardia with a rate of 140 per minute, and then the rhythm is converted by carotid sinus stimulation to sinus rhythm with anomalous A-V conduction, which was seen prior to the onset of the paroxysm of tachycardia. The QRS complex during the tachycardia is different from the QRS complex during sinus rhythm, in that it is wide and bizarre, a finding which may represent ordinary aberrant ventricular conduction (This case was previously presented in electrocardiographic form in Clinical Vectorcardiography and Electrocardiography by Edward Massie, M.D., and Thomas J. Walsh, M.D., Chicago, 1960, The Year Book Publishers, Inc.)

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aVR

aVF

Fig. 4. The vectorcardiogram (-4) and electrocardiogram (B) display Group B ventricular pre-excitation. There is marked conduction delay in the entire efferent limb of the QRSsfi loop. The Tsf? loop is 180 degrees discordant, and there is an ST vector. The lead strips in Cand D were taken on different occasions in this patient. The leads in C show paroxysmal atria1 tachycardia (PAT’) with a rate of 170 per minute and normal QRS complexes without anomalous conduction. The tracings in D demonstrate PAT with a slightly faster rate (175 per minute) than that in C, and the QRS complex is markedly aberrant.

cardia between Group A and Group B patients. The ventricular rates in the entire group with ectopic tachycardias varied between 160 and 200 per minute. Only one of our series had atria1 flutter (with 2:l atrioventricular response) (Fig. 6). This 58-year-old patient had arteriosclerotic heart disease; his electrocardiogram and vectorcardiogram presented the findings of Group A. A similar case has been reported previously.37 None of the Group B patients showed atria1 fibrillation or flutter (see Table II). It is impossible to evaluate the true incidence of atria1 flutter or fibrillation in the two groups (A and B) of the Wolff-Parkinson-White syndrome in the literature, since the majority of case reports fail to show precordial leads or vec-

torcardiographic findings that permit one to determine the group type. The QRS complex during paroxysmal tachycardia in the WPW syndrome is normal in the majority of cases of regular supraventricular tachycardia7~8J1J2~66 (see Fig. Z), although there are exceptions6~‘2~15*L6J7~40 (see Figs. 3 and 4); this is particularly true in atria1 fibrillation (see Figs. 5 and 7) or atria1 flutter1*5s6J6J’6,64 (see Fig. 6), in which the QRS deflection may simulate ventricular tachycardia.5*7,8@ Paroxysmal atria1 tachycardia with anomalous A-V excitation was reported by Rosenbaum.66 Scherf and Schonbrunner36 were the first to point out the occurrence of wide QRS complexes during paroxysmal atria1 fibrillation or flutter. Although the occurrence of ven-

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tricular tachycardia in the WPW syndrome has been reported by several observers,36s67-11 we have been unable to find a single unequivocal case of the arrhythmia in the WPW syndrome. Wolff4 has stated that the most likely diagnosis of the arrhythmias in these reports was rapid atria1 fibrillation or flutter with anomalous conduction instead of ventricular tachycardia (see Figs. 5 and 7). Ordinary aberrant ventricular conduction without anomalous conduction may occur in paroxysmal atria1 tachycardia5J6 (see Fig. 3), atria1 fibrillation (see Fig. S), or atria1 flutter because of the ra.pid rate. This aberration of the

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QRS complexes may occasionally simulate ventricular premature beats or ventricular tachycardia. 6.67,6gFig. 5 is a good example of atria1 fibrillation with rapid ventricular response (rate between 170 and 270 per minute), with marked aberrant ventricular conduction producing QRS complexes of a form different from that of those seen during sinus rhythm with the Wolff-ParkinsonWhite syndrome. These ventricular deflections closely resemble ventricular tachycardia in some portions of the electrocardiogram. The occurrence of more than one type of abnormal ventricular complex in different paroxysms of rapid heart action

