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Left bundle branch block: A predictor of poor left ventricular function in coronary artery disease
Left bundle branch block: A-predictor of poor left ventricular function in coronary artery disease Clinical, coronary arteriographic, and hemodynamic studies were performed in 55 patients with left bundle branch block (LBBB) and coronary artery disease and were compared with 110 patients consecutively matched for age and sex with ischemic heart disease but without LBBB. No significant differences were found in duration of symptoms or frequency of prlor myocardial infarction, hypertension, or diabetes mellitus; however, the LBBB patients had a significantly (p < 0.001) higher frequency of congestive heart failure (38.2% VI 11.8%) and cardiomegaly (63.6% vs 25.5%). An evaluation of severity of the coronary disease on the basis of subtotal vs total obstructive lesions, number of vessels involved, total coronary score, and individual coronary arteries involved revealed no significant differences between the groups. The LBBB patients had significantly @ < 0.001) greater impairment of left ventricular function as reflected by the end-diastolic volume (107 + 43 vs 79 & 30 ml/ml), ejection fraction (0.35 & 0.19 vs 0.59 ? 0.18), and frequency of an abnormal contractile pattern (91% vs 61%). Evaluating the LBBB patients on the basis of the QRS width and axis revealed no significant intragroup differences in clinical profile, severity of coronary disease, or left ventricular dysfunction. A prolonged PR interval (10.20 second) was associated with more severe coronary artery disease and an enlarged heart. This study indicates that coronary artery disease associated with LB66 identifies patients with severe left ventricular dysfunction. (AM HEART J 106:471, 1983.)
Robert I. Hamby, M.D., Ronald H. Weissman, M.D., M. N. Prakash, and Irwin Hoffman, M.D. Roslyn, New Hyde Park, Far Rockaway, and Stony Brook, N.Y.
Left bundle branch block (LBBB) in the clinical setting of heart disease is associated with a high frequency of hypertension, cardiomegaly, and heart failure.‘-l2 LBBB is most commonly associated with coronary artery disease. It is a marker of both a high mortality during an acute infarction and a poor long-term prognosis. 2,3,5*8,vvl1 Limited studies of the hemodynamic and coronary arteriographic findings in small numbers of patients with LBBB combined with coronary artery disease have been reported. 10*13-17 In the present study the clinical, hemodynamic, and coronary anatomy are reported in a large group of patients with ischemic heart disease and LBBB and are compared with matched patients without LBBB.
From the Heart Center, St. Francis Hospital; Department of Medicine, Division of Cardiology, Long Island Jewish-Hillside Medical Center; St. Johns Episcopal Hospital Affiliation; and School of Medicine, Health Sciences Center, State University of New York at Stony Brook. Received for publication March 11, 1982; accepted Apr. 26, 1982. Reprint requests: Robert I. Hamby, M.D., 100 Port Washington Blvd., Roslyn, NY 11576.
M.D.,
METHODS Patients. A review of all patients undergoing cardiac catheterization during an &year period (1973 to 1980) revealed 108 patients with ECG criteria for LBBB. This included 55 patients with coronary artery disease,27 with aortic valve disease,15 with cardiomyopathy, two with mitral valve disease,and nine patients with no hemodynamic or angiographic evidence of heart disease.The 55 patients with coronary artery diseasehad no evidence of primary valvular disease or complicating congenital anomaly, and they form the basis of this report. Each patient with coronary artery disease and LBBB was matched for age and sex with two patients with coronary artery diseasebut no LBBB. Random selection of this latter group wasbasedonly on the presenceof angiographic evidence of coronary artery disease.All patients were interviewed, examined, and evaluated by one of the authors. Information obtained directly from the patient, including a detailed history and physical examination, was coded. The history included onset of clinical diseaseas angina pectoris, myocardial infarction, or congestiveheart failure. A history of myocardial infarction wasaccepted if it wasdocumentedby the referring doctor or if the patient had a prior hospitalization for at least 3 weeks for prolonged chest pain. A positive history of congestive 471
472
Hamby et al.
Table
I. Clinical profile
September, 1883 Amarlcan ttaart Journel
Left
bundle
branch
Mean
block
(n = 55)
Control
Number
Males/females
%
Mean
46/9
Age(yr)
Number
%
92/18
59 * 8
Range Duration of symptoms (yr) Angina pectoris Congestive heart failure Prior myocardial infarction Hypertension Diabetes mellitus Cardiomegaly
(n = 110)
59 + 8
41-79
41-79
5.1 f 3.9
4.1 k 3.7 48*
87.3 38.2 69.1 43.6
21t 38 24
107*
97.3
1st
11.8
60 41
54.6 37.3
12
21.8
12
10.9
35t
63.6
28t
25.5
fp < 0.02. tp < 0.001.
Table
II. Coronary anatomy Left bundle branch block (n = 51) Number
Main left disease a Circumflex artery Subtotal obstruction 30 Total obstruction 8 Right coronary artery Subtotal obstruction 18 Total obstruction 20 Left anterior descending Subtotal obstruction 31 Total obstruction 10 Number of vessels involved Single 8 Double 15 Triple 28 Total coronary score (mean 2 1 S.D.) 9.9 +- 3.2
Control (n = 110)
%
Number
%
15.7
8
58.8 15.7
58 12
52.7 10.9
35.3 39.2
39 50
35.5 45.5
60.8
60
54.6
19.6
35
31.8
15.7 29.4
19
17.3
33 57
30.0 51.8
54.9
7.3
10.2 k 2.9
heart failure was basedon a prior hospital admissionfor congestive heart failure or shortnessof breath not associated with angina pectoris but requiring digitalis and/or diuretic therapy. A diagnosis of hypertension required either a history of antihypertensive therapy or a persistent diastolic pressureof 90 mm Hg or more when admitted for evaluation. A prior diagnosis of diabetes mellitus was made if either the appropriate diet or antidiabetic drug therapy was reported. LBBB criteria. A la-lead standard ECG was taken for all patients and was interpreted on the basis of accepted criteria.18 Criteria for LBBB included a QRS duration > 0.12 second,slurred R wave in the left precordial leads or lead I with a delayed intrinsicoid deflection, absenceof septal q waves in the left precordial leads, and small or absent r wavesin leadsV, and V,. The ECG pattern (QRS) of the control group was comparable in distribution to a
larger number of patients with coronary artery disease previously reportedI and included 45 with an infarction pattern, 12 with intraventricular conduction disturbances, left ventricular hypertrophy in four, and 49 patients with a normal QRS pattern. Radiologic evaluation and interpretation was performed by a radiologist to evaluate the presenceor absenceof cardiomegaly. Cardiac catheterization. All studieswere performed by standard cardiac catheterization methodslo Left ventricular cineangiogramswere obtained with the patient in a 40-degree right anterior oblique position and were followed by selective coronary angiograms performed in multiple projections using methods described by Sones and ShireyN or by Judkins.21Four patients with LBBB did not undergo coronary arteriography. The left ventricular volumeswere derived usingthe area-length method.22The normal end-diastolic volume and ejection fraction for this laboratory are 69 rt 21 ml/m2 and 0.66 + 0.12, respectively.1° The pattern of left ventricular contraction wasdetermined
by reviewing
the
superimposition
of the
end-
diaztolic and end-systolic silhouette and utilizing terminology as defined by Herman et al.= Significant coronary artery diseasewas defined as narrowing of a coronary artery lumen by more than 50%. The number of coronary arteries (right coronary artery, left anterior descending, and circumflex artery) involved with significant disease was noted. Total and subtotal obstruction of each of the three major coronary arteries were recorded. Each of the coronary arteries wasgraded on the basisof a scoresystem previously defined,‘Owith the sum of the scoresfor each coronary artery defining the total coronary score. The main left coronary artery wss considered separately. All information acquired was evaluated by a statistician utilizing the chi square and Fisher exact probability method as a test of significance for the LBBB-control comparisons. RESULTS Clinical profile. The clinical profile of both the LBBB and control groups is given in Table I. Both
Volume Number
106 3
LBBB and LV function
240
r
in CAD
473
fp<0.00'7
220 t
+-PC 0.001 7
.
