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Left bundle branch block and coronary artery disease
J. ELECTROCARDIOLOGY, 8 (4) 317-324
Left Bundle Branch Block and Coronary Artery Disease* BY WALTER H. HERBERT, M.D.t
SUMMARY This study tries the concept that left bundle-branch block (LBBB) connotes coronary artery disease (CAD). The findings indicate that prior studies both supporting of and in contradiction to the premise of a positive correlation have been biased by pre-selection of the patients reviewed. The data indicate, therefore, that LBBB is related to multiple entities. The major categories are CAD and/or hypertension, myocardiopathy and aortic valvular disease. In addition, LBBB may develop during the acute phase of myocardial infarction. Its existence as a wholly benign entity has been documented as well. Further, this study adds still another group with LBBB. Six of the nine LBBB patients were female. Five of these, in spite of typical anginal histories, had no arteriographically demonstrable CAD. The absence of disease was surprising and the incidence of women with LBBB was greater than anticipated, thus providing some basis for suggesting that these women may be representative of still another group with LBBB. Further, this study supports the findings of Lewis et al by confirming an association between LBBB and a statistically shorter LCA mainstem (p < 0.001).
From the Department of Medicine, New York Medical College, New York, N.Y. and the Cardiopulmonary Laboratory, Grasslands Hospital, Valhalla, N.Y. tAssociate Professor of Medicine, New York Medical College and Associate Director, Cardiopulmonary Laboratory, Grasslands Hospital. *This study was supported by a grant from the Westchester Heart Association. Reprint requests to: Walter H. Herbert, M.D., Associate Director, Cardiopulmonary Laboratory, Grasslands Hospital, Valhalla, NY 10595.
The controversy as to whether left bundle branch block (LBBB) connotes coronary artery d i s e a s e (CAD) is still unresolved. A reasonable approach to the assessment of the relationship is to postulate that if a positive correlation exists, then the incidence of the conduction disturbance in a group of patients specifically referred for coronary arteriography should be higher than that in the population at large, and, further, such patients should have significant demonstrable lesions. In one of the few arteriographic studies pertaining to this problem, Lewis et al 1 reported on 12 patients with LBBB out of a total study population of 366. Only 4 of these 12 patients had CAD. In an earlier study by Haft et al, 2 24 of 578 patients were demonstrated to have LBBB. Only 7 (29%) had angiographic evidence of CAD. A l t h o u g h the incidence of LBBB in these two studies, 3.2% and 4.1% respectively, was substantially higher than t h a t in t h e general population (less t h a n 1%), 84 only a small percentage in each group had demonstrable CAD (33% and 29% respectively). Certainly there is an inconsistency between these two very similar studies and the n u m e r o u s reports of the close correlation b e t w e e n L B B B a n d CAD a n d / o r hypertension .5-13 In one of the above reports I it was noted as well that the LBBB patients had extremely short left coronary artery (LCA) mainstems. Although another group of observers 14 was unable to substantiate this finding, should it prove to be correct even in some of the patients, then it may have an important bearing on the understanding of this clinical entity. This study was undertaken in an effort to define further the significance of LBBB in the several populations in which it is described:
MATERIALS AND METHODS Three hundred consecutive patient studies were reviewed. All subjects had undergone selective coronary arteriography with ventriculography by the transbrachial Sones and Shirey technique. 15 317
318
HERBERT
Ventriculograms were exposed in both the right and left anterior oblique positions. Each coronary artery was opacified in at least three separate projections which included both the left and right anterior obliques and a 60~ left anterior view. The arteriographic patterns were defined according to the criteria of Schlesinger. TM The film sequences were recorded with a North American Philips 6" image intensifier on 35 mm film at 50 frames/sec. For the purpose of this study, any coronary arterial luminal irregularity causing a distortion or encroachment greater than 25% was considered abnormal. Hemodynamic measurements were made with Statham P23db gauges and monitored on an Electronics for Medicine DR-12 recorder. The zero reference level was established 5 cm below the angle of Louis. The upper limit of normal for left ventricular end-diastolic pressure for (LVEDP) in this laboratory is 12mm Hg. All pressure measurements reported were the average of two full respiratory cycles. Nine patients fulfilled the New York Heart Association criteria for LBBB.1~Their ages ranged from 32 to 63 years. Six were women. Assessment of LCA mainstem length was by the method of Lewis et al.1
