(Circulation. 1997;96:2978-2986.)
© 1997 American Heart Association, Inc.
Articles |
Left Ventricular Pressure-Volume Relationships Before and After Cardiomyoplasty in Patients With Heart Failure
From the Departments of Anesthesiology and Cardiology, Cardiovascular Research Institute, University Hospital Maastricht, The Netherlands (J.J.S., F.H. v.d. V., S.A.A.P.H., H.-G.K., H.J.J.W.); Department of Cardiology, University Hospital Leiden, The Netherlands (E.T. v.d. V, J.B.); Departments of Cardiac Surgery and Cardiology, Lyon, France (F.D., O.J., G.F.); Department of Cardiac Surgery, Ospedale Civile, Brescia, Italy (O.A., R.L., M.V.); and Department of Pulmonary Diseases, Erasmus University Rotterdam, The Netherlands (J.R.C.J.)
Correspondence to J.J. Schreuder, MD, PhD, Department of Anesthesiology, University Hospital Maastricht, PO Box 5800, 6202 AZ Maastricht, The Netherlands. E-mail JSCHR{at}SANE.AZM.NL
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Abstract |
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Background The aim of this study was to elucidate whether beneficial effects of cardiomyoplasty (CMP) in patients with dilated cardiomyopathy are the result of a decrease in existing ventricular dilatation or a prevention of further dilatation.
Methods and Results Combined
micromanometer-conductance catheters were used to
evaluate left ventricular pressure-volume relationships in
six patients with dilated cardiomyopathy before and
at 6 and 12 months after CMP. Acute changes in preload and afterload
were induced by a standardized leg-tilting intervention and a bolus
infusion of nitroglycerin. After CMP,
end-diastolic volume (EDV) decreased from 138±10 to
103±18 mL/m2 (P<.01) at 6 months and to
83±17 mL/m2 (P<.01) at 12 months.
End-diastolic pressure (EDP) decreased from 20.2±6.4 to
13.9±7.7 mm Hg (P<.01) at 6 months after CMP.
Peak ejection rate and ejection fraction increased at 6 months after
CMP from 594±214 to 799±214 mL/s (P<.05) and from
26.6±4.7% to 40.1±8.3% (P<.05), respectively. Peak
-dP/dt decreased at 12 months after CMP from -842±142 to
-712±168 mm Hg/s (P<.05). Leg-tilting before
CMP increased EDP from 20.2±6.4 to 25.6±5.2 mm Hg
(P<.01), end-systolic pressure (ESP) from
118±17 to 122±17 mm Hg (P<.05), and 
from
50.8±2.8 to 53.8±2.3 ms (P<.05). Six months after
CMP, leg-tilting also increased EDV from 103±18 to 110±22
mL/m2 (P<.05) and ESV from 62±14 to 66±14
mL/m2 (P<.05). Before CMP,
nitroglycerin decreased EDP from 20.2±6.4 to
10.4±3.8 mm Hg (P<.01), ESP from 118±17 to
96±11 mm Hg (P<.05), ESV from 100±11 to 89±7
mL/m2 (P<.05), and from 50.8±2.8 to
44.5±3.7 ms (P<.05). Six months after CMP,
nitroglycerin decreased EDP, ESP, and to similar
values.
Conclusions Our findings show that up to 1 year after CMP, marked decreases in left ventricular volume are present. Our measurements suggest that CMP actively reduced the dilated ventricle but did not prevent a higher EDV on an increased venous return. The latissimus dorsi muscle wrap contraction results in better synchronization of contraction and more rapid emptying of the left ventricle.
Key Words: cardiomyoplasty • cardiomyopathy • ventricles
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Introduction |
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The mechanisms of possible clinically beneficial effects of CMP, as introduced by Carpentier and Chachques,1 in the treatment of heart failure have been a matter of debate for more than a decade.2 In a previous clinical study, we demonstrated a significant active contribution of the stimulated wrapped LD muscle on LV P-V relationships.3 At optimal stimulator settings, an increased contractile state of the LV LD muscle combination could be demonstrated by an increased PER, a leftward shift of the end-systolic P-V points, an increased SV, and increased peak -dP/dt. However, at clinically used cardiomyostimulator settings, no significant changes in SV or peak -dP/dt were observed. At the same time, LV systolic PER increased during LD stimulation, and an increase in EDP occurred directly after cessation of a 1:2 applied stimulation period, suggesting a decrease in workload of the heart muscle itself during LD stimulation and a dynamic effect that decreased LV EDP. Therefore, even in the nonoptimal clinical setting, CMP exerted an active hemodynamic effect on the systolic as well as the diastolic phase.
