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Vectorcardiographic study of the QRS loop in patients with left anterior focal block
Clinical communications
Vectorcardiographic with
left
anterior
study focal
of the
QRS loop
in patients
block
H. Kulbertus, M.D.* P. Collignon, M.D.** L. Humble& M.D.*** LGge, Belgium
I
n recent years, there has been general agreement that the most common cause of left axis deviation (L.A.D.) is the left anterior focal block.1-6 This opinion is substantiated by several clinical and electrocardiographic-pathologic correlative studiesl~3~4~6 and by experimental work on canine and primate hearts.‘eg While electrocardiographic criteria for diagnosis of this conduction abnormality have been proposed,‘+4 its vectorcardiographic aspects have so far received little attention.lO The present paper is concerned with the vectorcardiographic findings in 40 patients aged 45 or over whose electrocardiogram was suggestive of a left anterior focal block. Methods
Spatial vectorcardiograms were recorded using the McFee-Parungao axiai system.” (Hewlett Packard Vectorcardiograph System 1520 A). The frontal, horizontal, and left sagittal loops as well as the scalar tracings X, Y, and Z were photographed
by means of a Polaroid camera. ‘?he upper frequency response of the recorder was set at 200 c.p.s. and the loop was interrupted either every 2.5 msec. or 5 msec. The sensitivity was adjusted at 20 or 10 mm. per millivolt and the 3 orthogonal scalar tracings were recorded at a speed of 100 mm. per second. For better delineation of initial forces, a fivefold amplification of the isolated QRS loop was also recorded. Timing of the various points of the loop was obtained by counting dots on the photograph from the onset of QRS. Since inaccuracies of timing owing to haziness around the E point are inherent in this method of determining instantaneous vectors,12 the determinations were checked with the scalar tracings so that the three planar instantaneous vectors of the same timing coincided with one another in their coordinates. The duration of the QRS loop was measured and the direction and magnitude of the following vectors were determined in each of the three projection planes; the
From the Division of Cardiology. Department of Medical Clinic and Semiology. University Li&x, Belgium. Part of this work was presented as a free communication at the Fifth European Congress September, 1968. Received for publication Feb. 19, 1969. Reprint requests to: Dr. Kulbertus. Chargk de Recherches du F.N.R.S., Department LiPae. School of Medicine. Li&ze.-. Beleium. ~*Charge de Recherches du Fends National Belge de la Recherche Scientifique. **Assistant. Q*Collaborateur Scientifique de l’l;niversit&
Vol. 79, No. 3, pp. 293-304
March, 1970
of L&e
School
of Cardiology,
of Cardiology
of Medicine,
Athens.
University
American Heart Journal
Greece,
of
293
294
Kulbertus,
CollignoTl,
maximal QRS vector and the instantaneous vectors at 10, 20, 30, 40, 50, and 60 msec. after the onset of QRS. The measurements of vector angles~in~each plane were made with a frame of reference in which the right of the abscissa was taken as 0 degrees, and the inferior and superior directions of ordinate were + 90 or - 90 degrees, respectively. For statistical treatment of angular data,
Fig. 1. Electrocardiogram and peripheral vascular
Amer. Hmvf 1. Marih, 19io
and Humblet
and vectorcardiogram disease. Calibration:
the procedure suggested by Downs and associate+ was used. Among other advantages, this method avoids difficulties inherent to the numerical discontinuity point at f 180 degrees. The prevalent direction (A) of each timed vector is determined. An index d which varies from 0 to 1 measures the precision of the prevalent direction. The closer its value approaches 1, the greater is the cluster of
of a 63-year-old man with 500 pvv. The loop is interrupted
atherosclerosis, angina every l/400 sec.
pectoris,
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295
disclosed: arterial hypertension with diastolic pressure higher than 100 mm. Hg (23 cases), atherosclerosis with calcifications of the ascending aorta (21 cases), radiologic evidence of left ventricular hypertrophy (20 cases), peripheral vascular disease(15 cases), angina pectoris (9 cases), aortic valvular disease (2 cases), and mild mitral incompetence probably related to papillary muscle dysfunction (2 cases). No patient with pulmonary emphysema or chronic lung disease was included in the present group.
the angles. Furthermore, to take into account the size of the sample, a x2/df value is calculated and indicates the significance of clustering. If x2/df is greater than 3.00, 4.61, or 6.91, the clustering is significant at the 5, 1, or 1 per cent level, respectively. Description
study of QRS loop
of patients
The following electrocardiographic criteria were used for selection of the patients: (1) total QRS duration shorter than 120 msec.; (2) deviation of the mean QRS axis to the left and superior of -30 degrees in the frontal plane; (3) ventricular complexes showing a tall R wave in Leads I and aVr, and an rS morphology in Leads II, III, and aVF. The present series consists of 40 patients (25 male, 15 female) ranging in age from 45 to 82 years with an average of 61. They were clinically evaluated in our department and the following clinical features were
Results
The total duration of the QRS complex was 92.5 msec. f 12.4. Three main inflection points (Figs. 1, 2, and 5) were consistently observed in the loops. On the average, they occurred at 15 msec. (10 to 20), 35 msec. (30 to 40), and 65 msec. (50 to 70), respectively. The
“>“_
.’
.,
.-,
,
Fig. 2. Electrocardiogram and vectorcardiogram of a 63-year-old man with aortic stenosis regurgitation. These tracings wererecordedon the same day as the second electrocardiogram bration: 500 JN. The loop is interrupted every l/200 sec.
and mild mitral of Fig. 8#. Cali-
loop was thus divided into four parts which, for description purposes, have been designated as initial, early, midtemporal, and late portions of the QRS.r4 The frontal #lane loop was open-faced and inscribed counterclockwise in all cases. The initial vectors were nearly always directed inferiorly, either to the right or to the left. The efferent limb proceeded horizontally to the left. Between 30 and 40 msec., the loop abruptly swang superiorly and the midtemporal vectors xvere inscribed in the left superior quadrant. The
FRONTAL
third inflection point was located at about -90 degrees. Therefrom, the return to the E point was achieved with small delay, if any. The loop passed a little into the right superior quadrant in 14 cases. In 26 patients, 9 of whom had left ventricular the shape of the frontal hypertrophy, plane loop was nearly that of a rightangled triangle (Fig. 1). The remaining 14 patients (11 of whom had left ventricular hypertrophy) showed a more circular frontal loop (Fig. 3) with a midtemporal portion of the QRS bending
PLANE
-90’ I
0.01 set a d X2/d,
Fig. 3. Scattergram plane. The prevalent
86' 0.70 19.71
0.02
a035ec
set
32"
-
11’
0.81
a96
26.57
36.63
of the angular direction direction (A) is indicated
0.04 set
0.05 see
0.06 set
Vmax
-11’
- 50’
-77'
-25'
0.90 32.4
0.85 28.9
0.82
0.77
26.89
23.59
of the maximal and instantaneous by the sign C#J.See text for definition
timed vectors in the frontal of d and x2/df.
