Congenital and surgical atrioventricular block within the His bundle

Congenital and Surgical Atrioventricular

Block

Within the His Bundle

ANTOINE PAUL

T. NASRALLAH,

C. GILLETTE,

CHARLES

MD

MD

E. MULLINS,

MD,

FACC

Houston, Texas

From the Division of Cardiology, Texas Heart Institute, St. Luke’s Episcopal Hospital and the Texas Children’s Hospital and the Section of Cardiology, Department of Pediatrics, Baylor College of Medicine, Houston, Texas. This study was supported in part by Grant HL-5756 from the National Institutes of Health and by U. S. Public Health Service Grant RR-00166 from the General Clinical Research Branch, National Institutes of Health, Bethesda, Md. Manuscript accepted March 5, 1975. Address for reprints: Department 01 Pediatric Cardiology, Texas Children’s Hospital, 6621 Fannin, Houston, Texas 77025.

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In three patients with congenital heart disease the site of atrioventricular (A-V) block was localized within the His bundle with the aid of His bundle electrograms. In one patient with first degree A-V block and normal QRS configuration, electrophysiologic studies revealed “split” His potentials. The other two patients had complete A-V block, and their His bundle electrograms revealed His spikes both proximal and distal to the site of block. One of the two patients, who had a pattern of left bundle branch block in the electrocardiogram, had surgically induced complete A-V block after repair of an ostium primum atrial septal defect. The other patient with congepital A-U block had a narrow ORS complex and, in addition to complete block within the His bundle, prolonged A-V nodal conduction time but no associated cardiac anomaly. Both patients with complete heart block rqg&ed pacemaker insertion. The natural history of intra-His bundle block is not known, and it is difficult to recommend appropriate therapy. More electrophysiologic studies are needed in patients with A-V block to determine the prognostic significance of such block or conduction delay in the His bundle.

His bundle recordings have demonstrated’-:j that the sites of delay or block along the specialized conducting tissues between the sino-atria1 node and the ventricles may involve one or more of the following locations: the atria, atrioventricular (A-V) node, bundle of His, right or left bundle branch and the Purkinje network. The standard electrocardiogram sometimes fails to localize precisely the site of delay or block.‘mg Block in the His bundle has no representation in the surface electrocardiogram but has been deduced by clinical electrocardiographers.” Narula et a1.2 first documented block within the His bundle. They termed their findings “split” H potentials and suggested that one of these (HI) was recorded proximal to and the other (HZ) distal to an area of block. Others2-4,8-‘7 ha ve reported similar observations (Table I). This report deals with three patients with delay or block within the His bundle documented by His bundle recordings. The report (1) presents the first documented instance of surgically induced block within the His bundle, (2) demonstrates the second instance of congenital heart block within the His bundle with no associated cardiac anomaly, (3) documents two additional instances of congenital heart block occurring within the His bundle, and (4) tabulates the previous 20 reported cases of intra-His bundle block. Met hods His bundle electrograms were obtained in three children with congenital heart disease during the course of a prospective study of patients with conduction disturbances. The His bundle electrograms were obtained using conventional techniques. 1H-20The patient and all electrical equipment were securely grounded. Bipolar and tripolar electrode catheters were used with in-

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I

TABLE

Cases of Block Within the His Bundle

Reported

QRS Complex Age fvr) Study

H,-V (msec)

& Sex

Type of Block

1 2 3 4 5 6 7

B4M

Normal Normal Normal Normal

0.08 0.06 0.08

l’ii 23M

Mobitz I (3:2) Mobitz II (2:l) Complete 2:l Mobitz I I Complete Complete

Normal RBBB

d&

8

71 F

Mobitz

Normal

0.09

ASHD’ ASHD Congenital Penetrating trauma ASHD

9

27M

2:1

RBBB

0.13

ASHD

.

30

10

78M

Complete

Normal

0.09

ASHD

.

45

11

82M

Complete

RBBB

0.12

ASHD

12 13 14 15 16 17

iii 87M 85M 81M

Mobitz I I Mobitz I I Complete Complete Complete Mobitz I I

Normal Normal RBBB LBBB

ii6

18

56M

Mobitz

LBBB

0.17

19

67M

l”A-V

RBBB

0.12

Bharati et al.”