Lee et al4 and Bellotti et al5 demonstrated decreases in LV wall stress after CMP during LD stimulation in animal and patient studies, respectively. The prevention or decrease of acute or chronic ventricular dilatation may be another beneficial mechanism associated with dynamic cardiomyoplasty, as was suggested by Chachques et al6 and Kass et al.7
To evaluate these possible mechanisms, we studied LV P-V relationships in patients with dilated cardiomyopathy before CMP and at 6 and 12 months after CMP. To study the hemodynamic effects of CMP, we also performed quickly reversible changes in preload and afterload. To induce a state of acute increased preload and afterload, a standardized leg-tilting intervention was performed. An acute decrease in preload and afterload was induced by a bolus injection of NTG. The conductance catheter technique as described by Baan et al8 was used to measure instantaneous Vlv. Plv and PaO were measured simultaneously with micromanometers. The segmental volume signals of the conductance catheter were used to study wall motion.
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Methods |
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Patients
All patients (Table 1
) received
long-term treatment with diuretics, digoxin, and ACE
inhibitors at the time of CMP. Patient 2 also received
amiodarone for arrhythmias up to 6 months after CMP.
The dosing schedule of these drugs were either unchanged or reduced
after CMP.
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Cardiomyoplasty Procedure
The patients studied were operated in Lyon (France) and Brescia
(Italy). The surgical technique has been described by Chachques et
al.9 The left LD muscle was mobilized, keeping
the neurovascular pedicle intact. After the attachment of two
intramuscular stimulation electrodes (model SP 5528, Medtronic), the
muscle was introduced into the thoracic cavity and wrapped clockwise
around both ventricles. The stimulation electrodes and a sensing
electrode, attached to the right ventricular wall, were
connected to a cardiomyostimulator (model SP1005, Medtronic).
Preoperative and Postoperative Evaluations
The study was approved by the medical ethics committees of the
two hospitals. Informed patient consent was obtained for insertion of
the catheters, and for testing the cardiomyostimulator at different
settings and for the use of NTG.
Patients were sedated and heparinized before catheterization. A Swan-Ganz thermodilution catheter was placed in the pulmonary artery. A dual-micromanometer transducer conductance catheter (F7, Sentron) was inserted via the femoral artery into the LV for measurement of PaO, Plv, and Vlv. The correct position of the conductance catheter was verified by fluoroscopy and inspection of the segmental conductance signals.
The conductance catheter was connected to a Leycom Sigma-5DF signal conditioner/processor (CardioDynamics, Zoetermeer, The Netherlands) to measure Vlv.8,10,11 The method is based on measurement of the time-varying electrical conductances of five segments of blood in the LV. The five segmental conductances are measured from six adjacent electrodes, and total Vlv is calculated from the sum of the five segmental conductances. The dual-field modification, which has been shown to improve the accuracy of the method, was used in all patients.12
Ventricular function analysis by Ees was performed in three patients. A change in loading conditions was induced with an 8F balloon occlusion catheter (model SP9168, Cordis), which was positioned in the inferior caval vein.
From the individual segmental conductance signals, we were able to assess wall motion abnormalities. It has been shown previously that the time-varying segmental conductances reflect time-varying segmental Vlv values as obtained by cine CT in canine hearts.13
To obtain reliable estimates of CO by thermodilution, a computer-controlled injection system was used.11 CO was determined by use of a CO computer (COM-2, Baxter) and injections of 10 mL ice-cold 5% glucose. The simultaneously recorded conductance catheter SV was calibrated by thermodilution SV.
