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Ann Thorac Surg 1997;63:1706-1711
© 1997 The Society of Thoracic Surgeons

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Original Article: Cardiovascular

Effects of Wrapping Tightness on Acute Cardiac Function in Dynamic Cardiomyoplasty

First Department of Surgery, Gifu University School of Medicine, Gifu, Japan

Accepted for publication December 18, 1996.

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Background. It has not been clarified how tightly the heart should be wrapped for maximal augmentation of cardiac function in cardiomyoplasty.

Methods. Hearts in acute failure induced by propranolol were wrapped with the left latissimus dorsi muscle, loosely (loose CMP), moderately (moderate CMP), and tightly (tight CMP) in each of 5 pigs. To measure the pressure between the latissimus dorsi muscle and the left ventricle (LV), a Millar pressure catheter with a latex balloon was placed on the anterior wall of the LV. Left ventricular wall tension was calculated according to Laplace's law, using the difference between the LV pressure and the balloon pressure.

Results. In the loose CMP, moderate CMP, and tight CMP groups, the mean balloon pressures during unassisted beats were 8.2, 10.4, and 13.2 mm Hg, respectively. During unassisted beats, the mean LV wall tension values were 38,683, 29,938 (p < 0.05 versus loose CMP), and 26,652 (p < 0.05 versus loose CMP) dynes/cm, respectively, the peak LV pressures were 76.8, 73.8, and 65 (p < 0.05 versus loose CMP) mm Hg, respectively, and the stroke volumes were 12.8, 9.2, and 8.5 (p < 0.05 versus loose CMP) mL, respectively. During assisted beats, the mean LV wall tension values were 20,059, 11,290, and 7,893 (p < 0.05 versus loose CMP) dynes/cm, respectively, the peak LV pressures were 94.1, 98.1, and 92.0 mm Hg, respectively, and the stroke volumes were 13.8, 11.6, and 9.4 (p < 0.05 versus loose CMP) mL, respectively.

Conclusions. During unassisted beats, tight CMP (13 mm Hg) had the advantage of diminishing LV wall tension, but the disadvantage of diminishing LV pressure and stroke volume, compared with loose CMP (8 mm Hg). Moderate CMP (10 mm Hg), however, had the advantage of diminishing LV wall tension without a decrease in LV pressure and stroke volume.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
See also page 1711.

The first clinical dynamic cardiomyoplasty in the world was performed in 1985 [1], and this procedure is now being done in patients with dilated or ischemic cardiomyopathy and Chagas' disease [2–4]. Experimental studies have shown that cardiomyoplasty with the left latissimus dorsi muscle (LDM), the right LDM [5], or both LDMs [6] provides excellent hemodynamic augmentation. The preferred procedure for dynamic cardiomyoplasty has involved orientation of the LDM fiber circumferential to the heart and perpendicular to the ventricular septum [7]. It is unclear, however, how tightly the heart should be wrapped with the LDM for maximal augmentation of cardiac function in dynamic cardiomyoplasty, because objective parameters of wrapping tightness have not been clearly defined. This is considered to be one of the factors critical to the success of this procedure. We hypothesized that the pressure between the LDM and the heart, measured by a Millar pressure catheter equipped with a fluid-filled balloon, would provide an objective parameter of tightness. We conducted a study to clarify the optimal wrapping tightness in dynamic cardiomyoplasty by evaluating cardiac function in three grades of pressure between the LDM and the heart.

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Five pigs weighing 14 to 18 kg (mean, 15.9 ± 1.9 kg) were used in our experiment. For the induction of anesthesia, 25 mg/kg of ketamine hydrochloride and 5 mg/kg of pentobarbital sodium were administered, first intramuscularly and then intravenously. Tracheostomy was performed and mechanical positive-pressure ventilation was initiated. To maintain the anesthesia, pentobarbital sodium was administered intravenously, as needed.

Through a left lateral longitudinal thoracic incision, the left, unconditioned LDM was mobilized completely from all attachments except the thoracodorsal neurovascular pedicle. The entire LDM, except for the pedicle, was passed into the left thoracic cavity through a 3-cm window in the partially removed second rib, and its humeral insertion was fixed with a suture around the third rib. The pericardium was opened longitudinally through a median sternotomy. Both the left and right ventricles were wrapped with the LDM in a clockwise fashion by the placement of several mattress sutures at the pericardium.

