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Ann Thorac Surg 1999;67:1339-1344
© 1999 The Society of Thoracic Surgeons

Original Articles

A new method of double cardiomyoplasty: "contractile muscular sling"

Hidetoshi Furuta, MDa, Go Watanabe, MDa, Takuro Misaki, MDa, Katsushi Ueyama, MDa

a Department of Surgery (1), Toyama Medical and Pharmaceutical University, Toyama, Japan

Accepted for publication November 17, 1998.

Address reprint requests to Dr Furuta, Department of Surgery (1), Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama, Japan 930-0152


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 References
 
Background. In several experimental studies, double cardiomyoplasty using both latissimus dorsi muscles did not provide sufficient assist to the failing heart and did not clearly show improvement compared with single cardiomyoplasty. This study demonstrated the superior efficacy of our method of double cardiomyoplasty compared with single cardiomyoplasty.

Methods. In 16 dogs, the two latissimus dorsi muscles were crossed in front of the heart and directly sutured to each other behind the heart. Control hemodynamic measurements were obtained, and acute heart failure was induced by intravenous administration of propranolol. After the hemodynamic changes with bilateral latissimus dorsi muscle assistance were measured, single cardiomyoplasty was done in the same dog, and the hemodynamic variables were measured.

Results. With our double cardiomyoplasty, aortic systolic pressure increased by 25% (p < 0.001); pulmonary artery systolic pressure, by 40% (p < 0.001); end-systolic elastance, by 155% (p < 0.001); and cardiac output, by 55% (p < 0.001). There were significant increases in aortic pressure, pulmonary artery pressure, end-systolic elastance, stroke volume, and cardiac output with our double cardiomyoplasty compared with single cardiomyoplasty.

Conclusions. In this study, our double cardiomyoplasty provided significant hemodynamic improvement compared with single cardiomyoplasty.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 References
 
Several ways of using skeletal muscle to augment heart function have been reported. Kantrowitz and McKinnon [1] wrapped the diaphragm around the descending aorta of dogs and showed an increase in systemic blood pressure with phrenic nerve stimulation. Other groups [2, 3] studied the effect of skeletal muscle stimulation on hemodynamic variables. In these studies, the most serious problem related to use of skeletal muscle was muscle fatigue. In 1969, Salmons and Vrbova [4] reported that low-frequency stimulation of canine latissimus dorsi muscles effected a uniform transformation of fast muscles into slow muscles. On the basis of this report and other experimental studies [5–7], in 1985, Carpentier and Chachques [8] applied dynamic cardiomyoplasty clinically for the first time. Since then, dynamic cardiomyoplasty has been carried out in about 800 patients.

Reviews [9–12] of clinical data suggested that cardiomyoplasty improves the clinical symptoms of patients with dilated and ischemic cardiomyopathies but provides no direct cardiac assistance. With respect to direct cardiac assistance with cardiomyoplasty, we [13–15] have previously reported several experimental studies. We now have developed a double cardiomyoplasty that is a much more effective method of using skeletal muscle. Other groups [16–19] have also done animal studies using both latissimus dorsi muscles.

In this study, we applied our new double cardiomyoplasty, which is based on a very different concept of how to wrap the heart. Briefly, the two latissimus dorsi muscles are made into a "contractile muscular sling" by suturing their distal portions to each other. When the "sling" contracts, the vector of the force is directed toward the center of the sling. After the hemodynamic changes with bilateral latissimus dorsi muscle assistance were measured, the muscles were removed from the heart. Using the method described by Carpentier and Chachques [8], single cardiomyoplasty was carried out, and the hemodynamic variables were measured again. We then compared the hemodynamic effects with double versus single cardiomyoplasty.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 References
 
Sixteen adult mongrel dogs, each weighing between 8.5 and 20 kg (mean weight, 13.1 ± 5.9 kg), were studied. All animals received humane care in compliance with the "Principles of Laboratory Animal Care" formulated by the National Society for Medical Research and the "Guide for the Care and Use of Laboratory Animals" published by the National Institutes of Health (NIH publication 85-23, revised 1985).

Surgical procedures
Anesthesia was induced by intramuscular administration of ketamine hydrochloride (10 mg/kg) and maintained through the inhalation of Fluothane (halothane) (1% to 2%). Lactated Ringer’s solution was used for intravenous fluid replacement.

Skin incisions 10 cm long were made in the posterior edges of the axillary region on both sides. The two latissimus dorsi muscles were dissected from the chest wall with a hot knife [20]. The collateral blood vessels excepting the thoracodorsal neurovascular pedicles were divided from the chest wall. Electrodes especially designed for muscle stimulation (Myos; Biotronik, Berlin, Germany) were placed proximally near the thoracodorsal nerve branches of the two latissimus dorsi muscles. Bilateral windows into the chest were created by removing the lateral portion of the second ribs.

