Asian Cardiovasc Thorac Ann 2005;13:351-356
© 2005 Asia Publishing EXchange Ltd
Adaptive Cardiac Binding: A New Method for Treatment of Dilated Cardiomyopathy
Valeri Chekanov, MD,
Arimantas Dumcius, MD1,
Pavel Karakozov, MD2
Heart Care Associates, Milwaukee Heart Institute at Aurora Sinai Medical Center, Milwaukee, Wisconsin, USA
1 Institute for Biomedical Research, Clinic of Cardiac Surgery, Kaunas University of Medicine, Kaunas, Lithuania
2 Vakhidov Scientific Center of Surgery, Tashkent, Uzbekistan
For reprint information contact: Valeri Chekanov, MD Tel: 1 414 219 7899 Fax: 1 414 219 6252 Email: vchekanov{at}yahoo.com, 945 N. 12th Street, Rm. W301, PO Box 342, Milwaukee, WI 53201-0342, USA.
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ABSTRACT
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Adaptive cardiac binding, a new surgical procedure for advanced heart failure, allows a gradual increase in compression on the dilated heart, with separate loads on the left and right ventricles. A canine model of biventricular heart failure (anastomosis between the carotid artery and jugular vein and doxorubicin administration) was created. Twenty-four dogs were divided into 4 groups: control, adynamic cardiomyoplasty, plastic cardiac binding, and adaptive cardiac binding. In the adaptive cardiac binding group, fluid was added (35, 15, and 10 mL) to each side of the pouch at weeks 1, 2, and 3. Left ventricular ejection fraction was 59% ± 4% before induction of heart failure and 27% ± 2% 6 weeks later. Immediately after the main operation, left ventricular ejection fractions were 35 ± 3% (cardiomyoplasty), 34% ± 4% (plastic cardiac binding), and 35% ± 4% (adaptive cardiac binding). Four weeks later, left ventricular ejection fraction had not changed in the cardiomyoplasty (37% ± 3%) and plastic cardiac binding (32% ± 2%) groups, but significantly increased in the adaptive cardiac binding group (48% ± 5%); it had decreased to 23% ± 4% in controls. Adaptive cardiac binding is a promising new surgical approach for patients with end-stage heart failure.
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INTRODUCTION
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In the United States alone, the prevalence of chronic heart failure has risen steadily to approximately 4–5 million people, with 400,000 new cases annually (2,000 cases per 1.5 million people).1 Cardiac transplantation remains the proven therapeutic modality to achieve long-term survival in patients with end-stage heart failure.2 Unfortunately, the prospect of heart transplantation proves a false hope for many patients because of the small number of donors and the strict selection criteria for recipients. Artificial hearts and cardiac assist devices are promising approaches, but their clinical application is limited mainly to that of a bridge to transplantation.3 Cellular cardiomyoplasty is the emerging procedure.4
Two surgical methods with controversial results are reduction ventriculectomy and dynamic cardiomyoplasty. Data on ventriculectomy from 14 countries show a 75% hospital survival rate, but early and late failures preclude its widespread use, although it may be useful as a biological bridge to transplantation.5–8 The benefits of dynamic cardiomyoplasty depend on successful systolic augmentation by the stimulated latissimus dorsi muscle (LDM) wrapped around the heart, this significantly prevents progression of left ventricular dilatation.9 Real hemodynamic improvement has not been demonstrated in clinical trials, but there has been improvement in quality of life and functional status.10–12 Simple cardiac binding is the logical extension of the cardiomyoplasty girdling effect.13–14 The new ACORN cardiac support device provides high tensile strength while maintaining flexibility.15 This relatively simple technique is an alternative method to restrain the ventricles from progressive dilatation. However, the device and related procedure have a significant limitation: if it is necessary to repeat the remodeling, another operation is needed. We propose a new surgical technique: adaptive cardiac binding (ACB) of the left and right ventricles.
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MATERIALS AND METHODS
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Our investigation was performed in two centers: ACB and plastic cardiac binding (PCB) at the Vakhidov Scientific Center of Surgery, Tashkent, Uzbekistan; and adynamic cardiomyoplasty (CMP) at the Institute for Biomedical Research, Clinic of Cardiac Surgery, Kaunas University of Medicine, Kaunas, Lithuania. All animals received humane care in compliance with state, federal, and local laws, and policies governing animal experimentation. In Kaunas, care conformed to the approved guidelines of the Experimental Laboratory of Kaunas University, and in Tashkent, care was performed in compliance with guidelines of the Experimental Department of the Center of Surgery.