20

85F

Complete

Present report Present report Present report

21 22 23

22

I’A-V Complete Complete

LBBB, RBBB Normal LBBB Normal

Narula Narula Narula Rosen Rosen Rosen Rosen

et et et et et et et

al.2-4 al.lb4 al.*-4 al .9 al.“* al.” al.lz

Schuilenburg & Durrer” Schuilenburg & Durrer13 Schuilenburg & Durrer13 Schuilenbur & Durrer’ P Gupta el al.14* Gupta et al.l“* Gupta et al.]“ Gupta et al.ls Gupta et al.r6 Jacobson & Scheinman16 Jacobson & Scheinman16 Bharati et al.17

48i 70M

. . .

9F

Configuration

Associated Lesions

Case no.

II

.. ..

II

Cause

0.14

ii 60

NC%

i5’ 40 50

45

..

0.06 0.11 0.13

40

VSD

...

. . . .

.

.

0.08 0.12 0.08

DORV

= double outlet

.

sb’ 40 45 60

. Catheterinduced Catheterinduced Calcific and degenerative Calcific and degenerative Congenital Surgical Congenital

..

l Data obtained from abstract only rather than full paper. ASD = atrial septal defect; ASHD = arteriosclerotic heart disease; A-V = atrioventricular; bundle branch block; RBBB = right bundle branch block; VSD = ventricular septal defect.

terelectrode distances of 1 or 10 mm, or both. All records were obtained on a multichannel oscilloscopic photographic recorder (Electronics for Medicine DR-8) at paper speeds of 100 to 200 mm/set with filter frequencies of 0.1 to 200 hertz for electrocardiographic leads and 40 to 500 hertz for electrographic recording. Several potentials were recorded sequentially in the interval from the low right atrium to ventricle (LRA-V), but the potential after the low right atria1 (LRA) deflection that was farthest from the ventricular electrogram was designated the H potential. The potential between the H and V potentials is the right bundle (Rb) potential. The interval from the low right atrium to the His bundle potential (LRA-H) was measured from the onset of the low right atria1 depolarization to the onset of the first rapid deflection of the His bundle potential. The interval from the His bundle to the ventricle (H-V) was measured from the first rapid deflection of the His bundle potential to the earliest ventricular activity in either surface or intracardiac recordings. The interval from the right bundle to the ventricle (Rb-V) was measured from the initial rapid deflection of the first potential after the His deflection to the earliest ventricular activity. When split His bundle potentials were recorded with intact A-V conduction, measurements were made of the LRA-HI, HI-Hz and Hz-V intervals. When complete block occurred between Hr and Hz, only the LRA-Hr and Hz-V intervals were measured. All intervals were measured in milliseconds. The normal values for in-

... . . ..

.

61 .

48 48

DORV I0 ASD None

right ventricle;

ii! 45

LBBB = left

tervals from our laboratories20 are as follows: LRA-H interval 60 to 129 msec, H-V interval 30 to 55 msec, Rb-V interval 15 to 25 msec.

Clinical Cases and Results Case 1: The patient was a 2 year old boy with the diagnosis of double outlet right ventricle, infundibular pulmonary stenosis and persistent left superior vena cava draining into the coronary sinus. The electrocardiogram demonstrated sinus rhythm at a rate of lOO/min with a prolonged P-R interval of 0.20 second (Fig. 1). First degree A-V block was evident in the initial electrocardiogram obtained at age 2 months. The QRS complexes were narrow and 0.08 second in duration. Right axis deviation and right ventricular hypertrophy were evident.

His bundle electrograms were recorded during right heart catheterization. With the tripolar catheter positioned at the tricuspid valve, two high frequency electrograms were recorded between the atria1 and ventricular electrograms (Fig. 2), possibly representing “split” H potentials as defined by Narula et a1.2 Each atria1 depolarization was followed by a biphasic proximal His bundle potential (HI) at an LRA-Hi interval of 76 seconds. The HI-HZ intervai measured 49 msec and the Hz-V interval 34 msec. In addition, every ventricular depolarization was pre-

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ceded by a separate biphasic spike between HZ and V, which probably represented the right bundle branch (Rb) potential at an Rb-V interval of 16 msec.

