Latissimus dorsi and serratus anterior dynamic descending aortomyoplasty for ischemic cardiac failure

Latissimus Dorsi and Serratus Anterior Dynamic Descending Aortomyoplasty for Ischemic Cardiac Failure Aurel C. Cernaianu, MD, Teimouraz V. Vassilidze, MD, PhD, David R. Flum, MD, John G. Gallucci, MD, Andreas Olah, MD, Jonathan H. Cilley, Jr, MD, Michael A. Grosso, MD, and Anthony J. DelRossi, MD Division of Cardiothoracic Surgery, Department of Surgery, Cooper Hospital/University Medical Center, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School at Camden, Camden, New Jersey

Dynamic descending aortomyoplasty for cardiac assistance is a form of extraaortic, skeletal muscle-driven counterpulsation. Controversy exists regarding its clinical applicability and the most suitable muscle autograft for the procedure. Specifically, the ligation of intercostal vessels required for descending aortomyoplasty may not be tolerated clinically. This study compared the hemodynamic profiles and long-term function of latissimus dorsi (LD) aortomyoplasty to a split serratus anterior (SA) descending aortomyoplasty in which all intercostal vessels were preserved. Descending aortomyoplasty was performed in 11 goats. In 5, the SA was harvested and its distal end divided, facilitating a wrap of the aorta without ligation of intercostal arteries. In 6, the LD was used as a circumferential aortic wrap. At 90 days, an occluder placed on the left anterior descending artery created an ischemic event. H e m o d y n a m i c studies with and without

here are currently 2.3 million patients with chronic T heart failure in the United States. Medical therapy for these patients is associated with a 5-year mortality of 50% [1, 2]. Unfortunately, cardiac transplantation is available to only a small percentage because of a shortage of donor hearts. While the search continues for implantable cardiac assist devices, the use of skeletal muscle for cardiac assistance has been successful in animal and h u m a n models [3]. Cardiomyoplasty and ascending aortomyoplasty have been offered as therapeutic alternatives for cardiac assistance in end-stage heart disease. Successful cardiomyoplasty has been reported in animal and h u m a n subjects [4]. The degree of its clinical benefit and the physiologic mechanism of its assistance have been debated. Moreover, cardiomyoplasty m a y be contraindicated in those patients with morbidly dilated or hypertrophic cardiomyopathy. In addition, although Accepted for publication Dec 6, 1994. Presented at the Ninth International Congress Cardiostim 94, Nice, France, June 15--18,1994. Address reprint requests to Dr Cernaianu, Division of Cardiothoracic Surgery, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Cooper Hospital/University Medical Center, 3 Cooper Plaza, Suite 411, Camden, NJ 08103. © 1995 by The Society of Thoracic Surgeons

assistance were performed in the ischemic and nonischemic states. Latissimus dorsi aortomyoplasty improved cardiac output 24% and 5.6%, stroke volume 29% and 66%, left ventricular stroke work index 30% and 166%, and coronary flow 4% and 3% in the normal and ischemic heart, respectively. Serratus anterior aortomyoplasty improved cardiac output 36% and 10%, stroke volume 42.8% and 13.5%, left ventricular stroke work index 64% and 21%, and coronary flow 8% and 4.3%, in the normal and ischemic heart, respectively. Two of the SA autografts were fibrotic and nonfunctional at 3 months. Aortomyoplasty with either SA or LD muscle improves cardiac function in the normal and ischemic heart. However, divided SA is associated with a higher rate of fibrosis and may be less suitable for the procedure.

