Incomplete Right Bundle-Branch Block

An Electrocardiographic
Enigma

and Possible Misnomer

By E. NEIL MooRE, D.V.M., PH.D., JoHN P. BOINEAU, M.D., AND DONALD F. PATTWSON, D.V.M., D.Sc.
With
James

Alexander, M.D., and A. J. Kennel, M.D.

SUMMARY Incomplete right bundle-branch block (IRBBB) usually is thought to be associated with abnormalities of the peripheral Purkinje system. This paper discusses the results of a study of six dogs from the same family and three nonrelated dogs with congenital IRBBB. Cardiac catheterization data were normal, and no evidence or history of cardiac disease was found before or after death. The depolarization sequence of ventricular epicardial activation was determined, and delays in right ventricular (RV) epicardial activation times were observed. Multipoint intramural electrodes were used to study intramural activation of the ventricular septum and free walls. The "electrical thickness" near the base of the RV mass was more than double that of the normal RV mass (9 vs 4 mm). Conduction along the right bundle branch (RBB) was analyzed during cardiopulmonary bypass, and electrograms recorded simultaneously from six sites along the RBB demonstrated that conduction velocity down the bundle was normal. The normal time of activation of the endocardial RV Purkinje fibers demonstrated that conduction in the right peripheral Purkinje system also was normal. Therefore, IRBBB in these dogs did not result from conduction abnormalities within the RV specialized conduction system. Interestingly, six of these dogs were members of the F1 generation from a mating of a female beagle with pulmonary stenosis and a male beagle with ventricular septal defect. Both defects as well as IRBBB were observed in the F2 generation. The present findings suggest that IRBBB may be a developmental variation in thickness of the RV free wall rather than an abnormality of the RV conduction system in cases without apparent heart disease. The developmental variant appears to have a genetic basis.
Additional Indexing Words: Conduction delay Cardiac developmental variant Parietal block Right ventricular hypertrophy

Focal hypertrophy

INCOMPLETE RIGHT bundle-branch block or "parietal block" describes the electrocardiographic abnormality associated with a wide variety of heart diseases in which it is presumed that an abnormality exists in the peripheral Purkinje conduction system. However, the fact that the same electrocardiogram is recorded in a variety of dissimilar
From the Comparative Cardiovascular Studies Unit, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, and the Departments of Pediatrics, Medicine, and Surgery, Duke University Medical Center, Durham, North Carolina. Supported in part by grants from the American Heart Association and U. S. Public Health Service
678

clinical and experimental conditions raises a question about the specific etiology underlying incompflete right bundle-branch block (IRBBB). -.-10 There also have been a number of papers pi ublished in which individuals with electrocardii ographic evidence of IRBBB have been found to have no underlying cardiac
grants HE-4885, HE-10995, HE-11307, HE-5372, and HE-11309. Address for reprints: Dr. E. Neil Moore, Comparative Cardiovascular Studies Unit, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104. Received April 5, 1971; revision accepted for publication July 1, 1971.
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INCOMPLETE RIGHT BUNDLE-BRANCH BLOCK

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disease as demonstrated by clinical studies and by postmortem histologic studies.1-' 5 The present paper concerns electrophysiologic investigations on a family of dogs with definite electrocardiographic evidence of IRBBB in which no evidence of cardiac disease could be demonstrated, either antemortem or postmortem. Evidence is presented that the pattern of IRBBB resulted not from conduction abnormalities within the atrioventricular specialized conduction system, but rather was due to focal hypertrophy of the right ventricle which was a congenital developmental variant.
Materials and Methods Genetic Studies In the course of genetic studies of cardiovascular malformations in the dog, a female beagle with hereditary valvular pulmonic stenosis16 was mated to a male beagle with a small subaortic

ventricular septal defect. These dogs probably were not closely related as they were obtained

