Download Influence of Right Ventricular Filling Pressure on Left Ventricular

Influence of Right Ventricular Filling Pressure on Left Ventricular
Pressure and Dimension
By Charles E. Bemis, Juan R. Serur, David Borkenhagen, Edmund H. Sonnenblick, and
Charles W.Urschel
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ABSTRACT
The effects of alterations in the diastolic filling pressure of the right ventricle on left
ventricular (LV) geometry and filling pressure were studied in six isolated, supported
canine hearts. This experimental preparation permitted graded increments in right
ventricular (RV) end-diastolic pressure while LV cardiac output, heart rate, and mean
aortic pressure were held constant. Endocardial radiopaque markers were placed in the
ventricular septum, the anterior wall, the posterior wall, and the free wall in a plane perpendicular to the aortoapical axis. LV end-diastolic dimensions were recorded by x-ray
cinematography at 60 frames/sec. The effects of varied RV end-diastolic pressure (0-16
mm Hg) on LV end-diastolic pressure and dimensions were studied at several LV cardiac
outputs (780-2880 ml/min) and at several initial LV end-diastolic pressures (1-18 mm
Hg). Increments of 5 mm Hg in RV end-diastolic pressure increased LV end-diastolic
pressure 2.3 mm Hg. The septum-to-free wall distance decreased by 4.5% from the control distance, but the anterior-to-posterior dimension increased by 4.4%.Thus, LV enddiastolic pressure and LV end-diastolic dimensions were significantly related to RV enddiastolic pressure; LV end-diastolic geometry was increasingly distorted at elevated RV
end-diastolic pressure. These data suggest that the high RV filling pressures that characterize certain diseases can secondarily alter LV filling pressures and geometry.
KEY WORDS
ventricular compliance
ventricular diastolic geometry ventricular interaction
x-ray cinematography
radiopaque makers
• In the absence of factors which alter compliance
such as incomplete ventricular relaxation, stress
relaxation, or hypertrophy, left ventricular (LV)
end-diastolic pressure is a direct function of enddiastolic volume. Accordingly, ventricular enddiastolic pressure has been used as an index of enddiastolic volume, and the relation of stroke volume
or work to end-diastolic pressure has been used extensively to quantify ventricular performance. In
addition to the factors intrinsic to the left ventricle
that alter compliance, the LV pressure-volume relationship is influenced by the filling of the right
ventricle both in vivo and in the postmortem heart
(1-6). Furthermore, during experimental diastolic
From the Cardiovascular Division, Department of Medicine,
The Peter Bent Brigham Hospital and Harvard Medical School,
Boston, Massachusetts 02115.
This work was supported in part by U. S. Public Health Service Grants HL 11306 and HL 05890 from the National Heart
and Lung Institute and by U. S. Army Contract DADA 17-67C-7164.
Please address reprint requests to Charles W. Urschel, M.D.,
Department of Physiology, University of South Alabama,
Mobile, Alabama 36688.
Received January 15, 1973. Accepted for publication January 15, 1974.
498
pressure-volume relation
isolated, supported heart,
overloading of the right ventricle, LV function is
reduced relative to LV end-diastolic pressure (3,
4). Finally, during clinical overloading of the right
ventricle, LV end-diastolic pressure is elevated in
the absence of overt LV disease (7, 8).
Although the previous studies demonstrate that
LV compliance or function is apparently altered by
right ventricular (RV) diastolic overload, it is not
clear whether interaction occurs at physiological
ventricular pressures. It is also unclear whether
concomitant changes in LV geometry occur. Significant alterations in ventricular shape may further
alter ventricular performance and affect calculations of the stress-strain distribution in the ventricular wall.
In the present study LV filling pressures were
measured independent of reflex and humoral factors, because cardiac output, heart rate, mean aortic pressure, and RV filling pressure were controlled.
Methods
Data were obtained from six isolated hearts obtained
from mongrel dogs (22-25 kg). The dogs were anesthetized with sodium pentobarbital (25-30 mg/kg, iv),
intubated, and mechanically ventilated with room air.