Fig. 5. The vectorcardiogram (A) and electrocardiogram (B) show the Group A WPW syndrome. The lower two tracings (C) are continuous strips of Lead II during paroxysmal atria1 fibrillation with a rate of 170 to 270 per minute. In these strips, there are many different forms of QRS complexes. Some portions of Lead IIb show a very rapid ventricular rate (2’70 per minute) with marked aberrant ventricular conduction of the ventricular deflection which differs from the QRS complexes of the anomalous beats. These areas resemble ventricular tachycardia but probably are the result of markedly exaggerated anomalous A-V conduction. (Some QRS complexes, such as the second, ninth, and twenty-seventh beats of Lead I Ia, and the thirtieth beat of Lead I Ib, aresimilar to the QRS complexes during normal sinus rhythm.) The QRS complexes in the mid-portion of Lead IIa show normal QRS complexes without anomalous A-V conduction. The occurrence of QRS complexes of various configurations indicates that the impulses travel through the normal A-V pathway and/or the anomalous A-V pathway,

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Fig. 6. The vectorcardiogram and electrocardiogram drome. There is conduction delay in the initial 0.03 is almost 180 degrees discordant to the QRSsl? loop. tion, best seen in Lead VI. The atria1 rate is about paroxysms are similar to the QRS complexes during

has been observed previously,‘-6*g,21 and one example is shown in Fig. 4. In this figure, two tracings taken at different times show two different QRS complexes occurring with very similar rates in a case of paroxysmal atria1 tachycardia associated with the Wolff-Parkinson-White syndrome. Different kinds of atria1 arrhythmias (paroxysmal atria1 tachycardia, atria1 fibrillation, and atria1 flutter) have been observed on different occasions in the same individual who had the WPW syndrome.7fg Paroxysmal tachycardias in association with the Wolff-Parkinson-White syndrome have a much higher incidence in infants and young children than in adults, and usually they are very rapid regular supraventricular tachycardias.7,25a4n-42 Isolated nodal premature beats or nodal escape beats with normal QRScolnpleses,‘3,??,66,72-7”

(A and B) exhibit the Group .A WP\Y synsecond of the QRSsl? loop, and the Tsfi loop C shows atria1 flutter with 2:l A-V conduc400 per minute. (The QRS complexes during sinus rhythm.)

as well as with anomalous A-V conduction,7v26,75 have been reported in the WolffParkinson-White syndrome. In our series, there were 4 cases of nodal premature beats, and all showed normal QRS complexes. The occurrence of ventricular premature beats in the WPW syndrome has been reported,6J7*76 and one of our patients, a young healthy individual, presented continuous ventricular bigeminy and intermittent atrioventricular nodal rhythm (Fig. with atrioventricular dissociation &A). We found one ventricular parasystole (Fig. 8,B) in an elderly individual who had coronary heart disease associated with the Wolff-Parkinson-White syndrome, and this has been reported by others.7.13,15,17.77 One atria1 parasystole (Fig. 8,C) was also found in an elderly woman who had breast cancer and mild arteriosclerotic heart

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disease, and this is a rare combination in so far as we can ascertain. Ventricular parasystole, in general, occurs once in 900 to 1,200 (0.1 per cent) routine electrocardiograms ta.ken in a general hospital,7sr7g whereas the Wolff-Parkinson-White syndrome has an incidence of 0.15 to 0.2 per cent.7J6J7-1g Therefore, the combination of parasystole and the Wolff-ParkinsonWhite syndrome is very rare indeed. Various other arrhythmias, such as first-degree4 and second-degree A-V block 13,28,73,80-82complete atrioventricular dlo~k,~~ and atrioventricular nodal rhythm,8‘i have also been reported. Effect of drugs and other procedures on WPW syndrome and associated arrhythmias

If patients with the WPW syndrome develop paroxysmal tachycardia, they may require urgent medical treatment, and the paroxysm almost always induces congestive heart failure in infancy, early childhood,41 or in older patients with heart involvement. About one half of the patients in our series did not require any medical treatment for their paroxysmal tachycardia. In the remainder, quinidine (sometimes Pronestyl) or digitalis or a combination of the drugs, carotid sinus pressure, and atropine were used in the various arrhythmias associated with the WPW syndrome. Hejtmancik and associate+ reported 80 cases of paroxysmal tachycardia with the WPW syndrome, and in ,most of their patients the rapid ectopic tachycardia reverted spontaneously to sinus rhythm. WolfF2 observed that most of the ectopic tachycardias ended spontaneously, or as a result of the patient holding his breath, lying down or vomiting, or by stimulation of the c:arotid sinus or the use of drugs. Various medications, such as digitalis, quinidine, Pronestyl, acetylcholine, neostigmine, atropine, amyl nitrite, potassium salts, or any combination of these preparations, have been employed in the treatment of the ectopic tachycardias associated with the WPW syndrome.4~12~17*2L~84 However, the drugs are not always effective in the treatment of rapid heart action, and this is not surprising, since the underlying pathophysiology of the syndrome is not

