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Eur J Cardiothorac Surg 2001;19:174-178
© 2001 Elsevier Science NL

Hemodynamic evaluation of descending aortomyoplasty versus intra-aortic balloon pump performed in normal animals: an acute study

Gil Bolotina,b, Tamir Wolfa,b, R. Shachnera,b, Frederik H. van der Veenc, Rona Shoftia,b, Roberto Lorussoc, Jan J. Shreuderc, Gideon Uretzkya,b

a Department of Cardiothoracic Surgery, Tel Aviv Sourasky Medical Center, Rappaport Institute of Research in the Medical Sciences, Technion-Israel Institute of Technology, Haifa, Israel
b Department of Biomedical Engineering, Technion-Israel Institute of Technology, Haifa, Israel
c The Department of Cardiology, Maastricht University, Maastricht, The Netherlands

Received 18 September 2000; received in revised form 18 November 2000; accepted 27 November 2000.

Corresponding author. Tel.: +972-3-6973322; fax: +972-3-6974439
e-mail: bolotin{at}netvision.net.il


   Abstract
Top
 Abstract
1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 References
 
Objective: Aortomyoplasty is a surgical procedure that aims to induce hemodynamic benefits similar to those of the intra-aortic-balloon-pump (IABP). The objective of this study was to compare the coronary blood flow augmentation and afterload reduction produced by IABP and descending aortomyoplasty counterpulsation. Methods: From a series of fifteen mongrel dogs (18–35 kg), eight underwent acute descending aortomyoplasty and seven had IABP application. Left anterior descending (LAD) coronary artery blood flow was measured using a Doppler flow probe. Left ventricular pressure in addition to aortic pressures both proximal and distal to either the aortomyoplasty site or the IABP position were monitored continuously. All experiments were acute and performed in normal hearts. Results: Descending aortomyoplasty induced a 27% increase in the LAD blood flow integral during assisted beats (14.0±6 ml/min integral compared to 10.8±4 ml/min integral in unassisted beats [P<0.001]). This was comparable to an 18% rise in the LAD blood flow integral during IABP counterpulsation (from 8.6±3 ml/min to 10.2±4 ml/min [P<0.001]). Conversely, while IABP counterpulsation reduced the left ventricular afterload by 16% (from 102±23 mmHg to 86±26 mmHg [P<0.001]), descending aortomyoplasty did not result in afterload reduction. Conclusions: Descending aortomyoplasty produces coronary blood flow augmentation comparable to that achieved by the IABP. This may be important for end-stage ischemic patients. However, afterload reduction achieved by the IABP was not reproduced during descending aortomyoplasty counterpulsation. The surgical technique of descending aortomyoplasty should be modified to attain afterload reduction, thus improving treatment for congestive heart failure patients.

Key Words: Heart failure • Skeletal muscle • Aortomyoplasty • Intra-aortic-balloon pump


   1. Introduction
Top
 Abstract
 1. Introduction
2. Materials and methods
 3. Results
 4. Discussion
 References
 
The intra-aortic-balloon pump (IABP) is an important tool for the treatment of stage IV ischemic and/or heart failure patients [1]. The two main hemodynamic benefits of the IABP are coronary blood flow augmentation and afterload reduction (the difference between end-diastolic pressure during an assisted beat compared to that during an unassisted beat and the reduction in next beat's systolic pressure) [2]. However, long-term IABP support is not feasible due to the occurrence of infection and thromboembolic events [3]. Aortomyoplasty is a surgical technique that aims to achieve and maintain the hemodynamic benefits of IABP as a chronic treatment, without the morbidity associated with IABP counterpulsation [4].

Both ascending aortomyoplasty (i.e. wrapping of the right latissimus dorsi (LD) muscle around the ascending aorta) and descending aortomyoplasty (i.e. wrapping of the left LD muscle around the descending aorta) revealed significant hemodynamic improvements during stimulation of the wrapped LD muscle [5–7]. Chachques and associates demonstrated significant diastolic pressure augmentation in goats while the LD muscle was stimulated around the ascending aorta [5]. The same group presented experimental results 12 and 24 months postoperatively, using a conditioned LD muscle. Diastolic augmentation was maintained 2 years after the operation [8], implying potential long-term benefit for heart failure patients.

