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Left bundle branch block with left-axis deviation: An electrophysiologic approach
Left Bundle Branch Block with Left-Axis Deviation: An ElectrophysiologicApproach ALAIN GRESSARD, MD
In an attempt to explain QRS left-axis deviation (LAD) in left bundle branch block (LBBB), 69 patients with LBBB were studied. The patients were separated into 2 groups. Group A included 60 patients wlth a QRS axis of i-60’ to -55’ (average - 11” ) and Group B included 9 patients with a QRS axis of -60’. In all patients, a point was detected on the apex of the right ventricle at which activation was simultaneous with the beginning of ventricular depolarization (V-apex = 0). Ventricular stimulation at this point gave a monomorphic response with a QRS axis of -60’ and QS in D2 and DB. Minor conduction aberrations related to the relative refractory period of the His Purkinje network were found during atrial premature beats in 40 patients in Group A (and
always as LAD of the QRS axis [average 24.6’1) and in 4 patients in Group B. In Group B, these aberrations were in the form of a disappearance of the r2 wave with a QRS axis similar to that achieved through stimulation of the right ventricle apex. Given this aberration, one may conclude that the left bundle branch plays a role in the depolarization of the left ventricle. Blocking it brings the QRS axis closer to that obtained by stimulation of the point of primary depolarization of the right ventricle. Thus, LBBB must have a monomorphic morphology. lf not, the lefl branch is the location of slowed, but persistent, conduction.
Many investigators have tried to distinguish, among patients with left bundle branch block (LBBB), those whose axes remain normal (between +90° and -30”) from those with left-axis deviation (LAD) (deviation to the left more than -30’). Investigators who rely on anatomic-clinical and clinical considerations1-4 agree that a more cautious prognosis should be given to patients with LBBB and LAD than to those with LBBB and a normal axis. LAD is more frequent in idiopathic cardiomyopathy with severely impaired myocardial function, and is often accompanied by marked cardiomegaly. Some studies also show that the QRS is wider and the HV interval larger than in the group without LAD.5,6 The explanation for the LAD with LBBB is not clear. According to some investigators7-g the deviation could stem from the association of a conductive disturbance both on the left bundle branch trunk and on its upper frontal subdivisions. However, this hypothesis has been questioned.lOJ1 Laham and Gerbaux12 reported that LAD with LBBB appears in conjunction with right ventricular hypertrophy. Swiryn et a1,13 in a recent
comparative study of the QRS axis before and after an LBBB in a large sample of patients, showed that the QRS axis with LBBB was not necessarily dependent on the QRS axis without LBBB. They could not explain LAD by an associated left anterior hemiblock. De Pasquale and Bruno14 reported similar findings.
From the Hbpital Antoine Charial, Francheville, France. Manuscript received February 14, 1983; revised manuscript received July 8, 1983, accepted July 12, 1983. Address for reprints: l%pital Antoine Charial, 40. avenue de la Table de Pierre, 69340 Francheville, France.
(Am J Cardiol 1963;52:1013-1016)
Material and Methods Sixty-nine patients with LBBB defined according to New York Heart Association criteria15 were studied. Electrophysiologic testing was performed without premeditation. A bipolar catheter electrode (1 cm apart) was introduced into the right ventricular apex to record the local electrical potential and to pace the heart at this point. The position of the catheter was such that the V-apex interval (the delay between the local electrogram and the onset of QRS in the external lead where it was found to be the earliest) was 0 in all patients. Pacing of the right atrium was performed by extrastimulation. Other catheters were used to pace the right atrium and to record His bundle and right atria1 activity.
Results The patients were divided into 2 groups according to their QRS axis. Group A included 60 patients with a QRS axis of +80 to -55’ (average -11’). Group B included 9 patients with LAD of -60”.