N^ 200 E 2 6 180 -I: 2 1603 z 0 ;
..
.
;
.
*.. .
.
.:. 4 4
120-
I .I.C .
0 5 & loowc 80-
1. .: ?. : i -& 1: :
.
LBBB (N=551
Control !N= 110;
1406040I
LBBB (N-55)
Fig. 1. Ejection fraction coronary disease patients. Table
III. Left ventricular
Control (N=llO)
(left panel) and end-diastolic
(right panel)
volume
in LBBB
and control
function Left
Mean
End-diastolic volume (mllm2) Mean + 1 S.D. Number > 100 ml/m’ Ejection fraction Mean f 1 SD. Number < 0.5 End-diastolic pressure (mm Hg) Mean 5 1 S.D. Number > 11 mm Hg Abnormal contraction Generalized hypokinesia Aneurysm
(+
bundle branch (n = 55)
1 S.D.)
block Control
Number
%
29*
52.1
39*
70.9
42* 50* 25* 4
76.4 90.9 45.5 1.3
107 f 43*
0.35
Mean
(r
1 S.D.)
(n = 110) Number
5%
22+
20.0
38*
34.6
73* 65* 5* 7
66.4 59.6 4.6 6.4
79 f 30’
k 0.19*
0.56 rt 0.18*
18 f 8.7*
15 f 7.3+
‘p < 0.001.
groups of patients had a similar duration of symptoms; however, angina pectoris was more frequent in the controls (p < 0.0‘2). Congestive heart failure and cardiomegaly were significantly 0, < 0.001) more frequent in the LBBB group. The frequency of prior myocardial infarction or hypertension was not significantly different. Although diabetes mellitus was twice as frequent in the LBBB patients (21.8% vs 10.9%), the difference was not statistically significant. Coronary pathoanatomy. The coronary anatomy in both groups of patients is given in Table II. The
patterns of coronary dominance showed no significant group difference. The length of the main left coronary artery was not evaluated. When the severity of the coronary artery disease was evaluated on the basis of subtotal vs total obstructive lesions, number of vessels involved with significant disease, and total coronary score, no significant differences were found. The frequency of involvement of individual coronary arteries revealed no significant intergroup differences. Indeed, 80.4% of LBBB patients and 86.4% of the control group had involvement of the left anterior descending artery. Total
474
Hamby et al.
Table
IV. Left bundle
septmbw, American
branch
block ECG subgroups Number
PR interval I 0.20 second > 0.20 second QRS width 0.12 second > 0.12 second I 0.14 second > 0.14 second QRS axis I -30” > -30 5 3o” > 30”
%
44 11
80 20
24 23 8
43.6 41.8 14.5
14 22 19
25.5 40.0 34.5
obstructive disease of the left anterior descending artery was more frequent (not significant) in the control group (31.8% vs 19.6%). Although main left coronary artery disease was thought to be more frequent in the LBBB patients (15.7 % vs 7.3 % ), the difference was not statistically significant. LV function. The left ventricular function in both groups of patients is presented in Table III and Fig. 1. Left ventricular function as represented by enddiastolic volume, pressure, and ejection fraction was significantly more impaired in the LBBB group. Thus 52.7% of the LBBB group had end-diastolic volumes greater than 100 ml/m” compared to only 20% in the control group (p < 0.001). The majority (70.9%) of patients with LBBB had an ejection fraction less than 0.5 compared to only 34.6% in the control group (p < 0.001). Left ventricular contractile abnormalities were observed in 50 of 55 (91% ) of the patients with LBBB, compared to 59.6% in the control group 0, < O.OOl), with almost half (45.5%) the LBBB patients demonstrating di&tse generalized hypokinesia compared to only 5.6% in the control group 0, < 0.001). The frequency of localized aneurysms was similar in both groups. LBBB characteristics. The 55 patients with LBBB were further evaluated on the basis of the PR interval (PR I 0.20 second vs PR > 0.20 second), QRS width (QRS = 0.12 second vs QRS > O.-l2 but 10.14 second vs QRS > 0.14 second), and QRS frontal plane axis (QRS I -30 degrees vs QRS > 30 degrees). The number of patients in these various subgroups of LBBB is given in Table IV. Neither the clinical pro6le nor coronary artery anatomy revealed significant differences when subgroups of patients with LBBB were compared on the basis of QRS width or axis. Similarly, left ventricular function (end-diastolic volume and pressure, ejection fraction, and contractile pattern) was not signiscantly different when comparisons were made on the basis
HearI
1983 Journal
of QRS width or axis. The PR interval was 0.20 second or less in 44 patients and was prolonged (>0.20 second) in 11 patients with LBBB. Congestive heart failure and cardiomegaly were noted in 55% and 73%, respectively, of patients with a prolonged PR interval, compared to 32% and 55% in the remaining patients; however, these differences were not significant. The frequency of patients being on digitalis was greater (83 % vs 54 % ) in those with a prolonged PR interval (N.S.). The total coronary score was 9.3 -t 3.4 and 12.3 _+ 1.2 in the patients with normal (10.20 second) and prolonged 00.20 second) PR interval, respectively@ < 0.025). All patients with prolonged PR intervals had triplevessel disease compared to 50% in the remaining patients. The end-diastolic volume (ml/m2) was 96 f 35 and 141 f 61 in those with normal and prolonged PR intervals, respectively 0, < 0.005). No significant differences were found in the ejection fraction, end-diastolic pressure, or contractile pattern when patients with LBBB were compared on the basis of the PR interval. DISCUSSION LV dysfunction.The present study reviewed a select subset of patients referred because of symptomatic coronary artery disease not readily controlled by medical management. The criteria for selection were documented coronary artery disease and an ECG demonstrating LBBB. These patients represent only a small sample (1.4 % ) of our population of patients with ischemic heart disease seen during an &year period. Conclusions based on this study are thus limited by the patient referral and the criteria for selection. Although it is well appreciated that LBBB may occur in the absence of heart disease,2v3,6*14,24*25 the present study indicates that LBBB associated with symptomatic coronary artery disease is a marker of severe left ventricular dysfunction. This conclusion is necessary, since the findings noted in the LBBB patients were compared with an age-sex-matched population who also had symptomatic coronary artery disease, but without LBBB. This control population had a comparable duration of symptomatic disease when compared to the LBBB patients and represented a clinical cross section of our own experience with patients referred for symptomatic coronary disease. Our control population had ECG findings similar in distribution to a larger consecutive coronary population previously reported.le Clearly, LBBB in patients with coronary artery disease is an ominous finding consistent with a poor prognosis. Severity of CAD. The severe left ventricular dys-
