Pre-excitation dueto accessory sinoventricular A cases · Gerlis, Davies, Boyle, Williams, Scott...

Br Heart J 1985; 53: 314-22

Pre-excitation due to accessory sinoventricularconnexions associated with coronary sinus aneurysmsA report of two casesL M GERLIS,* M J DAVIES4 R BOYLE,t G WILLIAMS,t H SCOTT§

From the Departments of *Pathology and tCardiology, Killingbeck Hospital, Leeds; the tDepartment ofHistopathology, St George's Hospital, London; and the §Department of Paediatrics, West Suffolk Hospital,Bury St Edmunds, Suffolk

SUMMARY Ventricular pre-excitation occurred in two cases in which the accessory pathways betweenthe atria and the ventricles were histologically identified as being associated with aneurysmal mal-formations of the coronary sinus. In one case the connexions were in the posterior wall of thecoronary sinus aneurysm and were not related to the atrioventricular annulus; in the other, aconnexion was situated in the anterior wall of the aneurysm in close apposition to the annulus andsuperficially resembled a Kent fibre. These connexions were considered to be of sinus venosus originand to represent a modification of the muscular sheath that normally surrounds the coronary sinusbut does not continue along the coronary veins. One of the posterior wall connecting bundles wascomposed of abnormally large Purkinje-like fibres; this may have played some role in the manifesta-tion of the pre-excitation by reducing any mismatch impedance.

In normal circumstances the heart beat is initiated inthe sinoatrial node and the impulse spreads throughthe atrial muscle to reach the atrioventricular nodewhere it is delayed before passing on to the ventricularmuscle through the atrioventricular bundle of His andthe right and left bundle branches. This provides theonly functional connexion between the inlet and out-let chambers of the heart. Pre-excitation' is said tooccur when the ventricular response to the atrial con-traction occurs earlier than would be expected if theactivation had followed the usual pathway through thespecialised conduction system; it is manifested by anunduly shortened PR interval on the electrocardio-gram.

Various accessory pathways and connexions havebeen postulated or described as substrates of the vari-ous presentations of this condition (Fig. 1). Accessoryatrioventricular muscle fibres bridging the fibrous tis-sue between atrial and ventricular myocardium maybe parietal, as first described by Kent,27 or septal.8 9

Requests for reprints to Dr L M Gerlis, Cardiac Research Depart-ment, Killingbeck Hospital, Leeds LS14 6UQ.

Accepted for publication 23 October 1984

RA

Fig. 1 Diagram showing nonral and abnormalatrioventricular conduction pathways. The normal pathway isfrom the atrioventricular node (AVN) through theatrioventricular bundle ofHis (H) which penetrates the centralfibrous body (CFB) and divides into the right and left bundlebranches (RBB, LBB) in the ventricular septum (VS).Abnormal pathways include 1, Kentfibres; 2, Mahaimfibres;3, Jamesfibres, and 4, central atrioventricular pathway asdescribed by Krikler et al. 9 RA, right atrium; RV, rightventricle; LV, left ventricle.

314

on August 12, 2021 by guest. P

rotected by copyright.http://heart.bm

j.com/

Br H

eart J: first published as 10.1136/hrt.53.3.314 on 1 March 1985. D

ownloaded from

http://heart.bmj.com/

Pre-excitation due to accessory sinoventricular connexions associated with coronary sinus aneurysms

Accessory nodoventricular connexions, between partsof the atrioventricular node and the ventricularmyocardium, were first described by Mahaim.10-12Bypass tracts or atriofascicular fibres passing from theatrial muscle to the atrioventricular bundle of Hishave been described by James,'3 and fasciculoven-tricular connexions between the atrioventricularbundle and the ventricular muscle are included in theconnexions described by Mahaim. 10-12 The preferredanatomical terminology is that proposed by the Euro-pean Study Group on Pre-excitation,'4 as there is con-siderable confusion and inaccuracy in the use of thevarious eponymous terms.'5When the depolarising impulse reaches the ven-