from sources that were geographically distant from each other. No pedigree information was available however. The female had an electrocardiogram consistent with a mild degree of right ventricular hypertrophy (right ventricular pressure 72/0, main pulmonary artery pressure 26/18). The electrocardiogram of the male was within normal limits. This mating produced seven pups (fig. 1), none of which had evidence of structural malformation of the cardiovascular system by physical examination, thoracic radiography, cardiac catheterization, or angiocardiography. Six of the seven dogs were submitted to necropsy examination and were found to have no gross evidence of cardiovascular disease. Despite the absence of gross structural abnormalities, all members of the litter had electrocardiographic patterns of the incomplete right bundle-branch block (IRBBB) type. In three dogs, the pattern was well developed, and the QRS interval was near the upper limit of normal for the dog (0.07 sec). In four others, the pattern was less developed but the spatial orientation of the QRS forces was similar to that of dogs with fully developed IRBBB. Terminal QRS forces were

em

El 0

Normal Male
Normal Femole
IRBBB (well - developed)

+
*

Neonatal Deoth NO ECG Sacrificed f or Study

= =

VSD
PS

Ventricular Septal Defect Valvulor Pulmonic Stenosis

IROBB (lesser- degree)

Figure 1
Female beagle with pulmonic stenosis and a male beagle with a ventricular septal defect produced seven pups with varying degrees of incomplete right bundle-branch block (IRBBB) but no gross cardiovascular malformations. Both pulmonic stenosis and ventricular septal defect as well as IRBBB were observed in the F2 generation. See text for full description.
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680
directed ventrally, cranially, and to the right, producing R' waves in AVR and V1 and terminal S waves in leads V3, V6, and Vl0. Members of the litter were mated inter se to produce an F2 generation consisting of 17 pups (fig. 1). Electrocardiograms were recorded in only eight of the 17 members of the F2 generation, since the remaining nine died in the early neonatal period. Of the eight studied electrocardiographically, five had normal electrocardiograms, one dog with pulmonic stenosis and a ventricular septal defect had electrocardiographic signs of right ventricular hypertrophy, and two otherwise-normal dogs had an incomplete right bundle-branch block pattern. This report deals with findings in six offspring of the F, generation which were studied by electrophysiologic methods.
Electrophysiologic Studies

MOORE ET AL.
tions of the conduction system. Serial sections of 6-8 g in thickness were made by the method of Pickett and Sommer.'8 Three dogs with normal electrocardiographic findings were studied in a like manner. After fixation, multiple measurements were made of the thickness of the free walls of the right ventricle, of the free walls of the left ventricle, and of the septum. The weight of the free wall of the right ventricle was determined as a percentage of the total ventricular weight and compared with normal values obtained by Knight.'9 The following portions of the atrioventricular conduction system were examined in each case: portions of the interatrial septum including the approaches to the atrioventricular (A-V) node, the A-V node, the penetrating and bifurcating portions of the common A-V bundle (His bundle), the proximal 1 cm of the left bundle branch, the entire right bundle branch from its origin at the bifurcation to its termination at the base of the septal papillary muscle, the freerunning false tendons arising at the base of the papillary muscle through their attachment to the free wall of the right ventricle, that portion of the right ventricular free wall to which the freerunning false tendons attached, and, finally, adjacent atrial as well as ventricular and valvular structures.

The sequence of epicardial and intramural activation of the ventricles was determined using a bipolar electrode to scan 40 points on the right and left ventricular epicardium, and multipoint, plunge electrodes to define intramural activation. These techniques have been previously described in detail.'0 During the intramural activation studies using plunge electrodes, special emphasis was made to record from various right and left Purkinje fibers both within the free ventricular walls and septum. The onset of activation of the Purkinje fibers was correlated with the onset of the QRS complex. In addition, new techniques were developed to determine the sequence of excitation along the right bundle branch and HisPurkinje system.17 These investigations were performed after completing the epicardial-intramural activation studies. Both normal dogs and dogs with IRBBB were placed on cardiopulmonary bypass, and a right ventriculotomy was made. Then a 1.0- by 1.5-cm electrode plaque containing 30 separate monopolar electrode sites located about every 2 mm was gently sutured over the right bundle branch (RBB) (as indicated in figure 5 below). This electrode path enabled multiple RBB electrograms to be recorded simultaneously in either a bipolar or a unipolar mode. It was then possible to determine the conduction velocity along the RBB since the geometry of the recording sites on the electrode patch and the time of activation at these same electrodes was known. In 10 normal dogs, the conduction velocity along the RBB using this technique was 1-3 m/sec.17
Histologic Studies

