PEDIATRIC CARDIOLOGY
EchocardiographicAssessment of PulmonaryArterial Pressure
in Children With Complete Right Bundle Branch Block
GREGORY L. JOHNSON, MD
RICHARD A. MEYER, MD, FACC
JOAN KORFHAGEN, RDMS
DAVID C. SCHWARTZ, MD, FACC
SAMUEL KAPLAN, MD, F&C
Lexington, Kentucky
Cincinnati, Ohio
From the Department of Pediatrics, College of
Medicine, University of Cincinnati, Children’s
Hospital,Cincinnati,OhioandDepartmentof Ps
diaiics, College of Medicine,Universityof Kentuckv MedicalCenter. Lexintion, Kentucky.This
w&wassq+rtedI~partbytheAmericar;Hear?
Association, SouthwesternOhio Chapter, Cincinnati,Ohioandthe KentuckyHeartAssociation,
Louisvllie,Kentucky.hb~script recehredOctober
11,1977; rev&d rnanuscrlptreceivedDecember
6,1977, acoepted December 7,1977.
Addressfor reprints:Qe9ory L. Johnson,MD,
Deparbnentof Pediatrics,Universityof Kentucky
Medical Center, Lexington,Kentucky40506.
1264
June 1978
The time Interval between tricuspid valve closure and pulmonaryvalve
openlng,termed the lsovokrmlccontractlontime of the rightventricle,was
evaluated echographically In 38 normal children and within 24 hours of
cardiac catheterlzatlon in 83 children with congenital heart disease and
normal conductlon as assessed with the electrocardilbgram.In the 53
patients with congenital heart disease, lsovolumiccontractiontime was
stronglyinfluencedby rfghtventricularaflerload,as defined by pulmonary
arterial end-dlastollc pressure (r = 0.87). It was possibleto utilize Isovolumlc contraction time to separate patlents wtth normal or elevated
values for pufmonaryarterial end-diastolicpressure.Similar correlations
were demonstrated between lsovolumic contraction time and mean
pulmonaryarterialpressureand calculatedpulmonaryvascularreststance.
Evaluattonof 15 chiklrenwith completerightbundlebranchblockrevealed
values for lsovolumlccontractiontime that dld not signtflcantlydiffer from
those of patlents with similar pulmonary arterial end-dlastollc pressure
but no conductlon abnormalltles. These findings indicate that serial
echographic evaluatton of the interval from tricuspid valve closure to
pulmonaryvalve openingcan glve an accurate reproducibleassessment
of rightventrkxrlarafterloadIn many childrenwtth congenftalheart d&ease
and complete right bundle branch block.
Obstructive pulmonary vascular disease is a well known potentially lethal
complication of many forms of congenital heart disease. In patients at
risk of this complication, repeated invasive assessment of pulmonary
arterial pressures and pulmonary vascular resistance has frequently been
required to determine optimal timing of surgical intervention. Recent
that echocardiographic
studies by Hirschfeld et al. 112demonstrated
measurement of right ventricular systolic time intervals, performed
serially and without difficulty, can result in a reasonable noninvasive
estimation of pulmonary vascular resistance. In their studies the ratio
of the right ventricular preejection period to ejection time, recorded
echographically, correlated well with invasively determined values for
pulmonary arterial end-diastolic and mean pressure and calculated
pulmonary
vascular resistance. Because electromechanical
delay
prolongs the right ventricular preejection period in patients with complete right bundle branch block, the ratio cannot be used to evaluate
serial changes in pulmonary vascular dynamics in these patients. Many
children have postoperative complete right bundle branch block after
correction of their congenital heart lesion. It would be particularly
valuable to have a method ofserially evaluating the pulmonary vascular
bed noninvasively in these patients.
Right ventricular isovolumic contraction time may be defined echographically as the interval from coaptation of the tricuspid valve leaflets
to opening of the pulmonary valve. If this interval were found to be relatively independent of the prolongation of the right ventricular pre-
The American Journal of CARDIOLOGY
Vohme 41
ECHDCARDIDGBAM IN COMPLETE RIGHT BUNDLE BRANCH BLOCK-JOHNSON ETAL.
