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Dynamic aortomyoplasty to assist left ventricular failure
Dynamic Aortomyoplasty to Assist Left Ventricular Failure Juan C. Chachques, MD, Pierre A. Grandjean, MS, E. I. Cabrera Fischer, MD, Christian Latremouille, MD, Victor A. Jebara, MD, Ivan Bourgeois, MS, and Alain Carpentier, MD, PhD Department of Cardiovascular Surgery, HBpital Broussais, Paris, France, and the Bakken Research Center, Maastricht, the Netherlands
The efficacy of skeletal muscle contractile force to augment left ventricular function has been demonstrated experimentally and clinically by the cardiomyoplasty procedure. Another approach in biomechanical cardiac assistance is the use of electrostimulated skeletal muscle in an extracardiac position. We describe an autologous counterpulsating device using the native ascending aorta as a ventricular chamber wrapped by an electrostimulated latissimus dorsi muscle flap (LDMF). This model avoids thrombotic complications observed in skeletal muscle neo-ventricles associated with prosthetic chambers. In 8 goats, a right LDMF was transferred to the thoracic cavity by removal of the second rib. In 4 goats, the diameter of the aorta was enlarged by surgical implantation (using lateral clamping) of an autologous pericardial patch. The LDMF was wrapped around the ascending aorta and electrostimulated using an external diastolic pulse generator connected to a sensing myocar-
dial lead and to LDMF pacing electrodes. Hemodynamic studies were performed (left ventricular, aortic, and pulmonary artery pressures and rate of rise of left ventricular pressure). The LDMF diastolic counterpulsation was performed using a burst of 30 Hz, with a delay from the R wave adjusted to provide optimal diastolic augmentation. Percent increase in the subendocardial viability index was calculated during unassisted and assisted cardiac cycles (1:2) at baseline and after acute heart failure induced by the administration of high doses of propranolol hydrochloride (3 mg/kg intravenously). Diastolic aortic counterpulsation by the stimulated LDMF resulted in a significant improvement in the subendocardial viability index both at baseline and after induced cardiac failure in both groups, though the increase was greater in the group with aortic enlargement.
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contraindications to performance of the cardiomyoplasty technique (extremely dilated cardiomyopathies, previous cardiac operations, hypertrophic cardiomyopathies) or for use in conjunction with LV cardiomyoplasty. We report here the preliminary experimental results of dynamic aortomyoplasty in animal models with acute heart failure.
ortomyoplasty is a surgical procedure that consists of wrapping a latissimus dorsi pedicled muscle graft around the ascending aorta to compress it, with synchronous electrostimulation of the muscle mass in each diastole. The native ascending aorta, enlarged by an autologous pericardial patch, becomes a ventricular chamber. This model of assisted circulation avoids thrombotic complications and systemic emboli observed in skeletal muscle neo-ventricles associated with prosthetic chambers [14]. With dynamic aortomyoplasty, the autologous "neo-ventricle" is continuously washed out by the left ventricular (LV) output. Skeletal muscle plasticity and adaptive changes is the basic physiological concept of biomechanical assist devices. The efficacy of skeletal muscle contractile force to augment LV function has been documented experimentally and clinically using the cardiomyoplasty procedure [ 5 7 ] . Electrical induction of fatigue resistance in skeletal muscles may also be effective for long-term circulatory assistance using diastolic counterpulsation. With the aortomyoplasty procedure, we are seeking an extracardiac biomechanical assist device for hearts with Presented at the Twenty-fifth Anniversary Meeting of The Society of Thoracic Surgeons, Baltimore, MD, Sep 11-13, 1989. Address reprint requests to Dr Chachques, Department of Cardiovascular Surgery, HBpital Broussais, 96 rue Didot, 75014 Paris, France.
0 1990 by The Society of Thoracic Surgeons
(Ann Thorac Surg 1990;49:225-30)
Material and Methods Eight adult alpine goats weighing 36 to 45 kg were used. Anesthesia was induced with an intramuscular injection of 2% xylazine and maintained with intravenously administered alfaxalone-alfadolone acetate. Curariform drugs were contraindicated. All goats underwent a right vertical, lateral thoracic incision to facilitate dissection of the latissimus dorsi muscle. The right latissimus dorsi muscle was divided from its insertion on the lateral aspect of the last four ribs, iliac crest, and thoracolumbar fascia, and 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 latissimus dorsi muscle flap (LDMF), which was brought into the chest through an opening made by resecting a portion of the second rib [8]. Care was taken to preserve the neurovascular bundle. Sternotomy was performed. The ascending aorta, the 0003-4975/90/$3.50
/ SENSING LEAD
cephalic trunk. Muscle fibers lie perpendicular to the longitudinal axis of the aorta.
Fig 1. (A) The ascending aorta, the transverse aortic arch, and its branches are dissected. The aorta is enlarged by implantation of a patch of autologous pericardium. ( B ) The latissimus dorsi muscle flap (LDMF), its distal end split longitudinally, is positioned behind the aorta. (C) The aorta is wrapped with the LDMF in a counterclockwise fashion. (D) The aorta is covered on both sides of the brachio-
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transverse aortic arch, and its branches were dissected (Fig 1A). In 4 goats, the ascending aorta was enlarged by implantation of an elliptical patch of autologous pericardium treated with glutaraldehyde [9]. This was done by side-clamping the aorta and placing a continuous suture of polypropylene monofilament 5-0. In all animals, LDMF was positioned behind the aorta (Fig 1B). Then the ascending and transverse aorta was wrapped with the muscle flap in a counterclockwise fashion so that its fibers lay perpendicular to the longitudinal axis of the aorta (Fig 1C). To cover the aorta on both sides of the brachiocephalic trunk, the distal end of the LDMF was split longitudinally (Fig lD), with care taken to consider its intramuscular neurovascular anatomy [lo, 111. Skeletal muscle electrostimulation was performed using an external counterpulsator (Medtronic model SP 3076) connected to a sensing myocardial lead (Medtronicmodel SP 5548) and to LDMF pacing electrodes. The variables involved in muscle stimulation were as follows: pulse amplitude, 4 to 6 V; pulse width, 210 ps; burst rate, 30 Hz; and burst duration, 185 ms. Diastolic counterpulsation was performed using a delay from the R wave adjusted to provide optimal diastolic augmentation. Short-term cyclic skeletal muscle electrostimulation (ten minutes per cycle) was delivered to allow functional study of dynamic aortomyoplasty. The following hemodynamic studies were performed: measurement of LV, aortic, and pulmonary artery pressures and rate of rise of left ventricular pressure. The extent of diastolic augmentation was measured by the subendocardial viability index: diastolic pressure-time index/systolic tension-time index [12, 131. Percent increase in this ratio (diastolic pressure-time index/systolic tension-time index) was calculated during unassisted and assisted cardiac cycles (1:2) at baseline and after acute heart failure induced by high-dose propranolol hydrochloride (3 mgkg intravenously). The subendocardial viability index was derived from superimposed tracings of aortic arch and LV pressures. Statistical analysis was performed using the paired t test and analysis of variance. Data are reported as the mean f the standard deviation. A p value of less than 0.05 was considered significant. 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 No. 85-23, revised 1985).