Data Acquisition and Analysis
ECG (extremity leads), PaO,
Plv, and Vlv signals were
digitized at a sampling rate of 200 Hz and stored on hard disk for
subsequent analysis. A dedicated data acquisition and
analysis software package CONDUCT-PC (CardioDynamics) was used
to analyze conductance catheter data. The following
variables were calculated, among others, with the package: , the
time constant of exponential isovolumic Plv
relaxation, which was defined as the time from peak -dP/dt until the
pressure reaches half its value; PER and PFR, which were calculated as
maximal -dV/dt and maximal +dV/dt, respectively.
Parallel Conductance
The conductance catheter measures not only the conductance of
the blood inside the LV but also the conductance of the
myocardium and other surrounding tissues, the parallel
conductance. This parallel conductance introduces an offset term
(Vc), which can be estimated by injecting 5 mL
hypertonic saline (8%) into the pulmonary
artery.8 This method is, in fact, an indicator
dilution technique that uses the conductance of blood. The estimation
of Vc was performed with the dedicated package
CONDUCT-PC. The algorithm indicates the best Vc
values, thus avoiding an operator-dependent bias. A reliable estimation
of Vc together with matching thermodilution SV is
a prerequisite for the calibration of conductance catheter volume in
absolute terms.
Experimental Protocol
Blood resistance, parallel conductance, and five thermodilutions
were measured before all baseline measurements.
After the CMP procedures, the measurements were performed with the LD stimulator interval at the patient's clinically used setting and amplitude in a 1:2 ratio. Episodes of 15-second duration were recorded while the patients performed expiratory breath-holding to prevent respiration-related changes in venous return.
After the baseline measurements, an increase in preload and afterload was induced by a leg-tilting procedure. The legs were passively lifted to 50 cm, and measurements during tilting were performed within 45 seconds. In three patients, an acute preload reduction was established by occluding the inferior caval vein with the balloon catheter. In all patients, the hemodynamic effects were measured 60 seconds after a 0.5 µg/kg NTG injection into the pulmonary artery.
Statistical analysis was performed with Student's t test for paired variates, and comparison among the three data groups was also performed with randomized-block ANOVA. Values are presented as mean±SD; statistical significance was assumed at P<.05.
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Results |
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All data were measured during 15-second sampling periods, and the values of all beats were averaged. One patient (patient 6) died 1 week before the 12-month catheterization procedure, probably due to an arrhythmia. From another patient (patient 2) incomplete data are available due to a hemodynamic collapse during the measurement procedures at 12 months, most likely induced by the ventriculography contrast agent. This probably also affected the 12-month results of patients 1 and 3. Therefore, the results of the leg-tilting and NTG series for the 12 months after CMP are not presented.
Table 2 provides baseline data for all
six patients before and at 6 and 12 months after CMP. Compared with
before CMP, no significant changes in HR, CI, ESP, peak +dP/dt, , or
PFR were observed at 6 and 12 months after CMP.
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EF increased from 26.6±4.7% to 40.1±8.3% (P<.05)
and to 40±4% (P<.05) at 6 and 12 months after CMP,
respectively. Decreases in EDV from 138±10 to 103±18
mL/m2 (P<.01) and in ESV from 101±10
to 62±14 mL/m2 (P<.01) were
present 6 months after CMP. Further significant decreases compared
with pre-CMP values occurred at 12 months in EDV (to 83±17
mL/m2; P<.01) and ESV (to 50±7
mL/m2; P<.01). EDP decreased from
20.2±6.4 to 13.9±7.7 mm Hg (P<.01) at 6 months
after CMP, and the values at 12 months were similar to the 6-month
values. Peak -dP/dt was significantly (P<.05) less
negative at 12-month CMP compared with the pre-CMP values. PER
increased from 594±214 to 799±214 mL/s (P<.05) at 6
months after CMP, whereas PER at 12 months after CMP was not different
from the pre-CMP values. The parallel conductance component
Vc was not different after CMP (299±26 versus
296±35 mL). Fig 1 shows
representative P-V loops of the baseline measurements
of all patients before and at 6 and 12 months after CMP. An obvious
leftward shift of the end-systolic P-V points after CMP is
present in all patients, caused by the decreases in EDV and ESV. In
Table 3, results are presented of
the 50-cm leg-tilting procedures before and at 6 months after CMP. In a
comparison of the leg-tilting procedures before CMP with its baseline
values (Table 2
), revealed a slightly but significantly
(P<.05) increased HR; no significant change in CI, EF, EDV,
ESV, peak +dP/dt, -dP/dt, PER, or PFR; but significant increases in
EDP (from 20.2±6.4 to 25.6±5.2 mm Hg; P<.01), ESP
(from 118±17 to 122±17 mm Hg; P<.05), and (from
50.8±2.8 to 53.8±2.3 ms; P<.05). A comparison of the
leg-tilting procedures at 6 months after CMP with the corresponding
baseline values (Table 2) reveals no changes in HR, CI, EF, peak
+dP/dt, peak -dP/dt, PER, and PFR but significant increases in EDV
(from 103±18 to 110±22 mL/m2;
P<.05), ESV (from 62±14 to 66±14
mL/m2; P<.05), ESP (from 110±12 to
119±16 mm Hg; P<.05), EDP (from 13.9±7.7 to
20.5±5.8 mm Hg; P<.01), and (from 49.9±2.1 to
53.9±3.2 ms; P<.05).
