(Circulation. 1995;92:210-215.)
© 1995 American Heart Association, Inc.
Articles |
Clinical Study of the Effects of Latissimus Dorsi Muscle Flap Stimulation After Cardiomyoplasty
From the Department of Cardiology, Boucicaut Hospital, Paris, France, the Faculty of Medicine Necker-Enfants Malades, University Paris V, and the Department of Cardiovascular Surgery (J.C.C., A.C.), Broussais Hospital, Paris.
Correspondence to Dr A.A. Hagège, Boucicaut Hospital, 78 Rue de la Convention, 75730 Paris Cedex 15, France.
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Abstract |
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Background Beneficial hemodynamic effects after dynamic cardiomyoplasty have been inconsistently demonstrated, and the effects seen may be due to the wrap itself, to flap stimulation, or both. The aim of this study was to determine whether flap stimulation per se acts as a systolic active process after cardiomyoplasty.
Methods and Results Catheterizations were
performed in 13 patients 14.4±7 months after cardiomyoplasty. New York
Heart Association functional class decreased from 3.3 to 2.1 after the
procedure (P=.0005). Hemodynamic evaluations
were first performed with the stimulator on in the 2:1 mode and then
after the stimulator had been off for at least 24 hours. Left
ventricular (LV) ejection fraction increased from 25.1±6%
before surgery to 28.2±6.7% with the stimulator on after
cardiomyoplasty (P=.04). When stimulation was stopped, there
was no change (P>.05) in indexes of systolic or
diastolic LV function (peak systolic LV pressure,
LV ejection fraction, peak positive dP/dt, peak negative dP/dt, or
). Pulmonary capillary wedge pressure and cardiac index were
unchanged when stimulated and nonstimulated settings were compared
(P>.05). However, a remarkable
heterogeneity of individual responses was observed.
Ejection fraction and cardiac index decreased with the stimulator off
in 3 patients, but peak positive dP/dt decreased in 6 patients;
diastolic function deteriorated in 2 patients, but a slight
improvement was noted in 3 patients. Cardiothoracic ratio,
echocardiographic LV end-diastolic
dimension, and fractional shortening remained unchanged between
immediate (<1 month) and long-term (36.7±25.9 months)
postoperative evaluations.
Conclusions In the majority of our patients, there was no short-term hemodynamic benefit of flap stimulation; therefore, we conclude that the efficacy of cardiomyoplasty may be a consequence of a passive "girdling effect," which limits the progression of ventricular enlargement and further deterioration of ejection fraction.
Key Words: hemodynamics • clinical trials • muscles
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Despite remarkable improvement of symptoms in the majority of patients after dynamic cardiomyoplasty, objective hemodynamic beneficial effects have not been consistently demonstrated, and their mechanisms remain equivocal.1 The potential beneficial effects of this technique can be due to the wrap itself, to flap stimulation, or to both. Preoperative and postoperative hemodynamic evaluations have not consistently demonstrated even a slight improvement in systolic left ventricular (LV) function.2 3 4 5 6 Only one study4 has shown a deterioration in LV systolic function when postoperative hemodynamics are compared first with and then without stimulation; however, that report was based on isolated measurement of LV ejection fraction during 1:1 stimulation mode, which is actually avoided in current clinical practice. Thus, the exact hemodynamic effect of flap stimulation in patients stimulated long term has not been systematically studied. Moreover, a passive "girdling" effect of cardiomyoplasty, simply limiting the progression of LV enlargement and further deterioration of LV ejection fraction, and reduction in myocardial stress due to increased mural thickness have been recently suggested.1 7 8
The aim of this study was to determine whether flap stimulation per se is at least partly responsible for the hemodynamic improvement that is sometimes observed after cardiomyoplasty; thus, we compared systolic and diastolic LV hemodynamic parameters in patients after successful cardiomyoplasty during long-term ambulatory 2:1 stimulation mode and after stimulation had been discontinued for at least 24 hours.