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completely settleds4 and the effect of antiarrhythmic agents may vary in the presence of various types of myocardial and conduction abnormalities.86 Digitalis. Digitalis is the drug of choice in the treatment of regular paroxysmal supraventricular tachycardias, since it predominantly depresses the normal conduction system,5 that is, it is capable of prolonging or completely blocking conduction in the A-V node and bundle of His.5 There is some evidence that digitalis increases the excitability of the anomalous conduction system and may aggravate the arrhythmia.86v8’ Consequently, this medication usually fails to slow the rapid ventricular rate in atria1 fibrillation with WPW syndrome,5,11,12,*4,8*,89 Often, large dosesof digitalis are required for the treatment of rapid heart action and may induce digitalis toxicity, particularly in casesof refractory arrhythmias associated with the WPW syndrome.g0 Quinidine and procaine amide. In atria1 fibrillation, quinidine or procaine amide invariably causes the pre-excitation QRS complex to disappear, since it depresses conduction via the accessory pathway, thereby favoring normal A-V conduction without changing the transmission interva1.4t5v12Quinidine blocks the action of the vagus nerve on the heart, and its effect is similar to that of atropine, but less pronounced. Hejtmancik and associates*5treated successfully with intravenous injections of procaine amide 2 patients who had paroxysmal atria1 tachycardia associated with the WPW syndrome. It appears that the best results are achieved by giving digitalis and quinidine (or, occasionally, procaine amide) simultaneously for paroxysmal ectopic tachycardia associated with the WPW syndrome, particularly in the case of atria1 fibrillation or flutter.7-g Carotid sinus stimulation. Carotid sinus pressure can abolish the ventricular preexcitation*2~21 or, in occasional instances, may cause it to appear.‘J3r2i When carotid sinus pressure is applied in the presence of WPW syndrome, it can produce an A-V nodal rhythm with a normal QRS complex,gO since the vagal stimulation tends to prolong A-V conduction time or temporarily block the normal pathway and dis-

128

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Am. He& I. Jawary. 19h5

Fig. 7. Electrocardiogram A presents typical Group iz ventricular pre-excitation, and B exhibits atria1 fibrillation with rapid ventricular response (rate varies between 180 and 230 per minute). The QRS complexes during the paroxysms of rapid ventricular response predominantly demonstrate exaggerated anomalous conduction. Some QRS complexes, such as the third beat of Lead I, the twelfth and thirteenth beats of Lead II, the eleventh and thirteenth beats of Lead III, and the tenth and eleventh beats of Lead aVR, show a normal configuration without anomalous conduction. This is a very common finding before and/or after the onset of paroxysmal tachycardia in the WPW syndrome.

place the pacemaker from the S-A node to the A-V node.4 Pick and Katz9 observed that, in one patient with paroxysmal atria1 tachycardia with 1 :l conduction associated with the WPW syndrome, carotid sinus pressure induced paroxysmal atria1 tachycardia with varying A-V response, which subsequently changed to atria1 flutter and finally to atria1 fibrillation. One of the patients of our serieswho had paroxysmal atria1 tachycardia in association with the WPW syndrome (Fig. 3) was unaffected by a combination of digitalis and quinidine, but responded very well when carotid sinus stimulation was added. Exercise. Exercise may re-establish normal A-V conduction, since the abnormal pathway is usually unable to function above a critical heart rate.Y0

Wolff13 reported the disappearance of the WPW syndrome when exercise raised the heart rate to 120 to 140 per minute, whereas, Sanghvi 84 found that exercise caused WPW conduction in successive beats in one case. Sandberg,g1 in a study of 28 cases of WPW syndrome,? found that 10 patients were transitorily affected by exercise in variable fashion. Various other drugs. The administration of atropine has been commonly used to produce normal conduction in cases of WPW syndrome.13t17The development of A-V dissociation after the administration of atropine in WPW has been reported.‘? Belletgo observed that antithyroid drugs and Ii31 may be effective in some refractory cases of paroxysmal tachycardia with the WPW syndrome. In addition, neostigmine, acetylcholine, amyl nitrite, and potassium

