Epicardial Activation in Human Left Anterior Fascicular Block
CHRISTOPHER FRACP, MOOIDEEN THOMAS RICHARD
R. WYNDHAM,
FACC K. MEERAN, SMITH, MD M. ENGELMAN,
MD,
MB, MRCP”
MD+
SIDNEY LEVITSKY, MD, FACC KENNETH M. ROSEN, MD, FACC
Chicago, Illinois
From the Section of Cardiology, Department of Medicine, Abraham Lincoln School of Medicine, University of Illinois, Chicago, Illinois. This study was supported in part by Institutional Training Grant HL 07387, HL 18794 and HL23566 from the National Institutes of Health, Bethesda, Maryland, and University of Illinois Graduate Research Support Grant 7508, Chicago, Illinois. Manuscript received March 14, 1979. accepted May 2, 1979. Present address: Louisiana State University, New Orleans, Louisiana. t Present address: University of Connecticut, Section of Cardiovascular Surgery, Baystate Medical Center, Springfield, Massachusetts. Address for reprints: Christopher R. Wyndham, MB, Section of Cardiology, Department of Medicine, Abraham Lincoln School of Medicine, P.O. Box 6998, Chicago, Illinois 66680. l
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Four patients with coronary artery disease and chronic marked left axis deviation, defined as a frontal ORS axis more negative than -45’, were studied with epicardial mapping during coronary bypass surgery. All patients had normal right ventricular and inferior left ventricular epicardial breakthrough sites and activation sequence. Normal breakthrough in the basal anterolateral left ventricular epicardium was absent in all four patients. Two patients had breakthrough in the apical region of the anterolateral left ventricle. In the other two this region was activated from wave fronts emerging in the right ventricle and inferior left ventricle. The latest site of left ventricular activation was the basal segment of the anterolateral wall, a site never found to be the latest activated in our previously studied patients without conduction defects. This site was activated during or slightly after the terminal portion of the QRS complex. It is concluded that marked left axis deviation in patients with coronary artery disease reflects delayed activation of the basal anterolateral left ventricle, and is consistent with the presence of block or delay in the anterior “fascicle” of the left bundle branch.
The criteria for diagnosis of specific intraventricular conduction defects in human beings have largely been derived from serial electrocardiographic observations in patients and analysis of conduction defects produced during animal experimentation. In contrast, the electrocardiographic criteria for diagnosis of anatomic abnormalities, such as hypertrophy or infarction, are subject to postmortem verification. The criteria for diagnosis of left anterior fascicular block were derived from serial electrocardiographic observations1-4 and knowledge of the structure of the conduction system5 and results of surgical section of the anterior division of the left bundle branch in animals.612 In patients with diagnosed left anterior fascicular block, although pathologic studies frequently reveal lesions in the left bundle branch system,i3-ls it is impossible for the pathologist to determine whether diseased portions of the His-Purkinje system were able to conduct during life.rg Thus, the diagnosis of left anterior fascicular block is not subject to absolute pathologic confirmation, Another approach to the examination of the electrocardiographic diagnosis of left anterior fascicular block would be to evaluate the pattern of ventricular activation revealed by cardiac mapping in patients with this electrocardiographic abnormality. In this study, we examined the pattern of epicardial activation in patients with electrocardiographically diagnosed left anterior fascicular block in an attempt to understand further this intraventricular conduction defect. The epicardial maps obtained were consistent with conduction delay localized to the anterolateral left ventricle. Methods Patient selection: Four patients with electrocardiographic left anterior fascicular block undergoing open heart surgery were studied. The criteria for
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inclusion in the study were: (1) left anterior fascicular block on preoperative electrocardiogram as defined by a QRS duration of less than 0.12 second, a negative mean frontal plane QRS axis of -45O or more and a qR complex in lead I and an rS complex in leads II and II14; (2) absence of previous myocardial infarction as judged from the electrocardiogram and left ventriculogram (no wall motion abnormality); (3) absence of left or right ventricular hypertrophy by precordial lead voltage criteria; (4) indications for elective cardiac surgery (angina pectoris in all cases); and (5) the signing of preoperative informed consent for epicardial mapping, under a protocol approved by the Human Investigation Committee of the University of Illinois. Epicardial mapping: Epicardial mapping was performed before initiation of cardiopulmonary bypass using previously described techniques.20,21 Three of seven continuously monitored electrocardiographic leads (I, II, III, aVR, aVL, aVF and Vs) were displayed simultaneously with a bipolar right ventricular reference electrogram and two bipolar electrograms from the exploring probe, on an Electronics for Medicine recorder (model VR-6 or DR-8, Minneapolis, Minnesota). Recordings were made at 100 and 200 or 250 mm/set. The timing of local electrograms, in milliseconds, reflected the mean of 5 to 10 beats measured during stable sinus rhythm, from the onset of the earliest QRS deflection in multiple surface or reference leads to the point at which the first high frequency deflection crossed the baseline in the local electrogram. In all, 54 to 75 points were mapped on the epicardial surface of each heart, without displacement of the heart, utilizing landmarks as previously detailed.21 Stability of the map was ensured by noting (1) a stable sinus rhythm throughout monitoring, with sinus rate varying by no more than 10 beats/min, and (2) a stable QRS configuration during monitoring. The 12 lead postoperative electrocardiogram resembled the preoperative, in regard to QRS duration, configuration and axis. No morbidity was encountered from the mapping procedure. Definitions: Epicardial breakthrough was defined as the site of emergence of a radially propagating wave front at the epicardial surface, producing an island of early activation, completely surrounded by points of later activation. The site of latest epicardial activation was noted for the ventricles as a whole and was considered the site of latest recordable ventricular activation. The site of latest activation was also noted for each ventricle.
TABLE
I
Clinical
and Epicardial
ET AL.
Comparison with epicardial maps in patients with normal QRS complex: In an attempt to delineate the abnormalities associated with left anterior fascicular block, we compared the epicardial maps obtained in this study with patterns of activation seen in patients without intraventricular conduction defects. These data in 11 patients with a normal QRS complex were recently reported by our laboratory.21 For comparison purposes, the following features were noted for epicardial mapping data in all patients without conduction defects? (1) Earliest epicardial breakthrough in the anterior paraseptal right ventricle, 7 to 25 (mean 17) msec after onset of the QRS complex. (2) Two to four subsequent epicardial breakthroughs in all patients, at multiple sites in the inferior right ventricle, inferior left ventricle and the anterolateral left ventricle. Anterolateral left ventricular breakthrough was almost always present near the base of the left ventricle, and often at sites near the apex. (3) Latest epicardial activation contiguous to the atrioventricular (A-V) groove, at any site on the basal right or left ventricles except the anterolateral left ventricle. The timing of this latest epicardial activity occurred 63 to 96 (mean 77) msec after the onset of the QRS complex, and within 20 msec of the end of the QRS complex in all patients.