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ECG Fig 2. Hemodynamic recording after dynamic aortomyoplasty. Ascending aortic (AA)pressure at baseline. The stars mark diastolic augmentation in assisted cycles. Heart-to-muscle contraction ratio was 2:1. (ECG = electrocardiogram.)
The average peak ascending aortic pressure generated by dynamic aortomyoplasty under baseline conditions was 90 mm Hg (systemic blood pressure, 115/65 mm Hg) (Fig 2). In the 4 goats with aortic enlargement, the average peak pressure during LDMF stimulation was 105 mm Hg (systemic pressure, 105/70 mm Hg) (Fig 3). The hemodynamic data are shown in Tables 1 and 2. Diastolic aortic counterpulsation by the stimulated LDMF resulted in a significant increase in the subendocardial viability index both at baseline (+29.3%) (Fig 4) and after
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AA
Results Experimental results were obtained in the acute phase. Early electrostimulation was performed while muscle conditioning, collateral vascular supply, and LDMF adhesion to the aorta did not exist. As expected, muscle fatigability occurred four to six minutes after induction of stimulation. The diameter of the ascending aorta was 14.5 ? 2 mm, and its perimeter was 45.5 f 3 mm. The surface area of the pericardial aortic patch used in 4 goats was 260 f 30 mm2. The length of the aortic segment wrapped by the LDMF was 70 & 8 mm.
ECG Fig 3. Diastolic augmentation (stars) after enlargement of the ascending aorta (AA).(ECG = electrocardiogram.)
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Table 1. lncrease i n Subendocardial Viability lndex W i t h Dynamic Aortomyoplasty Diastolic Augmentation on Alternate (Heart-Muscle Stimulation Ratio, 2 : l ) Cardiac Cycles Control Animal No.
Mean Standard deviation
Without Stimulation
With Stimulation
Without Stimulation
1.35 1.22 1.29 1.32 1.40 1.38 1.18 1.42
0.98 0.86 1.08 0.84 1.05 0.99 0.95 1.00
1.40 1.25 1.38 1.32 1.31 1.33 1.20 1.22
0.998 0.117
1.322" 0.086
0.968 0.084
1.30Ib 0.072
Paired t test (two-tailed): degrees of freedom = 7, t = -7.339, p < 0.001 versus without stimulation. Paired t test (two-tailed): degrees of freedom = 7, t = -10.283, p < 0.001 versus without stimulation.
induced cardiac failure (+26.8%). In the group with aortic enlargement, the average increase in the index was +35.8% and +42.2%, respectively. During these experiments, we noted that the electrostimulated LDMF contracted vigorously. Its mechanical action over the aorta resulted in a homogeneous "systolic activity." No displacement of or angularities in the aortic arch and no aortic valve regurgitation were observed. Despite the fact that heparin sodium was not used during these experiments, no thrombus was noted in the aortic chambers.
Table 2 . lncrease in Subendocardial Viability lndex in Animals W i t h Aortic Enlargement
1 3 6 7
Mean Standard deviation
Without Stimulation
With Stimulation
Cardiac Failure Without Stimulation
With Stimulation
0.95 0.88 1.18 0.82
1.35 1.22 1.29 1.34
0.98 0.86 1.08 0.84
1.40 1.25 1.38 1.32
0.957 0.157
1.300" 0.059
0.940 0.112
1.337b 0.067
Paired t test (two-tailed): degrees of freedom = 3, t = -3.980, p < 0.005 Paired t test (two-tailed): degrees of versus without stimulation. freedom = 3, t = -10.6, p < 0.005 versus without stimulation.
a
100
mfnb
With Stimulation
a
Animal No.
Assisted
Cardiac Failure
0.95 0.88 1.18 0.82 1.02 1.05 0.98 1.11
Control
Unassisted
50
mmHp
Fig 4 . lncrease in subendocardial viability ratio (diastolic pressuretime index [DPTIllsystolic tension-time index [TTII), during assisted cycles after dynamic aortomyoplasty (experiment 8).