Then median sternotomy and pericardiotomy were performed, and the heart was exposed. A sensing screw-in epicardial electrode was placed on the right ventricular free wall to monitor the R wave. Both venae cavae were dissected and encircled with umbilical tapes. An 8F volume-conductance catheter (ANP 565; Sentron, Roden, the Netherlands) and a pressure micromanometer were placed into the left ventricle through its apex. The two catheters were connected to a Sigma 5 recorder (CardioDynamics, the Netherlands) to obtain the pressure–volume loops.

After the two latissimus dorsi muscles were transferred into the thorax, our double cardiomyoplasty was done. The left latissimus dorsi muscle was placed on the heart, the right latissimus dorsi muscle was put over the left latissimus dorsi muscle, and both muscles were crossed in front of the heart. The heart was wrapped with these muscles, in a counterclockwise direction with the left, and a clockwise direction with the right latissimus dorsi muscles. The two muscles were sutured to each other behind the heart (Fig 1). Other sutures were placed from the edge of the latissimus dorsi muscles to the myocardium just below the atrioventricular groove. The two muscles acted as a "contractile muscular sling." When the "sling" contracted, the vector of the force was directed toward the center of the sling.



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  		Fig 1. Our method of double cardiomyoplasty. Both latissimus dorsi muscles (LDM) are crossed in front of the heart and then wrapped around it, the left latissimus dorsi going counterclockwise and the right, clockwise. Then the two muscles are sutured to each other behind the heart, thereby forming a "sling". When this sling contracts, the force vector is directed toward the center of the sling.

 
The following variables were measured: aortic pressure (AoP), pulmonary artery pressure (PAP), central venous pressure, end-systolic elastance (Ees), arterial elastance, left ventricular end-diastolic pressure, stroke volume (SV), and cardiac output (CO). Baseline hemodynamic measurements (control) were made. Another set of control measurements was obtained after the muscles were wrapped around the heart. To induce acute heart failure, propranolol hydrochloride (3 mg/kg) was administered intravenously to the animals. After heart failure was induced, the hemodynamic measurements were re-peated. The muscles were then stimulated, and the measurements were obtained 1 minute after muscle stimulation. Thus, hemodynamic changes with and without bilateral latissimus dorsi muscle assistance were recorded. Then the muscles were allowed to rest for 30 minutes to prevent fatigue. After all measurements were completed, the muscles were removed from the heart. Using the method described by Carpentier and Chachques [8], single cardiomyoplasty by wrapping the heart with the left latissimus dorsi muscle was carried out, and the hemodynamic variables were measured again.

Stimulation protocol
Both latissimus dorsi muscles were stimulated synchronously with the R wave at a 2:1 ratio with a Myos multiprogrammable cardiomyoplasty stimulator. The synchronization interval was 30 ms, the pulse amplitude was 4.8 V, the pulse width was 0.15 ms, the burst frequency was 33 Hz, and the burst duration was 150 ms.

Statistical analysis
All data are shown as the mean ± the standard error of the mean. The comparisons were made by means of the paired t test. The significance level was set at a p value of less than 0.05.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 References
 
There were no significant hemodynamic differences before or after wrapping the heart. After acute heart failure was induced, systolic AoP decreased by 34% (p < 0.001), central venous pressure increased by 23% (p < 0.01), Ees decreased by 38% (p < 0.01), end-diastolic pressure increased by 28% (p < 0.01), SV decreased by 44% (p < 0.001), and CO decreased by 45% (p < 0.001) (Table 1). Systolic PAP and arterial elastance showed nearly no change. Pressure tracings and pressure–volume loops after contraction of both latissimus dorsi muscles are shown in Figures 2 and 3, respectively. Systolic AoP increased by 25% (from 60.3 ± 12.1 mm Hg to 75.2 ± 14.1 mm Hg; p < 0.001), systolic PAP increased by 40% (from 22.6 ± 4.1 mm Hg to 31.6 ± 7.1 mm Hg; p < 0.001), Ees increased by 155% (from 3.1 ± 1.1 mm Hg/mL to 7.9 ± 1.6 mm Hg/mL; p < 0.001), SV increased by 27% (from 11.0 ± 3.4 mL to 14.0 ± 7.0 mL; p < 0.01), and CO increased by 55% (from 1.1 ± 0.3 L/min to 1.7 ± 0.9 L/min; p < 0.001) (Fig 4). When the latissimus dorsi muscles were contracted after the wrapping of the heart by the method of Carpentier and Chachques [8], AoP increased by 16% (p < 0.05) and Ees, by 47% (p < 0.01). The PAP increased by 9%, SV increased by 10%, and CO increased by 27%, but these changes were not significant (Fig 5).


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  		Table 1. Hemodynamic Changes With Propranolola,b

 


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  		Fig 2. Pressure tracings with synchronous burst stimulation of both latissimus dorsi muscles after propranolol-induced heart failure. The solid arrow shows a point of starting stimulation. The asterisk shows assisted beat. (AoF = aortic flow; AoP = aortic pressure; CVP = central venous pressure; PAP = pulmonary artery pressure.)