Support dogs (average 25 kg) were similarly anCirculation Research, VoL XXXIV, April 1974
DIASTOLIC VENTRICULAR INTERACTION
IVCIKUIT
499
dium was incised at the base and pulled back; the sinus
node was crushed and pacing wires from a Grass stimulator were attached to the right atrium. Endocardial and
epicardial markers were then positioned as described in
the following sections. The pericardium was closed
without overlap using loose sutures. The heart was then
connected to the external hydraulic circuits.
The cardiac output of each ventricle was controlled
by a separate circuit.
LEFT VENTRICLE
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FIGURE 1
Isolated heart preparation. Arterial blood was supplied to the
left ventricular (L V) circuit reservoir from a support dog with a
return of excess blood to the femoral veins of the same dog. A
constant venous return to the left atrium was supplied by a
siphon draining a constant-height reservoir. This output was
easily regulated by altering the height (hi). The siphon drained
into a reservoir connected to the left atrium. In any steady-state
condition, the LV cardiac output was constant and equaled the
input from the siphon. The left atrial pressure (h2) varied according to the ventricular compliance and contractility. LV
afterload was controlled by a clamp on the aorta (Ci). Both aortic (AoP) and ventricular pressures (LVP) were measured.
Right ventricular (RV) pressure and cardiac output were regulated by the height of the reservoir in the RV circuit and by the
clamps on the pulmonary artery (C3) and right atrial inflow
(C2). The pericardium was intact (broken line), and the entire
preparation was placed beneath the image tube of a 60-framesl
sec cinematograph.
esthetized and ventilated. Both femoral arteries and
veins of the support dogs were cannulated to provide arterial blood for and to receive deoxygenated blood from
the isolated heart. Figure 1 illustrates the experimental
preparation. The sternum of the donor dog was
removed, and the innominate artery was cannulated
with large-bore Tygon tubing. The right ventricle was
cannulated via the superior vena cava to drain venous
return to the support dog. The major veins and arteries
were isolated and tied.
The donor dog was allowed to bleed rapidly into a
reservoir connected to the innominate cannula until
mean arterial blood pressure fell to 40-50 mm Hg. This
procedure required 1-3 minutes. The aorta was then
clamped distal to the first four or five intercostal arteries, which were ligated, and the heart was perfused
through the innominate cannula with arterial blood from
the support dog. The heart was then dissected free from
the lungs and mediastinum; the pericardium and the
descending aorta were left intact to the midthoracic
level. After the heart had been removed, the pericarCirculatton Research, Vol. XXXIV, April 1974
A siphon from a constant-height reservoir provided a
constant venous return to the left ventricle (Fig. 1). The
siphon drained into a left atrial reservoir and then into
the left atrium. Thus, the flow of blood into the atrial
reservoir was constant, and, except for brief transients, a
constant LV output was guaranteed, but atrial and LV
end-diastolic pressures were allowed to vary. The left
ventricle ejected normally into the residual aortic segment; the blood returned to the main reservoir through
a variable resistance. Mean aortic pressure was controlled by a clamp; the blood level in the main reservoir
was maintained constant by allowing the overflow to return to the support dog.
RIGHT VENTRICLE
The right atrium and the pulmonary artery were connected to a second reservoir set at a constant height. RV
end-diastolic filling was varied either by changing the
height of the reservoir or by changing RV outflow resistance. The overflow from the RV reservoir which comprised the coronary sinus flow was returned to the support dog.
PRESSURE MEASUREMENTS
Pressures were measured by short, wide-bore metal
cannulas placed in the apex of the left ventricle, the free
wall of the right ventricle, and the left subclavian artery. Pressures were measured with Statham P23Db
transducers and recorded on a multichannel recorder at
100 mm/sec. The cinematographic film and the paper
recordings were simultaneously marked by striking the
heart with a hemostat. The time of contact was localized
to within 1 frame on the film and to ± 5 msec from the
pressure artifact. The apical cannula also provided a
degree of fixation for the apex and ensured that the long
axis of the ventricle remained parallel to the x-ray beam.
VENTRICULOQRAPHIC MEASUREMENTS
The isolated heart was placed under a 9-inch image
intensifier (General Electric) with the plane of the atrioventricular groove perpendicular to the x-ray beam.
The shutters were positioned to use the center 4 x 4 inch field. The motion and relative position of the
markers were filmed on 16-mm film (Kodak double X) at
60 frames/sec while simultaneous pressure recordings
were made.