Comment Thirty-five thousand people per year in the United States need replacement of irreparable, sick natural hearts (141. Because no more than 2,000 donor hearts will be available, 33,000 artificial hearts will be necessary on a permanent basis, on top of the few hundred needed as a bridge to transplantation. None of the available treatments of severe cardiac failure can be expected to benefit a large number of patients in the near future. Physicians must search for alternative techniques [15-171. We have been investigating the use of the patient's own skeletal muscle to augment myocardial performance. Latissimus dorsi dynamic cardiomyoplasty has demonstrated experimentally and clinically its capacity to improve ventricular function on a long-term basis [5, 61. The aim of dynamic aortomyoplasty is to create a new hemocompatible contractile chamber in the ascending aorta using an autologous pericardial patch to enlarge its diameter. The electrostimulated LDMF is wrapped around the neo-chamber. The native aortic valve serves to close its afferent orifice, and hemodynamically this biological device acts as a new ventricle and the impaired left ventricle functionally becomes a left atrium. Therefore, LV afterload decreases and counterpulsation is effectively performed at the proximity of the coronary artery ostia. One of the advantages of dynamic aortomyoplasty is that it is performed without heart manipulation, aortic cross-clamping, or cardiopulmonary bypass. Moreover, contrary to another experimental model of muscular wrapping of the descending aorta [15], dynamic aortomyoplasty avoids the risk of paraplegia due to spinal cord ischemia. Results obtained with the model of dynamic aortomyoplasty associated with induced cardiac failure showed that when the aorta is enlarged the increase in subendocardial viability index is larger than when the aorta is left intact. This means that a dilated ventricle is better assisted by a larger aortic chamber volume. In patients with a large and long ascending aorta, it probably is not necessary to use patch enlargement of the aorta or to split the distal end of the LDMF, wrapping entirely the aorta before the origin
Ann Thorac Surg 1990;49:22530
of the brachiocephalic trunk. Aortic valve regurgitation, Marfan’s syndrome, and a calcified ascending aorta could be contraindications to dynamic aortomyoplasty. Routine preoperative computed tomographic scanning and nuclear magnetic resonance imaging are indicated to detect aortic calcifications in candidates before operation. On a hypothetical basis, dynamic aortomyoplasty can be viewed as a complementary technique in patients who have undergone LV cardiomyoplasty and in whom supplementary hemodynamic support is necessary. The extensive experience with the intraaortic balloon pump demonstrates considerable hemodynamic and physiological benefits of diastolic counterpulsation to the Efforts were made to reproduce these failing heart “1. effects using extraaortic ventricles wrapped with electrostimulated muscles [19], but were always limited by the thromboembolic potential of the prosthetic chambers because of interactions between the blood and artificial surfaces. Dynamic aortomyoplasty offers advantages similar to those of the intraaortic balloon pump. Moreover, because no prosthetic materials are used and blood flow is continuous, stasis and turbulence are avoided; hence no thromboembolic events are encountered. Consequently, the procedure could be viewed as a potential permanent perivascular assist device. Although short-term experimental dynamic aortomyoplasty led to significant diastolic augmentation, a longterm study using this procedure will allow us to evaluate the hemodynamic and functional effects of this biomechanical assist device to support chronic ventricular failure. The muscle we mobilized loses some of its blood supply, and we assume there is limited contractile function postoperatively. However, after a certain delay (2 weeks), sufficient blood flow will be reestablished by means of collateral circulation, and muscle function will recover. It is also important to consider the postoperative muscle training. Skeletal muscle receiving long-term electrostimulation undergoes metabolic transformation (glycolytic toward oxidative), with induction of fatigue resistance [20, 211. Before dynamic aortomyoplasty can be used in the clinical setting, upcoming experimental studies should answer three major questions. (1) What are the effects of long-term diastolic counterpulsation? (2) How do the local (aortic) and systemic circulations adapt to and tolerate dynamic aortomyoplasty? (3) What are the hemodynamic benefits of the procedure? We think these questions are partially clarified by the circulatory system of the kangaroo [22]. In this animal, the ascending aortic pressure waveform displays a very large secondary wave that begins in late systole or early diastole and continues throughout most of diastole. The peak of this secondary wave (which almost always occurs in diastole) is often greater than systolic peak pressure and results apparently from intense wave reflections from peripheral vascular beds in the lower part of the kangaroo’s body. These findings are explicable on the basis of body size and shape and the extreme eccentric location of the heart within the body. This permanent physiological counterpulsation system is very well tolerated and assists chronically the voluminous lower part of the kangaroo‘s body.
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Long-term experimental studies involving dynamic aortomyoplasty will elucidate the potential and clinical feasibility of this new, promising approach to biomechanical assisted circulation.
References 1. Mannion JD, Acker MA, Hammond RL, Faltemeyer W, Duckett S, Stephenson LW. Power output of skeletal muscle ventricles in circulation: short-term studies. Circulation 1987; 76:155-62. 2. Kochamba G, Desrosiers C, Dewar M, Chiu RC-J. The muscle-powered dual-chamber counterpulsator: rheologically superior implantable cardiac assist device. Ann Thorac Surg 1988;45:62C-5. 3. Mannion JD, Hammond R, Stephenson LW. Hydraulic pouches of canine latissimus dorsi. J Thorac Cardiovasc Surg 1986;91:53444. 4. Chiu RCJ, Walsh GL, Dewar ML, DeSimon JH, Khalafalla AS, Ianuzzo D. Implantable extra-aortic balloon assisted powered by transformed fatigue-resistant skeletal muscle. J Thorac Cardiovasc Surg 1987;94:694-701. 5. Chachques JC, Grandjean PA, Schwartz K, et al. Effect of latissimus dorsi dynamic cardiomyoplasty on ventricular function. Circulation 1988;78(Suppl 3):203-16. 6. Carpentier A, Chachques JC. Myocardial substitution with a stimulated skeletal muscle: first successful clinical case. Lancet 1985;1:1267. 7. Chachques JC, Grandjean PA, Bourgeois I, Carpentier A. Dynamic cardiomyoplasty to improve ventricular function. In: Unger F, ed. Assisted circulation 3. Heidelberg: SpringerVerlag, 1989:52541. 8. Chachques JC, Grandjean PA, Smits K. Method and apparatus including a sliding insulation lead for cardiac assistance. European patent 0,234,457, 1987; US patent 4,735,205, 1988. 9. Chachques JC, Vasseur B, Perier P, Balansa J, Chauvaud S, Carpentier A. A rapid method to stabilize biological materials for cardiovascular surgery. Ann NY Acad Sci 1988;529:184-6. 10. Tobin GR, Schusterman M, Peterson GH, Nichols G, Bland KI. The intramuscular neurovascular anatomy of the latissimus dorsi muscle: the basis for splitting the flap. Plast Reconstr Surg 1981;67:637-41. 11. Chachques JC, Mitz V, Hero M, et al. Experimental cardioplasty using the latissimus dorsi muscle flap. J Cardiovasc Surg (Torino) 1985;26:457-62. 12. Buckberg GD, Fixler DE, Archie JP, Hoffman JIE. Experimental subendocardial ischemia in dogs with normal coronary arteries. Circ Res 1972;30:67-81. 13. Neilson IR, Brister SJ, Khalafalla AS, Chiu RCJ. Left ventricular assistance in dogs using a skeletal muscle-powered device for diastolic augmentation. Heart Transplant 1985;4: 343-7. 14. Kolff WJ. The artificial heart, the inevitable development: will it be the U.S. or abroad? Artif Organs 1989;13:18?-4. 15. Kantrowitz A, McKinnon WMP. The experimental use of the diaphragm as an auxiliary myocardium. Surg Forum 1959;9: 266-8. 16. Spotnitz HM, Merker C, Malm JR. Applied physiology of the canine rectus abdominis. Trans Am SOCArtif Intern Organs 1974;20:747-55. 17. Chachques JC, Grandjean PA, Carpentier A. Latissimus dorsi dynamic cardiomyoplasty. Ann Thorac Surg 1989;47: 6004. 18. Kantrowitz A, Kantrowitz A. Experimental augmentation of coronary flow by retardation of the arterial pressure pulse. Surgery 1953;34:67%87.