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Vectorcnrdiogrnphic
outward. The incidence of this type of vectorcardiogram was significantly higher in the presence of left ventricular hypertrophy as judged from chest films (p < 0.01). The maximal frontal vector occurred at 45 msec. (=t 12) and its mean voltage was 1.56 mv. i 0.67. The scattergram and statistical analysis of the 40 patients’ tracings indicated a good degree of clustering for each timed vectors in the frontal projection (Fig. 3). The horizontal plane loop was inscribed counterclockwise in all cases. The initial vectors were directed anteriorly in all but 5 patients, 3 of whom exhibited advanced left ventricular hypertrophy. The loop soon moved posteriorly and occupied the
~iORlZONTAL
I 2
Fig. 4. plane.
0.01 SK
a.02 set
87’
44.
d
0.58
0.72
X2/df
1318
20.88
Scattergram
of the
angular direction
5’ 0.836
of the
297
left posterior quadrant. The late portion proceeded nearly along the 2 axis with minimal crossing to the right in 14 instances. The maximal vector occurred at 48 msec. f 10 and its mean voltage was 1.84 mv. f 0.82. Statistical analysis of the 40 tracings indicated that, the 10 msec. vectors being excepted, the instantaneous and maximal vectors were very clustered in the horizontal plane (Fig. 4). The left sagittal plane loop showed characteristic alterations (Fig. 5). It was inscribed entirely or mostly counterclockwise in all but 5 patients. The initial vectors were nearly always directed anteriorly and inferiorly and the loop soon passed behind the Y axis. At about 30 to 40 msec.,
PLANE
0.03sec
27.36
study of QRS loop
0.0 4 set
0.05St.C
-33’
-57’
0.87 30.7
maximal
0.06sec -78
0.31 3308
and instantaneous
VnUX - 51’
a92 34 18
timed
0.82 26.8
vectors
in the horizontal
298
Kulhertns,
.4mrr. Hem? J. March. 1970
C’ollignon, 11nd Humblet
Fig. 5. Examples of isolated sagittal plane loops showing the QRS loop and its four separate portions. In Cases 1, 2, 3, and 4, theposteriorlydirectedmovement of the earIy vectors is seen as a straight, easily identified segment. In Case 5, this movement is smaller and most of the early vectors are inscribed almost perpendicularly to the sagittal plane.
there was a rapid movement directed superiorly and the midtemporal vectors were inscribed in the posterosuperior quadrant. The loop was elongated. Its maximal vector occurred at 5.5 msec. & 8, was located at about -30 degrees, and had a mean voltage of 1.84 mv. Z!Z 0.66. It should be noted that the posteriorly directed movement of the early portion of the loop varied in amplitude. In the majority of cases, the early vectors constituted an easily identified horizontal straight segment (Fig. 5, parts 1 through 4), but in some instances the posterior displacement was smaller and most of the corresponding vectors were inscribed almost perpendicularly to the sagittal plane (Fig. 5, part 5). This feature accounts for the considerable scatter observed at 30 msec. in this projection while there was reasonably good cluster at 10 and 40 msec., and extremely good cluster at 50 and 60 msec. (Fig. 6). In summary, the important diagnostic features of these vectorcardiograms in-
clude: (1) initial vectors of ventricular depolarization directed anteriorly and inferiorly in most instances; (2) early vectors traveling horizontally to the left and, to a variable extent, posteriorly; (3) abrupt upward shift of the loop between 30 and 40 msec. and midtemporal vectors located in the left superior and posterior octant. In 5 patients although the standard electrocardiograms fulfilled all the selection criteria, the vectorcardiograms did not exhibit the characteristic features that have just been described. On the contrary, the rotation was entirely clockwise in the left sagittal projection and the early electromotive forces were directed anteriorly (Fig. 7). Finally, the following clinical observations deserve being reported: (1) three patients whose electrocardiograms initially showed a left axis deviation with a RIrSII1 pattern subsequently developed a complete left bundle branch block; (2) the characteristic electrocardiographic and vectorcardiographic features considered in this paper were sometimes observed to be intermittent (2 cases) or transitory (3 cases). They suddenly appeared for instance during an exercise test in 2 patients with angina pectoris. Fig. 8 illustrates a case of transitory left axis deviation. In this 63-year-old patient with congenital aortic stenosis we observed several abrupt shifts from normal QRS axis to left axis deviation. These changes took place without any attending clinical event. Furthermore, whenever left axis deviation developed, it was accompanied by inversion of the T wave in Leads I and aVr. The T-wave alteration, most likely secondary to change in ventricular excitation, mimicked the so-called pattern of left ventricular hypertrophy “with strain.” Discussion
Production of a septal laceration which interrupts the anterior rami of the left bundle branch in the baboon heart is attended by changes in the spread of activation into the anterior free wall of the left ventricle.8 The electrocardiographic expression of these changes is a leftward shift of the mean QRS axis to -30 degrees or higher. Similar observations have been reported in man after surgical injury to
Volwne Number
79 3
Vectorcardiographic
LEFT
Fig. 6. Scattergram plane.
of the angular
direction
SAGITTAL
of the maximal
the anterior division of the left branch during transventricular mitral4 or aortic commissurotomyi5 or during corrective incision of the left ventricular outflow tract in patients with idiopathic hypertrophic subaortic stenosis.4J6 Observations derived from direct epicardial recordings indicate the following pattern of excitation in experimental left anterior arborization block.g The earliest focus of epicardial depolarization is located near the anterior trabeculated zone of the right ventricle about halfway to the apex (15 to 20 msec.). Depolarization of the epicardial surface of the posterior portion of the left ventricle occurs between 30 and 40 msec. and the activation is much
study of QRS loop
299
PLAFIE
and instantaneous
timed
vectors
in the left sagittal
delayed in the laterobasal region of the left ventricle where excitation occurs between 50 and 70 msec. It seems very tempting to interpret our findings in the light of these experimental results. The initial anterior vectors of our cases would mainly represent the activation of septal and paraseptal masses. The early vectors horizontally directed to the left and posteriorly would be predominantly determined by the spread of activation into the posterodiaphragmatic portion of the left ventricular free wall. Finally, the midtemporal vectors located in the left posterior and superior octant would result from markedly delayed excitation of the laterobasal wall of the left ventricle.
Fig. 7. Electrocardiogram and vectorcardiogram of a 65year-old man with ischemic heart disease hypertension. Calibration: 500 pv. The loop is interrupted every l/400 sec. To be noted, the anterior tion of the initial and early vectors and the clockwise rotation of the aagittal plane loop.
