H-V interval in patients with bifascicular block (right bundle branch block and left anterior hemiblock)

H-V Interval in Patients with Bifascicular Block (Right Bundle Branch Block and Left Anterior Clinical, Electrocardiographic

PABLO DENES, MD RAMESH C. DHINGRA, MD DELON WU, MD RUBEN CHUQUIMIA, MD FERNANDO AMAT-Y-LEON, MD CHRISTOPHER WYNDHAM, MD KENNETH M. ROSEN, MD, FACC Chicago, Illinois

From the Cardiology Section, Abraham Lincoln School of Medicine, University of Illinois College of Medicine; West Side Veterans Administration Hospital: and Department of Adult Cardiology, Cook County Hospital, Chicago, III. This study was supported in part by National Institutes of Health Contract 71-2478 under the Myocardial Infarction Program, and U. S. Public Health Service Training Grant 05879-0551 National Heart and Lung Institute, National Institutes of Health, Bethesda, Md.; and West Side Veterans Administration Hospital, Chicago Basic Institutional Support, Chicago, Ill. Manuscript accepted July 1, 1974. Address for reprints: Pablo Denes, MD, Cardiology Section, University of Illinois Hospital, P. 0. Box 6998, Chicago, Ill. 60680.

and Electrophysiologic

Hemiblock)

Correlations

Electrophysiologic studies were performed in 119 adults with chronic bifascicular block manifested by right bundle branch block and left anterior hemibtock. The H-V interval was normal in 86 patients and prolonged in 33. The following clinical variables were more frequent (P <0.05) in patients with a prolonged H-V interval: cardiac third sound, mitral systolic murmur, cardiomegaly on chest roentgenogram, congestive heart failure and cardiac functional class Ill or IV (New York Heart Association criteria). The following differences in the electrocardiographic and electrophysiologic findings were found: Patients with a prolonged H-V interval had a longer mean P-R interval, QRS duration and A-H interval (P <0.02). All patients were followed up prospectively in a cardiac conduction disease clinic after initial evaluation. The mean follow-up periods were (mean f standard error of the mean) 514 f 49 and 563 f 34 days for the patients with a prolonged and normal H-V interval, respectively. Progression of conduction disease occurred in three patients (4 percent) with a normal H-V interval and in four (12 percent) with a prolonged interval. The cumulative 3 year mortality rate for the entire group was 25 percent. The patients with a prolonged H-V interval had a higher cumulative 2 year mortality rate than those with a normal H-V interval but the difference was not statistically significant. In summary, a prolonged H-V interval was often associated with serious myocardial dysfunction and a high mortality rate. The risk of progression of conduction disease was slight with either a prolonged or a normal H-V interval during this relatively short follow-up period.

The H-V interval is a measure of conduction time from His bundle depolarization to the onset of ventricular activation.‘t2 In patients with right bundle branch block and left anterior hemiblock, the H-V interval is a measure of conduction time in the His bundle and the posterior fascicles of the left bundle branch system. Prolongation of this interval in a patient with right bundle branch block and left anterior hemiblock should reflect the presence of conduction disease in the posterior fascicle or distal His bundle, or both. Pathologic studies suggest the presence of trifascicular disease in patients with bundle branch block and a prolonged H-V interval.” It is not known whether H-V prolongation in such a patient predicts a high risk of subsequent atrioventricular (A-V) block, Stokes-Adams attacks or sudden cardiac death.4-7 In this study we examined several clinical, electrocardiographic and electrophysiologic variables in patients with right bundle branch block and left anterior hemiblock with both normal and prolonged H-V intervals in an attempt to further define the significance of this interval. In addition, all patients studied were followed up prospectively in a cardiac conduction disease clinic. This report presents our detailed observations on the short-term prognostic significance of the H-V interval in these patients.

