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Ann Thorac Surg 2000;69:429-434
© 2000 The Society of Thoracic Surgeons

Original Articles

Composite cardiac binding in experimental heart failure

Himansu R. Shah, MDa, Mikhail Vaynblat, MDa, Louis Salciccioli, MDb, Paul Impellizzeri, MMSa, Joseph N. Cunningham, Jr, MDa, Mario Chiavarelli, MD, PhDa

a Division of Cardiothoracic Surgery, Department of Surgery and Medicine, State University of New York Health Science Center, Brooklyn, New York, USA
b Division of Cardiology, Department of Surgery and Medicine, State University of New York Health Science Center, Brooklyn, New York, USA

Address reprint requests to Dr Chiavarelli, Division of Cardiothoracic Surgery, SUNY Health Science Center at Brooklyn, 450 Clarkson Ave, Box 40, Brooklyn, NY 11203
e-mail: mchiavarelli{at}netmail.hscbklyn.edu


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 References
 
Background. Composite cardiac binding consists of wrapping the heart with a synthetic membrane and a pericardial interposition. The goal of the present study was to apply composite cardiac binding to a canine model of heart failure.

Methods. Twenty dogs were randomized to 2 groups: untreated heart failure (group 1, n = 13) and heart failure pretreated by composite cardiac binding (group 2, n = 7). They received a total dose of 1 mg x kg-1 of intracoronary doxorubicin over 4 weeks. Hemodynamic data were obtained at weeks 0, 7, and 12. All animals were followed up with weekly echocardiography for 12 weeks.

Results. Survival in group 1 was 54% and in group 2 was 100% at week 12 (p = 0.0438). Left ventricular end-diastolic pressure increased by 153% in group 1 and by 59% in group 2 (p = 0.0395) at week 12. Ejection fraction decreased by 27% in group 1 and by 19% in group 2 (p = 0.4401) at week 12.

Conclusions. Composite cardiac binding significantly prolongs survival and attenuates left ventricular dilatation and the increase in left ventricular end-diastolic pressure associated to chronic heart failure. Further evaluation in established heart failure is needed. Composite cardiac binding may be used for the prevention of recurrent dilatation following reduction ventriculoplasty.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 References
 
End-stage heart disease is a major medical and social issue. There are approximately 4,700,000 patients with chronic heart failure. Once heart failure develops, 6-year mortality approaches 80% in men and 65% in women [1]. Current treatment modalities have serious limitations. A well-established surgical treatment is cardiac transplantation which is limited by the shortage of the donor pool [2]. Cardiac assist devices and artificial hearts are promising areas of research [3], but at present their clinical application is limited to the bridge-to-transplantation modality. Reduction ventriculoplasty (Batista procedure) is currently undergoing clinical trials [4].

Cardiomyoplasty is being investigated as a surgical method for the treatment of heart failure [5]. The beneficial effects of dynamic cardiomyoplasty are attributed to two mechanisms: (1) systolic augmentation by the stimulated muscle wrap, and (2) limitation of progressive cardiac dilatation [6]. Unstimulated muscle wrapping, namely the "girdling effect," significantly prevents the progression of left ventricular dilatation in a canine model of heart failure [7]. Cardiomyoplasty attenuates both ventricular dilatation and remodeling process associated with severe progressive heart failure in a chronic canine model [8]. Hemodynamic improvement has not been demonstrated consistently in clinical trials using dynamic cardiomyoplasty even though the quality of life and functional status improve [9]. This may be attributed to the girdling effect of dynamic cardiomyoplasty.