Results Clinical data (Table I): The study group consisted of one woman and three men, aged 48 and 54,52 and 43 years, respectively. Their preoperative electrocardiograms are shown in Figure 1. The QRS duration ranged from 80 to 110 (mean 100) msec and the frontal plane QRS axis from -45” to -60” (mean -49’). All patients had a qR complex in lead I and an rS complex in leads II and III. Electrocardiographic criteria for myocardial infarction were not present in any patient, although three patients (Cases 1 to 3) gave a history of a previous heart attack, of unknown anatomic location. Left ventriculography revealed moderate generalized hypokinesia in one patient (Case 2) but a normal contractile pattern in the other three patients. Typical epicardial map (Fig. 2): The four epicardial maps obtained in this study were all similar (see later). A typical example (from Patient 1) is shown in Figure 2. The local activation times in milliseconds are shown
Data
QRS
QRS
Case no.
Age (yr) & Sex
Duration (msec)’
Axis
1
48F
110
-45
2
54M
110
-45
3
52M
80
-60
4 Mean
43M 49
100 100
-45 -49
(Y
Latest Epicardial
Epicardial Breakthrough Site and Timing (msec) BTI ARV 19 ARV 20 ARV A:: t:
RV BT2
BTs
BT1
IRV 34 IRV 29 IRV
IRV 35
ILV 19 ILV 29 ILV 1::
::
35
-
z;
LV BT, AALV 47 ILV 37 ILV 50 ILV 42’:
BTs -
A ALL
Activation Site and Timing (msec) RV LV RVOT RV:: 81 ARV 80 IRV
BALV 125 BALV 124 BALV BAZ
3”:
Epicardial events are timed (msec) from onset of the QRS complex. AALV = apical anterolateral left ventricle; ARV = anterior right ventricle; BALV = basal anterolateral left ventricle; B,, 82 and B3 = first, second and third epicardial breakthroughs, respectively; ILV = inferior left ventricle; IRV = inferior right ventricle; LV = lefl ventricle; RV = right ventricle; RVOT = right ventricular outflow tract. l
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I
II
m
OVR
OVL
ET AL
oVF
VI
VI3
‘6
FIGURE 1. Preoperative electrocardiograms of the four patients with left anterior fascicular block.
,
Anterior
Left
msec
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Lateral/
FIGURE 2. Epicardial map from Patient 1. Anterior, left lateral and inferior views are shown. A zone of overlap is present between the anterior and left lateral views in the region of the left anterior descending coronary artery. Numbers reflect the timing (msec) of arrival of local activation at each bipolar recording site. The QRS complex in lead II is displayed above the time scale in milliseconds. Normal anterior right ventricular (19 msec), inferior left ventricular (19 msec) and apical anterolateral left ventricular (47 msec) epicardial breakthrough sites are shown. The occurrence of the latest right ventricular (77 msec) and abnormal basal anterolateral left ventricular (125 msec) activation is shown.
QRS onset
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for each data point explored, time zero being the onset of the QRS complex. Right ventricular activation was normal, a single anterior right ventricular breakthrough being observed 19 msec after the onset of the QRS complex. Left ventricular activation was abnormal. The earliest left ventricular epicardial breakthrough was seen inferiorly 19 msec after onset of the QRS complex and considerably later in the anterolateral apical region at 47 msec (Fig. 2, left lateral). The normal left ventricular epicardial breakthroughs in the basal region of the anterolateral left ventricle were absent.21 The latest right ventricular epicardial activation occurred normally in the outflow tract region 77 msec after QRS onset (Fig. 2, anterior). The latest left ventricular activation was abnormal in site and occurred in the basal anterolateral left ventricle, 125 msec after onset of the QRS complex, which occurred 15 msec after the end of the visible QRS complex in the surface leads (Fig. 2, left lateral). Epicardial breakthrough (Table I, Fig. 3): All sites of epicardial breakthrough in the four patients are shown in Figure 3. Right ventricular epicardial breakthrough was normal in all four patients, occurring in the anterior wall adjacent to the septum, 19 to 28 (mean 22) msec after onset of the QRS complex; three of the four patients showed breakthrough in the inferior right ventricle at 29 to 37 (mean 34) msec (one patient demonstrated two inferior breakthroughs). Left ventricular epicardial activation was normal in the inferior wall in all patients, seven breakthroughs occurring in the four patients, 19 to 50 (mean 33) msec after onset of the QRS complex. Only two patients showed the apical anterolateral left ventricular breakthrough shown in Figure 2 (it occurred 38 and 47 msec, respectively, after onset
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ET AL.
of the QRS complex). None of the four patients manifested the normally present basal anterolateral left ventricular epicardial breakthrough. Latest epicardial activation (Table I, Fig. 4): The site of latest epicardial activation in the four patients is shown in Figure 4. The latest right ventricular activation was normal in site and timing in all patients, occurring in two patients in the outflow region, and in one patient each in the anterobasal and the posterobasal region, respectively, 77 to 88 (mean 82) msec after onset of the QRS complex. In two patients (Cases 3 and 4) who had a normal QRS duration, the site of latest right ventricular activation was also the latest area to be activated in the epicardium as a whole. The latest left ventricular epicardial activation was abnormal in all patients. The site of latest activation was invariably in the basal anterolateral left ventricle anterior to the obtuse margin (Fig. 4). This occurred 68 to 125 (mean 97) msec after onset of the QRS complex. In two patients (Cases 1 and 2) with a slightly prolonged QRS duration, this site on the left ventricle was also the latest site on the ventricular epicardium as a whole, and corresponded closely with the terminal forces of the QRS complexes, occurring within I5 msec of the end of the visible QRS inscription in the electrocardiogram. Rapidity of late epicardial activation: With the limitation that no spatial measurements were made between recording sites in this study, one can derive a crude estimate of wave front velocity on the epicardial surface by noting the relative spacing of successive isochrones.22 Crowding of isochrones has been thought to indicate slower conduction of impulses and widely spaced isochrones to imply more rapidly conducting
Sites of Epicardial Breakthrough
..:::.. .:.:.:: ::i;i:. lo
No.of patients
FIGURE 3. Summary of epicardial breakthrough events. Cardiac views as for Figure 2. Each circle represents a site where breakthrough occurred. The numbers represent the number of patients having an epicardial breakthrough event at each site. Note the absence of breakthroughs in the basal segments of the anterolateral left ventricle.
FIGURE 4. Summary of sites of latest epicardial activation. Cardiac views as for Figure 2. Each area encircled represents a site of latest epicardial activation on the right and left ventricles. The numbers represent the number of patients whose latest epicardial activation occurred at each site.