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Methods |
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Study Population
From 1988 to 1991, 22 patients with refractory congestive heart failure, in sinus rhythm, without significant mitral insufficiency (regurgitation less than 2+ on a scale of 1 to 4 by angiography) and with contraindication to cardiac transplantation underwent cardiomyoplasty. All were operated on in the same institution (Broussais Hospital, Paris, France) with the standardized reinforcement surgical technique previously described by Carpentier and Chachques.9 Two juxtaneural pacing electrodes were implanted in the muscle flap (Medtronic SP 5528 BV, Medtronic), an intramyocardial sensing lead (Medtronic SP 5548 BV) was implanted in the right ventricle (RV), and an intra-abdominal cardiomyostimulator (Medtronic SP 1005 BV) was used for muscle stimulation. Four patients died postoperatively (<1 month) and 5 patients died after 15±16 months (range, 2 to 36 months) and were therefore not included in this study.
Thus, 13 patients (12 men and 1 woman) formed the study group; patient age was 49±10 years (range, 21 to 61 years). Etiology was classified as idiopathic in 5 patients and ischemic in 8 patients. Preoperative LV ejection fraction on angiography was 25.1%. Associated surgical procedures were aneurysm resection in 2 patients coronary artery bypass grafts in 1 patient, and both aneurysm resection and coronary artery bypass grafts in 1 patient. Preoperative New York Heart Association functional class was 3.3±0.5 (NYHA III, 11 patients; NYHA IV, 2 patients). Written informed consent was obtained in all cases, and the study was approved by the ethics committee of our institution.
At time of postoperative catheterization, all patients were hemodynamically stable and in 2:1 chronic ambulatory stimulation mode. Stimulation parameters were the following: pulse amplitude 3 to 5 V, pulse width 210 µs, pulse frequency 30 Hz, burst duration 185 ms, and synchronization delay (up to 125 ms) was set to start flap stimulation after mitral valve closure on M-mode echocardiography as previously described.9
Evaluation of Patients
Clinical evaluation was based on NYHA
functional class. Chest
x-ray for measurement of cardiothoracic ratio and
echocardiographic examination for measurements of LV
end-diastolic dimension and fractional shortening were
performed and compared within 1 month (21±6 days; range, 16 to 28
days) after the cardiomyoplasty procedure (immediate results) and 8 to
78 months (mean, 36.7±25.9 months) after surgery (long-term
results) with the stimulator off. Such comparison may avoid the changes
seen between preoperative and immediate postoperative periods due to
associated procedures or muscle wrap. Echocardiographic
parameters were assessed from a parasternal M-mode
echocardiographic recording according to the
recommendations of the American Society of
Echocardiography. Measurements recorded were
the mean values of four consecutive cardiac cycles.
Cardiac catheterizations were performed 14.4±7 months (range, 7 to 27 months) after surgery. Hemodynamic evaluation was first performed with the stimulator on in the 2:1 mode. The stimulation was then stopped for at least 24 hours and the patient monitored in the coronary care unit. A second hemodynamic evaluation was then performed 25±0.9 hours (range, 24 to 26 hours) after the first one. Medical therapy (eg, diuretics, digoxin, and angiotensin-converting enzyme inhibitors) remained unchanged during the study.
Each procedure consisted of left heart catheterization with a micromanometer catheter (Millar Mikro-tip catheter pressure transducer, Millar Instruments Inc) introduced into the femoral artery and right heart catheterization with a 7F Swan-Ganz thermodilution catheter (Baxter Healthcare Corp, Edwards Division) introduced into the femoral vein.
We measured RV pressure, pulmonary artery pressure,
pulmonary capillary wedge pressure, and cardiac index by the
Fick thermodilution technique with a cardiac output computer (American
Edwards model 9520 A, Baxter Healthcare Corp). We recorded LV
pressure curve and measured (1) indexes of LV systolic
performance (LV peak systolic pressure and maximum rate
of LV pressure rise, peak positive dP/dt) and (2) indexes of LV
diastolic function (ie, LV end-diastolic
pressure; maximum rate of LV pressure decay, peak negative dP/dt; and
, the time constant of LV isovolumic pressure decline) with a
semilogarithmic model with zero asymptote of LV
pressure.10 Systolic and
end-diastolic LV volumes were assessed from
end-diastolic and end-systolic endocardial
contours from ventriculograms recorded at 30° right anterior
oblique projection and indexed to body surface area; global
angiographic LV ejection fraction was then calculated by the
area-length method.11 Measurements recorded were
the mean of six consecutive cardiac cycles, three assisted beats and
three unassisted ones, when in the 2:1 stimulation mode and the
mean of three consecutive cardiac cycles when the stimulator was off.