PLACEMENT OF MARKERS
Figure 2 schematically illustrates the position of the
markers in the heart.
The surgeon placed his finger into the left ventricle
through a purse-string incision in the left atrial appendage. Care was taken not to introduce air into the
500
BEMIS, SERUR, BORKENHAQEN, SONNENBLICK, URSCHEL
ing each experiment by filming a 10-cm2 grid with grid
lines every 1 cm. The grid was placed at each endocardial marker in the plane of the marker. A correction factor was derived from the average of ten measurements
in each directon.
EXPERIMENTAL PROTOCOL
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FIGURE 2
Schematic representation of the positions of the endocardial
markers. Four markers were routinely placed on the endocardial surface of the LV chamber.
ventricular cavity. By palpation, a spot between the papillary muscles was chosen, and the LV wall was then
pierced from the outside with a 0.038-inch Seldinger
wire directed toward the finger in the ventricle. The end
of the wire was then brought out retrograde across the
mitral valve following the finger and out the atrial appendage. Silastic tubing (1 mm in diameter) attached to
a steel marker was tied to the wire and pulled back
through the left atrium and the left ventricle so that it
extended through the wall of the ventricle to the epicardial surface. Palpation ensured that the marker in the
ventricle was firmly against the endocardium and not
trapped in the chordae tendinae or in the trabeculae. A
second marker was then attached to the tubing on the
epicardial surface with sufficient tension in the tubing to
hold both markers firmly against their respective surfaces. Coronary arteries were carefully avoided in this
process. The septal marker was placed in a similar manner by retracting the RV free wall and tricuspid valve
downward to permit visualization of the septum for insertion of the wire into the left ventricle. The plane of
the endocardial markers was perpendicular to the long
axis of the left ventricle and about 2 cm below the atrioventricular groove. Markers were placed on the septum,
the free wall between the papillary muscle, the anterior surface, and the posterior surface. Alignment of
the markers was ensured by careful placement of the
punctures in the ventricular wall. These points were
carefully lined up in the same plane. In addition, marker
position was confirmed following the experiment; one
experiment was discarded because the markers were not
firmly against the endocardium. Marker positions were
measured following filming with a Vanguard analyzer.
Four measurements of each marker position were made
in each of three consecutive beats; this technique
yielded a reproducibility of 0.25 mm, 0.5% of the average distance that was measured. The variability on repeated measurements was substantially less than the
smallest change observed during the experiment. The
cinematographic analysis system was calibrated follow-
Mean aortic pressure and heart rate were held constant during each experiment. Mean aortic pressure was
generally set at 80 mm Hg (range 70 to 95 mm Hg), and
heart rate ranged from 120 to 150 beats/min with atrial
pacing. Arterial blood gases and blood temperature
were periodically monitored and maintained in the
physiological range. For each experiment, LV cardiac
output and mean aortic pressure were held constant, and
the effects of both increments and decrements in RV filling were evaluated. Because LV cardiac output and
mean aortic pressure were constant, peak LV pressure
was unchanged before and after an intervention. Experiments were not analyzed if the conditions of constant
mean aortic pressure and constant LV pressure (± 2 mm
Hg) were not met. Cardiac output was controlled by the
flow of the siphon into the left atrial reservoir.
Therefore, brief transients in cardiac output occurred
during the period of readjustment to new diastolic
geometry and pressures, but these transients were not
analyzed. Following each change in RV filling, a 5minute equilibration period was observed after which
new hemodynamic and cinematographic measurements
were made. Several such experiments were performed
in each heart with constant LV output and varied RV filling.
Results
The effects of graded changes in RV pressure on
LV hemodynamics were measured during 22 experiments. These data include 62 separate changes
in RV end-diastolic pressure with LV cardiac output held constant. Figure 3 illustrates a typical ex20- ~! -
FIGURE 3
Effects of a change in right ventricular pressure (RVP) on LV
hemodynamics. At the midpoint of the tracing, RV pressure was
reduced from 40/10 to 12/0 with LV cardiac output held constant. There was a prompt fall in left ventricular end-diastolic
pressure (LVEDP) from 7.5 mm Hg to 2.5 mm Hg. Aortic
pressure (AoP) and peak left ventricular pressure (LVP) were
unchanged.