RESULTS Table 1 displays the hemodynamic, angiographic and pertinent historical findings in the nine patients with LBBB. It is noted t h a t the separation b y sex is also consistent with a difference in both clinical presentation and laboratory findings. Whereas each woman underwent study for the primary complaint of anterior chest pain with radiation into the neck, arms or jaw, usually precipitated by exertion, these complaints were not part of the male patients' histories. The men complained of severe shortness of breath. In addition, one had had episodes of paroxysmal nocturnal dyspnea and one had had a syncopal attack. Two men were diagnosed as having idiopathic, non-obstructive cardiomyopathy and the third severe aortic insufficiency on a rheumatic basis. By ventriculography all three men had grossly dilated and sluggishly contractile left ventricles. Only one woman (patient 5) had similar ventricular dysfunction. This patient was the only one of the entire group (male and female) to manifest CAD. Specifically, there was a 90% discrete narrowing in the proximal right coronary artery. In addition, there were significant linear changes in the proximal anterior descending artery involving the major septal perforators. All the remaining patients were considered to have normal coronary vascular trees. One m a n (patient 8) had a dominant left c o r o n a r y a r t e r y p a t t e r n w i t h t h e atrio-
ventricular nodal artery arising from the left coronary artery. One women (patient 3) had a balanced circulation with the sino-atrial nodal a r t e r y a r i s i n g from t h e circumflex branch of the left coronary artery. The remainder of the patients had dominant right circulation with both the sino-atrial and the atrio-ventricular nodal arteries arising from the right. Each of the five women with a normal coron a r y tree demonstrated a consistent ventriculographic pattern. That is, there was some degree of ventricular dilatation and what appeared to be some apical emptying delay. A representative end-systolic frame recorded on patient 6 is seen in Fig. 1A. Fig. 1B is a drawing of 1A to outline the apical dilatation at end-systole. The ventriculogram was recorded in the right anterior oblique projection. Three of these patients had normal LVEDP's prior to contrast media studies (patients 1, 3 and 6). Two patients had abnormal elevations in LVEDP (patients 2 and 4) (Table 1). E a c h p a t i e n t w i t h LBBB d e m o n s t r a t e d normal axis deviation. Neither the electrocardiographic nor the vectorcardiographic p a t t e r n s were consistent w i t h myocardial infarction. Typical records (patient 3) appear in Fig, 2. In two patients (3 and 8) the left anterior descending artery and the circumflex artery appeared to arise from a common orifice. The mean LCA m a i n s t e m length for the LBBB patients was 5.5 m m (Table 2). This differed significantly from the control values of 12.8 m m of Lewis et al 1 and 10.9 m m of De Mots et a114 (p < 0.001). Fig. 3 is an example of an extremely short left coronary artery mainstem (patient 1).
DISCUSSION A l t h o u g h t h e r e l a t i o n s h i p of CAD and LBBB has yet to be fully resolved, there is now some indication as to the nature of the solution. The multiple discrepancies between the reports of competent observers is in itself a clue. The primary disagreement has been, of course, is LBBB b e n i g n or otherwise. An analysis of reports favoring the latter concept indicates t h a t they share a common denominator. There is an important element of selectivity of the patients studied. Harper et a111 reported a good correlation between the histologic f i n d i n g s a n d the e l e c t r o c a r d i o g r a m (ECG). Their study was, however, a retrospective one of patients who had succumbed to CAD and then were selected for pathologic review only because of a conductance disturbance. Mulcahy et al 9 stated specifically t h a t J. ELECTROCARDIOLOGY, VOL. 8, NO. 4, 1975
LBBB AND CAD
319
TABLE I The Pertinent Clinical and Laboratory Findings in Nine LBBB Patients
mm Hg LVEDP Age/Sex Before* After*
Arteriography Vessels Ventriculogram Dominance S-A A-V 1"Volumes
1
61F
7
9
Normal
Emptying Delay
55F
18
24
Normal
Emptying Delay
R
R
R
10
13
Normal
Emptying Delay
60F
15
24
Normal
Emptying Delay
arm with exertion Epigastric pain with
R
R
R
1' Volumes 63F
Catheterization Diagnosis
Chest pain to left
~'Volumes 2
Symptoms
numbnessin left arm Chest pain to left arm
Balanced L
R
and back with exertion
R
left arm
Chest pain to jaw and 4
R
R
R-90% 5
56F
20
31
LAD
Tightness in chest and l"l"~Dilatation
R
R
R
neckwith exertion
ASHD, CS
Tightness in chest, 6
49F
7
B
Normal
Emptying Delay
R
R
R
neckand jaws Shortness of breath Paroxysmal nocturnal
-/
57M
36
36
Normal ~'~Biiatation
R
R
R
dyspnea
RHD, AI
8
46M
17
27
Normal l"l"~Dilatation
L
R
L
Dyspneaon exertion
myopathy
Dyspnea on exertion
Cardiq-
Cardio-
9
32M
23
29
Normal ~l"l"Dilatation
R
R
R
One syncopal episode
myopathy
*Before and after contrast media studies. M, F = Male, Female; R-90% = 90% narrowing of right coronary artery; LAD = Diseaseof left anterior descending artery (see text); R, L = Right, Left; S-A = Origin of sino-atrial nodal artery; A-V = Origin of atrioventricular nodal artery; ASHD = Arteriosclerotic heart disease; CS = Coronary sclerosis; RHD = Rheumatic heart disease; AI = Aortic insufficiency
their patient population consisted primarily of t h o s e w i t h h y p e r t e n s i o n and/or CAD. Bauer ~ in his study of the development of LBBB reported patients whose conduction disturbance was related to myocardial infarction, s e v e r e c o n g e s t i v e h e a r t f a i l u r e or pulmonary edema. Smith and Hayes is in a review of hospital ECGs concluded that LBBB J. ELECTROCARDIOLOGY, VOL. 8, NO. 4, 1975
was a poor prognostic sign. Certainly the many excellent pathologic studies, by definition, are pre-selected. 11'12,1~-21 Is there an element of pre-selection in the reports of the benignancy of LBBB? The studies of Beach et a122 were performed on a patient population chosen specifically because they had no sign or symptom of heart disease
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HERBERT
Fig. 1. A. A representative end-systolic frame record on patient No. 6 in the right anterior oblique projection.