Analysis of the data was blinded to the setting of the
cardiomyostimulator.
Data are expressed as mean±SD. We used a Student's paired t test to compare (1) data obtained in the preoperative period with the follow-up data (stimulator turned on); (2) cardiothoracic ratio and echocardiographic measurements obtained in the immediate postoperative period with the long-term data (stimulator turned off); (3) postoperative hemodynamic data obtained with the stimulator turned on and off; and (4) postoperative hemodynamic data between assisted and unassisted beats during the 2:1 stimulation mode. Results were considered to be significant when P<.05.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Effects of Dynamic Cardiomyoplasty: Preoperative Versus Postoperative Data
NYHA functional class decreased from 3.3±0.5 before surgery to 2.1±0.6 after the procedure (P=.0005). Improvement in functional class was observed in 10 of the 13 patients. Functional status did not change in 3 patients in class III who did not undergo associated procedures. Angiographic LV ejection fraction increased significantly from 25.1±6 (range, 8 to 35) before surgery to 28.2±6.7 (range, 16 to 39) with the stimulator on after cardiomyoplasty (P=.04). When patients with associated surgical procedures were removed so that only patients who had no associated procedures were compared, there was still significant postoperative improvement in functional status (3.2±0.4 versus 2.2±0.5, P=.001) and in ejection fraction (26.1±5% versus 28.4±6%, P=.04).
Effects of Dynamic Cardiomyoplasty: Immediate Versus Long-term
Postoperative Data
Cardiothoracic ratio remained unchanged when
immediate (<1 month)
and long-term postoperative evaluations were compared [0.56±0.06
mm (range, 0.52 to 0.66 mm) versus 0.57±0.06 mm (range, 0.52 to
0.67 mm), P=.28]. Immediate postoperative
echocardiographic LV end-diastolic
dimensions were unchanged when compared with long-term values
[68.4±6.8 mm (range, 62 to 84 mm) versus 70.5±8.0 mm
(range, 60 to
88 mm), P=.19] as was LV fractional shortening
[17.4±5.5
(range, 8 to 27) versus 15.3±3.3 (range, 9 to 20),
P=.15].
Effects of Flap Stimulation
No change in clinical status was
observed during the protocol with
the stimulator on (2:1 stimulation mode) or the protocol with the
stimulator off, and the hemodynamic status remained
stable throughout the 24-hour procedure (see the
Table
).
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Heart rate was not significantly different during the two different catheterizations with the stimulator either on or off.
When considering the results, hemodynamic indexes of
systolic LV function, such as peak systolic LV
pressure, ejection fraction (Fig 1), or
peak positive dP/dt (Fig 2), were
unchanged when stimulation was discontinued. Similarly,
hemodynamic indexes of diastolic LV
function, such as peak negative dP/dt (Fig 3) and (Fig
4), remained identical with or without
flap stimulation; moreover, LV end-diastolic pressure
remained high despite flap stimulation. LV
end-diastolic volume was unchanged with flap
stimulation. RV pressure, pulmonary artery pressure,
pulmonary capillary wedge pressure, and cardiac index were also
unchanged when stimulated and nonstimulated settings were compared
(Table
).
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However, if a 20% change from stimulated to
nonstimulated
hemodynamic data was considered to be clinically
significant in individual cases, individual responses would be
considered remarkably heterogeneous: (1) LV ejection
fraction never increased with the stimulator off, whereas it decreased
in 3 patients (Fig 1) who demonstrated parallel
decreases in peak positive dP/dt and cardiac indexes and a stability or
an increase in capillary pulmonary wedge pressure; (2) cardiac
index decreased in these 3 patients only and increased in 3 others; (3)
pulmonary capillary wedge pressure decreased in 1 patient and
increased in 5 patients; and (4) peak positive dP/dt increased in only
2 patients but decreased in 6 patients who could not be identified by
preoperative or postoperative clinical, hemodynamic, or
angiographic data.