The following observation might also support the latter assumption. From comparison between epicardial excitation maps and vectorcardiograms recorded in the same patients, Arntzeniusi7Js has recently showed that the main inflection points of the QRS loop reflect major occurrences in the excitation of the heart. In particular, the inflection points where the loop changes
and mild localiza-
first, from an anterior to posterior direction and, later, from a leftward to rightward direction were found to coincide with the breakthrough of the excitation fronts at the right anterior and left ventricular epicardium, respectively. Since epicardial recordings were not available in our series, we could only try to draw a parallel between our vectorcardiographic findings
Vectorcardiographic
study of QRS loop
301
1830.67.
A’R
01
I,
16.10.67. 01
,oz
03
t
aVF
2O.M,67. h
02
03
03
-
&JR
nvl”
aVR
aVL
‘aVF
aVF
V6
Fig. 8. Same patient as in Fig. 2. These five electrocardiograms were recorded a few days apart. The second and fourth tracings show left axis deviation with an inverted T wave in Leads I and aVL. The precordial leads of the last tracing are shown to allow comparison with those recorded in the presence of left axis deviation (Fig. 2).
302
Kulbertus,
Collignon,
und Humblet
and the epicardial data obtained in the primate heart after production of a left anterior arborization block. It is worth being noted that there is indeed a very satisfactory correlation in timing between the three successive inflection points seen in the vectorcardiograms of our patients and the arrival of excitation at the epicardial surface of the anterior, left posterior, and left laterobasal aspects of the primate heart in the presence of experimental left anterior arborization block. According to these data and although no pathologic or electrophysiologic data were actually obtained in our patients, it is assumed that the type of vectorcardiograms described in this paper corresponds to a left anterior focal block. The same opinion has been expressed by Testoni and associatesi who studied various forms of focal blocks, and by Cohen and coworkers’g who observed vectorcardiograms exactly similar to ours in cases where aberrant ventricular conduction was experimentally produced by introduction of atria1 premature beats. The observations that the electrocardiographic and vectorcardiographic patterns described here may be transitory or intermittent,10~1gJ4 that they may precede complete left bundle branch block, and, finally, that their association with right bundle branch block is a common forerunner of complete atrioventricular block21-25 represents further pieces of evidence to support the hypothesis according to which this type of left axis deviation are related to a focal conduction disturbance of the left bundle branch. The pathologic basis of these vectorcardiographic changes are not yet precisely known. They undoubtedly may vary in both location and extent.21*26 This assumption is substantiated by the experimental demonstration that the same axis shift may be obtained either by a proximal block (septal laceration)‘mg or by a distal block (cocaine solution injection into the left ventricular free wa11).5 Similarly in man, the anterior radiation of the left bundle branch may be proximally interrupted in the interventricular septum either by surgical injury,4,‘5*16 infarction,27 or fibrotic infiltration.1-4p6 The latter process seems rather frequent after
.-lrwr. Heart 1. March. 1970
50 years of age. It is known that fibrosis, hyalinization with or without calcification of the mitral valve, the pars membranacea, the central fibrous body, and/or the summit of the muscular ventricular septum may be observed in most hearts in the fifth and sixth decades.28-30 This sclerosis of the left side of the cardiac skeleton, which seems particularly frequent in hypertension and coronary heart disease30 may catch the adjacent left bundle branch or its major ramifications.21~28-30 In some autopsied cases of left axis deviation, histological examination of the heart revealed fibrotic lesions involving predominantly the fibers of the anterior division.4*6 In other instances, the whole left bundle branch appeared extensively involved.21J6 In the latter cases, it is most likely that a few undamaged specific fibers are sufficient to conduct the activation from the node to the left ventricle and that the anterior division of the left bundle has a greater conduction delay than that of the posterior ramification. On the other hand, a significant number of hearts from patients with left axis deviation exhibit on serial sectioning no anatomic abnormalities of the proximal portions of the conduction system.4J6J1 In those patients, the conduction delay probably results from diffuse or scattered myocardial lesions. Variations in the location of the lesions producing the block might account for the scatter of the initial vectors. To be noted that in 5 cases of the present series, the initial vectors start posteriorly. This sign usually suggests an anteroseptal infarction32 but is no longer reliable in the presence of advanced left ventricular hypertrophy.33z34 The present observations also confirm that a left anterior focal block is frequently associated with left ventricular hypertrophy (50 per cent of our cases). The presence of LVH results in changes in magnitude but not in direction of the instantaneous vectors and the loop maintains all its essential characteristics. It is likely that the left axis deviation is not due to LVH alone but suggests a conduction delay in addition.‘s4 The case illustrated in Fig. 8 is particularly interesting in that respect and shows that the electric
Volume Number
79 3
pattern of left ventricular hypertrophy with left axis deviation may be a transitory phenomenon. This feature already reported by Segers and associates35 in 1952 supports Pruitt’s opinion36 that both the abnormal direction of activation and some of the evidence of LVH might be due to conduction disturbances. Five patients of the present series showed anteriorly oriented initial and early electromotive forces, and an entirely clockwise rotation of the left sagittal plane loop. These cases would take place in type II of Testoni’s classification.iO The pathologic differences that could account for the peculiarities of those 5 tracings are unknown and deserve further study. Testoni’O assumes that the causative factor might be pathologic alterations involving the posteroseptal area or the posteroinferior wall of the left ventricle. This interpretation is admittedly purely speculative and its substantiation must await histologic proof. Summary
The authors have studied the vectorcardiograms of 40 patients, 45 years of age or over, whose electrocardiograms showed a QRS duration shorter than 120 msec., a leftward shift of the mean QRS axis and ventricular complexes with a tall R wave in Leads I and aVL, and an rS morphology in Leads II, III, and aVr. Most patients had atherosclerosis, hypertension, or ischemic heart disease. The following vectorcardiographic characteristics were disclosed: (1) The frontal plane loop was open-faced and turned counterclockwise in all cases; (2) the initial vectors were nearly always directed anteriorly and inferiorly; (3) the early vectors travelled horizontally to the left and, to a variable extent, posteriorly; (4) the midtemporal vectors were located in the left, posterior, and superior octant. These vectorcardiographic features were sometimes observed to be transitory or intermittent or to precede the development of a complete left bundle branch block. Their association with a complete right bundle branch block is known to be a common forerunner of complete atrioventricular block.