FIGURE 1. Echocardiograms of
pulmonary and tricuspid valves of
three patients demonstrating pulmonary valve opening and closure
and coaptation of tricuspid leaflets.
Numbers 235,230 and 220 refer to
right ventricular ejection time. ASD
= atrial septal defect; MS = mitral
stenosis: PHT = pulmonary hypertension; POST-W = postoperative;
QPO = interval from the 0 wave to
pulmonary valve opening; QT, =
interval from the Q wave to tricuspid
valve closure: RBBB= right bundle
branch blm RICT (rim isovolumic
contraction time) = (QPo - QT,);
VSD = ventricular septal defect.
ejection period induced by electromechanical delay, it
could be utilized to evaluate right ventricular afterload
in patients with complete right bundle branch block.
Additionally, the interval could be utilized in patients
without right ventricular conduction abnormalities in
whom difficulty in recording pulmonary valve closure
precludes use of the preejection period to ejection time
ratio to assess right ventricular afterload.
The purposes of this study were (1) to evaluate right
ventricular isovolumic contraction time echographically
in normal children and to establish a range of normal
values; (2) to evaluate right ventricular isovolumic
contraction time in a large series of children with a variety of congenital heart lesions, including several with
coexisting complete right bundle branch block, who
were undergoing elective cardiac catheterization; (3) to
compare right ventricular isovolumic contraction time
with values for pulmonary arterial end-diastolic and
mean pressure and calculated pulmonary vascular resistance determined invasively; and (4) to determine the
efficacy of using right ventricular isovolumic contraction
time in evaluating right ventricular aferload in the
presence of complete right bundle branch block.
Material and Methods
Echocardiograms were performed in 38
normal children aged 1 month to 17 years (median 8 years)
without signs of heart disease and within 24 hours of cardiac
catheterization in 68 children aged 1 month to 22 years (median 6 years) with congenital heart disease. Fifteen of these
66 children had electrocardiographic evidence of complete
right bundle branch block as indicated by a QRS interval
greater than 120 msec; the block was temporally related to
intracardiac surgery in 14 of the 15.
Case material:
Echocardiography:
Echocardiograms
were obtained
utilizing a Hoffrel 1OlBor 201 ultrasonoscope. The echographic tracing and electrocardiogram were recorded on a Cambridge multichannel
physiologic recorder or a Honeywell
model 1856 multichannel
recorder. Tracings were recorded
at a paper speed of 75 or 125 mm/set with time lines of lo,20
or 40 msec. At a paper speed of 75 mm/set, there was a po-
tential error of approximately 5 msec in measurement of time
intervals,s which was judged insignificant. An Aerotech 5.0
megahertz nonfocused or a 3.5 or 2.25 megahertz short internal
focus transducer was used. In older children, in whom the 2.25
megahertz transducer was used for left ventricular studies,
it was frequently helpful to change to a higher frequency
transducer to obtain optimal echoes from the right-sided
structures. The tricuspid valve was visualized echographically
by rotating the transducer medially and inferiorly along the
sternum from the aortic region. This position enabled the
ultrasonic beam to pass inferiorly through the valve. The ramp
was then set to peak at approximately the point of coaptation
of the anterior and posterior tricuspid valve 1eailet.s to visualize the point of valve leaflet closure. Similarly, the transducer was robted laterally and slightly superiorly from the
aortic area to visualize the pulmonary artery. Occasionally,
particularly in older children, it was necessary to move the
transducer one interspace superiorly and then rotate it laterally. If the ramp peak was then set at approximately the
center of the pulmonary arterial echo, both opening and closure of the pulmonary valve could be visualized.
