Ann Thorac Surg 2002;74:514-521
© 2002 The Society of Thoracic Surgeons
Original article: cardiovascular
Effects of chronic cardiomyoplasty on ventricular remodeling in a goat model of chronic cardiac dilatation: part 2
Hans G. Kaulbach, MDa,
Roberto Lorusso, MD, PhDb,
Gil Bolotin, MD, PhDc,
Jan J. Schreuder, MD, PhDd,
Frederik H. van der Veen, PhD*e
a Department of Cardiac Surgery, Bundes Krankenhaus, Koblenz, Germany
b Department of Cardiac Surgery, Civic Hospital, Brescia, Italy
c Department of Cardiothoracic Surgery, Tel Aviv Medical Center, Tel Aviv, Israel
d Department of Cardiac Surgery, St Raphael Hospital, Milan, Italy
e Department of Cardiothoracic Surgery, Academic Hospital, Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands
Accepted for publication April 21, 2002.
* Address reprint requests to Dr van der Veen, Department of Cardio-thoracic Surgery, Academic Hospital Maastricht, P. de Bijelaan 25, 6229 HX Maastricht, The Netherlands
e-mail: fvv{at}scpc.azm.nl
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Abstract
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Background. Reduction of ventricular dilatation, rather than direct improvement of pump function, has been suggested to be the main working mechanism of dynamic cardiomyoplasty (CMP). This working mechanism was examined in the goat using a chronic cardiac dilatation model induced by the creation of a cervical arteriovenous shunt and submitted to passive and active CMP.
Methods. Fourteen female goats underwent surgical creation of a shunt between the left carotid artery and the jugular vein. Seven goats had no additional operation (control group). The other 7 goats (CMP group) underwent CMP approximately 8 weeks after the creation of the shunt. The wrapped left latissimus dorsi muscle was left unstimulated for 2 weeks, and subsequently stimulated electrically for a 3-month period, using a 1:4 muscle-to-heart contraction ratio. Hemodynamic measurements included heart catheterization and determination of left ventricular (LV) pressure-volume relations by means of the conductance catheter method at baseline, after 8 weeks (only in the CMP group), and after 5 months. Transthoracic echocardiography was performed just before opening the AV shunt and every 2 weeks thereafter.
Results. Significant ventricular enlargement, as well as persistent increase in filling pressures, were observed after 8 weeks. Animals in the control group dilated further beyond 2 months (LV end-diastolic diameter from 39 ± 2 to 67 ± 6 mm). In contrast, the ongoing LV dilatation process was stopped by passive CMP, and LV end-diastolic diameter significantly decreased after electrical activation of the wrapped skeletal muscle (from 63 ± 7 to 42 ± 6 mm). Cardiomyoplasty also significantly increased the slope of the end-systolic pressure-volume relation (elastance) when compared with pre-CMP values (from 0.9 ± 0.2 to 1.7 ± 0.5 mm Hg/mL), which indicated an improvement of the LV contractile state. No significant hemodynamic effects could be observed at the tuned stimulation settings on a beat-to-beat basis during electrical muscle stimulation.
Conclusions. The contribution of CMP to LV dimension and contractility appeared to be either passive or active, and this study suggests the importance of stimulating the latissimus dorsi muscle to enhance the girdling effects of the wrapped latissimus dorsi muscle and to improve LV contractility.