1014
LEFT BUNDLE BRANCH BLOCK WITH LEFT-AXIS
DEVIATION
In all cases, regardless of the QRS axis, an area of primary ventricular depolarization could be detected in the region of the apex of the right ventricle (V-apex = 0) (Fig. 1). Leaving the same catheter in the same position, pacing of the right ventricle led to a monomorphic morphology of QRS; that is, its aspect, obviously with left delay, QRS > 0.12 second and no qi and qVs waves, LAD of -6O”, and a QS wave at Ds and Ds (thus, no initial positivity). QRS modifications were recorded in response to an atria1 premature beat. In group A, these modifications occurred in 40 cases (66%). They always appeared as LAD, ranging from 10” to 50“ (average 24.6). A decrease in the Rs and Rs waves was recorded, together with the appearance of an increase in the Ss or Ss wave. LAD was never greater than -60’ (Fig. 2). In group B, in 4 patients, the disappearance of a previously present rs wave was noted. In 1 case, a concomitant r3 wave also disappeared. Therefore, the QRS morphology was characterized by LAD of -60’ and an absence of R wave in the Dz and Ds leads (Fig. 3). Discussion In LBBB, the conduction of the left bundle branch should be stopped. Given this hypothesis, the depolar-
Dl,
r
.-
7/c/l
b-
-(If-
D--V_
ization of the ventricles is solely dependent on the conduction in the right bundle branch. Indeed, it is possible to locate the area of primary depolarization (V-apex = 0) through contact with the right ventricular endocardium. The 0 value of the V-apex agrees with what is known about ventricular depolarization in LBBB. Indeed, activation begins in the right ventricle with penetration of the septum from right to left.16-is Durrer et a1,20in their studies of whole heart endocardial depolarization, clearly established the site of right ventricular primary depolarization. This site appears to be unique. More recently, Cannom et a121showed that the occurrence of LBBB is accompanied by a reduction of the V-apex interval to 0. Pacing at this point should reproduce the LBBB corresponding to the supraventricular QRS. However, it does not. The monomorphic aspect of LAD obtained during right ventricular pacing is well known. This aspect is dependent only on the site of pacing and, in particular, is independent of the conducting status of the Purkinje network. Consequently, ventricular activation does not depend on possible conduction through the Purkinje network from the point of pacing, but rather on slow conduction through the myocardium. As the pacing is given in the lowest region of the heart, and on the right side, the depolarization can only spread upward and to the left, resulting in a QRS axis of -6O”, absence of r2-r3 waves, increased deviation of the QRS, and left-delay morphology. Thus, a part of the left Purkinje network participates in the depolarization of the left ventricle in most cases of LBBB. Cannom et a122noted, in 6 of 9 patients studied, LAD in response to an atria1 premature beat in the presence of LBBB with a normal axis. They concluded that a part of the Purkinje network of the left anterior division of the His bundle partipated in ventricular depolarization
vl--l/----vf-v+- + Apex -L
i
FIGURE 1. Left, measurement of conduction intervals in left bundle branch block. A = right atrial electrogram; H = His bundle lead; Apex = electrogram obtained at the apex of the right ventricle, simultaneous with the onset of ventricular activation (V-apex = 0). RfgM, morphofogy of QRS during ventricular pacing with electrode placed at the apex: left delay morphology, QRS axis deviated toward the left (-600), OS in D2 and Ds. The CBS is longer during ventricular pacing (0.19 second) than during sinus rhythm (0.16 second).
hi FIGURE 2. Electrocardiogram from a patient in group A. An atrial premature beat is conducted to the ventricles with a modification of QRS as left-axis deviation of about 25“.
November 1, 1983
in these cases of LBBB, but excluded any participation of the lower posterior subdivision. Indeed, a modification of the QRS axis must be interpreted as evidence of a conduction block somewhere in the Purkinje network (corresponding to its relative refractory period). It is unlikely that the Purkinje responsible depends on the right bundle branch, because it is not separated into individualized bundles and because its conduction disturbances do not appear as a QRS axis deviation. Therefore, the Purkinje network, whose blocking is responsible for LAD, may be derived from the left bundle branch and particularly from its upper and front subdivisions. As for the smaller group of patients with LBBB with LAD, the differences could correspond to the blocking of the lower posterior subdivisions of the left bundle branch, for the case in which the upper front subdivisions are already blocked (see preceding case). Under these conditions, the left conduction disturbance was not complete. Moreover, all of the morphologic variations after atria1 premature beat combined bring the QRS closer to that achieved by pacing of the right ventricular site of primary depolarization, which could be called “pure” LBBB (QRS axis -60”; QS in DP and Ds, exclusive R in Di). Among the factors that favor this “pure” LBBB morphology is the intraventricular reentry or ventricular double response with intermediate H potential sometimes achieved by premature right ventricular pacing (Fig. 4). Akhtar et alz3 showed that under these conditions, in the reentry circuit, depolarization follows the left bundle branch in the retrograde direction and then the right bundle in the anterograde direction. This comes after reflection of the influx at the His bundle division. The new ventricular depolarization, then, derives only from the arrival of the stimulus through the right branch. This phenomenon explains the “pure”
DI
THE AMERICAN JOURNAL OF CARDIOLOGY
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1015
“l “6 FIGURE 4. lntraventricular reentry after a right ventricular extrasystole. The extrasystole is delivered on a basic ventricular pacing. The extrasystole is followed by a late H potential, reflecting the retrograde conduction of the influx in the common part of the His bundle (from the left bundle branch). The second QRS arises from ventricular depolarization produced by the anterograde conduction of the influx through the right bundle branch alone after reflection at the His divide. This reentry can be regarded as a model of pure left bundle branch block. It possesses the same morphologic features as the QRS determined by pacing the apex of the right ventricle.