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salts may abolish the tachycardia.gO Fisch and associatesg2 have used external countershock successfully for supraventricular tachycardia associated with WPW syndrome, and, in light of present knowledge, it appears to be advisable to apply this form of therapy when urgent treatment is needed. Prognosis

The prognosis of uncomplicated WPW syndrome is generally good, unless rapid heart action occurs very frequently and

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the episodes are long in duration. Paroxysmal tachycardia may produce diminished mental alertness, lossof consciousness,and, in patients with underlying coronary heart disease, episodes of coronary insufficiency which require urgent medical attention. Sudden death during or after the episode of tachycardia has been reported,4*6J3J5,21 and the paroxysm itself may frequently cause congestive heart failure,35r42*44 and sometimes irreversible changes in the heart.g0 The occasional occurrence of tachycardia

-.-. _“II ;.t..

:

..GVR

Fig. 8. Parts A, B, and C are tracings from three different patients. A, This electrocardiogram* illustrates ventricular pre-excitation with frequent ventricular premature beats producing ventricular bigeminy and an intermittent A-V nodal rhythm (the eleventh, thirteenth, and fifteenth beats of Lead I; the first, third, fifth, and seventh beats of Lead II), causing A-V dissociation. (*Modified from Fig. 345, page 493 in Clinical Vectorcardiography and Electrocardiography by Edward Massie, M.D., and Thomas J. Walsh, M.D., Chicago, 1960, The Year Book Publishers, Inc.) B, Leads Vaa and Vab are continuous. These strips show ventricular pre-excitation with intermittent ventricular parasystole. The rate of the parasystole is 37 per minute. There is a ventricular fusion beat (marked FB). C, This tracing displays ventricular pre-excitation with intermittent atria1 parasystole. Note that the ventricular complexes of the parasystolic beats also show anomalous A-V conduction. The rate of the atria1 parasystole is 52 per minute.

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in individuals who have a normal heart and the WPW syndrome has no significant effect on the cardiovascular system, so that these persons usually lead normal active lives.87 The prognosis is almost always serious when the syndrome occurs during infancy or early childhood, or in adults with heart involvement when the attack of tachycardia is refractory to therapy and complications ensue. Summary

and

conclusions

Previous literature concerning the WPW syndrome has been reviewed. In addition, 40 of our caseshave been studied in detail, with particular emphasis on the occurrence of various arrhythmias and vectorcardiographic analysis. No difference was found in the incidence of regular supraventricular tachycardia (paroxysmal atria1 tachycardia) between patients with Group A ventricular pre-excitation and those with Group B type, but atria1 fibrillation or flutter was found only in Group A patients. There was a significant difference in both groups between the duration of the initial portion of conduction delay in the electrocardiogram and that in the vectorcardiogram. In addition, Group A electrocardiograms and vectorcardiograms tended to show more marked initial conduction delay. The spatial QRSsl?-TsE angle was much narrower in Group A (less than 60 degrees) than in Group B vectorcardiograms. However, we have been unable to establish that either a narrow or wide QRSsl?-Tsl? angle has any clinical significance. There is much evidence to justify acceptance of the accessory-pathway theory as the mechanism of the Wolff-ParkinsonWhite syndrome and of the associated arrhythmias, but other theories have been discussed. The treatment of choice for paroxysmal supraventricular tachycardia in WolffParkinson-White syndrome is either digitalis or quinidine in the majority of cases, whereas atria1 fibrillation and atria1 flutter usually require a combination of both medications. External countershock seems to be an appropriate treatment when the patient’s condition is apparently deteriorating. Twenty-six patients (65 per cent) in