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From comparison with experimental data reported in the literature, the characters of the loops observed in these cases are assumed to be related to a delayed activation of the anterolateral wall of the left ventricle and to correspond to left anterior focal block. We would like to sincerelythank Professor A. Nizet for his most helpful interest and for the opportunity to perform this study in his department. We also wish to thank Miss S. Smeets and Mrs. B. Vervier for their technical and secretarial assistance. REFERENCES 1. Grant, R. P.: Left axis deviation: An electrocardiographic-pathologic correlative study, Circulation 14:233, 1956. 2. Davies, H., and Evans, W.: The significance of deep S waves in leads II and III, Brit. Heart J. 22:551, 1960. 3. Corne, R. A., Parkin, T. W., Brandenburg, R. O., and Brown, A. L.: Significance of marked left axis deviation: electrocardiographic-pathologic correlative study, Amer. J. Cardiol. 15:605, 1965. 4. Pryor, R., and Blount, S. G.: The clinical significance of true left axis deviation, AMER. HEART J. 72:391, 1966. 5. Van Bogaert, A.: Valeur clinique de la sinistrodeviation de l’axe Clectrique dans le plan des derivations standard, Arch. Mal. Coeur. 60:337, 1967. R. L., and Pryor, R.: Quantitative and 6. Hawley, electrocardiographic correlation of the conduction system of the heart, Amer. J. Cardiol. 15:132, 1965. T. B., and Pruitt, R. D.: Electrocardio7. Watt, graphic findings associated with experimental arborization blocks in does. AMER. HEART "I. 69:642, 1965. 8. Watt, T. B., Murao, S., and Pruitt, R. D.: Left axis deviation induced experimentally in a nrimate heart. AMER. HEART 1. 70:381. 1965. 9. Watt, T. B., Freund, G. E., Purrer, b., and Pruitt, R. D.: Left anterior arborization block combined with right bundle branch block in canine and primate hearts. An electrccardiographic study, Circ. Res. 2257, 1968. 10. Testoni, F., Narbone, N. B., and Tommaselli, A.: Aspetti vettocardiographici nei blocchi sinistri con elettrocardiogramma di tippo RI-SII-SIII, Mal. Cardiov. 9:379, 1968. 11. McFee, R., and Parungao, A.: An orthogonal lead system for clinical electrocardiography, AMER. HEART J. 62:93, 1961. 12. Pipberger, H. V.: The normal orthogonal electrocardiogram with a critique on some commonly used analytic criteria, Circulation 17:1102, 1958. 13 Downs, Th. D., Liebman, J., Agusti, R., and Romberg, H. C.: The statistical treatment of angular data in vectorcardiography, Proc. Long Island Jewish Hosp. Vectorcardiography, Am.,
I
14.
1.5.
16.
17.
18.
19.
20.
21. 22.
23.
24.
sterdam, 1965, North Holland Publishing Company, p. 272. Burch, G. E., and DePasquale, N. I’.: Electrocardiography in the diagnosis of congenital heart disease. Philadelohia. 1967. Lea & Febiger, Publishers. ’ ’ ’ Samson, W. E., and Bruce, R. A.: Left ventricular parietal block produced by transventricular aortic commissurotomy, AMEK. HEART J. 63:41, 1962. Wigle, E. D., and Baron, R.: Electrocardiogram in muscular subaortic stenosis: effect of left atrial incision and right bundle branch block, Circulation 34:X5, 1966. Arntzenius, A. C.: Physiological basis for recognizing ventricular hypertrophy in the vectorcardiogram. Brit. Heart T. 30:421. 1968. (Abst.) Arntzemus, A. C.: A model of excitation‘of the human heart. Its value in establishing a link between pathway of excitation and clinical Thesis, ITniversity of vectorcardiography, Leiden, 1968. Cohen, S. I., Lau, S. H., Stein, E., Young, M. W., and Damato, A. W.: Variations of aberrant ventricular conduction in man: Evidence of isolated and combined block within the specialized conduction system: an electrocardiographic and vectorcardiographic study, Circulation 38:899, 1968. Taccola, A. F.: Left bundle branch semiblock. A clinical contribution, Ma]. Cardiov. 9:257, 1968. Lencgre, J.: Contribution ri l’etude des blocs de branche, Paris, 1958, J. B. Bailliere. Lasser, R. P., Haft, J. I., and Friedberg, C. I(.: The relationship of right bundle branch block with marked left axis deviation (with left anterior parietal or peri-infarction block) to complete heart block and syncope, Circulation 37:429, 1968. Slama, R., Marneffe, H., Gourgon, R., and Motte, G.: Aspect du ventriculogramme en rythme sinusal chez les malades atteints de blocs auriculo-ventriculaires chroniques, Ma]. Cardiov. 7:1, 1966. Salzmann, P., Linn, H., and Pick, A.: Right bundle branch block with left axis deviation, Brit. Heart J. 28:703, 1966.
2.5.
26.
27. 28.
29.
30. 31.
32.
33.
34.
3.5.
36.
Kulbertus, II., and Collignou, I’.: ‘Ihe association of right bundle branch block with left superior or inferior intraventricular block. Its relationship to complete heart block and StokesAdams syndrome, Brit. Heart J. 31:435, 1969. Entman, M. L., Estes, E. H., and Hackel, D. B.: The pathologic basis of the electrocardiographic pattern of parietal block, AMER. HEART J. 74:202, 1967. Grant, R. I’.: Peri-infarction block, Prog. Cardiov. Dis. 2:237, 1959. Lev, M.: The pathology of complete atrioventricular block, Prog. Cardiov. Dis. 6:317, 1964. Lev, M.: The normal anatomy of the conduction system in man and its pathology in atrioventricular block, Ann. N. Y. Acad. Sci. 111:817, 1964. Lev, M.: Pathology of bundle branch block, Heart Bull. 16:107, 1967. Lepeschkin, E.: Electrocardiographic diagnosis of bilateral bundle branch block in relation to heart block, Prog. Cardiov. Dis. 6:445, 1964. Hugenholtz, P. G., Whipple, G. H., and Levine, H. D.: A clinical appraisal of the vectorcardiogram in myocardial infarction, Circulation 24:808, 1961. Estes, E. H., Jr.: Left ventricular hypertrophy in acquired heart disease: a comparison of the vectorcardiogram in aortic stenosis and aortic insufficiency, Proc. Long Island Jewish Hospital symposium on vectorcardiography, Amsterdam. 1965. North Holland Publishing Company, p. 157. Bell, H., Pugh, D., and Dunn, M.: Vectorcardiographic evolution of left ventricular hypertrophy, Brit. Heart J. 30:70, 1968. Segers, M., Regniers, M., and Delatte, E.: L’installation brusque de l’image electrocardiographique de preponderance, Acta Cardiol. 7:63, 1952. Pruitt, R., Esser, H. E., and Burchell, M. B.: Studies on the spread of excitation through the ventricular myocardium, Circulation 24:808, 1951.