Hemodynamic indexes of LV diastolic
function (LV end-diastolic pressure, peak negative
dP/dt, and ) were simultaneously impaired with the
stimulator off in 2 patients only, but a slight improvement was
observed in 3 patients with the stimulator off.
When comparing assisted and unassisted beats during 2:1 stimulation mode, there was no statistically significant hemodynamic difference for the parameters previously measured.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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Since the first successful report in 1985,12 cardiomyoplasty has been performed in more than 400 patients with congestive heart failure; however, despite its extensive use and the remarkable improvement in symptoms seen in the majority of patients surviving surgery, the mechanisms of its beneficial effect remain controversial.1 Thus, objective hemodynamic beneficial effects have not been consistently demonstrated after the procedure.2 3 4 5 6 Moreover, it is still unknown to what extent improvements in symptoms and ejection fraction after cardiomyoplasty are due to the presence of an active systolic assist effect of the muscle wrap with stimulation.
The discrepancy between clinical outcome and frequent absence of objective important hemodynamic changes after cardiomyoplasty has been attributed to multiple hypothetical causes: inappropriate stimulator settings, cardiovascular compensatory mechanisms, poor resolution of applied techniques,13 improvement only at exercise13 —power of latissimus dorsi increasing experimentally with mechanical heart load14 —but not at rest, or muscle damage.15 Recently, a girdling effect, in which the flap prevents only progressive LV dilation and does not provide real systolic assistance,7 and a reduction in myocardial stress8 have also been suggested.
This study confirms the clinical improvement (77% of the patients) that persisted after a follow-up >1 year and the slight increase in ejection fraction after surgery with the stimulator on as demonstrated by numerous other clinical studies.2 3 4 5 13 16 This improvement was also demonstrated in patients who did not have associated surgical procedures; however, optimization of medical therapy may have been responsible for these results.
The protocol and technical modalities of clinical evaluation of flap stimulation vary and are scarce. Using ultrasonic techniques during long-term 2:1 stimulation mode, few clinical studies17 18 have shown increases in aortic and pulmonary flow velocities with stimulation, and the interpretation of these findings has been equivocal; the velocity of flap relaxation is experimentally slower than that of myocardium, and theoretically impairment of ventricular filling during the unassisted beat might explain these findings.1 14 In the current study, analysis that separated assisted and unassisted beats during 2:1 stimulation mode did not show any significant hemodynamic difference. When hemodynamics with the stimulator both on and off are compared in normal19 20 or failing21 animal hearts, improvement in LV function with flap stimulation has not been consistently demonstrated. Moreover, only one clinical study4 demonstrated, in a small group of patients, a slight decrease in ejection fraction when the stimulator was turned off; however, complete and detailed hemodynamic data have not been published, and the 1:1 stimulation mode that was used in the study of Bocchi et al has not been used long term in current clinical practice to avoid diastolic impairment and premature change of the stimulator.
The question of the active participation of muscle flap in ventricular systolic activity during the usual 2:1 stimulation mode may be highlighted by comparison of complete hemodynamics with the stimulator on and off; a protocol such as this may obviate the discrepancies in associated procedures and the influence of etiology or medications on postoperative hemodynamics. Using this protocol, we have not seen a deterioration in clinical status when the stimulator was turned off for at least 24 hours, with no changes made in medical treatment. On the other hand, although clinical deterioration after stimulator dysfunction has been rarely reported previously, the duration of dysfunction has been longer,1 13 usually >1 to 2 weeks; this represents evidence for the beneficial effect of stimulation on hemodynamics in some instances. The results from our hemodynamic parameters are in agreement with results of experimental studies performed in animal models of chronic heart failure, which showed no change in LV contractility as assessed by LV pressure-volume relations with the stimulator both off and on.22 However, in our study, individual analyses showed a minimum 20% increase in LV ejection fraction in 23% of the patients and an improvement in peak positive dP/dt, a more reasonable index of systolic function, in 46.1% of the patients, but in two patients there was a deterioration in this parameter. In a previous isolated analysis of ejection fraction4 that included eight patients and had a similar evaluation protocol but a 1:1 stimulation mode, one patient demonstrated an important decrease, five patients a slight decrease, and two patients an increase in this index with cessation of stimulation. Thus, in almost half of the cases, flap stimulation might participate to improve cardiac function.