To measure the pressure between the LDM and the left ventricle (LV), a 5F catheter pressure transducer (MPC-500; Millar Instruments, Inc, Houston, TX) with a fluid-filled latex balloon, 5 mm in diameter, was placed on the anterior wall of the LV midway between the apex and the base. Balloon pressure (P_B), equal to the pressure between the LDM and the LV, was amplified with a transducer control unit (TC-510; Millar Instruments, Inc) and a pressure amplifier (AP-641G; Nihon Kohden, Tokyo, Japan). A 7F conductance catheter (2-RF-517; Leycom, Ocgstgeet, the Netherlands) was placed along the long axis of the LV cavity through the apex. Volume measurements were obtained with a volumetric system (Sigma 5; Leycom). The volume measurements were calibrated by the injection of 5 mL of hypertonic saline solution (8%) into the pulmonary artery. An LV pressure (P_LV) catheter was placed through the right carotid artery, and P_LV was amplified with a pressure amplifier (AP-641G; Nihon Kohden). The data were transferred to a data acquisition and analysis system (MacLab/8 and Chart v3.4; Analog Digital Instruments, Castle Hill, Australia), and were analyzed with a computer (Power Macintosh 8500/120; Apple Computer, Inc, Cupertino, CA).

In all animals, insufficient LDM mass did not allow complete muscle wrapping. The anterior wall of the right ventricle, left without muscle covering, was covered by a triangle of polytetrafluoroethylene patch. This polytetrafluoroethylene patch was placed anteriorly on the right ventricle and connected to the LDM with sutures. Wrapping tightness of the LDM was regulated by pulling several monofilament sutures placed at the two sides of the patch. In each pig, the heart was wrapped with the LDM in the following three grades of tightness: loosely, by using 10 mm Hg in P_B (loose CMP); moderately, by using between 10 and 12 mm Hg (moderate CMP); and tightly, by using more than 12 mm Hg (tight CMP). Loose CMP was performed first without stimulation, and then 0.05 mg/kg of propranolol was administered intravenously as a bolus to diminish peak P_LV to 80 mm Hg. In cases in which peak P_LV did not diminish to 80 mm Hg, the same dose of propranolol was administered repeatedly until this occurred. The LDM was stimulated to provide five contractions in each grade of wrapping tightness and then given 3 minutes of rest. In the second step, moderate CMP was performed. Then, once the tightness of the LDM was returned to that of loose CMP, tight CMP was performed last.

Burst stimulation, using 3 V of pulse amplitude, 210 µs of pulse width, 30 Hz of burst rate, and 200 ms of burst duration (number of pulses = 7), was delivered by a thoracodorsal nerve bipolar cuff using an electronic stimulator (SEN3301; Nihon Kohden). Stimulation was performed with 4 ms of synchronization delay from the R wave on the body surface electrocardiogram. The heart-to-muscle contraction ratio was set at 2:1 to compare hemodynamic parameters achieved during unassisted beats with those of assisted beats.

Stroke volume (SV) was calculated as the difference between LV end-diastolic volume and end-systolic volume in a cardiac cycle. Ejection fraction was calculated as SV/LV end-diastolic volume. It was assumed that P_B at the anterior wall of the LV midway between the apex and the base was constant in any place between the LDM and the LV. It was further assumed that the heart was modeled by a sphere, and the wall tension was calculated as a function of the radius and the difference between the pressure inside and outside the wall. Based on that, we derived a modified form of Laplace's equation in the following form: P_LV - P_B = 2T_LV/R, where P_LV is LV pressure, P_B is balloon pressure equal to the pressure between the LDM and the LV, T_LV is LV wall tension, and R is the radius of the LV. Because it was assumed that the LV was a sphere, R was calculated with the following equation: V_LV = 4R³/3, where V_LV is LV volume and R is the radius of the LV. Instantaneous T_LV was calculated using both equations, and mean T_LV when a cardiac cycle was done.

All animals received humane care in compliance with the "Guide for the Care and Use of Laboratory Animals" published by the National Institutes of Health (NIH publication 85-23, revised 1985).

For comparison of multiple groups, analysis of variance was used for repeated measurements with the Bonferroni multiple-comparison test. All data are expressed as means plus or minus standard deviations. A p value of less than 0.05 was considered statistically significant.