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Introduction
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A small number of clinical studies have indicated that dynamic cardiomyoplasty (CMP) plays a beneficial effect in reversing the remodeling process of the dilated and functionally impaired left ventricle (LV), rather than providing evident systolic assist [1–3]. Besides this geometric modification, reduced LV wall stress and related myocardial energy demands have been also shown in experimental studies [4–7]. It is becoming increasingly evident, therefore, that previous experimental and clinical investigations of CMP most likely simplified the actual mechanisms of action, merely confining postoperative hemodynamic assessment and relative data interpretation to the so-called squeezing effect of the electrically activated wrapped latissimus dorsi (LD) muscle during cardiac systole [8–13]. The inconsistency of clinical results according to such a mechanism of action, despite objective evidence of functional and clinical improvement of CMP patients, has led to marked skepticism regarding the potentials of this surgical procedure and hampered its wider application as an accepted therapeutic option in the treatment of chronic heart failure. However, CMP may provide subtle and yet effective mechanical support to the impaired myocardium, leading to disparate and beneficial effects (reverse remodeling), even if no significant changes in conventional hemodynamic variables can be demonstrated. The difficulty in separately demonstrating and analyzing these various factors has most likely been related to the limited accuracy of the clinical investigational tools and to the appropriateness of experimental models when CMP was tested in the lab. To date, several experimental reports have been provided for delineation of the girdling effect of CMP using a chronic model of LV dilatation [4, 14–16], whereas the majority of research investigations used normal hearts, acute heart failure models, or unconditioned LD muscles [5, 6, 9, 17]. Experimental models of chronic heart dilatation and failure rely mainly on rapid ventricular pacing, which was also used in several laboratory reports of CMP with successful results [14–16]. To specifically address the effects of CMP on ventricular dilatation, we used an alternative animal model of chronic cardiac dilatation induced by the surgical creation of a high-flow arteriovenous (AV) fistula [18]. The actual role of passive or active cardiac reinforcement exerted by CMP represents an additional matter of debate and of experimental investigations. Therefore, our study was also designed to address this controversial topic and to evaluate these two different modalities of biologic cardiac binding.
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Material and methods
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Animal model
Fourteen female goats with a weight of 49 ± 11 kg were entered in this study, which was conducted in accordance with the "Guide for the Care and Use of Laboratory Animals," published by the National Institutes of Health (publication 85-23, revised 1985), and which was approved by the Animal Ethical Committee of the University of Maastricht, The Netherlands.
The study population consisted of two groups: in the control group (n = 7) an AV shunt was performed to induce volume cardiac overload during a period of 5 months, without additional operation. Also in the CMP group (n = 7) an AV shunt was made, and 8 weeks later a left LD muscle CMP was performed with a subsequent follow-up of 3 months. All animals (n = 14) were two new groups of goats undergoing AV shunt alone (control) or AV shunt subsequently associated with CMP, and, therefore, were not the ones used in the part 1 acute study [19]. All animals were studied before opening the AV fistula to assess baseline ventricular function and dimensions using the conductance catheter method and transthoracic echocardiography. During the 5-month study protocol LV dimensions were obtained every 2 weeks by echocardiography. Invasive measurements were obtained after 8 weeks just before the CMP procedure in the CMP group, and at the end of the study in both groups. In the CMP group hemodynamic measurements were first performed with the cardiomyostimulator off and then with different stimulation settings.
Animal instrumentation and hemodynamic monitoring
After overnight fasting, the animals were anesthetized with intravenous administration of thiopental (15 mg/kg), and subsequently intubated and ventilated (Pulmomat, Dräger, Lübeck, Germany). Anesthesia was maintained by inhalation of oxygen-nitrous oxide (1:2) and halothane (1% to 2%). Body temperature was kept constant with a heating blanket, and the animals were placed in the right recumbent position. An indwelling catheter was placed in the left saphenous vein for continuous infusion of 5% Ringer’s lactate solution during the experimental protocol. Standard electrocardiographic leads I, II, and III were recorded simultaneously. Transthoracic echocardiographic assessment (Hewlett Packard, Palo Alto, CA) of LV dimensions (LV end-diastolic diameter, LV end-systolic diameter) was then performed in all goats.
Heparin (5000 IU intravenously) was given preoperatively and for 5 days postoperatively (2 x 5000 IU subcutaneously). Prophylactic antibiotic regimen consisted of ampicillin 1000 mg and gentamycin 5 mg/kg body weight intravenously before the operation, and 1000 mg ampicillin postoperatively.