Results

Three dogs with electrophysiologically documented alterations of activation of the right ventricle (RV) had detailed histologic examina-

The X, Y, and Z scaler electrocardiograms and frontal and left sagittal vectorcardiograms inscribed using the McFee lead system are shown in figure 2 from one of the dogs with incomplete right bundle-branch block (IRBBB). The P-R interval is normal and the QRS duration is increased by about 10-15 (35 vs 45) msec. The initial forces are normal. The terminal forces, however, are directed cranially, dorsally, and toward the right. Note also that these later terminal forces are markedly slowed in their inscription. This is a characteristic feature of IRBBB in man. Figure 3 illustrates the epicardial sequence map of ventricular excitation correlated with the inscribed QRS complex in a normal dog. The heart is viewed frontally (Ant.) on the left in the same position as the heart would be observed upon a midsternotomy, and on the right it is positioned as observed in a left lateral thoracotomy (Lat.). The interventricular sulcus is indicated by the coronary arteries. Below the anterior and lateral views
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INCOMPLETE RIGHT BUNDLE-BRANCH BLOCK

681

X
y

LS

z
'Z

orA
2mv
100 msec.
Figure 2
X, Y, and Z scalar electrocardiograms and frontal (F) and left sagittal (LS) vectorcardiograms from a dog with IRBBB were recorded using the McFee lead system (dog 37). See text for discussion.

K
II

vs

Ant.

Lot.

V,

21
0
5

10

15

20

E?igure 3
Epicardial ventriciular depolarization in a normal dog. A frontal (left activation map) and left sagittal (right activation map) view of the pattern of epicardial excitation (breakthrough) are shown along with the lead II and pericardial lead V1 electrocardiograms. See text for

discussion.

of the heart is a time key with different

stippling representing the period of time within the QRS complex in which the
respective epicardial regions were activated. Lead II and precordial lead V1 QRS complexes are shown on the right with time lines indicated every 10 msec. The time of earliest
Circulation, Volume XLIV, October 1971

epicardial activity in this animal was noted at 10 msec after the onset of the reference ECG. The pattern of epicardial spread was basically similar in all normal dogs studied.-10 The earliest site of epicardial activity was located in the midright ventricle near the interventricular sulcus. Activity then spread centrifugally

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MOORE ET AL.

toward the atrioventricular groove, the inflow and outflow (conus) regions of the right ventricle (RV), and leftward across the interventricular sulcus. The left ventricular (LV) epicardium was also activated in a centrifugal fashion with earliest activity being observed in the midregions and late activity occurring at both the base and a small region near the anterior interventricular sulcus anteriorly. The late activity in the RV conus, which occurred during the same period of the QRS complex as did late activity in the LV base and anterior apex, resulted in considerable cancellation and a normal QRS complex being inscribed. The epicardial activation sequence maps and lead II and V, QRS complexes in figure 4 were recorded in a dog with IRBBB. The time key below the activation maps contains stippling corresponding to the time of activation of the respective regions of the epicardium. The rSR' QRS complex in the precordial lead V1 is characteristic of IRBBB. The frontal view of the dog's heart is shown on the left, and the left lateral view of the heart is presented on the right. In contrast to the normal dog (fig. 3) early activity was observed on the right epicardium near the interventricular sulcus and simultaneously at the apex of the LV indicating relatively later than normal RV breakthrough. Activity during the initial inscription of the R' wave in the