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The results of the 0.5 µg/kg NTG injections before and 6
months after CMP are given in Table 3. In a comparison of the NTG
injections before CMP with baseline values, HR, CI, EF, EDV, peak
+dP/dt, peak -dP/dt, PER, and PFR were unchanged, whereas significant
decreases occurred in ESV (from 100±11 to 89±7
mL/m2; P<.05), EDP (from 20.2±6.4 to
10.4±3.8 mm Hg; P<.01), ESP (from 118±17 to
96±11 mm Hg; P<.05), and (from 50.8±2.8 to
44.5±3.7 ms; P<.05). In a comparison of the 6-month NTG
data with the six corresponding baseline values (Table 2), there were
no changes in HR, CI, EF, EDV, ESV, peak +dP/dt, peak -dP/dt, PER, and
PFR but significant decreases in EDP (from 13.9±7.7 to 8.9±4.3
mm Hg; P<.05), ESP (from 110±12 to 99±9 mm Hg;
P<.05), and (from 49.9±2.1 to 45±3.4 ms;
P<.05).
In three patients, inferior caval vein occlusion was
performed before CMP as well as after CMP at the patient's individual
best LD stimulator setting. In only one patient could a sufficient
decrease in loading conditions be obtained to construct an
end-systolic P-V relationship. Failures were due to
insufficient decreases in preload and to arrhythmias. In Fig 2, the pre-CMP and 12-month post-CMP P-V
relationships are presented of patient 4 during temporary
inferior caval vein occlusion. Of all patients, this
patient had the lowest pre-CMP EDP, which may have facilitated the
decrease in EDV during the caval vein occlusion. The
Ees measured before CMP was similar to the
Ees of the unassisted post-CMP beats, but the
end-systolic P-V relationship was shifted to the left. However,
the Ees of the 1:2 LD-stimulated beats at the
patient's best stimulator setting was considerably lower than the
Ees of nonstimulated beats.
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In Table 4, the results of the
analysis of the five segmental conductance signals are
presented. Preoperatively, paradoxical motions of segmental
volume signals were observed in all patients in one or more segments.
After the NTG bolus in five patients, the paradoxical motions changed
into more synchronized segmental volume changes. After CMP, paradoxical
volume changes were reduced in all patients although at 12 months after
CMP, the baseline asynchrony returned in one patient. Fig 3 presents an example of the
segmental volume changes before and after NTG of one patient before
CMP. Fig 4 shows segmental volume changes
before and 6 months after CMP of two patients.
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Discussion |
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This study demonstrates the potential of cardiomyoplasty to reduce long-term dilated left heart chambers in size and in EDP up to 12 months after surgery. Moreover, PER and EF increased, and the incidence of abnormal wall motion decreased. However, at 12 months after CMP, peak -dP/dt decreased significantly. On the other hand, CO,
, and
PFR were not affected.