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wave fronts in the plane of the epicardial surface.22 In three of our four patients, we observed relative crowding of isochrones in the basal anterolateral left ventricle, compared with the basal areas of the remaining portions of the left and right ventricles (Fig. 2). However, in the fourth patient (Case 3) there was no evidence of pronounced slowing in this region relative to other basal regions of the heart. Discussion Experimental production of left anterior fascicular block: The popularization of the concept of a “trifascicular” intraventricular conduction system by Rosenbaum et a1.4 represents a synthesis of considerable experimental and clinical data collected over a period of 70 years, dating from the experimental production of bundle branGh blocks in the dog by Eppinger and R0thberger.c Rothberger and Winterberg subsequently demonstrated axis changes after severance of the anterior and posterior divisions of the canine left bundle branch. Smith et a1.,g in 1954, published results of acute segmental and diffuse lesions of the right and left bundle branches. Segmental lesions of the left bundle branch, although producing definite changes in epicardial activation sequence, had little effect on limb leads in most animals. However, Watt et al.il showed that experimental left anterior divisional block in dogs and primates, with or without right bundle branch block, resulted in a superior and anterior shift in mean QRS electrical axis, delay in anterior left ventricular epicardial activation by 30 to 40 msec and a shift in the normal anterior paraseptal left ventricular epicardial breakthrough toward the apex. Most recently, Gallagher et a1.,12 utilizing intramural, endocardial and epicardial recordings, showed that division of the anterior left bundle fibers in the dog uniformly produced delays of 6 to 20 msec in the blocked Purkinje fibers, 3 to 25 msec delays in the associated endocardial areas and 4 to 25 msec delays in the epicardial surface, confined to the lateral basal surface of the left ventricle. When lesions were placed in the septal ramifications of the left bundle branch, in addition to the left anterior division, epicardial surface delays of greater magnitude (7 to 35 msec) and area of distribution as well as marked left axis deviation were encountered. Clinical observations on left axis deviation and “hemiblock”: In regard to clinical electrocardiology, Wilson et al.’ suggested that the rS complexes in leads II and III in three patients might reflect the presence of block in the anterior division of the left bundle branch. Grant,2 and Pryor and Blount3 suggested that block or delay of the left anterior division is the most common cause of left axis deviation. Rosenbaum et a1.,4 in their clinical and electrocardiographic studies of patients with chronic Chagasic cardiomyopathy, and coronary, hypertensive and aortic valve disease, concluded that left axis deviation of -45’, or more negative, separated the greatest number of cases of left anterior “hemiblock” from the greatest number of cases of left axis deviation unrelated to conduction disturbances.
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Histopathologic studies in human beings2,‘“m1s have shown that marked left axis deviation is accompanied by widespread disease of the left bundle branch system, not necessarily restricted to the anterior fibers. Surgical injury to the anterior portion of the left bundle branch has produced left axis deviation.“:’ Controversy persists, however. Some experienced electrocardiographers have expressed doubt as to the validity of the widespread use of the term “left anterior hemiblock” to describe various patterns of left axis deviation.“4 Nevertheless others?” have stated that it is not even necessary to require that the electrocardiogram show initial Q waves in lead I and aVL for a diagnosis of left anterior hemiblock. It has also been shown2a that discrete lesions that affect the nonbranching portion of the bundle of His without affecting bundle branch tissue may produce functional disturbance in fascicles. Interpretation of present results: Our study was designed to show whether epicardial activation patterns in patients with marked left axis deviation would show changes consistent with left anterior fascicular block. We used for comparison our previously described pattern of epicardial activation in 11 patients without intraventricular conduction defects.21 In those patients, three to five epicardial breakthrough events were identified in all, the first invariably occurring in the anterior paraseptal right ventricle, 7 to 25 (mean 17) msec after onset of the QRS complex, followed by breakthroughs in the inferior right, inferior left and anterolateral left ventricle. Of particular relevance to this study is the fact that all but one patient without conduction defect had at least one breakthrough in the anterolateral left ventricle. Ten of the 13 anterolateral left ventricular breakthroughs in the 11 patients were in the basal region, near either the septum or the obtuse margin, the other 3 being near the apex. None of our four patients had a basal anterolateral left ventricular breakthrough. Two patients with left axis deviation had an apical anterolateral breakthrough (Fig. 2, Table I), a finding consistent with the previously cited short term experiment of Watt et al. 1l In our previously studied 11 patients with no conduction defect the latest epicardial activation was distributed along t,he basal rim of right or left ventricle at all sites with the exception of the anterolateral basal left ventricle. In contrast, in all four patients in the present series with left axis deviation the latest left ventricular activation occurred in the basal anterolateral left ventricle. Comparison of the corresponding recording sites in the 11 patients with no conduction defect2i and in the 4 with marked left axis deviation revealed that equivalent sites in the basal anterolateral left ventricle were activated a mean of 47 msec later in the latter group. These findings are best interpreted as reflecting a delay in initial endocardial activation of the basal anterolateral left ventricle, with late activation and local delay (as reflected by crowding of isochrones) in this region, after normal activation of the right ventricle and the inferior left ventricle. The findings are consistent with block or delay in the anterosuperior divisional fi-
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bers (anterior border fibers of Lazzara et al.27) of the left bundle branch as the cause of the marked left axis deviation in our four patients with coronary artery disease. We interpret the persistence of apical anterolateral left ventricular and inferior left ventricular breakthroughs as representing intact conduction by way of posterior or septal ramifications, or both, of the left bundle branch.27*2s The timing of the latest recordable epicardial activity in our patients, relative to the terminal forces of the QRS complex, deserves some comment. In the two patients (Cases 3 and 4) with normal QRS duration, terminal left ventricular epicardial activation preceded the end of the QRS complex by 10 and 32 msec, respectively. In these two patients, right ventricular epicardial activity accompanied the terminal QRS complex. Rosenbaum et a1.4 stated that uncomplicated left anterior “hemiblock” never increases the QRS duration by more than 0.02 second, and that in approximately half of their cases of left anterior “hemiblock” the QRS duration was 0.06 to 0.08 second.4 Our Cases 3 and 4 would seem to be typical of this group. However, more than one fourth of Rosenbaum’s patients with left anterior “hemiblock” had a QRS complex of 0.10 to 0.13 second. This degree of widening was attributed to a concomitant abnormality, such as left ventricular hypertrophy or infarction.4 In our two patients (Cases 1 and 2) with QRS widening of 0.11 second the latest recordable left ventricular activity occurred 15 and 14 msec, respectively, after the end of the QRS complex in surface leads. These two patients may well have had additional intraventricular delay secondary to diffuse left ventricular disease. Patient 1 (Fig. 2) had a long history of labile hypertension, and the left ventriculogram showed a hypercontractile ventricle. Patient 2 had a diffusely moderately hypocontractile left ventricle with an ejection fraction of 30 percent. In contrast, the two patients with normal QRS duration had a normal left ventriculogram. Comparison of human and canine data: Our data in human subjects with left anterior fascicular block compares and contrasts with data from the experi-
BLOCK-WYNDHAM
ET AL.