LBBB aspect of this second ventricular response described earlier. The HV interval, found more often in Group A than in Group B, also tends to confirm the more advanced character of the conduction disturbance of LBBB with LAD. The average HV was 70.68 ms in Group A (variance 10.77) and 81.1 ms in Group B (variance 13.41). Similar observations have been reported previously.5~cJ The following conclusions regarding the schematic possibilities of LBBB may be suggested: LBBB with normal axis is a conduction disturbance that alters left septal depolarization with persistence of slow conduction in the anterior and posterior rami of the left bundle branch. In LBBB with LAD and r2 wave (and possibly rs wave also), conduction is blocked in anterior ramus and is slow but persistent in posterior ramus of the left bundle branch. In LBBB with a right axis, conduction is blocked in posterior ramus and is slow but persistent in anterior ramus. In “pure” LBBB by complete block of conduction in the left branch, exclusive R in D1, QS in Ds and Ds and QRS axis at -60”. References Blondeau M. Le bloc complet de la branche gauche avec forte deviation ;;i:,le gauche de QRS. I. Etude clinique. Arch Mal Coeur 1974:67:621-
FIGURE 3. Electrocardiogram from a patient in group B. An atrial premature beat is conducted to the ventricles with a modification of QRS in the form of a disappearance of the r2 wave.
Blondeau M. Le bloc complet de la branche gauche avec forte deviation axiale gauche de QRS. Il. Etude anatomique. Arch Mal Coeur 1974;67: 635645. Dhlngra RC, *mat-y-Leon F, Wyndham C, Srldhar SS, Wu D, Denes P,
1018
4. 5.
8. 7. 8. 9. IO. Il.
LEFT BUNDLE BRANCH BLOCK WITH LEFT-AXIS
DEVIATION
Rosen KM. Sianificance of left axis deviation in oatients with chronic left bundle branch-block. Am J Cardiol 1978;42:551&8. Llchaleln E, Mahapatra R, Gupla PK, Chadda K. Significance of complete left bundle branch block with left axis deviation. Am J Cardiol 1979;44: 239-242. Spurrell RAJ, Krlkler DM, Sowton E. Study of intraventricular conduction times in patients with left bundle-branch block and left axis deviation and in patients with left bundle-branch block and normal QRS axis using His bundle electrograms. Br Heart J 1972;34:1244-1249. Rosen KM, Ehsanl A, Rahlmtoola SH. H-V intervals in left bundle branch block. Clinical and electrocardiographic correlations. Circulation 1972; 48:7l?-723. Pryor B, Blount SG Jr. The clinical significance of true left axis deviation. Lefl intraventricular blocks. Am Heart J 1988;72:391-413. Davies H, Evans W. The significance of deep S waves in leads II and Ill. Br Heart J 1960;22:551-581. Warembourg H, Lekleflre J, Thery C. Blocs parietaux et blocks p&i infarctus. Leur resoonsabilit6 dans l’aeoarition des blocs auriculoventriculaires. Coeur t&J Intern 1970;9:35-‘47. Rosenbaum MB, Ellzarl MV, Larzari JO. Los h8mibloqueos. Buenos Aires: Paidos. 1988. Wall JB Jr, Prultt RD. Incomplete EBB, arborization block and intramural block: electrocardi~rap~ic expressions of experimentally produced single ;;;,compound lesions In the canine heart. Cardiovasc Res 1987;5:91-
12. Laham J,._-. Gerbaux __ A..-Les blocs de branche gauche atypiques. Ann Cardiol Angelo1 lY74;23:1-17. 13. Swltyn S, Abben R, Genes P, Rosen KM. Electrocardiographic determinants of axis during left bundle branch block: study in patients with intermittent
14. 15. 18. 17. 18. 19.