Techniques
To estimate absolute Vlv, we determined the
parallel conductance factor according to the hypertonic saline method.
This factor was used to calibrate intraventricular
volume measured by the conductance catheter; subsequently, the
conductance SV volume was matched to the mean SV of five thermodilution
measurements. Next, EDV and ESV were adjusted accordingly. Possible
overestimations or underestimations of thermodilution SV in the
presence of severe tricuspid and/or pulmonary valve
regurgitation should affect the results of this study
only when a major change in these disorders occurred after CMP. Kass et
al7 used contrast-ventriculography to estimate
EF; with its value and while matching conductance SV to thermodilution
SV, they assessed absolute LV P-V relations.
The hypertonic saline method is an indicator dilution technique and therefore independent of heart motion and shape changes due to CMP. Delahaye et al14 demonstrated in CMP patients that LD muscle wrap stimulation may have a geometric distorting influence on the heart by pulling the inferior and posterior LV wall up, which will result in inaccuracies for techniques using diameters or planes to estimate ventricular volume. The value of the parallel conductance can be obtained objectively with a dedicated computer algorithm; therefore we preferred the hypertonic saline method as an operator-independent method to measure EF to the use of echocardiography and contrast ventriculography.
In a previous study, we observed that the parallel conductance factor of LD-stimulated beats was similar to that of the unassisted beats.3 In the present study, we found comparable values before and after CMP, although the LD muscle was wrapped around the heart. This might be explained by realizing that the parallel conductance resides mainly in the ventricular wall and right ventricular blood content and is only marginally influenced by extracardiac tissues such as lungs and LD muscle.
Baseline Hemodynamics
The pronounced decreases in EDV, with a mean of 26% at 6 months
and 40% at 12 months after CMP, and EDP, with a mean of 6 mm Hg,
with unchanged CO, are indicative for marked changes in
diastolic properties. Kass et al7
measured similar decreases in EDV and EDP, even in absolute values, in
their CMP study in three patients. Jatene et al15
observed decreases in pulmonary wedge pressure in 10 patients
with a mean of 8 mm Hg after CMP. With a right LD CMP in
patients, Magovern et al16 observed a 18%
decrease in EDV 6 months after surgery. Also, Lorusso et
al17 observed a significant decrease in LV
end-diastolic diameter up to 2 years after CMP. A relative
dehydration status at the time of catheterization to
explain the decreased EDV after CMP is not likely because most patients
gained weight after CMP (Table 1). Moreover, their diuretic
drug regimen was essentially unaltered.
The unchanged peak -dP/dt, the unchanged time constant of
Plv decline (), and unchanged PFR values at 6
months after CMP are in contradiction to observations by Corin et
al18 in an acute CMP animal study. They observed
a prolonged both with and without LD stimulation and a decreased
peak -dP/dt due to CMP and concluded that CMP acutely hampers
diastolic properties. In a previous study, we observed an
increased peak -dP/dt in LD-stimulated beats at the best setting in
patients evaluated up to 24 months after CMP.3 In
an acute animal study with right LD CMP, Magovern et
al16 did not observe any difference in
between stimulated and nonstimulated beats. Moreover, we observed
similar values of PFR before and after CMP. Therefore, CMP seems not to
be associated with an impairment of diastolic properties.
The finding that the peak -dP/dt at 12 months after CMP was decreased
significantly compared with pre-CMP values might be related to preload
dependence of this variable.19
No significant changes in peak +dP/dt, SV, and LV ESP were present after CMP, whereas PER and EF increased and ESV decreased. EF increased by 13.5% at 6 months after CMP, which is in accordance with the 12.5%, 10%, and 9% net increases as reported by Kass et al,7 Jatene et al,15 and Lorusso et al,17 respectively. Bocchi et al20 reported a significant 4% increase in EF, whereas Magovern et al16 and Delahaye et al14 reported no significant changes after right and left LD CMP, respectively.
The mean 33% increase in PER in this study can be attributed in part to systolic effects of the stimulated LD muscle, as was also demonstrated in a previous study.3 Even at nonoptimally tuned clinical settings, PER increased with a mean of 30% during assisted beats, whereas at the best stimulator settings, a mean increase of 68% was observed.