mental acute left anterior divisional blocks in dogs, best exemplified by the study of Gallagher et a1.12 Absolute activation times to equivalent recording sites tend to be longer in the normal human heart than in the heart of the dog. 2g The normal epicardial breakthrough events are less complex in the dog, as reflected by the preoperative epicardial maps in the study of Gallagher et a1.,12 which typically did not show anterolateral left ventricular breakthrough. Thus, the absence of normal early activation of the anterolateral left ventricle, characterizing human left anterior fascicular block, is not so easily detectable in the dog, if one relies solely on epicardial breakthrough phenomena. However, there is good agreement between the canine data and our results regarding the site of late left ventricular activation, namely, the basal portion of the anterolateral wall. As with normal epicardial data in human beings, the absolute timing of this late activation is distinctly later than in the dog with acute left anterior fascicular block. Because we obtained no data from the endocardium or intramural sites within the blocked segment of the left ventricle, we are unable with certainty to differentiate true anterior fascicular block or delay from an identical epicardial activation sequence due to localized intramural block,12,30 and we agree with otherst6~1s~2e~“8 that it is probably an oversimplification to consider the left intraventricular conduction system as consisting of two discrete subdivisions as popularly taught.4 Clinical implications: Our findings lend further weight to the concept of electrocardiographic left anterior fascicular block. Electrocardiograms showing the pattern of left anterior fascicular block correlate with the presence of focal delay in activation of the basal anterolateral left ventricular wall. A further implication of this study is relevant to the surgical management of ventricular tachycardia. Spurrell et a1.2s reported the abolition of a reentrant left ventricular tachycardia by an incision in the left ventricle that probably severed the anterior divisional fibers of the left bundle branch. Postoperative epicardial mapping of conducted beats in such patients should provide evidence of damage to or interruption of the fibers of the anterior fascicle.
References 1. Wilson FN, Johnston FD, Barker PS: Electrocardiograms of an unusual type in right bundle branch block. Am Heart J 9:472-479, 1934 Grant RP: Left axis deviation. An electrocardiographic-pathologic correlative study. Circulation 14:233-249, 1956 Pryor R, Blount SG: The clinical significance of true left axis deviation. Am Heart J 72:391-413, 1966 Rosenbaum MB, Elizari MV, Lazrari JO: The Hemiblocks. Oldsmar, FL, Tampa Tracings, 1970, p 7 l-93 Lev M: The normal anatomy of the conduction system in man and its pathology in atrioventricular block. Ann NY Acad Sci 111: 817-829, 1964 6. Eppinger H, Rothberger CJ: ijber die Folgen der Durchschneidung der Tawarschen Schenkel des Reizleitungssystems. Z Klin Med 70:1-20, 1910 7. Rothberger CJ, Winterberg H: Experimentelle Beitrage zur Kenntnis der Reizleitungsstorungen in den Kammern des Saugertierherzens. Z Ges Exp Med 51246-320, 1917
8. Wilson FN, Herrmann GR: Experimental study of incomplete bundle branch block and of the refractory period of the heart of the dog. Heart 8:229-296, 1921 9. Smith LA, Kennamer R, Prinzmetal M: Studies on the mechanism of ventricular activity. Circ Res 2:221-230. 1954 10. Pruitt RD. Watt RB. Murao S: Left axis deviation: its relation to experimentally induced lesions of the anterior left bundle branch system in canine and primate hearts. Ann NY Acad Sci 127: 204-223, 1965 11. Watt TB Jr, Freud GE, Durrer P, Pruitt RD: Left anterior arborization block combined with right bundle branch block in canine and primate hearts. Circ Res 22:57-63, 1968 12. Gallagher JJ, Tfczon AR, Wallace AG, Kasell J: Activation studies following experimental hemiblock in the dog. Circ Res 35:752-763, 1974 13. Sugiura M, Okada R, Horaoka K, Ohkawa S: Histological studies on the conduction system in 14 cases of right bundle branch block associated with left axis deviation. Jpn Heart J 10:121-132,
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1969 14. Rosen KM, Rahimtoola SH, Gunnar RM, Lev M: Site of heart block as defined by His bundle recording. Pathologic correlations in three cases. Circulation 45:965-987, 1972 15. Lev M, Bharati S: Lesions of the conduction system and their functional significance. In, Pathology Annual (Sommers CS, ed). New York, Appleton-Century-Crofts, 1974, p 157-207 16. Kulbertus H: Concept of left hemiblocks revisited. A histopathological and experimental study. Adv Cardiol 14:126-135, 1975 17. Rossi L: Histopathology of conducting system in left anterior hemiblock. Br Heart J 38:1304-1311, 1976 18. Demoulin JC, Simar LJ, Kulbertus HE: Quantitative study of left bundle branch fibrosis in left anterior hemiblock. A stereologic approach. Am J Cardiol 36:751-756, 1975 19. Rosen KM, Wu D, Kanakis C, Denes P, Bharati S, Lev M: Return of normal conduction after paroxysmal heart block. Report of a case with major discordance of electrophysiological and pathological findings. Circulation 51:197-204, 1975 20. Wyndham CRC, Amat-y-Leon F, Denes P, Dhingra RC, Burman SO, Pouget JM, Rosen KM: Posterior left ventricular preexcitation. Arch Intern Med 134:243-249, 1974 21. Wyndham CR, Meeran MK, Smith T, Saxena A, Engelman RM, Levitsky S, Rosen KM: Epicardial activation of the intact human heart without conduction defect. Circulation 59:161-168, 1979 22. van Dam RT: Ventricular activation in human and canine bundle branch block. In, The Conduction System of the Heart. (Wellens
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HJJ, ed). Philadelphia, Lea & Febiger, 1976, p 377-392 23. Spurrell RAJ, Sowton E, Deuchar DC: Ventricular tachycardia in 4 patients evaluated by programmed electrical stimulation of heart and treated in 2 patients by surgical division of anterior radiation of left bundle branch. Br Heart J 35:1014-1025, 1973 24. Burch GE: Of hemiblock propaganda. Am Heart J 94532-533, 1977 25. Jacobson LB, LaFollete L, Cohn K: An appraisal of initial QRS forces in left anterior fascicular block. Am Heart J 94:407-413, 1977 26. Fabregas R, Tse W, Han J: Conduction disturbances of the bundle branches produced by lesions in the nonbranching portion of His bundle. Am Heart J 92:356-362, 1976 27. Lazzara R, Yeh BK, Samet P: Functional anatomy of the canine left bundle branch. Am J Cardiol 33:623-632, 1974 28. lwamura N, Kodama I, Shimizu T, Hirata Y, Toyama J, Yamada K: Functional properties of the left septal Purkinje network in premature activation of the ventricular conduction system. Am Heart J 95:60-69, 1978 29. Durrer D, van Dam RT, Freud GE, Janse MJ, Meijler FL, Arzbaecher RC: Total excitation of the isolated human heart. Circulation 41:899-912, 1970 30. Daniel T, Boineau JP, Sabiston DC: Comparison of human ventricular activation with a canine model in chronic myocardial infarction. Circulation 44:741-756, 1971
Volume 44
CHRISTOPHER FRACP, MOOIDEEN THOMAS RICHARD
R. WYNDHAM,
FACC K. MEERAN, SMITH, MD M. ENGELMAN,
MD,
MB, MRCP”
MD+
SIDNEY LEVITSKY, MD, FACC KENNETH M. ROSEN, MD, FACC
Chicago, Illinois