rigid criteria was that LBBB did not imply a high mortality. These studies, by design, have pre-selected those patients in whom LBBB was more likely to be a benign entity. Certainly the acute development of LBBB d u r i n g m y o c a r d i a l i n f a r c t i o n h a s still a d i f f e r e n t p r o g n o s t i c i m p o r t . 6'25 In s u c h c i r c u m s t a n c e s u s u a l l y t h e r e is associated congestive heart failure, cardiac enlargement and a high mortality. The intra-ventricular c o n d u c t i o n d i s t u r b a n c e is a m e c h a n i c a l phenomenon be it secondary to necrosis or edema. There are numerous reports of the association of cardiomyopathy 2'7'1~26'27 and aortic valvular disease 2'7'1~27'2s with LBBB unrelated to CAD (patients 7-9). These entities, too, must be accepted as etiologic bases for the conduction disturbance. To date, there is no evidence that the presence of LBBB modifies the clinical or prognostic picture in such cases, and the outlook m u s t be predicated therefore on that anticipated for the underlying valvular or myopathic entity. The present study suggests that there is still another group of LBBB patients. These patients (in this study, at least, all women) presented with the classic clinical picture of CAD and yet angiographically proved to be free of the disease. A comparison of the patient population reported herein with those described in other angiographic studies substantiates two major observations. There are a g r e a t e r n u m b e r of female patients t h a n would be anticipated from the total population from which they were drawn and further,
\ TABLE 2 Left Coronary Artery Mainstem Lengths in Nine LBBB Patients
Fig. 1. B. A drawing of the same frame to outline the apical dilatation at end-systole.
other than the incidental detection of LBBB. Smith et a128 specifically screened over 1000 healthy aviators. Seven of these men manifested a change from a normal intraventricular conduction pattern to LBBB and 22 men developed RBBB, all while in routine service. In 24 of the 29 men there was no evidence of CAD at all. Rodstein et a124 reviewed 30,000 ECGs to determine the mortality associated with LBBB. They specifically excluded all individuals with any stigmata of h e a r t disease whatsoever. All those included were deemed insurable. Their assessment of the group remaining after the application of these
Patient
LCA mm
1
3.1
2
14.4
3
0.0
4
2.0
5
9.0
6
10.6
7
4.5
8
0.0
9
5.8
Total
49.4
Mean
5.49
LCA = Left coronary artery rnainstem. J. ELECTROCARDIOLOGY, VOL. 8, NO. 4, 1975
LBBB AND CAD
321
penetrating branches of the left anterior descending artery, thereby subjecting them to increased shearing stress. Trevino and Beller s~ described an u n k n o w n process affecting bundle branches causing fibrosis. They considered t h a t an insufficiency of the microcirculation m a y prove to be a major factor and suggested t h a t s h e a r i n g forces m a y cause occlusion of the minute vessels traversing bet w e e n m u s c l e b u n d l e s . T h e only demonstrated abnormality of coronary vessel structure to date is the unusually short left mainstem, a finding at least consistent with the postulates of Lewis et al 1 and Trevino and Beller. zo
,
............
I] .......... ,
..............
I
....................................
The effect of LBBB on left ventricular contraction has been a m a t t e r of contention for some time. The controversy has been, specifically, does LBBB cause a delay in left vent r i c u l a r contraction, TM a d y s y n c h r o n o u s contraction, 32'~4 both, 36'43 or n e i t h e r Y The ventriculographic patterns of the five women without CAD described above tend to Support the position of those investigators who report t h a t LBBB produces a dysynchronous left v e n t r i c u l a r contraction. 32-4s Our p a t i e n t s manifested some ventricular dilatation with an apical emptying delay, findings which certainly are consistent with late apical activation, s~ Although the angiographic abn o r m a l i t i e s in t h e s e p a t i e n t s are e a s i l y recognized, it is a moot point whether they
Fig. 2. Thirteen lead ECG demonstrating left bundle branch block and a normal electrical axis -patient 3.
the incidence of abnormal coronary arteriograms in these patients was unusually low. These data are tabulated in Tal~le 3. Patients referred to a cardiac laboratory for coronary arteriography are predominantly male, yet there were more women t h a n men with LBBB in two of the four studies now reported. As described above, males predominated by 2:1 yet, six of t h e n i n e LBBB p a t i e n t s were women. In addition, the incidence of coronary arteriographic abnormalities ranged from a low of 11% to a high of only 46%. Even this latter level is far less t h a n anticipated in a "coronary population" with the further "stigma" of LBBB. It is tempting to invoke the concept of small vessel disease to account for the findings, even though this entity is considered to be somewhat rare. 29 This would be consistent with the observations of Lewis et al 1 who suggested t h a t the effect of the extreme shortening of the LCA mainstem was to cause a reduction in the support of the fine J. ELECTROCARDIOLOGY, VOL. 8, NO. 4, 1975
Fig. 3. A right anterior oblique projection (patient 1) demonstrating an extremely short left coronary artery mainstem.