0.12 second. The ventricular escape focus may have originated in the right bundle branch system, producing the left bundle branch block configuration.

Case 2: The patient was a 20 year old woman with a history of syncopal attacks of 2 weeks’ duration and a pulse rate of 34/min. She had surgically induced complete heart block of 13 years’ duration with repair of an ostium primum atria1 septal defect at age 6 years. The electrocardiogram (Fig. 3) revealed a complete A-V block with an atria1 rate of 62 and a ventricular rate of 34/min. There was a left bundle branch block configuration with a QRS duration of

Recording of the His bundle electrogram showed that every atria1 depolarization was followed 100 msec later by a His potential (HI) and that every escape ventricular complex &as preceded by 35 msec by a second His potential (Hz) (Fig. 4). In addition, a second smaller deflection (Rb) preceded the ventricular complex between HP and V at an Rb-V interval

_

LI[ Lf?A-HI HI -Hz

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FIGURE 2. Case 1. Representative strip of His bundle electrogram (HBE). From top to bottom: electrocardiographic lead II, and His bundle electrograms with respective interelectrode distances of 10 and 1 mm. Paper speed is 200 mm/set, time lines are at 1,000 msec intervals. Sinus rhythm is evident at a cycle length of 600 msec. Each atrial beat is followed 76 msec later by a His potential (HI). This potential is followed at 49 msec later by a second potential (Hz) that precedes a ventricular complex with a constant interval of 34 msec. The right bundle branch potential (Rb) recorded simultaneously precedes the QRS complex at an Rb-V interval of 16 msec. HBE = His bundle electrocardiograms. LRA = low right atrium.

76 msec. 49msec.

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A

I

LRA- HI = 100 mroc 1 Hf V= 35mrrc

FIGURE 3. Case 2. Electrocardiogram reveals complete A-V block. The escape rhythm is characterized by a left bundle branch block pattern with a QRS duration of 0.12 second.

of 20 msec. Atria1 pacing had no effect on the ventricular rate. Intravenous administration of 0.5 mg of atropine sulfate increased the atria1 rate from 61 to lOO/min and the ventricular rate from 41 to 50/min. A permanent pacemaker was later inserted. Case 3: The patient was a 9 year old girl with congenital complete heart block first noted at age 8 months. The electrocardiogram revealed complete A-V block with an atria1 rate of 100 and a ventricular rate of 32/min. The QRS complex had a normal configuration and a duration of 0.08 second (Fig. 5). With exercise, the atria1 rate increased to 150 and the ventricular rate to 50/min. Hemodynamic and angiographic studies of the right and left sides of the heart revealed no abnormalities. There were no signs suggesting corrected transposition of the great vessels. His bundle electrograms revealed that every atrial depolarization was followed 220 msec later by a His bundle potential (HI) and that every ventricular escape complex was preceded by 45 msec by a second deflection (Fig. 6). In addition, a third deflection (Rb) preceded the ventricular complex at an Rb-V interval of 19 msec. Right atria1 pacing was carried out at rates of 120 to 19O/min. As the atria1 rate was increased, the LRA-Hi interval was prolonged with 1:l conduction being maintained to H1 up to a paced rate of 190/min. Intravenous administration of atropine sulfate (0.3 mg) increased the atria1 rate from 100 to 139/min and the ventricular rate from 32 to 5O/min. A permanent pacemaker was inserted, primarily because of the patient’s slow heart rate, premature ventricular contractions and poor exercise response.

FIGURE 4. Case 2. Electrocardiographic lead II and representative strips (A and B) from the His bundle electrogram. Complete A-V block is evident with an atrial rate of 62 and a ventricular rate of 4lImin. Each low right atrial (LRA) potential in B is followed by a high frequency potential (HI). Each QRS complex is preceded by a high frequency potential (Hz) recorded from the His bundle catheter as well as an Rb potential preceding the ventricular complex. Time lines are at 1 second intervals: paper speed is 200 mm/set.