20.
left bundle branch block: study in patients with intermittent left bundle branch block. Am J Cardiol 1980;48:53-58. De Pasquale NP, Bruno MS. Left bundle branch block and abnormal left axis deviation without left anterior hemiblock. Am J Cardiol 1973;32: 98-100. Criteria Committee of the New York Heart Association. Nomenclature and Criteria for the Diaanosis of Diseases of the Heart and Great Vessels. Boston: Little, Brown, 1973:270. Becker RA, Scher AM, Erkkson RV. Ventricular excitation in experimental left bundle branch block. Am Heart J 1958;55:547-556. Kennamer R, Prlnzmetal M. Depolarization of the ventricle with bundle branch block. Studies on the mechanism of ventricular activity. Am Heart J 1954:47:789-779, Erlcks& RV, Scher AM. Becker RA. Ventricular excitation in exoerimantal bundle branch blqck. Circ Res 1957;5:5-10. Venerose RS, Seldensleln M, Stuckey JH, Hoffman BF. Activation of subendocardial Purkinje fibers and muscle fibers on the left septal surface before and after left bundle branch block. Am Heart J 1982;83:346-361. Durrer D, Van Dam RT, Freud GE, Janse MJ, Meljler FL, Arzbaecher R. Total excitation of the isolated human heart. Circulation 1970;41:899A._ Y IL.
21. Cannom OS, Wyman MG, Golcfreyer BN. Initial ventricular activation in left sided intraventricular conduction defects. Circulation 1980;82:821-631. 22. Cannom GS, Golaeyer BN, Dam&o AN. Atrioventricular conduction system in left bundle branch block with normal QRS axis. Circulation 1972:46: 129-137. 23. Akhtar M, Gllberl C, Wall FG, Schmldl DH. Reentry within the His Purkinje system. Elucidation of reentrant circuit using right bundle branch and His bundle recordings. Circulation 1978;58:295-304.
In an attempt to explain QRS left-axis deviation (LAD) in left bundle branch block (LBBB), 69 patients with LBBB were studied. The patients were separated into 2 groups. Group A included 60 patients wlth a QRS axis of i-60’ to -55’ (average - 11” ) and Group B included 9 patients with a QRS axis of -60’. In all patients, a point was detected on the apex of the right ventricle at which activation was simultaneous with the beginning of ventricular depolarization (V-apex = 0). Ventricular stimulation at this point gave a monomorphic response with a QRS axis of -60’ and QS in D2 and DB. Minor conduction aberrations related to the relative refractory period of the His Purkinje network were found during atrial premature beats in 40 patients in Group A (and
always as LAD of the QRS axis [average 24.6’1) and in 4 patients in Group B. In Group B, these aberrations were in the form of a disappearance of the r2 wave with a QRS axis similar to that achieved through stimulation of the right ventricle apex. Given this aberration, one may conclude that the left bundle branch plays a role in the depolarization of the left ventricle. Blocking it brings the QRS axis closer to that obtained by stimulation of the point of primary depolarization of the right ventricle. Thus, LBBB must have a monomorphic morphology. lf not, the lefl branch is the location of slowed, but persistent, conduction.
Many investigators have tried to distinguish, among patients with left bundle branch block (LBBB), those whose axes remain normal (between +90° and -30”) from those with left-axis deviation (LAD) (deviation to the left more than -30’). Investigators who rely on anatomic-clinical and clinical considerations1-4 agree that a more cautious prognosis should be given to patients with LBBB and LAD than to those with LBBB and a normal axis. LAD is more frequent in idiopathic cardiomyopathy with severely impaired myocardial function, and is often accompanied by marked cardiomegaly. Some studies also show that the QRS is wider and the HV interval larger than in the group without LAD.5,6 The explanation for the LAD with LBBB is not clear. According to some investigators7-g the deviation could stem from the association of a conductive disturbance both on the left bundle branch trunk and on its upper frontal subdivisions. However, this hypothesis has been questioned.lOJ1 Laham and Gerbaux12 reported that LAD with LBBB appears in conjunction with right ventricular hypertrophy. Swiryn et a1,13 in a recent
comparative study of the QRS axis before and after an LBBB in a large sample of patients, showed that the QRS axis with LBBB was not necessarily dependent on the QRS axis without LBBB. They could not explain LAD by an associated left anterior hemiblock. De Pasquale and Bruno14 reported similar findings.
