(Chest. 2002;121:1628-1633.)
© 2002
American College of Chest Physicians
Perioperative Hemodynamic and Geometric Changes of the Left Ventricle During Cardiomyoplasty in Goats With Dilated Left Ventricle*
Gil Bolotin, MD, PhD;
Roberto Lorusso, MD, PhD;
Jan J. Schreuder, MD, PhD;
Nahum Nesher, MD;
Hans Kaulbach, MD;
Gideon Uretzky, MD and
Frederick van der Veen, PhD
* From the Department of Cardiothoracic Surgery (Drs. Bolotin, Nesher, and Uretzky), Tel Aviv Sourasky Medical Center, Division of Cardiac Surgery, Tel Aviv, Israel; and the Cardiovascular Research Institute (Drs. Lorusso, Schreuder, Kaulbach, and van der Veen), Maastricht University Hospital, Maastricht, the Netherlands.
Correspondence to: Gil Bolotin, MD, PhD, the Department of Cardiothoracic Surgery, Tel Aviv Sourasky Medical Center, 6 Weizmann St, Tel Aviv 64239, Israel; e-mail: bolotin{at}netvision.net.il
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Abstract
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Objective: Clinical data have suggested the occurrence of temporary short-term deterioration of the heart following cardiomyoplasty. The purpose of this study was to monitor the short-term hemodynamic effects of cardiomyoplasty in a goat model of a dilated left ventricle, using conductance catheters (ie, pressure-volume loops) and cardiac output measurements.
Methods: Eight female goats underwent acute cardiomyoplasty 8 to 12 weeks after left ventricular (LV) dilatation was induced by a carotid jugular arteriovenous shunt. The cardiomyoplasty procedure was monitored using a Swan-Ganz catheter for cardiac output measurements and a 12-electrode (dual-field) conductance catheter to LV pressure-volume loops.
Results: After wrapping the heart with the latissimus dorsi muscle, there was a significant reduction in both cardiac output and LV end-diastolic volume (LVEDV) at 10 min. Partial recovery was observed 45 min later.
Conclusion: A decrease in both cardiac output and LVEDV was observed following myocardial wrapping. This may explain some of the perioperative and postoperative morbidity and mortality observed following cardiomyoplasty.
Key Words: cardiomyoplasty • conductance catheters • heart failure model
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Introduction
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The short-term perioperative hemodynamic and geometric changes after cardiomyoplasty are not fully understood.1
Corin and coworkers2
demonstrated early postoperative impairment of left ventricular (LV) diastolic function in a healthy dog model following cardiomyoplasty. In contrast, Lazzara and associates3
reported little effect on LV end-diastolic volume (LVEDV) in healthy dogs that underwent cardiomyoplasty. The aim of this study was to evaluate the short-term hemodynamic and geometric changes of the LV during and immediately after the cardiomyoplasty procedure. The arteriovenous (AV) shunt was chosen to induce heart dilatation in a goat model in order to simulate end-stage dilated cardiomyopathy.
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Materials and Methods
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Carotid Jugular AV Shunt Model
Eight female goats, weighing 51 to 80 kg, were used for the experiments. All experiments were performed in accordance with the Guide for the Care and Use of Laboratory Animals.4
In the AV shunt surgical procedure, general anesthesia was induced by thiopental sodium (Pentothal; Abbott SPA; Rome, Italy), 15 mg/kg body weight IV, and after endotracheal intubation was maintained with oxygen/nitrous oxide (1:2) and 1.5% halothane (Fluothane; Zeneca Ltd; Macclesfield, Cheshire, UK). During the experiments, the lungs were ventilated with a positive-pressure respirator (Harvard Apparatus Inc; South Natick, MA), and body temperature was maintained constant with a heating mattress. A single dose of 10,000 U IV heparin was administered. Through a left cervical incision, the left jugular vein and the left carotid artery were exposed for a length of approximately 5 cm and were ligated distally. After cross-clamping of the left carotid artery, an end-to-side anastomosis of about 1 cm in diameter between the free end of the vein and the side of the artery was performed, using 6–0 polypropylene nonabsorbable running sutures (Ethicon; Edinburgh, Scotland, UK). The clamps were removed, and the patency of the fistula was confirmed by the pulsating filling of the jugular vein. The entire surgical procedure was completed in approximately 120 min.
Baseline measurements included cardiac output before and after performing the AV shunt (eight goats). Left-sided heart pressure-volume loops were attained by the conductance catheter method before and after performing the AV shunt (three goats). Baseline LV dimensions and wall thicknesses were measured by means of transthoracic echocardiography. Follow-up studies were performed 2 and 4 weeks after establishing the AV shunt to examine ECG, LV dimensions (short and long axis), and LV thickness (free wall and septum) by means of transthoracic echocardiography.