Discussion Electrophysiology: Electrophysiologic studies suggested that our patients had His bundle disease, with HI being recorded proximal to and Hs distal to an area of conduction delay in the His bundle. In Case 1,

FIGURE 5. Case 3. Electrocardiogram reveals complete A-V block. The escape rhythm.at a rate of 32/min is characterized by a normal QRS configuration with a duration of 0.08 second.

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1

1000

))

mare.

LRA-HI 220msec. H2- V

L5msek.

5:

FIGURE 6. Case 3. Lead II of the electrocardiogram and His bundle electrograms. Complete A-V block is evident with an atrial rate of 100 and a ventricular rate of 32/min. A, two bundle of His deflections (H, and H2) are recorded. The LRA-H, interval is prolonged. B, note the right bundle potential preceding the QRS complex recorded with the catheter advanced farther into the ventricle.

HBE,

I

’

I

if one accepts HI as a His bundle potential, then H:, is presumably a His bundle potential recorded distal to HI or a right bundle branch electrogram. The catheter electrode was presumed to be in the usual position for recording the His potential since both atria1 and ventricular electrograms were identifiable at the same position in which the HI and Hs potentials were recorded. In addition, each QRS complex was preceded by another potential, probably a right bundle branch (Rb) potential occurring 18 msec after Hz and 16 msec before the QRS complex. In Case 2, the pattern of splitting was somewhat different from that of Case 1. The most likely explanation is that a proximal His potential (HI) followed every low right atria1 deflection and was not conducted to the ventricles. The distal HZ potential was seen preceding escape beats with a left bundle branch block pattern. The Hs-V interval was normal. The subsidiary pacemaker probably arose in the bundle of His just proximal to its bifurcation but distal to the focal block. The QRS configuration in the surface electrocardiogram of the resulting ventricular beats indicated an additional impairment of impulse conduction to or in the left bundle branch. One might anticipate a prolonged H-V interval in the presence of left bundle branch block. In keeping with this possibility, the Hz potential in this case may have originated from the proximal right bundle branch, in which case one could postulate surgical injury to the

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distal bundle of His or to the most proximal portion of both main divisions, with a right bundle branch impulse origin. However, a normal H-V interval as in this case has been reported in the presence of left bundle branch block.21m23 In addition, a right bundle branch (Rb) potential was recorded between the HZ and V potentials. It is sometimes not possible to record clear HI, Hz and Rb potentials simultaneously, as in this case and those reported by Schuilenburg and Durrer.24 We did not succeed in localizing the site of origin of the H2 deflection by stimulating the heart by way of the His bundle recording electrodes because the ventricles were always activated immediately on stimulation. We believe that the His bundle lesion producing A-V block in this patient was related to surgical trauma. The likelihood of a traumatic lesion involving the proximal left bundle branch is obvious. This case is the first known instance in which His bundle recording identified the site of surgical A-V block within the bundle of His. Case 3 is unique in several aspects. It is the second reported case of congenital A-V block with no associated anomaly in which intra-His bundle block was documented by His bundle electrogram (Table I). In addition, the findings represent an exception to the general rule relating the level of block to the configuration of the QRS complex. Each of the nonconducted atria1 impulses is followed by a His deflection. The complete block is not within the A-V node although

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the LRA-HI interval is prolonged. The QRS complexes are normal and are preceded by a single His deflection with a normal Hz-V interval. The findings are compatible with intra-His bundle block in which the pacemaker for the ventricles resides within the bundle of His but below the level of block. Diagnosis of intra-His bundle block: Block within the His bundle cannot be distinguished by surface electrocardiograms from block within the A-V node.15 In either instance, if the block is complete, the QRS configuration is of a supraventricular type, unless an associated bundle branch block is properties of the escape present. l3 Functional rhythms may be of some value in determining their site of origin. It is possible that the association of the slow ventricular rate with a narrow QRS complex indicates block within the His bundle. Unlike patients with A-V nodal block, patients with intra-His bundle block have no or only a small increment in ventricular rate after intravenous administration of atropine.24~13This is possibly because of the lack of parasympathetic control of a more distal His bundle pacemaker. However, the ventricular rate increased slightly after atropine in our Cases 2 and 3 and in two patients with intra-His bundle block described by Gupta et a1.15The response of the subnodal A-V conduction to cholinergic stimulation is still controversial and needs to be resolved. Two patterns of “splitting” are described in this report, one occurring with intact conduction (Case 1) and the other occurring with complete A-V block (Cases 2 and 3). In Cases 1 and 3 the splitting was presumably due to focal lesions in the His bundle. Pathologic correlation is not available but the patients are presumed to have developmental disruptive lesions in the His bundle. Etiology: The origin of complete heart block in the His bundle has been attributed to traumatic causes,12 lecoronary occIusion,1o calcific and degenerative sions,17 postsurgical status (Case 2) and congenital lesions (Cases 1 and 3).11 Congenital A-V block maybe an isolated abnormality of the conduction system as in our Case 3 or may be associated with other congenital cardiac malformations. Pathologic findings noted in reviews of congenital A-V block by Levz5 and Carter et a1.26 include imperfect formation of, or lack of, the His bundle, and inflammatory or noninflammatory degeneration of the bundle, possibly resulting from an intrauterine inflammatory process. Carter et a1.26reviewed the histologic features of