From the Hbpital Antoine Charial, Francheville, France. Manuscript received February 14, 1983; revised manuscript received July 8, 1983, accepted July 12, 1983. Address for reprints: l%pital Antoine Charial, 40. avenue de la Table de Pierre, 69340 Francheville, France.
(Am J Cardiol 1963;52:1013-1016)
Material and Methods Sixty-nine patients with LBBB defined according to New York Heart Association criteria15 were studied. Electrophysiologic testing was performed without premeditation. A bipolar catheter electrode (1 cm apart) was introduced into the right ventricular apex to record the local electrical potential and to pace the heart at this point. The position of the catheter was such that the V-apex interval (the delay between the local electrogram and the onset of QRS in the external lead where it was found to be the earliest) was 0 in all patients. Pacing of the right atrium was performed by extrastimulation. Other catheters were used to pace the right atrium and to record His bundle and right atria1 activity.
Results The patients were divided into 2 groups according to their QRS axis. Group A included 60 patients with a QRS axis of +80 to -55’ (average -11’). Group B included 9 patients with LAD of -60”.
1014
LEFT BUNDLE BRANCH BLOCK WITH LEFT-AXIS
DEVIATION
In all cases, regardless of the QRS axis, an area of primary ventricular depolarization could be detected in the region of the apex of the right ventricle (V-apex = 0) (Fig. 1). Leaving the same catheter in the same position, pacing of the right ventricle led to a monomorphic morphology of QRS; that is, its aspect, obviously with left delay, QRS > 0.12 second and no qi and qVs waves, LAD of -6O”, and a QS wave at Ds and Ds (thus, no initial positivity). QRS modifications were recorded in response to an atria1 premature beat. In group A, these modifications occurred in 40 cases (66%). They always appeared as LAD, ranging from 10” to 50“ (average 24.6). A decrease in the Rs and Rs waves was recorded, together with the appearance of an increase in the Ss or Ss wave. LAD was never greater than -60’ (Fig. 2). In group B, in 4 patients, the disappearance of a previously present rs wave was noted. In 1 case, a concomitant r3 wave also disappeared. Therefore, the QRS morphology was characterized by LAD of -60’ and an absence of R wave in the Dz and Ds leads (Fig. 3). Discussion In LBBB, the conduction of the left bundle branch should be stopped. Given this hypothesis, the depolar-
Dl,
r
.-
7/c/l
b-
-(If-
D--V_
ization of the ventricles is solely dependent on the conduction in the right bundle branch. Indeed, it is possible to locate the area of primary depolarization (V-apex = 0) through contact with the right ventricular endocardium. The 0 value of the V-apex agrees with what is known about ventricular depolarization in LBBB. Indeed, activation begins in the right ventricle with penetration of the septum from right to left.16-is Durrer et a1,20in their studies of whole heart endocardial depolarization, clearly established the site of right ventricular primary depolarization. This site appears to be unique. More recently, Cannom et a121showed that the occurrence of LBBB is accompanied by a reduction of the V-apex interval to 0. Pacing at this point should reproduce the LBBB corresponding to the supraventricular QRS. However, it does not. The monomorphic aspect of LAD obtained during right ventricular pacing is well known. This aspect is dependent only on the site of pacing and, in particular, is independent of the conducting status of the Purkinje network. Consequently, ventricular activation does not depend on possible conduction through the Purkinje network from the point of pacing, but rather on slow conduction through the myocardium. As the pacing is given in the lowest region of the heart, and on the right side, the depolarization can only spread upward and to the left, resulting in a QRS axis of -6O”, absence of r2-r3 waves, increased deviation of the QRS, and left-delay morphology. Thus, a part of the left Purkinje network participates in the depolarization of the left ventricle in most cases of LBBB. Cannom et a122noted, in 6 of 9 patients studied, LAD in response to an atria1 premature beat in the presence of LBBB with a normal axis. They concluded that a part of the Purkinje network of the left anterior division of the His bundle partipated in ventricular depolarization
vl--l/----vf-v+- + Apex -L
i
FIGURE 1. Left, measurement of conduction intervals in left bundle branch block. A = right atrial electrogram; H = His bundle lead; Apex = electrogram obtained at the apex of the right ventricle, simultaneous with the onset of ventricular activation (V-apex = 0). RfgM, morphofogy of QRS during ventricular pacing with electrode placed at the apex: left delay morphology, QRS axis deviated toward the left (-600), OS in D2 and Ds. The CBS is longer during ventricular pacing (0.19 second) than during sinus rhythm (0.16 second).
