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CIRCULATION
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Echocardiographic Measurement
of Right Ventricular Wall Thickness
A New Application of Subxiphoid Echocardiography
HARUO MATSUKUBO, M.D., TOHRU MATSUURA, M.D., NAOTO ENDO, M.D.,
JUN ASAYAMA, M.D., TOSHIMITSU WATANABE, M.D., KEIZO FURUKAWA, M.D.,
HIROSHI KUNISHIGE, M.D., HIROSHI KATSUME, M.D., AND HAMAO IJICHI, M.D.
SUMMARY The feasibility of subxiphoid echocardiography to
measure the thickness of the right ventricular wall (RVWT) was investigated. In 87 (90.6%) of the 96 patients studied, adequate
visualization of the echoes from the right ventricular wall was obtained using the subxiphoid technique.
RVWT averaged 0.34 ± 0.08 cm (mean ± 1 SD), ranging from
0.2 to 0.5 cm in 25 normal individuals. This was not significantly
different from the values in the left ventricular overload group
(0.36 ± 0.10 cm). However, the RVWT was increased significantly
(P < 0.001) in the combined group (0.62 ± 0.18 cm), the right ventricular (RV) pressure overload group (0.60 ± 0.13 cm) and the RV
volume overload group (0.53 ± 0.11 cm).
Thirty-two patients underwent diagnostic right heart catheterization which revealed a good correlation between the RVWT
measured echocardiographically and the right ventricular peak
systolic pressure (r = 0.84).
Subxiphoid echocardiography was considered to be useful in
diagnosing right ventricular hypertrophy in adults.
THE RECENT DEVELOPMENT AND IMPROVEMENT of echocardiographic instruments has facilitated
noninvasive assessment of cardiac function and evaluation of
anatomical abnormalities of the heart. One of the most important achievements has been echocardiographic assessment of the dimensions of cardiac structures.1' 2 However,
evaluation of ventricular wall thickness has been limited to
the left ventricle. Assessment of the right ventricular wall
remains outside the scope of echocardiographic study, except
in infants and young patients who have a thin chest wall,3 4
because of interference by the gaseous tissue of the lung and
because of problems due to the physical properties of ultrasound. Only the right ventricular dimension described by
Popp et al.6 was found to be a clue to the estimation of the
size of the right ventricle, the value of which increases in
patients with atrial septal defect or tricuspid insufficiency.
Chang et al.6 reported that subxiphoid echocardiography
was useful in emphysematous or aged patients for recordings
of the mitral valve and the left ventricular posterior wall. The
present study was undertaken to examine the feasibility of
echocardiographic measurement of right ventricular wall
thickness by the subxiphoid method.
From the Second Department of Internal Medicine, Kyoto Prefectural
University of Medicine, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602,
Japan.
Address for reprints: Haruo Matsukubo, M.D., The Second Department
of Internal Medicine, Kyoto Prefectural University of Medicine,
Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602, Japan.
Received November 4, 1976; revision accepted March 18, 1977.
Patients and Methods
Ninety-six patients were examined; nine were excluded
due to unsatisfactory echocardiographic visualization of the
right ventricular wall. The clinical data of the remaining 87
patients are summarized in table 1. The patients were divided
into four groups: normal, left ventricular overload, combined, and right ventricular overload. The normal group included 25 patients with no evidence of cardiopulmonary disorders. There were 15 males and 10 females ranging in age
from 17 to 58 years (mean 32.9 years). The left ventricular
(LV) overload group included 15 males and seven females
aged 20-77 years (mean 56.4 years). The combined group
ECHO OF RV WALL THICKNESS/Matsukubo et al.
279
TABLE 1. Clinical Data
Group
Normal
No.