28 reported cases and provided an anatomic classification of congenital lesions of the cardiac conduction system. Incidence: Intra-His bundle blocks have been described infrequently in English language reports. In contrast, French investigators reported a 20 percent incidence rate of intra-His bundle lesions in patients after acute myocardial infarction.27 Guerot et a1.2s reported that in 11 (18 percent) of 60 cases of chronic A-V block the site of block was localized within the His bundle by His bundle electrograms. A similar incidence rate (19 percent) was reported by Puech et a1.2g Life history: Very little is known about the clinical evolution of lesions within the His bundle in man. El-Sherif et a1.30provided an experimental validation of the pathophysiologic findings after ligation of the anterior septal artery in dogs. They. .demonstrated that the evolution of His bundle block is a progressive phenomenon, and that Mobitz II block represents the initial stage of failure of impulse propagation in intra-His bundle lesions. The duration of block in our Cases 2 and 3 was 13 and 8 years, respectively. It has previously been shown31 that the site of block resides in the A-V node in patients with congenital A-V block with narrow QRS complexes. In our Cases 1 and 3, as well as in a case of congenital A-V block described by Rosen et al.,l’ the site of congenital block was demonstrated to be within the His bundle by His bundle electrograms. In our Case 3, the prolonged LRA-HI interval indicated an additional conduction abnormality in the A-V node. It is evident from the reported cases (Table I) that intraHis bundle conduction delay or block could simulate types I, II, III and high degree A-V block. By surface electrocardiogram the diagnosis of block within the His bundle cannot be made with certainty particularly when mixed conduction lesions exist. Block within the His bundle is more common than reported and, furthermore, His bundle recording in children with A-V block is of value to localize precisely the site of delay or block. It is anticipated that this technique may be of value in assessing the clinical evolution and pathophysiology of intra-His bundle lesions, their prognosis and the need for prophylactic pacemaker therapy. Acknowledgment We acknowledge the secretarial aid of Ms. Christine Abrams, and the technical assistance of Dean Harrelson.

References 1. Haff JI: The His bundle electrogram. Circulation 47:897-911, 1973 2. Narula OS, Scherlag BJ, Samet P, et al: Atrioventricular block. Am J Med 50:146-165. 1970 3. Narula OS, Scherlag SJ, Samet P: l&venous pacing of the specialized conducting system in man. His bundle and A-V nodal stimulation. Circulation 41:77-87, 1970 4. Narula OS, Samet P: Wenckebach and Mobitz type II A-V block

due to block within the His bundle and bundle branches. Circulation 41:947-965, 1970 5. Dam&o AN, Gallagher JJ, Lau SH: Application of His bundle recordings in diagnosing conduction disorders. Prog Cardiovasc Dis 14:601-620, 1972 6. Scherlag SJ, Samet P, Helfant RH: His bundle electrogram: a critical appraisal of its uses and limitations. Circulation 46: 601-613. 1972

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7. Yassumi R, Ali N: Determination

6.

9. 10. 11.

12.

13. 14.

15.

16.

17.

16.

19.

20.

