Vol. 91, Issue 1, 435-440, July 2001
Impaired distensibility of the left ventricle after stiffening
of the right ventricle
Masanori
Shirakabe,
Seiji
Yamaguchi,
Yoshiaki
Tamada,
Gajendra
Baniya,
Akio
Fukui,
Hiroshi
Miyawaki, and
Hitonobu
Tomoike
First Department of Internal Medicine, Yamagata University
School of Medicine, Yamagata 990-9585, Japan
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ABSTRACT |
Acute and chronic alterations of right
ventricular (RV) wall properties can change left ventricular (LV)
performance. We investigated whether and how stiffening of the RV free
wall alters LV diastolic distensibility. We used cross-circulated
isolated hearts, in which the LV and RV were independently
controllable. Stiffness of the RV free wall was altered by
intramuscular injections of glutaraldehyde into the RV free wall after
right coronary artery ligation. We measured circumferential and
longitudinal regional lengths in the septum and LV free wall. During
data acquisition, RV volume was held constant. After the RV free wall
was stiffened by glutaraldehyde, the LV diastolic pressure-volume
relation shifted upward and became steeper. Importantly, stiffening of
the RV free wall increased the diastolic regional area in the septum
and LV free wall under constant LV volume. The augmented regional
dimensions may result in enhanced regional tension under constant LV
volume and may be related to the observed increase in LV diastolic
intracavitary pressure. The impaired LV diastolic distensibility by
stiffening of the RV free wall may be at least partly explained by
myocardial stretch, probably due to LV deformation.
ventricular interdependence; ventricular geometry; left ventricular
stiffness; diastolic function; length-tension relation
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INTRODUCTION |
DIASTOLIC
DYSFUNCTION IS GENERALLY classified as abnormal distensibility
and abnormal relaxation (5). Myocardial diastolic distensibility is impaired in the presence of left ventricular (LV)
myocardial ischemia (9), LV hypertrophy
(8), and congestive heart failure (20). LV
diastolic distensibility is also determined by ventricular
interdependence between the LV and the right ventricle (RV) (1,
13, 21, 27) and by pericardial pressure (6, 10).
Conceivably, acute or chronic change in mechanical properties of the RV
modifies LV distensibility or the LV diastolic pressure-volume relation
through ventricular interdependence (14, 19, 29), the
mechanism of which has not been examined rigorously.
Transfer of forces between the ventricles, termed ventricular
interdependence, has been believed to occur primarily through the
septum (2, 3, 12, 20, 28), i.e., shifting of the septum
leftward by increasing RV volume. Several models have been developed on
the basis of simple definitions for volume and regional elastance
(14, 15, 22). The models (14, 15, 22) imply that all interactions occur through the septum and are not influenced through the ventricular free walls. We reported that ventricular interdependence not only altered septal position but also caused regional myocardial stretch in the whole ventricle (30,
31). For example, increasing RV volume enhanced regional LV
diastolic dimensions in the septum and LV free wall, even at constant
LV volume and increased LV chamber pressures (30). The
augmented myocardial diastolic stretch, that is, the increased regional preload, results in the increased resting and active regional forces
under the same LV volume, and then the increased forces inevitably
elevate LV intracavitary pressure (30, 31). Although the
septum is important in ventricular interdependence, ventricular interdependence affects the whole heart: the RV free wall, the LV free
wall, and the septum (7, 30). However, it is unclear whether changes in mechanical properties of one ventricle alter the
myocardial dimension of the other ventricle when both ventricular volumes are fixed.
Changes in LV distensibility may be affected by RV material properties,
that is, RV hypertrophy caused by pulmonary hypertension (14), RV myocardial infarction, and constrictive
pericarditis restricted to the right side of the heart. We hypothesized
that stiffening of the RV free wall may cause overall LV deformation and that LV deformation may increase LV myocardial fiber stretch, resulting in enhanced LV diastolic pressure (Fig.
