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Ann Thorac Surg 1995;60:417-421
© 1995 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Benefits of Aortic and Pulmonary Counterpulsation Using Dynamic Latissimus Dorsi Myoplasty

Edmundo I. Cabrera Fischer, MD, Juan-Carlos Chachques, MD, PhD, Alejandra I. Christen, MD, Marcelo R. Risk, EEng, Alain F. Carpentier, MD, PhD

Basic Research Center, University Institute of Biomedical Sciences, Favaloro Foundation, Buenos Aires, Argentina, and Department of Cardiovascular Surgery, Broussais Hospital, Paris, France

Accepted for publication April 8, 1995.


   Abstract
Top
 Footnotes
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 References
 
Background. Intraaortic and pulmonary artery counterpulsation are useful techniques to support circulation during either left or right ventricular dysfunction. Electrically stimulated skeletal muscles wrapped around the aorta, used as means of cardiac failure treatment, have proved to be an effective method of handling experimental left ventricular failure. In this article we report an induced cardiac failure model in acute open chest dogs and describe the hemodynamic improvement of simultaneous aortic and pulmonary artery counterpulsation.

Methods. This was achieved with a bilateral latissimus dorsi muscle flap, stimulated with a software written in C++ for Windows. Dynamic aortomyoplasty was performed using the left latissimus dorsi muscle flap around the descending aorta, and dynamic pulmonaromyoplasty was achieved wrapping the pulmonary trunk with the right latissimus dorsi muscle flap. In all animals blood pressures and cardiac output were measured after cardiac failure induced by a high-dose of propranolol hydrochloride (3 mg/kg intravenously) before and after latissimus dorsi muscle flap stimulation.

Results. Aortopulmonary counterpulsation resulted in a significant increase in mean aortic pressure, mean pulmonary pressure, and cardiac output. In addition, a significant decrease was observed in end-diastolic left ventricular pressure, systemic vascular resistance, and pulmonary vascular resistance. Subendocardial viability index (diastolic pressure-time index/systolic tension-time index) in aortomyoplasty and tension time index in pulmonaromyoplasty showed significant improvement when cardiac assistance was performed by electrical stimulation of both muscles (p = 0.037 and p = 0.001, respectively).

Conclusions. Treatment of experimentally induced cardiac failure using aortopulmonary counterpulsation allows effective hemodynamic improvement in open-chest dogs.


   Introduction
Top
 Footnotes
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 References
 
The intraaortic balloon pump is a mechanical assist device that has been used widely for treating severe left ventricular failure [1]. Systemic counterpulsation also has been obtained by using skeletal muscles wrapped around the distal portion of the thoracic aorta [2]. On the other hand, hemodynamic benefits of pulmonary artery balloon counterpulsation for right ventricular failure have been observed in experimental animals as well as in patients [3, 4]. Furthermore, biventricular mechanical support of the failing heart is required to reverse severe global failure [5–7].

In this article (1) we describe a new technique for counterpulsating both systemic and pulmonary circulation, by wrapping the the pulmonary trunk with the right latissimus dorsi muscle flap (LDMF), and wrapping the descending aorta with the left LDMF; and (2) we present electromyostimulation software devised to produce double mechanical synchronized assistance.


   Material and Methods
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 References
 
Surgical Procedure
Nine adult mongrel dogs weighing 23 to 28 kg and aged between 24 and 48 months were chosen at the beginning of this study. General anesthesia was induced with sodium thiopentone (20 mg/kg, intravenously), followed by intubation and maintenance of anesthesia with 2.5% enflurane delivered through a Bain tube connected to a Bird Mark 8 ventilator.

In all dogs a right lateral thoracic skin incision was performed to facilitate dissection of the right latissimus dorsi muscle. It was derived from its insertion on the lateral side of the last four ribs and thoracolumbar fascia, and it was mobilized proximally as a pedicled flap. Pacing electrodes were implanted (two leads, model SP 5528; Medtronic, Maastricht, the Netherlands) into the proximal part of the right LDMF, which was brought into the chest through an opening made by resecting a portion of the right second rib. Special care was taken to preserve the neurovascular bundle. Then, a dissection of the left latissimus dorsi muscle similar to the one described above was performed. The left latissimus dorsi was mobilized proximally as a pedicled flap. A pair of pacing electrodes similar to those used in the right side were implanted into the proximal part of the left LDMF, which was brought into the chest through an opening made by resecting a portion of the left second rib. Special care was taken to preserve the neurovascular bundle.