Vectorcardiographic with
left
anterior
study focal
of the
QRS loop
in patients
block
H. Kulbertus, M.D.* P. Collignon, M.D.** L. Humble& M.D.*** LGge, Belgium
I
n recent years, there has been general agreement that the most common cause of left axis deviation (L.A.D.) is the left anterior focal block.1-6 This opinion is substantiated by several clinical and electrocardiographic-pathologic correlative studiesl~3~4~6 and by experimental work on canine and primate hearts.‘eg While electrocardiographic criteria for diagnosis of this conduction abnormality have been proposed,‘+4 its vectorcardiographic aspects have so far received little attention.lO The present paper is concerned with the vectorcardiographic findings in 40 patients aged 45 or over whose electrocardiogram was suggestive of a left anterior focal block. Methods
Spatial vectorcardiograms were recorded using the McFee-Parungao axiai system.” (Hewlett Packard Vectorcardiograph System 1520 A). The frontal, horizontal, and left sagittal loops as well as the scalar tracings X, Y, and Z were photographed
by means of a Polaroid camera. ‘?he upper frequency response of the recorder was set at 200 c.p.s. and the loop was interrupted either every 2.5 msec. or 5 msec. The sensitivity was adjusted at 20 or 10 mm. per millivolt and the 3 orthogonal scalar tracings were recorded at a speed of 100 mm. per second. For better delineation of initial forces, a fivefold amplification of the isolated QRS loop was also recorded. Timing of the various points of the loop was obtained by counting dots on the photograph from the onset of QRS. Since inaccuracies of timing owing to haziness around the E point are inherent in this method of determining instantaneous vectors,12 the determinations were checked with the scalar tracings so that the three planar instantaneous vectors of the same timing coincided with one another in their coordinates. The duration of the QRS loop was measured and the direction and magnitude of the following vectors were determined in each of the three projection planes; the
From the Division of Cardiology. Department of Medical Clinic and Semiology. University Li&x, Belgium. Part of this work was presented as a free communication at the Fifth European Congress September, 1968. Received for publication Feb. 19, 1969. Reprint requests to: Dr. Kulbertus. Chargk de Recherches du F.N.R.S., Department LiPae. School of Medicine. Li&ze.-. Beleium. ~*Charge de Recherches du Fends National Belge de la Recherche Scientifique. **Assistant. Q*Collaborateur Scientifique de l’l;niversit&
Vol. 79, No. 3, pp. 293-304
March, 1970
of L&e
School
of Cardiology,
of Cardiology
of Medicine,
Athens.
University
American Heart Journal
Greece,
of
293
294
Kulbertus,
CollignoTl,
maximal QRS vector and the instantaneous vectors at 10, 20, 30, 40, 50, and 60 msec. after the onset of QRS. The measurements of vector angles~in~each plane were made with a frame of reference in which the right of the abscissa was taken as 0 degrees, and the inferior and superior directions of ordinate were + 90 or - 90 degrees, respectively. For statistical treatment of angular data,
Fig. 1. Electrocardiogram and peripheral vascular
Amer. Hmvf 1. Marih, 19io
and Humblet
and vectorcardiogram disease. Calibration:
the procedure suggested by Downs and associate+ was used. Among other advantages, this method avoids difficulties inherent to the numerical discontinuity point at f 180 degrees. The prevalent direction (A) of each timed vector is determined. An index d which varies from 0 to 1 measures the precision of the prevalent direction. The closer its value approaches 1, the greater is the cluster of
of a 63-year-old man with 500 pvv. The loop is interrupted
atherosclerosis, angina every l/400 sec.
pectoris,
Volume Number
79 3
Vectorcardiographic
295
disclosed: arterial hypertension with diastolic pressure higher than 100 mm. Hg (23 cases), atherosclerosis with calcifications of the ascending aorta (21 cases), radiologic evidence of left ventricular hypertrophy (20 cases), peripheral vascular disease(15 cases), angina pectoris (9 cases), aortic valvular disease (2 cases), and mild mitral incompetence probably related to papillary muscle dysfunction (2 cases). No patient with pulmonary emphysema or chronic lung disease was included in the present group.
the angles. Furthermore, to take into account the size of the sample, a x2/df value is calculated and indicates the significance of clustering. If x2/df is greater than 3.00, 4.61, or 6.91, the clustering is significant at the 5, 1, or 1 per cent level, respectively. Description
study of QRS loop
of patients
The following electrocardiographic criteria were used for selection of the patients: (1) total QRS duration shorter than 120 msec.; (2) deviation of the mean QRS axis to the left and superior of -30 degrees in the frontal plane; (3) ventricular complexes showing a tall R wave in Leads I and aVr, and an rS morphology in Leads II, III, and aVF. The present series consists of 40 patients (25 male, 15 female) ranging in age from 45 to 82 years with an average of 61. They were clinically evaluated in our department and the following clinical features were
Results
The total duration of the QRS complex was 92.5 msec. f 12.4. Three main inflection points (Figs. 1, 2, and 5) were consistently observed in the loops. On the average, they occurred at 15 msec. (10 to 20), 35 msec. (30 to 40), and 65 msec. (50 to 70), respectively. The
“>“_
.’
.,
.-,
,
Fig. 2. Electrocardiogram and vectorcardiogram of a 63-year-old man with aortic stenosis regurgitation. These tracings wererecordedon the same day as the second electrocardiogram bration: 500 JN. The loop is interrupted every l/200 sec.
and mild mitral of Fig. 8#. Cali-
loop was thus divided into four parts which, for description purposes, have been designated as initial, early, midtemporal, and late portions of the QRS.r4 The frontal #lane loop was open-faced and inscribed counterclockwise in all cases. The initial vectors were nearly always directed inferiorly, either to the right or to the left. The efferent limb proceeded horizontally to the left. Between 30 and 40 msec., the loop abruptly swang superiorly and the midtemporal vectors xvere inscribed in the left superior quadrant. The
FRONTAL
third inflection point was located at about -90 degrees. Therefrom, the return to the E point was achieved with small delay, if any. The loop passed a little into the right superior quadrant in 14 cases. In 26 patients, 9 of whom had left ventricular the shape of the frontal hypertrophy, plane loop was nearly that of a rightangled triangle (Fig. 1). The remaining 14 patients (11 of whom had left ventricular hypertrophy) showed a more circular frontal loop (Fig. 3) with a midtemporal portion of the QRS bending
PLANE
-90’ I
0.01 set a d X2/d,
Fig. 3. Scattergram plane. The prevalent
86' 0.70 19.71
0.02
a035ec
set
32"
-
11’
0.81
a96
26.57
36.63
of the angular direction direction (A) is indicated
0.04 set
0.05 see
0.06 set
Vmax
-11’
- 50’
-77'
-25'
0.90 32.4
0.85 28.9
0.82
0.77
26.89
23.59
of the maximal and instantaneous by the sign C#J.See text for definition
timed vectors in the frontal of d and x2/df.