Volume Number
106 3
function reflected by congestive heart failure, cardiomegaly, increased end-diastolic volume, diminished ejection fraction, and abnormal contractile pattern cannot be fully explained by the severity of the coronary artery disease (CAD). No indicator of coronary disease severity-i.e., subtotal vs total obstructive lesions, the number of the vessels involved, or coronary artery score-distinguished the patients with LBBB from our control coronary population (Table II). The LBBB patients had significantly more impairment of left ventricular function than the control coronary patients (Table III and Fig. 1). We found no other study which compared patients with LBBB and CAD with an age-sex-matched coronary population to ascertain if the extent of the CAD is related to LBBB. Some reports dealt with small numbers of patients and no attempt was made to determine if the extent of the CAD could be related to LBBB. In a total of 41 patients compiled from these reports,‘Os 14-16, 2otriplevessel disease was noted in 26 (63.4% ), compared to 54.9% observed in our LBBB patients and 51.8% found in our control coronary patients. Left bundle branch has a dual blood supply derived from septal perforating arteries arising from both the left anterior descending and the posterior descending arteries.27 Significant disease of both coronary arteries (right coronary and left anterior descending) supplying the left bundle branch was found in both LBBB patients (60%) and in control groups (60%). Thus the distribution of the CAD present in patients with coexistent LBBB is not unique and can neither explain-or predict the conduction disturbance. Hypertension. Reports on newly acquired LBBB have noted a large percentage of patients with preexisting hypertension, cardiomegaly, CAD, or a combination of hypertension and coronary disease.*T6*7 In the present study the frequency of hypertension in the LBBB patients was comparable to that in the controls. It is possible that some of our patients with LBBB had prior undiagnosed hypertension, which was masked by the severe left ventricular impairment. In studies excluding patients with primary conduction system disease (LBBB without demonstrable heart disease), LBBB was almost invariably associated with cardiomegaly.“,l*ll Both Master et al.,4 and Bauer7 concluded that LBBB in such instances is due to diffuse ventricular damage. It was further speculated that ECG evolutionary changes from left ventricular hypertrophy (LVH) to LBBB accompanied diffuse myocardial disease.4 Bauer7 noted that 7 of 15 patients with LBBB had prior ECGs demonstrating LVH. It is
LBBB and LV function
in CAD
475
well recognized that the QRS may be widened up to 0.12 second in the presence of ECG-LVH.’ Not infrequently ECG-LVH and incomplete LBBB coexist (tall R wave over the left precordium and absence of initial Q waves and early slurring). This ECG pattern may at times be difficult to distinguish from complete LBBB. Master et al.,4 as well as Rasmussen and Moe,% have even suggested that ECG-LVH and LBBB represent different degrees of impaired conduction in the left ventricle. Recently, Piccolo et al.2g observed that in some patients with ECG-LVH conduction in the left bundle branch system was slowed. This interrelationship between ECG-LVH and LBBB and the findings in the present study are consistent with prior workm demonstrating that ECG-LVH in CAD is associated with severe left ventricular dysfunction which cannot be entirely explained by the presence of hypertension. Thus ECG-LVH and LBBB in patients with CAD defines a group of patients with increased frequency of left ventricular dysfunction. The ECG patterns in both instances probably reflect varying degrees of conduction disturbance resulting from similar pathologic processes in the conducting system. QRS width and axis. We also evaluated subsets of our patients with LBBB based on the PR interval, QRS width, and QRS axis (Table IV) in order to ascertain any special correlations (Tables I to III). Johnson, Messer,and White” noted in a large patient population with LBBB that patients with the widest QRS durations had the shortest survival times, and they also found a slight correlation between QRS duration and heart size. This study, however, included only 36% of patients with CAD. In our 55 patients with LBBB, no clinical (Table II), coronary arteriographic (Table II), or hemodynamic (Table III) variable could be related to the width of the QRS. The left ventricular end-diastolic volume (ml/m2) was greater in the seven patients with the widest (>0.14 second) QRS compared to the 24 with a QRS of 0.12 second (115 vs 99); however, the differences noted were not statistically significant. Prior investigators24p31*32 have indicated that LBBB combined with left axis deviation (QRS I -30 degrees) is associated with a greater incidence of myocardial dysfunction. Dhingra et a131 observed that congestive heart failure and cardiomegaly were significantly more frequent in patients with LBBB associated with left axis deviation. However, that study included patients with primary conduction system disease, who usually present a normal QRS axis. Thus of the patients reported by Beach et al.24 and by Dhingra et al.,31 all patients with LBBB (n = 18) but no heart disease had normal QRS axes.
476
Sepbmber, 1983 American Hoart Journal
Hamby et al.