Cardiomyoplasty Procedure
The cardiomyoplasty procedure was performed 8 to 10 weeks after the AV shunt procedure. General anesthesia was induced using the same drugs and equipment as in the AV shunt procedure. A left-sided midaxillary incision was made, and all collateral blood vessels to the distal part of the latissimus dorsi (LD) muscle underwent coagulation. All attachments of the muscle were disconnected, taking care to preserve the axillary pedicle, in order to keep the thoracodorsal artery, vein, and nerve intact. Two IM electrodes (model IML-04B; Telectronics; Overland Park, KS) were implanted in the upper part of the LD muscle flap, perpendicular to the main branches of the thoracodorsal nerve, as described by Chachques and coworkers.5
To assure proper positioning, threshold values (0.3 to 0.6 V), total recruitment values (1.0 to 2.5 V), and impedance values (220 to 300 ohm) for the stimulation electrodes were measured by connecting these electrodes to a pacing system analyzer (model PSA 2401; Telectronics). A 5-cm segment of the anterior portion of the third rib, including the periosteum, then was resected to allow transposition of the LD muscle flap into the thorax. The muscle was inserted into the chest cavity, and its tendon was cut and sutured to the periosteum of the fourth rib while closing the thoracic window. The thoracic cavity was opened at the fourth left intercostal space, and the pericardium was opened. A sensing, pacing electrode (model 033-S72; Telectronics) was implanted in the LV wall, and sensing measurements (4.5 to 16.4 V) and impedance measurements (210 to 290 ohm) were recorded. The left LD muscle flap then was wrapped in a counterclockwise fashion around both ventricles. The muscle was first positioned around the right ventricle and was fixed near the atrioventricular groove at the base of the heart with interrupted sutures, after which the remaining part of the muscle was wrapped around the LV. This distal portion then was sutured to the proximal part of the muscle (Fig 1
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Monitoring
To monitor the surgical procedure, cardiac output and pressure-volume loops were taken before and after each step of the surgical procedure, including the introduction of the muscle into the chest cavity through the chest window (only cardiac output was measured at that time) and the wrapping of the heart. The same measurements were made 10 and 45 min after the heart wrapping was finished. These measurements included cardiac output and central venous pressure (which were obtained by means of a Swan-Ganz catheter), LV pressure and volume values (which were obtained by a dual-micromanometer transducer conductance catheter [7F; Sentron; Roden, the Netherlands]), and aortic pressure measured with a catheter (7F; Sentron).
For right-sided heart catheterization, an incision in the skin was made laterally to the right external jugular vein. Through a 2-mm longitudinal phlebotomy incision in the external jugular vein, a Swan-Ganz thermodilution catheter was introduced into the pulmonary artery. The catheter was secured in the external jugular vein by purse-string sutures. Central venous pressure and wedge pressure were monitored throughout the experiments in order to assure stable preloads to both ventricles. To obtain reliable estimates of cardiac output by thermodilution, a computer-controlled injection system was used. Cardiac output was determined by injections of 10 mL ice-cold glucose 5% using a cardiac output computer (COM-2; Baxter; Deerfield, IL). The balloon of an occluding catheter was inserted, under fluoroscopic guidance, into the upper part of the inferior vena cava through the left femoral vein.
For left-sided heart catheterization, a 12-electrode (duel-field) conductance catheter (7F; Sentron) was placed, via the left femoral artery and under fluoroscopic guidance, along the long axis of the LV cavity. An aortic pressure catheter was placed via the right femoral artery.
The position of the conductance catheter was verified by inspection of the segmental conductance signals. The appropriate location of the conductance catheter was assumed if the signals from at least the four most distal segments displayed a typical phasic LV volume tracing. If the most proximal segment reflected typical phasic atrial volume changes, this segment was excluded from the calculation of the total ventricular volume. Correct positioning of the conductance catheter was further facilitated by the online display of the LV contour, which was derived from the four or five segmental conductance signals.
The conductance catheter determines ventricle volume online by measuring time-varying electrical conductance of segments of intraventricular blood. Total ventricular volume was calculated from these measurements using formulas that have been described previously.6
The pigtail catheter was specially designed, equipped with electrodes that were 1 mm long and were placed 10 mm from each other. An alternating current of 0.03 mA at 20 KHz was passed through the first two electrodes, and voltages were measured between the four or five adjacent electrode pairs (electrodes 2 to 3 through 6 to 7), from which five conductance values were calculated. Electrodes 9 and 10 were not used. A signal conditioner-processor (Leycom Sigma-5DF; CardioDynamics; San Diego, CA) provided the current source and processed the segmental conductance values, producing an online display of the LV contour as well as a continuous and instantaneous volume signal. The volume signal of the ventricle was combined with the LV pressure signal on an X-Y oscilloscope in order to continuously display pressure-volume loops in real time.