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The American Journal of CARDIOLOGY

Volume 35

23

H-V INTERVAL IN BIFASCICULAR

Material

BLOCK-DENES

ET AL.

and Methods

Patient Selection Since February 1970, our laboratory has been engaged in a prospective study of patients with intraventricular conduction disease whose condition has been detected in the inpatient and outpatient facilities of the Cook County Hospital, the West Side Veterans Hospital and the University of Illinois Hospital, Chicago. Additional patients are referred to us for electrophysiologic studies and follow-up in our cardiac conduction clinics by private physicians in the greater Chicago area. To be entered in the study, patients must give informed consent for electrophysiologic studies and must agree to be followed up in a cardiac conduction disease clinic. This report describes our findings in 119 adults (aged 18 or over) with chronic right bundle branch block and left axis deviation (mean axis more negative than -3OO) whose condition was detected between February 1970 and August 1973 and who were followed up through June 1974. Patients who had second or third degree block before or at the time of study are excluded from this report.

initial Evaluation Electrophysiologic diagnosis: All patients were hospitalized upon entering the study. A complete history and physical examination were obtained by a cardiac fellow and reviewed by one of the senior authors. Serial electrocardiograms were obtained. The diagnosis of complete right bundle branch block and left anterior hemiblock was based on a modification of the criteria of Rosenbaum.8 The following criteria were used: (1) QRS duration of 0.12 second or greater, (2) RSR or qR configuration of the QRS in lead VI, and (3) left axis deviation with a mean frontal QRS axis more negative than -30’. QRS duration was defined as the longest QRS interval in the standard and augmented limb leads. The P-R interval was defined as the longest interval from the onset of the P wave to the onset of the QRS complex in the standard and augmented limb leads. Significant Q waves were defined by standard electrocardiographic criteria.” Clinical diagnosis: On the basis of the history, physical examination, electrocardiogram, chest roentgenogram and laboratory findings, a clinical diagnosis was reached. Arteriosclerotic heart disease was diagnosed if the patient had (1) a history of exertional chest pain suggestive of angina pectoris, or (2) a previous diagnosis of definite myocardial infarction, or both. Hypertension was diagnosed if two or more blood pressure recordings indicated a systolic pressure greater than 140 mm Hg and diastolic pressure greater than 90 mm Hg. Patients with both arteriosclerotic and hypertensive heart disease were classified for analysis as patients with arteriosclerotic heart disease. Valvular heart disease was diagnosed when a significant valvular lesion could be detected by auscultation or cardiac catheterization, or both. Primary myocardial disease was diagnosed if cardiomegaly (on routine posteroanterior chest roentgenogram, using cardiothoracic ratio) was present without demonstrable cause. Primary conduction disease was diagnosed if heart size was normal and there was no evidence of organic heart disease, with the exception of intraventricular conduction defect. Third and fourth heart sounds were diagnosed by auscultation. His bundle electrocardiogram: Cardiac drugs were withheld for at least 48 hours before the initial study. His bundle electrograms were recorded by previously described l-10 at the time of each patient’s entry catheter techniques

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The American Journal of CARDIOLOGY

into the study. Refractory periods were measured with the atria1 extrastimulus technique, as previously reported.” The following intervals were measured: (1) P-A (mean f 2 standard deviations; normal 27 f 18 msec), from the onset of the P wave on the surface electrocardiogram to the onset of the first high frequency potential of the low atria1 electrogram recorded by the His bundle catheter. This interval reflected conduction time from the high to the low right atrium. (2) A-H (normal 92 f 38 msec), from the first high frequency potential of the low atria1 electrogram to the first high frequency potential of the His bundle electrogram. This interval reflected A-V nodal conduction time. (3) H-V (normal 43 f 12 msec), from the first high frequency potential of the His frequency potential of the His electrogram to the earliest deflection of the QRS complex detected on multiple surface leads. The measurements were made at a paper speed of 200 mm/set and reflect the average of 10 consecutive beats. Atria1 pacing was used to validate H potentials.12

Patient Follow-Up All patients were prospectively followed-up in a conduction clinic at intervals of 1 to 2 months after the initial study, or at shorter intervals if clinically indicated. Clinic examinations consisted of a history, physical examination and a 12 lead electrocardiogram. Portable tape recorder monitoring of electrocardiograms was used in symptomatic patients for detection of transient bradyarrhythmias. Patients who missed appointments were followed up by mail, telephone or house call if necessary. When patients moved from Chicago, electrocardiograms and data from clinical evaluat,ions were obtained from local physicians. No patient was lost to follow-up during the study period. If death occurred outside the hospital, details of the death as well as a copy of the death certificate was obtained. Deaths were classified as either sudden or not sudden. Sudden death was defined as unexpected death occurring instantaneously or within an estimated 3 hours of the onset of acute symptoms.