The purpose of this study was to assess coronary blood flow and afterload reduction during assistance with acute descending aortomyoplasty, as compared to the current gold standard, IABP counterpulsation.


   2. Materials and methods
Top
 Abstract
 1. Introduction
 2. Materials and methods
3. Results
 4. Discussion
 References
 
Fifteen mongrel dogs weighing 18–35 kg were used for this study. Eight underwent acute descending aortomyoplasty and seven had IABP application. The experiments were performed in accordance with the ‘Guide for the Care and Use of Laboratory Animals’ [9]. All the experiments were acute and were performed in normal hearts.

2.1. Aortomyoplasty surgical procedure and IABP insertion
Both groups underwent general anesthesia, induced by i.v. sodium thiopental (Penthotal) 15 mg/kg, and maintained following endotrachial intubation with O2:NO (1:2) and 1.5% Fluothane. Throughout the experiments, lung ventilation was achieved using a positive pressure respirator (Harvard). Body temperature was kept constant using a heating mattress. Prior to surgery, a single dose of 5000 units i.v. heparin was administered.

2.1.1. Aortomyoplasty
A left-sided mid-axillary incision was performed above the LD muscle and all collateral blood vessels to the distal part of the muscle were coagulated. All attachments of the muscle were disconnected, except for the axillary pedicle, to keep the thoracodorsal artery, vein, and nerve intact. Two intramuscular electrodes (Medtronic SP 5590 stimulation leads) were implanted in the upper part of the LD muscle flap, perpendicular to the main branches of the thoracodorsal nerve, as described previously by Chachques and coworkers [10]. To ensure proper positioning of the electrodes, satisfactory threshold (0.3–0.6 V) and total recruitment (1.0–2.5 V) values were obtained following connection of the electrodes to the stimulator system (Medtronic Cardio-Myo Stimulator SP 3076). A 5 cm segment of the anterior portion of the second rib was then resected, including the periosteum, to allow transposition of the LD muscle flap into the thorax. The muscle was inserted into the chest cavity, its tendon cut and sutured to the periosteum of the third rib, prior to closing the thoracic window. The thorax was then opened at the fourth left intercostal space and the pericardium was cut open. A sensing electrode (Medtronic 6500 sensing lead) was implanted in the right ventricular wall (adjacent to the septum) and the sensing threshold (4.5–16.4 mV) was measured.

A segment of approximately 8–10 cm of the descending aorta (1.5–2.5 cm in diameter), distal to the left subclavian artery, was then mobilized. All intercostal arteries arising from the aorta in this particular portion were ligated and divided. The left LD muscle flap was subsequently wrapped around the exposed descending aorta (single layer) using Prolene 2/0 sutures. The configuration required tight wrapping of the latissimus dorsi around the aorta in a counter clockwise orientation (best configuration from previous study [11]).

The IABP catheter (pediatric Datascope IABP catheter 30 ml) was inserted through the femoral artery and its exact position was determined using fluoroscopic guidance. The IABP was activated in a 1:3 ratio, to allow comparison between the assisted beats and the previous, unassisted beats. The balloon was inflated at different delays following the QRS complex (from 200 to 400 ms) and with different inflation duration (from 150 to 250 ms). The best delay and duration were explored by increments of 50 ms and the decision was made according to the plotted proximal blood pressure curve.

2.2. Instrumentation and data collection
A Millar (Millar Instruments, Texas, USA) solid state pressure catheter was inserted via the left carotid artery and advanced into the left ventricle (LV). The pressure curve of the LV was used to avoid inflation of the IABP or contraction of the skeletal muscle prior to closure of the aortic valve. Two additional solid state pressure catheters were inserted via the right and left femoral arteries and advanced into the aorta, proximally and distally to the wrapping site, respectively. Pressure data presented in this study were measured using the proximal intra-aortic pressure catheter.

Following a left thoracotomy, the pericardium was opened and a Doppler flow probe (Transonic Systems, NY) was placed around the left anterior descending (LAD) coronary artery, proximal to the first diagonal, for measurement of coronary blood flow. Surface ECG was monitored continuously throughout the experiments.

2.3. LD muscle stimulation
Stimulation commenced following the wrapping of the latissimus dorsi muscle around the aorta. The first part of this protocol comprised a 6-pulse burst (5V, 165 µs pulse width, 150, 200, and 250 ms burst duration) using different delays (150, 200, 250, 300, 350, 400 or 450 ms) after the QRS complex, in order to cover the entire diastolic range. Best delay and duration were chosen based on the plotted proximal blood pressure curve.