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19. Acker MA, Anderson WA, Hammond RL, et al. Skeletal muscle ventricles in circulation. J Thorac Cardiovasc Surg 1987;94:16%74. 20. Salmons S, Henriksson J. The adaptative response of skeletal muscle to increased use. Muscle Nerve 1981;4:94-105.
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21. Pette D, Vrbovi G. Neural control of phenotypic expression in mammalian muscle fibers. Muscle Nerve 1985;8:67&89. 22. Nichols WW, Avolio AP, O’Rourke MF. Ascending aortic impedance patterns in the kangaroo: their explanation and relation to pressure waveforms. Circ Res 1986;59:247-55.
DISCUSSION DR ADRIAN KANTROWITZ (Detroit, MI): It might be of some value to point out that we have done similar experiments and reported them about 25 years ago. A series of experiments was done in our laboratory in Brooklyn by Dr Nose in which he demonstrated essentially the same thing, that the closer you make a counterpulsating device to the aortic valve, the more effective it is. The second thing that we did was to wrap a leaf of the diaphragm around the thoracic aorta and stimulate it in a counterpulsation mode. We had results that were not too different from those of Chachques and associates. The reason that we abandoned that approach was twofold: (1) we were not able to figure out how to overcome the fatigue problem, and (2) the stroke of that ventricle around the descending thoracic aorta was too small-it was about 3 or 4 mL. I would be interested to ask the question, first, do you know what the stroke volume of your aortic wrap device is? And, second, you implied that you felt it had better effects because it was closer to the coronary ostia. I would have to respectfully disagree with that. I think it has no relationship to how close it is to the coronary ostia. The flow during diastole through the left coronary artery is totally dependent on the pressure, or on the difference between intramyocardial pressure and aortic pressure. Nevertheless, I think this is a very nice piece of work and I congratulate you. DR CHACHQUES: We know very well the preliminary work by Dr Kantrowitz that opened the door for these kind of biological assist devices. Our choice of the ascending aorta myoplasty instead of the descending aorta was, first, to avoid paraplegia due to spinal cord ischemia, and, second, because the diameter of the ascending aorta and hence the volume of blood counterpulsated were more important. On the other hand, as you have mentioned earlier, Dr Nos6 and others have demonstrated that the closer you make a counterpulsation device to the aortic valve the more effective it is and the higher peak pressure wave you therefore obtain. Consequently the coronary circulation, which is directly proportional to the pressure during diastole, will improve if the device is closer to the aortic valve. Concerning the stroke volume, our hemodynamic studies did not include this variable. DR JOHN A. JACOBEY (Mountain Lakes, NJ): Dr Chachques, I believe I heard you mention that there was some unloading of afterwork of the left ventricle. I did not see that presented in your graphs. Perhaps there is another graph that shows where left ventricular systolic pressure does indeed come down which, as we all know, is one of the two basic components of counterpulsation, leaving the single effect approaches to be called either diastolic augmentation or systolic unloading. Again, I appreciate your paper, and I would like to ask what you think your particular device can do to unload the left ventricle. DR CHACHQUES: To demonstrate the effectiveness of the diastolic augmentation provided by the aortomyoplasty proce-
dure and to demonstrate the decrease in the left ventricular afterload we have used the subendocardial viability index that was derived from superimposed tracings of the aortic arch and left ventricular pressures. It was perhaps a mistake not to show directly a more simple and straightforward assessment of left ventricular pressure. However, if we look at the aortic pressure curves (see Figs 2, 3) we note that muscular relaxation is rapid and acts like balloon deflation in the intraaortic balloon pump. This “diastole” of the aortomyoplasty chamber could explain the decrease in LV afterload.
DR GEORGE J. MAGOVERN (Pittsburgh, PA): Was this a chronic model, and how did you induce chronic congestive heart failure? I think that seems to be a key to evaluating whether this procedure will work over a long period of time. One problem in our work has been the stimulation of the muscle, and we find that it is pretty difficult to thread the electrode through and get a uniform distribution of the current with uniform contractions. We have been putting the electrode on the nerve per se and find that we use much less current and obtain better distribution. But I think you will continue, and you should continue on this, because we have followed muscles that have been stimulated like this now for over 2 years and they do stay viable and biopsies do show that conversion occurs, as you well know. So, I think if you can get a long-term model, then it will be much more effective. DR CHACHQUES: Our present model was not a chronic one because the implantable diastolic pulse generator was not available at that time. We agree that chronic experiments are necessary. Concerning the skeletal muscle pacing electrodes we respectfully disagree with Dr Magovern as we obtain homogeneous, diffuse, and strong contractions with the electrodes we are using (Medtronic SP 5528) implanted into the muscle very close to the nerve branches. We have demonstrated that irreversible nerve damage, due to compression and fibrosis, may occur if electrodes are placed around the nerve itself. DR GREGORY A. MISBACH (Seattle, WA): I think that this is a very important frontier to be pursued, but I have one question. One of the limitations of skeletal muscle is lack of left ventricular afterload reduction, because you do not have a rapid deflation of a balloon as you do in an intraaortic balloon device. It also seems that it is the left ventricle that has to reinflate this counterpulsation device, which is your neo-ventricle. Do you think that there is work lost by the left ventricle in distending the ascending aorta and neo-ventricle, and does the compliance of your new aorta have some long-term effect that would influence this? DR CHACHQUES: Dynamic aortomyoplasty will be a chronic biomechanical support to the irreversibly diseased left ventricle. This sick left ventricle will then act as a left atrium and the enlarged ascending aorta acts as a neo-left ventricle. However if the left ventricular impairment is too serious for the left ventricle to be able to pump the blood to the neo-chamber it would be interesting to consider an associated cardiomyoplasty procedure using the left latissimus dorsi to assist the failing left ventricle.