Cardiac binding [10] is the logical extension of the cardiomyoplasty girdling effect. It consists of wrapping the failing heart with a synthetic membrane to prevent dilatation. In a canine model of chronic heart failure, cardiac binding reduces ventricular dilatation without exacerbating left ventricular dysfunction [10]. In the present study, composite cardiac binding is accomplished by interposing a flap of pericardium in the synthetic membrane wrap. This modification is designed to prevent cardiac constriction, while preserving cardiac function.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 References
 
A canine model of doxorubicin cardiomyopathy was used [11]. Twenty adult male mongrel dogs weighing 20 to 34 kg (27 ± 1 kg) were randomly assigned to 2 groups: untreated heart failure (group 1, n = 13), or heart failure pretreated by composite cardiac binding (group 2, n = 7) with a Gore-Tex surgical membrane (expanded polytetrafluoroethylene, 0.1 mm; W. L. Gore & Associates Inc, Flagstaff, AZ) and autologous pericardial interposition. All animals received humane care in accordance with the "Guide for the Care and Use of Laboratory Animals" published by National Institutes of Health (NIH publication No. 85-23, revised 1985).

Procedure
The animals were premedicated with acepromazine maleate (Aveco Co, Inc, Fort Dodge Laboratories, Inc, Fort Dodge, IA) and were anesthetized with intravenous thiopental (15 mg/kg, Abbott Laboratories, North Chicago, IL) [11]. Anesthesia was maintained after endotracheal intubation with oxygen and halothane (0.5 to 1 percent).

Animals were placed in a supine position and a bilateral anterior thoracotomy was performed through the fifth intercostal space. A percutaneous vascular access port (model GPV, Access Technologies, Skokie, IL) was positioned in the subcutaneous tissue in the posterior aspect of the incision. The pericardium was opened and the heart was suspended in a cradle. After the coronary vasculature was examined, the first or second diagonal branch was identified and mobilized. A 4F catheter was introduced retrogradely until the tip was in the left main coronary artery. The catheter was flushed with 1,000 U of heparin and then secured to the epicardium with several sutures.

In group 2, composite cardiac binding was performed after placement of the intracoronary catheter. The composite wrap was constructed with 90% synthetic membrane and 10% pericardium, which in our animals was approximately 1-cm wide (Fig 1). The pericardium was incorporated in the wrap as a pedicle flap to maintain its vascular supply. A surgical membrane was shaped and sized according to the animal’s heart. The heart was lifted gently and the membrane was wrapped around both the ventricles and the atria up to the pericardial reflection. The right lateral edge of the synthetic membrane was sutured with interrupted 5-0 Prolene (Ethicon, Somerville, NJ) stitches to the base of the flap. The left edge of the synthetic membrane was carefully trimmed to make the binding tight enough to follow the contour of the heart without altering hemodynamic parameters. It was sewn to the free edge of the pericardial flap with 5-0 Prolene suture. The thoracotomy incision was closed anatomically. Postoperative pain was controlled with intramuscular buprenorphine (0.01 to 0.02 mg x kg-1, Aveco Co, Inc). All animals were sacrificed at 12 weeks and necropsy was performed in cases of sudden death.



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  		Fig 1. A schematic diagram of composite cardiac binding.

 
Heart failure was induced by weekly infusions of doxorubicin (Adria Laboratories, Columbus, OH) for 4 weeks as described by Shah and colleagues [11]. Doxorubicin dosing was started 1 week after operation. Intracoronary doxorubicin administration takes advantage of the direct cardiotoxicity of doxorubicin, while minimizing its systemic effects. A significant decrease in left ventricular ejection fraction and cardiac index, and a significant increase in left ventricular end-diastolic pressure and volume, were demonstrated [11].

Cardiac hemodynamics
Right and left cardiac catheterization was performed prior to the operation (baseline) and repeated at 7 and 12 weeks following the first dose of doxorubicin. A Swan-Ganz catheter (Arrow International, Inc, Reading, PA) was inserted into the external jugular vein, and right atrial, right ventricular, pulmonary arterial, and pulmonary capillary wedge pressures were measured. Cardiac output was measured in triplicate using the thermodilution method (model 9520A; American Edwards Laboratories, Irvine, CA). Left ventricular pressure was obtained by insertion of a pigtail catheter (Cordis Corporation, Miami, FL) into the right femoral artery at week 7. At week 0 and 12, left ventricular pressure was obtained by direct puncture with an 18-gauge needle into the left ventricle. After instrumentation, arterial and mixed venous blood gas levels were obtained. Hemodynamic and oximetric parameters were calculated using standard formulas for cardiac and stroke volume indices, systemic and pulmonary vascular resistance indices, left and right ventricular stroke work indices, left ventricular minute work index and oxygen delivery and consumption.