After this procedure, a left lateral thoracotomy in the fourth intercostal space was made in every animal and an aortomyoplasty was performed, wrapping the left LDMF around the upper third of the descending thoracic aorta in a clockwise fashion. Afterward, the pulmonary trunk, the ascending aorta, the transverse aortic arch, and its branches were dissected. In all animals, the right LDMF was positioned around the pulmonary trunk in a counterclockwise fashion so that its fibers lay perpendicular to the longitudinal axis of the vascular pedicle (Fig 1Go).



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  		Fig 1. . The pulmonary trunk and the descending aorta are wrapped with the right and left latissimus dorsi muscle flaps, respectively.

 
All electrodes were coupled to a stimulation interface charged with two 9 V alkaline batteries. This interface was driven with a personal computer charged with software developed in our laboratory, written in C++ for Windows, to obtain accurate synchronization with cardiac rhythm. This software was designed primarily to be applied in animal models of cardiac failure with stimulated skeletal muscles, so as to improve hemodynamic parameters. The electronic circuit was arranged to pick up the surface electrocardiogram and deliver a stimulus into both right and left LDMFs. In this experimental preparation the muscle stimulation parameters were synchronization delay using the R wave of a surface electrocardiogram, pulse amplitude, pulse width, burst rate, and burst duration. All of them could be modified according to the characteristics of the hemodynamic parameters in both arteries to avoid competition with the natural systole. In this way, the stimulation system was divided into two outputs: (1) aortomyoplasty stimulation with synchronization delay adjusted to provide optimal diastolic aortic pressure augmentation, a pulse amplitude of 15 V, pulse width of 210 µs, burst rate of 30 Hz, burst duration of 180 ms, and maximal cardiac-sensing sensitivity of 1 mV; and (2) pulmonaromyoplasty stimulation with synchronization delay adjusted to provide optimal pulmonary diastolic pressure augmentation, pulse amplitude of 7 V, pulse width of 210 µs, burst rate of 30 Hz, burst duration of 200 ms, and maximal cardiac-sensing sensitivity of 1 mV. The values of the parameters described above are approximates, because changes in heart rate necessitated changes in both pulmonaromyoplasty and aortomyoplasty (Fig 2Go).



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  		Fig 2. . Block diagram showing a surface electrocardiogram (EKG) connected to an optocoupler that separates it from a compatible IBM PC computer. This computer, charged with an analog to digital (A/D) converter and stimulation software written in C++, is connected to two interfaces. Each of them is electrically separated from the computer and the latissimus dorsi muscle flap. Both interfaces are supplied with a pair of 9 V batteries. The interface stimulates the muscles directly. In this way, the electronic circuit picks up the electrocardiogram R wave and delivers a pair of pulse bursts for each latissimus dorsi muscle flap.

 
Hemodynamic Measurements
Aortic and left ventricular pressures were measured by using two catheters introduced through the left and right femoral arteries. Pulmonary and right ventricular pressures were measured by using two catheters introduced through the left and right jugular veins. All catheters were size 8F. Cardiac output was measured by using a Swan-Ganz catheter, which was positioned in the pulmonary trunk through the right femoral vein, and thermodilution signal was processed with an Edwards Model 9520 A cardiac output computer. All dogs were given heparin (300 units/kg). Pressure signals were registered on millimetered paper on a Gould multichannel recorder (Model 2600 S; Gould, Inc, Cleveland, OH) with Statham transducers and Gould 4600 series preamplifiers.

In all animals blood pressures and cardiac output were measured after cardiac failure induced by a high dose of propranolol hydrochloride (3 mg/kg intravenously), before and after LDMF stimulation. As we used untrained LDMFs, muscle fatigue and ischemia due to repetitive contractions would occur approximately 5 minutes after induction of stimulation. Therefore, we performed LDMF stimulations for periods shorter than 3 minutes.

The first derivative of left ventricular pressure was monitored in all cases to determine propranolol effect. Cardiac output and mean pressures were used to obtain systemic and pulmonary vascular resistance values.

The extent of the aortic diastolic augmentation was measured by the subendocardial viability index: diastolic pressure-time index (DPTI)/systolic tension-time index (TTI) [8, 9]. The efficacy of pulmonary counterpulsation was evaluated by the TTI [8]. After cardiac failure induction, aortopulmonary counterpulsation was monitored by both indexes during stimulated and nonstimulated cardiac cycles.