This suggests that left axis deviation combined with LBBB indicates only superimposed heart disease. Spurrell et al.32 suggested that LBBB associated with left axis deviation indicates only more extensive disease of the left bundle branches. Lichstein et al.33 observed that 9 of 24 (37.5%) patients with LBBB and left axis deviation showed left axis deviation in the ECG preceding the development of LBBB, compared to only 3 of 25 (12%) showing LBBB with a normal axis. Dhingra et a131 observed that the PR interval was significantly 0, < 0.001) longer in those with left axis deviation (0.23 vs 0.19 second). Of the 14 patients in the present study with left axis deviation, the PR interval was prolonged (>0.20 second) in five (35%) compared to 15 % in the remaining patients having a normal QRS axis. Perhaps left axis deviation associated with LBBB indicates more extensive disease of the conduction system. However, observations of others1o*33 as well as the present study do not indicate that left axis deviation with LBBB reflects more severe left ventricular dysfunction. The adverse prognosis of patients with left axis deviation associated with LBBB reported by Dhingra et a131 may simply reflect more severe conduction system disease. Furthermore, the conclusions of others24,31,32 that left axis deviation reflects more severe myocardial disease is based on a mixed patient population with various types of heart disease. In the present study of patients with CAD and LBBB the QRS axis was not observed to correlate with the frequency of congestive heart failure, cardiomegaly, severity of coronary disease (Table II), or the degree of left ventricular dysfunction (Table III). PI? interval. An unexpected finding in the present study was the observation that patients with a prolonged PR interval (>0.20 second) had significantly more severe CAD, reflected in both the coronary score and in the number of coronary arteries involved. In all such patients triple-vessel disease was present, compared to only 50% in the remaining patients with a normal PR interval. Furthermore, the patients with prolonged PR intervals had a greater frequency of cardiomegaly (88% vs 55%) and significantly (p < 0.005) greater enddiastolic volumes. It is difficult to speculate on these findings, since the blood supply to the atrioventricular node and the proximal left bundle are similar. Thus although LBBB alone correlates well with severe left ventricular dysfunction, the presence of PR prolongation in addition indicates triple-vessel disease, presumably the result of poor perfusion to the atrioventricular node. These observations support the concept that myocardial disease and dys-
function are responsible for the LBBB, regardless of the coronary anatomy in any given patient. Conclusions. The present study indicates that LBBB associated with CAD identifies patients with marked impairment in left ventricular function. The severity of the CAD in these patients was not significantly different from an age-sex-matched patient group with ischemic heart disease. In the patients with LBBB neither left axis deviation or QRS width could be correlated with the coronary disease severity or with the degree of left ventricular dysfunction; however, a prolonged PR interval correlated with more severe coronary disease and left ventricular dilatation. The authors thank Ms. Dacia B. Horowitz, Bruce Hamby, and Mrs. Brenda Hamby for their invaluable assistance. REFERENCES
1. Schneider JF, Thomas HE Jr, Sorlie P, Kreger BE, McNamara PM, Kannel WB: Comparative features of newly acquired left and right bundle branch block in the general population: The Framingham study. Am J Cardiol 47:931, 1981. 2. Smith S, Hayes WL: The prognosis of complete left bundle branch block. AM HEART J 78~157, 1965. M: The outlook with bundle-branch block. Br 3. Campbell Heart J 31:575, 1969. 4. Master AM, Kalter H, Dack S, Jaffe H L: The relation between bundle branch block and cardiac enlargement. AM HEART J 20:186, 1940. clinical assessment. 5. Scott RC: Left bundle branch block-A Part III. AM HEART J 70:813, 1965. 6. Schneider JF, Thomas HE Jr, Kreger, BK, McNamara PM, Kannel WB: Newly acquired left bundle branch block: The Framingham study. Ann Intern Med 90:303, 1977. of bundle branch block. Am J 7. Bauer GE: Development Cardiol 14~346, 1964. 8. Goodman MJ, Lassers BW, Juliam DG: Complete bundlebranch block complicating acute myocardial infarction. N Engl J Med 282:237, 1970. 9. Scheidt S, Killip T: Bundle-branch block complicating acute myocardial infarction. JAMA 222:919, 1972. 10. Haft JI, Herman MV, Gorlin R: Coronary arteriographic and left ventricular motion studies in left bundle branch block (abstr). Am J Cardiol 23:117, 1969. 11. Johnson RP, Messer AL, Shreenivas, White PD: Prognosis in bundle branch block. II. Factors influencing the survival period in left bundle branch block. AM HEART J 41:225, 1951. 12. 13.
14.
15.
16.
17.
Mulcahy R, Hickey N, Maurer B: Aetiology of bundle-branch block. Br Heart J 30:34, 1968. Ginks W, Sutton R, Siddons H, Leathom A: Unsuspected coronary artery disease as cause of chronic atrioventricular block in middle age. Br Heart J 44:699, 1980. Dizadji H, Tahmooressi P, Cernack WF: Etiology of left bundle branch block. Hemodynamic and angiographic studies. J Electrocardiol 7:221, 1974. Haft JI, Herman MV, Gorlin R: Left bundle branch block. Etiologic, hemodynamic, and ventriculographic considerations. Circulation 43:279, 1971. Lewis CM, Dagenais GR, Friesinger GC, Ross RS: Coronary arteriographic appearances in patients with left bundlebranch block. Circulation 41:299, 1970. Hamby RI, Tabrah F, Gupta M: Intraventricular conduction disturbances and coronary artery disease. Am J Cardiol 32:758,
1973.
Volume Number
18.
19.
20. 21. 22.
23.
24. 25. 26.
27.
106 3
Massie E, Walsh TJ: Clinical vectorcardiography and electrocardiography. Chicago, 1960, Year Book Medical Publishers, Inc. Hamby RI: Angina pectoris: A clinical-electrocardiographicangiographic correlative study in 510 patients. In Rios JC, editor: Cardiovascular clinics: Clinical electrocardiographic correlation. Philadelphia 1977, F.A. Davis Company, p 79. Sones FM Jr, Shirey EK: Cine-coronary arteriography. Mod Concepts Cardiovasc Dis 31:735, 1962. Judkins MP: Percutaneous transfemoral selective coronary arteriography. Radio1 Clin North Am 6:467, 1968. Dodge HT, Sandler H, Ballew DW: The use of biplane angiocardiography for the measurement of left ventricular volume in man. AM HEART J 60:762, 1960. Herman MV, Heinle RA, Klein MD, Gorlin, R: Localized disorders in myocardial contraction. Asynergy and its role in congestive heart failure. N Engl J Med 277:222, 1967. Beach TB, Gracey JG, Peter RH, Grunenwald PW: Benign left bundle branch block. Ann Intern Med 70:269, 1969. Wolfram J: Bundle branch block without significant heart disease. AM HEART J 41:656, 1961. Hamby RI, Tabrah F, Gupta M: Intraventricular conduction disturbances and coronary artery disease. Am J Cardiol 321758, 1973. Lev M: Anatomic basis for atrioventricular block. Am J Med 37~742, 1964.