FIRST OPERATION
For the heart failure model, 24 male dogs weighing 20–25 kg were fasted for 18–24 hours prior to surgery. In Tashkent, anesthesia was induced with sodium pentothal 25 mg·kg–1 and maintained with 1–1.5% halothane. Each dog was mechanically ventilated with 5 L·min–1 of oxygen via a 9 mm endotracheal tube using a Harvard Respirator (Harvard Apparatus, South Natick, MA, USA). The electrocardiogram (leads I, II, and VI) was monitored during the procedure. In Kaunas, each animal was premedicated with intramuscular atropine sulfate 0.04 mg·kg–1 and ketamine hydrochloride 10–20 mg·kg–1. In Tashkent, occasionally intramuscular acepromazine maleate (0.11–0.22 mg·kg–1) was added to the atropine sulfate and ketamine hydrochloride. To create the arteriovenous anastomosis, a 10 cm incision was made on the right side of the neck just above the clavicle, along the sternocleidomastoid muscle. The right jugular vein and right common carotid artery were isolated and a side-by-side anastomosis (8–10 mm) was created. Patency of the anastomosis was evaluated by auscultation (to detect a continuous systolic/ diastolic murmur) and palpation (to detect a systolic thrill). When this procedure was completed, the first injection of doxorubicin (2.5 mg·kg–1) was administered intravenously. Another 5 injections were given weekly over the next 5 weeks. Six weeks after creation of the arteriovenous anastomosis and 6 doxorubicin injections, the PCB (Tashkent), ACB (Tashkent), or CMP (Kaunas) procedures were performed. Six control animals did not undergo the second operation. Test dogs were randomly divided into 3 groups of 6 each. Controls were evaluated in Kaunas. All dogs survived both operations.
SECOND OPERATION
Plastic cardiac binding was undertaken in 6 animals. After anesthetic induction (as for the first operation), a median sternotomy was performed. The pericardium was opened and the heart was suspended in a cradle. A binding surgical pouch was shaped and sized according to the animal’s heart. The pouch was made by suturing together two 100 mL Viaflex PL 146 intravenous bags (Baxter, Deerfield, IL, USA). The heart was lifted gently and the pouch was wrapped around both ventricles up to the pericardial reflection. One bag was placed close to the left ventricle (LV) and the other close to the right ventricle (RV). The two lateral ends of the bags were sutured together to compress the heart just above the anterior border between the LV and RV. The binding was made tight enough to follow the contour of the heart without altering hemodynamic parameters. The free upper edge of the pouch was sutured to the pericardial flap, which anchored the pouch and prevented it from sliding down.
Adaptive cardiac binding was performed in another 6 animals. This procedure allows a gradual increase in compression on the dilated heart with separate loads on the LV and RV.16 A special pouch for binding the dilated heart, sutured from two plastic bags, allows repeated volume increases inside the pouch (Figure 1
). All surgical procedures were carried out as described above. The pouch was infused with Ringer’s solution through ports on the ends of the bags to change the volume for adaptive heart compression. One week after binding, the first portion of Ringer’s solution was administrated (35 mL into each chamber). One week later, additional solution was added (15 mL in each chamber). In the 3rd week, the final 10 mL of solution was added to each chamber. The total amount of fluid injected into the pouch over this period was 120 mL (60 mL in both left and right chambers).
Adynamic cardiomyoplasty was performed in 6 animals. The dogs were placed on their sides, and a 25 cm cutaneous incision was made from the left axilla towards the costovertebral angle at the level of the lateral border of the scapula to the intersection between the iliac crest and the paravertebral muscles. The LDM was dissected from the iliac crest, vertebra, inferior scapular angle, and the 9th to 12th rib attachments. Collateral blood vessels arising from the intercostal arteries were ligated. The muscle flap was freed of its distal attachments, with the neurovascular pedicle carefully preserved. A 4 cm segment of the anterior portion of the 2nd rib was resected and the LDM flap was transposed into the thoracic cavity. Cardiomyoplasty was performed through a median sternotomy with the pericardium wide open. The LDM flap was not sutured directly to the myocardium; rather, all sutures were placed into the pericardium. The first 2 sutures were placed close to the left branches of the pulmonary artery and the inferior vena cava. Next, the apex of the LV was elevated 2–3 cm, and the mid-portion of the LDM was placed under the heart. The heart was immediately returned to its natural position, and the electrocardiogram was monitored. If no severe arrhythmias were noted, the next suture was placed as deeply as possible at the level of the RV. The free edges of the LDM flap were sutured together.