Echographic
measurements
(Fig. 1): The interval from
the Q wave to tricuspid valve closure was measured from the
onset of ventricular depolarization, as defined by the Q or R
wave of the simultaneous electrocardiogram, to coaptation of
the tricuspid valve leaflets. When only the anterior tricuspid
leaflet could be accurately visualized, leaflet coaptation was
determined to have occurred at the point of transition of the
fine anterior leaflet echo to a thicker closed valve echo in early
systole. Immediately after valve closure there was a consistent
abrupt posterior movement of the valve echo before the
gradual anterior movement in systole. The interval Q to pulmonary valve opening was measured from the onset of ventricular depolarization to the point of rapid departure of fine
cusp echoes from the thick closed valve echoes recorded during
diastole. This method was also used when only the posterior
pulmonary cusp could be recorded adequately. Right ventricular ejection time was determined as the time from the
onset of ventricular ejection to the termination of ejection
noted by junction of the fine leaflet echo with the thick closed
valve echo. The difference of Q to pulmonary valve opening
less Q to tricuspid valve closure was arbitrarily termed right
ventricular isovolumic contraction time. Measurements were
June 1878
The Amlcan
Journal of CARDIOLGGY
Vofume 41
1285
EC!lOCARDlOGRAM IN COMPLETE RIGHT BUNDLE BRANCH BLOCK-JOHNSON
ET AL.
r= -.I9
n = 36
ym 14.5-.04x
0
l
m
l
16
I
l
l
ee
l
l
l
0
50
I
60
1
70
I
SO
I
60
I
100
HEART RATE
I
I IO
I
120
Results
Normal children: Right ventricular
isovolumic
contraction time in the 38 normal children ranged from
1 to 20 msec (mean f standard derivation 10.2 f 5.2
msec). There was no correlation (r = -0.05) between
values observed and patient age, and only a weak correlation (r = -0.19) between values observed for isovolumic contraction time and heart rate (Fig. 2). Data
for normal subjects as well as for study patients were
rate-corrected
by two separate methods to determine
whether rate correction would alter correlation of the
isovolumic contraction time with signs of obstructive
pulmonary vascular disease. The first of these involved
dividing the observed isovolumic contraction time by
the square root of the R-R interval. The mean value for
this interval in the normal group was 12.9 f 6.5 msec.
It has been reported2 that the ratio of right ventricular
preejection period to right ventricular ejection time is
relatively uninfluenced by heart rate in children. Because the right ventricular isovolumic contraction time
is the mechanical component of the right ventricular
June 1878
I
140
(bcatr/min.)
performed at similar R-R intervals and were made during
end-expiration in older children. in the infants with a rapid
respiratory rate in whom respiratory monitoring was not
available, the shortest R-R intervals were arbitrarily selected
to minimize the influence of respiratory variation on the intervals. Five separate complexes were measured and averaged
to obtain the final intervals.
Hemodynamic measurements: All patients were premedicated with pentobarbital or droperidol before cardiac
catheterization and children between 2 and 5 years of age received ketamine anesthesia. Right ventricular and pulmonary
arterial pressure curves were measured to the nearest 1 mm
Hg. Pulmonary vascular resistance was calculated in units of
mm Hg/liter per min per m2 utilizing assumed oxygen consumption in approximately half the patients and measured
oxygen consumption using a continuous flow-through system
in the remainder.
1288
I
130
‘TAT
FIGURE 2. Correlation between right ventricular
isovolumic contraction time (RICT) and heart rate in
38 normal chikken. Sdkl line is the line of regression.
n = number of children: r = correlation coefficient.
preejection period, the ratio of the right ventricular
isovolumic contraction time to the ejection time was also
analyzed as an alternative method of eliminating the
possible effect of heart rate from our data. The mean
value for this ratio in the normal subjects was 0.037 f
0.015.
Congenital heart disease without right bundle
branch block: In the 53 patients without electrocardiographic evidence of complete right bundle branch
block, right ventricular isovolumic contraction time
provided excellent separation of those patients with
normal pulmonary arterial end-diastolic pressure, all
of whom demonstrated values for isovolumic contraction time within the range defined by the normal population, from those with catheterization
findings consistent with pulmonary vascular obstructive disease
(Fig. 3). The latter group all demonstrated values for
isovolumic contraction time greater than 2 standard
deviations above the normal range, with the lowest value
of 25 msec observed in a patient with pulmonary arterial
end-diastolic pressure greater than 20 mm Hg. Although
there was considerable scatter in the data, particularly
at high values for end-diastolic pressure, a significant
positive linear correlation (r = 0.87) was demonstrable
between right ventricular isovolumic contraction time
and pulmonary arterial end-diastolic pressure. Significant correlations were also demonstrated
between
isovolumic contraction time and mean pulmonary arterial pressure (r = 0.88) and calculated pulmonary
vascular resistance (r = 0.68).