The efficacy of skeletal muscle contractile force to augment left ventricular function has been demonstrated experimentally and clinically by the cardiomyoplasty procedure. Another approach in biomechanical cardiac assistance is the use of electrostimulated skeletal muscle in an extracardiac position. We describe an autologous counterpulsating device using the native ascending aorta as a ventricular chamber wrapped by an electrostimulated latissimus dorsi muscle flap (LDMF). This model avoids thrombotic complications observed in skeletal muscle neo-ventricles associated with prosthetic chambers. In 8 goats, a right LDMF was transferred to the thoracic cavity by removal of the second rib. In 4 goats, the diameter of the aorta was enlarged by surgical implantation (using lateral clamping) of an autologous pericardial patch. The LDMF was wrapped around the ascending aorta and electrostimulated using an external diastolic pulse generator connected to a sensing myocar-
dial lead and to LDMF pacing electrodes. Hemodynamic studies were performed (left ventricular, aortic, and pulmonary artery pressures and rate of rise of left ventricular pressure). The LDMF diastolic counterpulsation was performed using a burst of 30 Hz, with a delay from the R wave adjusted to provide optimal diastolic augmentation. Percent increase in the subendocardial viability index was calculated during unassisted and assisted cardiac cycles (1:2) at baseline and after acute heart failure induced by the administration of high doses of propranolol hydrochloride (3 mg/kg intravenously). Diastolic aortic counterpulsation by the stimulated LDMF resulted in a significant improvement in the subendocardial viability index both at baseline and after induced cardiac failure in both groups, though the increase was greater in the group with aortic enlargement.
A
contraindications to performance of the cardiomyoplasty technique (extremely dilated cardiomyopathies, previous cardiac operations, hypertrophic cardiomyopathies) or for use in conjunction with LV cardiomyoplasty. We report here the preliminary experimental results of dynamic aortomyoplasty in animal models with acute heart failure.
ortomyoplasty is a surgical procedure that consists of wrapping a latissimus dorsi pedicled muscle graft around the ascending aorta to compress it, with synchronous electrostimulation of the muscle mass in each diastole. The native ascending aorta, enlarged by an autologous pericardial patch, becomes a ventricular chamber. This model of assisted circulation avoids thrombotic complications and systemic emboli observed in skeletal muscle neo-ventricles associated with prosthetic chambers [14]. With dynamic aortomyoplasty, the autologous "neo-ventricle" is continuously washed out by the left ventricular (LV) output. Skeletal muscle plasticity and adaptive changes is the basic physiological concept of biomechanical assist devices. The efficacy of skeletal muscle contractile force to augment LV function has been documented experimentally and clinically using the cardiomyoplasty procedure [ 5 7 ] . Electrical induction of fatigue resistance in skeletal muscles may also be effective for long-term circulatory assistance using diastolic counterpulsation. With the aortomyoplasty procedure, we are seeking an extracardiac biomechanical assist device for hearts with Presented at the Twenty-fifth Anniversary Meeting of The Society of Thoracic Surgeons, Baltimore, MD, Sep 11-13, 1989. Address reprint requests to Dr Chachques, Department of Cardiovascular Surgery, HBpital Broussais, 96 rue Didot, 75014 Paris, France.
0 1990 by The Society of Thoracic Surgeons
(Ann Thorac Surg 1990;49:225-30)
Material and Methods Eight adult alpine goats weighing 36 to 45 kg were used. Anesthesia was induced with an intramuscular injection of 2% xylazine and maintained with intravenously administered alfaxalone-alfadolone acetate. Curariform drugs were contraindicated. All goats underwent a right vertical, lateral thoracic incision to facilitate dissection of the latissimus dorsi muscle. The right latissimus dorsi muscle was divided from its insertion on the lateral aspect of the last four ribs, iliac crest, and thoracolumbar fascia, and 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 latissimus dorsi muscle flap (LDMF), which was brought into the chest through an opening made by resecting a portion of the second rib [8]. Care was taken to preserve the neurovascular bundle. Sternotomy was performed. The ascending aorta, the 0003-4975/90/$3.50
/ SENSING LEAD
cephalic trunk. Muscle fibers lie perpendicular to the longitudinal axis of the aorta.
Fig 1. (A) The ascending aorta, the transverse aortic arch, and its branches are dissected. The aorta is enlarged by implantation of a patch of autologous pericardium. ( B ) The latissimus dorsi muscle flap (LDMF), its distal end split longitudinally, is positioned behind the aorta. (C) The aorta is wrapped with the LDMF in a counterclockwise fashion. (D) The aorta is covered on both sides of the brachio-
A
m
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Ann Thorac Surg 1990;49225-30
transverse aortic arch, and its branches were dissected (Fig 1A). In 4 goats, the ascending aorta was enlarged by implantation of an elliptical patch of autologous pericardium treated with glutaraldehyde [9]. This was done by side-clamping the aorta and placing a continuous suture of polypropylene monofilament 5-0. In all animals, LDMF was positioned behind the aorta (Fig 1B). Then the ascending and transverse aorta was wrapped with the muscle flap in a counterclockwise fashion so that its fibers lay perpendicular to the longitudinal axis of the aorta (Fig 1C). To cover the aorta on both sides of the brachiocephalic trunk, the distal end of the LDMF was split longitudinally (Fig lD), with care taken to consider its intramuscular neurovascular anatomy [lo, 111. Skeletal muscle electrostimulation was performed using an external counterpulsator (Medtronic model SP 3076) connected to a sensing myocardial lead (Medtronicmodel SP 5548) and to LDMF pacing electrodes. The variables involved in muscle stimulation were as follows: pulse amplitude, 4 to 6 V; pulse width, 210 ps; burst rate, 30 Hz; and burst duration, 185 ms. Diastolic counterpulsation was performed using a delay from the R wave adjusted to provide optimal diastolic augmentation. Short-term cyclic skeletal muscle electrostimulation (ten minutes per cycle) was delivered to allow functional study of dynamic aortomyoplasty. The following hemodynamic studies were performed: measurement of LV, aortic, and pulmonary artery pressures and rate of rise of left ventricular pressure. The extent of diastolic augmentation was measured by the subendocardial viability index: diastolic pressure-time index/systolic tension-time index [12, 131. Percent increase in this ratio (diastolic pressure-time index/systolic tension-time index) was calculated during unassisted and assisted cardiac cycles (1:2) at baseline and after acute heart failure induced by high-dose propranolol hydrochloride (3 mgkg intravenously). The subendocardial viability index was derived from superimposed tracings of aortic arch and LV pressures. Statistical analysis was performed using the paired t test and analysis of variance. Data are reported as the mean f the standard deviation. A p value of less than 0.05 was considered significant. 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 No. 85-23, revised 1985).