Cimilatkm Remrch, VoL XXXIV. April 1974
DIASTOLIC VENTRICULAR INTERACTION
501
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periment. The arrow indicates the reduction in RV
pressure from 40/10 to 12/0. There was a prompt
fall in LV end-diastolic pressure from 7.5 mm Hg to
2.5 mm Hg despite constant aortic pressure, peak
LV pressure, and cardiac output.
Figure 4 illustrates data from 62 changes in RV
end-diastolic pressure with LV cardiac output held
constant. The resulting regression was statistically
significant (ALV end-diastolic pressure = 0.454
[ARV end-diastolic pressure] + 0.68) (F< 0.05, r =
0.74). The change in LV end-diastolic pressure averaged 45% of the change in RV end-diastolic
pressure. Only 2 of 62 alterations in RV enddiastolic pressure resulted in an inverse or inconsistent change in LV end-diastolic pressure. The
data were obtained over a range of LV enddiastolic pressure from 0.8 mm Hg to 18.4 mm Hg
and at cardiac outputs ranging from 0.8 liters/min
to 2.9 liters/min. The slopes of the lines relating the
absolute change in LV end-diastolic pressure to
that in RV end-diastolic pressure were not different
at high and low LV end-diastolic pressures (Fig. 5).
In Figure 6, the ratio of the change in LV enddiastolic pressure to RV end-diastolic pressure was
calculated for each of the 62 changes and plotted
as a function of the LV cardiac output at the time of
the change. There was no significant correlation
between the ratio of the change in LV end-
RVEDP
mm Hg
FIGURE 5
Influence of a change in right ventricular end-diastolic pressure
(RVEDP) on left ventricular end-diastolic pressure (LVEDP).
Each set of points connected by a line is at a common LV cardiac output. The slope of the lines relating LV end-diastolic
pressure to RV end-diastolic pressure was not affected significantly by either the level ofLV end-diastolic pressure or RV
end-diastolic pressure.
a.
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2
2-
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0
2
4
A
RVEDP
6
8
10
mm Hg
FIGURE 4
Response of left ventricular end-diastolic pressure (LVEDP)
to a change in right ventricular end-diastolic pressure
(A RVEDP). Each point represents one change in RV enddiastolic pressure with LV cardiac output held constant. The
corresponding change in LV end-diastolic pressure is plotted.
The regression is significant (P< 0.05, r = 0.74). The equation
for the line is A LVEDP-0.45 (bRVEDP) + 0.68. The data
were obtained over a range ofLV cardiac output of 0.8 liters/
min to 2.9 liters/min.
Circulation Research, Vol. XXXIV, April 1974
0
a5
1-0
Cardiac Output
1-5
2.0
2.5
3^>
L/min
FIGURE 6
Influence of left ventricular cardiac output on the interaction of
left (LVEDP) and right ventricular end-diastolic pressures
(RVEDP). The ratio of the change in LV end-diastolic pressure
to the change in RV end-diastolic pressure is plottedas a function ofLV cardiac output. There was no significant trend in the
interaction of the two ventricles as cardiac output increased.
502
BEMIS, SERUR, BORKENHAGEN, SONNENBLICK, URSCHEL
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diastolic pressure to the change in RV end-diastolic
pressure with LV cardiac output over a range of 0.8
liters/min to 2.9 liters/min.
For analysis of changes in geometry, two diameters were calculated for the left ventricle. The
distances between endocardial markers on the septum and the free wall and that between the
markers on the anterior and posterior walls were
calculated for changes in RVfillingwith LV cardiac
output held constant. Figure 7 shows the average
percent change in the distance between the septum and the free wall as a function of the change in
RV end-diastolic pressure. Figure 8 illustrates the
corresponding data for the distance between anterior and posterior markers. Both distances
changed significantly with increments in RV enddiastolic pressure. The distance between the septum and the free wall decreased (percent change in
the septum-to-free wall distance = — 0.89[ARV
end-diastolic pressure] -3.78) (P<0.05, r=0.59).