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Figure 1 shows mean P_B during both unassisted and assisted beats in three grades of tightness. During unassisted beats, mean P_B in loose CMP, moderate CMP, and tight CMP was 8.2 ± 0.9, 10.4 ± 0.7, and 13.2 ± 1.5 mm Hg, respectively. During assisted beats, compared with unassisted beats, mean P_B increased significantly (p < 0.01). Mean P_B in loose CMP, moderate CMP, and tight CMP was 17.7 ± 5, 23.8 ± 7.8, and 27.5 ± 4.3 mm Hg, respectively. During assisted beats, mean P_B in tight CMP was significantly greater, compared with loose CMP (p < 0.05).

View larger version (15K): [in this window] [in a new window]   Fig 1. . Mean balloon pressure (PB) during both unassisted and assisted beats in three grades of wrapping tightness. (CMP = cardiomyoplasty.)

View larger version (15K): [in this window] [in a new window]   Fig 2. . Stroke volume (SV) during both unassisted and assisted beats in three grades of wrapping tightness. (CMP = cardiomyoplasty; NS = not significant.)

View larger version (13K): [in this window] [in a new window]   Fig 3. . Ejection fraction (EF) during both unassisted and assisted beats in three grades of wrapping tightness. (CMP = cardiomyoplasty; NS = not significant.)

View larger version (15K): [in this window] [in a new window]   Fig 4. . Peak left ventricular pressure (PLV) during both unassisted and assisted beats in three grades of wrapping tightness. (CMP = cardiomyoplasty.)

View larger version (16K): [in this window] [in a new window]   Fig 5. . Mean left ventricular wall tension (TLV) during both unassisted and assisted beats in three grades of wrapping tightness. (CMP = cardiomyoplasty.)

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Since clinical dynamic cardiomyoplasty first was performed by Carpentier and Chachques [1], it has been accepted that LDM (left, right, or bilateral) is preferred for maximal augmentation of cardiac function [5, 6] and muscle fiber orientation, whether parallel or perpendicular to the ventricular septum [7]. How tightly the heart is wrapped with the LDM in dynamic cardiomyoplasty is one of the factors critical to the success of this procedure, even though objective parameters of tightness have yet to be established. Our study evaluated the optimal wrapping tightness of the LDM in dynamic cardiomyoplasty. We used P_B measured with a Millar pressure catheter using a fluid-filled balloon placed between the LDM and the LV as an objective parameter of tightness. Because tightness of wrapping in dynamic cardiomyoplasty is related to the increase in P_B, depending on how much is used, P_B is considered to be useful as an objective parameter of wrapping tightness. Balloon pressure was more than 7 mm Hg even with the loosest wrapping, and P_LV decreased to lower than 60 mm Hg with more than 15 mm Hg of P_B. Originally, we had attempted to assess cardiac function with a random order of wrapping tightness in each animal to make proper comparisons of the different tightness levels. The range of P_B that was reached was very narrow, between 7 and 15 mm Hg. Therefore, we regulated P_B with wrapping tightness, proceeding sequentially from loose to moderate to tight instead of in a random order.

We assumed that P_B measured on the anterior wall of the LV midway between the apex and the base was constant in any place between the LDM and the LV in our study. LV wall tension calculated in our study, however, was just the tension at the point where P_B was measured. Although we assumed that P_B measured on the LV anterior wall was the same for all points between the LDM and the LV because of our decision to model the LV as a sphere, P_B measured at different points may not be the same. The investigation of the effects of dynamic cardiomyoplasty on regional LV wall motion by LV angiography showed improvement in anterobasal (19%), anterolateral (22%), apical (17%), diaphragmatic (22%), and posterobasal (21%) regions, compared with regional wall motion before the procedure [8]. Radionuclide angiographic studies showed that regional wall motion of the low lateral region was significantly higher than during nonstimulation [9]. Further investigations to determine whether there are any differences among the LDM compressions at various points using Millar pressure catheters with balloons will be necessary to clarify systolic augmentation in dynamic cardiomyoplasty.