Hemodynamic evaluation was performed before the first operation (baseline), immediately after the second operation and 4 weeks later. For right cardiac catheterization, a Swan-Ganz catheter (Edwards Life Sciences, Irving, CA, USA) was inserted into the internal jugular vein. The right atrial, RV and pulmonary artery wedge pressures were measured. Two-dimensional echocardiography was carried out using a Model 1500 echocardiography system (Hewlett-Packard, Andover, MA, USA) with a 2.5 MHz transducer. All animals were anesthetized with intravenous thiopental (25 mg·kg–1) and placed in the left lateral decubitus position. Long- and short-axis views were obtained at the apex, left sternal border, and subcostal margin. Three sets of measurements were made in each echocardiography view. The mean value of the 3 measurements was used to describe the quantitative data for each animal at each of the 13 data points. Calculated parameters included LV end-systolic and end-diastolic areas, volume, and ejection fraction.
Results are expressed as mean ± 1 standard error of the mean. All analyses were performed using StatView software (SAS Institute, Inc., Cary, NC, USA). All continuous variables were studied using one-way analysis of variance. If a resultant fraction was found to be significant, i.e., established at p < 0.05, a Schiff test was used to specify pair-wise differences.
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RESULTS
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The data before and 6 weeks after creation of the arteriovenous anastomosis and doxorubicin injections are given in Table 1. Immediately after the heart wrapping procedures, all test animals showed improvement in LV performance, but none had better right heart performance (Table 2). No differences were noted among the 3 procedures immediately after heart wrapping. Four weeks after the second operation, the surgical conditions for controls and test animals remained the same. All values of LV and RV function in the CMP and PCB groups were comparable with data immediately after the 2nd operation (Table 3). In contrast, the animals who underwent ACB had improved left heart parameters; all left heart data were significantly better than in the other 2 test groups. LV end-systolic and end-diastolic volumes and ejection fractions were significantly better than the values before ACB. All right heart systolic pressures in the ACB group were similar to data immediately after the operation; however, statistically significant changes were noted in the diastolic pressure in the right atrium and in pulmonary wedge pressure.
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DISCUSSION
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A major goal in the treatment of heart failure is prevention or reduction of ventricular dilatation. Several years of clinical trials with dynamic cardiomyoplasty revealed that prevention of future ventricular dilatation is the first benefit of cardiomyoplasty. Most studies support a beneficial girdling effect of cardiomyoplasty in limiting the dilatation associated with heart failure.9–11 Nevertheless, objective evidence of a hemodynamic benefit is difficult to trace. Unfortunately, a 10-year clinical experience with cardiomyoplasty showed that after an initial elevation of LV ejection fraction (LVEF) and decrease in LV end-diastolic volume, both parameters returned to baseline.10 The lack of hemodynamic improvement has been attributed to skeletal muscle damage and cardiomyoplasty-induced heart displacement, especially during contraction. We think that demand stimulation or stimulation with a regimen of 1:3 or 1:4 will offer better results after dynamic cardiomyoplasty.12
It is our opinion that the current consensus to discard dynamic cardiomyoplasty as a method of treatment for pre-end-stage congestive heart failure is a mistake. If a patient with heart failure has a poor prognosis without surgical intervention, why would cardiomyoplasty not be an option if this procedure could offer the patient an additional 10 or more years of life? If heart transplants become available for all patients in need of them, there would be no reason to search for alternatives. However, with the deficit of donor hearts, thousands of patients are dying without any other surgical options, simply because of the conclusion that "cardiomyoplasty did not improve LVEF after 10 years". There is an urgent need for a viable option to support the failing heart, not as a replacement for heart transplantation, but to offer some alternative to those patients for whom heart transplantation is not available.