The distance between the anterior and posterior
markers increased (percent change in the anteriorto-posterior distance = 0.88 [A RV end-diastolic
pressure] -0.84) (P<0.05, r=0.74). Figure 9
shows the ratio of the percent change in anteriorto-posterior distance to the change in RV enddiastolic pressure plotted as a function of cardiac
output; Figure 10 shows the ratio of the change in
septum-to-free wall distance to the change in RV
A
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RVEDP mm Hg
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FIGURE 8
Change in anterior-to-posterior distance as a function of increased right ventricular end-diastolic pressure (RVEDP). Data
were plotted for the anterior-to-posterior distance as they were
for the septum-to-free wall distance in Figure. 7. The regression
is significant at the 0.05 level and r — Q. 74. The equation for this
line is %A A-P = 0.88 (ARVEDP) -0.84.
end-diastolic pressure plotted as a function of cardiac output. There was no significant dependence
of the increment in the distance between anterior
and posterior markers on initial cardiac output, but
the decrement in the septum-to-free wall distance
definitely depended on cardiac output ([percent
Cardiac Output L/min
1.5
2.0
-10
1 ~n
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FIGURE 7
Change in the sepum-to-free wall distance as a function of increased right ventricular end-diastolic pressure (RVEDP). Each
point represents one change in RV end-diastolic pressure with
LV cardiac output held constant. The vertical axis is the corresponding change in the distance between the septal and the free
wall markers. The regression is statistically significant (P < 0.05,
r - 0.59), and the equation for the line is %A S-F —0.89
(ARVEDP) -3.8.
FIGURE 9
Influence of LV cardiac output on the degree of shape changes
seen after increases in right ventricular end-diastolic pressure
(RVEDP). The ratio of the percent change in the septum-to-free
wall distance to the change in R V end-diastolic pressure is plotted as a function ofLV cardiac output. The decrease in this distance for a given increase in RV end-diastolic pressure is significantly less at high LV cardiac output (P < 0.05, r - 0.63). The
equation for the line is (% A S-F/ARVEDP) ~1.09(LV cardiac
output) -2.79.
Circulation Research, Vol. XXXIV. April 1974
503
DIASTOLIC VENTRICULAR INTERACTION
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Cardiac Output
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FIGURE 10
Influence of left ventricular cardiac output on the degree of
shape change following increments in right ventricular enddiastolic pressure (hVEDPl The ratio of the percent change in
the anterior-to-posterior distance to the change in RV enddiastolic pressure is plotted as a function of LV cardiac output.
There is no significant correlation between the degree of shape
change in this axis with LV cardiac output.
change in the septum-to-free wall distance]/
[change in RV end-diastolic pressure] = 1.09 [LV
cardiac output] -2.79) (P<0.05, r=0.63).
Discussion
The present data demonstrate that LV enddiastolic pressure and geometry are significantly
altered by changes in the filling pressure of the
right ventricle. Although augmented RV filling
results in an apparent decrease in LV compliance,
its direct effect is to shift the interventricular septum toward the left ventricle. The result is a
decrease in the septum-to-free wall hemiaxis of the
left ventricle with a corresponding increase in the
distance between the anterior and posterior walls.
Although the magnitude of the change in shape
is small, there is a substantial change in LV filling
pressure. Since the anterior-to-posterior wall and
the septum-to-free wall distances change in opposite directions, the calculated cross-sectional
area of the ventricle does not change significantly.
Thus, the change in geometry alone does not sufficiently explain the shift in the ventricular pressurevolume relation. These data suggest, however, that
an increase in RV pressure stiffens or buttresses the
interventricular septum. The overall ventricular
pressure-volume relation is a summation of separate areas of the ventricle. An increased stiffness of
one portion of the ventricle, i.e., the septum, leads
to an apparent decline in ventricular compliance.
Circulation Research, Vol XXXIV, April 1974
Previous data (3) have suggested that RV filling
affects LV compliance only at higher levels of RV
end-diastolic pressure. The present data do not
confirm this finding but demonstrate alterations in
LV geometry and pressure by RV filling over the
entire range of RV and LV end-diastolic pressures
(Fig. 5). One possibility for this disparity is that the
pericardium was retained intact in the present
study. Several observations, however, suggested
that the observed interaction was independent of
the pericardium. First, except at the highest ventricular filling pressures, the pericardium was
slack. Second, increments in LV end-diastolic
pressure in the absence of changes in RVfillingalways substantially augmented the stroke volume. It
is generally acknowledged that, in the presence of
significant pericardial restriction, stroke volume
cannot easily be increased by increments in LV
end-diastolic pressure. Third, if the pericardium is
in fact restrictive, increments in RV filling pressure
should result in equal or larger increments in LV
filling pressure. Fourth, pericardial restriction
should enhance the degree of interaction between
the two ventricles at a high ventricular filling
pressure. However, interaction was observed over
a wide range offillingpressures with similar slopes
at high and low end-diastolic pressures (Fig. 5).