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ECG Fig 2. Hemodynamic recording after dynamic aortomyoplasty. Ascending aortic (AA)pressure at baseline. The stars mark diastolic augmentation in assisted cycles. Heart-to-muscle contraction ratio was 2:1. (ECG = electrocardiogram.)
The average peak ascending aortic pressure generated by dynamic aortomyoplasty under baseline conditions was 90 mm Hg (systemic blood pressure, 115/65 mm Hg) (Fig 2). In the 4 goats with aortic enlargement, the average peak pressure during LDMF stimulation was 105 mm Hg (systemic pressure, 105/70 mm Hg) (Fig 3). The hemodynamic data are shown in Tables 1 and 2. Diastolic aortic counterpulsation by the stimulated LDMF resulted in a significant increase in the subendocardial viability index both at baseline (+29.3%) (Fig 4) and after
.*
AA
Results Experimental results were obtained in the acute phase. Early electrostimulation was performed while muscle conditioning, collateral vascular supply, and LDMF adhesion to the aorta did not exist. As expected, muscle fatigability occurred four to six minutes after induction of stimulation. The diameter of the ascending aorta was 14.5 ? 2 mm, and its perimeter was 45.5 f 3 mm. The surface area of the pericardial aortic patch used in 4 goats was 260 f 30 mm2. The length of the aortic segment wrapped by the LDMF was 70 & 8 mm.
ECG Fig 3. Diastolic augmentation (stars) after enlargement of the ascending aorta (AA).(ECG = electrocardiogram.)
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Ann Thorac Surg 1990;49:225-30
Table 1. lncrease i n Subendocardial Viability lndex W i t h Dynamic Aortomyoplasty Diastolic Augmentation on Alternate (Heart-Muscle Stimulation Ratio, 2 : l ) Cardiac Cycles Control Animal No.
Mean Standard deviation
Without Stimulation
With Stimulation
Without Stimulation
1.35 1.22 1.29 1.32 1.40 1.38 1.18 1.42
0.98 0.86 1.08 0.84 1.05 0.99 0.95 1.00
1.40 1.25 1.38 1.32 1.31 1.33 1.20 1.22
0.998 0.117
1.322" 0.086
0.968 0.084
1.30Ib 0.072
Paired t test (two-tailed): degrees of freedom = 7, t = -7.339, p < 0.001 versus without stimulation. Paired t test (two-tailed): degrees of freedom = 7, t = -10.283, p < 0.001 versus without stimulation.
induced cardiac failure (+26.8%). In the group with aortic enlargement, the average increase in the index was +35.8% and +42.2%, respectively. During these experiments, we noted that the electrostimulated LDMF contracted vigorously. Its mechanical action over the aorta resulted in a homogeneous "systolic activity." No displacement of or angularities in the aortic arch and no aortic valve regurgitation were observed. Despite the fact that heparin sodium was not used during these experiments, no thrombus was noted in the aortic chambers.
Table 2 . lncrease in Subendocardial Viability lndex in Animals W i t h Aortic Enlargement
1 3 6 7
Mean Standard deviation
Without Stimulation
With Stimulation
Cardiac Failure Without Stimulation
With Stimulation
0.95 0.88 1.18 0.82
1.35 1.22 1.29 1.34
0.98 0.86 1.08 0.84
1.40 1.25 1.38 1.32
0.957 0.157
1.300" 0.059
0.940 0.112
1.337b 0.067
Paired t test (two-tailed): degrees of freedom = 3, t = -3.980, p < 0.005 Paired t test (two-tailed): degrees of versus without stimulation. freedom = 3, t = -10.6, p < 0.005 versus without stimulation.
a
100
mfnb
With Stimulation
a
Animal No.
Assisted
Cardiac Failure
0.95 0.88 1.18 0.82 1.02 1.05 0.98 1.11
Control
Unassisted
50
mmHp
Fig 4 . lncrease in subendocardial viability ratio (diastolic pressuretime index [DPTIllsystolic tension-time index [TTII), during assisted cycles after dynamic aortomyoplasty (experiment 8).