(Ann Thorac Surgery 1995;59:639-43)

subsequent cardiac transplantation after cardimyoplasty has been reported, the operation becomes more technically challenging. Ascending aortomyoplasty has been advocated as a form of biomechanichal assistance [5]. The procedure, as described by Chachques and colleagues [6], includes an aortotomy and aortic patch (neo-ventricle) to facilitate the displacement of sufficient blood volume during counterpulsation. The morbidity of such a procedure m a y be unacceptable in clinical use. However, descending aortomyoplasty may be a more attractive alternative because it does not require an aortotomy or significantly manipulate the heart. Descending aortomyoplasty has been performed in animal models with success [7]. The descending portion of the thoracic aorta allows a longer free segment for myoplasty and therefore, m a y provide more effective counterpulsation. In this report we describe descending aortomyoplasty in the ischemic animal model and offer it as an option for cardiac assistance based on the principles of the intraaortic balloon pump. A technical barrier to clinical trials remains the fact that a complete wrap of the descending aorta requires ligation of intercostal arteries. In h u m a n subjects it is likely that interrupting the vascular supply 0003-4975/95/$9.50 0003-4975(94)01053-F

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C E R N A I A N U ET AL D E S C E N D I N G AORTOMYOPLASTY

Table 1. Muscle Conditioning Schedule

Parameter

Fig 1. Schematic representation of latissimus dorsi descending aortomyoplasty with ligated intercostal arteries.

to the spinal cord to facilitate aortomyoplasty m a y result in paralysis. It has been suggested that dividing the fibers of a serratus anterior (SA) muscle flap and interdigitating them a r o u n d the intercostal arteries m a y preserve the spinal cord's vascular supply. This study compared aortomyoplasty with latissimus dorsi (LD) and split SA muscle flaps to assess the utility of a spinal cord preserving aortomyoplasty.

Material and Methods Eleven adult alpine goats weighing 42 + 8 kg were anesthetized with thiopental and halothane. In all animals a longitudinal left chest incision was created. Either the LD or SA was harvested by sharp dissection preserving the neurovascular pedicle. In each case the muscle was dissected free of its b o n y insertions and left intact at its origin. A bipolar pacing electrode was placed adjacent to the proximal neurovascular bundle (Medtronic model 4003; Medtronic, Minneapolis, MN). The second rib was partially resected to facilitate transfer of the muscle flap into the chest. Through a fifth interspace left lateral thoracotomy, a single, clockwise wrap of the descending aorta adjacent to the origin of left subclavian artery was completed. Latissimus dorsi aortomyoplasty required ligation of several pairs of intercostal vessels (Fig 1). In 5 animals the SA muscle was transferred into the chest in a similar fashion. The distal end of the SA muscle was divided longitudinally into several muscular bands allowing the muscle to interdigitate with the aorta while preserving the intercostal arteries (Fig 2). A single, circumferential wrap was performed in all cases. A unipolar, epicardial screw-in sensing lead (Medtronic model 6917A-53T) was placed on the right ventricle and a

Pulse width (ms) Sensitivity (mV) Amplitude (V) Delay (ms) Burst rate (Hz) Pulses/burst

Weeks 1-6

Week 7

Week 8

Week 9

Off Of Off Off Of Off

0.05 0.6 2.5 400 10 1

0.6 1.0 4.0 400 10 3

1.5 1.25 5.0 400 10 6

cardiomyostimulator (Medtronic model 1005) was inserted into a subcutaneous pocket. After a 6-week "vascular healing" period, the cardiomyostimulator was p r o g r a m m e d (Medtronic model 9710) to condition the muscle flap. The voltage, pulse frequency, and rate of the electrical stimulation were gradually increased (Table 1). The muscle stimulation was obtained with six-pulse bursts, pulse amplitude 4 to 6 V, pulse width 1.5 ms, burst rate 10 Hz. Diastolic counterpulsation was delayed 400 ms from the R wave of the electrocardiogram. At 3 months postoperatively the animals were evaluated under general anesthesia. Baseline hemodynamic measurements were made with a pulmonary artery catheter and a femoral artery cannula. Through a median sternotomy the pericardium was incised and the left anterior descending (LAD) artery was isolated. After prophylactic administration of intravenous lidocaine for arrhythmia, an occlusion of the LAD greater than 50% was created with an external vascular occluder (model OC5; In Vivo Metric, Healdsburg, CA). Diminished flow was confirmed with an extravascular sonographic flowprobe (Transonic Systems Inc, Ithaca, NY) distal to the occluder. After baseline data were obtained, the cardiomyostimulator was activated to compare assisted and nonassisted hemodynamic profiles. Measurements included left ventricular stroke work index (LVSWI), stroke v o l u m e (SV), left ventricular end-diastolic pressure (LVEDP), cardiac output, mean arterial pressure (MAP), and coronary blood flow. Thermodilution cardiac outputs in triplicate were computed and indirect measurements of cardiac function were assessed with a SpaceLabs Computer Analysis System (Spacelabs, Seattle, WA). Statistical analysis was performed using an IBM SPSS PC PLUS (Version 3.0) statistical analysis package. Paired t test and X2 test were used for statistical comparison between groups. Each animal served as its own control. A p value of less than 0.05 was considered statistically significant. Data are presented as mean + standard deviation where appropriate. All animals received h u m a n e 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).