tricular muscle other than through the---atrioventricu-lar bundle and its branches, the spread is abnormal;this is reflected in an abnormal slurring of the firstpart of the electrocardiographic ventricular complex,the so called delta wave. This, together with-the shortPR interval, is characteristic of the Wolff-Parkinson-White syndrome.'6 The nature of thepolarity of the delta wave in the various electrocar-diographic leads enables the site of the epicardialatrioventricular connexion to be determined.'7 Whenthe atrioventricular node is bypassed, but the spreadof stimulus within the ventricle is through theatrioventricular bundle and bundle branches, then theshort PR interval is followed by normal ventricularelectrocardiographic complexes as in the Lown-Ganong-Levine syndrome. 18 Apart from the ventricu-lar pre-excitation these various accessory pathwaysalso provide the substrate for re-entry phenomena;these can lead to arrhythmias, which are the usualmode of clinical presentation of these syndromes.Associated anomalies have been noted, especially Ebs-tein's malformation of the tricuspid valve19 andhypertrophic cardiomyopathy.20We studied two cases of clinically documented ven-

tricular pre-excitation syndrome of the Wolff-Parkinson-White type, in which there were unusualaneurysmal malformations of the coronary sinus. Inboth cases accessory muscular atrioventricular con-nexions were found within these lesions. As far as weare aware neither the coronary sinus anomaly nor thistype of accessory connexion has been described previ-ously.

Case reports

CASE 1Clinical featuresA 16 year old male dyestuffs laboratory technicianpresented with an eight month history of episodes ofpalpitation accompanied by retr9oternal cbest pain.The first episode lasted for about four hours. Theduration of the attacks had dimished to about 30 to 45

minutes, but the frequency had increased to everythree or four weeks, usually occurring after exercise.There was no relevant medical or family history; hesmoked 10-15 cigarettes a day and his consumption oftea, coffee, and alcohol was moderate. Physicalexamination, chest radiography, and M mode andcross sectional echocardiography were all normal.Standard electrocardiography (Fig. 2) showed theappearances of a Wolff-Parkinson-White pre-excitation syndrome with a short PQ interval, and thepolarity of delta waves in the various leads was inaccord with anomalous atrioventricular conductionthrough an accessory pathway in the posterior aspect,according to the table of Gallagher et al'7 (Fig. 3).

Treatment was started with disopyramide 100 mgand amiodarone 200 mg twice a day, and he remainedwell for three months when he had a further spon-taneous episode of supraventricular tachycardia thatrequired electrocardioversion. His medication wasincreased to disopyramide and amiodarone 200 mgeach three times a day and he remained symptom freefor a further six months, when he experienced anotherepisode of supraventricular tachycardia; thisresponded to 5 mg verapamil intravenously. The doseof amiodarone was increased to 200 mg four times aday, and he remained well apart from two briefepisodes of supraventricular tachycardia which ceasedspontaneously. No episodes of atrial fibrillation oratrioventricular dissociation were noted. Graded exer-cise did not provoke arrhythmia.

In view of the satisfactory response to medicaltreatment surgery was not contemplated and elec-trophysiological studies were not performed. In Janu-ary 1982, three years after the onset of his symptoms,he suddenly collapsed and died while walking in thestreet. He was 18Y2 years old.

NecropsyfindingsApart from the presence of a 125 g benign thymomain the upper part of the anterior mediastinum,abnormal findings were limited to the heart. Thiswas of normal shape, slightly enlarged(130x 100x 70 mm) and weighed 360 g. The apex wasdirected normally to the left. The pulmonary and sys-temic venous connexions appeared to be normal.The atria were of solitus configuration and of equal

size and normal anatomy. A 5 mm diameter 12 mmlong tunnel passed upwards from the fossa ovale intothe septal wall of the right atrium, but there was nocommunication with the left atrium. The atrioven-tricular valves were normal.The right ventricle wall was slightly thickened to

8 mm and the trabeculations were well marked. Theposterior papillary muscle was very small. The leftventricular myocardium and the ventricular septum-*evre-Wfiformly thickened to 20 mm. The free wall

315



j.com/

Br H


ownloaded from


Gerlis, Davies, Boyle, Williams, Scott

Fig. 2 Case 1: (a) standard lead ofelectrocardiogram and (b) rhythm strip.

V6

I3S

O.2

Seconds

Fig. 3 Diagram of heart base showing position of variousparietal atrioventricular accessory connexions. The asteriskindicates the position of the accessory connexion in cases I and 2according to the electrocardiographic delta wave polarity. A,aorta; P, pulmonary artery; MV, mitral valve; TV, tricuspidvalve; CS, coronary sinus.