Correcting the isovolumic contraction time for heart
rate by dividing the observed interval by the square root
of the R-R interval also provided excellent separation
of patients with normal and elevated values for pulmonary arterial end-diastolic pressure, but the separation was not noticeably improved nor was the correlation coefficient significantly changed (r = 0.85) from
The Amerkan Journal of CARDlOLOQY Volume 41
ECHOCARDIOGRAM IN COMPLETE RIGHT BUNDLE BRANCH BLOCK-JOHNSON
-CRSEE
80
l Present
0 AS(12)
70
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PDAIB)
0
COA(5)
.
ECD
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MI (21
t
70
-
60
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-
(15)
oAbsent (53)
(51
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ET AL.
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40k
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r=.87
IO
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a/”
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y= 1.06(x)+2.82
r= .SI
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6
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40
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40
I5
“=1.31(x1-1.67
1
56
RICT (msec)
01’
FIGURE 3. Correlation between ri&t ventricular isovolumic contraction
time (RICT)and pulmonary arterial end-diastolic pressure (PA& in 53
chilcken with congenital heart disease but without complete rtght bundle
branch block. Solid Me is the line of regression. AS = aortlc stenosis;
COA = coarctation of the aorta; ECD = endocardial cushion defect;
MI = mitral insufficiency; n = number of patients; PDA = patent ductus
arteriosus; VSD = ventricular septal defect.
results observed utilizing the uncorrected data. Similar
findings were demonstrated in the correlations between
the rate-corrected interval and mean pulmonary arterial
pressure (r = 0.86) and calculated pulmonary vascular
resistance (r = 0.65).
Comparison
of pulmonary
arterial end-diastolic
pressure with the ratio of right ventricular isovolumic
contraction
time to right ventricular ejection time
yielded results similar to those utilizing isovolumic
contraction time alone (r = 0.87). Similar correlations
were observed between this ratio and mean pulmonary
arterial pressure (r = 0.85) and calculated pulmonary
vascular resistance (r = 0.71).
Patients with congenital heart disease and right
bundle branch block: In all patients with complete
right bundle branch block and normal pulmonary arterial end-diastolic pressure, values for right ventricular
isovolumic contraction time were within the range defined by the normal population. These values observed
were not notably different from those in patients with
similar pulmonary arterial end-diastolic pressures and
normal intraventricular
conduction (Fig. 4). As in the
patients with normal conduction, elevation of the pulmonary arterial end-diastolic pressure prolonged right
ventricular isovolumic contraction time in the patients
with complete right bundle branch block, and the interval clearly separated patients with normal pressures
from those with pressures indicative of hypertensive
’
8
I
16
1
24
RICT
I
I
I
I
32
40
40
56
lmsecl
FIGURE 4. Ccrrelation between rtght ventricular isovolumic contraction
time (RICT)and pulmonary arterial enddlastolic pressure (PA& in 15
children with congenital heart disease and complete rtght bundle branch
block (CRBBB) compared with that observed in 53 children without
complete right bundle branch block. SolId and dashed lines are regression lines in children with and without complete right bundle branch
block, respectively.
pulmonary vascular disease. A linear correlation relating
isovolumic contraction time and pulmonary arterial
end-diastolic pressure in patients with complete right
bundle branch block was demonstrable (r = 0.81), and
there was no statistically significant difference between
this regression equation and that relating isovolumic
contrastion time and pulmonary arterial end-diastolic
pressure in patients without complete right bundle
branch block. Similar correlations were demonstrable
relating right ventricular isovolumic contraction time
in patients with complete right bundle branch block to
mean pulmonary arterial pressure (r = 0.84) and calculated pulmonary vascular resistance (r = 0.86).