Age
mean ± 1 SD
(range)
25
32.9
LV overload
22
Combined
18
RV overload
22
=
11.5
(17-58)
56.4 A= 16.5
(20-77)
45.9 15.7
(24-70)
40.5 - 12.6
(10-70)
z
Sex
male:female
15:10
15:7
4:14
7:15
BSA (m2)
mean :4 1 SD
(range)
1.55
=
Diagnosis
0.15
(1.27-1.81)
1.57 = 0.18
(1.26-1.81)
1.44 = 0.14
(1.09-1.61)
1.49 A 0.22
(1.25-2.09)
Hypertension: 18, AS: 1,
ASI: 2, Aortitis: 1
MS+AI: 9, MS+ASI: 1, MSI: 2,
VSD: 3, COLD: 3
ASD: 10, TI: 2, MS: 9,
VSD+PS: 1
Abbreviations: LV = left ventricular; RV = right ventricular; AS = aortic stenosis; AI = aortic insufficiency; ASI = mixed
aortic stenosis and insufficiency; MS = mitral stenosis; MSI = mixed mitral stenosis and insufficiency; VSD = ventricular septal
defect; COLD = chronic obstructive lung disease; ASD = atrial septal defect; TI = tricuspid insufficiency; PS = pulmonary stenosis;
BD - standard deviation.
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consisted of four males and 14 females aged 24-70 years
(mean 45.9 years). The right ventricular (RV) overload
group was subdivided into two groups; RV volume overload
(12 patients) and RV pressure overload (10 patients). One
patient with pericardial effusion was also examined to confirm echoes from the endocardium and epicardium of the
right ventricular wall.
All echocardiograms were done with an Aloka SSD-90
using a 2.25 MHz, 10 mm diameter transducer. They were
recorded on a strip chart recorder at 50 or 100 mm/sec with
simultaneous recordings of the electrocardiogram and
phonocardiogram.
For estimation of the right ventricular dimension (RVD),
and the thickness of the left ventricular posterior wall
(LVPWT) and interventricular septum (IVST), the transducer was placed at the left fourth intercostal space and
angled inferiorly and laterally until a satisfactory echocardiogram could be recorded according to the standard
method of Popp et al.6
Echocardiographic visualization of the right ventricular
wall was accomplished by placing the transducer in the subxiphoid region and directing it superiorly and laterally
toward the heart (fig. 1). The interventricular septum was
easily visualized but the left ventricular wall and the mitral
valve could be detected less frequently. The direction of the
transducer was then carefully changed to obtain echoes from
the right ventricular wall.
The RVD was measured between the right ventricular epicardium or, if not feasible, a depth of 0.5 cm from the chest
wall and the right side of the interventricular septum. The
LVPWT was measured between the endocardium and the
epicardium of the left ventricular posterior wall. The IVST
was measured between the right and left side of the interventricular septum. The RVWT was measured between the
epicardium and the endocardium of the right ventricular
wall. All measurements were made at the peak of the R wave
of the electrocardiograms.
IVST in all patients but one who had atrial septal defect.
Echocardiographic measurements of this patient were made
with the subxiphoid technique alone.
An M-mode scan with the transducer placed in the subxiphoid region and scanned from the base to the apex of the
heart is useful to the examiner in interpreting subxiphoid
echocardiograms and in determining the correct direction of
the transducer for measurement of the RVWT. As seen in
figure 2, the left two-thirds of the tracing where the tricuspid
valve leaflets or the chordae tendineae attached to them can
be visualized, are suitable for measurement of the RVWT.
The echo beam passes through the right ventricular wall
obliquely and the papillary muscles (arrow) can be visualized
in the right one-third.
Figure 3 is a subxiphoid echocardiogram obtained from a
Results
Of the 96 patients examined, adequate visualization of the
right ventricular wall was possible in 87 (90.6%) patients. Of
the nine patients in whom visualization was unsatisfactory,
three had mitral stenosis and six were normal. All of them
were young and cardiac enlargement was mild or absent.
Echocardiograms obtained by the standard method were
available for measuring the RVD, the LVPWT, and the
FIGURE 1. The anterior aspect of the heart and the direction of
the transducer are shown. The echo beam passes through the abdominal wall, the wall of the right ventricular inflow tract and the
interventricular septum and then traverses the left ventricle.