1). To test this hypothesis, we injected
glutaraldehyde into the RV free wall after ligation of the right
coronary artery to stiffen the RV free wall (19, 29). We
used cross-circulated canine hearts and controlled the volumes of the
LV and RV independently. We measured diastolic circumferential and
longitudinal segment lengths in the interventricular septum and LV free
wall along with the LV diastolic pressure-volume relation. We evaluated
the LV geometrical effects derived from stiffening of the RV free wall
on the LV diastolic pressure-volume relation. The observed dimensional
alterations may be considered small; however, the dimensional changes
may explain the observed LV diastolic pressure increase after
stiffening of the RV free wall.
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Fig. 1.
A
hypothetical biventricular cross section after right ventricular (RV)
free wall stiffening. Stiffening of the RV free wall may cause left
ventricular (LV) deformation (B). RV free wall stiffening
may flatten the RV free wall, resulting in increased distance of the
junctions of the RV free wall on the LV. The LV free wall and septum
may assume a more crescentlike shape because of the stretched
junctions. Then the regional myocardial length may be elongated in the
LV free wall (from LC to LG) and septum under
constant LV volume. If the regional myocardial length increases, the
resting tension should increase. Because LV volume is held constant,
the increase in resting tension can increase diastolic ventricular
pressure.
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METHODS |
Surgical procedure and experimental preparation.
The methods are similar to those described previously
(30). Seven isolated cross-circulated heart preparations
were used. In each experiment, dogs for a donor heart (13.0 ± 0.3 kg) and a larger support dog (25.2 ± 1.5 kg) were anesthetized
with pentobarbital sodium (25 mg/kg iv), intubated, and ventilated
using room air. The femoral artery and vein of the support dog were
cannulated, and the cannula in the femoral artery was connected to the
perfusion line for an isolated heart. The heart of the smaller dog was
isolated from the systemic and pulmonary circulation.
The aortic valve cusps were sewn, and a rubber patch was sutured below
the aortic valve. A thin latex balloon (i.e., condom, 0.03 mm thick)
attached to a rigid cannula was inserted into the LV cavity via the
mitral orifice. A pacing wire was sewn into the His bundle, and two
pairs of ultrasonic crystals (see Placement of ultrasonic
crystals) were inserted into the interventricular septum through
the tricuspid orifice. The pulmonary valve was sutured. Another balloon
attached to a rigid cannula was inserted into the RV cavity through the
tricuspid orifice. The tips of 6-F micromanometer catheters (Millar
Instruments, Houston, TX) were positioned in the LV and RV balloons
through the cannulas. The balloons were filled with saline. Vents were
set in the apex of the LV and RV to decompress these chambers from any
Thebesian drainage. To ensure proper positioning of the balloons,
strings were attached to the apical portion of each balloon and
withdrawn through the drainage ports. The ascending aorta was
cannulated and connected to the perfusion line. The circuit included a
roller pump and a Starling resistor to produce constant perfusion
pressure. Five minutes after the perfusion line was opened, the
isolated heart was defibrillated on the atria. The heart was paced at a constant rate of 120-140 beats/min.
Cannulation-type electromagnetic flow probes (type 20T, lumen size 3 mm, Nihon Koden) were inserted into the perfusion and drainage
circuits, and the flows were measured by a square-wave electromagnetic
flowmeter (model ME-27, Nihon Koden). The return flow to the support
dog was set to the same flow from the support dog. The blood
temperature of the circuit was maintained at 37°C with a
thermostatically controlled bath. Sodium bicarbonate and pentobarbital
sodium (1-2
mg · kg
1 · h1) were infused
throughout the experiment to maintain arterial pH within the
physiological range and to maintain a constant level of anesthesia,
respectively. Heparin was infused into the support dog.
Placement of ultrasonic crystals.