our series showed no evidence of organic heart disease, which is similar to the findings reported by others.15f16Most of the patients with organic heart disease were more than 45 years of age, and the majority of these had some evidence of arteriosclerotic heart disease and/or hypertensive cardiovascular disease. There were 4 other patients, including one who had mitral stenosis due to rheumatic fever (this patient had atria1 fibrillation with rapid ventricular response on many occasions), 2 with thyrotosicosis, and 1 with congenital heart disease (interatrial septal defect). One of the more interesting findings in this study was that 10 patients with the WPW syndrome (25 per cent) had psychiatric disorders (mainly manic-depressive psychosis). This finding may be a coincidental manifestation, since we cannot explain the reason for such an association, but a similar observation was described by Hejtmancik and associates15in 1957, and deserves further investigation. Two instances of the very rare combination of parasystole and Wolff-ParkinsonWhite syndrome have been described, and in so far as we are able to ascertain, the example of a combination of atria1 parasystole with the Wolff -Parkinson-White syndrome may be among the first such cases reported. VVe gratefully acknowledge the able technical assistance of Mrs. Edna Comfort, Mrs. Glenna Wissner, Mrs. Shirley Gonzalez-Rubio, and Miss Sandra L. Steinhauser. We are also indebted to the personnel of the Department of Illustration. REFERENCES 1. Wolff, L., Parkinson, J., and White, P. D.: Bundle branch block with short P-R interval in healthy young people prone to paroxysmal tachvcardia. AM.HEART7.5685.1930. 2. Wilson, F. N.: A case in which the vagus influenced the form of two ventricular complexes of the electrocardiogram, Arch. Int. Med. 16:1008, 1915. 3. Wedd, A. M.: Paroxysmal tachycardia, with reference to normotropic tachycardia and the role of the extrinsic cardiac nerves, Arch. Int. Med. 2757, 1921. 4. Wolff, L. : Anomalous atrioventricular excitation (Wolff-Parkinson-White syndrome), Circulation 19:14, 1959. 5. Langendorf, R., Lev, M., and Pick, A.: Auricular fibrillation with anomalous A-V excitation (WPW syndrome) imitating ventricular parox-

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ysmal tachycardia. A case report with clinical and autopsy findings and critical review of the literature, Acta cardiol. 7:241, 1952. Wolff, L.: Syndrome of short P-R interval with abnormal QRS complexes and paroxysmal tachycardia (W-P-W syndrome), Circulation 10:282, 1954. Katz, L. N., and Pick, A.: Clinical electrocardiography. I. The arrhythmias, Philadelphia, 1956, Lea & Febiger. Massie, E., and Walsh, T. J.: Clinical vectorcardiography and electrocardiography, Chicago, 1960. The Year Book Publishers, Inc. Pick, A., and Katz, L. N.: Disturbances of impulse formation and conduction in the preexcitation (W.P.W.) syndrome-Their bearing on its mechanism, Am. J. Med. 19:759, 1955. Wolff, L., and White, P. D.: The cardinal aspects of paroxysmal rapid heart action, New England J. Med. 226:640, 1942. Wolff, L.: The WPW syndrome, AM. HEART J. 63:284, 1962. Wolff, L., and White, P. D.: Syndrome of short P-R interval with abnormal QRS complexes and paroxysmal tachycardia, Arch. Int. Med. 28:446, 1948. Hecht, H. H., Kennamer, R., Prinzmetal, M., Rosenbaum, F. F., Sodi-Pallares, D., Wolff, L., Brooks, C., Pick, A., Rijlant, P., and Robb, J. S.: Anomalous atrioventricular excitation. Panel discussion, Ann. New York Acad. SC. 65:826, 1956. Clagett, A. H., Jr.: Short P-R interval with prolonged QRS complex: Allergic manifestation a.nd unusual electrocardiographic abnormality, AM. HEART J. 26:55, 1943. Heitmancik. M. T.. and Herrmann. G. R.: The electrocardiographic syndrome ‘of short P-R interval and broad QRS complexes: a clinical study of 80 cases, AM. HEART J. 54:708, 1957. Willus, F. A., and Carryer, H. M.: Electrocardiograms displaying short P-R intervals with prolonged QRS complexes: An analysis of sixty-five cases, Proc. Staff Meet. Mayo Clin. 21:438, 1946. Averill, K. H., Fosmoe, R. J., and Lamb, L. E.: Electrocardiographic findings in 67,575 asymptomatic subjects. IV. W-P-W syndrome, Am. J. Cardiol. 6:108, 1960. Manning, G. W.: Electrocardiography in the selection of Royal Canadian Air Force Aircrew, Circulation 10:401, 1954. Packard, J. M., Graettinger, J. W., and Graybiel, A.: Analysis of the electrocardiograms obtained from 1,000 young healthy aviators. Ten years follow-up, Circulation 16:384, 1954. Ohnell., R. F.: Pre-excitation. a cardiac abnormality, Stockholm, 1944, P. A. Norstedt and Loner. Wolff, L.: Electrocardiography. Fundamentals and clinical application, Philadelphia. 1956. W. B. Saunders Company, p. 250. . Lepeschkin, E.: Modern electrocardiography, Baltimore, 1951, Williams & Wilkins, pp. 3.53, 355, 361. Master, A. M., Jaffe, H. E., and Dack, S.:

