Ann Thorac Surg 1999;68:1668-1675
© 1999 The Society of Thoracic Surgeons
Original Articles
Acute descending aortomyoplasty induces coronary blood flow augmentation
Gil Bolotin, MDa,
Tamir Wolf, BSca,
Frederik H. van der Veen, PhDa,b,
Rona Shofti, DVMb,
Roberto Loruso, MDa,b,
Jan J. Shreuder, MDa,b,
Gideon Uretzky, MDa
a Department of Cardiothoracic Surgery, Carmel Medical Center, Rappaport Institute of Research in the Medical Sciences, Haifa, Israel
b Department of Biomedical Engineering, Technion-Israel Institute of Technology, Haifa, Israel
Address reprint requests to Dr Bolotin, Department of Cardiothoracic Surgery, Carmel Medical Center, 7 Michal St, Haifa, 34362, Israel
e-mail: bolotin{at}netvision.net.il
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Abstract
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Background. Aortomyoplasty is a procedure aimed to improve cardiac output in patients suffering from heart failure. Stimulation of the latissimus dorsi muscle around the aorta produces hemodynamic effects similar to those of the intraaortic balloon pump. These may be maintained without the accompanying complications or the need for anticoagulation. The objective of this study was to test the acute effects of aortomyoplasty on coronary artery blood flow.
Methods. Eight mongrel dogs (18 to 30 kg) underwent acute descending aortomyoplasty. Several stimulation protocols were applied after wrapping of the latissimus dorsi muscle around the aorta in different surgical configurations. The left anterior descending coronary blood flow was measured using a transonic Doppler flow probe. Left ventricular and aortic pressures, proximal and distal to the aortomyoplasty site, were monitored continuously.
Results. Significant aortic diastolic pressure augmentation was expressed both as an increase in peak values, from 110 ± 24 mm Hg to 120 ± 24 mm Hg (p < 0.001) and as an increase in the diastolic integral, from 64 ± 23 mm Hg x s to 84 ± 37 mm Hg x s (p < 0.001). Concomitantly, peak left anterior descending coronary blood flow increased from 26 ± 10 mL/min to 32 ± 12 mL/min (p < 0.001). This was associated with an increase in the diastolic flow integral from 11 ± 4 mL to 14 ± 6 mL (p < 0.001).
Conclusions. Descending aortomyoplasty induces significant augmentation of coronary blood flow. Optimal timing of muscle stimulation is important in achieving the best assist. This procedure may prove beneficial for end-stage ischemic patients.
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Introduction
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Intraaortic balloon pump (IABP) counterpulsation has proved to be a useful clinical tool in supporting heart failure patients and was found to be especially effective in cases of acute ischemia. The IABP causes a decrease in both peak systolic pressure and myocardial oxygen consumption while simultaneously increasing mean diastolic blood pressure and coronary blood flow [1–3]. However, long-term IABP support is not possible due to the occurrence of various complications, such as infection and thromboembolic events [4].
Aortomyoplasty is a surgical approach that aims to mimic the advantageous hemodynamic effects of the IABP and maintain them permanently without the accompanying complications or the need for anticoagulation. Since first described by Chachques and coworkers in 1990 [5], experimental, as well as preliminary clinical data concerning dynamic aortomyoplasty have been gathered [6, 7].
Both ascending aortomyoplasty (ie, wrapping of the right latissimus dorsi [LD] muscle around the ascending aorta) and descending aortomyoplasty (ie, wrapping of the left LD muscle around the descending aorta) revealed significant hemodynamic improvements during stimulation of the wrapped LD muscle [7–9]. Chachques and associates [5] demonstrated significant diastolic pressure augmentation in goats while the LD muscle was stimulated around the ascending aorta. 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 [10], implying a potential long-term benefit for patients with heart failure.
One of the main advantages of IABP counterpulsation is the increase in coronary blood flow in ischemic patients [1, 3]. The purpose of this study was to assess coronary blood flow during assistance with descending aortomyoplasty. This was performed by examining four different surgical configurations: the LD muscle wrapped clockwise and counterclockwise around the aorta, both tightly and loosely in both configurations.
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Material and methods
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Eight mongrel dogs weighing 18 to 30 kg were used for this study. The experiments were performed in accordance with the "Guide for the Care and Use of Laboratory Animals" published by the National Institutes of Health (NIH publication 85-23, revised 1985).
Surgical procedure
General anesthesia was induced by intravenous sodium thiopental (Penthotal, Thiopentone sodium, Abbot S.p.a.) 15 mg/kg, and maintained after endotracheal intubation with O2:NO (1:2) and 1.5% fluothane. Throughout the experiments lung ventilation was achieved using a positive pressure respirator (Harvard Apparatus Inc, South Natick, MA). Body temperature was kept constant using a heating mattress. Before operation, a single dose of 5,000 U of intravenous heparin was administered.