precordial lead V1 (10-15 msec) occurred at the right and left ventricular bases. However, unlike the activation sequence in normal dogs, there was a late 10-msec period of time at 20-30 msec in which activation occurred only in the outflow tract of the RV (conus) without any activity being recorded on the LV epicardium. The peak of the R' wave coincided in time with this unopposed surface of activation in the RV. There are several possible causes of delayed activation of the RV conus region including alterations in conduction velocity of the right His-Purkinje system as well as possible variation in wall thickness of the RV free wall. Even with normal radial conduction velocity, the increased thickness of the RV free wall could result in delayed activation of the thick region due to increased time for epicardial breakthrough. To investigate the mechanism of delayed epicardial activation, intramural activation was analyzed using plunge electrodes. Figure 5 contains simultaneously recorded intramural RV electrograms obtained from a normal dog (A), and from a dog with an electrocardiogram characteristic of IRBBB (B). Using a constant reference electrogram, the lead II electrocardiogram was time normalized with the simultaneously recorded intramural ventricular activation data as described previously. The intramural plunge electrodes had 15 monopolar electrode sites

1'

II

VI

Ant.

I
6

ZwEEE
0

,,'

_1

10

15

20

25

30

Figure 4
Epicardial ventricular depolarization in incomplete right bundle-branch block (IRBBB). Frontal (Ant.) and left sagittal (Lat.) activation maps are presented along with the lead II and precordial lead V1 electrocardiogram (dog 37). See text for discussion.
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A
Lead II V

'
Pj

Lead II

1-2
2-3 1-2 2-3 3-4 4-5 -- 5-6

3-4
4-5

100 msec.

6-7 7-8 8-9

Figure 5

A and B contain simultaneously recorded ventricular intramural electrograms recorded using plunge-type electrodes. The lead II ECG was time normalized with the simultaneously recorded ventricular electrograms. A was recorded from the base of the right ventricle in a normal dog. B was recorded in a dog with incomplete right bundle-branch block (IRBBB) (dog 37). See text for discussion.

located at 1-mm intervals along the electrode shaft. In A, recorded from a normal dog, it can be observed that four bipolar electrograms were recorded between five monopolar electrodes sites, and the "electrical thickness" of the RV free wall at this conus region therefore was 4 mm. Note also that the Purkinje depolarization spike denoted by Pj in figure 5 recorded on the endocardial surface of the RV free wall occurred at the onset of the inscription of the R wave in the lead II ECG. The activation sequence was also from endocardium to epicardium as indicated by the progressive delay in onset of activation of bipolar site 1-2 to bipolar site 4-5. In figure 5B, the endocardial bipolar electrode site 1-2 was activated earliest. A small Purkinje spike was recorded in this electrogram (Pj) and the onset of depolarizaCirculation, Volume XLIV, October 1971

tion of the Purkinje fiber was again at the initiation of the R wave as normally observed. The "electrical thickness" of the RV free wall in this dog with IRBBB varied between 8 and 9 mm in the basilar regions and pulmonary conus region. This is nearly double the normal "electrical thickness" in this region as determined in over 30 normal dogs. The spread of activation radially through the free wall occurred at a normal conduction velocity. Note that the endocardial site (site 1-2) was activated during the R wave in the lead II ECG while the outermost epicardial site (site 8-9) was activated during the S wave. Similar increased thickness of the RV free wall in the conus region was observed in eight other dogs with electrocardiographic manifestation of IRBBB.