The correlation between right ventricular isovolumic
contraction time and pulmonary arterial end-diastolic
pressure in patients with complete right bundle branch
block was not notably improved by correction of the
observed interval for heart rate (F = 0.82) or by evaluation of the isovolumic contraction time to ejection time
ratio (r = 0.86).
Discussion
Isovolumic contraction time has classically been defined as that phase of the preejection period from closure of the atrioventricular valve to onset of ventricular
ejection.s*4 Although opening of the pulmonary valve
June 1979
The Amwkan
Joumal of CARDIOLOGY
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ECHOCARDIOGRAM
IN COMF’LETE RIGHT BUNDLE BRANCH BLOCK-JOHNSON
visualized echographically has generally been thought
to coincide with the onset of right ventricular ejection,
the exact timing of closure of the tricuspid valve and its
relation to right ventricular events has been controversial. However, it was recently demonstrated with
phonocardiographic-echocardiographic techniques5-7
that coaptation of the tricuspid valve leaflets visualized
echographically corresponds with the second group of
high frequency vibrations in the first heart sound, that
is, with tricuspid valve closure. By convention, isovolumic contraction time of the left ventricle has been
measured from the phonocardiographic mitral valve
closure to the onset of left ventricular ejection (determined from the rapid upstroke of the carotid pulse
tracing, and then corrected for the time delay of pulse
transmission).It appears reasonableto propose that the
echographic correlate of the corresponding period in the
right ventricle could be defined by the coaptation of the
tricuspid valve leaflets and the point of initial opening
of the pulmonary valve.
Echographic right ventricular isovolumic contraction time as an assessment of pulmonary arterial end-diastolic pressure: In the present study, the
echographic right ventricular isovolumic contraction
time thus defined was evaluated in children with and
without conduction abnormalities affecting the right
ventricle to determine whether the interval could provide the same assessmentof the status of the pulmonary
vascular bed afforded by evaluation of the right ventricular preejection period to right ventricular ejection
time ratio and, if so, whether this interval could be used
to assesspulmonary vascular disease in the presence of
right ventricular conduction abnormalities. Our results
confirm that right ventricular isovolumic contraction
time, evaluated echographically, provides excellent
separation of patients with normal pulmonary arterial
pressures from those with pressures indicative of hypertensive pulmonary vascular disease. Although a
highly significant linear correlation was demonstrated
between isovolumic contraction time and pulmonary
arterial diastolic and mean pressures, as well as with
calculated pulmonary vascular resistance, there was
considerable scatter in the data, and one should not
attempt to extrapolate precise hemodynamic data from
echographic evaluation of the isovolumic contraction
time. We believe that the principal utility of our data
will be in the serial evaluation of patients at risk of developing pulmonary vascular changes as a result of their
congenital heart lesion, particularlyin patients in whom
technical difficulty in echographically defining pulmonary valve closure precludes use of the right preejection period to right ventricular ejection time
ratio.
Effect of right bundle branch block: In patients
with complete right bundle branch block, values for
right ventricular isovolumic contraction time were not
significantly different from values in patients with
similar indexes of pulmonary vascular disease but
without right ventricular conduction abnormalities.
Isovolumic contraction time appears to provide a noninvasive method of serially evaluating the pulmonary
1268
June 1978
The American Journal ol CARDIOLOGY
ET AL.
vascular bed in this group of patients. In our patients
the presence of incomplete right bundle branch block
was usually an index of right ventricular hypertrophy,
and these patients were not separately evaluated.
Among children, complete right bundle branch block
usually is not a sign of generalized conduction system
disease but is presumably secondary to an isolated,
often surgically induced, proximal lesion. Leech and
Brooks (personal communication) found that in these
patients, right ventricular isovolumic contraction time
is normal, but that in the presence of normal afterload,
the interval is often prolonged in patients with generalized conduction system disease and distal or arborization block. It would follow that, without a high degree
of suspicion regarding the site of the block, the method
cannot be applied to all instances of complete right
bundle branch block. If these findings are confirmed,
the usefulness of the echographic evaluation of isovolumic contraction time in assessing the status of the
pulmonary vascular bed would be limited somewhat by
these considerations, particularly in adult patients.