A left-sided midaxillary incision was performed above the LD muscle and all collateral blood vessels to the muscle’s distal part were coagulated. All attachments of the muscle, except for the axillary pedicle, were disconnected 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 co-workers [11]. To assure proper positioning of the electrodes, satisfactory threshold (0.3 to 0.6 V) and total recruitment (1.0 to 2.5 V) values were obtained after connection of the electrodes to the stimulator system (Medtronic Cardio-Myo Stimulator SP 3076; Medtronic, Kerkrade, The Netherlands). A 5-cm segment of the anterior portion of the second rib, including the periosteum, was then resected 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, before closing the thoracic window. The thorax was then opened at the fourth left intercostal space and the pericardium cut open. A sensing electrode (Medtronic 6500 sensing lead; Medtronic, Kerkrade, The Netherlands) was implanted in the right ventricular wall (adjacent to the septum) and the sensing threshold (4.5 to 16.4 mV) was measured.
A segment of approximately 8 to 10 cm of the descending aorta (1.5 to 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) and four surgical wrapping configurations (clockwise, counterclockwise, loose, and tight) were applied (throughout all experiments) using Prolene 2-0 sutures (Ethicon Ltd, Edinburgh, Scotland). Tight wrapping was defined as the maximal tightening of the LD muscle around the aorta that did not induce pressure reduction in the distal aorta. Loose wrapping required 1.5 cm (one finger space) between the aorta and the LD muscle.
Instrumentation and data collection
A Millar solid-state pressure catheter (Millar Instruments, Houston, TX) was inserted through the left carotid artery and advanced into the left ventricle. Two additional Millar solid-state pressure catheters were inserted through the right and left femoral arteries and advanced into the aorta, proximally and distally to the wrapping site, respectively.
After left thoracotomy, the pericardium was opened and a transonic Doppler flow probe (Transonic Systems, Ithaca, NY) was placed around the left anterior descending (LAD) coronary artery, proximal to the first diagonal, for measurement of coronary blood flow. The electrocardiogram was continuously monitored throughout all experiments.
Latissimus dorsi muscle stimulation
Stimulation commenced immediately after application of each surgical configuration. The first part of this protocol comprised a six-pulse burst (5 V, 165 µs pulse width, 200 ms burst duration) using different delays (150, 200, 250, 300, 350, 400, and 450 ms) after the QRS complex, to cover the entire diastolic range. The stimulation burst was given every third or fourth spontaneous heart beat. Additional measurements were obtained using a six-pulse burst at 10-V pulse amplitude, in conjunction with what was considered to be the best delay (based on the maximal increase in coronary blood flow and proximal aortic pressure augmentation) as seen while using the 5-V stimulation during the first part of the experiment.
Data and statistical analysis
The hemodynamic data was gathered on an IBM personal computer (IBM, Greenock, UK) using CODAS software (DATAQ, Akron, OH). Additional software was designed to detect peak diastolic pressure and coronary blood flow and to calculate diastolic pressure and coronary blood flow curve integrals (area under the curve). Aortomyoplasty-assisted beats were compared to before nonassisted beats using Student’s paired t test. Results are expressed as mean ± standard deviation. Differences were accepted to be significant at p value less than 0.05.
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Results
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Diastolic pressure augmentation
Contraction of the LD muscle around the descending aorta induced diastolic pressure augmentation in the proximal aorta in all of the applied surgical configurations throughout all the experiments. When the delay was shorter (150 ms after the QRS complex), the LD muscle contracted during ventricular systole and before complete closure of the aortic valve. Thus, pressure changes were induced inside the left ventricle (ie, a higher left ventricular end-systolic pressure) and a change in peak systolic pressure (proximal aorta) was observed, increasing from 122 ± 6 mm Hg in the unassisted beats to 134 ± 6 mm Hg in the assisted beats (p < 0.05). Induction of LD muscle contraction during the latter part of ventricular diastole (450 ms after the QRS complex) resulted in a less profound diastolic pressure augmentation. Moreover, this long delay caused partial obstruction of the aorta during the next systole. This phenomenon induced an increase in the afterload during the next beat, and the systolic pressure in the proximal aorta increased from 128 ± 8 mm Hg in the unassisted beats up to 139 ± 7 mm Hg in the assisted beats (p < 0.001). At the same time, distal aortic pressure decreased. The mean diastolic augmentation of the optimal stimulation delay (for each animal) is shown in Tables 1 and 2. This was expressed as an overall increase in the peak diastolic pressure, from 110 ± 24 mm Hg in the unassisted beats up to 120 ± 24 mm Hg in the assisted beats in the proximal aorta (p < 0.001). Pressure augmentation was significantly maintained throughout the diastole, as evidenced by the proximal aortic diastolic pressure integral (area under the pressure curve), which was 64 ± 23 mm Hg x s in the unassisted beats and 84 ± 37 mm Hg x s in the assisted beats (p < 0.001) (Fig 1).