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EKG

T3 V,
~4

~~~~~~5

20 msec. Figure 6 A schematic diagram of the right ventricular septal surface is shown with the tricuspid valve (TV) and pulmonary artery (PA) labeled. The arrows numbered 1 through 5 indicate regionls along the right bundle branch (dark structure on the septal surface) at which simultaneous electrograms 1 through 5 were recorded using a multielectrode plaque. The five simultaneously recorded right bundle-branch electrograms are shown on the right of the figure along with the lead II ECG (dog 37). See text for discussion.

The intramural activation data demonstrated a delay in RV activation which was due to focal right ventricular hypertrophy. To investigate whether conduction delays within the RV specialized conduction system might also be involved in producing the electrocardiographic picture of IRBBB in those dogs, a technique was developed in which an electrode patch was sutured over the right bundle branch (RBB) during cardiopulmonary bypass, and multiple electrograms were recorded simultaneously from the specialized conduction tissue. In this way it was possible to determine the conduction velocity along the His-Purkinje system. Using this method it was found that conduction velocity was 1-3 m/sec along the RBB in 10 normal dogs.'7 In figure 6, a schematic diagram of the right septal surface of the heart of one of the dogs with IRBBB (number 37) is illustrated along with the sites from which the proximal and distal RBB electrograms on the right of figure 6 were recorded. Note that activation progressed from the first site to the fifth site in a uniform sequence. The propagation velocity in this heart with electrocardiographic evidence of incomplete right bundle-branch block was

2.5 m/sec. Therefore, since conduction velocity in normal hearts using these techniques was between 1 and 3 m/sec, there was no conduction delay in the main septal RBB in this heart with IRBBB. In three other dogs with electrocardiographic evidence of IRBBB, the same results were obtained with complete-

ly normal conduction velocity along the RBB. Interestingly, the RV septum was depolarized in the opposite direction (large depolarization complexes occurring after the rapid bundlebranch spikes) from apex to base. Also, additional evidence that there is not a conduction delay within the RBB system is that all of the RBB electrograms occur at the beginning of depolarization of the ventricles as displayed in the ECG (top trace). Figure 7 is a time-aligned illustration of depolarization along the RV specialized conduction system. The lead II ECG is shown (top trace) along with electrograms recorded from the proximal right bundle branch (RB Pj), right ventricular endocardial Purkinje fiber (RV EnPj), and a right ventricular epicardial electrogram recorded from the right ventricular conus region. The lead II ECG exhibits a prominent S wave, which is
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INCOMPLETE RIGHT BUNDLE-BRANCH BLOCK

68-05

Lead ]I

RB Pj

RV EnPj

RV Ep P
50 msec. Figure 7
Time-normalized illustration of the sequence and activation times of the proximal right bundle branch (RB Pj), endocardial right Purkinje system (RV EnPj), and the right ventricular epicardial conus region (RV EpP) during inscription of the electrocardiogram (lead II) in a dog with IRBBB (dog 37). See text for discussion.

characteristic of IRBBB. Note that the proximal right bundle branch was depolarized normally prior to inscription of the QRS complex during the P-R interval. The right ventricular endocardial Purkinje fiber (Rv EnPj) was likewise depolarized at a normal time just after the start of the R wave. The right ventricular epicardial point (RV EpP), on the other hand, was activated much later than normal during the S wave of the lead II electrocardiogram. Therefore, despite the fact that there is delayed activation of the conus region, there does not appear to be any electrophysiologic evidence of conduction delays along the right ventricular specialized conduction system. Although no electrophysiologic evidence of conduction abnormalities could be found in the RV specialized conduction system in the dogs with IRBBB, nevertheless it was considered important to examine, by serial histologCirculation, Volume XLIV, October 1971