322
HERBERT
TABLE 3 The Relationship of LBBB to CAD in Four Separate Patient Studies 1 No. of Patients LBBB
LBBB and CAD
3
4
366*
578*
Not Reported
M
200
F
100
M
3
8
13
6
F
6
4
11
7
M
0
4
6
6*
F I ncidence *
2
1
0
1
11%
33%
29%
46%
Sex division not stated
M,F = Male, Female 1.
This study
2.
Lewis et al (1970)
3. 4.
Haft et al (1969) De Mots et al (1973)
could affect ventricular function during exercise or daily activities sufficiently to produce their symptoms. Extreme left axis deviation (LAD) when associated with LBBB has been reported to enhance the correlation with CAD, 12'1a2~ although others have not been able to substantiate this observation. ~21'27 The present study included only one patient with CAD and the frontal plane axis recorded from this patient, as well as all the others, was within normal limits. Lewis et al I found that their LBBB patients had, in addition to a short LCA mainstem, a greater incidence of left dominance. In this regard, however, our observations were consistent with those of DeMots et al, who reported the usual distribution. 14 The present study and review are in support of the concept o f multiple etiologies for the electrocardiographic p a t t e r n of LBBB. CAD can and has unequivocally been demons t r a t e d to be associated with LBBB. The correlation of LBBB with myocardiopathy and aortic valvular disease is sufficient to w a r r a n t their inclusion as important etiologic factors as well. The development of LBBB
during the acute phase of MI, usually associated with congestive heart failure and cardiac enlargement, has been well documented. In addition, it would appear that LBBB exists as an isolated and wholly benign entity. A long-term e v a l u a t i o n of t h e s e individuals would be of interest. In addition, this study is consistent with that of Lewis et al I in that LBBB was found to be associated with a statistically shorter LCA mainstem (p < 0.001). Six of the nine LBBB patients reported above were female, thus representing an incidence suggestively higher t h a n anticipated in a predominantly (2:1) male population. These patients with rather typical anginal histories and normal coronary arteriographic findings m a y p r o v e to be r e p r e s e n t a t i v e of still another group with LBBB and their course and prognosis warrants further study as well.
Acknowledgments: The author acknowledges with gratitude the help of Deborah Telesco, R.N., Philomena Adinaro, P.N., Catherine Doyle, Pattie Baskette, Kathleen Dwyer, Deborah Pomier and Alberta Varble in the preparation of this manuscript. J. ELECTROCARDIOLOGY, VOL. 8, NO. 4, 1975
LBBB AND CAD
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70:157, 1965 19. LEV, M: The conduction system. In Pathology of the Heart, S E GOULD, ed. Charles C Thomas, Springfield, IL, 2nd ed, 1960 20. LEV, M: The anatomic basis for disturbances in conduction and cardiac arrhythmias. Prog Cardiovasc Dis 2:360, 1960 21. LEV, M, UNGER, P N, ROSEN, K M AND BHARATI, S: The anatomic base of left bundlebranch block. Am J Cardiol 33:151, 1974 22. BEACH, T B, GRACY, J G, PETER, R H AND GRUNEWALD, P W: Benign left bundle-branch block. Ann Intern Med 70:269, 1969 23. SMITH, R F, JACKSON, D H, HARTHORNE, J W AND SANDERS, C A: Acquired bundle-branch block in a healthy population. Am Heart J 80:746, 1970 24. RODSTEIN,M, GUBNER, R, MILLS, J P, LOVELL, J F AND UNGERLEIDER,H E: A mortality study in bundle-branch block. Arch Intern Med, 87:663, 1951 25. SCHEIDT, S AND KILLIP, T: Bundle-branch block complicating acute myocardial infarction. JAMA 222:919, 1972 26. MARRIOTT, H J L: Electrocardiographic abnormalities, conduction disorders and arrhythmias in primary myocardial disease. Prog Cardiovasc Dis 7:99, 1964 27. HAFT, J I, HERMAN, M V AND GORLIN,R: Coronary arteriographic and left ventricular motion studies in left bundle-branch block. Am J Cardiol 23:117, 1969 28. WOOD, P: Aortic stenosis. Am J Cardiol 1:553, 1958 29. JAMES, T N: Angina without coronary disease (sic). Circulation 42:189, 1970 30. TREVINO, A J AND BELLER, B M: Conduction disturbances of the left bundle-branch system and their relationship to complete heart block. Am J Med 51:374, 1971 31. MEDRANO, G A, BISTENI, A, BRANCATO, R W, PILEGGI, F AND SODI-PALLARES, D: The activation of the interventricular septum in the dog's heart under normal conditions and in bundle-branch block. Ann New York Acad Sci, 65:804, 1957 32. BRAUNWALD, E AND MORROW, A G: Sequence of ventricular contraction in h u m a n bundlebranch block; a study based on simultaneous catheterization of both ventricles. Am J Med 23:205, 1957 33. LEATHAM, A: Splitting of heart sounds and a classification of systolic murmurs. In Symposium on Cardiovascular Sound. II Clinical Aspects, McKuSICK, V A, ed. Circulation 16:417, 1957 34. BRAUNWALD, E AND MORROW, A G: Origin of heart sounds as elucidated by analysis of the sequence of cardiodynamic events. Circulation 18:971, 1958 35. BECKER, R A, SCHER, A M AND ERICKSON,R V: Ventricular excitation in experimental left bundle-branch block. Am Heart J 55:547, 1958 36. WOLFORTH,C C AND MARGOLIES,A: Asynchronism in contraction of the ventricles in the socalled common type of bundle-branch block: Its bearing on the determination of the size of the significant lesion and on the mechanism of split first and second heart sounds. Am Heart
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J 10:425, 1935 37. KENNAMER, R AND PRINZMETAL, M: Depolarization of the ventricle with bundlebranch block. Studies on the mechanism of ventricular activity. X. Am Heart J 47: 769, 1954 38. GRANT, R P AND DODGE, n T: Mechanisms of QRS complex prolongation in man. Left ventricular conduction disturbances. Am J Med 20:834, 1956 39. BOURASSA, M G, BOITEAU, G M AND ALLENSTEIN, B J: Hemodynamic studies during intermittent left bundle-branch block. Am J Cardiol 10:792, 1962 40. SABER, E AND LEATHAM, A: Splitting of heart sounds from ventricular asynchrony in
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J. ELECTROCARDIOLOGY, VOL. 8, NO. 4, 1975
Left Bundle Branch Block and Coronary Artery Disease* BY WALTER H. HERBERT, M.D.t
SUMMARY This study tries the concept that left bundle-branch block (LBBB) connotes coronary artery disease (CAD). The findings indicate that prior studies both supporting of and in contradiction to the premise of a positive correlation have been biased by pre-selection of the patients reviewed. The data indicate, therefore, that LBBB is related to multiple entities. The major categories are CAD and/or hypertension, myocardiopathy and aortic valvular disease. In addition, LBBB may develop during the acute phase of myocardial infarction. Its existence as a wholly benign entity has been documented as well. Further, this study adds still another group with LBBB. Six of the nine LBBB patients were female. Five of these, in spite of typical anginal histories, had no arteriographically demonstrable CAD. The absence of disease was surprising and the incidence of women with LBBB was greater than anticipated, thus providing some basis for suggesting that these women may be representative of still another group with LBBB. Further, this study supports the findings of Lewis et al by confirming an association between LBBB and a statistically shorter LCA mainstem (p < 0.001).
From the Department of Medicine, New York Medical College, New York, N.Y. and the Cardiopulmonary Laboratory, Grasslands Hospital, Valhalla, N.Y. tAssociate Professor of Medicine, New York Medical College and Associate Director, Cardiopulmonary Laboratory, Grasslands Hospital. *This study was supported by a grant from the Westchester Heart Association. Reprint requests to: Walter H. Herbert, M.D., Associate Director, Cardiopulmonary Laboratory, Grasslands Hospital, Valhalla, NY 10595.