Analysis of Data All information obtained during initial evaluation and subsequent visits was keypunched and stored on disk (IRS database system). Specifically designed programs were used for data recall. Statistical analysis was performed with use of a Biomedical Statistical Program (BMD X 76). Standard t test was used for testing the significance of differences in means. In a contingency table of 2 X 2, the chisquare method with Yates correction for continuity was used for frequency data analysis. Survival data were analyzed by previously described life table methods.ls,14

Results Clinical

data: On the basis of the initial electro-

physiologic study, the 119 patients were separated into two groups: (1) 86 patients had a normal H-V interval (31 to 55 msec) and are referred to as the normal H-V group. (2) 33 patients had a prolonged H-V interval (56 to 100 msec) and are referred to as the prolonged H-V group. The age and sex distribution of both groups are presented in Table 1. The mean age f standard error of the mean was 61.9 f 1.8 years for the normal H-V group and 62.6 f 2.9 years for the prolonged H-V group of patients. The difference was not statistically significant (NS, P

Volume 35

H-V INTERVAL

TABLE

I

TABLE

Age and Sex Distribution of 119Patients with Right Bundle Branch Block and Left Anterior Hemiblock

Age Group (yr) 18-20 21-30 31-40 41-50 51-60 61-70 71-80 81-90 91-100

Normal H-V (86 patients) -~ Sex no. 1 6 2 6 20 24 18 8 1

1M. 6M, lM, 5M, 15M, 17M, 15M, 6M, lM,

OF OF 1F 1F 5F 7F 3F 2F OF

lM, OM, 2M, 3M, 4M, 4M, lOM, lM, OM,

BLOCK-DENES

ET Al.

II

Classification of Heart Disease in 119 Patients with Right Bundle Branch Block and Left Atrial Hemiblock

Prolonged H-V (33 patients) ~ ____..~~~.~~~ no. Sex 1 0 2 3 5 9 12 1 0

IN 5lFASClCULAR

OF OF OF OF 1F 5F 2F OF OF

Classiflcatlon of Heart Disease Hypertensive Arteriosclerotic Valvular Primary myocardial disease Primary conduction disease Other NS = not significant;

>O.lO). There were 57 men and 19 women in the normal H-V group and 25 men and 8 women in the prolonged H-V group (NS). The clinical classification of heart disease in the 119 patients is presented in Table II. There was no significant difference in the prevalence of different types of disease between normal and prolonged H-V groups. Symptoms and physical findings: The frequency of cardiovascular symptoms and selected historical findings are presented in Table III. There was a greater prevalence of dyspnea (P 0.20 second); 12 of these were in the normal and 13 in the prolonged HV group. Forty-three patients had a QRS duration of 0.16 second or greater; 29 of these were in the normal and 14 in the prolonged H-V group. Electrophys,iologic data: Conduction intervals and other electrophysiologic data are presented in Table VI. Only the A-H interval was significantly longer in the prolonged H-V group (P <0.02). Block

TABLE

Normal H-V (86 patients)

Prolonged H-V (33 patients)

110.

g

;o.

33 22 1

38 26 1

9 11 2

27 34 6

NS NS NS

3

3

3

9

NS

23 4

27 5

4 4

12 12

NS NS

-iA

P

P = probability.

III

Cardiac Symptoms and Selected Historical Findings in 119 Patients with Right Bundle Branch Block and Left Anterior Hemiblock Normal H~V (86 patients) Symptcms Dizziness Syncope Angina Dyspnea NYHA class I-II III-IV Congestive heart failure Previous myocardial infarction Diabetes mellitus NYHA fication.

TABLE

class

=

New

York

Prolonged H-V (33 patients) P

no.

%

no.