From the Section of Cardiology, Department of Medicine, Abraham Lincoln School of Medicine, University of Illinois, Chicago, Illinois. This study was supported in part by Institutional Training Grant HL 07387, HL 18794 and HL23566 from the National Institutes of Health, Bethesda, Maryland, and University of Illinois Graduate Research Support Grant 7508, Chicago, Illinois. Manuscript received March 14, 1979. accepted May 2, 1979. Present address: Louisiana State University, New Orleans, Louisiana. t Present address: University of Connecticut, Section of Cardiovascular Surgery, Baystate Medical Center, Springfield, Massachusetts. Address for reprints: Christopher R. Wyndham, MB, Section of Cardiology, Department of Medicine, Abraham Lincoln School of Medicine, P.O. Box 6998, Chicago, Illinois 66680. l
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Four patients with coronary artery disease and chronic marked left axis deviation, defined as a frontal ORS axis more negative than -45’, were studied with epicardial mapping during coronary bypass surgery. All patients had normal right ventricular and inferior left ventricular epicardial breakthrough sites and activation sequence. Normal breakthrough in the basal anterolateral left ventricular epicardium was absent in all four patients. Two patients had breakthrough in the apical region of the anterolateral left ventricle. In the other two this region was activated from wave fronts emerging in the right ventricle and inferior left ventricle. The latest site of left ventricular activation was the basal segment of the anterolateral wall, a site never found to be the latest activated in our previously studied patients without conduction defects. This site was activated during or slightly after the terminal portion of the QRS complex. It is concluded that marked left axis deviation in patients with coronary artery disease reflects delayed activation of the basal anterolateral left ventricle, and is consistent with the presence of block or delay in the anterior “fascicle” of the left bundle branch.
The criteria for diagnosis of specific intraventricular conduction defects in human beings have largely been derived from serial electrocardiographic observations in patients and analysis of conduction defects produced during animal experimentation. In contrast, the electrocardiographic criteria for diagnosis of anatomic abnormalities, such as hypertrophy or infarction, are subject to postmortem verification. The criteria for diagnosis of left anterior fascicular block were derived from serial electrocardiographic observations1-4 and knowledge of the structure of the conduction system5 and results of surgical section of the anterior division of the left bundle branch in animals.612 In patients with diagnosed left anterior fascicular block, although pathologic studies frequently reveal lesions in the left bundle branch system,i3-ls it is impossible for the pathologist to determine whether diseased portions of the His-Purkinje system were able to conduct during life.rg Thus, the diagnosis of left anterior fascicular block is not subject to absolute pathologic confirmation, Another approach to the examination of the electrocardiographic diagnosis of left anterior fascicular block would be to evaluate the pattern of ventricular activation revealed by cardiac mapping in patients with this electrocardiographic abnormality. In this study, we examined the pattern of epicardial activation in patients with electrocardiographically diagnosed left anterior fascicular block in an attempt to understand further this intraventricular conduction defect. The epicardial maps obtained were consistent with conduction delay localized to the anterolateral left ventricle. Methods Patient selection: Four patients with electrocardiographic left anterior fascicular block undergoing open heart surgery were studied. The criteria for
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inclusion in the study were: (1) left anterior fascicular block on preoperative electrocardiogram as defined by a QRS duration of less than 0.12 second, a negative mean frontal plane QRS axis of -45O or more and a qR complex in lead I and an rS complex in leads II and II14; (2) absence of previous myocardial infarction as judged from the electrocardiogram and left ventriculogram (no wall motion abnormality); (3) absence of left or right ventricular hypertrophy by precordial lead voltage criteria; (4) indications for elective cardiac surgery (angina pectoris in all cases); and (5) the signing of preoperative informed consent for epicardial mapping, under a protocol approved by the Human Investigation Committee of the University of Illinois. Epicardial mapping: Epicardial mapping was performed before initiation of cardiopulmonary bypass using previously described techniques.20,21 Three of seven continuously monitored electrocardiographic leads (I, II, III, aVR, aVL, aVF and Vs) were displayed simultaneously with a bipolar right ventricular reference electrogram and two bipolar electrograms from the exploring probe, on an Electronics for Medicine recorder (model VR-6 or DR-8, Minneapolis, Minnesota). Recordings were made at 100 and 200 or 250 mm/set. The timing of local electrograms, in milliseconds, reflected the mean of 5 to 10 beats measured during stable sinus rhythm, from the onset of the earliest QRS deflection in multiple surface or reference leads to the point at which the first high frequency deflection crossed the baseline in the local electrogram. In all, 54 to 75 points were mapped on the epicardial surface of each heart, without displacement of the heart, utilizing landmarks as previously detailed.21 Stability of the map was ensured by noting (1) a stable sinus rhythm throughout monitoring, with sinus rate varying by no more than 10 beats/min, and (2) a stable QRS configuration during monitoring. The 12 lead postoperative electrocardiogram resembled the preoperative, in regard to QRS duration, configuration and axis. No morbidity was encountered from the mapping procedure. Definitions: Epicardial breakthrough was defined as the site of emergence of a radially propagating wave front at the epicardial surface, producing an island of early activation, completely surrounded by points of later activation. The site of latest epicardial activation was noted for the ventricles as a whole and was considered the site of latest recordable ventricular activation. The site of latest activation was also noted for each ventricle.
TABLE
I
Clinical
and Epicardial
ET AL.
Comparison with epicardial maps in patients with normal QRS complex: In an attempt to delineate the abnormalities associated with left anterior fascicular block, we compared the epicardial maps obtained in this study with patterns of activation seen in patients without intraventricular conduction defects. These data in 11 patients with a normal QRS complex were recently reported by our laboratory.21 For comparison purposes, the following features were noted for epicardial mapping data in all patients without conduction defects? (1) Earliest epicardial breakthrough in the anterior paraseptal right ventricle, 7 to 25 (mean 17) msec after onset of the QRS complex. (2) Two to four subsequent epicardial breakthroughs in all patients, at multiple sites in the inferior right ventricle, inferior left ventricle and the anterolateral left ventricle. Anterolateral left ventricular breakthrough was almost always present near the base of the left ventricle, and often at sites near the apex. (3) Latest epicardial activation contiguous to the atrioventricular (A-V) groove, at any site on the basal right or left ventricles except the anterolateral left ventricle. The timing of this latest epicardial activity occurred 63 to 96 (mean 77) msec after the onset of the QRS complex, and within 20 msec of the end of the QRS complex in all patients.