The controversy as to whether left bundle branch block (LBBB) connotes coronary artery d i s e a s e (CAD) is still unresolved. A reasonable approach to the assessment of the relationship is to postulate that if a positive correlation exists, then the incidence of the conduction disturbance in a group of patients specifically referred for coronary arteriography should be higher than that in the population at large, and, further, such patients should have significant demonstrable lesions. In one of the few arteriographic studies pertaining to this problem, Lewis et al 1 reported on 12 patients with LBBB out of a total study population of 366. Only 4 of these 12 patients had CAD. In an earlier study by Haft et al, 2 24 of 578 patients were demonstrated to have LBBB. Only 7 (29%) had angiographic evidence of CAD. A l t h o u g h the incidence of LBBB in these two studies, 3.2% and 4.1% respectively, was substantially higher than t h a t in t h e general population (less t h a n 1%), 84 only a small percentage in each group had demonstrable CAD (33% and 29% respectively). Certainly there is an inconsistency between these two very similar studies and the n u m e r o u s reports of the close correlation b e t w e e n L B B B a n d CAD a n d / o r hypertension .5-13 In one of the above reports I it was noted as well that the LBBB patients had extremely short left coronary artery (LCA) mainstems. Although another group of observers 14 was unable to substantiate this finding, should it prove to be correct even in some of the patients, then it may have an important bearing on the understanding of this clinical entity. This study was undertaken in an effort to define further the significance of LBBB in the several populations in which it is described:
MATERIALS AND METHODS Three hundred consecutive patient studies were reviewed. All subjects had undergone selective coronary arteriography with ventriculography by the transbrachial Sones and Shirey technique. 15 317
318
HERBERT
Ventriculograms were exposed in both the right and left anterior oblique positions. Each coronary artery was opacified in at least three separate projections which included both the left and right anterior obliques and a 60~ left anterior view. The arteriographic patterns were defined according to the criteria of Schlesinger. TM The film sequences were recorded with a North American Philips 6" image intensifier on 35 mm film at 50 frames/sec. For the purpose of this study, any coronary arterial luminal irregularity causing a distortion or encroachment greater than 25% was considered abnormal. Hemodynamic measurements were made with Statham P23db gauges and monitored on an Electronics for Medicine DR-12 recorder. The zero reference level was established 5 cm below the angle of Louis. The upper limit of normal for left ventricular end-diastolic pressure for (LVEDP) in this laboratory is 12mm Hg. All pressure measurements reported were the average of two full respiratory cycles. Nine patients fulfilled the New York Heart Association criteria for LBBB.1~Their ages ranged from 32 to 63 years. Six were women. Assessment of LCA mainstem length was by the method of Lewis et al.1
RESULTS Table 1 displays the hemodynamic, angiographic and pertinent historical findings in the nine patients with LBBB. It is noted t h a t the separation b y sex is also consistent with a difference in both clinical presentation and laboratory findings. Whereas each woman underwent study for the primary complaint of anterior chest pain with radiation into the neck, arms or jaw, usually precipitated by exertion, these complaints were not part of the male patients' histories. The men complained of severe shortness of breath. In addition, one had had episodes of paroxysmal nocturnal dyspnea and one had had a syncopal attack. Two men were diagnosed as having idiopathic, non-obstructive cardiomyopathy and the third severe aortic insufficiency on a rheumatic basis. By ventriculography all three men had grossly dilated and sluggishly contractile left ventricles. Only one woman (patient 5) had similar ventricular dysfunction. This patient was the only one of the entire group (male and female) to manifest CAD. Specifically, there was a 90% discrete narrowing in the proximal right coronary artery. In addition, there were significant linear changes in the proximal anterior descending artery involving the major septal perforators. All the remaining patients were considered to have normal coronary vascular trees. One m a n (patient 8) had a dominant left c o r o n a r y a r t e r y p a t t e r n w i t h t h e atrio-
ventricular nodal artery arising from the left coronary artery. One women (patient 3) had a balanced circulation with the sino-atrial nodal a r t e r y a r i s i n g from t h e circumflex branch of the left coronary artery. The remainder of the patients had dominant right circulation with both the sino-atrial and the atrio-ventricular nodal arteries arising from the right. Each of the five women with a normal coron a r y tree demonstrated a consistent ventriculographic pattern. That is, there was some degree of ventricular dilatation and what appeared to be some apical emptying delay. A representative end-systolic frame recorded on patient 6 is seen in Fig. 1A. Fig. 1B is a drawing of 1A to outline the apical dilatation at end-systole. The ventriculogram was recorded in the right anterior oblique projection. Three of these patients had normal LVEDP's prior to contrast media studies (patients 1, 3 and 6). Two patients had abnormal elevations in LVEDP (patients 2 and 4) (Table 1). E a c h p a t i e n t w i t h LBBB d e m o n s t r a t e d normal axis deviation. Neither the electrocardiographic nor the vectorcardiographic p a t t e r n s were consistent w i t h myocardial infarction. Typical records (patient 3) appear in Fig, 2. In two patients (3 and 8) the left anterior descending artery and the circumflex artery appeared to arise from a common orifice. The mean LCA m a i n s t e m length for the LBBB patients was 5.5 m m (Table 2). This differed significantly from the control values of 12.8 m m of Lewis et al 1 and 10.9 m m of De Mots et a114 (p < 0.001). Fig. 3 is an example of an extremely short left coronary artery mainstem (patient 1).