Echocardiography
A change in the left ventricular ejection fraction is a good indication of developing cardiomyopathy [12]. Two-dimensional echocardiographic studies were performed using a 1500 echocardiographic system (Hewlett-Packard, Andover, MA) with a 2.5-MHz transducer. All animals were anesthetized with intravenous thiopental (15 mg/kg) and placed in the left lateral decubitus position. Long-axis and short-axis views were obtained at the apex, left sternal border, and subcostal margin. Three sets of measurements were made in each echocardiographic view at the baseline, and then weekly for 12 weeks in both groups of animals. The mean value of three measurements was used to describe the quantitative data for each animal at each of the thirteen data points. The same echocardiographer analyzed all the images. Calculated parameters included left ventricular end-systolic and end-diastolic area and volume and ejection fraction.

Statistical analysis
Data were expressed as mean ± standard error of mean, and analyzed by repeated-measures analysis of variance with multiple comparisons (Scheffe’s test). Baseline data of survivors and nonsurvivors in the untreated group were analyzed by unpaired Student’s t-test. Actuarial survival was calculated by the Kaplan-Meier method and difference in survival were determined by the log-rank test. A p value of 0.05 or less was considered to represent statistical significance.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 References
 
Survival in untreated heart failure group was 54% and in composite cardiac binding group was 100% at week 12 ({chi}2 = 4.06, p = 0.0438, Fig 2). There were no intraoperative deaths. Necropsy performed in cases of sudden death showed neither evidence of myocardial infarction nor signs of liver or pulmonary congestion. Sudden cardiac death in the untreated group was attributed to malignant ventricular arrhythmia [11]. Baseline parameters of survivors and nonsurvivors in the untreated group were compared in Table 1 and no significant difference was found. Clinical signs of heart failure, including peripheral edema, ascites, or respiratory distress, were not detected during the 12 weeks of follow-up. Body weight increased by 2.8% in untreated heart failure group and by 5.7% in composite cardiac binding group (F = 0.18, p = 0.6806) at week 12. There were 5 cases of superficial wound infection, which were successfully treated with intramuscular cefazolin (1 g/day for 10 days). Two animals had wound dehiscence, which required debridement and reclosure.



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  		Fig 2. Actuarial survival curve (Kaplan-Meier method) for the untreated heart failure (n = 13) and the composite cardiac binding (n = 7) groups. The untreated animals had a 12 week survival of 54 percent (log-rank test, p = 0.0438). Sacrificed dogs were censored alive at week 12.

 

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  		Table 1. Comparison of Baseline Parameters Between Survivors and Nonsurvivors of the Untreated Group

 
Right atrial and right ventricular end-diastolic pressure, mean pulmonary arterial pressure, and pulmonary capillary wedge pressure increased and right and left ventricular stroke work index decreased in both groups, however, the difference between groups did not achieve statistical significance at week 12. Left ventricular end-diastolic pressure increased by 153% in untreated heart failure group and by 59% in composite cardiac binding group at week 12 (F = 5.33, p = 0.0395; Fig 3, Table 2). Cardiac index fell by 41% in untreated heart failure group and by 44% in composite cardiac binding group at week 12 (F = 0.90, p = 0.3606).



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  		Fig 3. Effect of composite cardiac binding on left ventricular end-diastolic pressure. An increase by 153% occurred in untreated heart failure group and by 59% in composite cardiac binding group (F = 5.33, p = 0.0395).