LBBB and LV function
in CAD
471
28. Rasmussen H, Moe T: Pathogenesis of left bundle branch block. Br Heart J 10~141, 1948. 29. Piccolo E, Raviele A, Delise P, Dainese F, Pascotto P, Totaro G, Sartori F, D’Este D: The role of left ventricular conduction in the electrogenesis of left ventricular hypertrophy. An electrophysiologic study in man. Circulation 59:1044, 1979. 30. Hamby RI, Prakash MN, Wyne UA, Hoffman I: Electrocardiographic left ventricular hypertrophy and coronary artery disease: Clinical, hemodynamic and angiographic correlates. AM HEART J 100:784, 1980. 31. Dhingra RC, Amat-Y-Leon F, Wyndham C, Spidhar SS, Wu D, Denes P, Rosen KM Significance of left axis deviation in patients with chronic left bundle branch block. Am J Cardiol 42:551, 1978. 32. Spurrell RAJ, Krikler 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 34~1244, 1972. 33. Lichstein E, Mahapatra R, Gupta PK, Chadda KD: Significance of complete left bundle branch block with left axis deviation. Am J Cardiol 44~239, 1979. 34. Wiberg TA, Richman HG, Gohel FL: The significance and prognosis of chronic bifascicular block. AM HEART J 71:329, 1977.
Robert I. Hamby, M.D., Ronald H. Weissman, M.D., M. N. Prakash, and Irwin Hoffman, M.D. Roslyn, New Hyde Park, Far Rockaway, and Stony Brook, N.Y.
Left bundle branch block (LBBB) in the clinical setting of heart disease is associated with a high frequency of hypertension, cardiomegaly, and heart failure.‘-l2 LBBB is most commonly associated with coronary artery disease. It is a marker of both a high mortality during an acute infarction and a poor long-term prognosis. 2,3,5*8,vvl1 Limited studies of the hemodynamic and coronary arteriographic findings in small numbers of patients with LBBB combined with coronary artery disease have been reported. 10*13-17 In the present study the clinical, hemodynamic, and coronary anatomy are reported in a large group of patients with ischemic heart disease and LBBB and are compared with matched patients without LBBB.
From the Heart Center, St. Francis Hospital; Department of Medicine, Division of Cardiology, Long Island Jewish-Hillside Medical Center; St. Johns Episcopal Hospital Affiliation; and School of Medicine, Health Sciences Center, State University of New York at Stony Brook. Received for publication March 11, 1982; accepted Apr. 26, 1982. Reprint requests: Robert I. Hamby, M.D., 100 Port Washington Blvd., Roslyn, NY 11576.
M.D.,
METHODS Patients. A review of all patients undergoing cardiac catheterization during an &year period (1973 to 1980) revealed 108 patients with ECG criteria for LBBB. This included 55 patients with coronary artery disease,27 with aortic valve disease,15 with cardiomyopathy, two with mitral valve disease,and nine patients with no hemodynamic or angiographic evidence of heart disease.The 55 patients with coronary artery diseasehad no evidence of primary valvular disease or complicating congenital anomaly, and they form the basis of this report. Each patient with coronary artery disease and LBBB was matched for age and sex with two patients with coronary artery diseasebut no LBBB. Random selection of this latter group wasbasedonly on the presenceof angiographic evidence of coronary artery disease.All patients were interviewed, examined, and evaluated by one of the authors. Information obtained directly from the patient, including a detailed history and physical examination, was coded. The history included onset of clinical diseaseas angina pectoris, myocardial infarction, or congestiveheart failure. A history of myocardial infarction wasaccepted if it wasdocumentedby the referring doctor or if the patient had a prior hospitalization for at least 3 weeks for prolonged chest pain. A positive history of congestive 471
472
Hamby et al.
Table
I. Clinical profile
September, 1883 Amarlcan ttaart Journel
Left
bundle
branch
Mean
block
(n = 55)
Control
Number
Males/females
%
Mean
46/9
Age(yr)
Number
%
92/18
59 * 8
Range Duration of symptoms (yr) Angina pectoris Congestive heart failure Prior myocardial infarction Hypertension Diabetes mellitus Cardiomegaly
(n = 110)
59 + 8
41-79
41-79
5.1 f 3.9
4.1 k 3.7 48*
87.3 38.2 69.1 43.6
21t 38 24
107*
97.3
1st
11.8
60 41
54.6 37.3
12
21.8
12
10.9
35t
63.6
28t
25.5
fp < 0.02. tp < 0.001.
Table
II. Coronary anatomy Left bundle branch block (n = 51) Number
Main left disease a Circumflex artery Subtotal obstruction 30 Total obstruction 8 Right coronary artery Subtotal obstruction 18 Total obstruction 20 Left anterior descending Subtotal obstruction 31 Total obstruction 10 Number of vessels involved Single 8 Double 15 Triple 28 Total coronary score (mean 2 1 S.D.) 9.9 +- 3.2
Control (n = 110)
%
Number
%
15.7
8
58.8 15.7
58 12
52.7 10.9
35.3 39.2
39 50
35.5 45.5
60.8
60
54.6
19.6
35
31.8
15.7 29.4
19
17.3
33 57
30.0 51.8
54.9
7.3
10.2 k 2.9
heart failure was basedon a prior hospital admissionfor congestive heart failure or shortnessof breath not associated with angina pectoris but requiring digitalis and/or diuretic therapy. A diagnosis of hypertension required either a history of antihypertensive therapy or a persistent diastolic pressureof 90 mm Hg or more when admitted for evaluation. A prior diagnosis of diabetes mellitus was made if either the appropriate diet or antidiabetic drug therapy was reported. LBBB criteria. A la-lead standard ECG was taken for all patients and was interpreted on the basis of accepted criteria.18 Criteria for LBBB included a QRS duration > 0.12 second,slurred R wave in the left precordial leads or lead I with a delayed intrinsicoid deflection, absenceof septal q waves in the left precordial leads, and small or absent r wavesin leadsV, and V,. The ECG pattern (QRS) of the control group was comparable in distribution to a
larger number of patients with coronary artery disease previously reportedI and included 45 with an infarction pattern, 12 with intraventricular conduction disturbances, left ventricular hypertrophy in four, and 49 patients with a normal QRS pattern. Radiologic evaluation and interpretation was performed by a radiologist to evaluate the presenceor absenceof cardiomegaly. Cardiac catheterization. All studieswere performed by standard cardiac catheterization methodslo Left ventricular cineangiogramswere obtained with the patient in a 40-degree right anterior oblique position and were followed by selective coronary angiograms performed in multiple projections using methods described by Sones and ShireyN or by Judkins.21Four patients with LBBB did not undergo coronary arteriography. The left ventricular volumeswere derived usingthe area-length method.22The normal end-diastolic volume and ejection fraction for this laboratory are 69 rt 21 ml/m2 and 0.66 + 0.12, respectively.1° The pattern of left ventricular contraction wasdetermined
by reviewing
the
superimposition
of the
end-
diaztolic and end-systolic silhouette and utilizing terminology as defined by Herman et al.= Significant coronary artery diseasewas defined as narrowing of a coronary artery lumen by more than 50%. The number of coronary arteries (right coronary artery, left anterior descending, and circumflex artery) involved with significant disease was noted. Total and subtotal obstruction of each of the three major coronary arteries were recorded. Each of the coronary arteries wasgraded on the basisof a scoresystem previously defined,‘Owith the sum of the scoresfor each coronary artery defining the total coronary score. The main left coronary artery wss considered separately. All information acquired was evaluated by a statistician utilizing the chi square and Fisher exact probability method as a test of significance for the LBBB-control comparisons. RESULTS Clinical profile. The clinical profile of both the LBBB and control groups is given in Table I. Both
Volume Number
106 3
LBBB and LV function
240
r
in CAD
473
fp<0.00'7
220 t
+-PC 0.001 7
.