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Atypical bundle branch block with short P-R interval in Grave’s disease, Mount Sinai Hosp. J. 4:100, 1937. Strong, J. A.: Thyrotoxicosis with ophthalmoplegia, myopathy, Wolff-Parkinson-White syndrome, and pericardial friction, Lancet 1:959, 1949. Harnischfeger, W. W.: Hereditary occurrence of the pre-excitation (Wolff-Parkinson-White) syndrome with re-entry mechanism and concealed conduction, Circulation 19:28, 1959. Rosenbaum, F. F., Hecht, H. H., Wilson, F. F. D.: The ootential variN.. and Tohnston. ations of the thorax and the esophagus in anomalous atrioventricular excitation (W-P-W syndrome), AM. HEART J. 29:281, 1945. Wolferth, C. C., and Wood, F. C.: The mechanism of production of short P-R intervals and prolonged QRS complexes in patients with presumably undamaged hearts; hypothesis of an accessory pathway of auriculoventricular conduction (bundle of Kent), AM. HEART J. 8~297, 1933. Scherf, D., Blumenfeld, S., and Mueller, P.: A-V conduction disturbance in the presence of the pre-excitation syndrome, AM. HEART J. 43:829, 1952. Grant, R. B., Tomlinson, F. B., and Van Buren, J. K.: Ventricular activation in the pre-excitation syndrome (Wolff-Parkinson-White), Circulation 18:355, 1958. Holzmann. M.. and Scherf. D.: iiber Elektrokardiogramme ’ mit verkvdrzter Vorhof-Kammer-Distanz and positiven P-Zacken, Ztschr. klin. Med. 121:404, 1932. Kent, A. F.: Researches on the structure and function of the mammalian heart, J. Physiol. 14:233, 1893. Wood, F. C., Wolferth, C. C., and Geckeler, G. D.: Histologic demonstration of accessory muscle connection between auricle and ventricle in a case of short P-R and prolonged QRS complex, AM. HEART J. 25:454, 1943. Segers, M., Sanabria, T., Lequime, J., and Denolin, H.: Le syndrome de Wolff-ParkinsonWhite. Mise en evidence d’une connexion A-V septale directe, Acta cardiol. 2:21, 1947. Kent, A. F. S.: Observations on the auriculoventricular junction of mammalian hearts, J. Physiol. 7:193, 1913. Kent, A. F. S.: The right lateral auriculoventricular junction of the heart, J. Physiol. 48:22, 1914. Scherf, D., and Schonbrunner, E.: Beitrage zum Problem der verkurzten Vorhof-KammerLeitung, Ztchr. klin. Med. 128:750, 1935. Campbell, M., and Turner-Warwick, M.: Two more families with cardiomegaly, Brit. Heart J. 8:393, 1956. Schiebler, G. L., Adams, P., Jr., and Anderson, R. C.: Familial cardiomegaly in association with the Wolff-Parkinson-White syndrome, AM. HEART I. 58:113. 1959. Soulie, P., di Matteo; J., Abaza, A., Nouaille, J., and Thibert, M. M.: Cardiomegalie familiale, Arch. mal. coeur. 50:22, 1957. Gleckler, W. J., and Lay, J. V. M.: WolffI

27.

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1.32

41.

42.

43.

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45.

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47.

48.

49.

50.

51. 52.

53.

54.

5.5.

56.

57.

58. 59.