hi FIGURE 2. Electrocardiogram from a patient in group A. An atrial premature beat is conducted to the ventricles with a modification of QRS as left-axis deviation of about 25“.
November 1, 1983
in these cases of LBBB, but excluded any participation of the lower posterior subdivision. Indeed, a modification of the QRS axis must be interpreted as evidence of a conduction block somewhere in the Purkinje network (corresponding to its relative refractory period). It is unlikely that the Purkinje responsible depends on the right bundle branch, because it is not separated into individualized bundles and because its conduction disturbances do not appear as a QRS axis deviation. Therefore, the Purkinje network, whose blocking is responsible for LAD, may be derived from the left bundle branch and particularly from its upper and front subdivisions. As for the smaller group of patients with LBBB with LAD, the differences could correspond to the blocking of the lower posterior subdivisions of the left bundle branch, for the case in which the upper front subdivisions are already blocked (see preceding case). Under these conditions, the left conduction disturbance was not complete. Moreover, all of the morphologic variations after atria1 premature beat combined bring the QRS closer to that achieved by pacing of the right ventricular site of primary depolarization, which could be called “pure” LBBB (QRS axis -60”; QS in DP and Ds, exclusive R in Di). Among the factors that favor this “pure” LBBB morphology is the intraventricular reentry or ventricular double response with intermediate H potential sometimes achieved by premature right ventricular pacing (Fig. 4). Akhtar et alz3 showed that under these conditions, in the reentry circuit, depolarization follows the left bundle branch in the retrograde direction and then the right bundle in the anterograde direction. This comes after reflection of the influx at the His bundle division. The new ventricular depolarization, then, derives only from the arrival of the stimulus through the right branch. This phenomenon explains the “pure”
DI
THE AMERICAN JOURNAL OF CARDIOLOGY
Volume 52
1015
“l “6 FIGURE 4. lntraventricular reentry after a right ventricular extrasystole. The extrasystole is delivered on a basic ventricular pacing. The extrasystole is followed by a late H potential, reflecting the retrograde conduction of the influx in the common part of the His bundle (from the left bundle branch). The second QRS arises from ventricular depolarization produced by the anterograde conduction of the influx through the right bundle branch alone after reflection at the His divide. This reentry can be regarded as a model of pure left bundle branch block. It possesses the same morphologic features as the QRS determined by pacing the apex of the right ventricle.
LBBB aspect of this second ventricular response described earlier. The HV interval, found more often in Group A than in Group B, also tends to confirm the more advanced character of the conduction disturbance of LBBB with LAD. The average HV was 70.68 ms in Group A (variance 10.77) and 81.1 ms in Group B (variance 13.41). Similar observations have been reported previously.5~cJ The following conclusions regarding the schematic possibilities of LBBB may be suggested: LBBB with normal axis is a conduction disturbance that alters left septal depolarization with persistence of slow conduction in the anterior and posterior rami of the left bundle branch. In LBBB with LAD and r2 wave (and possibly rs wave also), conduction is blocked in anterior ramus and is slow but persistent in posterior ramus of the left bundle branch. In LBBB with a right axis, conduction is blocked in posterior ramus and is slow but persistent in anterior ramus. In “pure” LBBB by complete block of conduction in the left branch, exclusive R in D1, QS in Ds and Ds and QRS axis at -60”. References Blondeau M. Le bloc complet de la branche gauche avec forte deviation ;;i:,le gauche de QRS. I. Etude clinique. Arch Mal Coeur 1974:67:621-
FIGURE 3. Electrocardiogram from a patient in group B. An atrial premature beat is conducted to the ventricles with a modification of QRS in the form of a disappearance of the r2 wave.