Results Clinical data (Table I): The study group consisted of one woman and three men, aged 48 and 54,52 and 43 years, respectively. Their preoperative electrocardiograms are shown in Figure 1. The QRS duration ranged from 80 to 110 (mean 100) msec and the frontal plane QRS axis from -45” to -60” (mean -49’). All patients had a qR complex in lead I and an rS complex in leads II and III. Electrocardiographic criteria for myocardial infarction were not present in any patient, although three patients (Cases 1 to 3) gave a history of a previous heart attack, of unknown anatomic location. Left ventriculography revealed moderate generalized hypokinesia in one patient (Case 2) but a normal contractile pattern in the other three patients. Typical epicardial map (Fig. 2): The four epicardial maps obtained in this study were all similar (see later). A typical example (from Patient 1) is shown in Figure 2. The local activation times in milliseconds are shown
Data
QRS
QRS
Case no.
Age (yr) & Sex
Duration (msec)’
Axis
1
48F
110
-45
2
54M
110
-45
3
52M
80
-60
4 Mean
43M 49
100 100
-45 -49
(Y
Latest Epicardial
Epicardial Breakthrough Site and Timing (msec) BTI ARV 19 ARV 20 ARV A:: t:
RV BT2
BTs
BT1
IRV 34 IRV 29 IRV
IRV 35
ILV 19 ILV 29 ILV 1::
::
35
-
z;
LV BT, AALV 47 ILV 37 ILV 50 ILV 42’:
BTs -
A ALL
Activation Site and Timing (msec) RV LV RVOT RV:: 81 ARV 80 IRV
BALV 125 BALV 124 BALV BAZ
3”:
Epicardial events are timed (msec) from onset of the QRS complex. AALV = apical anterolateral left ventricle; ARV = anterior right ventricle; BALV = basal anterolateral left ventricle; B,, 82 and B3 = first, second and third epicardial breakthroughs, respectively; ILV = inferior left ventricle; IRV = inferior right ventricle; LV = lefl ventricle; RV = right ventricle; RVOT = right ventricular outflow tract. l
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I
II
m
OVR
OVL
ET AL
oVF
VI
VI3
‘6
FIGURE 1. Preoperative electrocardiograms of the four patients with left anterior fascicular block.
,
Anterior
Left
msec
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Lateral/
FIGURE 2. Epicardial map from Patient 1. Anterior, left lateral and inferior views are shown. A zone of overlap is present between the anterior and left lateral views in the region of the left anterior descending coronary artery. Numbers reflect the timing (msec) of arrival of local activation at each bipolar recording site. The QRS complex in lead II is displayed above the time scale in milliseconds. Normal anterior right ventricular (19 msec), inferior left ventricular (19 msec) and apical anterolateral left ventricular (47 msec) epicardial breakthrough sites are shown. The occurrence of the latest right ventricular (77 msec) and abnormal basal anterolateral left ventricular (125 msec) activation is shown.
QRS onset
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for each data point explored, time zero being the onset of the QRS complex. Right ventricular activation was normal, a single anterior right ventricular breakthrough being observed 19 msec after the onset of the QRS complex. Left ventricular activation was abnormal. The earliest left ventricular epicardial breakthrough was seen inferiorly 19 msec after onset of the QRS complex and considerably later in the anterolateral apical region at 47 msec (Fig. 2, left lateral). The normal left ventricular epicardial breakthroughs in the basal region of the anterolateral left ventricle were absent.21 The latest right ventricular epicardial activation occurred normally in the outflow tract region 77 msec after QRS onset (Fig. 2, anterior). The latest left ventricular activation was abnormal in site and occurred in the basal anterolateral left ventricle, 125 msec after onset of the QRS complex, which occurred 15 msec after the end of the visible QRS complex in the surface leads (Fig. 2, left lateral). Epicardial breakthrough (Table I, Fig. 3): All sites of epicardial breakthrough in the four patients are shown in Figure 3. Right ventricular epicardial breakthrough was normal in all four patients, occurring in the anterior wall adjacent to the septum, 19 to 28 (mean 22) msec after onset of the QRS complex; three of the four patients showed breakthrough in the inferior right ventricle at 29 to 37 (mean 34) msec (one patient demonstrated two inferior breakthroughs). Left ventricular epicardial activation was normal in the inferior wall in all patients, seven breakthroughs occurring in the four patients, 19 to 50 (mean 33) msec after onset of the QRS complex. Only two patients showed the apical anterolateral left ventricular breakthrough shown in Figure 2 (it occurred 38 and 47 msec, respectively, after onset
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of the QRS complex). None of the four patients manifested the normally present basal anterolateral left ventricular epicardial breakthrough. Latest epicardial activation (Table I, Fig. 4): The site of latest epicardial activation in the four patients is shown in Figure 4. The latest right ventricular activation was normal in site and timing in all patients, occurring in two patients in the outflow region, and in one patient each in the anterobasal and the posterobasal region, respectively, 77 to 88 (mean 82) msec after onset of the QRS complex. In two patients (Cases 3 and 4) who had a normal QRS duration, the site of latest right ventricular activation was also the latest area to be activated in the epicardium as a whole. The latest left ventricular epicardial activation was abnormal in all patients. The site of latest activation was invariably in the basal anterolateral left ventricle anterior to the obtuse margin (Fig. 4). This occurred 68 to 125 (mean 97) msec after onset of the QRS complex. In two patients (Cases 1 and 2) with a slightly prolonged QRS duration, this site on the left ventricle was also the latest site on the ventricular epicardium as a whole, and corresponded closely with the terminal forces of the QRS complexes, occurring within I5 msec of the end of the visible QRS inscription in the electrocardiogram. Rapidity of late epicardial activation: With the limitation that no spatial measurements were made between recording sites in this study, one can derive a crude estimate of wave front velocity on the epicardial surface by noting the relative spacing of successive isochrones.22 Crowding of isochrones has been thought to indicate slower conduction of impulses and widely spaced isochrones to imply more rapidly conducting
Sites of Epicardial Breakthrough
..:::.. .:.:.:: ::i;i:. lo
No.of patients
FIGURE 3. Summary of epicardial breakthrough events. Cardiac views as for Figure 2. Each circle represents a site where breakthrough occurred. The numbers represent the number of patients having an epicardial breakthrough event at each site. Note the absence of breakthroughs in the basal segments of the anterolateral left ventricle.
FIGURE 4. Summary of sites of latest epicardial activation. Cardiac views as for Figure 2. Each area encircled represents a site of latest epicardial activation on the right and left ventricles. The numbers represent the number of patients whose latest epicardial activation occurred at each site.