Lee and associates [10] measured the pressure, wall thickness, and minor and major axis dimensions of the LV, and demonstrated that dynamic cardiomyoplasty diminished mean systolic LV wall stress significantly. They calculated the LV wall stress with a formula based on the thin-walled ellipsoid model of the LV described by Sandler and Dodge [11], using P_LV. In dynamic cardiomyoplasty, however, pressures against the LV wall are not only P_LV, but also LDM compression of the LV equal to the pressure between the LDM and the LV that was measured as P_B in our study. Therefore, it is understood that the differences between P_LV and P_B have to be used in calculating LV wall stress. We chose to model the LV as a sphere rather than as an ellipsoid because we could then determine the radius based on conductance catheter measurements and, as a result, compute T_LV. This probably is not accurate, but it is acceptable for comparative measurements. We were able to calculate only T_LV and not the LV wall stress because the LV wall thickness was not measured. Because the LV wall thickness increases at end-systole [11], it is assumed that the mean LV wall stress during assisted beats diminishes, unlike during unassisted beats in dynamic cardiomyoplasty. Decrease of the LV wall stress suggests that myocardial oxygen consumption (VO₂) is diminished. In an isolated cross-circulated dog-heart model, however, dynamic cardiac compression by a compression device augmented LV pump function without increasing myocardial VO₂ [12]. Although Cho and associates [13] demonstrated that assisted beats during 1:2 stimulation in dynamic cardiomyoplasty produced an increase in end-systolic elastance of the heart, the end-systolic elastance they described is considered to be that of both the LV and the LDM, and not that of the LV only. Theoretically, the end-systolic elastance of the LV can be calculated only with the difference between P_LV and P_B that we measured. Because pressure–volume area correlates well with myocardial VO₂ [14], pressure–volume area calculated with this difference is considered to correlate with myocardial VO₂ in dynamic cardiomyoplasty. Direct measurement of myocardial VO₂ in dynamic cardiomyoplasty still will be needed. So far, it has been difficult to dissect out the LV component of the contractility of the LV–LDM unit. With measurements of P_B, it may be possible to calculate the end-systolic elastance of the LV alone. When the P_LV and the V_LV are measured under varying stages of preload or afterload for the LV, we can see the effects of the wrap on contractility and T_LV, both of which are major determinants of myocardial VO_2.

During unassisted beats, tight CMP had the advantage of diminishing mean T_LV, but the disadvantage of diminishing SV and peak P_LV, compared with loose CMP. Moderate CMP, however, had the advantage of diminishing mean T_LV without significantly decreasing SV and peak P_LV. During assisted beats, tight CMP had the advantage of diminishing mean T_LV, but the disadvantage of diminishing SV, compared with loose CMP. During assisted beats, moderate CMP was not significantly different from loose CMP in all measured parameters. Our results suggest the following. During unassisted beats, the cardiomyoplasty in which the pressure between the LDM and the LV is 10 mm Hg is superior to the cardiomyoplasty in which the pressure between the LDM and the LV is 8 mm Hg, because of diminishing myocardial VO₂. During assisted beats, the cardiomyoplasty of 13 mm Hg is superior to the cardiomyoplasty of 8 mm Hg, because of diminishing myocardial VO₂, but is also inferior to it because of diminishing hemodynamics. In our preliminary study, acute heart failure induced by ß-blockers was investigated, not chronic heart failure such as dilated cardiomyopathy. Because ß-blockers were administered after the heart was wrapped with the LDM, the comparisons were made not with the unwrapped failing heart, but with the loosely wrapped failing heart.

The data presented are based on numerous assumptions. These include trying to achieve a certain P_LV by titration with a ß-blocker that was rather unstable during the course of the experiment. However, there were no significant differences in peak P_LV among the three grades of tightness during assisted beats. Other assumptions include the use of a spherical model for the calculation of T_LV, and the assumption of a uniform interface pressure between the muscle wrap and the epicardium. Another assumption was that the choice of the size of the balloon placed in this interface could affect the interface pressure (P_B) recorded [15]. It is believed that fixing the size of the balloon makes P_B useful as a parameter of wrapping tightness.