The concept of surgically modulating the ventricular remodeling process in heart failure was an offshoot of the experience with dynamic cardiomyoplasty. In some cardiomyoplasty patients, the cardiothoracic ratio was stabilized or even appeared to decrease over time (reverse remodeling).10 Capouya and colleagues9 confirmed that adynamic cardiomyoplasty might delay ventricular dilatation. It was proposed that the elastic stretch of the skeletal muscle allowed it to provide dynamic constraint against progressive cardiac dilatation. However, even synthetic material wrapped around the heart reduced ventricular dilatation in doxorubicin-induced failure.13 Using a Marlex sheet for cardiac binding, Oh and colleagues14 showed that LVEF was better preserved with adynamic cardiomyoplasty and cardiac binding with Marlex mesh, than without. In our experiments, LVEF immediately improved from 26% to 35% with cardiomyoplasty and from 27% to 34% with plastic cardiac binding. The same improvement was seen in LV end-systolic and end-diastolic volumes. Of course, in addition to elasticity, skeletal muscles undergo conformation changes by the addition or deletion of the number of sarcomeres in the muscle fibers. This leads to a change in the pressure of the muscle on the ventricles and its resultant remodeling. Oh and colleagues14 concluded that passive restraint against further dilatation alone is not sufficient to reverse remodeling, and that this may necessitate the added benefit of active systolic assist available through dynamic cardiomyoplasty. We agree with this conclusion, but in time, when cardiomyoplasty has survived the Hamlet question: "to be or not to be", we hypothesize that it will be necessary to replace stable static heart compression with adaptive binding correlating with the heart’s condition.16 This provides hemodynamically correct remodeling of the dilated heart. First, it is necessary to create a pouch to wrap the heart. Oh and colleagues14 used a special Marlex sheet. Power and colleagues17 used a custom polyester jacket. These devices were sutured around the heart and had one layer only; none was able to change its form nor to increase or decrease the pressure on the heart. Moreover, this operation could be performed one time only, and there was no way to modulate the heart size postoperatively.
Preclinical studies showed that a passive cardiac constraint could promote reverse remodeling and improve cardiac function. Using the ACORN cardiac support device in 48 patients, Oz and colleagues18 showed improvement in LVEF 6 months postoperatively. Actuarial survival was 73% at 12 months, and 68% at 24 months. With these encouraging results, we created a special preliminary pouch from two plastic bags, which allowed repeated increases of the volume inside the pouch. After the pouch reached a volume of 120 mL, the parameters of LV function were significantly better than in the groups with plastic cardiac binding or adynamic cardiomyoplasty. Every week, these adaptations to LV and RV hemodynamics were performed to increase the load, and each new addition of fluid had a beneficial effect. As a model of biventricular heart failure, we used an arteriovenous anastomosis with doxorubicin administration. In preliminary studies, this model was tested in sheep.19 When comparing this model with anastomosis creation only and doxorubicin administration only: bilateral heart insufficiency was more stable and profound after the combination. In 2003, Tessier and colleagues20 also recommended this combination for creation of experimental cardiomyopathy. An interesting effect was described in our original proposition.16 LVEF increased from 28% to 35% after binding and to 42% after the addition of 60 mL of liquid to the pouch. When the liquid in the pouch reached 120 mL, LVEF increased to 50%; however, any further addition of liquid compressed the heart too much and LVEF dropped to 34%. When this extra amount of solution was removed, LVEF again increased to 49%. After adaptive cardiac binding and step-by-step increases in the volume of liquid in the pouch, there were no ventricular arrhythmias. However, when the loading was more than 60 mL, bigemina, trigemina, and a run of ventricular tachycardia was noted in 3 of the 6 animals. We think that additional compression of the heart must be performed carefully and the possibility of ventricular arrhythmia must be considered. It is important to note that in these 3 cases, after decreasing the volume of liquid in the chamber, cardiac rhythm reverted to normal.
An adaptive heart binding device for clinical use must be created. The device must have a non-distensible jacket to prevent the heart from expanding beyond a preselected volume (Figure 2). In operation, the differing stiffness and distensibility of the inner wall (distensible) and external wall (non-distensible) enables heart remodeling. Once the device is wrapped around the heart to match its initial volume, and sutured together, the external layer does not distend but acts as an unyielding barrier to prevent any heart dilatation that would be detrimental to lung expansion. The distensible inner wall should conform to the heart’s surface. When one or both chambers has an increased amount of liquid, the pressure on the ventricle will increase (Figure 3). The outer non-distensible wall will resist the additional pressure, while the inner distensible wall will increase the pressure on the ventricle.16 While realizing that additional investigation is needed, we feel that this new procedure might offer hope to patients with end-stage congestive heart failure who do not have the option of a heart transplant.
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Figure 3. A surgical pouch with separate chambers wrapped around the right ventricle (RV) and left ventricle (LV) up to the pericardial reflection. (A) After the first portion of liquid is administrated to each chamber. (B) With the final portions of liquid, there is greater heart compression and decreasing volumes of the ventricles.
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- Power JM, Raman J, Dornom A, Farish SJ, Burrell LM, Tonkin AM, et al. Passive ventricular constraint amends the course of heart failure: a study in an ovine model of dilated cardiomyopathy. Cardiovasc Res 1999;44:549–55.[Abstract/Free Full Text]
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ABSTRACT
INTRODUCTION