280
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FIGURE 2. An M-mode scan with the subxiphoid- technique. Scan was performed by directing the transducer
superiorly and to the left laterally. Measurement of the thickness of the right ventricular wall should be made where the
tricuspid valve ( TV) or the chordae tendineae are visualized (left two-thirds of the tracing). Ifmeasured on the right onethird of the tracing. the presence of the echoes from the papillary m uscle (arrow) and the obliq ue passage of the echo
beam cause an erroneous measurement. IVS
interventricular septum; MV = mitral valve; L VW left ventricular
wall; R VW = right ventricular wall.
=
patient in the normal group (the right ventricular peak
systolic pressure was 25 mm Hg). The right ventricular wall
is seen below the thick multiple echoes originating from the
abdominal wall and moves slowly toward the transducer during ventricular diastole and away from the transducer during
systole. The left ventricular wall moves toward the transducer during ventricular systole. The interventricular septum
moves toward the left ventricular wall during systole and
reverses the direction of its motion during diastole as seen in
an echocardiogram using the standard method. The RVWT
of this patient was 0.4 cm.
Figure 4 shows a subxiphoid echocardiogram from a
£
fta
Ta
ical septal motion). The RVWT of this patient was 0.4 cm.
A subxiphoid echocardiogram obtained from a patient
with PS associated with VSD with a right ventricular peak
systolic pressure of 74 mm Hg is shown in figure 5. The right
ventricular wall had thickened to an estimated 0.9 cm.
Figure 6 shows a standard M-mode scan of a patient with
pericardial effusion of long duration. An echo-free space is
clearly shown behind the left ventricular posterior wall. The
right ventricular wall could not be visualized clearly in this
RVWT 0.4
Epi.
End.
_r_
MMWANNOO
~
patient with ASD. The motion of the interventricular septum
is in a direction opposite to that of the right ventricular wall
and parallels the motion of the left ventricular wall (paradox-
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.-_-po
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FIGURE 3. A subxiphoid echocardiogram obtainedfrom a healthy subject. The right ventricular wall moves toward
the transducer gradually during ventricular diastole until the P wave of the electrocardiogram. There is a more abrupt
motion toward the transducer during the P-R interval. Shortly after the R wave, the right ventricular wall begins to
move away from the transducer or toward the left ventricular wall which moves in a direction opposite to the right ventricular wall. After the maximum movement away from the transducer before the second heart sound of the phonocardiogram. the right ventricular wall moves in an opposite direction toward the transducer. The motion of the interventricular septum shows a similar pattern to that of the right ventricular wall although it i.s more complex. The right
ventricular peak systolic pressure was 25 mm Hg and the R VWT was measured as 0.4 cm. ECG electrocardiogram:
PCG phonocardiogram; Epi epicardium; End endocardium; R VWT= thickness of the right ventricular wall.
ECHO OF RV WALL THICKNESS/Matsukubo et al.
281
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RVWT0.9
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_
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FIGURE 4. A subxiphoid echocardiogram obtained from a
patient with atrial septal defect. The interventricular septum moves
paradoxically. The patterns of motion of the right ventricular wall
and the left ventricular wall do not differ from the pattern in the
healthy subject in figure 3. Therefore, the right ventricular cavity is
dilated more rapidly during ventricular diastole. The R VWT was
measured as 0.4 cm.
tracing but became clearer when the transducer was angled
more accurately, as is experienced often in pericardial effusion (fig. 7A). Figure 7B is a subxiphoid echocardiogram
from the same patient, which clearly revealed the right ventricular wall. In both panels, the echo from the epicardium of
the right ventricular wall was denser than that from the
endocardium and the effusion fluid separated the epicardium from the pericardium throughout the whole cardiac
phase. The epicardium was visualized as a smooth echo in
figure 7A although it appeared as rough, multiple echoes in
some places in figure 7B. This is possibly due to the attachment of inflammatory products to the epicardial surface of
the inferior portion of the right ventricular wall. The RVWT
was measured as 0.6 cm in figure 7A and figure 7B.