%

29 9 12 27

34 11 14 31

9 3 6 17

27 9 18 52

NS NS NS
83 3 19

97 3 22

24 9 16

73 27 49


11

13

5

15

NS

13

15

10

30

NS

Heart

Association

functional

classi-

IV

Selected Physical and Chest Roentgenographic Findings in 119Patients with Right Bundle Branch Block and Left Anterior Hemiblock Normal H-V (86 patients)

Systolic murmur mitral area Protodiastolic gallop (S3) Atria1 gallop (S4) Cardiomegaly on chest roentgenogram

January 1975

Prolonged H-V (33 patients)

no.

%

no.

%

P

11

13

12

36


5

6

8

24


48 41

56 48

21 24

64 72

NS <0.05

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H-V INTERVAL

TABLE

IN BIFASCICULAR

BLOCK-DENES

ET AL.

V Findings in 119Patients with Right Bundle Branch Block and Left Anterior

Electrocardiographic

Normal H-V (86 patients)

Hemiblock

Prolonged H-V (33 patients)

Patients Mean i 0.177 0.141 -67.27

P-R interval (set) QRS duration (set) QRS axis (degrees) Significant Q waves Atrial fibrillation Ventricular premature SEM

= standard

i * i ...

SEM 0.003 0.002 2.62

... complexes

...

Patients

no.

%

.. ... .... 35 3 10

... ... ... 41 3.5 12

Mean * 0.21 0.149 -73.64

SEM

no.

%

zt 0.002 i 0.003 i 5.29

... ... ... 17 0 6

... ... ... 52 0 18

.. . .

...

P
error of the mean.

TABLE VI Conductjon

Times and Refractory

Periods in 119Patients with Right Bundle Branch Block and Left Anterior Normal H-V

P-A (msec) A-H (msec) Atrial ERP (msec) A-V nodal ERP (msec) HPS ERP (msec) SA nodal recpvery time ERP = etfective

(msec)

refractory

period;

29.82 100.18 264.12 360.40 402.50 984.79

i 1.17 -f 2.89 f 6.58 i 10.39 zk 17.5 Lf 26.98

HPS = His.Purkinje

83 83 40 25 2 64

system;

to the His potential during atria1 pacing occurred in two patients in the pormal H-V group (at paced heart rates of lOO/min and 17l/min, respectively) and in two patients from the prolonged H-V group (at paced heart rates of 140 and 180/min, respectively). None of these patients had progression of conduction disease during the follow-up period. Follow-up data: The mean follow-up periods for the normal and prolonged H-V groups were (mean f standard error of the mean) 563 f 34 and 514 f 49 days, respectively. The total cumulative 3 year mortality rates and mortality rates due to sudden death in all the patients studied are presented in Table VII and Figure 1. Four of the patients who died suddenly had arteriosclerotic heart disease. The cumulative 3 year mortality rates, comparing the normal and prolonged H-V groups, are shown in Table VIII and Figure 2. The prolonged H-V group had a higher mortality rate at 2 and 3 years, but the differences were not statistically significant. The 2 year cumulative mortality for sudden death was similar in the normal and prolonged H-V gxoups. Twenty-two of the 119 patients died, 14 in the normal H-V group (6 suddenly) and 8 in the prolonged H-V group (2 suddenly). The 14 patients who did not die suddenly died of congestive heart failure or cardiogenic shock, or both (7 patients), pneumonia (3 patients), cerebrovascular accident (1 patient), postopdistal

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Prolonged H-V no. of patients

Mean & SEM

Hemiblock

Mean & SEM 31.36 113.40 267.50 343.18 472.50 1041.6

I!Z i z!z z!z xt z!z

2.09 7.02 14.60 15.78 52.52 56.30

no. of patients 33 33 18 11 2 30

P NS (0.02 NS NS NS NS

SA = sinoatrial.