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Parkinson-White syndrome and paroxysmal tachycardia in infancy, J.A.M.A. 150:683, 1952. Schieve, J. F.: Paroxysmal tachycardia in an infant with Wolff-Parkinson-White syndrome, Am. J. Dis. Child. 77:474, 1949. Kreidbere. M. B.. and Dushan. T. .A.: Paroxvsma1 au&lar tachycardia associated with Wolff-Parkinson-White syndrome in a newborn infant, J. Pediat. 43:92, 1953. Butterworth, J. S., and Poindexter, C. A.: Short P-R interval associated with a prolonged QRS complex. A clinical and experimental study, Arch. Int. Med. 69:437, 1942. Bleifer, S., Kahn, M., Grishman, A4., and Donoso, E.: Wolff-Parkinson-White syndrome; a vectorcardiographic, electrocardiographic and clinical study, Am. J. Cardiol. 4:321, 1959. Lev, M., Gibson, S., and Miller, R. -4.: Ebstein’s disease with Wolff-Parkinson-White syndrome. Report a case with histopathologic study of possible conduction pathways, AM. HEART J. 49:724, 1955. Bodlander, J. W.: Wolff-Parkinson-White syndrome in association with congenital heart disease, AM. HEART J. 31:785, 1946. Stein, M. H.: Wolff-Parkinson-White syndrome in case of congenital heart disease, AM. HEART J. 35:140, 1948. Kleiber, E. E.: Wolff-Parkinson-White syndrome with congenital heart disease, Pediatrics 4:210, 1949. Prinzmetal, M., Kennamer, R., Corday, E., Osborne, J. A., Fields, J., and Smith, L. A.: Accelerated conduction, New York, 1952, Grune & Stratton, Inc. Sondergaard, G.: The Wolff-Parkinson-White syndrome in infants, Acta med. scandinav. 145:386, 1953. Chung, K. Y., Walsh, T. J., and Massie, E.: Unpublished observation. Frank, E.: An accurate clinically practical system for spatial vectorcardiography, Circulation 13:736, 1956. Helm, R. A., and Fowler, N. O., Jr.: A simplified method for determining the angle between two spatial vectors, AM. HEART J. 45:835, 1953. Lamb, L. E.: Multiple variations of WPW conduction in one subject: Intermittent normal conduction and a false positive exercise tolerance test, Am. J. Cardiol. 4:346, 1959. Lepeschkin, E.: Observations on the mechanisms of the Wolff-Parkinson+White syndrome (WPW) and other types of pre-excitation, AM. HEART J. 37:646, 1949. Burch, G. E., and De Pasquale, N.: Electrocardiographic and vectorcardiographic detection of heart disease in the presence of preexcitation (W-P-W) syndrome, Ann. Int. Med. 54:387, 1961. Tranchesi, J., Gruimaraes, A. C., Texeira, V., and Pileggi, F.: Vectorial interpretation of the ventricular complex in Wolff-Parkinson-White syndrome, Am. J. Cardiol. 4:334, 1959. Duchosal, I’. W., and Sulzer, R.: La vertorcardiographie, Basle, 1949, S. Karger. Donzelot, E., Milovanovich, J. B., and Plavsic, C. : Vectographic spatiale frontale et horizontale

60.

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du syndrome de LVolff, I’arkinson, et W’hite. Arch. mal. coeur 8:781, 1949. Grishman, A., and Jaffe, H. L.: Spatial vectorcardiography : Wide QRS complexes with short P-R interval (the Wolf-Parkinson-White syndrome), J. Mt. Sinai Hosp. 18:208, 1951. Genohorsky, J.: Vector analysis of the W-P-W syndrome, Cardiologia 29:278, 1956. Friedberg, C. K.: Disease of the heart, ed. 2, Philadelphia, 1956, W. B. Saunders Company. Odier, JI, Montouchet, M., and Duchosal, P. W.: Etude spatiale de la compasante prematurCe dans le syndrome de Wolff-ParkinsonWhite, Cardiologia 30:182, 19.57. Laneendorf. R.: Auricular fibrillation with anomalous A-V conduction (W-P-W syndrome) imitating ventricular paroxysmal tachycardia, AM. HEART J. 37:645,-1949.. Cooke. W. T.. and White. P. D.: Auricular fibrillation foliowing the injection of acetylbeta-methyl choline chloride (Mecholyl) during an attack of paroxysmal auricular tachycardia or flutter, Cardiologia 4:313, 1940. Rosenbaum, F. F.: The nature of paroxysmal tachycardia in anomalous A-V excitation, AM. HEART J. 37:668, 1949. Levine, S. A., and Beeson, P. B.: The WolffParkinson-White syndrome with paroxysms of ventricular tachycardia, AM. HEART J. 22:401, 1941. Missal, M. E., Wood, D. J., and Leo, S. D.: Paroxysmal ventricular tachycardia associated with short P-R intervals and prolonged QRS complexes, Ann. Int. Med. 24:911, 1946. Arana, R., and Cossio, P.: Fibrilacion auricular y taquicardia ventricular coma eventualizidad posible en el P-R corto con QRS ancho y mellado, Rev. argent. de cardiol. 5:43, 1938. Palatucci, 0. A., and Knighton, J. E.: Short P-R interval associated with prolongation of QRS complex; a clinical study demonstrating interesting variations, Ann. Int. Med. 21:58, 1944. Klainer, M. J., and Joffe, H. H.: ,4 case of short P-R interval and uroloneed ORS complex with a paroxysm of ven%-ic&r tachyrardia, Ann. Int. Med. 24:920, 1946. Mallinow, M. R., and Langendorf, R.: Different mechanisms of fusion beats, AM. HEART J. 35:449, 1948. Fox, T. T., Weaver, J., and March, H. W.: On the mechanism of the arrhythmias in aberrant ventricular conduction (Wolff-ParkinsonWhite), AM. HEART T. 43507, 1952. Barker; J. M. : The unipolar electrocardiogram ; a clinical interoretation. New York. 1952. Appleton-Centur‘y-Crofts. Segers, M., Lequine, J., and Denolin, H.: L’activation ventriculaire precoce de certains coeurs hvperexcitables. Etude de l’onde de I’electroca;diogramme, Cardiologia 8:113, 1944. Fox, T. T.: Aberrant atrio-ventricular conduction in a case showing a short P-R interval and an abnormal but not prolonged QRS complex, Am. J, M. SC. 209:199, 1945: Eirhert. H.: Wolff-Parkinson-White svndrome simulating myocardial infarction, :\nn. Int. Med. 21:907, 1944.