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Table 1. Peak Proximal Aortic Diastolic Pressures Before and During Latissimus Dorsi Muscle Stimulation in Different Surgical Configurations
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Table 2. Proximal Aortic Diastolic Pressure Integral Before and During Latissimus Dorsi Muscle Stimulation in Different Surgical Configurations
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Fig 1. Tracing of proximal aortic pressure illustrating pressure augmentation after latissimus dorsi stimulation (delay, 350 ms). (ECG = electocardiogram.)
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Coronary flow measurement
Coronary blood flow (LAD) increased after LD muscle stimulation simultaneously with diastolic augmentation. In summation of all configurations, peak coronary flow increased from 26 ± 10 mL/min in the unassisted beats to 32 ± 12 mL/min in the assisted beats (p < 0.001). This increase was associated with a significant increase in the diastolic flow integral (area under the coronary blood flow curve) from 11 ± 4 mL to 14 ± 6 mL in the assisted beats (p < 0.001) (Fig 2).
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Fig 2. A typical tracing illustrating the concomitant increase in both proximal aortic pressure (A) and coronary blood flow (B) during latissimus dorsi muscle stimulation. (ECG = electocardiogram.)
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Surgical configurations
The results of the different surgical configurations, namely, clockwise and counterclockwise, loose and tight wrapping of the LD muscle around the descending aorta, are summarized in Tables 1 to 4 (clinically applicable delays; ie, the whole burst was confined to the diastolic phase). Comparing between the tight and loose wrapping techniques reveals a trend toward greater diastolic augmentation of coronary blood flow (Fig 3) when using the tight configuration, although no statistical significance was observed. Counterclockwise wrapping achieved better coronary blood flow augmentation (Fig 4), compared to clockwise wrapping of the LD muscle. There was no significant difference in the diastolic pressure augmented between clockwise and counterclockwise wrapping.
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Table 3. Peak Coronary Blood Flow Before and During Latissimus Dorsi Muscle Stimulation in Different Surgical Configurations
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Table 4. Coronary Blood Flow Diastolic Integral Before and During Latissimus Dorsi Muscle Stimulation in Different Surgical Configurations
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Fig 3. Tight wrapping technique resulted in greater coronary blood flow diastolic integral augmentation. With respect to the proximal aortic pressure area, tight wrapping was more effective throughout the shorter delays. Data are shown as mean ± standard error of the mean. (LAD = left anterior descending coronary artery.)
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Fig 4. Counterclockwise wrapping of the latissimus dorsi resulted in a more profound coronary blood flow diastolic integral augmentation. Data are shown as mean ± standard error of the mean (*p < 0.05). (CCW = counterclockwise wrapping; CW = clockwise wrapping; LAD = left anterior descending coronary artery.)
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Afterload
Reduction in the end-diastolic pressure in the proximal aorta was demonstrated in most of the experiments, implying a decrease in the left ventricular afterload (Fig 5). However, no statistical significance was observed and the results were not sufficiently consistent to indicate either a preferred configuration or an effective delay that would lead to afterload reduction. Moreover, in some of the experiments, the LD muscle was not sufficiently relaxed around the aorta during the next systole, implying an untimely aortic narrowing (ie, an increase in the left ventricular afterload). A further tendency toward an increase in the next beat’s afterload was observed both when using longer delays and when using the tight wrapping configuration.
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Fig 5. An illustration of proximal aortic pressure afterload reduction (delay, 250 ms). (ECG = electocardiogram.)
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Comment
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Augmentation of coronary blood flow is an important mechanism in IABP support in ischemic patients with heart failure [1, 3]. A review of the literature reveals a paucity of information regarding coronary blood flow in aortomyoplasty counterpulsation. Cardone and associates [12] induced regional ischemia with LAD coronary artery occlusion in a canine model. They observed an improvement in regional wall motion during counterpulsation with descending aortomyoplasty. These improvements might represent the favorable effects of aortomyoplasty on coronary blood flow. Cernaianu and colleagues [13] compared the use of the LD muscle with that of the serratus anterior muscle in chronic descending aortomyoplasty. They used a model of ischemia induced by external LAD occlusion in alpine goats. In both normal and ischemic hearts, stroke volume and left ventricular stroke work index increased significantly during LD muscle stimulation. However, no significant increase in mean LAD flow was observed in either the normal or the ischemic heart.