ic sectioning, the right atrioventricular specialized conduction tissues. It is not possible, of course, even with serial sectioning to permit quantitative conclusions to be made regarding all of the peripheral arborizations of the RBB fibers and peripheral Purkinje network which for obvious reasons could not be studied in their entirety. The area included in our histologic examination was that in which activation abnormalities have been previously demonstrated to result in electrocardiographic evidence for incomplete and complete right bundle-branch block and included the entire right bundle and Purkinje fibers in the freerunning false tendons. The atrioventricular node and common bundle of His were completely normal. Histologic serial sections showed that the RBB was intact throughout its entire length. The free-running false tendons and the arborization of Purkinje fibers in the free wall of the right ventricle likewise appeared normal in all specimens. No quantitative or qualitative differences were apparent between cases having electrocardiographic evidence of IRBBB and those designated normal. Areas of fresh hemorrhage were found in scattered portions of the specialized tissues of the dogs with IRBBB in which electrophysiologic studies were also carried out. These resulted from intramural electrode penetrations, and in no case did hemorrhage appear to interrupt the pathway of the specialized tissue. Ventricular muscle fibers were studied throughout the heart, and no abnormalities were encountered.
Discussion

The term incomplete right bundle-branch block (IRBBB) is defined in most electrocardiographic textbooks as a QRS configuration consisting of an rSr' or rsR' in V1 with or without associated s or S waves in the standard leads I), II III, and aVF. The QRS duration is usually prolonged in adults to 0.09-0.11; correspondingly less prolongation occurs in children. IRBBB is a somewhat ambiguous term due to the wide variation observed in QRS configuration and duration as well as the numerous clinical conditions in which ECG's with this abnormality are

686

MOORE ET AL.
IRBBB in man. However, they do indicate at least one basis for this electrocardiographic pattern other than the classically accepted theory of parietal block of the right Purkinje network. Strong additional support for focal regions of right ventricular hypertrophy giving rise to an ECG pattern of IRBBB is the fact that two other unrelated dogs of different breeds (keeshond and a mongrel) also had a focal right ventricular hypertrophy associated with an electrocardiographic pattern of IRBBB. It should be mentioned that when the ratio of the total weight of the right ventricular free wall was compared to total heart weight in these dogs, the ratio was at the upper limits of normal found by Knight in a series of 38 normal dogsl9 (24% of total heart weight in IRBBB dogs vs an average of 22% in normal dogs). The fact that there was not a significant increase in right ventricular wall weight as determined by this method points out that activation delays in only a small region of the right ventricle can result in changes in phase relationships of a sufficient degree to alter the usual balance of forces, thereby permitting delayed right ventricular activation to be expressed as IRBBB. The thickened right ventricular wall not only results in phasic changes in right and left ventricular activation, but also permits the activation wavefront to occupy a greater area of the right ventricular wall, thereby causing the amplitude of the late right ventricular forces to be increased in the electrocardiogram.20 Perhaps of greater significance is the finding that mild localized right ventricular hypertrophy was present in the family of beagles in the absence of any obvious hemodynamic stimulus. This suggests that the distribution of right ventricular mass is determined not only by the hemodynamic state, but also by genetic factors which govern the morphogenesis of the ventricular walls. Such intrinsic mechanisms may determine to some extent the capacity of the individual to react to hemodynamic loads and may account for the variation in right ventricular hypertrophy encountered in patients with similar degrees of hemodynamic
Circulation, Volume XLIV, October 1971

encountered. The term IRBBB implies that there is block in the peripheral right Purkinje system, and cases of IRBBB associated with acquired, congenital, or experimental lesions within the right ventricular Purkinje network have been clearly demonstrated. However, other instances of IRBBB without demonstrable cardiovascular lesions have also been reported. Thus, there is clearly a need to examine the right bundle branch-Purkinje system using direct electrophysiologic techniques to determine the sequence of right ventricular myocardial activation, as well as activation studies on the right ventricular specialized conduction system in cases of IRBBB. These types of investigations are difficult and, in many instances, impossible to perform in patients. The