erative complications (2 patients) and bronchogenic carcinoma (1 patient). Progression of conduction disease: In three patients (4 percent) with a normal H-V interval, second or third degree A-V block developed: in one, at an unknown site, secondary to transient hyperkalemia (on day 6 after entry into the study); in one, distal to the His potential, without precipitating cause (on day 2); and in one, at an unknown site, detected during portable tape recorder monitoring (on day 17). In four patients (12 percent) with a prolonged H-V interval, second or third degree block developed: in one, distal to the His potential, secondary to acute anteroseptal infarction (on day 351); in one, at an undetermined site, after cardiac surgery (on day 58); and in one, proximal to the His potential, without precipitating cause (on day 71); and in one, proximal to the His potential, secondary to digitalis (on day 136). Idiopathic progression of conduction disease occurred in only three patients, two with a normal and one with a prolonged H-V interval. Discussion The H-V interval in patients with right bundle branch block and left anterior hemiblock is a measure of conduction time in the His bundle and posterior fascicles of the left bundle branch system. Pathologic studies in a limited number of cases suggest that

Volume 35

H-V

TABLE

VII

IN BIFASCICULAR

BLOCK-DENES

ET AL

TABLE VIII

Cumulative Mortality Rate for 119 Patients with Right Bundle Branch Block and Left Anterior Hemiblock

Mortality Rate * Standard Error (%) Total

INTERVAL

Comparative Cumulative Prolonged H-V Groups

14 f 21 f 25 f

(no.)

3 4 6

6&2 9f3 913

112 63 19

107 62 19 -

Years

0

a prolonged H-V interval in these patients reflects the presence of trifascicular conduction disease.3J5 The reported incidence of a prolonged H-V interval (>55 msec) in patients wit,h right bundle branch block and left anterior hemiblock ranges from 17 to 50 percent.4,7J6p17 In the study by Narula et a1.,4 31 of 68 patients with this conduction defect had an H-V interval greater than 55 msec. In our study 36 percent of patients had a prolonged H-V interval. Clinical, Electrocardiographic Correlations

Total mortality 1st year 2nd year 3rd year Mortality due to sudden death 1st year 2nd year 3rd year

of follow-up

FIGURE 1. Mortality curves for 119 patients with right bundle branch block and left anterior hemiblock (actuarial method) representing the yearly cumulative mortality rates after His bundle study from sudden and nonsudden deaths combined (x- - -x) and from sudden death alone (a-----*).

and Electrophysiologic

In our series, a prolonged H-V interval was associated with a significantly increased prevalence of signs and symptoms of myocardial dysfunction, such as dyspnea, apical systolic murmuis, third heart sound, cardiomegaly and congestive heart failure. This was surprising in view of the pathologic studies of Lenegre I8 and Lev,lg who suggested that the most common pathologic process responsible for bilateral bun-

Rates of the Normal

Normal H-V (86 patients)

Patients Exposed to Risk of Dying

mortality

1st year 2nd year 3rd year Mortality due to sudden death 1st year 2nd year 3rd year

Mortality

I

Years

and

Prolonged H-V (33 patients)

Mortality Rate + Standard Error

Patients Exposed to Risk of Dying

Mortality Rate -ir Standard Error

Patients Exposed to Risk of Dymg

(%)

(no.)

(%)

(no.)

P

32 18 9

NS NS NS

30 17 4

NS NS NS

14 i 18 & 23 f

4 5 7

80 46 16

7f3 8zIz3 8f3

2 of follow-up

16 $I 6 30 zt 9 3Oi9

77 45 15

3

3z!z 9& 9f6

3 6

0

I Years

2 of follow-up

3

FIGURE 2. Comparative mortality curves of the groups with a normal and prolonged H-V interval. Lefl, yearly cumulative mortality rates. Right, yearly cumulative mortality rates from sudden death. NHV (x--x) = normal H-V interval; PHV (*- - -0) = prolonged HV interval.

dle branch disease (trifascicular disease) was primary sclerodegenerative disease involving the cardiac skeleton and the intraventricular conduction system. However, neither of these workers excluded the presence of additional organic heart disease or other etiologic mechanisms for the production of bilateral bundle branch block. Several mechanisms may explain the high incidence of myocardial dysfunction in the patients with a prolonged H-V interval: (1) The same disease process, arteriosclerotic or hypertensive, for example, directly involves both the working myocardium and the conduction system. (2) The same etiologic factors are responsible for both sclerodegenerative bilateral hundle branch disease and ventricular muscle disease. (3) The prolonged H-V interval in patients with bifascicular block may reflect stretch of the left ventricle, in a manner similar to that in which incomplete right bundle branch block occurs in patients with diastolic overload of the right ventricle.