In the seven isolated hearts, circumferential and longitudinal segment
lengths in the LV free wall and interventricular septum were measured
with four pairs of sonomicrometer crystals (5 MHz, 2-mm diameter). LV
free wall crystals were placed at approximately one-third the depth of
the wall from the LV epicardium. Septal crystals were placed at
approximately one-third the depth of the wall from the RV cavity side.
The long axis of the LV was defined as the line connecting the
bifurcation of the left main coronary artery and the apical dimple. At
the midpoint of the base and the apex and the midpoint of each wall in
the circumferential plane, the four pairs of crystals were implanted.
In six of the seven hearts, RV circumferential and longitudinal segment
lengths were also measured, with crystals placed at the midpoint
between the tricuspid valve and the pulmonary valve. The distance
between a pair of crystals was ~1 cm. Regional area was calculated by multiplying the longitudinal end-diastolic length by the
circumferential end-diastolic length. The reproducibility of these
measurements was confirmed repeatedly by increasing and decreasing LV
(or RV) volume.
Experimental protocol.
While RV volume was fixed at a relatively low level (10.1 ± 1.6 ml), LV volume was increased in 2-ml increments from 15.1 ± 2.1 to 23.6 ± 2.0 ml and the resultant pressures and segment lengths
were recorded. Small and large LV volumes were defined as the volume at
which LV end-diastolic pressure was ~4 and 12 mmHg, respectively.
After measurement of the pressures and lengths in the control
condition, the proximal portion of the right coronary artery and
visible collateral vessels draining to the RV free wall were ligated
(29). Ten minutes after the ligation, 25% glutaraldehyde was injected into the ischemic myocardium of the epicardial
portion of the RV free wall with a 26-gauge syringe. The area of
glutaraldehyde injection was ~65% of the RV free wall. Then, the
glutaraldehyde-injected area of the RV free wall became stiff and
discolored. Ten minutes after injection of glutaraldehyde, the
pressures and lengths were recorded according to the same protocol
described for the control condition.
The investigation conforms with the Guide for the Care and Use of
Laboratory Animals [DHHS Publication No. (NIH) 85-23, Revised 1985, Office of Science and Health Reports, Bethesda, MD 20892].
Statistical analysis.
Values are means ± SE. Student's t-test was used to
assess the significance of the differences for paired observations.
P < 0.05 was considered a statistically significant difference.
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RESULTS |
Figure 2 represents the RV diastolic
pressure-volume relation (A) and the diastolic pressure-RV
free wall regional area relation (B) before and after
glutaraldehyde injection. The RV diastolic pressure-volume relation
shifted upward after glutaraldehyde, which corresponds well with a
marked stiffening of the RV free wall.
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Fig. 2.
RV
diastolic pressure (RVDP)-RV volume relation (A) and RV
diastolic pressure-regional area relation in RV free wall (RVFW) under
varying RV volume (B). After injection of glutaraldehyde,
the relation showed a steeper upstroke than under the control
condition.
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Figure 3 shows the effect of decreased
distensibility of the RV free wall on LV diastolic pressure. After
stiffening of the RV free wall, LV diastolic pressure significantly
increased at low, intermediate, and high LV volume. Stiffening of the
RV free wall caused an upward shift of the LV diastolic pressure-volume relation while the RV volume was held constant. The extent to which LV
diastolic pressure was enhanced after glutaraldehyde was greater in
high than in low LV volume (4.1 ± 0.7 vs. 1.1 ± 0.4 mmHg,
P < 0.01; Fig. 3, Table
1). RV volume was set at the low level,
and therefore RV diastolic pressure after glutaraldehyde showed no
remarkable change (Fig. 1, Table 1). Thus the effects of RV pressure on
the LV can be neglected.
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Fig. 3.