DISCUSSION A l t h o u g h t h e r e l a t i o n s h i p of CAD and LBBB has yet to be fully resolved, there is now some indication as to the nature of the solution. The multiple discrepancies between the reports of competent observers is in itself a clue. The primary disagreement has been, of course, is LBBB b e n i g n or otherwise. An analysis of reports favoring the latter concept indicates t h a t they share a common denominator. There is an important element of selectivity of the patients studied. Harper et a111 reported a good correlation between the histologic f i n d i n g s a n d the e l e c t r o c a r d i o g r a m (ECG). Their study was, however, a retrospective one of patients who had succumbed to CAD and then were selected for pathologic review only because of a conductance disturbance. Mulcahy et al 9 stated specifically t h a t J. ELECTROCARDIOLOGY, VOL. 8, NO. 4, 1975
LBBB AND CAD
319
TABLE I The Pertinent Clinical and Laboratory Findings in Nine LBBB Patients
mm Hg LVEDP Age/Sex Before* After*
Arteriography Vessels Ventriculogram Dominance S-A A-V 1"Volumes
1
61F
7
9
Normal
Emptying Delay
55F
18
24
Normal
Emptying Delay
R
R
R
10
13
Normal
Emptying Delay
60F
15
24
Normal
Emptying Delay
arm with exertion Epigastric pain with
R
R
R
1' Volumes 63F
Catheterization Diagnosis
Chest pain to left
~'Volumes 2
Symptoms
numbnessin left arm Chest pain to left arm
Balanced L
R
and back with exertion
R
left arm
Chest pain to jaw and 4
R
R
R-90% 5
56F
20
31
LAD
Tightness in chest and l"l"~Dilatation
R
R
R
neckwith exertion
ASHD, CS
Tightness in chest, 6
49F
7
B
Normal
Emptying Delay
R
R
R
neckand jaws Shortness of breath Paroxysmal nocturnal
-/
57M
36
36
Normal ~'~Biiatation
R
R
R
dyspnea
RHD, AI
8
46M
17
27
Normal l"l"~Dilatation
L
R
L
Dyspneaon exertion
myopathy
Dyspnea on exertion
Cardiq-
Cardio-
9
32M
23
29
Normal ~l"l"Dilatation
R
R
R
One syncopal episode
myopathy
*Before and after contrast media studies. M, F = Male, Female; R-90% = 90% narrowing of right coronary artery; LAD = Diseaseof left anterior descending artery (see text); R, L = Right, Left; S-A = Origin of sino-atrial nodal artery; A-V = Origin of atrioventricular nodal artery; ASHD = Arteriosclerotic heart disease; CS = Coronary sclerosis; RHD = Rheumatic heart disease; AI = Aortic insufficiency
their patient population consisted primarily of t h o s e w i t h h y p e r t e n s i o n and/or CAD. Bauer ~ in his study of the development of LBBB reported patients whose conduction disturbance was related to myocardial infarction, s e v e r e c o n g e s t i v e h e a r t f a i l u r e or pulmonary edema. Smith and Hayes is in a review of hospital ECGs concluded that LBBB J. ELECTROCARDIOLOGY, VOL. 8, NO. 4, 1975
was a poor prognostic sign. Certainly the many excellent pathologic studies, by definition, are pre-selected. 11'12,1~-21 Is there an element of pre-selection in the reports of the benignancy of LBBB? The studies of Beach et a122 were performed on a patient population chosen specifically because they had no sign or symptom of heart disease
320
HERBERT
Fig. 1. A. A representative end-systolic frame record on patient No. 6 in the right anterior oblique projection.
rigid criteria was that LBBB did not imply a high mortality. These studies, by design, have pre-selected those patients in whom LBBB was more likely to be a benign entity. Certainly the acute development of LBBB d u r i n g m y o c a r d i a l i n f a r c t i o n h a s still a d i f f e r e n t p r o g n o s t i c i m p o r t . 6'25 In s u c h c i r c u m s t a n c e s u s u a l l y t h e r e is associated congestive heart failure, cardiac enlargement and a high mortality. The intra-ventricular c o n d u c t i o n d i s t u r b a n c e is a m e c h a n i c a l phenomenon be it secondary to necrosis or edema. There are numerous reports of the association of cardiomyopathy 2'7'1~26'27 and aortic valvular disease 2'7'1~27'2s with LBBB unrelated to CAD (patients 7-9). These entities, too, must be accepted as etiologic bases for the conduction disturbance. To date, there is no evidence that the presence of LBBB modifies the clinical or prognostic picture in such cases, and the outlook m u s t be predicated therefore on that anticipated for the underlying valvular or myopathic entity. The present study suggests that there is still another group of LBBB patients. These patients (in this study, at least, all women) presented with the classic clinical picture of CAD and yet angiographically proved to be free of the disease. A comparison of the patient population reported herein with those described in other angiographic studies substantiates two major observations. There are a g r e a t e r n u m b e r of female patients t h a n would be anticipated from the total population from which they were drawn and further,
\ TABLE 2 Left Coronary Artery Mainstem Lengths in Nine LBBB Patients
Fig. 1. B. A drawing of the same frame to outline the apical dilatation at end-systole.
other than the incidental detection of LBBB. Smith et a128 specifically screened over 1000 healthy aviators. Seven of these men manifested a change from a normal intraventricular conduction pattern to LBBB and 22 men developed RBBB, all while in routine service. In 24 of the 29 men there was no evidence of CAD at all. Rodstein et a124 reviewed 30,000 ECGs to determine the mortality associated with LBBB. They specifically excluded all individuals with any stigmata of h e a r t disease whatsoever. All those included were deemed insurable. Their assessment of the group remaining after the application of these
Patient
LCA mm
1
3.1
2
14.4
3
0.0
4
2.0
5
9.0
6
10.6
7
4.5
8
0.0
9
5.8
Total
49.4
Mean
5.49
LCA = Left coronary artery rnainstem. J. ELECTROCARDIOLOGY, VOL. 8, NO. 4, 1975
LBBB AND CAD
321
penetrating branches of the left anterior descending artery, thereby subjecting them to increased shearing stress. Trevino and Beller s~ described an u n k n o w n process affecting bundle branches causing fibrosis. They considered t h a t an insufficiency of the microcirculation m a y prove to be a major factor and suggested t h a t s h e a r i n g forces m a y cause occlusion of the minute vessels traversing bet w e e n m u s c l e b u n d l e s . T h e only demonstrated abnormality of coronary vessel structure to date is the unusually short left mainstem, a finding at least consistent with the postulates of Lewis et al 1 and Trevino and Beller. zo
,
............