was appreciably trabeculated, the papillary muscles illdefined, and many of the mitral valve chordaeinserted directly into the ventricular wall.On the posterior aspect of the heart at the base of

the right ventricle immediately below the atrioven-

tricular sulcus, there was an area of cyst-like softeningdiscernible only by palpation and without any visibleindication. This occupied an ill defined area approxi-mately 20 mm in diameter and appeared to have notension within. Incision and subsequent completeopening showed this to be a rather more extensivelesion, extending 50 mm laterally to the right fromthe midline, 20 mm downwards from the atrioven-tricular sulcus and up to 10 mm in depth. There waspartial division of the cavity by incomplete septa be-tween the anterior and posterior walls, and the cavitywas lined by a thin smooth membrane. At the upperleft margin, that is approximately in the midline of theheart, this cavity communicated with the lumen of theapparently normal coronary sinus which was 4 mm indiameter and opened into the right atrium through adilated coronary sinus orifice of 8 mm in diameter.This lesion appeared to be an abnormal (aneurysmal)posterior coronary vein (Fig. 4). The posterior wallwas thin and membranous but contained extensiveareas of muscle which appeared to continue into themyocardium of the wall of the right ventricle. Dissec-tion and transillumination showed some apparentstrands of muscular continuity between the posteriorwall of the right atrium, the posterior wall of thecoronary sinus, and the posterior wall of this ventricu-lar venous "cyst." Dissection and transillumination ofthe atrioventricular rings elsewhere showed no evi-dence of atrioventricular muscle continuity whenviewed macroscopically or with a x 5 dissecting lens.The great arteries arose normally and the pulmo-

nary artery and aorta were each 20 mm in diameter

II

III

316



j.com/

Br H


ownloaded from



Fig. 4 Case 1: morphologicalappearance of the posteror aspect of theheart. (a) The visceral pericardium hasbeen stripped from an area approximatelyequal to the extent of the coronary sinusaneurysm, the dotted area indicates theblock of tissue which was taken forhistological sections. (b) The posteriorwall ofthe aneurysm has been incised andreflected upwards showing the smoothpartially septated inner aspect. Theopening into the right atrium is indicatedby the open arrow; openings of thecoronary veins are indicated by the smallarrows. CS, coronary sinus; RA, rightatrium; LA, left atrium; RV, rightventricle; LV, left ventricle; IVC,inferior vena cava; AVS, atrioventricularsulcus.

and had normal valves. The coronary arteries werenormal in distribution and structure.

HistologySerial sections showed the atrioventricular node, theatrioventricular bundle (of His), and the left bundlebranch fascicles to be normal. The right bundlebranch was slightly abnormal in that its origin andcourse were situated entirely intramuscularly, andthere were early tenuous connexions between it andthe working myocardium of the upper part of the

atrioventricular septum. A block of tissue wasremoved from the posterior wall of the coronary sinusaneurysm, as indicated in Fig. 4, extending from theleft atrium to the left ventricle. Serial histological sec-tions showed three bands of direct atrioventricularmuscular connexion, two of which are illustrated inFigs. 5 and 6. One of these accessory connexions wasof special interest as it was composed of very largefibres up to 50 IL in diameter, almost four times thewidth of the adjacent normal myocardial fibres (10-14 ,u). These fibres also showed increased spacing of

317



j.com/

Br H


ownloaded from



Fig. 5 Case 1: serial histological sectionsfrom the blockindicated in Fig. 4a. (a) The musclefibres of the coronary sinus Fig. 6 Case 1: serial histological sections at 10 IL intervals(CS) and the ventricle (V) are separated by afibrous zone (F). ((a)-(c)) showing progressive bridging of thefibrous gap by(b) The same area as (a) at an interval of40 jt showing the coalescence oftwo portions ofa prominent and discrete musclebriding continuity ofa muscle strand. (Masson's trichrome stain band (arrowed). (Masson's trichrome stain x 20.) CS, coronaryx 20.) sinus; F,fibrous zone; V, ventricle.

the myofibrils and some clear vacuolation, and theywere surrounded and separated by conspicuousfibrosis. The appearances were somewhat similar tothose of Purkinje fibres (Fig. 7).

CASE 2A young girl had had a normal history apart fromrecurrent urinary infections associated with slightureteric reflux since the age of 7 years. When she was10 years old she fainted after running uphill butremained well otherwise. Six months later, however,while running at play, she suddenly collapsed, stop-ped breathing, and went into a tonic convulsion. Shewas given mouth to mouth artificial respiration duringtransport to hospital, where on arrival she was pulse-less and without an audible apex beat. Respirationswere gasping and there had been some inhalation ofvomit and she was immediately intubated.- An elec--

trocardiogram showed ventricular fibrillation; thisreverted to sinus rhythm after electrocardioversionand an initial sinus bradycardia responded toatropine. She remained in sinus rhythm with a goodcardiac output and made a full clinical recovery within24 hours.Over the next year she experienced several episodes

of feeling faint, associated with pallor and palpitation,always after exercise. Several attempts were made toreproduce an attack with exercise in the hospital out-patient clinic, but without success. The resting elec-trocardiogram did, however, show the classicalappearances associated with the Wolff-Parkinson-White pre-excitation syndrome with a posterior acces-sory atrioventricular connexion (Fig. 8).Almost a year after her initial cardiac arrest she

again felt faint while playing in the garden, and thiswas accompanied by central chest pain. She was