 


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  		Fig 3. Pressure–volume loops. The slope of end-systolic elastance and stroke volume increased with double cardiomyoplasty (CMP).

 


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  		Fig 4. Hemodynamic changes with double cardiomyoplasty (DCMP): aortic pressure (AoP) (upper = systolic and lower = diastolic); pulmonary artery pressure (PAP) (upper = systolic and lower = diastolic); end-systolic elastance (Ees); arterial elastance (Ea); end-diastolic pressure (EDP); cardiac output (CO); and stroke volume (SV). (NS = not significant.)

 


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  		Fig 5. Hemodynamic changes with single cardiomyoplasty (SCMP); aortic pressure (AoP) (upper = systolic and lower = diastolic); pulmonary artery pressure (PAP) (upper = systolic and lower = diastolic); end-systolic elastance (Ees); arterial elastance (Ea); end-diastolic pressure (EDP); cardiac output (CO); and stroke volume (SV). (NS = not significant.)

 
There were significant increases in systolic AoP (p < 0.01), systolic PAP (p < 0.001), Ees (p < 0.001), SV (p < 0.05), and CO (p < 0.05) with our double cardiomyoplasty compared with single cardiomyoplasty (Table 2).


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  		Table 2. Comparison of Double and Single Cardiomyoplastya

 

   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
References
 
Four mechanisms have been postulated to explain the efficacy of dynamic cardiomyoplasty [21]. The first is a squeezing effect [22]. When a latissimus dorsi muscle that is wrapped around the heart contracts, the heart is squeezed directly, and consequently cardiac function may improve. The second mechanism is a sparing effect [23, 24]. Because of the latissimus dorsi muscle contractions, the work load of the myocardium may decrease after cardiomyoplasty. The third mechanism is a girdling effect [25]. The latissimus dorsi muscle wrapped around the heart may prevent enlargement of the failing heart. The fourth mechanism is a collateral effect [26]. Increase in collateral flow from the latissimus dorsi muscle to the ischemic heart may improve cardiac function.

Dynamic cardiomyoplasty has been proposed for the treatment of dilated cardiomyopathies. We thought that it would induce direct hemodynamic improvement (squeezing effect), but several reports [9–12] indicated that dynamic cardiomyoplasty did not directly improve cardiac function. However, symptoms could be improved by the indirect effects (sparing, girdling, collateral) of this method [23–26]. Recently, three different types of double cardiomyoplasty to reinforce the squeezing effect were studied in three institutions [16–19]. The results were not satisfactory.

To achieve more effective hemodynamic assistance, we propose a new wrapping technique for double cardiomyoplasty that can optimize the muscle power. The heart is wrapped with the latissimus dorsi muscles, the left one in a counterclockwise direction and the right one in a clockwise direction. Then both muscles are sutured to each other behind the heart, thereby creating a belt, which we call the "contractile muscular sling." When the "sling" contracts, the force vector is directed to the center of the sling, thus achieving the maximum squeezing effect on the heart.

In this study, the sling increased in systolic AoP, Ees, SV, and CO significantly. After the heart was wrapped using the method of Carpentier and Chachques [8], AoP and Ees increased significantly on stimulation of the left latissimus dorsi muscle. Further, the sling also increased systolic PAP significantly, which means that one method provides the squeezing effect for the right ventricle. The comparison between double cardiomyoplasty and single cardiomyoplasty showed a significant increase in systolic AoP, systolic PAP, Ees, SV, and CO with double cardiomyoplasty. It was evident that our double cardiomyoplasty was more effective than single cardiomyoplasty. In particular, our double cardiomyoplasty provided not only left ventricular support but also right ventricular support.

We also found differences in hemodynamic improvement between our method and methods of others [16–19]. Our double cardiomyoplasty increased systolic AoP by 25%, systolic PAP by 40%, Ees by 155%, and CO by 55%. The double cardiomyoplasty method used at the Allegheny General Hospital increased AoP by 11%, PAP by 35%, and CO by 10% [16]. The Wayne State University method increased AoP by 21% and CO by 22%, and Ees improved to 7.1 mm Hg/mL. The Baylor College of Medicine method increased CO by 32%, and AoP was unchanged [19]. Comparing these data suggests our double cardiomyoplasty has superior efficacy.

This study has limitations as well as clinical implications. In terms of limitations, we did not use preconditioned skeletal muscles. Transformed muscles generate less force than nontransformed muscles [17]. Using preconditioned skeletal muscles, we are currently investigating the long-term effects of our method. In terms of clinical implications, we demonstrated that our double cardiomyoplasty provides significantly improved hemodynamic support compared with single cardiomyoplasty. In particular, double cardiomyoplasty provides not only left ventricular support but also right ventricular support. Therefore, we expect our double cardiomyoplasty may be effective in patients with biventricular failure.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

  1. Kantrowitz A., McKinnon W.M.P. The experimental use of the diaphragm as an auxiliary myocardium. Surg Forum 1959;9:266-268.
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