Volume Number
79 3
Vectorcnrdiogrnphic
outward. The incidence of this type of vectorcardiogram was significantly higher in the presence of left ventricular hypertrophy as judged from chest films (p < 0.01). The maximal frontal vector occurred at 45 msec. (=t 12) and its mean voltage was 1.56 mv. i 0.67. The scattergram and statistical analysis of the 40 patients’ tracings indicated a good degree of clustering for each timed vectors in the frontal projection (Fig. 3). The horizontal plane loop was inscribed counterclockwise in all cases. The initial vectors were directed anteriorly in all but 5 patients, 3 of whom exhibited advanced left ventricular hypertrophy. The loop soon moved posteriorly and occupied the
~iORlZONTAL
I 2
Fig. 4. plane.
0.01 SK
a.02 set
87’
44.
d
0.58
0.72
X2/df
1318
20.88
Scattergram
of the
angular direction
5’ 0.836
of the
297
left posterior quadrant. The late portion proceeded nearly along the 2 axis with minimal crossing to the right in 14 instances. The maximal vector occurred at 48 msec. f 10 and its mean voltage was 1.84 mv. f 0.82. Statistical analysis of the 40 tracings indicated that, the 10 msec. vectors being excepted, the instantaneous and maximal vectors were very clustered in the horizontal plane (Fig. 4). The left sagittal plane loop showed characteristic alterations (Fig. 5). It was inscribed entirely or mostly counterclockwise in all but 5 patients. The initial vectors were nearly always directed anteriorly and inferiorly and the loop soon passed behind the Y axis. At about 30 to 40 msec.,
PLANE
0.03sec
27.36
study of QRS loop
0.0 4 set
0.05St.C
-33’
-57’
0.87 30.7
maximal
0.06sec -78
0.31 3308
and instantaneous
VnUX - 51’
a92 34 18
timed
0.82 26.8
vectors
in the horizontal
298
Kulhertns,
.4mrr. Hem? J. March. 1970
C’ollignon, 11nd Humblet
Fig. 5. Examples of isolated sagittal plane loops showing the QRS loop and its four separate portions. In Cases 1, 2, 3, and 4, theposteriorlydirectedmovement of the earIy vectors is seen as a straight, easily identified segment. In Case 5, this movement is smaller and most of the early vectors are inscribed almost perpendicularly to the sagittal plane.
there was a rapid movement directed superiorly and the midtemporal vectors were inscribed in the posterosuperior quadrant. The loop was elongated. Its maximal vector occurred at 5.5 msec. & 8, was located at about -30 degrees, and had a mean voltage of 1.84 mv. Z!Z 0.66. It should be noted that the posteriorly directed movement of the early portion of the loop varied in amplitude. In the majority of cases, the early vectors constituted an easily identified horizontal straight segment (Fig. 5, parts 1 through 4), but in some instances the posterior displacement was smaller and most of the corresponding vectors were inscribed almost perpendicularly to the sagittal plane (Fig. 5, part 5). This feature accounts for the considerable scatter observed at 30 msec. in this projection while there was reasonably good cluster at 10 and 40 msec., and extremely good cluster at 50 and 60 msec. (Fig. 6). In summary, the important diagnostic features of these vectorcardiograms in-
clude: (1) initial vectors of ventricular depolarization directed anteriorly and inferiorly in most instances; (2) early vectors traveling horizontally to the left and, to a variable extent, posteriorly; (3) abrupt upward shift of the loop between 30 and 40 msec. and midtemporal vectors located in the left superior and posterior octant. In 5 patients although the standard electrocardiograms fulfilled all the selection criteria, the vectorcardiograms did not exhibit the characteristic features that have just been described. On the contrary, the rotation was entirely clockwise in the left sagittal projection and the early electromotive forces were directed anteriorly (Fig. 7). Finally, the following clinical observations deserve being reported: (1) three patients whose electrocardiograms initially showed a left axis deviation with a RIrSII1 pattern subsequently developed a complete left bundle branch block; (2) the characteristic electrocardiographic and vectorcardiographic features considered in this paper were sometimes observed to be intermittent (2 cases) or transitory (3 cases). They suddenly appeared for instance during an exercise test in 2 patients with angina pectoris. Fig. 8 illustrates a case of transitory left axis deviation. In this 63-year-old patient with congenital aortic stenosis we observed several abrupt shifts from normal QRS axis to left axis deviation. These changes took place without any attending clinical event. Furthermore, whenever left axis deviation developed, it was accompanied by inversion of the T wave in Leads I and aVr. The T-wave alteration, most likely secondary to change in ventricular excitation, mimicked the so-called pattern of left ventricular hypertrophy “with strain.” Discussion
Production of a septal laceration which interrupts the anterior rami of the left bundle branch in the baboon heart is attended by changes in the spread of activation into the anterior free wall of the left ventricle.8 The electrocardiographic expression of these changes is a leftward shift of the mean QRS axis to -30 degrees or higher. Similar observations have been reported in man after surgical injury to
Volwne Number
79 3
Vectorcardiographic
LEFT
Fig. 6. Scattergram plane.
of the angular
direction
SAGITTAL
of the maximal
the anterior division of the left branch during transventricular mitral4 or aortic commissurotomyi5 or during corrective incision of the left ventricular outflow tract in patients with idiopathic hypertrophic subaortic stenosis.4J6 Observations derived from direct epicardial recordings indicate the following pattern of excitation in experimental left anterior arborization block.g The earliest focus of epicardial depolarization is located near the anterior trabeculated zone of the right ventricle about halfway to the apex (15 to 20 msec.). Depolarization of the epicardial surface of the posterior portion of the left ventricle occurs between 30 and 40 msec. and the activation is much
study of QRS loop
299
PLAFIE
and instantaneous
timed
vectors
in the left sagittal
delayed in the laterobasal region of the left ventricle where excitation occurs between 50 and 70 msec. It seems very tempting to interpret our findings in the light of these experimental results. The initial anterior vectors of our cases would mainly represent the activation of septal and paraseptal masses. The early vectors horizontally directed to the left and posteriorly would be predominantly determined by the spread of activation into the posterodiaphragmatic portion of the left ventricular free wall. Finally, the midtemporal vectors located in the left posterior and superior octant would result from markedly delayed excitation of the laterobasal wall of the left ventricle.
Fig. 7. Electrocardiogram and vectorcardiogram of a 65year-old man with ischemic heart disease hypertension. Calibration: 500 pv. The loop is interrupted every l/400 sec. To be noted, the anterior tion of the initial and early vectors and the clockwise rotation of the aagittal plane loop.