Results Fig 2. Serratus anterior descending aortomyoplasty with distal end divided to allow for preservation of intercostal arteries.

Six goats underwent LD aortomyoplasty. All animals tolerated the procedure well. On average, two to three

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Table 2. Hemodynamic Changes in the Normal Heart LD Variable

CMS Off

MAP (mm Hg) Cardiac output (L/min) SV (mL/min) LVSWI (g- min/beat/m 2) Coronary flow (mL/rnin)

69 4.5 38 26 78

+ 21 ± 2.5 ± 15 -+ 22 ± 32

SA

73 5.6 49 34 82

CMS On a

CMS Off

+ ± + + -

46 3.3 42 14 74

20 (5.7%) 2.3 (24%) b 13 (29%) b 20 (30%) b 28 (5.1%)

a Parentheses represent percentage improvement, b p < 0.05. CMS = cardiomyostimulator; LVSWI= left ventricular stroke work index;

+ ± ~ + +

CMS On a 49 4.5 60 23 80

3 4.1 10 5 20

MAP = mean arterial pressure;

+- 5 (6.5%) + 1.5 (36%) + 12 (42.8%) ± 4 (64%) ± 15 (8%)

SV = stroke volume.

tional at 3 m o n t h s a n d w e r e fibrotic o n a u t o p s y . Both failures w e r e w i t h i n the S A a o r t o m y o p l a s t y g r o u p . T h e r e w a s a statistically significant difference in failure rates b e t w e e n t h e SA g r o u p (2 of 5, 40%) a n d t h e LD g r o u p (0 of 6, 0%). N o t e c h n i c a l difficulties w e r e n o t e d in this g r o u p . M o r b i d i t y i n v o l v e d p r o l o n g e d w o u n d h e a l i n g in 2 a n i m a l s a n d t h e d e v e l o p m e n t of s e r o m a r e q u i r i n g d r a i n age in 4 a n i m a l s . N o f u n c t i o n a l deficit w a s i d e n t i f i e d as a r e s u l t of m u s c l e autografting.