N^ 200 E 2 6 180 -I: 2 1603 z 0 ;
..
.
;
.
*.. .
.
.:. 4 4
120-
I .I.C .
0 5 & loowc 80-
1. .: ?. : i -& 1: :
.
LBBB (N=551
Control !N= 110;
1406040I
LBBB (N-55)
Fig. 1. Ejection fraction coronary disease patients. Table
III. Left ventricular
Control (N=llO)
(left panel) and end-diastolic
(right panel)
volume
in LBBB
and control
function Left
Mean
End-diastolic volume (mllm2) Mean + 1 S.D. Number > 100 ml/m’ Ejection fraction Mean f 1 SD. Number < 0.5 End-diastolic pressure (mm Hg) Mean 5 1 S.D. Number > 11 mm Hg Abnormal contraction Generalized hypokinesia Aneurysm
(+
bundle branch (n = 55)
1 S.D.)
block Control
Number
%
29*
52.1
39*
70.9
42* 50* 25* 4
76.4 90.9 45.5 1.3
107 f 43*
0.35
Mean
(r
1 S.D.)
(n = 110) Number
5%
22+
20.0
38*
34.6
73* 65* 5* 7
66.4 59.6 4.6 6.4
79 f 30’
k 0.19*
0.56 rt 0.18*
18 f 8.7*
15 f 7.3+
‘p < 0.001.
groups of patients had a similar duration of symptoms; however, angina pectoris was more frequent in the controls (p < 0.0‘2). Congestive heart failure and cardiomegaly were significantly 0, < 0.001) more frequent in the LBBB group. The frequency of prior myocardial infarction or hypertension was not significantly different. Although diabetes mellitus was twice as frequent in the LBBB patients (21.8% vs 10.9%), the difference was not statistically significant. Coronary pathoanatomy. The coronary anatomy in both groups of patients is given in Table II. The
patterns of coronary dominance showed no significant group difference. The length of the main left coronary artery was not evaluated. When the severity of the coronary artery disease was evaluated on the basis of subtotal vs total obstructive lesions, number of vessels involved with significant disease, and total coronary score, no significant differences were found. The frequency of involvement of individual coronary arteries revealed no significant intergroup differences. Indeed, 80.4% of LBBB patients and 86.4% of the control group had involvement of the left anterior descending artery. Total
474
Hamby et al.
Table
IV. Left bundle
septmbw, American
branch
block ECG subgroups Number
PR interval I 0.20 second > 0.20 second QRS width 0.12 second > 0.12 second I 0.14 second > 0.14 second QRS axis I -30” > -30 5 3o” > 30”
%
44 11
80 20
24 23 8
43.6 41.8 14.5
14 22 19
25.5 40.0 34.5
obstructive disease of the left anterior descending artery was more frequent (not significant) in the control group (31.8% vs 19.6%). Although main left coronary artery disease was thought to be more frequent in the LBBB patients (15.7 % vs 7.3 % ), the difference was not statistically significant. LV function. The left ventricular function in both groups of patients is presented in Table III and Fig. 1. Left ventricular function as represented by enddiastolic volume, pressure, and ejection fraction was significantly more impaired in the LBBB group. Thus 52.7% of the LBBB group had end-diastolic volumes greater than 100 ml/m” compared to only 20% in the control group (p < 0.001). The majority (70.9%) of patients with LBBB had an ejection fraction less than 0.5 compared to only 34.6% in the control group (p < 0.001). Left ventricular contractile abnormalities were observed in 50 of 55 (91% ) of the patients with LBBB, compared to 59.6% in the control group 0, < O.OOl), with almost half (45.5%) the LBBB patients demonstrating di&tse generalized hypokinesia compared to only 5.6% in the control group 0, < 0.001). The frequency of localized aneurysms was similar in both groups. LBBB characteristics. The 55 patients with LBBB were further evaluated on the basis of the PR interval (PR I 0.20 second vs PR > 0.20 second), QRS width (QRS = 0.12 second vs QRS > O.-l2 but 10.14 second vs QRS > 0.14 second), and QRS frontal plane axis (QRS I -30 degrees vs QRS > 30 degrees). The number of patients in these various subgroups of LBBB is given in Table IV. Neither the clinical pro6le nor coronary artery anatomy revealed significant differences when subgroups of patients with LBBB were compared on the basis of QRS width or axis. Similarly, left ventricular function (end-diastolic volume and pressure, ejection fraction, and contractile pattern) was not signiscantly different when comparisons were made on the basis
HearI
1983 Journal
of QRS width or axis. The PR interval was 0.20 second or less in 44 patients and was prolonged (>0.20 second) in 11 patients with LBBB. Congestive heart failure and cardiomegaly were noted in 55% and 73%, respectively, of patients with a prolonged PR interval, compared to 32% and 55% in the remaining patients; however, these differences were not significant. The frequency of patients being on digitalis was greater (83 % vs 54 % ) in those with a prolonged PR interval (N.S.). The total coronary score was 9.3 -t 3.4 and 12.3 _+ 1.2 in the patients with normal (10.20 second) and prolonged 00.20 second) PR interval, respectively@ < 0.025). All patients with prolonged PR intervals had triplevessel disease compared to 50% in the remaining patients. The end-diastolic volume (ml/m2) was 96 f 35 and 141 f 61 in those with normal and prolonged PR intervals, respectively 0, < 0.005). No significant differences were found in the ejection fraction, end-diastolic pressure, or contractile pattern when patients with LBBB were compared on the basis of the PR interval. DISCUSSION LV dysfunction.The present study reviewed a select subset of patients referred because of symptomatic coronary artery disease not readily controlled by medical management. The criteria for selection were documented coronary artery disease and an ECG demonstrating LBBB. These patients represent only a small sample (1.4 % ) of our population of patients with ischemic heart disease seen during an &year period. Conclusions based on this study are thus limited by the patient referral and the criteria for selection. Although it is well appreciated that LBBB may occur in the absence of heart disease,2v3,6*14,24*25 the present study indicates that LBBB associated with symptomatic coronary artery disease is a marker of severe left ventricular dysfunction. This conclusion is necessary, since the findings noted in the LBBB patients were compared with an age-sex-matched population who also had symptomatic coronary artery disease, but without LBBB. This control population had a comparable duration of symptomatic disease when compared to the LBBB patients and represented a clinical cross section of our own experience with patients referred for symptomatic coronary disease. Our control population had ECG findings similar in distribution to a larger consecutive coronary population previously reported.le Clearly, LBBB in patients with coronary artery disease is an ominous finding consistent with a poor prognosis. Severity of CAD. The severe left ventricular dys-