Blondeau M. Le bloc complet de la branche gauche avec forte deviation axiale gauche de QRS. Il. Etude anatomique. Arch Mal Coeur 1974;67: 635645. Dhlngra RC, *mat-y-Leon F, Wyndham C, Srldhar SS, Wu D, Denes P,
1018
4. 5.
8. 7. 8. 9. IO. Il.
LEFT BUNDLE BRANCH BLOCK WITH LEFT-AXIS
DEVIATION
Rosen KM. Sianificance of left axis deviation in oatients with chronic left bundle branch-block. Am J Cardiol 1978;42:551&8. Llchaleln E, Mahapatra R, Gupla PK, Chadda K. Significance of complete left bundle branch block with left axis deviation. Am J Cardiol 1979;44: 239-242. Spurrell RAJ, Krlkler DM, Sowton E. Study of intraventricular conduction times in patients with left bundle-branch block and left axis deviation and in patients with left bundle-branch block and normal QRS axis using His bundle electrograms. Br Heart J 1972;34:1244-1249. Rosen KM, Ehsanl A, Rahlmtoola SH. H-V intervals in left bundle branch block. Clinical and electrocardiographic correlations. Circulation 1972; 48:7l?-723. Pryor B, Blount SG Jr. The clinical significance of true left axis deviation. Lefl intraventricular blocks. Am Heart J 1988;72:391-413. Davies H, Evans W. The significance of deep S waves in leads II and Ill. Br Heart J 1960;22:551-581. Warembourg H, Lekleflre J, Thery C. Blocs parietaux et blocks p&i infarctus. Leur resoonsabilit6 dans l’aeoarition des blocs auriculoventriculaires. Coeur t&J Intern 1970;9:35-‘47. Rosenbaum MB, Ellzarl MV, Larzari JO. Los h8mibloqueos. Buenos Aires: Paidos. 1988. Wall JB Jr, Prultt RD. Incomplete EBB, arborization block and intramural block: electrocardi~rap~ic expressions of experimentally produced single ;;;,compound lesions In the canine heart. Cardiovasc Res 1987;5:91-
12. Laham J,._-. Gerbaux __ A..-Les blocs de branche gauche atypiques. Ann Cardiol Angelo1 lY74;23:1-17. 13. Swltyn S, Abben R, Genes P, Rosen KM. Electrocardiographic determinants of axis during left bundle branch block: study in patients with intermittent
14. 15. 18. 17. 18. 19.
20.
left bundle branch block: study in patients with intermittent left bundle branch block. Am J Cardiol 1980;48:53-58. De Pasquale NP, Bruno MS. Left bundle branch block and abnormal left axis deviation without left anterior hemiblock. Am J Cardiol 1973;32: 98-100. Criteria Committee of the New York Heart Association. Nomenclature and Criteria for the Diaanosis of Diseases of the Heart and Great Vessels. Boston: Little, Brown, 1973:270. Becker RA, Scher AM, Erkkson RV. Ventricular excitation in experimental left bundle branch block. Am Heart J 1958;55:547-556. Kennamer R, Prlnzmetal M. Depolarization of the ventricle with bundle branch block. Studies on the mechanism of ventricular activity. Am Heart J 1954:47:789-779, Erlcks& RV, Scher AM. Becker RA. Ventricular excitation in exoerimantal bundle branch blqck. Circ Res 1957;5:5-10. Venerose RS, Seldensleln M, Stuckey JH, Hoffman BF. Activation of subendocardial Purkinje fibers and muscle fibers on the left septal surface before and after left bundle branch block. Am Heart J 1982;83:346-361. Durrer D, Van Dam RT, Freud GE, Janse MJ, Meljler FL, Arzbaecher R. Total excitation of the isolated human heart. Circulation 1970;41:899A._ Y IL.
21. Cannom OS, Wyman MG, Golcfreyer BN. Initial ventricular activation in left sided intraventricular conduction defects. Circulation 1980;82:821-631. 22. Cannom GS, Golaeyer BN, Dam&o AN. Atrioventricular conduction system in left bundle branch block with normal QRS axis. Circulation 1972:46: 129-137. 23. Akhtar M, Gllberl C, Wall FG, Schmldl DH. Reentry within the His Purkinje system. Elucidation of reentrant circuit using right bundle branch and His bundle recordings. Circulation 1978;58:295-304.