pairs of i n t e r c o s t a l a r t e r i e s w e r e l i g a t e d in e a c h animal. N o i m m e d i a t e or c h r o n i c n e u r o l o g i c s e q u e l a e w e r e i d e n tified. Five goats u n d e r w e n t S A a o r t o m y o p l a s t y . N o intercostal a r t e r i e s w e r e l i g a t e d in this g r o u p . T w o of five S A a u t o g r a f t s w e r e n o n f u n c t i o n a l at 3 m o n t h s . T h e s e m u s c l e flaps w e r e o b s e r v e d to b e fibrotic a n d n o n f u n c t i o n a l at a u t o p s y . T h e s e a n i m a l s w e r e excluded from hemodynamic evaluations. H e m o d y n a m i c profiles in t h e n o n i s c h e m i c a n d ische m i c states are listed in T a b l e s 2 a n d 3, r e s p e c t i v e l y . Acute myocardial ischemia was characterized by a dec r e a s e in m e a n L A D flow of 57% in the LD g r o u p a n d 48% in t h e S A g r o u p . D e c r e a s e s in c o r o n a r y flow w e r e a s s o c i a t e d w i t h a 24% i n c r e a s e in L V E D P (9.2 -+ 4.0 to 12 + 3.1 m m Hg, p < 0.05) in t h e LD g r o u p a n d a 34% i n c r e a s e in L V E D P in t h e S A g r o u p (8.7 + 2.7 to 13.0 + 1.0 m m Hg, p < 0.05). T h e M A P a n d L V S W I d e c r e a s e d 47% a n d 43%, r e s p e c t i v e l y , a s s o c i a t e d w i t h n o n s i g n i f i c a n t v a r i a t i o n s in cardiac o u t p u t a n d SV d u r i n g t h e i s c h e m i c state in the LD g r o u p . T h e M A P , cardiac output, a n d SV d e c r e a s e d 13%, 12%, a n d 12%, r e s p e c t i v e l y , in t h e SA group during ischemia. Hemodynamic data during counterpulsation are s h o w n in T a b l e s 2 a n d 3. All cardiac v a r i a b l e s i m p r o v e d w i t h e i t h e r t y p e of a o r t o m y o p l a s t y w h e n t h e c a r d i o m y o s t i m u l a t o r w a s activated. I m p r o v e m e n t s w e r e significant in t h e i s c h e m i c a n d n o n i s c h e m i c states in t h e g r o u p w i t h LD a o r t o m y o p l a s t y . T h e r e w a s a t r e n d t o w a r d i m p r o v e d h e m o d y n a m i c s in t h e S A g r o u p ; h o w e v e r , a t t r i b u t a b l e to t h e s m a l l s u b g r o u p w i t h f u n c t i o n a l S A autografts, t h e statistical significance of t h e s e results w a s r e d u c e d . T w o of 11 m u s c l e w r a p s w e r e c o n s i d e r e d n o n f u n c -

Comment

In t h e U n i t e d States, 35,000 p a t i e n t s p e r y e a r r e q u i r e h e a r t t r a n s p l a n t a t i o n for c h r o n i c cardiac failure. Yearly, f e w e r t h a n 2,000 d o n o r h e a r t s b e c o m e a v a i l a b l e for t r a n s p l a n t a t i o n [8]. This m a k e s t h e s e a r c h for a l o n g t e r m , effective, a n d practical cardiac assist d e v i c e e s s e n tial. Skeletal m u s c l e - d r i v e n cardiac assist d e v i c e s are t h e o r e t i c a l l y ideal b e c a u s e t h e y are i n d e p e n d e n t of ext e r n a l p o w e r s o u r c e s a n d are n o n i m m u n o r e a c t i v e . T h e u s e of a u t o l o g o u s skeletal m u s c l e for cardiac assistance has b e e n u n d e r i n v e s t i g a t i o n for c a r d i o m y o p l a s t y a n d a o r t o m y o p l a s t y a n d has a c h i e v e d v a r i a b l e d e g r e e s of success. In 1959, K a n t r o w i t z a n d M c K i n n o n [9] first u s e d skeletal m u s c l e for cardiac assistance. By w r a p p i n g a n o n c o n d i t i o n e d s e g m e n t of d i a p h r a g m a r o u n d t h e d e s c e n d i n g aorta of a n i m a l s t h e s e i n v e s t i g a t o r s w e r e a b l e to d e m o n s t r a t e diastolic c o u n t e r p u l s a t i o n until m u s c l e fat i g u e d e v e l o p e d . This c o u n t e r p u l s a t i o n a u g m e n t e d M A P

Table 3. Hemodynamic Changes in the Ischemic Heart LD Variable

CMS Off

MAP (mm Hg) Cardiac output (L/min) SV (mL/min) LVSWI (g. min/beat/m 2) Coronary flow (mL/min)

44 5.3 42 15 34

+ 7 + 3.4 ___8 + 1 + 16

SA

59 5.6 70 40 35

CMS On a

CMS Off

+ + + ± +

40 2.9 37 14 46

10 (34%) b 3.3 (5.6%) 40 (66%) b 32 (166%) b 18 (3%)

represent percentage improvement, b p < 0.05. CMS = cardiomyostimulator; LVSWI= left ventricular stroke work index;

+2 _+ 0.5 + 11 _+ 5 _+ 18

CMS On a 52 3.2 42 17 48

+ + + + +

5 (30%) 0.8 (10%) 15 (13.5%) 6 (21%) 9 (4.3)

a Parentheses

MAP = mean arterial pressure;

SV = stroke volume.