The stimulation burst was applied every third or fourth spontaneous heartbeat.

2.4. Data and statistical analysis
Hemodynamic data was gathered on an IBM personal computer using CODAS (DATAQ, Akron, OH, USA) and HDAS (Maastricht, The Netherlands) software. Additional software was designed to detect diastolic pressure and coronary blood flow peaks and to calculate their curve integrals (area under the curve). Assisted beats were compared to prior, unassisted beats, using Student's paired t-test. Results are expressed as mean±SD. The correlation between the three variables: diastolic pressure augmentation integral (i.e. area under the diastolic pressure curve), peak diastolic pressure augmentation (assisted beat compared to unassisted beat), and coronary blood flow augmentation (area under the coronary blood flow curve, assisted beat compared to unassisted beat) was analyzed using Pearson's correlation. Differences were considered significant at a P-value <0.05.


   3. Results
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
4. Discussion
 References
 
The mean descending aortic diameter was 19±3 mm and the mean length of the aortic segment to be wrapped was 92±6 mm, resulting in 26±2 ml volume of wrapped descending aorta. No deleterious effect on the aorta was observed during the experiments.

3.1. Proximal aortic pressure and coronary blood flow measurement
Descending aortomyoplasty counterpulsation induced a 27% increase in the LAD coronary blood flow integral (14±6 ml/min in assisted beats compared to 10.8±4 ml/min in unassisted beats [P<0.001]). This is higher (P=0.022) than the 18% rise in the LAD coronary blood flow integral during the IABP counterpulsation assisted beats (10.2±4 ml/min compared to 8.6±3 ml/min in unassisted beats [P<0.001]). In addition to the advantage of aortomyoplasty in terms of coronary blood flow augmentation, the procedure also induced a higher diastolic pressure integral than that attained with the IABP (Table 1).


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  		Table 1. Left anterior descending coronary blood flow integral, peak and integral diastolic pressures, and aortic end-diastolic pressurea.

 
3.2. Afterload reduction
Reduction of end diastolic pressure in the proximal aorta was demonstrated with the IABP in the proper timing settings (Fig. 1A), and in some of the aortomyoplasty experiments. However, while the afterload reduction induced by the IABP demonstrated statistical significance (from 102±23 to 86±26 mmHg [P<0.001]), descending aortomyoplasty failed to induce repetitive afterload reduction (from 91±12 to 93±14 mmHg [NS], P-value between the two groups <0.001). Moreover, in some of the experiments, the LD muscle was not sufficiently relaxed around the aorta during the next systole, implying an aortic narrowing, and a subsequent increase in LV afterload (Fig. 1B,C).



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  		Fig. 1. Proximal aortic pressure curves during IABP and descending aortomyoplasty counterpulsation. Note that while IABP utilization repeatedly caused afterload reduction (A), aortomyoplasty did not induce afterload reduction (B), and in some cases even induced an undesired increase in afterload (C).

 
Another parameter of afterload reduction, namely, the reduction of the following beat's systolic pressure, was not demonstrated in either of the counterpulsatory techniques applied.

3.3. Correlation between hemodynamic variables
In the IABP group, a significant correlation was observed between the diastolic pressure augmentation integral and coronary blood flow augmentation (Fig. 2). This data was gathered from different stimulation settings in the IABP group, resulting in three or four measurements for each animal. However, coronary blood flow was not found to correlate with peak diastolic pressure augmentation. Furthermore, in the descending aortomyoplasty group, no correlation was demonstrated between the hemodynamic variables assessed.



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  		Fig. 2. Correlation between augmentation in coronary blood flow integral and proximal aortic diastolic pressure integral.

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
References
 
In the study presented herein, we compared the hemodynamic effects of acute descending aortomyoplasty with the current gold standard, IABP counterpulsation. The results indicate the advantage of the descending aortomyoplasty procedure in achieving coronary blood flow augmentation. In contrast, descending aortomyoplasty did not induce aortic end diastolic pressure reduction, a major component of afterload reduction.