Comment Thirty-five thousand people per year in the United States need replacement of irreparable, sick natural hearts (141. Because no more than 2,000 donor hearts will be available, 33,000 artificial hearts will be necessary on a permanent basis, on top of the few hundred needed as a bridge to transplantation. None of the available treatments of severe cardiac failure can be expected to benefit a large number of patients in the near future. Physicians must search for alternative techniques [15-171. We have been investigating the use of the patient's own skeletal muscle to augment myocardial performance. Latissimus dorsi dynamic cardiomyoplasty has demonstrated experimentally and clinically its capacity to improve ventricular function on a long-term basis [5, 61. The aim of dynamic aortomyoplasty is to create a new hemocompatible contractile chamber in the ascending aorta using an autologous pericardial patch to enlarge its diameter. The electrostimulated LDMF is wrapped around the neo-chamber. The native aortic valve serves to close its afferent orifice, and hemodynamically this biological device acts as a new ventricle and the impaired left ventricle functionally becomes a left atrium. Therefore, LV afterload decreases and counterpulsation is effectively performed at the proximity of the coronary artery ostia. One of the advantages of dynamic aortomyoplasty is that it is performed without heart manipulation, aortic cross-clamping, or cardiopulmonary bypass. Moreover, contrary to another experimental model of muscular wrapping of the descending aorta [15], dynamic aortomyoplasty avoids the risk of paraplegia due to spinal cord ischemia. Results obtained with the model of dynamic aortomyoplasty associated with induced cardiac failure showed that when the aorta is enlarged the increase in subendocardial viability index is larger than when the aorta is left intact. This means that a dilated ventricle is better assisted by a larger aortic chamber volume. In patients with a large and long ascending aorta, it probably is not necessary to use patch enlargement of the aorta or to split the distal end of the LDMF, wrapping entirely the aorta before the origin
Ann Thorac Surg 1990;49:22530
of the brachiocephalic trunk. Aortic valve regurgitation, Marfan’s syndrome, and a calcified ascending aorta could be contraindications to dynamic aortomyoplasty. Routine preoperative computed tomographic scanning and nuclear magnetic resonance imaging are indicated to detect aortic calcifications in candidates before operation. On a hypothetical basis, dynamic aortomyoplasty can be viewed as a complementary technique in patients who have undergone LV cardiomyoplasty and in whom supplementary hemodynamic support is necessary. The extensive experience with the intraaortic balloon pump demonstrates considerable hemodynamic and physiological benefits of diastolic counterpulsation to the Efforts were made to reproduce these failing heart “1. effects using extraaortic ventricles wrapped with electrostimulated muscles [19], but were always limited by the thromboembolic potential of the prosthetic chambers because of interactions between the blood and artificial surfaces. Dynamic aortomyoplasty offers advantages similar to those of the intraaortic balloon pump. Moreover, because no prosthetic materials are used and blood flow is continuous, stasis and turbulence are avoided; hence no thromboembolic events are encountered. Consequently, the procedure could be viewed as a potential permanent perivascular assist device. Although short-term experimental dynamic aortomyoplasty led to significant diastolic augmentation, a longterm study using this procedure will allow us to evaluate the hemodynamic and functional effects of this biomechanical assist device to support chronic ventricular failure. The muscle we mobilized loses some of its blood supply, and we assume there is limited contractile function postoperatively. However, after a certain delay (2 weeks), sufficient blood flow will be reestablished by means of collateral circulation, and muscle function will recover. It is also important to consider the postoperative muscle training. Skeletal muscle receiving long-term electrostimulation undergoes metabolic transformation (glycolytic toward oxidative), with induction of fatigue resistance [20, 211. Before dynamic aortomyoplasty can be used in the clinical setting, upcoming experimental studies should answer three major questions. (1) What are the effects of long-term diastolic counterpulsation? (2) How do the local (aortic) and systemic circulations adapt to and tolerate dynamic aortomyoplasty? (3) What are the hemodynamic benefits of the procedure? We think these questions are partially clarified by the circulatory system of the kangaroo [22]. In this animal, the ascending aortic pressure waveform displays a very large secondary wave that begins in late systole or early diastole and continues throughout most of diastole. The peak of this secondary wave (which almost always occurs in diastole) is often greater than systolic peak pressure and results apparently from intense wave reflections from peripheral vascular beds in the lower part of the kangaroo’s body. These findings are explicable on the basis of body size and shape and the extreme eccentric location of the heart within the body. This permanent physiological counterpulsation system is very well tolerated and assists chronically the voluminous lower part of the kangaroo‘s body.
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Long-term experimental studies involving dynamic aortomyoplasty will elucidate the potential and clinical feasibility of this new, promising approach to biomechanical assisted circulation.
References 1. Mannion JD, Acker MA, Hammond RL, Faltemeyer W, Duckett S, Stephenson LW. Power output of skeletal muscle ventricles in circulation: short-term studies. Circulation 1987; 76:155-62. 2. Kochamba G, Desrosiers C, Dewar M, Chiu RC-J. The muscle-powered dual-chamber counterpulsator: rheologically superior implantable cardiac assist device. Ann Thorac Surg 1988;45:62C-5. 3. Mannion JD, Hammond R, Stephenson LW. Hydraulic pouches of canine latissimus dorsi. J Thorac Cardiovasc Surg 1986;91:53444. 4. Chiu RCJ, Walsh GL, Dewar ML, DeSimon JH, Khalafalla AS, Ianuzzo D. Implantable extra-aortic balloon assisted powered by transformed fatigue-resistant skeletal muscle. J Thorac Cardiovasc Surg 1987;94:694-701. 5. Chachques JC, Grandjean PA, Schwartz K, et al. Effect of latissimus dorsi dynamic cardiomyoplasty on ventricular function. Circulation 1988;78(Suppl 3):203-16. 6. Carpentier A, Chachques JC. Myocardial substitution with a stimulated skeletal muscle: first successful clinical case. Lancet 1985;1:1267. 7. Chachques JC, Grandjean PA, Bourgeois I, Carpentier A. Dynamic cardiomyoplasty to improve ventricular function. In: Unger F, ed. Assisted circulation 3. Heidelberg: SpringerVerlag, 1989:52541. 8. Chachques JC, Grandjean PA, Smits K. Method and apparatus including a sliding insulation lead for cardiac assistance. European patent 0,234,457, 1987; US patent 4,735,205, 1988. 9. Chachques JC, Vasseur B, Perier P, Balansa J, Chauvaud S, Carpentier A. A rapid method to stabilize biological materials for cardiovascular surgery. Ann NY Acad Sci 1988;529:184-6. 10. Tobin GR, Schusterman M, Peterson GH, Nichols G, Bland KI. The intramuscular neurovascular anatomy of the latissimus dorsi muscle: the basis for splitting the flap. Plast Reconstr Surg 1981;67:637-41. 11. Chachques JC, Mitz V, Hero M, et al. Experimental cardioplasty using the latissimus dorsi muscle flap. J Cardiovasc Surg (Torino) 1985;26:457-62. 12. Buckberg GD, Fixler DE, Archie JP, Hoffman JIE. Experimental subendocardial ischemia in dogs with normal coronary arteries. Circ Res 1972;30:67-81. 13. Neilson IR, Brister SJ, Khalafalla AS, Chiu RCJ. Left ventricular assistance in dogs using a skeletal muscle-powered device for diastolic augmentation. Heart Transplant 1985;4: 343-7. 14. Kolff WJ. The artificial heart, the inevitable development: will it be the U.S. or abroad? Artif Organs 1989;13:18?-4. 15. Kantrowitz A, McKinnon WMP. The experimental use of the diaphragm as an auxiliary myocardium. Surg Forum 1959;9: 266-8. 16. Spotnitz HM, Merker C, Malm JR. Applied physiology of the canine rectus abdominis. Trans Am SOCArtif Intern Organs 1974;20:747-55. 17. Chachques JC, Grandjean PA, Carpentier A. Latissimus dorsi dynamic cardiomyoplasty. Ann Thorac Surg 1989;47: 6004. 18. Kantrowitz A, Kantrowitz A. Experimental augmentation of coronary flow by retardation of the arterial pressure pulse. Surgery 1953;34:67%87.