318



j.com/

Br H


ownloaded from


Pre-excitation due to accessory sinoventnicular connexions associated with coronary sinus aneurysms 319

arrest, again associated with a tonic convulsion. The_- electrocardiogram again showed ventricular fibrilla-

tion; this did not respond to electrocardioversion, sheproceeded to asystole, and all attempts at resuscitationfailed. She was 11 years old when she died.

Necropsyfidings|~ No major abnormalities were noted other than in theheart. The heart was not enlarged, and the cavities,valves, and great vessels were normal. An incisionacross the posterior wall of the left atrioventricular

->2R~_:RU4 ring showed a thin walled aneurysmal sac 1 cm across9 + ** i i which communicated with the coronary sinus through

a narrow slt (Fig. 9). Lateral to this sac the sinus waspt.ti absent, and the posterior cardiac vein was enlarged

* and extended towards the apex of the ventricle.v~jbt >ig a N N E | S Histological sections traced a very large muscle

connexion which slanted diagonally on the posterior* -;bt5wallof the heart, from the posterior wall of the leftatrium to the left ventricle across the aneurysmal por-tion of the coronary sinus (Fig. 10).

', / f tiDiscussion

Accessory atrioventricular connexions and bypass*(i)#{<13/ + S ^ tracts, of the types previously described, are common

vestigial remnants of embryonic structures, but only asmall proportion of these cause ventricular pre-Fig. 7 Histological sections: (a) high power view of the excitation detectable by electrocardiography and very

bridging band (affows) shown in Fig. 6b showing the contrastbetween it and the adjacent working muscke. ( x 80.) (b) detailed few cause symptomatic disease. 19-21 It is not gener-higherpower view ofpartofthe anomalous band (arrows) shown ally realised that apart from atrioventricular connex-in Fig. 6a showing the greatly enlarged muscular elements ions, normal or anomalous, of specialised or non-separated byfibrous stroma. (x 200.) specialised myocardium, there is another potential

lmVm

| I I | I 2 | :; ! ~~~~~~~~~~A ,!:.LA!II M aVR Vl.....r- |V4 -

O2s~~~~~~~~~~~~~~~~~~~~~~~~~~~N

II aVL V2 V5

Fig. 8 Case 2: standard lead electrocardiogram. (Note leads _ _ _V3 and V4 are recorded at half sensitivity.) Fig. 9 Case 2: morphological appearance of the posteroraspect of the atrioventicularjunction sectioned in the sagittalimmediately taken to hospital and on arrival she was plane showing the coronary sinus aneurysm (asterisk) and the slit

pale and restless, and her pulse was noted to be slow like orifice into the coronary sinus (CS). LA, left atrium; LV,and irregular. While being examined she had a cardiac left ventricle; A, aorta.



j.com/

Br H


ownloaded from



Fig. 10 Case 2: (a) a lngitudinal histological sectin through the coronary sinus (CS) aneurysm and the adjacent atrioventricularjunction. (Masson's trichrome stain x 4.) (b) Microscopical appearance ofthe atrioventricularjunction in an area adjacent to that in(a) showing the accessory connexion (arrows). (Masson's trichrome stain x 20.) AVA, atnioventricular annulus; MV, mitral valve;LA, left atrium, LV, left ventricle. *, aneurysm cavity.

avenue of communication between the proximal car-diac chamber and the ventricles and that is throughthe musculature of the sinus venosus. In many verte-brates the sinus venosus is a distinct contractilechamber. In. mammals this separate identity is lostduring fetal development, and the sinus venosusbecomes absorbed into the right atrium and its musclebecomes continuous with that of the atrium. Theright extension of the primitive sinus venosus, orcuvierian duct, becomes the cardiac end of thesuperior vena cava, and the left extension becomes thecoronary sinus (Fig. 11). The proximal portion of thecoronary sinus is surrounded by a spiral sheath ofmyocardium which is continuous with that of themorphological right atrium and is clearly a remnant ofthe sinus venosus musculature (Fig. 12). This musclesheath normally stops abruptly at or shortly beyondthe orifices of the entering coronary veins, but as theseveins progress into intimate anatomical relation withthe ventricles it remains possible that extensions ofthis sinus venosus muscle could be responsible for aphysiological connexion. Such a circumstance mightwell be more likely to occur in association with a mal-formation of the coronary sinus. This appears to have