k'ohmc 69 1

Wolf-Parkinson- White syndrome

Number

78.

79. 80.

81.

82.

83.

84.

Chung, K. Y., Walsh, T. J., and Massie, E.: Double ventricular parasystole, AM. HEART J. 67:162, 1964. Scherf, D., Yilid, M., and De Armas, D.: Atria1 parasystole, AM. HEART J. 57507, 1959. Levine, H. D., and Burge, J. C.: Septal infarction with complete heart block and intermittent anomalous atrio-ventricular excitation (Wolff-Parkinson-White syndrome). Histologic demonstration of a right lateral bundle, AM. HEART J. 36:431, 1948. Hoffman, I., Morris, M. H., Friedfeld, L., and Gittler, D.: Aberrant beats of Wolff-ParkinsonWhite configuration in arteriosclerotic heart disease, Brit. Heart J. 18:301, 1956. Coelho, F.: Nova contribuicao para o estudo sindroma de Wolff-Parkinson-White (W-P-W). Amatus Lusitanus 4:603, 1945. ’ ” Gottsegen, G., and Bodrogi, G.: On the mechanism of the W-P-W syndrome, Acta cardiol. 16529, 1961. Sanghvi, L. M., Banerjie, K. B., Misra, S. N., Wolff-Parkinson-White synand Bose, Ii.: drome. Report of a case with several types of P waves. varvine ORS contour and A-V nodal rhythm ‘with d&iation, Am. J. Cardiol. 4:341, 1959.

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Ask-Upmark, E.: Coarctatio aortae, Acta med. scandinav. 112:7, 1942. Fox, T. T., Travell, J., and Molorsky, L.: Action of digitalis on conduction in the svndrome of short P-R interval and prolonged ORS comolex. Arch. Int. Med. 71:206. 1943. Wolff, L.: \colff-Parkinson-White syndrome; historical and clinical features, Prog. Cardiovas. Dis. 2:677, 1960. Levine, S. A., and Curtis, A. N.: A case of ventricular tachycardia and auricular fibrillation. Unusual problem in therapy, AM. HEART J. 1:413, 19251926. Movitt, E. R.: Some observation on the syndrome of short P-R interval with long QRS, AM. HEARTJ.~~:~~, 1945. Bellet, S.: Clinical disorders of the heart beat, Philadelohia. 1963. Lea & Febieer. Sandberg, L.: The effect of exercise on the electrocardiogram of pre-excitation, Acta med. scandinav., Suppl. 365, 1961. Knoebel, S. B.. King, H., and Fisch, C.: Termination of supraventricular tachycardia complicating the Wolff-Parkinson-White syndrome with external countershock, Circulation 28:111, 1963.