The correction of the volume signal for the parallel conductance caused by tissues surrounding the ventricular cavities was performed by injecting a bolus of 7.5 mL hypertonic NaCl (9%) into the central venous compartment via the Swan-Ganz catheter. As the bolus mixes with the fluid in the ventricular cavity, its conductivity increases, causing the overall conductance signal to increase while the parallel component remains constant. End-systolic overall conductance then was plotted as a function of the end-diastolic overall conductance during the mixing of the bolus. The parallel conductance was equal to the intersection point between the regression line of these values and the line of identity.
Statistical analysis was performed with Student’s t test for paired variants. Values are presented as the mean ± SD. Significance was assumed at p < 0.05.
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Results
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Carotid Jugular AV Shunt Model
The carotid jugular AV shunt induced both immediate and long-term hemodynamic effects. The immediate results of the shunt consisted of a marked increase in the cardiac output to 7.9 ± 1.7 L/min, only a few minutes after the AV shunt was opened, compared to the average baseline cardiac output of 4.9 ± 1.4 L/m.
The long-term results of the shunt were monitored by echocardiography and cardiac output measurements. Compared to baseline measurements, a consistent significant increase in the LV end-diastolic diameter was observed 2, 4, and 8 weeks following the AV shunt procedure. Eight weeks after placing the shunt, a further increase in cardiac output was observed (to 9.9 ± 2.7 L/m).
Cardiomyoplasty Procedure
During the cardiomyoplasty procedure, cardiac output decreased slightly but significantly after the LD muscle was introduced into the chest (6%). However, it decreased by an additional 18% immediately after the wrapping procedure and was partially improved 45 min later. The average cardiac output results measured during the cardiomyoplasty procedure are presented in Figure 2 .
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Figure 2.. Average cardiac output measured by Swan-Ganz catheters at different stages of the cardiomyoplasty procedure. Baseline = following anesthesia; Muscle in = after introducing the LD muscle into the thorax; 10 min postwrapping = after the LD muscle was attached to the ventricles; 45 min postwrapping = after a recovery period of 45 min.
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The wrapping procedure was monitored with conductance catheters showing the pressure-volume loops before and after the wrapping. After the wrapping, a significant reduction was observed in the mean LVEDV, and 45 min later a partial recovery was noted (Fig 3
). An example of pressure-volume loops before, immediately after, and 45 min after the wrapping is presented in Figure 4 .
Heart rate, LV end-systolic volume, stroke volume, ejection fraction, and negative first derivative of pressure (dP/dt) before and after the wrapping are presented in Table 1
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Discussion
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Carotid Jugular AV Shunt Model
The AV shunt model is capable of producing immediate, stable, and long-term high cardiac output (overload) LV dilatation. None of the eight goats demonstrated clinical signs of pulmonary congestion. Our findings are in contrast with the high mortality rates (77%) and signs of pulmonary congestion that commonly occur within 24 h of placing the AV shunt in small animals, as reported by Flaim and coworkers.7
This discrepancy is probably due to the relatively small AV shunt (approximately 10 mm) that was used in our study in goats weighing 51 to 80 kg. Moreover, in the present study, the animals did not present clinical or hemodynamic signs of heart failure, such as tachycardia, or an increase in LV end-diastolic pressure, as was observed with the inferior vena cava aortic AV shunt applied in mongrel dogs.8
The successful compensatory mechanism in the goat carotid jugular AV shunt model is the reason for the lack of signs of renal failure, such as were demonstrated in a rat aortocaval fistula by Wegner and coworkers.9
Therefore, the model described should be considered a compensatory overload dilatation model rather than a heart failure model.