The results of the echocardiographic measurements are
shown in table 2. In the normal group, the mean RVWT was
0.34 + 0.08 cm (mean ± ISD) and was not significantly
different from that in the LV overload group (0.36 ± 0.10
cm). The combined group, the RV pressure overload group
and the RV volume overload group had increased RVWT
values. They were 0.62 ± 0.18 cm, 0.60 + 0.13 cm, and
0.53 ± 0.11 cm, respectively. For the RVD index (calculated
from the RVD divided by the body surface area), the mean
value in the normal group was 0.96 ± 0.27 Cm/M2. Only the
RV volume overload group showed an increased mean value
(2.49 + 0.67 cm/M2). The remaining groups had normal or
slightly increased values. The LVPWT was 0.78 ± 0.10 cm
in the normal group and was increased significantly only in
the LV overload group (1.16 ± 0.30 cm). The IVST was
0.82 ± 0.12 cm in the normal group and was also increased
significantly in the LV overload group (1.18 + 0.32 cm). The
ratios of RVWT/LVPWT were calculated. The ratio was
0.44 ± 0.12 for the normal group and 0.33 ± 0.10 for the LV
overload group. The ratios for the other three groups were
increased but there were no significant differences among
them.
Of the patients studied, 32 underwent diagnostic right
heart catheterization within one month before or after the
FI GURE 5. A thicken ed righ t ven tricular wall is no ted in a pa tien t
with pulmonary stenosis associated with ventricular septal defect
(R V WT 0.9 c m). Th e righ t ven tric ular p eak sys tolic p ress ure was
74 mm Hg. The echoes fromn the interventricular septum are not
visualized clearly in the direction of the echo beam in this tracing.
echocardiographic examinations. The RVWT was
significantly correlated with the right ventricular peak
systolic pressure (r = 0.84) as seen in figure 8.
Discussion
Echocardiographic measurements of the size of cardiac
structures such as the left atrial dimension,7 the left ventricular internal dimension' 8 9 and the thickness of the left ventricular posterior wall" 10, 11 have been reported by many investigators, and their accuracy has been confirmed by
angiography2 or at surgery.1 However, echocardiographic estimation of the thickness of the right ventricular wall has not
$,I
4
S
a
FIGURE 6. A standard M-mode scan obtained from a patient
with pericardial effusion. Echo-free spaces are present behind the
left ventricular posterior wall and in front of the right ventricular
anterior wall. S Echo-free space due to effusion fluid;
RVA W = Right ventricular anterior wall; LVPW = Left ventricular posterior wall.
VOL 56, No 2, AUGUST 1977
CI RCULATION
282
'-A.i
-%,O
I
II
I I
_kr,.
_
,
-.--
em111S
_r
FIGURE 7. Echocardiograms obtained from the
patient as in figure 6. Panel A shows the right
ventricular wall with the standard method and panel
B shows it with the subxiphoid method. The right
ventricular wall can be detected easily with both
methods because effusion fluid separates the epicardium from the pericardium during the whole cardiac
phase. The thickness of the right ventricular wall was
measured as 0.6 cm equally with both methods. Epi
Abdominal wail
Ne;End<**
N.<
N "I *I.
;0
same
N4
; S s
Ep
Epicardium; End
Endocardium.
LV PW
I
I
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t
.
we
w
-
Rup,
-,
ular wall thickness, and the interventricular septum with the
standard and the subxiphoid techniques. They made no
reference to measuring the right ventricular wall with this
new method.