After the experimental session all animals were euthanized with an overdose of sodium thiopentone. All animals received humane care in the preoperative period 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).

Statistical Treatment
All results were subjected to the paired difference t test to determine differences between assisted and unassisted values. Values reported are expressed as mean ± standard deviation. Pressure values considered here are the mean of five consecutive cardiac cycles; cardiac output, TTI, and DPTI/TTI values are the mean of three consecutive determinations. A 95% confidence limit was chosen as indicator of statistical significance (p < 0.05).


   Results
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 References
 
Of the 9 dogs initially operated on, data from 2 animals were discarded due to technical mistakes during the recording. No animal deaths occurred during the course of any surgical or experimental session, and no aortic or pulmonary regurgitation was observed. No cardiac arrhythmias or significant blood pressure variations were found during the LDMF placements or while double electromyostimulation was performed. Aortopulmonary counterpulsation monitored on the oscilloscope always showed a high degree of diastolic pressure augmentation both in aortic and in pulmonary vessels (as high as systolic pressure), as shown in Figure 3Go.



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  		Fig 3. . Example of the effect of stimulation of the latissimus dorsi muscle flaps recorded from a dog. In the first panel we can observe the electrical stimuli* obtained with the pulse trains, 1:1 on the electrocardiogram (EKG) signal. Simultaneously, the aortic and pulmonary pressure signals show diastolic augmentation.

 
Aortopulmonary counterpulsation resulted in a significant increase in mean aortic pressure (68.66 ± 9.80 to 80.73 ± 10.40 mm Hg; p = 0.004), mean pulmonary artery pressure (9.34 ± 0.83 to 10.31 ± 0.93 mm Hg; p = 0.006), and cardiac output (1.16 ± 0.17 to 1.46 ± 0.16 L/min; p = 0.001). In addition, a significant decrease was observed in end-diastolic left ventricular pressure (15.66 ± 2.28 to 6.56 ± 0.70 mm Hg; p = 0.001), systemic vascular resistance (59.7 ± 5.98 to 55.5 ± 4.92 mm Hg • L-1 • min-1; p = 0.001), and pulmonary vascular resistance (8.21 ± 1.29 to 7.16 ± 1.17 mm Hg • L-1 • min-1; p = 0.007) (Table 1Go). Aortic diastolic pressure changes in cardiac failure, evaluated through the DPTI/TTI index during aortic counterpulsation by stimulated LDMF, showed a significant increase compared with unassisted values (1.31 ± 0.37 to 1.65 ± 0.29; p = 0.037), as can be seen in Table 2Go. Pulmonary assistance in cardiac failure, obtained during pulmonary counterpulsation with LDMF stimulation, showed a significant decrease in the TTI index in comparison with unassisted values (2,385.44 ± 126.44 to 2,303 ± 131.71 mm Hg • s • min-1; p = 0.001) (Table 3Go).


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  		Table 1. . Hemodynamic Parameters in Assisted Cardiac Failure (n = 7)a
 

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  		Table 2. . Subendocardial Viability Index (Diastolic Pressure-Time Index/Systolic Tension-Time Index) in Aortomyoplasty
 

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  		Table 3. . Tension-Time Index in Pulmonaromyoplastya
 

   Comment
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
References
 
Heart failure is a syndrome in which right and left ventricular assistances are required to preserve hemodynamic parameters [10–12]. During recent years, mechanical circulatory assistance systems have been used as alternative treatments to provide recovery support in patients suffering from severe cardiac failure refractory to drug therapy [13]. However, these methods of heart failure assistance usually are performed by using mechanical devices and rarely applied simultaneously. Actually, heart transplantation remains the best treatment for end-stage cardiac failure, without taking into account the cause; nevertheless, immunosuppression and scarcity of organ donors restrict this option [14]. Because none of the available treatments of severe heart failure could be expected to benefit a large number of patients in the near future, new alternative techniques should be developed [15].

Since Leriche and Fontaine [16] succeeded in repairing left ventricular aneurysms in dogs in 1933, the cardiac application of skeletal muscle has undergone major progress to become a clinically feasible procedure. Furthermore, it has been demonstrated that skeletal muscles are capable of generating four times the force per cross-sectional area that cardiac muscle does [17]. Counterpulsation of a vessel, created by Kantrowitz and Kantrowitz [18] in 1953, is a method thought to assist cardiac failure. In early experiments, arterial counterpulsation was obtained by stimulating a hemidiaphragm wrapped around the distal thoracic aorta [2]. Since then, augmentation of diastolic aortic pressure has been considered a useful tool for cardiac failure treatment. Counterpulsation was described as the mechanical removal of blood during systole and the subsequent reinfusion in diastole. Even though counterpulsation in patients is obtained with the intraaortic balloon pump, it is an invasive alternative with an external power source that can only be used as a temporary method.