The following observation might also support the latter assumption. From comparison between epicardial excitation maps and vectorcardiograms recorded in the same patients, Arntzeniusi7Js has recently showed that the main inflection points of the QRS loop reflect major occurrences in the excitation of the heart. In particular, the inflection points where the loop changes
and mild localiza-
first, from an anterior to posterior direction and, later, from a leftward to rightward direction were found to coincide with the breakthrough of the excitation fronts at the right anterior and left ventricular epicardium, respectively. Since epicardial recordings were not available in our series, we could only try to draw a parallel between our vectorcardiographic findings
Vectorcardiographic
study of QRS loop
301
1830.67.
A’R
01
I,
16.10.67. 01
,oz
03
t
aVF
2O.M,67. h
02
03
03
-
&JR
nvl”
aVR
aVL
‘aVF
aVF
V6
Fig. 8. Same patient as in Fig. 2. These five electrocardiograms were recorded a few days apart. The second and fourth tracings show left axis deviation with an inverted T wave in Leads I and aVL. The precordial leads of the last tracing are shown to allow comparison with those recorded in the presence of left axis deviation (Fig. 2).
302
Kulbertus,
Collignon,
und Humblet
and the epicardial data obtained in the primate heart after production of a left anterior arborization block. It is worth being noted that there is indeed a very satisfactory correlation in timing between the three successive inflection points seen in the vectorcardiograms of our patients and the arrival of excitation at the epicardial surface of the anterior, left posterior, and left laterobasal aspects of the primate heart in the presence of experimental left anterior arborization block. According to these data and although no pathologic or electrophysiologic data were actually obtained in our patients, it is assumed that the type of vectorcardiograms described in this paper corresponds to a left anterior focal block. The same opinion has been expressed by Testoni and associatesi who studied various forms of focal blocks, and by Cohen and coworkers’g who observed vectorcardiograms exactly similar to ours in cases where aberrant ventricular conduction was experimentally produced by introduction of atria1 premature beats. The observations that the electrocardiographic and vectorcardiographic patterns described here may be transitory or intermittent,10~1gJ4 that they may precede complete left bundle branch block, and, finally, that their association with right bundle branch block is a common forerunner of complete atrioventricular block21-25 represents further pieces of evidence to support the hypothesis according to which this type of left axis deviation are related to a focal conduction disturbance of the left bundle branch. The pathologic basis of these vectorcardiographic changes are not yet precisely known. They undoubtedly may vary in both location and extent.21*26 This assumption is substantiated by the experimental demonstration that the same axis shift may be obtained either by a proximal block (septal laceration)‘mg or by a distal block (cocaine solution injection into the left ventricular free wa11).5 Similarly in man, the anterior radiation of the left bundle branch may be proximally interrupted in the interventricular septum either by surgical injury,4,‘5*16 infarction,27 or fibrotic infiltration.1-4p6 The latter process seems rather frequent after
.-lrwr. Heart 1. March. 1970
50 years of age. It is known that fibrosis, hyalinization with or without calcification of the mitral valve, the pars membranacea, the central fibrous body, and/or the summit of the muscular ventricular septum may be observed in most hearts in the fifth and sixth decades.28-30 This sclerosis of the left side of the cardiac skeleton, which seems particularly frequent in hypertension and coronary heart disease30 may catch the adjacent left bundle branch or its major ramifications.21~28-30 In some autopsied cases of left axis deviation, histological examination of the heart revealed fibrotic lesions involving predominantly the fibers of the anterior division.4*6 In other instances, the whole left bundle branch appeared extensively involved.21J6 In the latter cases, it is most likely that a few undamaged specific fibers are sufficient to conduct the activation from the node to the left ventricle and that the anterior division of the left bundle has a greater conduction delay than that of the posterior ramification. On the other hand, a significant number of hearts from patients with left axis deviation exhibit on serial sectioning no anatomic abnormalities of the proximal portions of the conduction system.4J6J1 In those patients, the conduction delay probably results from diffuse or scattered myocardial lesions. Variations in the location of the lesions producing the block might account for the scatter of the initial vectors. To be noted that in 5 cases of the present series, the initial vectors start posteriorly. This sign usually suggests an anteroseptal infarction32 but is no longer reliable in the presence of advanced left ventricular hypertrophy.33z34 The present observations also confirm that a left anterior focal block is frequently associated with left ventricular hypertrophy (50 per cent of our cases). The presence of LVH results in changes in magnitude but not in direction of the instantaneous vectors and the loop maintains all its essential characteristics. It is likely that the left axis deviation is not due to LVH alone but suggests a conduction delay in addition.‘s4 The case illustrated in Fig. 8 is particularly interesting in that respect and shows that the electric
Volume Number
79 3
pattern of left ventricular hypertrophy with left axis deviation may be a transitory phenomenon. This feature already reported by Segers and associates35 in 1952 supports Pruitt’s opinion36 that both the abnormal direction of activation and some of the evidence of LVH might be due to conduction disturbances. Five patients of the present series showed anteriorly oriented initial and early electromotive forces, and an entirely clockwise rotation of the left sagittal plane loop. These cases would take place in type II of Testoni’s classification.iO The pathologic differences that could account for the peculiarities of those 5 tracings are unknown and deserve further study. Testoni’O assumes that the causative factor might be pathologic alterations involving the posteroseptal area or the posteroinferior wall of the left ventricle. This interpretation is admittedly purely speculative and its substantiation must await histologic proof. Summary
The authors have studied the vectorcardiograms of 40 patients, 45 years of age or over, whose electrocardiograms showed a QRS duration shorter than 120 msec., a leftward shift of the mean QRS axis and ventricular complexes with a tall R wave in Leads I and aVL, and an rS morphology in Leads II, III, and aVr. Most patients had atherosclerosis, hypertension, or ischemic heart disease. The following vectorcardiographic characteristics were disclosed: (1) The frontal plane loop was open-faced and turned counterclockwise in all cases; (2) the initial vectors were nearly always directed anteriorly and inferiorly; (3) the early vectors travelled horizontally to the left and, to a variable extent, posteriorly; (4) the midtemporal vectors were located in the left, posterior, and superior octant. These vectorcardiographic features were sometimes observed to be transitory or intermittent or to precede the development of a complete left bundle branch block. Their association with a complete right bundle branch block is known to be a common forerunner of complete atrioventricular block.