One of the limitations of our study is that we investigated acute dynamic cardiomyoplasty with the unconditioned LDM in a drug-induced model of acute heart failure. Although our study demonstrated that the ejection fraction was unchanged and the peak P_LV was significantly increased by acute dynamic cardiomyoplasty with the unconditioned LDM in acute heart failure, long-term cardiomyoplasty with the conditioned LDM in chronic heart failure improved the ejection fraction significantly, and peak P_LV remain unchanged [16]. In long-term cardiomyoplasty with the conditioned LDM in chronic heart failure conditions such as dilated cardiomyopathy, wrapping tightness will have to be examined further. The way in which the wrapping tightness of the LDM affects the "girdling" effect of cardiomyoplasty [17] also is believed to affect the long-term results of dynamic cardiomyoplasty (eg, which grade of tightness is more beneficial in the setting of progressive cardiac dilatation).

It is important to acknowledge that LDM tension will change over time as the muscle adjusts to its new resting tension, making the initial wrapping tightness a rather transitory consideration. If the LDM relaxes within a few hours after the operation, its initial tightness may not be a critical factor in the recovery of the patient. It will be necessary to measure P_B over a more extended period, ranging from 30 minutes to a few hours, to determine how fast the muscle accommodates to the wrapped configuration. The ability of the skeletal muscle to adapt gradually to the changes in resting tension by sarcomere addition or depletion [18, 19], known as conformational change [20], would make the initial tension applied by the LDM on the myocardium at the time of operation irrelevant to the later function of the cardiomyoplasty. In the early postoperative period, before the conformational changes of the LDM wrap, clinically the LDM is not fully stimulated. It usually is given no stimulation to contract at all for the first week or two for "vascular delay," and for several more weeks to allow skeletal muscle transformation to occur. By the time the full burst stimulation is applied, the resting length and tension have changed considerably from the initial conditions. Therefore, our findings obtained at the time of acute operation are relevant only to the early postoperative period in clinical dynamic cardiomyoplasty. Further investigation of cardiac function in later stages, such as after conformational changes take place, with different wrapping tightnesses at the time of operation is necessary.

The wrapping tightness of the LDM, without any stimulation, is pertinent at the time of the operation primarily for its effect on venous return, because it may restrict the ventricular filling analogous to constrictive pericarditis. Because the skeletal muscle is not stimulated to contract at this stage, the effect of resting tension on the Frank-Starling relation is not relevant. It previously had been reported that wrapping of the LDM per se, without stimulation, can cause an immediate decrease in cardiac function, presumably as a result of reduced diastolic filling. Therefore, it will be valuable to study the effects of muscle wrapping tightness, without stimulation, on ventricular diastolic filling and other hemodynamic changes using our model.

If this technique of measuring wrapping tightness were to be applied to humans, we would have to take into account the effects on P_B of the catecholaminergic state of the patient. If the wrap was performed intraoperatively while the patient was receiving large doses of inotropic agents, we could assume that when the infusion was discontinued, P_B would increase. However, P_B of the catecholaminergic state was not investigated in our study. Because P_B of the noncatecholaminergic state is considered to be correlated with that of the catecholaminergic state, we can safely predict the former with intraoperative measurements of the latter. Our method for measuring tightness at the initial operation does not adequately reproduce the essentials of clinical cardiomyoplasty, namely, a long-term, conditioned LDM wrap in dilated cardiomyopathy. It is well known that over a certain number of weeks, whether conditioned or not, the LDM flap becomes smaller and more fibrotic. In neither chronic experimental preparations nor clinical cases does tamponade physiology arise as the wrap and the LV shrink in size, as if wrapping tightness and intracavitary P_LV autoregulate. It will be necessary to evaluate the significance of wrapping tightness after the customary conditioning or healing period, and to determine the functional consequences of each degree of tightness. Clinical cardiomyoplasty produces remodeling in a failing heart primarily for geometric reasons, such as dilation in diffuse Chagas' disease or scarred ischemic myocardium, whereas our model uses a heart failing primarily from altered contractility. Moreover, we must be cautious when making inferences about myocardial VO₂ based on indices of wall stress only, while using ß-blockers or one of the other major determinants of myocardial VO₂, contractility.

	Acknowledgments

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
We thank Mr Hideo Yokoyama for his excellent technical assistance.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Address reprint requests to Dr Takagi, First Department of Surgery, Gifu University School of Medicine, 40 Tsukasa, Gifu 500, Japan.

	References

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Takagi, H. Articles by Mori, Y. Search for Related Content PubMed PubMed Citation Articles by Takagi, H. Articles by Mori, Y.