Heart catheterization and instrumentation for pressure-volume analysis have been reported in our part 1 study [19]. Pressure-volume analysis was performed according to the principles of Baan and collaborators [20]. Left ventricular baseline measurements in all goats included end-diastolic and end-systolic pressure, end-diastolic and end-systolic volume, stroke volume and stroke work, peak ejection rate (maximum rate of increase of LV volume) and peak filling rate, positive and negative maximum rate of increase of LV pressure, ejection fraction, cardiac output, and LV relaxation time, as well as end-systolic elastance (slope of the end-systolic pressure-volume relationship) using transient inferior vena cava inflow occlusion. Electrocardiogram and LV, central venous, and pulmonary pressures were digitally sampled at 200 Hz in real time and stored on a microprocessor. These data were analyzed off-line with the software package HDAS-PC (Hemodynamic Data Acquisition System, University of Maastricht, Maastricht, The Netherlands).
Surgical procedure and wrapped muscle stimulation protocol
Once the baseline hemodynamic measurements were completed, an AV shunt was created between the left carotid artery and the jugular vein. The technical details of the AV shunt model and CMP procedure have been described in the accompanying article [19].
In the CMP group (n = 7), a left LD CMP was performed 8 weeks after the creation of the shunt using the technique described by Chachques and colleagues [10].
After CMP, the wrapped muscle flap was left unstimulated for the first 2 weeks postoperatively. Thereafter, the wrapped muscle flap was stimulated with a single pulse (150-µs pulse duration, 5-V amplitude, 50-ms delay, 1:4 contraction ratio) for 2 weeks. The number of stimuli progressed to two pulses, three pulses, and, finally, to four pulses per burst (99-ms burst duration, 30-Hz frequency) after each successive 2-week period. The prudent LD muscle-to-heart contraction ratio as compared with conventional stimulation pattern was used in accordance with experimental and clinical evidence of reduced muscle damage and preserved mechanical properties [21, 22]
Transthoracic echocardiography studies for LV dimension and wall thickness estimation were performed every 2 weeks after the creation of the shunt and before the onset of muscle stimulation, whereas it was carried out every 2 to 4 weeks during the wrapped LD conditioning protocol and thereafter. Invasive hemodynamic investigations, including LV pressure-volume loops, were performed at baseline and after 5 months in the control group, whereas CMP animals underwent additional invasive studies after 8 weeks, before the wrapping procedure.
Statistics
The Student’s paired t test was used to compare preoperative and postoperative values among animals within one group. The unpaired Student’s t test was used for comparison between the control group and CMP group. Results are presented as mean ± standard deviation, and p values less than 0.05 are regarded as statistically significant.
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Results
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The relatively large AV shunt was well tolerated in all animals, and no mortality occurred throughout the 5 months of follow-up. However, 2 animals (control group, 1; CMP group, 1) died because of cardiac decompensation during the very last step of the experimental protocol before conductance catheter measurements could be performed.
Echocardiography showed a significant increase in LV dimensions at 8 weeks after AV shunt creation, with further dilatation in the control group (Fig 1).
This increase was comparable in the CMP group at 8 weeks after opening the AV fistula (Fig 2). However, LV end-diastolic and end-systolic diameters did not modify during the transposed LD recovery period of 2 weeks after CMP operation, before starting the electrical stimulation (passive reinforcement state). Once the cardiomyostimulator was turned on (active reinforcement state) and the conditioning protocol was initiated just with one pulse every four cardiac beats, both LV end-diastolic and end-systolic diameters progressively decreased in all animals of the CMP group, and this trend persisted throughout the subsequent 3 months.
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Fig 1. Left ventricular short axis as measured by transthoracic echocardiography at baseline and during 20-week follow-up after an arteriovenous shunt procedure in the control group (n = 7) is shown. Both left ventricular end-systolic (LVESD) and end-diastolic diameters (LVEDD) are reported (mean ± SD).
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Fig 2. Left ventricular short axis as measured by transthoracic echocardiography is presented at baseline during 8 weeks following an arteriovenous shunt procedure, and after a cardiomyoplasty (CMP) procedure. The onset of latissimus dorsi muscle stimulation is indicated 2 weeks after the cardiomyoplasty operation. Both left ventricular end-systolic (LVESD) and end-diastolic diameters (LVEDD) are shown (mean ± SD).