Leg-Tilting
A relatively small increase in afterload and unchanged preload of
the LV was the effect of the leg-tilting procedure before CMP,
resulting in a sharp increase in EDP and . After CMP, however, EDP
increased to a mean value equal to the mean baseline value before CMP.
Although an increase in afterload itself may increase , the small
rise in PaO before CMP during leg-tilting suggests that the
compromised second part of the ventricular relaxation, as
expressed by the increase in , is merely the result of an
inappropriate reaction to volume loading or increased venous
return.
An inability to increase SV by augmenting EDV is demonstrated in the present study through the use of the leg-tilting test before surgery. There even was a tendency toward decreased LV EDV values due to leg-tilting, albeit not significant. This abnormal preload reserve mechanism in dilated cardiomyopathy was also demonstrated by Volpe et al21 through acute isotonic volume expansion in patients in New York Heart Assocation functional classes I or II. It might be due to cross-talk between the ventricles, because dilatation of the right ventricle during rapid filling may affect filling of the LV,22 inducing a higher LV EDP at a lower LV EDV. After CMP, however, LV EDV increased during leg-tilting in all patients, which is indicative of some recruitment of the preload reserve mechanism. Comparable effects of ACE inhibitors and NTG were observed in the study of Volpe et al.21
The results of the leg-tilting procedures do not allow the conclusion that CMP prevents further acute cardiac dilatation, but the decreased EDV and EDP after CMP will at least provide a safer range. Capouya et al23 have shown in an animal study that a nonstimulated LD wrap attenuated the progression of LV enlargement. However, in the present study, an acute increase in EDV induced by an increased venous return due to leg-tilting was not prevented by the 1:2 stimulated LD muscle.
Preoperatively, the effect of leg-tilting on the diastolic
phase was more pronounced than the effect on the systolic
phase. After CMP, however, ESP increased significantly with a mean of
10 mm Hg due to tilting, whereas before CMP, almost no (mean,
4 mm Hg) change was observed. Together with the increased EDV,
this may be indicative of improved pump function to an increased load.
Thus, CMP to some extent corrected preload reserve afterload mismatch.
In Fig 5, the results of the leg-tilting
are presented schematically with the use of mean EDP, EDV, ESV,
and ESP values for the six patients before and 6 months after CMP.
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), mean EDV did not change significantly due to
leg-tilting (
), whereas 6 months after CMP (
), EDV and ESV
increased significantly due to leg-tilting (
).
In the present study, leg-tilting was considered a rather light
exercise maneuver. Increases in maximum oxygen consumption during
exercise testing after CMP have been observed.20
Other studies, however, failed to demonstrate such an
increase.14 It can be argued that testing at the
maximal exercise level is not appropriate in CMP patients because
maximal exercise may evoke a high afterload and increased wall stress,
, and EDP, overruling the possible beneficial effects of CMP.
NTG
EDP and decreased to similar values in both the pre- and
post-CMP procedures after a standardized 0.5 µg/kg NTG
injection, although the post-CMP series started at a significantly
lower EDP.
NTG improved EF only before CMP, with a mean net increase of 7%; however, this change did not reach statistical significance. Sharir et al24 observed a mean 16% increase in EF due to intravenous injections of 400 µg NTG in patients with dilated cardiomyopathy; in their study, as in our series, EDV did not decrease significantly in response to NTG. Pre-CMP ESV decreased significantly, which means the increased EF is merely the result of an improvement of the systolic ejection phase. After CMP, NTG did not change EF, which points to an ejection-improving effect due to CMP that is not augmented by NTG.