The present study indicates that the thickness of the right
ventricular wall can be measured with this method in 87 of 96
patients examined. The nine patients in whom good echocardiograms could not be obtained with the subxiphoid technique were all young and had thin thoraxes with no cardiac
enlargement or had a tight abdominal wall as experienced by
Chang et al.t'
Identification of the epicardium and endocardium of the
right ventricular wall was easier with the subxiphoid technique than with the standard technique. If good visualization
of echoes from the right ventricular wall using the standard
technique can be made, systolic separation of the epicardium from the pericardium or the chest wall should be
noticed frequently without any evidence of pericardial
effusion.'2 This finding also was observed frequently with the
subxiphoid technique, and both systolic and diastolic
separations were found in a patient with pericardial effusion.
This further supports the theory that an echo below the mul-
been documented in adults. With the standard technique,
that is, with the transducer positioned in the left fourth intercostal space, successful echocardiographic recording of the
right ventricular wall has been disappointing in most adult
patients, especially those with pulmonary emphysema. There
are several reasons for this. The most important one is that
with age the lung overinflates into the space between the
chest wall and the heart, thus interfering with the penetration
of the echo beam. Another reason is that multiple echoes
from the chest wall are usually denser than the echo from the
epicardium; thus, distinguishing between them is often
difficult even with careful adjustment of near gain. Even if
these difficulties are overcome, the echoes from the right ventricular wall often interfere with the chest wall echoes and
measurement of the thickness of the right ventricular wall
results in a lower value.
Chang et al.P found that in emphysematous or aged
patients detection of the heart valves and visualization of the
left ventricular wall became easier when the transducer was
in the subxiphoid region and there was little or no interference by the lung. They also noted comparable
measurements of left ventricular dimensions, left ventricTABLE 2. Echocardiographic Data
Group
Normal
No.
25
LV overload
22
Combined
18
RV volume
overload
12
RV pressure
10
RVDI (cm/m2)
0.27t
(0.60-1.71):
0.96
-
0.25
(0.66-1.51)
1.10 d4 0.31
(0.65-1.84)
2.49 - 0.67*
1.04
-
(1.54-3.96)
1.02 4 0.28
(0.67-1.46)
overload
*Significantly different from the normal group (P
RVWT (cm)
0.08
0.34
a-
IVST (cm)
0.78 fi- 0.10
0.82 =i 0.12
(0.6-1.0)
(0.2-0.5)
0.36
LVPWT (cm)
0.10
1.16
(0.2-0.5)
i
0.30*
(0.8-2.0)
(0.6-1.1)
1.18 - 0.32*
(0.8 1.9)
0.91 =* 0.21
0.62 =i 0.18*
0.91
(0.4-1.2)
0.53 0.11*
0.84 i 0.22
0.85
0.13*
0.60
(0.4-0.9)
0.84
(0.5-1.6)
0.22
(0.5 1.6)
0.85
(0.4-0.7)
-
0.21
(0.7-1.3)
(0.7-1.3)
0.19
(0.6-1.4)
,
0.19
(0.6-1.4)
RVWT/LVPWT
0.44 - 0.12
(0.22-0.67)
0.33 ) 0.10
(0.13-0.50)
0.70 * 0.23*
(0.40-1.33)
0.71 , 0.30*
(0.25 -1.40)
0.74 - 0.18*
(0.45-1.13)
<0.001).
tMean ± 1 SD.
$Range.
Abbreviations: RVDI - right ventricular dimension index; RVWT
thickness of the right ventricular wall; LVPWT
ness of the left ventricular posterior wall; IVST
thickness of the interventricular septum.
=
=
=
thick-
ECHO OF RV WALL THICKNESS/Matsukubo et al.
RVWT
(cm)
N =
32
r =
0.84
283
volume overload had increased mean values of both right
ventricular wall thickness and right ventricular dimension index. This is considered to be due partly to secondary
pulmonary hypertension, as shown in the good correlation
between right ventricular wall thickness and right ventricular peak systolic pressure. Diamond et al.1 observed an increased right ventricular dimension index in patients with
right ventricular volume overload, such as atrial septal defect
or tricuspid insufficiency. But investigations concerning the
thickness of the right ventricular wall have not been
reported. In order to make a diagnosis of right ventricular
hypertrophy, it is necessary to know the right ventricular
wall thickness as well as the size of the right ventricular
cavity. The present study indicates that subxiphoid echocardiography provides adequate visualization of echoes from
the right ventricular wall facilitating the measurement of its
thickness.