Cardiomyoplasty Procedure
The wrapping procedure monitored in our study induced a major reduction in both cardiac output and LV volume followed by partial recovery 45 min later. These results are consistent with the clinical reports of short-term deterioration in the immediate postoperative period for which Carpentier et al10
and Mesana et al11
proposed the extensive use of an intra-aortic balloon pump and inotropic support before and after the operation. In an attempt to deal with the short-term hemodynamic changes, the cardiomyoplasty procedure has undergone major technical changes since the first clinical experience.12
Two major changes in the surgical technique were the "noncardiac suture" technique13
and the "flap sliding maneuver."10
These technical improvements were one of the main factors that contributed to a reduction of up to 12% in operative mortality rate.14
Efforts have been made to identify the optimal length of the LD muscle (compared to its original resting length) that is necessary for more effective mechanical performance15
as well as the best LD muscle orientation for dynamic cardiomyoplasty.16
Gealow and coworkers17
demonstrated the adaptive changes of skeletal muscle conformation after the wrapping procedure, suggesting the lack of need for stretching the LD muscle to reproduce in situ muscle tension and length. Pericardial suspenders, which were described by Lorusso and Alfieri18
and were introduced during right-sided cardiomyoplasty, not only enabled this procedure to be carried out using the flap sliding maneuver but, perhaps more importantly, enabled the wrapping tightness to be controlled. Under direct transesophageal echocardiographic observation, the adjustment of the wrapping tightness was achieved by pulling the pericardial strips connected to the LD muscle flap.
Monitoring the cardiomyoplasty procedure under direct transesophageal echocardiographic observation also gave important data in real time, enhancing the control of certain steps in the surgical procedure. However, exact quantitative hemodynamic data concerning the effects of the wrapping are still missing in the literature. In this study, efforts were made to monitor the hemodynamic effects of the wrapping procedure. The monitoring of both cardiac output and LV volumes before, during, and after the surgical procedure provided new data about the immediate physiologic changes.
Both cardiac output and LVEDV decreased slightly, yet with statistical significance, after introducing the LD muscle into the thorax through the intercostal window and prior to the thoracotomy. Our data demonstrated that this step of the surgical procedure exerts dangerous hemodynamic effects, most probably due to the slight elevation in left chest internal pressure and direct heart compression. However, it is important to note that the harmful influence that this stage usually has on respiratory function was not monitored in this study. The wrapping, in contrast, had a major effect on both cardiac output and the LVEDV. Immediately after the wrapping there was an 18% reduction in cardiac output and a total cardiac output reduction of 22%, including the reduction due to the introduction of the LD muscle into the chest. These extreme results can be explained by analyzing the data recorded by the conductance catheter. The 24% reduction of the LVEDV measured 10 min after wrapping indicates a major change in left-sided heart hemodynamics due to the external pressure of the LD muscle around the heart. The slight reduction in stroke volume represents a partial compensatory mechanism, with the rise in LV ejection fraction due to the reduction in LV end-systolic volume. The slower heart rate after the wrapping emphasizes the nonphysiologic hemodynamic situation 10 min after the wrapping. The major reduction of LVEDV measured 10 min after wrapping is in contrast with the findings of other investigators,2
3
19
who have shown some reduction in LV diastolic function but without any reduction in volumes. The explanation for this discrepancy may be the combination of the LV dilatation model and the sensitive methods of hemodynamic monitoring used in this study. This assumption is supported by the clinical data published by Barbier and coworkers,20
demonstrating short-term modification of the LV and right ventricular geometry, as monitored by echocardiography immediately after cardiomyoplasty. These findings underscore some potential risks of cardiomyoplasty and might explain some of the perioperative mortality associated with the procedure, especially in patients with markedly dilated hearts and severely impaired LV function who might lack the reserve to overcome this dangerous phase of the cardiomyoplasty procedure.21
The partial recovery within 45 min in both cardiac output (86%) and LVEDV (88%) seems to be relatively quick, but in our study it might be related to the compensated, not the failed, dilated heart model. The AV shunt probably moved the LV to a new balanced position on the Frank-Starling curve. Based on clinical information, one can estimate that this recovery process might take days in heart failure patients.22
A negative dP/dt accounts for the compliance of the LV. The significant reduction of the negative dP/dt following the wrapping procedure is another physiologic result of the muscle being wrapped around the ventricle. However, this parameter stayed stable 45 min after the procedure, an indication that partial recovery was achieved even though LV compliance still appeared to be affected.
In conclusion, our data suggest that in the short-term postcardiomyoplasty phase the heart attains a new tension/length balance with a smaller LVEDV before the stimulation protocol is commenced. This may explain the clinical improvements sometimes seen in these patients at that early postoperative stage. However, since the immediate postwrapping LVEDV reduction may reflect incorrect tightness of the wrapping, we recommend a routine monitoring of the wrapping tightness by means of transesophageal echocardiography.
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Footnotes
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Abbreviations: AV = arteriovenous; dP/dt = first derivative of pressure; LD = latissimus dorsi; LV = left ventricle, ventricular; LVEDV = left ventricular end-diastolic volume
Received for publication June 20, 2001.
Accepted for publication November 28, 2001.
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References
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Abstract
Introduction