ACE inhibitors, diuretics, and digoxin have become the standard therapy for dilated cardiomyopathy. ACE inhibitors attenuate progressive cardiac enlargement and improve survival.25 Beneficial effects of nitrates in patients with dilated cardiomyopathy during exercise were observed by Hecht et al.26
Wall Stress
In patients with dilated cardiomyopathy,
Hayashida et al27 demonstrated a markedly
elevated wall stress throughout the cardiac cycle. Decreases in wall
stress during LD stimulation were observed in animal and patient CMP
studies.4,5 The net decrease in wall stress will
depend on the decrease in EDV and on the contraction/relaxation cycle
of the LD muscle. In the present study, Vlv
values were markedly reduced after CMP, and with the addition of the
1:2 active LD muscle, the wall stress after CMP will be substantially
lowered in this patient group. In an acute CMP animal study, Chen et
al28 measured the pressure between LD muscle and
the heart and demonstrated a considerable decrease in transmural LV
pressure during LD-stimulated beats. Decreases in transmural pressure
will have a wall stress–and afterload-decreasing effect during
systole. The afterload-decreasing effect will be operative when the
aortic valves are opened. The timing and configuration of the applied
LD stimulus therefore determine the extent to which the LD muscle will
exert a dynamic wall stress–and afterload-decreasing effect.
Wall Motion Asynchrony
In Fig 4, the segmental conductance signals are presented
of two patients before and 6 months after CMP. Before CMP, marked
paradoxical movements in four ventricular volume segments
can be observed, which were converted into synchronous segmental volume
signals after CMP. NTG also reduced asynchronous wall motion in five of
six patients during the preoperative measurement procedures (Fig 3).
After CMP, NTG decreased asynchrony in one of the two patients with
persistent wall motion asynchrony. Asynchronous wall motion is observed
even in normal ventricles and is more pronounced in patients with
healed myocardial infarction.29 Nonuniformity
reduces the mechanical efficiency of ventricular ejection
by inducing a premature onset of relaxation and decreasing the rate of
Plv fall.30 Previously, we
showed that during LD stimulation at the optimal setting the rate of
Plv fall increased.3 Both
NTG and CMP may improve segmental synchronism by reducing myocardial
wall stress, especially in the abnormal contracting segments. In the
previous study, we observed in one patient that during LD muscle
stimulation at the optimal setting, an aneurysmal apical
segment was forced in synchrony with global volume changes only during
the LD assisted beats.3
P-V Relationships
The pathophysiology of the lower Ees during
optimal LD stimulation in patient 4 may reveal part of the working
mechanism of CMP (Fig 2). Kass et al7 observed in
three patients a leftward shift of the ESPVR at 12 months after CMP,
but in two patients Ees decreased and no
differences were observed in Ees between assisted
and unassisted beats. The leftward shift of the end-systolic
P-V points in all patients after CMP in the present study also
indicates a leftward shift of the ESPVR. However, in an animal study, a
higher Ees was reported after CMP in an
ischemic animal model, without a change between assisted and
unassisted beats.31 In another animal study,
increased Ees during LD-stimulated beats was
reported.32
The load dependence of myocardial relaxation is a fundamental property of mammalian cardiac muscle, and evidence in the intact heart has been provided in several studies.19 Sudden increases in afterload, when applied late in the ejection phase, induce a premature pressure decline, whereas when the sudden increase in afterload is applied early in the cardiac cycle, the onset of pressure fall is delayed.33 However, unloading the ventricle during the second half of the ejection phase resulted in some extra active shortening and improved emptying by delaying the onset of relaxation.34,35
Under physiological circumstances, the ventricle shortens against a varying afterload. The stimulated LD muscle might work as a time-varying wall stress reducer and a time-varying afterload reducer. The observed worst LD stimulator settings as presented in a previous patient study occurred mostly with short delays.3 This might be due to a too-early relaxation of the LD muscle, causing a pseudoafterload increase late in the ejection phase. Also, an afterload decrease during early contraction may shorten the ejection phase.19 The best LD stimulation setting should be the moment at which maximal LD force coincides with late ejection, inducing a lowest afterload in this period and delaying relaxation. At the optimal stimulator settings, which were the settings with the longest delays, SV increased with a mean of 20% and PER increased with a mean of 68%; the subsequent initial rate of pressure fall (-dP/dtmax) was faster.3 This is analogous to the effects of an afterload decrease during the second half of the ejection phase. One might consider this effect of LD stimulation as a limiting effect on shortening deactivation of ventricular muscle. Recently, Watkins et al35 demonstrated in isolated rabbit hearts through rapid volume withdrawal at end systole the existence of shortening activation as a third mechanism that mediates cardiac contractility during ejection, together with length-dependent activation and shortening deactivation.