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H-V INTERVAL IN BIFASCICULAR

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ET AL.

We believe there is a significant prevalence of undiagnosed trifascicular disease in the normal H-V group (Lev’s disease, Lenegre’s disease), which has not produced H-V prolongation. This possibility is supported by the spontaneous occurrence of block distal to the His potential in patients with bundle branch block and a normal H-V interval. Although P-R intervals and QRS durations were significantly longer in the ‘prolonged H-V group, these findings alone or in combination had little value in predicting the H-V interval. This observation was in contrast to results of a previously reported study” in patients with left bundle branch block, in which a P-R interval greater than 0.20 second in combination with a QRS duration greater than 0.16 second predicted H-V prolongation. The prevalence of a prolonged A-H interval was significantly greater in the prolonged H-V group, suggesting an association of A-V nodal and intraventricular conduction disease that contributed to the frequent P-R prolongation found in this group. There was no significant difference in intraatrial conduction time (P-A interval), or atria1 and A-V nodal effective refractory periods in the groups with a normal and prolonged H-V interval. The number of patients whose effective refractory period of the His-Purkinje system was determined was too small to permit a conclusion to be reached. Follow-Up (Natural History) The progression of bifascicular block to complete heart block has been demonstrated in previous studies.8J7,20-23 The reported incidence of development of heart block in patients with right bundle branch block and left anterior hemiblock ranges from 6 to 30 percent over a period of several months to several decades. All previous reported studies concerning progression of bifascicular block have been retrospective. The present study is the first prospective study on the natural history of these patients. Documented progression of conduction disease was uncommon, occurring in only 6 percent of patients during a mean follow-up period of approximately 1 l/2 years. Surprisingly, the site of A-V block was not always distal to the His bundle. The risk of progression of conduction disease was similar in both the prolonged and normal H-V groups during the relatively short follow-up period.

Mortality The cumulative mortality rate in our total group of patients with bifascicular block was high, being 14 percent in the 1st year, 21 percent in the 2nd year, and 25 percent in the 3rd year. These statistics were similar to those reported by DePasquale and Bruno,23 who noted a 23 percent mortality rate with a follow-up period ranging from 0 to 15 years. In this series, the patients with a prolonged H-V interval had a greater cumulative mortality. This observation appears to reflect the higher incidence of myocardial disease in this group, most of these patients dying of cardiac failure. Patients in both the normal and prolonged H-V groups had a relatively high incidence of sudden cardiac death. Sudden death in both groups of patients could reflect either progression of conduction disease or ventricular fibrillation. We believe the latter to be a frequent causative mechanism of sudden death in our patients. A recent report2* revealed a high rate of ventricular arrhythmias manifested in the electrocardiograms of patients with intraventricular conduction defects. Also, in our study patients in both the normal and prolonged H-V groups had a high incidence of ventricular premature beats. In addition, we recently reported 25 that the majority of patients with bifascicular block, when subjected to graded treadmill exercise, manifested premature beats and, occasionally, ventricular tachycardia. However, sudden death due to asystole secondary to progression of intraventricular conduction disease cannot be excluded in either of our two groups of patients. Therapeutic Implications Our data do not allow us to recommend prophylactic pacing in patients with right bundle branch block and left anterior hemiblock and either a normal or a prolonged H-V interval. We emphasize that the mean follow-up period in this prospective series was approximately 1 l/2 years and that, with continued study, it may be possible to delineate a group with significant risk of progression of conduction disease. Acknowledgment We thank Mrs. Jo Price for secretarial assistance, Mrs. Loretta Kasparas, RN, for assistance in both the laboratory and the conduction disease clinic, and Mr. Minu Pate1 and the Research Resources Laboratory of the University of Illinois for statistical and computer support.