LV diastolic pressure (LVDP)-LV volume relation before
and after injection of glutaraldehyde into RV free wall. LV diastolic
pressure increased at low, intermediate, and high LV volumes. Values
are means ± SE. *P < 0.05 vs. control;
**P < 0.01 vs. control.
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Figure 4 shows original traces of a
representative case showing changes in segment lengths at the
interventricular septum and LV free wall and LV diastolic pressures
before and after glutaraldehyde. Despite fixed RV and LV volumes,
diastolic segment lengths of the interventricular septum and LV free
wall increased circumferentially as well as longitudinally after
injection of glutaraldehyde into the RV free wall. The change in
diastolic segment length and the regional area of the interventricular
septum and LV free wall of seven hearts is summarized in Table 1 and
Fig. 5. After stiffening of the RV free
wall by injection of glutaraldehyde into the RV free wall, segment
lengths in the interventricular septum generally increased
circumferentially and longitudinally. The regional area in the
interventricular septum increased by 2.5% in high LV volume (Fig. 5).
Segment lengths in the LV free wall increased circumferentially and
longitudinally. The regional area in the LV free wall increased by
2.1% in high LV volume (Fig. 5).
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Fig. 4.
Original traces of a representative case showing changes
in segment lengths at interventricular septum (IVS) and LV free wall
(LVFW) and RV and LV diastolic pressures before and after
glutaraldehyde injection into the RV free wall. RV diastolic pressure
was similar before and after glutaraldehyde (5 mmHg). The model used in
this study was an isovolumically contracting heart. Segmental systolic
shortening and bulging occur concomitantly. Arrowhead, end diastole.
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Fig. 5.
Regional area change in interventricular septum (A) and
LV free wall (B) before (C) and after injection of
glutaraldehyde into RV free wall (G) with LV and RV volumes held
constant. Values are means ± SE.
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DISCUSSION |
In the present study, when injection of glutaraldehyde stiffened
the RV free wall, the LV diastolic pressure-volume curve shifted upward
and became steeper. The diastolic dimensions of the interventricular
septum and LV free wall increased after stiffening of the RV free wall
under constant LV volume, implying that the increase in LV diastolic
dimensions is probably due to changes in overall LV geometry. The LV
myocardial stretch at constant LV volume may at least in part explain
the reduced LV distensibility caused by the stiffened RV free wall.
Modulation of the LV diastolic pressure-volume relation by the RV.
It has been demonstrated that an increase in the volume of one
ventricle shifts the diastolic pressure-volume relation of the other
ventricle upward and leftward in the intact heart. Changes in
myocardial properties of a component of the heart such as the free wall
or the interventricular septum have been reported to alter the
magnitude of ventricular interdependence (14, 19, 29).
Decreased elastance due to hypertrophy of the RV free wall after
chronic pulmonary artery banding enhanced the effect of RV pressure on
the diastolic LV pressure-volume relation (14). Santamore
et al. (19) demonstrated a significant upward shift in the
LV pressure-volume relation in an arrested heart after RV free wall
distensibility was decreased by injection of glutaraldehyde into the
right coronary artery. These findings were consistent with the present
observation that intramuscular injections of glutaraldehyde into the RV
free wall caused an upward shift of the LV pressure-volume relation in
isolated beating hearts. Even though RV diastolic pressures were
similar before and after injection of glutaraldehyde because RV was
fixed at low volume, the coupling in the diastolic ventricular
interdependence was stronger with the stiffened RV free wall.
Furthermore, we observed that the LV diastolic regional dimensions
increased after hardening of the RV free wall.
Mechanism.
The septum has been proposed as a key element for ventricular
interdependence. For instance, increasing RV volume and/or pressure causes a leftward septal shift in normal hearts by echocardiography (3, 11, 12), radiography (1, 21, 25), or
sonomicrometry (6, 17, 28). However, it was uncertain how
the leftward shift of the septum alters the LV chamber pressure at
fixed LV volume. Several models have been developed to explain the
ventricular interdependence (2, 14, 15, 22, 26). A
three-element elastance model has been proposed to explain direct
ventricular interdependence (14, 15, 22). In this model,
the heart is viewed as three walls, LV and RV free walls and septum,
composing the two ventricles. All the mechanical properties of each
wall were expressed in terms of elastance (14, 15, 22).