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As expected, in the control group cardiac output increased from 4.4 ± 0.9 to 9.8 ± 1.7 L/min after the shunt had been opened for 5 months. Also in the CMP group, cardiac output increased from the time of pre-CMP invasive studies (4.7 ± 1.3 to 10.5 ± 4.7 L/min; p < 0.001). In both groups an increase in central venous pressure, pulmonary artery pressure, and pulmonary capillary wedge pressure was observed after 5 months and 8 weeks. On the left side of the heart, the LV end-diastolic pressure increased significantly in the control group and in the CMP group (17 ± 5 mm Hg, and 16 ± 5 mm Hg, respectively), and remained increased at 3 months after the wrapping procedure in the CMP group. In the control group, arterial diastolic pressure decreased to 85 ± 5 mm Hg after 5 months, whereas arterial systolic pressure did not change. In the CMP group, no significant changes were observed (Table 1).
Comparison of the hemodynamics between the two groups revealed a significantly higher ejection fraction at 3 months in the CMP group (59% ± 4% versus 49% ± 5%) and a concomitant lower cardiac output (6.2 ± 0.7 versus 9.8 ± 1.7 L/min). Other hemodynamic characteristics were not significantly different between the two groups (Table 2).
Together with an increase in stroke volume, the end-diastolic and end-systolic volumes were increased at 5 months after opening of the AV shunt in the control group. Also in the CMP group, these characteristics were increased at 8 weeks after AV fistula operation, whereas, after a period of geometric stabilization before the onset of muscle stimulation, these volumes had decreased significantly to baseline values at 3 months after CMP.
Figure 3
represents typical plots of LV pressure-volume relations from one animal before opening the AV shunt, 2 months later, and 3 months after CMP with the cardiomyostimulator turned off. There is a pronounced reduction both in pressure-volume area and stroke volume without apparent changes in filling pressures when compared with pre-CMP values. However, the rate of maximum diastolic pressure decay and the time constant of diastolic relaxation did not differ from baseline and pre-CMP values.
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Fig 3. Left ventricular pressure (Plv)-volume (Vlv) loops of one representative animal of the cardiomyoplasty group is shown before opening the arteriovenous shunt (a), after 8 weeks of arteriovenous shunt opening (b), and 3 months after performing cardiomyoplasty and subsequent latissimus dorsi muscle stimulation (c).
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Acute hemodynamic indices of systolic augmentation derived from the left LD wrap with the cardiomyostimulator turned on were present in only 3 of the 6 CMP animals studied at 5 months. However, the differences between stimulator off and several on settings in a 1:4 contraction ratio at 10 V were not significant. In the animals in which the beat-to-beat changes of the LV performance could be documented, variable extent of LD muscle contribution to the LV systole was observed in direct relation to the number of pulses per burst (Fig 4)
as well as to the pulse amplitude delivered (Figs 5 and 6)
during assisted beats. Adjustment of the LD muscle contraction timing also determined variable changes in hemodynamic values, ranging from clear systolic benefits to negative effects on the supported beats or to the diastolic phase of the subsequent beat.
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Fig 4. The effects on the pressure-volume relationship according to the number of pulses per burst during latissimus dorsi assistance at 4:1 heart-to-wrapped muscle contraction ratio are shown. Note that by increasing the number of pulses per burst (from 1 to 3 pulses, from top to bottom) there are evident increases in left ventricular systolic pressure and increases in stroke volume, more relevant with higher pulse number (bottom).
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Fig 5. Beat-to-beat pressure-volume tracings and relations at clinical stimulation setting (5 V, heart-to-latissimus dorsi muscle contraction ratio 4:1) after chronic cardiomyoplasty. Evident increase in stroke volume with little change in left ventricular systolic pressure is shown during assisted beats (arrows).
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Fig 6. Beat-to-beat pressure-volume tracings at forced stimulation setting (10 V, heart-to-latissimus dorsi muscle contraction ratio 4:1). At this stimulus strength, although significant increases in stroke volume and left ventricular systolic pressure are shown during assisted beats (arrows), the postassisted stroke volume is significantly reduced.