References 1. Scherlag BJ, Lau SH, Helfant RH, et al: Cathetertechnique for recording His bundle activity in man. Circulation 39: 13-18, 1969 2. Rosen KM: Catheter recording of His bundle electrograms. Mod Concepts Cardiovasc Dis 42:23-28, 1973 3. Rosen KM, Rahimtoola SH, Bharati S, et al: Bundle branch block with intact atrioventricular conduction. Electrophysiologic and pathologic correlation in three cases. Am J Cardiol 32: 783-792, 1973 4. Narula OS, Samet P: Right bundle branch block with normal, left or right axis deviation. Am J Med 51:432-455, 1971 5. Rosen KM, Ehsani A, Rahimtoola SH: H-V intervals in the left

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bundle branch block. Clinical and electrocardiographic correlations. Circulation 46:717-723, 1972 6. Gupta PK, Lichstein E, Chadda KD: lntraventricular conduction time (H-V interval) during antegrade conduction in patients with heart block. Am J Cardiol 32:27-31, 1973 7. Haft JI, Weinstock M, DeGuia R, et al: Assessment of atrioventricular conduction in left and right bundle branch block using His bundle electrograms and atrial pacing. Am J Cardiol 27:474489 1971 8. Rosenbaum MB, Elizari MV, Lazzari JO: The Hemiblocks. Oldsmar, Fla, Tampa Tracings, 1970, p 97, 130

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9. Lipmen BS, Massle E: Clinical Scalar Electrocardiography. Chicago, Year Book Publishers, 1965, p 263 10. Dhlngra RC, Rosen KM, Rehlmtoola SH: Normal conduction intervals and responses in 61 patients using His bundle recording and atrial pacing. Chest 6455-59, 1973 11. Denes P, Wu D, Dhlngra RC, et al: The effect of cycle length on cardiac refractory periods in man. Circulation 49:32-41, 1974 12. Rosen KM: Evaluation of cardiac conduction in the cardiac catheterization laboratory. Am J Cardiol30:701-703, 1972 13. Cutler SJ, Ederer F: Maximum utilization of the life table method in analyzing survival. J Chronic Dis 6:699-712, 1958 14. National Office of Vital Statistics: Standard error of the age-adjusted death rate. Vital Statistics-Special Report Vol 47, no. 9, 1961 15. Rosen KM, Rahlmtoola SH, Gunner RM, et al: Site of heart block as defined by His bundle recordings. Pathological correlation in three cases. Circulation 45:965-987, 1972 16. Berkowitz WD, Lau SH, Patton RD, et al: The use of His bundle recordings in the analysis of unilateral and bilateral bundle branch block. Am Heart J 81:340-350, 1971 17. Rangenathan H, Dhurandhar R, Phillips JH, et al: His bundle electrogram in bundle branch block. Circulation 45:282-293, 1972 18. Lenegre J: Etiology and pathology of bilateral bundle branch

19. 20.

21.

22.

23.

24.

25.

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ET AL.

block in relation to complete heart block. Prog Cardiovasc Dis 61409-444, 1964 Lev M: Anatomic basis for atrioventricular block. Am J Med 37: 742-748, 1964 Lasser RP, Heft JI, Frladberg CK: Relationship of right bundle branch block and marked left axis deviation (with left parietal or peri-infarction block) to complete heart block and syncope. Circulation 37:429-437, 1968 Schloff LD, Adler L, Donoso E, et al: Bilateral bundle branch block. Clinical and electrocardiographic aspects. Circulation 35790-801, 1967 Scanlon PG, Pryor R, Blount SG: Right bundle branch block associated with left superior or inferior intraventricular block. Clinical setting, prognosis, and relation to complete heart block. Circulation 421123-l 133, 1970 DePasquale NP, Bruno MS: Natural history of combined right bundle branch block and left anterior hemiblock (bilateral bundle branch block). Am J Med 54:297-303, 1973 Watanabe Y, Pamlntuan JC, Dreltus LS: Role of intraventricular conduction disturbances in ventricular premature systoles. Am J Cardiol32:188-195, 1973 Hesanaln J, Ashley WW, Denes P, et al: Effect of exercise on cardiac conduction in patients with bifascicular block (abstr). Circulation 48: Suppl IV: IV-175, 1973

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