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19. Acker MA, Anderson WA, Hammond RL, et al. Skeletal muscle ventricles in circulation. J Thorac Cardiovasc Surg 1987;94:16%74. 20. Salmons S, Henriksson J. The adaptative response of skeletal muscle to increased use. Muscle Nerve 1981;4:94-105.
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21. Pette D, Vrbovi G. Neural control of phenotypic expression in mammalian muscle fibers. Muscle Nerve 1985;8:67&89. 22. Nichols WW, Avolio AP, O’Rourke MF. Ascending aortic impedance patterns in the kangaroo: their explanation and relation to pressure waveforms. Circ Res 1986;59:247-55.
DISCUSSION DR ADRIAN KANTROWITZ (Detroit, MI): It might be of some value to point out that we have done similar experiments and reported them about 25 years ago. A series of experiments was done in our laboratory in Brooklyn by Dr Nose in which he demonstrated essentially the same thing, that the closer you make a counterpulsating device to the aortic valve, the more effective it is. The second thing that we did was to wrap a leaf of the diaphragm around the thoracic aorta and stimulate it in a counterpulsation mode. We had results that were not too different from those of Chachques and associates. The reason that we abandoned that approach was twofold: (1) we were not able to figure out how to overcome the fatigue problem, and (2) the stroke of that ventricle around the descending thoracic aorta was too small-it was about 3 or 4 mL. I would be interested to ask the question, first, do you know what the stroke volume of your aortic wrap device is? And, second, you implied that you felt it had better effects because it was closer to the coronary ostia. I would have to respectfully disagree with that. I think it has no relationship to how close it is to the coronary ostia. The flow during diastole through the left coronary artery is totally dependent on the pressure, or on the difference between intramyocardial pressure and aortic pressure. Nevertheless, I think this is a very nice piece of work and I congratulate you. DR CHACHQUES: We know very well the preliminary work by Dr Kantrowitz that opened the door for these kind of biological assist devices. Our choice of the ascending aorta myoplasty instead of the descending aorta was, first, to avoid paraplegia due to spinal cord ischemia, and, second, because the diameter of the ascending aorta and hence the volume of blood counterpulsated were more important. On the other hand, as you have mentioned earlier, Dr Nos6 and others have demonstrated that the closer you make a counterpulsation device to the aortic valve the more effective it is and the higher peak pressure wave you therefore obtain. Consequently the coronary circulation, which is directly proportional to the pressure during diastole, will improve if the device is closer to the aortic valve. Concerning the stroke volume, our hemodynamic studies did not include this variable. DR JOHN A. JACOBEY (Mountain Lakes, NJ): Dr Chachques, I believe I heard you mention that there was some unloading of afterwork of the left ventricle. I did not see that presented in your graphs. Perhaps there is another graph that shows where left ventricular systolic pressure does indeed come down which, as we all know, is one of the two basic components of counterpulsation, leaving the single effect approaches to be called either diastolic augmentation or systolic unloading. Again, I appreciate your paper, and I would like to ask what you think your particular device can do to unload the left ventricle. DR CHACHQUES: To demonstrate the effectiveness of the diastolic augmentation provided by the aortomyoplasty proce-
dure and to demonstrate the decrease in the left ventricular afterload we have used the subendocardial viability index that was derived from superimposed tracings of the aortic arch and left ventricular pressures. It was perhaps a mistake not to show directly a more simple and straightforward assessment of left ventricular pressure. However, if we look at the aortic pressure curves (see Figs 2, 3) we note that muscular relaxation is rapid and acts like balloon deflation in the intraaortic balloon pump. This “diastole” of the aortomyoplasty chamber could explain the decrease in LV afterload.
DR GEORGE J. MAGOVERN (Pittsburgh, PA): Was this a chronic model, and how did you induce chronic congestive heart failure? I think that seems to be a key to evaluating whether this procedure will work over a long period of time. One problem in our work has been the stimulation of the muscle, and we find that it is pretty difficult to thread the electrode through and get a uniform distribution of the current with uniform contractions. We have been putting the electrode on the nerve per se and find that we use much less current and obtain better distribution. But I think you will continue, and you should continue on this, because we have followed muscles that have been stimulated like this now for over 2 years and they do stay viable and biopsies do show that conversion occurs, as you well know. So, I think if you can get a long-term model, then it will be much more effective. DR CHACHQUES: Our present model was not a chronic one because the implantable diastolic pulse generator was not available at that time. We agree that chronic experiments are necessary. Concerning the skeletal muscle pacing electrodes we respectfully disagree with Dr Magovern as we obtain homogeneous, diffuse, and strong contractions with the electrodes we are using (Medtronic SP 5528) implanted into the muscle very close to the nerve branches. We have demonstrated that irreversible nerve damage, due to compression and fibrosis, may occur if electrodes are placed around the nerve itself. DR GREGORY A. MISBACH (Seattle, WA): I think that this is a very important frontier to be pursued, but I have one question. One of the limitations of skeletal muscle is lack of left ventricular afterload reduction, because you do not have a rapid deflation of a balloon as you do in an intraaortic balloon device. It also seems that it is the left ventricle that has to reinflate this counterpulsation device, which is your neo-ventricle. Do you think that there is work lost by the left ventricle in distending the ascending aorta and neo-ventricle, and does the compliance of your new aorta have some long-term effect that would influence this? DR CHACHQUES: Dynamic aortomyoplasty will be a chronic biomechanical support to the irreversibly diseased left ventricle. This sick left ventricle will then act as a left atrium and the enlarged ascending aorta acts as a neo-left ventricle. However if the left ventricular impairment is too serious for the left ventricle to be able to pump the blood to the neo-chamber it would be interesting to consider an associated cardiomyoplasty procedure using the left latissimus dorsi to assist the failing left ventricle.