The lower Ees during LD stimulation at the
optimal LD muscle stimulation setting of patient 4 (Fig 2) can be
explained by a relatively stronger afterload decrease at lower preload,
because the contribution of the LD muscle may be similar at lower
preload, inducing lower ESV values. Therefore, the
Ees concept erroneously characterized the
simultaneous actions of heart and LD muscle during LD
stimulation as a lower cardiac contractile state compared with the
unassisted heart beats.
In an assessment of the LV contractile state of these patients by preload-adjusted maximal power, an ejection phase index of contractile state hardly influenced by loading conditions as proposed by Kass and Beyar,36 would provide highly significant increases in contractile state after CMP because PER increased and EDV decreased significantly and LV pressure was unchanged after CMP.
Active Versus Passive Girdling Effects of CMP
During diastole, the wrapped LD muscle will exert a
tension on the cardiac wall, even in total relaxed state; therefore,
the measured absolute decreases in LV EDPs due to CMP implicate even
lower transmural values. This passive effect may be the basis of the
limiting effect of a nonstimulated LD muscle wrap to the progression of
LV enlargement in an animal model.23 However, we
observed in a previous study an acute significant rise in EDP when the
1:2 LD stimulation was blocked. Moreover, in some patients, a
concomitant direct increase in EDV was measured, and one patient in the
present study (patient 6) deteriorated each time the LD stimulator
was blocked, as demonstrated by sharp increases in EDP. In all
patients, PER increased during LD muscle stimulation at each stimulator
setting that was applied. The increase in PER is probably explained by
the active segmental synchronizing effects of the stimulated LD muscle
and may contribute to the striking decreases in LV dimensions after
CMP. Therefore, the so-called passive elastic girdling effect of CMP as
speculated by Kass et al7 may be of secondary
significance.
Conclusions
When making conclusions about this limited group of patients, it
must be considered that patient selection, the surgical procedure, and
the LD muscle conditioning protocol may vary substantially among
different institutions. On the other hand, a major advantage of the
present patient group was that no additional cardiac surgery was
performed.
LV EDV and EDP decreased markedly after CMP, whereas CO was unchanged. Concomitant increases in PER and EF were observed. CMP was not associated with impairment of diastolic properties at 6 months after CMP because the indices of ventricular relaxation and PFR were not affected. At 12 months after CMP, however, peak -dP/dt was less negative than the pre-CMP values.
The leg-tilting maneuver resulted in unchanged EDV before CMP and in small increases after CMP, indicating some recruitment of the preload reserve mechanism and decreasing the preload reserve afterload mismatch. CMP reduced the dilated ventricle but did not prevent acute increases in LV EDV.
Nitrate administration resulted in a decrease in EDP and and
increased wall motion synchrony.
Asynchrony in ventricular contraction of the dilated LV diminishes LV function in dilated cardiomyopathy. This asynchrony decreased in all patients after CMP, probably because the LD contraction caused more synchronization of LV contraction. The increase in synchrony might be the rationale behind the working mechanism of CMP by improving the mechanical efficiency of ventricular ejection. Because we observed immediate rises in EDP and occasionally in EDV after cessation of LD stimulation, we suppose that these results are due to an active synchronizing effect of the stimulated LD muscle. This implies that optimally tuned stimulator settings are a prerequisite for optimal segmental synchronization.
The Ees as an index for contractile state cannot be applied in cardiomyoplasty when the LD muscle is stimulated because the stimulated muscle changes the ESPVR in an unpredictable fashion.
The stimulated LD muscle might work as a time-varying wall stress and afterload reducer; the decrease in wall stress induces a more synchronized contraction/relaxation pattern, and the decrease in afterload applied at the end of the ejection phase may induce an accelerated ejection and a delayed relaxation.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was supported by Telectronics Pacing Systems (Denver, Colo). We wish to thank Th. van der Nagel for excellent technical assistance and M.C. Stuart, MD, FFARCSI, for correction of the manuscript.
Received February 23, 1997; revision received June 12, 1997; accepted June 19, 1997.
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