The three-element elastance model was sophisticated for explaining
ventricular interdependence; however, there was no interaction or force
transmission from one ventricle to the free wall of the other ventricle
in the model. Although the septum is important in ventricular
interdependence, the geometrical alterations of the whole heart may
account for ventricular interdependence.
We observed that RV volume overload increased diastolic segment lengths
in the septum and LV free wall at constant LV volume (30).
The increase in segment length elevates the resting tension of the
segment. The augmented resting tension inevitably increases the LV
chamber pressure. In the present study, stiffening of the RV free wall
increased the diastolic segment area of the septum and LV free wall,
which corresponded well with the increase in LV diastolic pressure. The
increased diastolic area elevates the LV regional tension. Because LV
dimensions after stiffening of the RV free wall increase with fixed LV
volume, the elevated LV diastolic tension probably causes the observed
increase in LV diastolic pressure. Therefore, the LV pressure-volume
curve is shifted upward. The LV shape change observed in this study may be derived from flattening of the RV free wall after hardening of the
RV free wall (Fig. 1). Consequently, the distance of the junctions of
the RV free wall and septum on the LV may be elongated, resulting in an
increase in septal dimensions. The stretched junctions may also cause a
more crescent shape of the LV free wall in circumferential and
longitudinal cross sections. When a sphere deforms to an ellipsoid (or
an ellipsoid to further elliptical geometry) under constant volume, the
overall surface area necessarily increases. It is likely that the
overall myocardial fiber length may be increased by the LV deformation.
One may consider that the dimensional changes elicited by stiffening of
the RV free wall are too small to explain the observed increase in LV
diastolic pressure. A small percentage of the increase in the LV free
wall area may cause a significant increase in LV diastolic pressure. On
the basis of the relation between the regional area and LV diastolic
pressure, we calculated the predicted increase in LV diastolic pressure
from the observed increase in regional area. The predicted pressure
increase was similar to the measured pressure increase caused by
stiffening of the RV free wall (data not shown). The dimensional
stretch due to ventricular deformation may be an important factor for
explaining the observed increase in LV diastolic pressure, although the
significance of the dimensional stretch should be thoroughly elucidated
in further studies.
Clinical implication.
The effect of alterations in RV material properties on the LV diastolic
pressure-volume relation may be recognized in the following clinical
situations: RV hypertrophy resulting from pulmonary hypertension,
constrictive pericarditis restricted to the right side of the heart
after an operative procedure, and chronic RV myocardial infarction,
which resulted in fibrotic change in the RV free wall. For example, the
upward shift of the LV diastolic pressure-volume relation may occur in
constrictive pericarditis primarily on the right side of the heart. RV
distensibility may decrease because of severe adhesion of constrictive
pericardium restricted to the right side of the heart. This situation
is similar to our experiment, in which the RV free wall was stiffened
by injection of glutaraldehyde into the RV free wall. According to the
present study, the impaired RV distensibility in constrictive pericarditis may cause LV geometrical change. Subsequently, LV diastolic regional stretch may occur even at constant LV volume, and
thus an upward shift of the LV diastolic pressure-volume relation may
ensue. Our observation in this study may also imply other clinical
situations such as those mentioned above, although the stiffening of
the RV by glutaraldehyde is an artificial circumstance. In addition to
the fact that LV diastolic stiffness is affected by molecular
alterations of the LV (24), it should be considered that
the other chambers contribute to LV diastolic stiffness.
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FOOTNOTES |
Address for reprint requests and other correspondence: S. Yamaguchi, First Department of Internal Medicine, Yamagata University School of Medicine, 2-2-2 Iida-Nishi, Yamagata 990-9585, Japan (E-mail:
syamaguc{at}med.id.yamagata-u.ac.jp).
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement"
in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 5 April 2000; accepted in final form 13 February 2001.
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ABSTRACT
INTRODUCTION