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No deterioration of the LV diastole could be detected either in the long term (ie, as compared with baseline values) or at a beat-to-beat level after CMP, provided that appropriate muscle tuning was programmed.
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Comment
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In the present study, the AV shunt model appeared to be useful to induce a dilated heart within approximately 2 months in large animals. This overload-induced progressive LV dilatation process could be stopped by wrapping the left LD muscle around the ventricles without muscle graft contractions (passive cardiac reinforcement). The subsequent activation of the wrapped muscle flap synchronously to the LV contractions (active cardiac reinforcement) gradually reversed the ventricular dilatation to the original cardiac dimensions within 3 months despite the ongoing AV fistula. Significant beat-to-beat hemodynamic benefits from CMP comparing assisted versus unassisted beats could not be fully shown in this study, also at forceful stimulation regimens (10 V amplitude), although objective contribution of the wrapped LD muscle mechanics to the LV systolic performance could be clearly documented in some animals.
Passive and active left ventricular girdling: the dynamism of cardiomyoplasty
The benefits from chronic passive cardiac reinforcement were elegantly demonstrated by Capouya and associates [14], who showed that unstimulated CMP significantly reduced LV enlargement in an animal model of cardiac dilatation using rapid ventricular pacing. Recently, the use of an inactive prosthetic cardiac binding device has been proposed and compared with passive CMP with apparently less efficacy in terms of reverse remodeling [23]. However, a few experimental studies of CMP have shown that, besides the demonstrated passive LV containment, the use of electrically driven LD contractions, either synchronous or asynchronous to LV systole, is critical to provide more efficient results. Indeed, Mott and coworkers [15] showed that both passive (unstimulated CMP) and active (stimulated CMP) wrapping were able to halt the progressive LV enlargement produced by rapid ventricular pacing, but only active cardiac reinforcement was capable of bringing LV volumes to baseline values. Our findings confirmed that the passive ventricular reinforcement, although in place for a short time, represented a valuable constraint to the ongoing ventricular enlargement secondary to the working AV fistula. However, actual LV reverse remodeling could be achieved only after activation of the LD muscle flap by electrical stimulation. It has been also suggested that the evident benefits secondary to CMP activation may come from the LD shrinkage related to structural muscle changes induced by permanent electrical stimulation (increased muscle stiffness secondary to increased fibrotic and fat tissue components), which usually lead also to increased relaxation time of muscle fibers because of muscle phenotype transformation (more type 1 fibers). This purely restrictive effect is in contrast to the observed hemodynamics, as no deterioration of diastolic function could be detected after CMP in the long term.
In our previous study [2], we did not observe an increase in end-systolic elastance after CMP. However, in the goat study, end-systolic elastance was increased significantly 3 months after the CMP procedure, suggesting that the wrapped LD muscle enhanced LV contractile mechanics. The LV contractile characteristics have been shown to improve in the long term after chronic CMP. It is therefore likely that myocardial recovery or improvement in mechanical performance does occur for multifactorial benefits. More efficient energy transfer, more favorable working state according to Starling’s law because of shortened sarcomere length, or reduced wall stress because of more efficient radius-to-length ratio (Laplace’s law) and reduced myocyte oxygen demands are all probable components of relevant changes, although subtle and not easy to document, secondary to long-standing biologic and dynamic support.
The LV diastole was not affected by the LD muscle in this study, but, again, the lack of overt chronic heart failure state obviously hampers any discussion on this matter, also taking into account the marked diastolic changes that usually occur during permanent impairment of LV function and are potentially induced also by peculiar myocardial pathology.