Recently, cardiac assistance with aortic counterpulsation was achieved by using native ascending aorta as a ventricular chamber wrapped with electrostimulated LDMF in an animal model of cardiac failure [19, 20]. In isolated right ventricular failure, pulmonary diastolic pressure augmentation also has proved to be a useful treatment [3, 4]. In addition, mechanical devices, dynamic cardiomyoplasty, and aortomyoplasty have been considered of great interest during the last few years [19, 21, 22].

As heart failure would involve biventricular support, the final aim of our work was to obtain simultaneous right and left ventricular assistance and to verify its effect on hemodynamic parameters. On the basis of earlier studies [19], we designed our protocol to analyze the effects of combined aortic and pulmonary counterpulsation with both autologous LDMFs in an animal model of cardiac failure. The model of pharmacologically induced heart failure used in our experiments was developed previously to mimic as closely as possible human impairment of cardiac function [22, 23].

As shown in the Results section, instantaneous dynamic diastolic aortopulmonary counterpulsation, obtained with two LDMFs synchronized with the cardiac cycle for short periods of time, is capable of restoring hemodynamic parameters in our model of cardiac failure. As the LDMFs were not trained in this acute experimental animal model, muscle fatigue and ischemia would occur approximately 5 minutes after induction of stimulation. Therefore, we performed the LDMF stimulation for periods shorter than 3 minutes. As formerly reported, fatigue-resistant muscular fibers are the consequence of an electrical stimulation program of 8 weeks. It is understood that we used untrained skeletal muscles in this acute animal preparation only for technical reasons, and it is not an alternative to trained muscles [24]. The pulse amplitude used in these experiments was three times the usual voltage we apply in chronic animal experiments, because it was found to be well tolerated in acute preparations.

The subendocardial viability index (DPTI/TTI) is a standard method that allows an accurate evaluation of aortic counterpulsation [8, 9], and the tension time index (TTI) is an appropriate tool to demonstrate the efficacy of pulmonary counterpulsation; besides, this index previously has been used to show changes in cardiac performance [8, 25]. Therefore, the mentioned indexes were chosen, and statistical significance of improvements was observed when bilateral assistance was performed.

The dynamic aortopulmonary counterpulsation described here is a simple method that avoids the possible risk of thrombus in the arterial tree, as previously observed in aortic wrapping [19]. Besides, this method has the advantage of being a bilateral modality for heart failure assistance. As aortic and pulmonary artery counterpulsation involved a pair of pulse bursts synchronized with the cardiac rhythm, specific software written in C++ for Windows was developed. Synchronization of LDMF stimulation with cardiac rhythm was achieved using the R wave of a surface electrocardiogram. As shown in the Results section, the software allowed stimulation of skeletal muscles with a wide range of synchronization delays and pulse amplitudes, which are parameters required for appropriate stimulation if cardiovascular assistance is performed simultaneously in two or more places.

In conclusion, treatment of experimentally induced cardiac failure using both aortomyoplasty and pulmonaromyoplasty artery counterpulsation resulted in effective improvement of hemodynamic parameters in open-chest dogs. More experimental studies would be useful to evaluate the long-term effects of this technique.


   Footnotes
Top
 Footnotes
Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 
Address reprint requests to Dr Cabrera Fischer, Basic Research Center, Favaloro Foundation, Solís 453, 1078 Buenos Aires, Argentina.