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CERNAIANU ET AL DESCENDINGAORTOMYOPLASTY

by 27% [10] and prompted additional research in this field, avoiding the use of hydraulic or pneumatic drives and transferring animal-driven longitudinal force into a potential cardiac assist device. Other investigators followed with similar concepts of skeletal muscle-driven assist devices; however, the barrier of muscle fatigue remained an obstacle to success [11, 12]. The ability to convert skeletal muscle into a more "cardiac-like" muscle was an important technical link that prompted investigators to use conditioned fatigueresistant muscle in various models of cardiac assistance. There are significant biochemical distinctions between cardiac and skeletal muscle that account for differences in fatigability. Although cardiac muscle is composed of a syncytium of low-fatigue fibers, skeletal muscle is organized into distinct muscle units that contract separately and fatigue at variable rates. Skeletal muscle is composed of a combination of type I, slow-twitch and fatigueresistant fibers with a variable percentage of type II, less fatigue-resistant, fast-twitch muscle fibers. Mannion and Stephenson [13] demonstrated that through chronic electrical conditioning type II muscle fibers can be converted to type I fibers, which are similar to cardiac muscle fibers in stimulation and fatigue characteristics. Macoviak and colleagues [14] used preconditioned muscle to provide several hours of effective cardiac assistance. DelRossi and co-workers [15] documented a histologic biotransformation of electrically preconditioned muscle in an animal model of descending aortomyoplasty. In 1985, Neilson and colleagues [16] used a skeletal muscle-driven extraaortic pump to compress a polyurethane bulb placed in circuit with the heart. Other investigators have addressed the use of a hydraulic pouch powered by the rectus abdominis [12], latissimus dorsi [3], or serratus anterior muscles. However, thrombogenicity and foreign body reaction have been associated with these models. In the mid-1980s Carpentier and associates [3] reported the use of cardiomyoplasty in human subjects. Chronic data demonstrate effective fatigue-resistant cardiac assistance [17]. The mechanism of this augmentation has not been clarified and reproducible data are difficult to obtain [18]. Moreover, the operation may be contraindicated in many of the patients for whom it might be helpful. Specifically, patients with extremely dilated and hypertrophic cardiomyopathy are not candidates. Although technically feasible, extensive adhesions after cardiomyoplasty may complicate future heart transplantation [191. Ascending aortomyoplasty was advocated by Chachques and colleagues [5] as a promising approach to assisted biomechanical circulation. Because the length of ascending aorta available for aortomyoplasty is limited by anatomic considerations, these investigators have suggested an enlargement of the ascending aorta through an aortotomy and the application of a pericardial patch (neo-ventricle). Acute [5] and chronic data [6] have been reported but the technical feasibility of this neo-ventricle in humans has not been addressed. Moreover, the morbidity of aortotomy may exceed the practical benefits of the procedure.