present investigations afforded an unusual opportunity to examine the basis of spontaneous IRBBB in a group of beagle dogs which were siblings of an F1 breeding of two dogs with congenital heart disease (fig. 1). In the present study, six canine siblings were found to have an electrocardiographic pattern of IRBBB, but no cardiovascular abnormalities could be found on clinical examination or upon histologic examination of the heart. The etiology of the IRBBB pattern was a focal hypertrophy of regions of the right ventricular free wall near the atrioventricular margin and pulmonary conus. Myocardial conduction velocity through these thickened regions of right ventricular myocardium was found to be normal; however, the longer distance that the wavefront had to travel from the endocardium to epicardium resulted in delay in the onset of activation of the right ventricular epicardium at these hypertrophied regions. Therefore, IRBBB resulted from a prolonged phase of activation in certain regions of the right ventricular free wall caused by focal hypertrophy, rather than from delay caused by conduction abnormalities within the peripheral right ventricular Purkinje system. Of course, the explanation for the surface ECG pattern of IRBBB in these animals cannot be generalized to explain all cases of

INCOMPLETE RIGHT BUNDLE-BRANCH BLOCK

687

overload. Also, the present findings suggest that the frequent occurrence of late anteriorrightward QRS forces (rSr' and S1S2S3) in apparently healthy people may in part represent normal variation in thickness and distribution of the RV mass.
Acknowledgments The authors wish to thank Ralph Iannuzzi, William Schnarr, J. H. Kasell, and C. B. Clark for invaluable technical assistance.
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5.
6.

7.

References GRANT RP: Clinical Electrocardiography, the Spatial Vector Approach. New York, McGrawHill Book Co., Inc., 1957 LEDBETTER MK, CANNON AB, COSTA AF: The electrocardiogram in diphtheritic myocarditis. Amer Heart J 68: 599, 1964 BiRiNiK AJ, NEILL CA: The electrocardiogram in congenital heart disease. Circulation 12: 604, 1955 HuTH ES, SQUIRES RD: The relation of cardiovascular phenomena to metabolic changes in a patient with chronic hypokalemia. Circulation 14: 60, 1965 PAYNE CA, GREENFIELD JC: Electrocardiographic abnormalities associated with myotonic dystrophy. Amer Heart J 65: 436, 1963 GRANT RP: Left axis deviation. Circulation 14: 233, 1956 UHLEY HN, RIVKIN L: Electrocardiographic patterns following interruption of main and peripheral branches of the canine right bundle of His. Amer J Cardiol 7: 810, 1961

8. MOORE EN, HOFFMAN BF, PATTERSON DF,

STJUCKEY JH: Electrocardiographic changes due to delayed activation of the wall of the right ventricle. Amer Heart J 68: 347, 1964 9. WATT TB, PRurrr RD: Electrocardiographic findings associated with experimental arborization block in dogs. Amer Heart J 69: 642, 1965

10. BOINEAU JP, SPACH MS, AYREs CR: Genesis of the electrocardiogram in atrial septal defect. Amer Heart J 68: 637, 1964 11. STEWART CB, MANNING GW: A detailed analysis of electrocardiograms of 500 R.C.A.F. air crew. Amer Heart J 27: 502, 1944 12. PACKARD JM, GRAETrINGER JS, GRAYBIEL A: Analysis of the electrocardiogram obtained from 1,000 young healthy aviators. Circulation 10: 384, 1954 13. Hiss RG, LAMB LF, ALLEN MF: Electrocardiographic findings in 67,375 asymptomatic subjects: Normal values. Amer J Cardiol 6: 209, 1960 14. ELIOT RS, MILLHAM WA, MILLHAM J: The clinical significance of marked left axis deviation in man without known disease. Amer J Cardiol 12: 767, 1963 15. ENTMAN ML, ESTES EH, HACKEL DB: The pathologic basis of the electrocardiographic pattern of parietal block. Amer Heart J 74: 202, 1967 16. PATTERSON DF: Epidemiologic and genetic studies of congenital heart disease in the dog. Circ Res 23: 171, 1968 17. WALSTON A, BOINEAU JP, ALEXANDER JA, SEALY WC: A study of functional dissociation in the right bundle branch. In preparation 18. PICKETT JP, SOMMER JR: Thirty-five mm film as mounting base and plastic spray as cover glass for histologic sections. Arch Path (Chicago) 69: 239, 1960 19. KNIGHT DH: Effects of spontaneous cor pulmonale in dogs (Dirofilaria immitis infestation) on the gross morphology and hemodynamics of the lung circulation and ventricles. Masters thesis, University of iPennsylvania 20. BOINEAU JP, HILL EN, SPACH MS, MOORE EN: Basis of the electrocardiogram in right ventricular hypertrophy: Relationship between ventricular depolarization and body surface potentials in dogs with spontaneous RVH-contrasted with normal dogs. Amer Heart J 76: 605, 1968

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