AzV

Ivc PCv

Fig. 11 Diagrams showing the development of the coronarysinus: (a) schematic early embryonic stage and (b) filly developedcondition, as viewedfrom behind. The sinus venosus componentis coarsely stippled. A, atrium, LA, left atrium; RA, rightatrium, V, ventricle; LV, left ventricle; RV, right ventricle; SV,sinus venosus; AVA, atrioventricular annulus; SVC, superiorvena cava; IVC, inferior vena cava; AzV, azygos vein; CS,coronary sinus; ACV, antrior cardinal vein; PCV, posteriorcardinal vein. Asterisks indicate the positions of the sinoatrialand atrioventncular nodes.

320



j.com/

Br H


ownloaded from



Fig. 12 Histological sections (a) longitudinally through a normal coronary sinus and adjacent structures and (b) through the origin ofa coronary vein from the coronary sinus showing the level of discontinuity of the coronary sinus muscle coat (arrow). (Masson'strichrome stain x 5 (a) and x 20 (b).) CS, coronary sinus; CSM, coronary sinus muscle; AM, atrial muscle; VM, ventricular muscle;AVA, atrioventricular annulus; LA, left atrium; CV, coronary vein; CA, coronary artery.

been the situation in the two cases which we havestudied. In the first case the muscular connexion waslocated in the posterior aspect of the aneurysm andwas not related to the atrioventricular annulus. In thesecond case the connexion was on the anterior wall ofthe aneurysm and was in close apposition to thefibrous atrioventricular annulus and presented a his-tological picture very similar to that of the more usualatrioventricular connexion or bundle of Kent;nevertheless, we consider that the underlyingsinoventricular nature was common to both cases(Fig. 13).The presence of other accessory connexions was not

excluded; this would have required serial histologicalsections throughout the whole of the atrioventricularjunction which would have been a formidable task.Dissection with transillumination in the patient incase 1 excluded major connexions, but fibres ofmicroscopic size would not have been identified.Nevertheless, as the electrocardiographic delta wavepolarity patterns indicated that the accessory conduc-tion pathways were precisely at the position of thecoronary sinus aneurysms, we consider that there is

little doubt that the connexions that we identifiedwere responsible for the clinical features in both cases.The large size of the fibres of one of the accessory

connexion bundles in the patient in case 1 is of specialinterest as a possible contributory factor in the evolu-tion of the clinical abnormality from a pre-existingsymptomless anatomical malformation. Accessorytracts are not necessarily used, and Krikler and Row-land have pointed out that narrow pathways may beineffective in stimulating a ventricular responsebecause of mismatch impedance, in which the "cablecapacity" is inadequate to depolarise the large mass ofmyocardium into which it is inserted.22 Enlargementof the tracts by muscle disorders such as hypertrophiccardiomyopathy may be a possible cause of activationof such latent pathways by cancelling this mismatchimpedance.23 It is not possible to know whether thePurkinje-type structure of the tract in question hadalways been so or whether this was an adaptivedevelopment in response to the abnormal conductionactivity in which it was involved, but in either casesuch enlargement would be likely to enhance both theconduction rate and the cable capacity. Such changes

321



j.com/

Br H


ownloaded from


322

Svc

@

RAA CS

F AVA.* . TV

RV

Fig. 13 Diagrams showing the relation of the coronary sinus

muscle to the atrial and ventricular muscle (a) in a normal case,

(b) in case 1, and (c) in case 2. The asterisks indicate thecoronary sinus aneurysms and the arrmows the accessory pathways.AVA, atrioventricular annulus; CS, coronary sinus; CV,coronary vein; F,fibrous discontinuity; RA, right atrium RV,right ventricle; TV, tricuspid valve.

have not been described in other accessory pathways,and it is possible that they may be related to theunusual anatomical location.

Although the combination of coronary sinus aneur-ysm and ventricular pre-excitation is a rare condition,the finding of two almost identical examples within ashort period suggests that it is worth bearing in mindespecially when cases that are being considered forsurgical intervention are investigated, and that duringdetailed electrophysiological studies placement of thecoronary sinus electrode lead could quite convenientlybe combined with coronary sinus contrast angio-graphy.