The absence of evidence of systolic improvement in the remaining patients may support the hypothesis of a passive girdling effect of cardiomyoplasty, simply limiting the progression of LV enlargement and further deterioration of LV ejection fraction by modulating the remodeling process of the failing heart.1 7 23 Thus, when a canine model of heart failure was used,7 even an unstimulated latissimus dorsi muscle flap was able to attenuate LV dilation and deterioration in ejection fraction. In the current study, the absence of significant increases in the cardiothoracic ratio and in the echocardiographic LV dimension and fractional shortening after a mean follow-up of 3 years may confirm this hypothesis. Serial analysis of LV performance by invasive LV pressure-volume relation analysis24 has recently demonstrated in three patients a progressive leftward shift in pressure-volume loop after the procedure with the stimulator off but no significant effect of flap stimulation; however, a progressive effect of long-term drug therapy such as angiotensin-converting enzyme inhibitors could not be eliminated as a cause.
Another possible mechanism of the efficacy of cardiomyoplasty has been postulated, based on the hypothesis that dynamic cardiomyoplasty constitutes the creation of an iatrogenic cardiac hypertrophy, with increased myocardial thickness distributing and reducing the myocardial stress in accordance with Laplace's law.23 For this to occur, the muscle wrap has to develop and share tension with the myocardium even though the systolic work of the LV remains unchanged. Cessation of muscle wrap contraction may then increase the native myocardial stress, which may take longer than 24 hours to demonstrate hemodynamic deterioration measurable by the technique used23 ; experimental studies support this explanation.8
Previous experimental19 25 and clinical2 3 4 5 reports failed to show constrictive or restrictive myopathy after cardiomyoplasty. However, clinical studies were usually based only on LV end-diastolic pressure measurements, and at least one experimental study failed to show deterioration in diastolic function shortly after the procedure.26 In our current study, diastolic function evaluated with more reasonable indexes was unchanged. Meanwhile, individual analysis showed that LV diastolic function improved in only two patients and deteriorated in three patients. These changes were not correlated to parallel changes in systolic function.
The present evaluation has some limitations: small number of patients, inhomogeneity in preoperative clinical status, individual setting of the cardiomyostimulator, averaging of stimulated and nonstimulated beats during 2:1 stimulation mode, absence of assessment of pressure-volume relation, and absence of evaluation during stress. Moreover, the 24-hour delay between the two hemodynamic evaluations is in fact arbitrary; however, this delay was also chosen in a previous study,4 is convenient for repeat hemodynamic evaluations, and could be sufficient to bring to the fore a potential active systolic effect. Finally, the variations seen between patients may also be related to the quantity and quality of the latissimus dorsi muscle available for the wrap, to the nature of cardiac disease, or to associated surgical procedures.
Thus, LV ejection fraction is usually mildly increased after cardiomyoplasty, but interpretation of this finding remains controversial. In some instances, active systolic effect of chronic latissimus dorsi muscle flap stimulation is observed when assessed by peak positive dP/dt. In the majority of the cases, there is no short-term benefit of flap stimulation on LV function, but it is possible that long-term flap stimulation, which obviates muscle atrophy and fibrosis, may be an important stimulus to the chronic girdling effect that results from cardiomyoplasty without beat-to-beat benefit. Therefore, several mechanisms may explain the efficacy of cardiomyoplasty; many could be the consequence of a passive girdling effect of muscle wrap or the consequence of sparing myocardial stress, and some could be due to a dynamic systolic assist.
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