4.1. Proximal aortic pressure and coronary blood flow measurement
The advantage of coronary blood flow augmentation in stenotic vessels is still under debate in the literature [12,13]. Several authors demonstrate its importance, especially for compromised left ventricular contraction, and in combination with drug-induced reduction of coronary resistance [14,15]. In the present study, the coronary blood flow augmentation induced by descending aortomyoplasty is encouraging. In our acute animal model, applying the proper surgical configuration resulted in higher coronary blood flow augmentation than that demonstrated in the IABP control group. This finding is most probably due to the higher diastolic pressure integral (area under the curve) achieved with descending aortomyoplasty. Both findings (coronary blood flow and diastolic pressure integral augmentation) result from the direction of the muscle fibers, and therefore the contraction, which squeezes blood retrogradely into the coronary arteries. This may indicate that the very mechanism of pressure augmentation in the aorta, and not solely the extent (peak) of its enhancement, is responsible for the augmentation of coronary blood flow. The higher coronary blood flow augmentation cannot be explained by the volume of the aorta wrapped by the muscle, since this volume was approximately 26 ml, smaller then that of the IABP catheter (mean aortic diameter is 1.9 cm and the wrapped segment can be up to 9.2 cm in length).

4.2. Afterload reduction
The lack of afterload reduction in the aortomyoplasty group can be explained by the relaxation rate of the latissimus dorsi muscle, which may be too slow to induce a measurable decrease in the aortic pressure, such as that produced by the active deflation of the IABP. Proximal aortic end-diastolic pressure reduction was clearly obtained in some of the aortomyoplasty experiments; however, in the majority of the experiments, end-diastolic pressure reduction was not induced, despite careful adjusting of the stimulation settings. This inconsistency may be resolved by modifying the surgical configuration. Two surgical strategies that merit consideration are the ascending aortomyoplasty technique and the introduction of a recoil device between the aorta and the skeletal muscle.

The diameter of the descending aorta in both groups was relatively small (mean 1.9 cm). This constitutes a hemodynamic advantage to the IABP group (higher balloon/aorta diameter ratio) and reduces the aortomyoplasty effect, which depends on blood volume changes in the aorta. To address this, Chachques and coworkers assessed the use of a pericardial patch to increase the aortic volume at the aortomyoplasty site using a goat model [4]. However, if this is the main reason for the lack of end-diastolic pressure reduction, human clinical aortomyoplasty should render better results. In the current study, the additional component of afterload reduction, namely, the decrease in the next beat's peak systolic pressure, was absent in both the aortomyoplasty and the IABP groups. This was most likely due to the animal model with the small aortic diameter and high aortic compliance, as has been demonstrated in the pediatric population [16]. The afterload reduction induced by the IABP may have a negative influence on coronary flow due to the effect of auto regulation.

4.3. Correlation between hemodynamic variables
In this study, no correlation was found between peak diastolic pressure augmentation and coronary blood flow augmentation in either the aortomyoplasty or the IABP group. However, there was a strong correlation (Pearson's correlation coefficient r2=0.6) between proximal aortic diastolic pressure integral augmentation and coronary blood flow augmentation in the IABP. This data has clinical implications and should be addressed when adjusting the IABP setting.

4.4. Study limitations
Healthy mongrel dogs served for the animal model used in the current study. Generally, it is difficult to demonstrate in healthy hearts the benefits of innervations conceived to assist the failing heart. However, since the IABP was capable of inducing both diastolic augmentation and afterload reduction in such a healthy animal model, and since this study was designed as a comparison with the IABP, the drawbacks of using a healthy animal model can be considered minimal.

Another limitation of the study is the use of an untrained skeletal muscle. The conditioning protocol results in reduction of muscle power and speed of contraction. However, it may be assumed that a trained muscle would not induce more significant afterload reduction than that induced by an untrained muscle.

An additional problem of the acute experiment may be that the distal, ischemic part of the muscle is not critical in aortomyoplasty studies, since this part of the muscle is not used in the wrapping [17].

4.5. Conclusions
In conclusion, afterload reduction achieved by the IABP was not demonstrated during descending aortomyoplasty counterpulsation. However, descending aortomyoplasty induced greater coronary blood flow augmentation than that achieved by the IABP. This may be of significance for end-stage ischemic patients. Long term follow-up in an experimental heart failure model and possible modification of the surgical technique in descending aortomyoplasty are important to clearly study the effects and hemodynamic benefits of this new left ventricular assist system.