1.0
0
Other Echocardiographic Measurements
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50
100
RVPSP (mmBg)
FIGURE 8. Correlation between the right ventricular peak
systolic pressure (RVPSP) and the thickness of the right ventricular wall (R VWT).
tiple echoes from the abdominal wall originates from the epicardium. Moreover, echoes originating from the abdominal
wall are not so dense as those from the right ventricular wall
and the depth at which echoes from the right ventricular wall
could be visualized using the subxiphoid technique ranged
from 2 to 8 cm from the transducer, but is less than 2 cm in
depth with the standard technique. In the present study the
mean value was 5 cm. Therefore, gain control could be done
more easily to obtain an echo from the epicardium of the
right ventricular wall. Identification of the endocardium is
also difficult with the standard technique because of a narrow
window through which the right ventricular wall can be
detected and because of a weaker echo than that originating
from the epicardium causing difficulties in the adjustment of
gain or output. By the subxiphoid technique, the window is
wide enough that an M-mode scan may be performed if
necessary to obtain satisfactory echo from the endocardium. Moreover, gain adjustment is easier at a greater
depth and the epicardium can be recorded without interference from the echoes from the chest wall or the abdominal surface.
The Thickness of the Right Ventricular Wall
In the present study the average normal value of the right
ventricular wall thickness was 0.34 cm. This was not so
different from the values in neonates using the standard technique.8' 4 18 The right ventricular wall was shown to increase
in thickness in patients with right ventricular pressure overload without significant increases in the right ventricular
dimension index. However, patients with right ventricular
The thickness of the left ventricular posterior wall and that
of the interventricular septum were increased only in patients
with left ventricular overload. But the thickness of the left
ventricular posterior wall exceeded 1.2 cm in two patients
with right ventricular overload; one with atrial septal defect
and the other with mitral stenosis. Neither showed any
evidence suggesting associated abnormalities causing left
ventricular hypertrophy. The patient with atrial septal defect
was 70 years old and the echocardiographic examination
could be made only with the subxiphoid technique. The other
was also an aged patient and had frequent episodes of
chronic bronchitis. Therefore, chronic hypoxemia due to
respiratory disorders may be a cause of the increased
thickness of the left ventricular wall secondary to left ventricular dysfunction although the possibility of mistaking
papillary muscle echoes for the endocardium cannot be
eliminated completely.
Critiques of the Subxiphoid Method
Two problems should be considered in applying this
method to evaluate right ventricular hypertrophy. In the Mmode scan the right ventricular wall appears to increase in
thickness from the base to the apex because of visualization
of the papillary muscles and the oblique passage of the echo
beam. An erroneous measurement can result if the thickness
of the right ventricular wall is measured near the apex. Thus
a criterion to determine the proper site for this measurement
is necessary. In the present study, the direction of the transducer was set so as to visualize echoes from the tricuspid
valve or the chordae tendineae attached to it in the same
manner as the thickness of the left ventricular posterior wall
is measured, because at such a location the right ventricular
wall is uniform in its thickness and the endocardium is easily
distinguished from the chordae tendineae.
The other problem is that when the transducer is placed in
the subxiphoid region, the echo beam transects the portion of
the wall of the right ventricular inflow tract. In the course of
right ventricular hypertrophy, the wall of the outflow tract or
the parts around the crista supraventricularis hypertrophies
first, especially in patients with right ventricular pressure
overload; these hypertrophic changes subsequently extend to
CIRCULATION
284
the other parts of the right ventricular wall. Hence, estimation of the thickness only of the wall of the right ventricular
inflow tract may not be accurate enough for diagnosis of
early stage right ventricular hypertrophy. But even if this is
the case, right ventricular wall thickness in the present study
was closely correlated with right ventricular peak systolic
pressure which could not be measured in most adult patients
using the standard method, but which could be measured
easily with the subxiphoid technique.