I] .......... ,
..............
I
....................................
The effect of LBBB on left ventricular contraction has been a m a t t e r of contention for some time. The controversy has been, specifically, does LBBB cause a delay in left vent r i c u l a r contraction, TM a d y s y n c h r o n o u s contraction, 32'~4 both, 36'43 or n e i t h e r Y The ventriculographic patterns of the five women without CAD described above tend to Support the position of those investigators who report t h a t LBBB produces a dysynchronous left v e n t r i c u l a r contraction. 32-4s Our p a t i e n t s manifested some ventricular dilatation with an apical emptying delay, findings which certainly are consistent with late apical activation, s~ Although the angiographic abn o r m a l i t i e s in t h e s e p a t i e n t s are e a s i l y recognized, it is a moot point whether they
Fig. 2. Thirteen lead ECG demonstrating left bundle branch block and a normal electrical axis -patient 3.
the incidence of abnormal coronary arteriograms in these patients was unusually low. These data are tabulated in Tal~le 3. Patients referred to a cardiac laboratory for coronary arteriography are predominantly male, yet there were more women t h a n men with LBBB in two of the four studies now reported. As described above, males predominated by 2:1 yet, six of t h e n i n e LBBB p a t i e n t s were women. In addition, the incidence of coronary arteriographic abnormalities ranged from a low of 11% to a high of only 46%. Even this latter level is far less t h a n anticipated in a "coronary population" with the further "stigma" of LBBB. It is tempting to invoke the concept of small vessel disease to account for the findings, even though this entity is considered to be somewhat rare. 29 This would be consistent with the observations of Lewis et al 1 who suggested t h a t the effect of the extreme shortening of the LCA mainstem was to cause a reduction in the support of the fine J. ELECTROCARDIOLOGY, VOL. 8, NO. 4, 1975
Fig. 3. A right anterior oblique projection (patient 1) demonstrating an extremely short left coronary artery mainstem.
322
HERBERT
TABLE 3 The Relationship of LBBB to CAD in Four Separate Patient Studies 1 No. of Patients LBBB
LBBB and CAD
3
4
366*
578*
Not Reported
M
200
F
100
M
3
8
13
6
F
6
4
11
7
M
0
4
6
6*
F I ncidence *
2
1
0
1
11%
33%
29%
46%
Sex division not stated
M,F = Male, Female 1.
This study
2.
Lewis et al (1970)
3. 4.
Haft et al (1969) De Mots et al (1973)
could affect ventricular function during exercise or daily activities sufficiently to produce their symptoms. Extreme left axis deviation (LAD) when associated with LBBB has been reported to enhance the correlation with CAD, 12'1a2~ although others have not been able to substantiate this observation. ~21'27 The present study included only one patient with CAD and the frontal plane axis recorded from this patient, as well as all the others, was within normal limits. Lewis et al I found that their LBBB patients had, in addition to a short LCA mainstem, a greater incidence of left dominance. In this regard, however, our observations were consistent with those of DeMots et al, who reported the usual distribution. 14 The present study and review are in support of the concept o f multiple etiologies for the electrocardiographic p a t t e r n of LBBB. CAD can and has unequivocally been demons t r a t e d to be associated with LBBB. The correlation of LBBB with myocardiopathy and aortic valvular disease is sufficient to w a r r a n t their inclusion as important etiologic factors as well. The development of LBBB
during the acute phase of MI, usually associated with congestive heart failure and cardiac enlargement, has been well documented. In addition, it would appear that LBBB exists as an isolated and wholly benign entity. A long-term e v a l u a t i o n of t h e s e individuals would be of interest. In addition, this study is consistent with that of Lewis et al I in that LBBB was found to be associated with a statistically shorter LCA mainstem (p < 0.001). Six of the nine LBBB patients reported above were female, thus representing an incidence suggestively higher t h a n anticipated in a predominantly (2:1) male population. These patients with rather typical anginal histories and normal coronary arteriographic findings m a y p r o v e to be r e p r e s e n t a t i v e of still another group with LBBB and their course and prognosis warrants further study as well.
Acknowledgments: The author acknowledges with gratitude the help of Deborah Telesco, R.N., Philomena Adinaro, P.N., Catherine Doyle, Pattie Baskette, Kathleen Dwyer, Deborah Pomier and Alberta Varble in the preparation of this manuscript. J. ELECTROCARDIOLOGY, VOL. 8, NO. 4, 1975
LBBB AND CAD
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J. ELECTROCARDIOLOGY, VOL. 8, NO. 4, 1975