   References
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 

  1. Kantrowitz A. Introduction of left ventricular assistance. Trans Am Soc Artif Organs 1987;33:39–48.
  2. Kantrowitz A, McKinnon WMP. The experimental use of the diaphragm as an auxiliary myocardium. Surg Forum 1959;9:266–8.
  3. Jett KG, Siwek LG, Picone AL, Applebaum RE, Jones M. Pulmonary artery balloon counterpulsation for right ventricular failure. J Cardiovasc Surg 1983;86:364–72.
  4. Miller CD, Moreno-Cabral RJ, Stinson EB, Shinn JA, Shumway NE. Pulmonary artery balloon counterpulsation for acute right ventricular failure. J Thorac Cardiovasc Surg 1980;80:760–3.[Abstract]
  5. Pennock JL, Pierce WS, Wisman CB, Bull AP, Waldhausen JA. Survival and complications following ventricular assist pumping for cardiogenic shock. Ann Surg 1983;198:469–78.[Medline]
  6. Pennington DG, Lawrence R, McBride LR, et al. Use of the Pierce-Donachy ventricular assist device in patients with cardiogenic shock after cardiac operations. Ann Thorac Surg 1989;47:130–5.[Abstract]
  7. Brugger JP, Bonandi L, Meli M, Lichsteiner M, Odermatt R, Hahn C. SWAT team approach to ventricular assistance. Ann Thorac Surg 1989;47:136–41.[Abstract]
  8. Buckberg GD, Fixler DE, Archie JP, Hoffman JIE. Experimental subendocardial ischemia in dogs with normal coronary arteries. Circ Res 1972;30:67–81.[Abstract/Free Full Text]
  9. 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;4:343–7.
  10. Costanzo-Nordin MR, Cooper DKC, Jessup M, Renlund DG, Robinson JA, Rose EA. Task Force 6: future developments. J Am Coll Cardiol 1993;22:54–64.[Medline]
  11. Cabrera Fischer EI, Willshaw P, Armentano RL, Bensansón Delbo MI, Pichel RH, Favaloro RG. Experimental acute right ventricular failure and right ventricular assist in the dog. J Thorac Cardiovasc Surg 1985;90:580–5.[Abstract]
  12. Cabrera Fischer EI, Chachques JC, Garcia A, Pichel RH, Morales MC, Carpentier A. Temporary mechanical circulatory support for severe cardiac failure: experimental study. Int J Artif Organs 1991;14:466–72.[Medline]
  13. Hetzer R, Hennig E, Schiessler A, Friedel N, Warnecke H, Adt M. Mechanical circulatory support and heart transplantation. J Heart Lung Transplant 1992;11:S175–81.[Medline]
  14. Boullon F, Sinagra A, Riarte A, et al. Experimental cardiac transplantation and chronic Chagas' disease in dogs. Transplant Proc 1988;20(Suppl 1):432–7.
  15. Chachques JC, Grandjean PA, Carpentier A. Patient management and clinical follow-up after cardiomyoplasty. J Cardiac Surg 1991;6:89–99.[Medline]
  16. Leriche R, Fontaine R. Essai expérimental de traitement de certains infarctus du myocarde et de l'anéurysme du coeur par une graffe muscle strié. Bull Soc Nat Chir 1933;9:229–32.
  17. Mommaerts WFHM. Heart muscle. In: Fishman AP, Richard DW, eds. Circulation of the blood. Baltimore: American Physiological Society, 1964:152–7.
  18. Kantrowitz A, Kantrowitz A. Experimental augmentation of coronary flow by retardation of the arterial pressure pulse. Surgery 1953;34:678–87.[Medline]
  19. Chachques JC, Grandjean PA, Cabrera Fischer EI, et al. Dynamic aortomyoplasty to assist left ventricular failure. Ann Thorac Surg 1990;49:225–30.[Abstract]
  20. Chachques JC, Haab F, Cron C, et al. Long-term effects of dynamic aortomyoplasty. Ann Thorac Surg 1994;58:128–34.[Abstract]
  21. Lee KF, Dignan RJ, Parmar JM, et al. Effects of dynamic cardiomyoplasty on left ventricular performance and myocardial mechanics in dilated cardiomyopathy. J Thorac Cardiovasc Surg 1991;102:124–31.[Abstract]
  22. Chagas ACP, Moreira LFP, da Luz PL, et al. Stimulated preconditioned skeletal muscle cardiomyoplasty. An effective means of cardiac assist. Circulation 1989;80(Suppl 3):202–8.
  23. Cabrera Fischer EI, Chachques JC, García A, et al. Effect of cardiomyoplasty on left ventricular diastolic function. Basic Appl Myology 1991;1:253–8.
  24. Chachques JC, Grandjean P, Schwartz K et al. Effect of latissimus dorsi dynamic cardiomyoplasty on ventricular function. Circulation 1988;78(Suppl 3):203–16.
  25. Sonnenblick EH, Ross J Jr, Covell JW, Kaiser GA, Braunwald E. Velocity of contraction as a determinant of myocardial oxygen consumption. Am J Physiol 1965;209:919–27.[Abstract/Free Full Text]



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