References
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4. Hagan AD, Deely WJ, Sahn DJ, Friedman WF: Echocardiographic
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The Effect of Propranolol
Canine Myocardial CPK Distribution Space
and Rate of Disappearance
JOHN A. CAIRNS, M.D., F.R.C.P.(C),
AND
GERALD A. KLASSEN, M.D., F R.C.P., (C)
SUMMARY Canine myocardial CPK was partially purified and
injected into 11 conscious mongrel dogs. From serial serum CPK
measurements in each dog, mean Kd was calculated as
0.0047 ± 0.0009 (±SD) mIinm. Correlation coefficients indicated
that CPK disappearance rate was well described by a single exponential expression. Kd measured on consecutive days in four dogs
varied minimally. CPK distribution space ranged from 74 to 134% of
plasma volume. Propranolol loading with 0.3 mg/kg or 2 mg/kg,
followed by hourly maintenance doses, resulted in increased Kd in
eight of ten dogs, mean Kd rising from .0048 min-' to .0059 min-'
(P < 0.02). Propranolol appeared to increase plasma volume but
had no significant effect on the relationship of CPK distribution
space to plasma volume. If the serial CPK technique were used to
measure infarct size, using an average Kd, propranolol might
produce artifactual reduction of infarct size measurement by increasing Kd and possibly by increasing plasma volume. The obligation to assess the effect upon CPK Kd and distribution space of an
agent designed to limit infarct size is apparent.
SOBEL AND SHELL have described a technique for estimating the depletion of myocardial creatine phosphokinase (CPK) occurring in the course of acute myocardial infarction.'-5 The technique is based on the kinetics of the CPK
released by the damaged tissue. The estimate of myocardial
CPK depletion is dependent on the use of an appropriate
parameter characterizing CPK disappearance from the
vascular compartment and verification that a valid approximation of the parameter can be obtained in order to
calculate aggregate release of CPK from serial serum CPK
values. The CPK disappearance from the vascular compart-
ment (Kd) has been found to be monoexponential.8 The
aggregate release is assumed to have a constant relationship
to the amount of myocardium damaged. An attempt has
been made to express the extent of myocardial damage quantitatively as infarct size." s Interventions designed to modify
infarct size are assumed not to alter the variables which
relate the serial serum CPK values to the amount of
damaged myocardium. Recently, Sobel et al.' have used the
initial portion of the serial serum CPK curve to predict the
entire curve. The effect of a therapeutic intervention initiated
after the first few hours of CPK rise is then assessed by comparison of the actual to the predicted aggregate CPK release
curve.
The purpose of our study was to re-examine the original
observations of CPK disappearance rate (Kd) and distribution space, the variability of Kd in the same animal and
between animals, and the effect of CPK Kd and distribution
space of propranolol, a drug known to have an effect on the
process of myocardial infarction in the dog.2
From the Cardiovascular Division, McGill University Clinic, Royal Victoria Hospital, Montreal, Quebec.
Supported by grants from the Medical Research Council of Canada (MT3238), Ayerst Laboratories, Montreal, and the Joseph Edwards Foundation.
Address for reprints: John A. Cairns, M.D., Division of Cardiology,
McMaster University Medical Centre, 1200 Main Street West, Hamilton,
Ontario L8S 4J9, Canada.
Received September 15, 1975; revision accepted February 10, 1977.
Echocardiographic measurement of right ventricular wall thickness. A new application of
subxiphoid echocardiography.
H Matsukubo, T Matsuura, N Endo, J Asayama and T Watanabe
Downloaded from http://circ.ahajournals.org/ by guest on April 29, 2017
Circulation. 1977;56:278-284
doi: 10.1161/01.CIR.56.2.278
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1977 American Heart Association, Inc. All rights reserved.
Print ISSN: 0009-7322. Online ISSN: 1524-4539
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