Effect of heart rate: An unexpected finding in our
study was that right ventricular isovolumic contraction
time was minimally affected by heart rate, and correction of the interval for heart rate did not appreciably
change its usefulness in evaluating the status of the
pulmonary vascular bed. Because the isovolumic contraction time was found to normally be exceedingly
short (mean value in the normal group 10 msec), it may
be that the changes associated with changing heart rate
are not sufficient to produce the type of changes seen
with increased right ventricular afterload. Similarly,
division of the isovolumic contraction time by right
ventricularejection time, an intervalthat is significantly
correlated with heart rate,2 did not improve our data.
Effect of right ventricular
contractile
state,
preload and afterload: The principal determinants of
the duration of left ventricular isovolumic contraction
time have been described as (1) contractile state of the
myocardium; (2) preload, or left ventricular end-diastolic volume or pressure; and (3) afterload, or aortic
impedance.3vsContractile state of the right ventricular
myocardium is difficult to assess;however, none of our
patients demonstrated clinical findings of right heart
failure at the time of study. Until further data regarding
the effect of right ventricular myocardial contractility
on right ventricular isovolumic contraction time are
available, we believe that any attempt to utilize echocardiographic systolic time intervals to assess right
ventricular afterload (pulmonary vascular resistance)
in patients in whom right heart failure is suspected
should be viewed with extreme caution. Similarly, the
effects of preload on the isovolumic contraction time
were not evaluated in our study; however, right ventricular end-diastolic pressure was less than 10 mm Hg
in all patients in whom this measurementwas available.
Despite the potential effect of these factors, our study
demonstrates that right ventricular isovolumic contraction time, determined echographically, is significantly affected by right ventricularafterload in patients
with a wide variety of congenital heart defects.
Volume 41
ECHOCARDIOGRAM
Implications: Much additional work is necessary to
define more completely factors that can influence right
ventricular isovolumic contraction time. Our study may
provide an accurate reproducible method of noninvasively defining this interval. In our patient group,
marked prolongation of the interval was consistent with
the presence of pulmonary hypertension, and this correlation was not affected by the presence of complete
right bundle branch block. The serial evaluation of the
interval would appear to afford a reasonably accurate
IN COMPLETE RIGHT BUNDLE BRANCH BLOCK-JOHNSON
ET AL.
assessment of the pulmonary vascular bed in selected
pediatric patients, particularly those with conduction
abnormalities that preclude use of the right ventricular
preejection period to right ventricular ejection time
ratio. As further experience is gained, serial echographic
assessment of right ventricular isovolumic contraction
time should enhance the clinical management and reduce the need for repeated cardiac catheterization
in
many children prone to develop hypertensive pulmonary vascular disease.
References
1. Hlrschfeld S, Meyer R, Schwartz DC, et al: Measurement of right
and left systolic time intervals by echocardiography. Circulation
51:304-309,1975
2. Hlrschfeld S, Meyer R, Schwartz DC, et al: The echocerdiographic
assessment of pulmonary artery pressure and pulmonary vascular
resistance. Circulation 52642-650,
1975
3. Welaaler AM, Lewis RP, Lelghtcn RF: The systolic time intervals
as a measure of left ventricular performance in man. In, Progress
in Cardiology, Vol 1 (Vu PN, Goodwin JF, ed). Philadelphia, Lea &
Feblger, 1972, p 155
4. Spcdlck SH, Kuman S: lsovolumic contraction period of the left
ventricle. Am Heart J 76:498-503, 1968
5.
6urggrafGW, Cralge E: The
YgF
first heart sound in complete heart
phono-echocardlographic correlations. Circulation 50: 17-24,
6. Walder W, Cralge E: The first heart soundand ejection sounds:
echo-phonocardlographic correlation with valvular events. Am J
Cardiol35:346-356,
1975
7. Mllner S, Meyer RA, VenablesAW, et al: Mitral and tricuspid valve
closure in congenital heart disease. Circulation 53513-518.
1976
8. Wallace AG, MitchellJH, Skinner NS, et al: Duration of the phases
of left ventricular systole. Circ Res 12:6 1 l-6 19, 1963
June 1978
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