Ann ThoracSurg 1995;59:639-43

Several investigators have been involved with models of descending aortomyoplasty. The feasibility and efficacy of this procedure have been demonstrated in acute [20] and chronic [21] animal studies. The technique is modeled on the intraaortic balloon pump. In both cases, effective counterpulsation is based on (1) the generation of a force to displace blood volumes and assist systemic perfusion, (2) augmentation of coronary flow during diastole, and (3) precise timing to decrease afterload. The hemodynamic benefits of counterpulsation are an increased cardiac contractility and coronary flow. Lazarra and colleagues [22] have evaluated the hemodynamic benefits of descending aortomyoplasty compared with those yielded by an IABP in an animal model. These investigators found that LD aortomyoplasty has a beneficial effect on left ventricular contractility that is independent of its effects on preload and afterload. The hemodynamic effects were comparable to those achieved with an IABP. An improvement in diastolic relaxation time was identified and has been advocated as an important factor in the hemodynamic changes associated with descending aortomyoplasty. The descending aorta permits a longer length for myoplasty than the ascending aorta and therefore should provide more effective displacement of blood volume. However, the mobilization of a large segment of descending aorta may compromise spinal cord blood flow. No animals in the LD group demonstrated paraplegia after ligation of several pairs of intercostal arteries. Our animal model may have a more developed collateral circulation. It is generally considered that ligation of these vessels in humans may interrupt the vascular supply to the spinal cord. In this study we have addressed the use of divided SA muscle fibers to achieve aortomyoplasty without division of intercostal branches. Our data demonstrate evidence of improved hemodynamic profiles with both models of aortomyoplasty. Specifically, in both the normal and ischemic heart an increase in cardiac output, SV, and LVSWI were identified. It is likely that LVSWI improved dramatically as a result of the decrease in afterload demonstrated with descending aortomyoplasty. A similar effect has been demonstrated by other authors [22]. Although the operations were technically successful in both groups, there is a statistically significant difference in failure rate between the groups. In our series, SA muscle assistance was a less effective technique. Our results may be explained by the extensive dissection required for harvest, mobilization, and splitting of the muscle fibers in the SA group. The segmental vascular anatomy of the SA has been described by Tobin and colleagues [23] who have advocated it as a theoretical alternative to the LD in aortomyoplasty. However, in practice, when the SA is harvested and divided for wrapping around the aorta additional dissection is required. Moreover, despite careful consideration of the vascular anatomy, nonanatomic splitting of the muscle fibers may be associated with ischemia and therefore fibrosis. Both LD and SA muscle flaps were otherwise treated in a similar fashion and it is unlikely that the

Ann Thorac Surg 1995;59:639-43

neurovascular pedicle was compromised in either group. Although no histologic confirmation was performed, fibrosis was evident on gross examination d u r i n g necropsy. The presence of fibrosis was not evident in the functional SA or the LD aortomyoplasty group, although no quantitative analysis was performed. Therefore, the benefit of SA muscle flaps in this configuration is equivocal. The procedure was tolerated well in both groups a n d m i n i m a l complications were noted. Although our model of ischemia used to evaluate the h e m o d y n a m i c effects of aortomyoplasty was d o c u m e n t e d by reductions of the LAD flow a n d global h e m o d y n a m i c impairment, no direct contractility assessments, wall motion abnormalities, or laboratory evidence of ischemia were i n c l u d e d in the study. O u r data demonstrate the efficacy of descending aortomyoplasty in the ischemic animal model. The SA aortomyoplasty, although experimentally effective, m a y not be a clinically practical choice based on its higher rate of fibrosis. The preservation of intercostal arteries, therefore, r e m a i n s an investigational issue to advance this technique to clinical trials. Clearly, there is a clinical d e m a n d for a n effective a n d practical cardiac assist device. Skeletal muscle autografts demonstrate m a n y of these i m p o r t a n t qualities. Further investigation is r e q u i r e d to determine if descending aortomyoplasty is a potentially effective a n d practical cardiac assist device.