Finally, the contour of the LV pressure tracing was
consistently normal and, even at the highest filling
pressure, did not exhibit the pattern typically seen
with pericardial restriction.
Several major inferences are evident from these
data. The data confirm previous findings (1-3) that
LV end-diastolic pressure may be a misleading index of volume or function of the left ventricle when
RVfillingvaries. If a pressure-volume curve is used
to estimate LV volume, an error of 30-50% may
result from changes in RV end-diastolic pressure of
only 5 mm Hg (1). An absolute translation of the
present findings to the heart in situ is difficult, and
the variability in the changes observed precludes
use of these averages to predict precise changes in
ventricular geometry following changes in RV filling. It is interesting, however, that the interaction
observed between RV and LVfillingand geometry
occurred over a physiological range of transmural
filling pressures. Thus, there are several possible
situations in which these data may have significance.
Recently, attempts have been made to define LV
compliance for clinical use. The present data suggest that variables other than muscle compliance
affect the LV pressure-volume relation (6-8). If a
504
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similar interaction of LV and RVfillingis present in
man, then LV end-diastolic pressure and apparent
compliance will be directly affected by RV diastolic overload in the absence of LV disease. Alternatively, in the presence of severe RV distention,
an elevation in LV end-diastolic pressures does not
reflect augmented volume.
Also, attention should be focused on the use of
the ventricular function curve as an index of LV
performance. Generally, stroke volume and work
are plotted as functions of LV end-diastolic pressure. End-diastolic pressure itself is commonly
varied by volume infusion. Since volume infusion
will raise RV end-diastolic pressure as well as LV
end-diastolic pressure, a new variable is introduced
that can affect the relation between LV enddiastolic pressure and stroke volume or work.
The present data describe only the diastolic
geometry of the left ventricle. It is not possible to
predict specific patterns by which an alteration in
diastolic geometry will affect the subsequent contraction. Data from Kelly and co-workers (4) suggest that LV peak dP/dt and peak contractile element velocity are depressed in the presence of RV
diastolic overload, even after a correction is made
for the apparent change in compliance. It is attractive to postulate that this decline in peak dP/dt
directly reflects impaired ventricular performance
resulting from the altered geometry.
The present data illustrate that LV end-diastolic
BEMIS, SERUR, BORKENHAGEN, SONNENBLICK, URSCHEL
pressure and geometry are affected by the dynamic
interaction of the two ventricles. This interaction
complicates the analysis of data based on ventricular end-diastolic pressure and compliance and
emphasizes the need for caution in the interpretation of such data.
References
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JR.: Dependence of ventricular distensibility onfillingof
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MOULOPOULOS, S.D., SAHCAS, A., STAMATELOPOULOS, S., AND
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KELLY, D.T., SPOTNITZ, H.M., BEISER, G.D., PIERCE, J.E., AND
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TAQUINI, A., FERMOSO, I., AND ARAMENDIA, P.: Behavior of the
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7. HERBERT, W.H., AND YELLIN, E.: Left ventricular diastolic
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Circulation 40:887-892,1969.
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RAO, B.S., COHN, K.E., ELDRIDGE, F.L., AND HANCOCK, E.W.:
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Circulation Research, VoL XXXIV, April 1974
Influence of Right Ventricular Filling Pressure on Left Ventricular Pressure and Dimension
CHARLES E. BEMIS, JUAN R. SERUR, DAVID BORKENHAGEN, EDMUND H.
SONNENBLICK and CHARLES W. URSCHEL
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Circ Res. 1974;34:498-504
doi: 10.1161/01.RES.34.4.498
Circulation Research is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1974 American Heart Association, Inc. All rights reserved.
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