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wave fronts in the plane of the epicardial surface.22 In three of our four patients, we observed relative crowding of isochrones in the basal anterolateral left ventricle, compared with the basal areas of the remaining portions of the left and right ventricles (Fig. 2). However, in the fourth patient (Case 3) there was no evidence of pronounced slowing in this region relative to other basal regions of the heart. Discussion Experimental production of left anterior fascicular block: The popularization of the concept of a “trifascicular” intraventricular conduction system by Rosenbaum et a1.4 represents a synthesis of considerable experimental and clinical data collected over a period of 70 years, dating from the experimental production of bundle branGh blocks in the dog by Eppinger and R0thberger.c Rothberger and Winterberg subsequently demonstrated axis changes after severance of the anterior and posterior divisions of the canine left bundle branch. Smith et a1.,g in 1954, published results of acute segmental and diffuse lesions of the right and left bundle branches. Segmental lesions of the left bundle branch, although producing definite changes in epicardial activation sequence, had little effect on limb leads in most animals. However, Watt et al.il showed that experimental left anterior divisional block in dogs and primates, with or without right bundle branch block, resulted in a superior and anterior shift in mean QRS electrical axis, delay in anterior left ventricular epicardial activation by 30 to 40 msec and a shift in the normal anterior paraseptal left ventricular epicardial breakthrough toward the apex. Most recently, Gallagher et a1.,12 utilizing intramural, endocardial and epicardial recordings, showed that division of the anterior left bundle fibers in the dog uniformly produced delays of 6 to 20 msec in the blocked Purkinje fibers, 3 to 25 msec delays in the associated endocardial areas and 4 to 25 msec delays in the epicardial surface, confined to the lateral basal surface of the left ventricle. When lesions were placed in the septal ramifications of the left bundle branch, in addition to the left anterior division, epicardial surface delays of greater magnitude (7 to 35 msec) and area of distribution as well as marked left axis deviation were encountered. Clinical observations on left axis deviation and “hemiblock”: In regard to clinical electrocardiology, Wilson et al.’ suggested that the rS complexes in leads II and III in three patients might reflect the presence of block in the anterior division of the left bundle branch. Grant,2 and Pryor and Blount3 suggested that block or delay of the left anterior division is the most common cause of left axis deviation. Rosenbaum et a1.,4 in their clinical and electrocardiographic studies of patients with chronic Chagasic cardiomyopathy, and coronary, hypertensive and aortic valve disease, concluded that left axis deviation of -45’, or more negative, separated the greatest number of cases of left anterior “hemiblock” from the greatest number of cases of left axis deviation unrelated to conduction disturbances.
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Histopathologic studies in human beings2,‘“m1s have shown that marked left axis deviation is accompanied by widespread disease of the left bundle branch system, not necessarily restricted to the anterior fibers. Surgical injury to the anterior portion of the left bundle branch has produced left axis deviation.“:’ Controversy persists, however. Some experienced electrocardiographers have expressed doubt as to the validity of the widespread use of the term “left anterior hemiblock” to describe various patterns of left axis deviation.“4 Nevertheless others?” have stated that it is not even necessary to require that the electrocardiogram show initial Q waves in lead I and aVL for a diagnosis of left anterior hemiblock. It has also been shown2a that discrete lesions that affect the nonbranching portion of the bundle of His without affecting bundle branch tissue may produce functional disturbance in fascicles. Interpretation of present results: Our study was designed to show whether epicardial activation patterns in patients with marked left axis deviation would show changes consistent with left anterior fascicular block. We used for comparison our previously described pattern of epicardial activation in 11 patients without intraventricular conduction defects.21 In those patients, three to five epicardial breakthrough events were identified in all, the first invariably occurring in the anterior paraseptal right ventricle, 7 to 25 (mean 17) msec after onset of the QRS complex, followed by breakthroughs in the inferior right, inferior left and anterolateral left ventricle. Of particular relevance to this study is the fact that all but one patient without conduction defect had at least one breakthrough in the anterolateral left ventricle. Ten of the 13 anterolateral left ventricular breakthroughs in the 11 patients were in the basal region, near either the septum or the obtuse margin, the other 3 being near the apex. None of our four patients had a basal anterolateral left ventricular breakthrough. Two patients with left axis deviation had an apical anterolateral breakthrough (Fig. 2, Table I), a finding consistent with the previously cited short term experiment of Watt et al. 1l In our previously studied 11 patients with no conduction defect the latest epicardial activation was distributed along t,he basal rim of right or left ventricle at all sites with the exception of the anterolateral basal left ventricle. In contrast, in all four patients in the present series with left axis deviation the latest left ventricular activation occurred in the basal anterolateral left ventricle. Comparison of the corresponding recording sites in the 11 patients with no conduction defect2i and in the 4 with marked left axis deviation revealed that equivalent sites in the basal anterolateral left ventricle were activated a mean of 47 msec later in the latter group. These findings are best interpreted as reflecting a delay in initial endocardial activation of the basal anterolateral left ventricle, with late activation and local delay (as reflected by crowding of isochrones) in this region, after normal activation of the right ventricle and the inferior left ventricle. The findings are consistent with block or delay in the anterosuperior divisional fi-
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bers (anterior border fibers of Lazzara et al.27) of the left bundle branch as the cause of the marked left axis deviation in our four patients with coronary artery disease. We interpret the persistence of apical anterolateral left ventricular and inferior left ventricular breakthroughs as representing intact conduction by way of posterior or septal ramifications, or both, of the left bundle branch.27*2s The timing of the latest recordable epicardial activity in our patients, relative to the terminal forces of the QRS complex, deserves some comment. In the two patients (Cases 3 and 4) with normal QRS duration, terminal left ventricular epicardial activation preceded the end of the QRS complex by 10 and 32 msec, respectively. In these two patients, right ventricular epicardial activity accompanied the terminal QRS complex. Rosenbaum et a1.4 stated that uncomplicated left anterior “hemiblock” never increases the QRS duration by more than 0.02 second, and that in approximately half of their cases of left anterior “hemiblock” the QRS duration was 0.06 to 0.08 second.4 Our Cases 3 and 4 would seem to be typical of this group. However, more than one fourth of Rosenbaum’s patients with left anterior “hemiblock” had a QRS complex of 0.10 to 0.13 second. This degree of widening was attributed to a concomitant abnormality, such as left ventricular hypertrophy or infarction.4 In our two patients (Cases 1 and 2) with QRS widening of 0.11 second the latest recordable left ventricular activity occurred 15 and 14 msec, respectively, after the end of the QRS complex in surface leads. These two patients may well have had additional intraventricular delay secondary to diffuse left ventricular disease. Patient 1 (Fig. 2) had a long history of labile hypertension, and the left ventriculogram showed a hypercontractile ventricle. Patient 2 had a diffusely moderately hypocontractile left ventricle with an ejection fraction of 30 percent. In contrast, the two patients with normal QRS duration had a normal left ventriculogram. Comparison of human and canine data: Our data in human subjects with left anterior fascicular block compares and contrasts with data from the experi-
BLOCK-WYNDHAM
ET AL.