References 1. Kannel WB, Thom TG. Incidence, prevalence and mortality of cardiovascular disease. In: Hurst JW, ed. The heart, 6th ed. New York: McGraw-Hill, 1986:562-3. 2. Smith WM. Epidemiology of congestive heart failure. Am J Cardiol 1985;55:3A-8A. 3. Carpentier A, Chachques JC, Grandjean PA. Cardiomyoplasty. Mount Kisco, NY: Futura, 1991. 4. Lee KF, Wechsler AS. Dynamic cardiomyoplasty. Adv Card Surg 1993;4:207-36. 5. Chachques JC, Grandjean PA, Fischer EC, et al. Dynamic aortomyoplasty to assist left ventricular failure. Ann Thorac Surg 1990;49:225-30. 6. Chachques JC, Haab F, Cron C, et al. Long-term effects of dynamic aortomyoplasty. Ann Thorac Surg 1994;58:128-34. 7. Constance CG, Sabini G, Turi GK, et al. Descending thoracic

CERNAIANUET AL DESCENDINGAORTOMYOPLASTY

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aortomyoplasty: effect of chronically conditioned muscle on heart failure. Cardiovasc Surg 1993;1:291-5. 8. Kolff WJ. The artificial heart; the inevitable development: will it be the U.S. or abroad? Artif Organs 1989;13:183-4. 9. Kantrowitz A, McKinnon WMP. The experimental use of the diaphragm as an auxiliary myocardium. Surg Forum 1959;9: 266. 10. Kantrowitz A, Krakauer J, Rubenfine M, et al. Functioning autogenous muscle used experimentally as an auxiliary ventricle. Trans Am Soc Artif Intern Organs 1960;6:305-10. 11. Kusserow BK, Clapp JF. A small ventricle-type pump for prolonged perfusions: construction and initial studies, including attempts to power a pump biologically with skeletal muscle. Trans Am Soc Artif Intern Organs 1964;10:74-8. 12. Spotnitz HM, Merker C, Malm JR. Applied physiology of the canine rectus abdominis: force-length curves correlated with functional characteristics of a rectus powered ventricle-potential for cardiac assistance. Trans Am Soc Artif Intern Organs 1974;20:747-56. 13. Mannion JD, Stephenson LW. Potential uses of skeletal muscle for myocardial assistance. Surg Clin N Am 1985;65: 679-987. 14. Macoviak TA, Stephenson LW, Spielman S, et al. Replacement of ventricular myocardium with diaphragmatic skeletal muscle: short-term studies. J Thorac Cardiovasc Surg 1981;81:519-27. 15. DelRossi AJ, Cernaianu AC, Vertrees RA, Cilley JH Jr, Baldino WA, Camishion RC. Biotransformation of skeletal muscle cord for long-term dynamic aortomyoplasty. BAM 1991;1:311-6. 16. Neilson IR, Brister SJ, Khalafalla AS, Chiu RC-J. Left ventricular assistance in dogs using a skeletal muscle powered device for diastolic augmentation. Heart Transplant 1985;6: 343-7. 17. Carpentier A, Chachques JC, Acar C, et al. Dynamic cardiomyoplasty at 7 years. J Thorac Cardiovasc Surg 1993;106: 42-54. 18. Fernandez F, Desnos M, Chachques JC, Guerot C, Carpentier A. Dynamic cardiomyoplasty: hemodynamic study of 3 patients. Arch Mal Coeur Vaiss 1990;83:1515-9. 19. Jegaden O, Delahaye F, Montagna P, et al. Cardiomyoplasty does not preclude heart transplantation. Ann Thorac Surg 1992;53:875-80. 20. Hines GL, Mishinki Y, Williams L, Monroe K, Metwally N. Physiologic and pathologic evaluation of chronic extra-aortic counterpulsation with latissimus dorsi flap. J Cardiovasc Surg 1991;382:485-90. 21. Vertrees RA, Cernaianu AC, Camishion RC, Cilley JH Jr, Baldino WA, DelRossi AJ. A surgical approach to chronic aortomyoplasty in the goat model. J Invest Surg 1993;6: 419-29. 22. Lazarra RR, Trumble DR, Magovern J. Dynamic descending aortomyoplasty: comparison with intraortic balloon pump in a model of heart failure. Ann Thorac Surg 1994;58:366-71. 23. Tobin AL, Barker JH, Slater D, Gray LA, Tobin, GR. The anatomic basis for serratus anterior aortic counterpulsations in humans. Am Coll Surg Surgical Forum 1993;44:657-60.