Beat-to-beat analysis of chronic cardiomyoplasty
The limited consistency of improvement in conventional hemodynamic variables, but especially during the beat-to-beat assessment, as shown in many clinical series of CMP [2, 24], has been a major limitation for such a technique to be accepted and widely applied in patients affected by dilated cardiomyopathy and chronic heart failure. Experimental data, however, have been rather controversial [5, 7–9], sometimes documenting evident and hemodynamically significant LD support during LV systole [15, 16]. Our group showed, in several patients, that only forceful stimulation (clinically inapplicable in the long run for patient discomfort) could generate slight, yet hemodynamically relevant, improvement [2]. This experimental study provides findings that are in accordance with our previous clinical conclusions, although a substantial increase in acute LV contractile state was observed in 3 of the 6 CMP animals. Furthermore, the correct skeletal muscle tuning to activate LD contraction synchronously to LV systole has been shown to play a critical role also in chronic CMP [24], not only to efficiently modulate LD contribution, but also to prevent the potentially negative influence of inappropriate muscle contraction timing on the ongoing ejective phase or on the subsequent diastolic filling. Therefore, the need for appropriate LD tuning should be considered as an additional indirect proof of the beat-to-beat influence and of the dynamism of CMP.
Our data are unfortunately not conclusive in this respect, but confirm, as many other experimental and clinical reports, that if the chronic active girdling is the main effect of dynamic CMP, the permanent LD contractile compression, regardless of the beat-to-beat hemodynamic significance, represents the basic principle of such a biologic cardiac support for effective LV reverse remodeling to be achieved in the long term.
Study limitation
The AV fistula was shown to induce marked and stable cardiac dilatation. However, despite the fact that decreased contractile function was also documented after 8 weeks by pressure-volume data, overt chronic heart failure was not systematically induced (only 2 animals showed frank signs of myocardial impairment). It is conceivable that this limitation may affect the clinical relevance of this study. Furthermore, owing to the peculiar cardiocirculatory conditions induced by the AV shunt, additional hemodynamic factors, ie, peripheral resistance, could inevitably influence actual CMP effects and related interpretation. However, the capability of reversing the dilatation process triggered by the AV fistula might even be underestimated, inasmuch as dynamic CMP was able to actively and efficiently counteract an extremely powerful cardiocirculatory condition that usually induces severe cardiac dilatation, as shown in the control group. Accordingly, the beat-to-beat analysis, which theoretically warrants full or, at least, relevant preservation of the original mechanical and structural properties of the electrically stimulated LD muscle [25, 26], conducted in a model that represents a potential obstacle for a squeezing effect to be performed with significant hemodynamic changes, was nonetheless documented in some animals. The passive CMP was in place for 2 weeks only. This short time, although sufficient to halt the ongoing LV dilatation, was not evaluated for a longer period, because LD electrical activation was subsequently carried out. It is possible, therefore, that a longer period of passive cardiac containment could have led to reduced LV sizes, although other studies [14–16, 23] have clearly shown that the usual result of adynamic CMP is a stabilization of LV dimensions and not a reduction of LV sizes.
Wrapped muscle histology was not performed systematically; therefore, despite observation of preserved muscle structure in the muscle biopsies performed, no conclusive information could be provided with regards to structural preservation of the muscle graft. Accordingly, no definitive conclusions can be drawn about the efficacy of the stimulation protocol used in the study to avoid or reduce notorious long-term muscle degeneration [27].
The hemodynamics of the right side of the heart was not fully elucidated, although some data regarding the performance of the right ventricle could be extrapolated.
Finally, the high flow conditions may have affected the transformational process of the chronically stimulated muscle graft, hence its structural and mechanical properties, but this aspect was not assessed in our study and may require specific investigation.
In conclusion, this study investigated some of the working mechanisms of CMP in the presence of a dilated heart. The passive wrapping of a transposed muscle flap around an enlarged LV appeared to halt progressive LV dilatation. The LD muscle activation by electrical stimulation, however, was crucial to reverse ongoing cardiac dilatation. The acute effects of chronic CMP on cardiac hemodynamics were less substantial, although clearly documented in some cases. Recent advances in the electrical stimulation pattern of wrapped muscles will most likely provide a significant advantage in terms of structural preservation and, hence, of mechanical properties of skeletal muscle graft with predictable benefits on biomechanical cardiac support results.
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Acknowledgments
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We thank Jo Habets and Theo van der Nagel for excellent technical assistance. This study was financially supported by the European Community Institutional grant (ERBCHBGCT 930414), as part of the Human Capital and Mobility Program, and by Telectronics Pacing Systems, Inc. (Denver, CO).
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Abstract
Introduction