920

of the site of impaired conduction in atrio-ventricular block. J Electrocardiol 3: 193-20 1, 1970 Nasrallah AT, Gillette PC, Mullins CE, et al: Concealed His bundle extrasystoles in congenital heart disease. Am J Cardiol 35: 266-292, 1975 Rosen KM, Loeb HS, Chuquimia M, et al: Site of heart block in acute myocardial,infarction. Circulation 42:925-933, 1970 Rosen KM, Loeb HS, Chuqulmia M, et al: Mobitz type II block wthout bundle branch block (abstr). Am J Cardiol 26:657, 1970 Rosen KM, Mehta A, Rahlmtoola SH, et al: Sites of congenital and surgical heart block as defined by His bundle electrocardiography. Circulation 44:633-64 1, 197 1 Rosen KM, Heller R, Ehsani A, B1 al: Localization of site of traumatic heart block with His bundle recordings. Am J Cardiol 30: 412-417, 1972 Schuilenburg RM, Durrer D: Conduction disturbances located within the His bundle. Circulation 45:612-626, 1972 Gupta P, Chadda K, Lichstein E, et al: His bundle lesions producing heart block-electrophysiological documentation (abstr). Clin Res 20:375, 1972 Gupta PK, Lichstein E, Chadda K: Electrophysiological features of complete A-V block within the His bundle. Br Heart J 35: 610-615, 1973 Jacobson LB, Scheinman M: Catheter-induced intra-Hisian and infrafascicular block during recording of His bundle electrograms. Circulation 49:579-564, 1974 Bharatl S, Lev M, Wu D, et al: Pathophysiologic correlaGons in two cases of split His bundle potentials. Circulation 49:615-623. 1974 Scherlag BJ, Lau SH, Helfant RH, et al: A catheter technique for recording His bundle activity in man. Circulation 39:13-16, 1969 Damato AN, Lau SH, Berkowitz WD, et al: Recording of specialized conduction fibers (A-V nodal His bundle and right bundle branch) in man using an electrode catheter technique. Circulation 39:435-477, 1969 Gillette PC, Reitman MJ, Gutgesell HP, et al: Intracardiac electrography in children and young adults. Am Heart J 69:36-44,

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1975 2 1. Rosen KM, Rahimtoola SH, Slnno MZ, et al: Bundle branch and ventricular activation in man. A study using catheter recordings of left and right bundle branch potentials. Circulation 43:193203, 1971 22. Rosen KM, Ehsani A, Rahimtoola SH: H-V interval in left bundle branch block. Circulation 46:7 17-723, 1972 23. Spurrell RA, Krinkler DM, Sowton E: Study of intraventricular conduction times in patients with left bundle branch block and left axis deviation and in patients with left bundle branch block and normal QRS axis using His bundle electrograms. Br Heart J 34:1244-1249,1972 24. Schuilenburg RM, Durrer D: Problems in the recognition of conduction disturbances in the His bundle. Circulation 51:66-74, 1975 25. Lev M: Pathogenesis of congenital atrioventricular block. Prog Cardiovasc Dis 15145-157. 1972 26. Carter JB, Blieden LC, Edwards JE: Congenital heart block: anatomic correlations and review of the literature. Arch Pathol 97:51-57. 1974 27. Touboul P, Clement C, Porte J, et al: Etude electrophysiologique des troubles de conduction auriculo-ventriculaire dans I’infar&s myocardique recent. Arch Mal Coeur 65:1267-1291. 1972 26. Guerot C, Valere P, Coste A, et al: Bloc auriculo-ventriculaire localis& au tronc du faisceau de His: Le block tronculaire. Ann Cardiol Angeiol 2 1: 143- 152, 1972 29. Puech P, Grolleau-Raoux R, Latour H, et al: Diagnostic des blocks tronculaires hisiens par I’energist-rement endocavitaire et la stimulation du faisceau de His. Arch Mal Coeur 65:315322, 1972 30. El-Sherif N, Scherlag BJ, Lazzara R: Conduction disorders in the canine proximal His-Purkinje system following acute myocardial ischemia: the pathophysiology of intra-His block. Circulation 491637-647, 1974 31. Kelly DT, Brodsky SJ, Mlrowski M, et al: Bundle of His recordings in congenital complete heart block. Circulation 45:277261, 1972

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