Vectorcardiographic study of QRS loop
303
From comparison with experimental data reported in the literature, the characters of the loops observed in these cases are assumed to be related to a delayed activation of the anterolateral wall of the left ventricle and to correspond to left anterior focal block. We would like to sincerelythank Professor A. Nizet for his most helpful interest and for the opportunity to perform this study in his department. We also wish to thank Miss S. Smeets and Mrs. B. Vervier for their technical and secretarial assistance. REFERENCES 1. Grant, R. P.: Left axis deviation: An electrocardiographic-pathologic correlative study, Circulation 14:233, 1956. 2. Davies, H., and Evans, W.: The significance of deep S waves in leads II and III, Brit. Heart J. 22:551, 1960. 3. Corne, R. A., Parkin, T. W., Brandenburg, R. O., and Brown, A. L.: Significance of marked left axis deviation: electrocardiographic-pathologic correlative study, Amer. J. Cardiol. 15:605, 1965. 4. Pryor, R., and Blount, S. G.: The clinical significance of true left axis deviation, AMER. HEART J. 72:391, 1966. 5. Van Bogaert, A.: Valeur clinique de la sinistrodeviation de l’axe Clectrique dans le plan des derivations standard, Arch. Mal. Coeur. 60:337, 1967. R. L., and Pryor, R.: Quantitative and 6. Hawley, electrocardiographic correlation of the conduction system of the heart, Amer. J. Cardiol. 15:132, 1965. T. B., and Pruitt, R. D.: Electrocardio7. Watt, graphic findings associated with experimental arborization blocks in does. AMER. HEART "I. 69:642, 1965. 8. Watt, T. B., Murao, S., and Pruitt, R. D.: Left axis deviation induced experimentally in a nrimate heart. AMER. HEART 1. 70:381. 1965. 9. Watt, T. B., Freund, G. E., Purrer, b., and Pruitt, R. D.: Left anterior arborization block combined with right bundle branch block in canine and primate hearts. An electrccardiographic study, Circ. Res. 2257, 1968. 10. Testoni, F., Narbone, N. B., and Tommaselli, A.: Aspetti vettocardiographici nei blocchi sinistri con elettrocardiogramma di tippo RI-SII-SIII, Mal. Cardiov. 9:379, 1968. 11. McFee, R., and Parungao, A.: An orthogonal lead system for clinical electrocardiography, AMER. HEART J. 62:93, 1961. 12. Pipberger, H. V.: The normal orthogonal electrocardiogram with a critique on some commonly used analytic criteria, Circulation 17:1102, 1958. 13 Downs, Th. D., Liebman, J., Agusti, R., and Romberg, H. C.: The statistical treatment of angular data in vectorcardiography, Proc. Long Island Jewish Hosp. Vectorcardiography, Am.,
I
14.
1.5.
16.
17.
18.
19.
20.
21. 22.
23.
24.
sterdam, 1965, North Holland Publishing Company, p. 272. Burch, G. E., and DePasquale, N. I’.: Electrocardiography in the diagnosis of congenital heart disease. Philadelohia. 1967. Lea & Febiger, Publishers. ’ ’ ’ Samson, W. E., and Bruce, R. A.: Left ventricular parietal block produced by transventricular aortic commissurotomy, AMEK. HEART J. 63:41, 1962. Wigle, E. D., and Baron, R.: Electrocardiogram in muscular subaortic stenosis: effect of left atrial incision and right bundle branch block, Circulation 34:X5, 1966. Arntzenius, A. C.: Physiological basis for recognizing ventricular hypertrophy in the vectorcardiogram. Brit. Heart T. 30:421. 1968. (Abst.) Arntzemus, A. C.: A model of excitation‘of the human heart. Its value in establishing a link between pathway of excitation and clinical Thesis, ITniversity of vectorcardiography, Leiden, 1968. Cohen, S. I., Lau, S. H., Stein, E., Young, M. W., and Damato, A. W.: Variations of aberrant ventricular conduction in man: Evidence of isolated and combined block within the specialized conduction system: an electrocardiographic and vectorcardiographic study, Circulation 38:899, 1968. Taccola, A. F.: Left bundle branch semiblock. A clinical contribution, Ma]. Cardiov. 9:257, 1968. Lencgre, J.: Contribution ri l’etude des blocs de branche, Paris, 1958, J. B. Bailliere. Lasser, R. P., Haft, J. I., and Friedberg, C. I(.: The relationship of right bundle branch block with marked left axis deviation (with left anterior parietal or peri-infarction block) to complete heart block and syncope, Circulation 37:429, 1968. Slama, R., Marneffe, H., Gourgon, R., and Motte, G.: Aspect du ventriculogramme en rythme sinusal chez les malades atteints de blocs auriculo-ventriculaires chroniques, Ma]. Cardiov. 7:1, 1966. Salzmann, P., Linn, H., and Pick, A.: Right bundle branch block with left axis deviation, Brit. Heart J. 28:703, 1966.
2.5.
26.
27. 28.
29.
30. 31.
32.
33.
34.
3.5.
36.
Kulbertus, II., and Collignou, I’.: ‘Ihe association of right bundle branch block with left superior or inferior intraventricular block. Its relationship to complete heart block and StokesAdams syndrome, Brit. Heart J. 31:435, 1969. Entman, M. L., Estes, E. H., and Hackel, D. B.: The pathologic basis of the electrocardiographic pattern of parietal block, AMER. HEART J. 74:202, 1967. Grant, R. I’.: Peri-infarction block, Prog. Cardiov. Dis. 2:237, 1959. Lev, M.: The pathology of complete atrioventricular block, Prog. Cardiov. Dis. 6:317, 1964. Lev, M.: The normal anatomy of the conduction system in man and its pathology in atrioventricular block, Ann. N. Y. Acad. Sci. 111:817, 1964. Lev, M.: Pathology of bundle branch block, Heart Bull. 16:107, 1967. Lepeschkin, E.: Electrocardiographic diagnosis of bilateral bundle branch block in relation to heart block, Prog. Cardiov. Dis. 6:445, 1964. Hugenholtz, P. G., Whipple, G. H., and Levine, H. D.: A clinical appraisal of the vectorcardiogram in myocardial infarction, Circulation 24:808, 1961. Estes, E. H., Jr.: Left ventricular hypertrophy in acquired heart disease: a comparison of the vectorcardiogram in aortic stenosis and aortic insufficiency, Proc. Long Island Jewish Hospital symposium on vectorcardiography, Amsterdam. 1965. North Holland Publishing Company, p. 157. Bell, H., Pugh, D., and Dunn, M.: Vectorcardiographic evolution of left ventricular hypertrophy, Brit. Heart J. 30:70, 1968. Segers, M., Regniers, M., and Delatte, E.: L’installation brusque de l’image electrocardiographique de preponderance, Acta Cardiol. 7:63, 1952. Pruitt, R., Esser, H. E., and Burchell, M. B.: Studies on the spread of excitation through the ventricular myocardium, Circulation 24:808, 1951.