mental acute left anterior divisional blocks in dogs, best exemplified by the study of Gallagher et a1.12 Absolute activation times to equivalent recording sites tend to be longer in the normal human heart than in the heart of the dog. 2g The normal epicardial breakthrough events are less complex in the dog, as reflected by the preoperative epicardial maps in the study of Gallagher et a1.,12 which typically did not show anterolateral left ventricular breakthrough. Thus, the absence of normal early activation of the anterolateral left ventricle, characterizing human left anterior fascicular block, is not so easily detectable in the dog, if one relies solely on epicardial breakthrough phenomena. However, there is good agreement between the canine data and our results regarding the site of late left ventricular activation, namely, the basal portion of the anterolateral wall. As with normal epicardial data in human beings, the absolute timing of this late activation is distinctly later than in the dog with acute left anterior fascicular block. Because we obtained no data from the endocardium or intramural sites within the blocked segment of the left ventricle, we are unable with certainty to differentiate true anterior fascicular block or delay from an identical epicardial activation sequence due to localized intramural block,12,30 and we agree with otherst6~1s~2e~“8 that it is probably an oversimplification to consider the left intraventricular conduction system as consisting of two discrete subdivisions as popularly taught.4 Clinical implications: Our findings lend further weight to the concept of electrocardiographic left anterior fascicular block. Electrocardiograms showing the pattern of left anterior fascicular block correlate with the presence of focal delay in activation of the basal anterolateral left ventricular wall. A further implication of this study is relevant to the surgical management of ventricular tachycardia. Spurrell et a1.2s reported the abolition of a reentrant left ventricular tachycardia by an incision in the left ventricle that probably severed the anterior divisional fibers of the left bundle branch. Postoperative epicardial mapping of conducted beats in such patients should provide evidence of damage to or interruption of the fibers of the anterior fascicle.
References 1. Wilson FN, Johnston FD, Barker PS: Electrocardiograms of an unusual type in right bundle branch block. Am Heart J 9:472-479, 1934 Grant RP: Left axis deviation. An electrocardiographic-pathologic correlative study. Circulation 14:233-249, 1956 Pryor R, Blount SG: The clinical significance of true left axis deviation. Am Heart J 72:391-413, 1966 Rosenbaum MB, Elizari MV, Lazrari JO: The Hemiblocks. Oldsmar, FL, Tampa Tracings, 1970, p 7 l-93 Lev M: The normal anatomy of the conduction system in man and its pathology in atrioventricular block. Ann NY Acad Sci 111: 817-829, 1964 6. Eppinger H, Rothberger CJ: ijber die Folgen der Durchschneidung der Tawarschen Schenkel des Reizleitungssystems. Z Klin Med 70:1-20, 1910 7. Rothberger CJ, Winterberg H: Experimentelle Beitrage zur Kenntnis der Reizleitungsstorungen in den Kammern des Saugertierherzens. Z Ges Exp Med 51246-320, 1917
8. Wilson FN, Herrmann GR: Experimental study of incomplete bundle branch block and of the refractory period of the heart of the dog. Heart 8:229-296, 1921 9. Smith LA, Kennamer R, Prinzmetal M: Studies on the mechanism of ventricular activity. Circ Res 2:221-230. 1954 10. Pruitt RD. Watt RB. Murao S: Left axis deviation: its relation to experimentally induced lesions of the anterior left bundle branch system in canine and primate hearts. Ann NY Acad Sci 127: 204-223, 1965 11. Watt TB Jr, Freud GE, Durrer P, Pruitt RD: Left anterior arborization block combined with right bundle branch block in canine and primate hearts. Circ Res 22:57-63, 1968 12. Gallagher JJ, Tfczon AR, Wallace AG, Kasell J: Activation studies following experimental hemiblock in the dog. Circ Res 35:752-763, 1974 13. Sugiura M, Okada R, Horaoka K, Ohkawa S: Histological studies on the conduction system in 14 cases of right bundle branch block associated with left axis deviation. Jpn Heart J 10:121-132,
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1969 14. Rosen KM, Rahimtoola SH, Gunnar RM, Lev M: Site of heart block as defined by His bundle recording. Pathologic correlations in three cases. Circulation 45:965-987, 1972 15. Lev M, Bharati S: Lesions of the conduction system and their functional significance. In, Pathology Annual (Sommers CS, ed). New York, Appleton-Century-Crofts, 1974, p 157-207 16. Kulbertus H: Concept of left hemiblocks revisited. A histopathological and experimental study. Adv Cardiol 14:126-135, 1975 17. Rossi L: Histopathology of conducting system in left anterior hemiblock. Br Heart J 38:1304-1311, 1976 18. Demoulin JC, Simar LJ, Kulbertus HE: Quantitative study of left bundle branch fibrosis in left anterior hemiblock. A stereologic approach. Am J Cardiol 36:751-756, 1975 19. Rosen KM, Wu D, Kanakis C, Denes P, Bharati S, Lev M: Return of normal conduction after paroxysmal heart block. Report of a case with major discordance of electrophysiological and pathological findings. Circulation 51:197-204, 1975 20. Wyndham CRC, Amat-y-Leon F, Denes P, Dhingra RC, Burman SO, Pouget JM, Rosen KM: Posterior left ventricular preexcitation. Arch Intern Med 134:243-249, 1974 21. Wyndham CR, Meeran MK, Smith T, Saxena A, Engelman RM, Levitsky S, Rosen KM: Epicardial activation of the intact human heart without conduction defect. Circulation 59:161-168, 1979 22. van Dam RT: Ventricular activation in human and canine bundle branch block. In, The Conduction System of the Heart. (Wellens
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HJJ, ed). Philadelphia, Lea & Febiger, 1976, p 377-392 23. Spurrell RAJ, Sowton E, Deuchar DC: Ventricular tachycardia in 4 patients evaluated by programmed electrical stimulation of heart and treated in 2 patients by surgical division of anterior radiation of left bundle branch. Br Heart J 35:1014-1025, 1973 24. Burch GE: Of hemiblock propaganda. Am Heart J 94532-533, 1977 25. Jacobson LB, LaFollete L, Cohn K: An appraisal of initial QRS forces in left anterior fascicular block. Am Heart J 94:407-413, 1977 26. Fabregas R, Tse W, Han J: Conduction disturbances of the bundle branches produced by lesions in the nonbranching portion of His bundle. Am Heart J 92:356-362, 1976 27. Lazzara R, Yeh BK, Samet P: Functional anatomy of the canine left bundle branch. Am J Cardiol 33:623-632, 1974 28. lwamura N, Kodama I, Shimizu T, Hirata Y, Toyama J, Yamada K: Functional properties of the left septal Purkinje network in premature activation of the ventricular conduction system. Am Heart J 95:60-69, 1978 29. Durrer D, van Dam RT, Freud GE, Janse MJ, Meijler FL, Arzbaecher RC: Total excitation of the isolated human heart. Circulation 41:899-912, 1970 30. Daniel T, Boineau JP, Sabiston DC: Comparison of human ventricular activation with a canine model in chronic myocardial infarction. Circulation 44:741-756, 1971
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