Several methodologic differences exist between the studies performed by the groups of Cardone and Cernaianu and our current study. Both investigators compared the hemodynamic profile obtained during an unassisted time period with that of a period assisted by LD muscle stimulation every spontaneous heart beat (1:1). However, in the present study, the LD muscle was stimulated every third or fourth spontaneous heart beat. Comparison of hemodynamic effects was performed in a beat-to-beat manner between the assisted beats and the corresponding previous unassisted beats. Use of a constant delay of 400 ms after the R wave and a 1:1 stimulation protocol may be responsible for the nonsignificant increases observed by Cernaianu and coworkers in the LAD blood flow. Moreover, the stimulation protocol used herein (ie, of either 1:3 or 1:4 stimulation) is in accordance with the clinical setting, and therefore, may accurately resemble the possible hemodynamic advantage. Tailoring these variables for compatibility with the specific heart rate of each animal and conducting a beat-to-beat comparison enables us to ascertain the optimal stimulation parameters for each animal, thus refining the procedure.
The results of the current study demonstrate a significant increase in the LAD blood flow induced by contraction of the LD muscle wrapped around the descending aorta. Simultaneously with this increase in coronary blood flow, diastolic pressure augmentation in the proximal aorta was observed, as described previously in other studies [14, 15].
We found that the delay between the QRS and the stimulation of the muscle is crucial to the diastolic augmentation, with respect to the animal’s heart rate (110 to 140 beats/min). A delay of 450 ms appeared to be too long; implying the LD muscle was still in a contractile state around the aorta when the next beat’s systole initiated. Thus, the next beat’s afterload was higher. Delays of less than 250 ms caused occlusion of the aorta, indicating a sudden increase in the afterload before the end of the systolic phase. There exists a time window throughout which stimulation of the LD muscle is hemodynamically optimal. Deviation from this time window, in either direction, produces transient aortic constriction, resulting in a high afterload. However, this optimal delay varies with heart rate, underling the importance of a physiologic stimulator, which includes the ability to adjust the stimulatory delay and duration in conjunction with the patient’s changing heart rate.
Another important goal regarding the efficacy of aortomyoplasty is to find the optimal surgical configuration. Chachques and colleagues [5, 7, 10] demonstrated diastolic pressure augmentation in ascending aortomyoplasty. They succeeded in enhancing counterpulsation effects by enlarging the ascending aorta with a pericardial patch. Pattison and coworkers [8] reported significant diastolic augmentation using the LD wrap around the descending aorta. In the current study, effective diastolic pressure and coronary blood flow augmentation were demonstrated in both clockwise and counterclockwise wrapping techniques. However, the increase in coronary blood flow was significantly higher in counterclockwise wrapping as compared to clockwise wrapping. This difference may be attributable to the change in orientation of the LD muscle myofilaments relative to the descending aorta. In addition to the increase in coronary blood flow, afterload reduction is an important factor in the mechanism of counterpulsation. Hymes and associates [15] noted the pivotal role of afterload reduction in aortomyoplasty; however, in their acute canine model, no afterload reduction was demonstrated. Slow LD muscle relaxation may hinder afterload reduction. Thus, we hypothesized that better afterload reduction may be achieved using a loose, rather than tight, configuration, due to earlier dilatation of the compressed aorta. Nonetheless, no significant advantage concerning afterload reduction was observed using the loose configuration. Tight wrapping induced better coronary blood flow augmentation using different delays, and was superior in inducing pressure augmentation throughout the shorter delays (250 and 300 ms). Loose wrapping suggests that a slightly longer delay exists between muscle stimulation and aortic compression.
There are several differences between the experimental model, as described in our study, and a clinical situation. No reduction in the skeletal muscle’s force and contractile velocity as demonstrated by Salmons and colleagues [16, 17] after muscle conditioning was observed, as in the acute model presented herein, the LD muscle did not undergo a training period. In addition, the use of a healthy rather than a failing heart model is also not compatible with the clinical situation. However, on the basis of previous studies of aortomyoplasty, one may assume that it is more difficult to achieve augmentation of pressure and coronary blood flow in a healthy heart rather than in a failing heart [9].
In conclusion, acute descending aortomyoplasty has been shown to induce both proximal diastolic pressure and coronary blood flow augmentation. Optimal timing of muscle stimulation is important in achieving the best assist. The diversity of results obtained when applying different surgical configurations, as well as the occasional demonstration of afterload reduction indicates a need for further investigation, and an emphasis on a chronic setting using trained skeletal muscle, to optimize this surgical modality.
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Acknowledgments
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We acknowledge Ami Weizer, BA, for his expert assistance in developing the software used throughout this study.
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References
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Accepted for publication May 21, 1999.
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Abstract
Introduction