   Footnotes
 
Presented at the 13th Annual Meeting of the European Association for Cardio-thoracic Surgery, Glasgow, Scotland, UK, September 5–8, 1999.


   References
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 References
 

  1. Fuchs R.M., Brin K.P., Brinkern J.A., Guzman P.A., Herzer R.R., Yin F.C.P. Augmentation of regional coronary blood flow by intra-aortic balloon counterpulsation in patients with unstable angina. Circulation 1983;68:117-123.[Abstract/Free Full Text]
  2. Mundth E.D. Mechanical and surgical interventions for the reduction of myocardial ischemia. Circulation 1976;53(Suppl 3)):I176-I183.
  3. Freed P.S., Wasfie T., Zado B., Kantrowitz A. Intra-aortic balloon pumping for prolonged circulatory support. Am J Cardiol 1988;61:554-557.[Medline]
  4. Chachques J.C., Grandjean P.A., Fischer E.I.C., Latremouille C., Jebara V.A., Bourgeois I., Carpentier A. Dynamic aortomyoplasty to assist left ventricular failure. Ann Thorac Surg 1990;49:225-230.[Abstract]
  5. Chachques J.C., Radermercker M., Tolan M.J., Fischer E.I.C., Grandjean P.A., Carpentier A. Aortomyoplasty counterpulsation: experimental results and early clinical experience. Ann Thorac Surg 1996;61:420-425.[Abstract/Free Full Text]
  6. Pattison C.W., Cumming D.V.E., Williamson A., Clayton-Jones D.G., Dunn M.J., Goldspink G., Yacoub M. Aortic counterpulsation for up to 28 days with autologous latissimus dorsi in sheep. J Thorac Cardiovasc Surg 1991;102:766-773.[Abstract]
  7. Lazzara R.R., Trumble D.R., Magovern J.A. Chronic counterpulsation with descending thoracic aortomyoplasty improved cardiac function in animals with heart failure. J Heart Lung Transplant 1994;13:652-660.[Medline]
  8. Chachques J.C., Haab F., Cron C., Fischer E.I.C., Grandjean P.A., Bruneval P., Acar C., Jebara V.A., Fontaliran F., Carpentier A. Long-term effects of dynamic aortomyoplasty. Ann Thorac Surg 1994;58:128-134.[Abstract]
  9. National Academy of Sciences: Guide for the Care and Use of Laboratory Animals. DHHS Publication No. NIH 85-23, revised 1985.
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  11. Bolotin G., Wolf T., Van Der Veen F.H., Shofti R., Lorusso R., Schreuder J.J., Uretzky G. Acute descending aortomyoplasty induces coronary blood flow augmentation. Ann Thorac Surg 1999;68:1668-1673.[Abstract/Free Full Text]
  12. Williams D.O., Korr K.S., Rewirtz H., Most A.S. The effect of intraaortic balloon counterpulsation on regional myocardial blood flow and oxygen consumption in the presence of coronary artery stenosis in patients with unstable angina. Circulation 1982;66(3):593-597.[Abstract/Free Full Text]
  13. Angerpointer T.A., Jackson P.G., Williams B.T. The long-term effect of intra-aortic balloon counterpulsation on left ventricular performance. J Cardiovasc Surg (Torino) 1980;21(4):399-404.[Medline]
  14. Zehetgruber M., Mungigler G., Christ G., Merhaut C., Klaar U., Kratochwill C., Neunteufl T., Hofmann S., Heinz G., Maurer G., Siostrzonek P. Relation of hemodynamic variables to augmentation of left anterior descending coronary flow by intra-aortic balloon pulsation in coronary artery disease. Am J Cardiol 1997;80(7):951-955.[Medline]
  15. Jett G.K., Dengle S.K., Barnett P.A., Platt M.R., Willerson J.T., Watson J.T., Eberhart R.C. Intra-aortic balloon counterpulsation: its influence alone and combined with various pharmacological agents on regional myocardial blood flow during experimental acute coronary occlusion. Ann Thorac Surg 1981;31(2):144-154.[Abstract]
  16. Veasy L.G., Blalock R.C., Orth J.L., Boucek M.M. Intra-aortic balloon in infants and children. Circulation 1983;68(5):1095-1100.[Abstract/Free Full Text]
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