Volume Number
106 3
function reflected by congestive heart failure, cardiomegaly, increased end-diastolic volume, diminished ejection fraction, and abnormal contractile pattern cannot be fully explained by the severity of the coronary artery disease (CAD). No indicator of coronary disease severity-i.e., subtotal vs total obstructive lesions, the number of the vessels involved, or coronary artery score-distinguished the patients with LBBB from our control coronary population (Table II). The LBBB patients had significantly more impairment of left ventricular function than the control coronary patients (Table III and Fig. 1). We found no other study which compared patients with LBBB and CAD with an age-sex-matched coronary population to ascertain if the extent of the CAD is related to LBBB. Some reports dealt with small numbers of patients and no attempt was made to determine if the extent of the CAD could be related to LBBB. In a total of 41 patients compiled from these reports,‘Os 14-16, 2otriplevessel disease was noted in 26 (63.4% ), compared to 54.9% observed in our LBBB patients and 51.8% found in our control coronary patients. Left bundle branch has a dual blood supply derived from septal perforating arteries arising from both the left anterior descending and the posterior descending arteries.27 Significant disease of both coronary arteries (right coronary and left anterior descending) supplying the left bundle branch was found in both LBBB patients (60%) and in control groups (60%). Thus the distribution of the CAD present in patients with coexistent LBBB is not unique and can neither explain-or predict the conduction disturbance. Hypertension. Reports on newly acquired LBBB have noted a large percentage of patients with preexisting hypertension, cardiomegaly, CAD, or a combination of hypertension and coronary disease.*T6*7 In the present study the frequency of hypertension in the LBBB patients was comparable to that in the controls. It is possible that some of our patients with LBBB had prior undiagnosed hypertension, which was masked by the severe left ventricular impairment. In studies excluding patients with primary conduction system disease (LBBB without demonstrable heart disease), LBBB was almost invariably associated with cardiomegaly.“,l*ll Both Master et al.,4 and Bauer7 concluded that LBBB in such instances is due to diffuse ventricular damage. It was further speculated that ECG evolutionary changes from left ventricular hypertrophy (LVH) to LBBB accompanied diffuse myocardial disease.4 Bauer7 noted that 7 of 15 patients with LBBB had prior ECGs demonstrating LVH. It is
LBBB and LV function
in CAD
475
well recognized that the QRS may be widened up to 0.12 second in the presence of ECG-LVH.’ Not infrequently ECG-LVH and incomplete LBBB coexist (tall R wave over the left precordium and absence of initial Q waves and early slurring). This ECG pattern may at times be difficult to distinguish from complete LBBB. Master et al.,4 as well as Rasmussen and Moe,% have even suggested that ECG-LVH and LBBB represent different degrees of impaired conduction in the left ventricle. Recently, Piccolo et al.2g observed that in some patients with ECG-LVH conduction in the left bundle branch system was slowed. This interrelationship between ECG-LVH and LBBB and the findings in the present study are consistent with prior workm demonstrating that ECG-LVH in CAD is associated with severe left ventricular dysfunction which cannot be entirely explained by the presence of hypertension. Thus ECG-LVH and LBBB in patients with CAD defines a group of patients with increased frequency of left ventricular dysfunction. The ECG patterns in both instances probably reflect varying degrees of conduction disturbance resulting from similar pathologic processes in the conducting system. QRS width and axis. We also evaluated subsets of our patients with LBBB based on the PR interval, QRS width, and QRS axis (Table IV) in order to ascertain any special correlations (Tables I to III). Johnson, Messer,and White” noted in a large patient population with LBBB that patients with the widest QRS durations had the shortest survival times, and they also found a slight correlation between QRS duration and heart size. This study, however, included only 36% of patients with CAD. In our 55 patients with LBBB, no clinical (Table II), coronary arteriographic (Table II), or hemodynamic (Table III) variable could be related to the width of the QRS. The left ventricular end-diastolic volume (ml/m2) was greater in the seven patients with the widest (>0.14 second) QRS compared to the 24 with a QRS of 0.12 second (115 vs 99); however, the differences noted were not statistically significant. Prior investigators24p31*32 have indicated that LBBB combined with left axis deviation (QRS I -30 degrees) is associated with a greater incidence of myocardial dysfunction. Dhingra et a131 observed that congestive heart failure and cardiomegaly were significantly more frequent in patients with LBBB associated with left axis deviation. However, that study included patients with primary conduction system disease, who usually present a normal QRS axis. Thus of the patients reported by Beach et al.24 and by Dhingra et al.,31 all patients with LBBB (n = 18) but no heart disease had normal QRS axes.
476
Sepbmber, 1983 American Hoart Journal
Hamby et al.