LMG is supported by the National Heart ResearchFund.

References

1 Ohnell RF. Pre-excitation, a cardiac abnormality. ActaMed Scand 1944; 152 (suppl): 1-167.

2 Kent AFS. Researches on the structure and function ofthe mammalion heart.J Physiol (Lond) 1983; 14: 233-54.

3 Kent AES. Observations on the auriculo-ventricularjunction of the mammalion heart. QJ Exp Physiol 1913;7: 193-5.

4 Kent AFS. The structure of the cardiac tissues at theauriculo-ventricular junction.I Physiol (Lond) 1913; 47:


XVu-XVm.5 Kent AFS. The right lateral auriculo-ventricular junc-

tion of the heart [Abstract]. J Physiol (Lond) 1914; 48:xxi-xxiv.

6 Kent AFS. A conducting path between the right atriumand the external wall of the right ventricle of the heart ofthe mammal [Abstract].J Physiol (Lond) 1914; 48: lvii.

7 Kent AFS. Illustrations of the right lateral auriculo-ventricular junction in the heart [Abstract]. J Physiol(Lond) 1914; 48: lxiii-lxiv.

8 Spurrell RAJ, Krikler DM, Sowton E. Problems con-cerning assessment of anatomical site of accessory path-way in Wolff-Parkinson-White syndrome. Br Heart J1975; 37: 127-35.

9 Krikler DM, Davies MJ, Rowland E, Goodwin JF,Evans RC, Shaw DB. Sudden death in hypertrophic car-diomyopathy: associated accessory atrioventricularpathways. Br HeartJ 1980; 43: 245-51.

10 Mahaim I. Nouvelles recherches sur les lesions du fais-ceau de His-Tawara: le bloc bilateral manque. Nouvelleform anatomique de bloc du coeur a substituer au blocdit "d'arborisations". Annales de Medicine 1932; 32:347-77.

11 Mahaim I, Benatt A. Nouvelles recherches sur les con-nexions sup6rieures de la branche gauche du faisceau deHis-Tawara avec la claison interventriculaire. Cardiologia1937; 1: 61-73.

12 Mahaim I. Kent's fibres and the A-V paraspecific con-duction through the upper connections of the Bundle ofHis-Tawara. Am HeartJ 1947; 33: 651-3.

13 James TN. Morphology of the human atrioventricularnode, with remarks pertinent to its electrophysiology.Am Heart J 1961; 62: 756-71.

14 Anderson RH, Becker AE, Brechenmacher C, DaviesMJ, Rossi L. Ventricular pre-excitation, a proposednomenclature for its substrates. Eur J Cardiol 1975; 3:27-36.

15 Anderson RH, Becker AE. Stanley Kent and accessoryatrioventricular connections. J Thorac Cardiowsc Surg1981; 81: 649-58.

16 Wolff L, Parkinson J, White PD. Bundle-branch blockwith short P-R interval in healthy young people prone toparoxysmal tachycardia. Am Heart 1930; 5: 685-704.

17 Gallagher JJ, Prichett ELC, Sealy WC, Kasell J, WallaceAG. The pre-excitation syndromes. Prog Cardiovasc Dis1978; 20: 285-327.

18 Lown B, Ganong WF, Levine SA. The syndrome ofshort P-R interval, normal QRS complex and parox-ysmal rapid heart action. Circulation 1952; 5: 693-706.

19 Schiebler GL, Adams P Jr, Anderson RC. The Wolff-Parkinson-White syndrome in infants and children.Pediatrics 1959; 24: 585-603.

20 Pernod J, Ferrane J, Quinot B, Vasile N, Carre R. Car-diomyopathie obstructive et syndrome de Wolff-Parkinson-White. Presse Med 1966; 42: 2135-7.

21 Ray D, Danino EA. Wolff-Parkinson-White syndrome.A review of forty-two cases. Indian Heart J 1975; 27:13-8.

22 Krikler D, Rowland E. Concealed pre-excitation.J Elec-trocardiol 1978; 11: 209-11.

23 Goodwin JF, Krikler DM. Arrhythmia as a cause of sud-den death in hypertrophic cardiomyopathy. Lancet 1976;ii: 937-40.



j.com/

Br H


ownloaded from


Pre-excitation dueto accessory sinoventricular A cases · Gerlis, Davies, Boyle, Williams, Scott...

Documents

Transcript of Pre-excitation dueto accessory sinoventricular A cases · Gerlis, Davies, Boyle, Williams, Scott...