This suggests that left axis deviation combined with LBBB indicates only superimposed heart disease. Spurrell et al.32 suggested that LBBB associated with left axis deviation indicates only more extensive disease of the left bundle branches. Lichstein et al.33 observed that 9 of 24 (37.5%) patients with LBBB and left axis deviation showed left axis deviation in the ECG preceding the development of LBBB, compared to only 3 of 25 (12%) showing LBBB with a normal axis. Dhingra et a131 observed that the PR interval was significantly 0, < 0.001) longer in those with left axis deviation (0.23 vs 0.19 second). Of the 14 patients in the present study with left axis deviation, the PR interval was prolonged (>0.20 second) in five (35%) compared to 15 % in the remaining patients having a normal QRS axis. Perhaps left axis deviation associated with LBBB indicates more extensive disease of the conduction system. However, observations of others1o*33 as well as the present study do not indicate that left axis deviation with LBBB reflects more severe left ventricular dysfunction. The adverse prognosis of patients with left axis deviation associated with LBBB reported by Dhingra et a131 may simply reflect more severe conduction system disease. Furthermore, the conclusions of others24,31,32 that left axis deviation reflects more severe myocardial disease is based on a mixed patient population with various types of heart disease. In the present study of patients with CAD and LBBB the QRS axis was not observed to correlate with the frequency of congestive heart failure, cardiomegaly, severity of coronary disease (Table II), or the degree of left ventricular dysfunction (Table III). PI? interval. An unexpected finding in the present study was the observation that patients with a prolonged PR interval (>0.20 second) had significantly more severe CAD, reflected in both the coronary score and in the number of coronary arteries involved. In all such patients triple-vessel disease was present, compared to only 50% in the remaining patients with a normal PR interval. Furthermore, the patients with prolonged PR intervals had a greater frequency of cardiomegaly (88% vs 55%) and significantly (p < 0.005) greater enddiastolic volumes. It is difficult to speculate on these findings, since the blood supply to the atrioventricular node and the proximal left bundle are similar. Thus although LBBB alone correlates well with severe left ventricular dysfunction, the presence of PR prolongation in addition indicates triple-vessel disease, presumably the result of poor perfusion to the atrioventricular node. These observations support the concept that myocardial disease and dys-
function are responsible for the LBBB, regardless of the coronary anatomy in any given patient. Conclusions. The present study indicates that LBBB associated with CAD identifies patients with marked impairment in left ventricular function. The severity of the CAD in these patients was not significantly different from an age-sex-matched patient group with ischemic heart disease. In the patients with LBBB neither left axis deviation or QRS width could be correlated with the coronary disease severity or with the degree of left ventricular dysfunction; however, a prolonged PR interval correlated with more severe coronary disease and left ventricular dilatation. The authors thank Ms. Dacia B. Horowitz, Bruce Hamby, and Mrs. Brenda Hamby for their invaluable assistance. REFERENCES
1. Schneider JF, Thomas HE Jr, Sorlie P, Kreger BE, McNamara PM, Kannel WB: Comparative features of newly acquired left and right bundle branch block in the general population: The Framingham study. Am J Cardiol 47:931, 1981. 2. Smith S, Hayes WL: The prognosis of complete left bundle branch block. AM HEART J 78~157, 1965. M: The outlook with bundle-branch block. Br 3. Campbell Heart J 31:575, 1969. 4. Master AM, Kalter H, Dack S, Jaffe H L: The relation between bundle branch block and cardiac enlargement. AM HEART J 20:186, 1940. clinical assessment. 5. Scott RC: Left bundle branch block-A Part III. AM HEART J 70:813, 1965. 6. Schneider JF, Thomas HE Jr, Kreger, BK, McNamara PM, Kannel WB: Newly acquired left bundle branch block: The Framingham study. Ann Intern Med 90:303, 1977. of bundle branch block. Am J 7. Bauer GE: Development Cardiol 14~346, 1964. 8. Goodman MJ, Lassers BW, Juliam DG: Complete bundlebranch block complicating acute myocardial infarction. N Engl J Med 282:237, 1970. 9. Scheidt S, Killip T: Bundle-branch block complicating acute myocardial infarction. JAMA 222:919, 1972. 10. Haft JI, Herman MV, Gorlin R: Coronary arteriographic and left ventricular motion studies in left bundle branch block (abstr). Am J Cardiol 23:117, 1969. 11. Johnson RP, Messer AL, Shreenivas, White PD: Prognosis in bundle branch block. II. Factors influencing the survival period in left bundle branch block. AM HEART J 41:225, 1951. 12. 13.
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Mulcahy R, Hickey N, Maurer B: Aetiology of bundle-branch block. Br Heart J 30:34, 1968. Ginks W, Sutton R, Siddons H, Leathom A: Unsuspected coronary artery disease as cause of chronic atrioventricular block in middle age. Br Heart J 44:699, 1980. Dizadji H, Tahmooressi P, Cernack WF: Etiology of left bundle branch block. Hemodynamic and angiographic studies. J Electrocardiol 7:221, 1974. Haft JI, Herman MV, Gorlin R: Left bundle branch block. Etiologic, hemodynamic, and ventriculographic considerations. Circulation 43:279, 1971. Lewis CM, Dagenais GR, Friesinger GC, Ross RS: Coronary arteriographic appearances in patients with left bundlebranch block. Circulation 41:299, 1970. Hamby RI, Tabrah F, Gupta M: Intraventricular conduction disturbances and coronary artery disease. Am J Cardiol 32:758,
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106 3
Massie E, Walsh TJ: Clinical vectorcardiography and electrocardiography. Chicago, 1960, Year Book Medical Publishers, Inc. Hamby RI: Angina pectoris: A clinical-electrocardiographicangiographic correlative study in 510 patients. In Rios JC, editor: Cardiovascular clinics: Clinical electrocardiographic correlation. Philadelphia 1977, F.A. Davis Company, p 79. Sones FM Jr, Shirey EK: Cine-coronary arteriography. Mod Concepts Cardiovasc Dis 31:735, 1962. Judkins MP: Percutaneous transfemoral selective coronary arteriography. Radio1 Clin North Am 6:467, 1968. Dodge HT, Sandler H, Ballew DW: The use of biplane angiocardiography for the measurement of left ventricular volume in man. AM HEART J 60:762, 1960. Herman MV, Heinle RA, Klein MD, Gorlin, R: Localized disorders in myocardial contraction. Asynergy and its role in congestive heart failure. N Engl J Med 277:222, 1967. Beach TB, Gracey JG, Peter RH, Grunenwald PW: Benign left bundle branch block. Ann Intern Med 70:269, 1969. Wolfram J: Bundle branch block without significant heart disease. AM HEART J 41:656, 1961. Hamby RI, Tabrah F, Gupta M: Intraventricular conduction disturbances and coronary artery disease. Am J Cardiol 321758, 1973. Lev M: Anatomic basis for atrioventricular block. Am J Med 37~742, 1964.
LBBB and LV function
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28. Rasmussen H, Moe T: Pathogenesis of left bundle branch block. Br Heart J 10~141, 1948. 29. Piccolo E, Raviele A, Delise P, Dainese F, Pascotto P, Totaro G, Sartori F, D’Este D: The role of left ventricular conduction in the electrogenesis of left ventricular hypertrophy. An electrophysiologic study in man. Circulation 59:1044, 1979. 30. Hamby RI, Prakash MN, Wyne UA, Hoffman I: Electrocardiographic left ventricular hypertrophy and coronary artery disease: Clinical, hemodynamic and angiographic correlates. AM HEART J 100:784, 1980. 31. Dhingra RC, Amat-Y-Leon F, Wyndham C, Spidhar SS, Wu D, Denes P, Rosen KM Significance of left axis deviation in patients with chronic left bundle branch block. Am J Cardiol 42:551, 1978. 32. Spurrell RAJ, Krikler 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 34~1244, 1972. 33. Lichstein E, Mahapatra R, Gupta PK, Chadda KD: Significance of complete left bundle branch block with left axis deviation. Am J Cardiol 44~239, 1979. 34. Wiberg TA, Richman HG, Gohel FL: The significance and prognosis of chronic bifascicular block. AM HEART J 71:329, 1977.