 

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  		Table 2. Comparison of Weeks 0 and 12 Parameters Between Groups 1 (Untreated) and 2 (Cardiac Binding)

 
Left ventricular end-diastolic volume increased by 42% in untreated heart failure group and decreased by 3% in composite cardiac binding group at week 12 (F = 9.22, p = 0.0103; Fig 4, Table 2). Left ventricular end-diastolic diameter increased by 14% in untreated heart failure group and by 7% in composite cardiac binding group at week 12 (F = 8.32, p = 0.0137). Ejection fraction decreased by 27% in untreated heart failure group and by 19% in composite cardiac binding group at week 12 (F = 0.64, p = 0.4401; Fig 5, Table 2).



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  		Fig 4. Heart failure caused a marked increase in left ventricular end-diastolic volume (p = 0.0103). Composite cardiac binding effectively prevented ventricular dilatation.

 


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  		Fig 5. Heart failure was associated with substantial depression of ejection fraction in both untreated and composite cardiac binding group.

 

   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
References
 
Reduction or prevention of ventricular dilatation is a major goal in the treatment of heart failure. A new clinical therapeutic modality for dilated cardiomyopathy, reduction ventriculoplasty (Batista procedure [4]), is based on the concept of restoring normal left ventricular diameters, thus improving cardiac function. Although the heart function does not return to normal, this procedure offers significant clinical improvement [13]. Redilatation has been described following reduction ventriculoplasty and it has been attributed to the progression of cardiac disease and inadequate removal of left ventricular muscle at time of operation [4]. Currently, it has not been determined whether the Batista procedure is a biological bridge or an alternative to transplantation.

Dynamic cardiomyoplasty has undergone clinical trials including more than 500 patients worldwide [14]. Improvement in patient’s functional status, survival, and quality of life are reported [15, 16]. Nevertheless, objective evidence of hemodynamic benefit is difficult to trace. A 10-year experience with clinical cardiomyoplasty reported an initial elevation of left ventricular ejection fraction and a decrease in left ventricular end-diastolic volume [17]. Later in the follow-up period, however, both parameters returned to baseline levels. In another study hemodynamic evaluation or exercise stress test variables did not demonstrate an advantage from muscle stimulation beyond 6 months [18]. Thus, prevention of cardiac dilatation was considered the principal benefit of the procedure. The lack of hemodynamic improvement has been attributed to skeletal muscle damage and cardiomyoplasty induced heart displacement [19].

Failure to demonstrate significant hemodynamic changes occurred in a recent experimental study, which tested different stimulation ratios [20]. Conversely, an additional benefit from skeletal muscle stimulation was inferred by Patel and associates, since synchronous stimulation of the conditioned wrap reduced myocardial workload [8]. Most clinical and experimental studies support a beneficial girdling effect of cardiomyoplasty in limiting cardiac dilatation associated to heart failure.

The concept of applying a synthetic girdle to prevent cardiac dilatation is appealing. The use of synthetic material instead of skeletal muscle would avoid the prolonged operative procedure of dynamic cardiomyoplasty, and would be easily tolerated by patients with heart failure. Wrapping the heart with a synthetic membrane can also avoid some other negative aspects of cardiomyoplasty, namely the burden and inertia of the muscle. Cardiac binding was designed to prevent ventricular dilatation in an animal model of heart failure [10]. Biventricular dilatation was effectively avoided and the increase in left ventricular end-diastolic pressure was attenuated. Cardiac binding with a Marlex sheet (C. R. Bard, Inc, Murray Hill, NJ) reduced cardiac enlargement and functional deterioration after rapid pacing, and attenuated the deleterious ventricular remodeling process [21]. Long-term follow-up with cardiac binding suggested that some degree of cardiac constriction might develop. To minimize potential constrictive effects we introduced the concept of composite cardiac binding. The interposed pericardial flap offers the potential of controlled growth of the wrap while limiting cardiac dilatation. This represents an advantage over both the uncontrolled growth of the pericardium and a fixed cardiac binding.

Composite cardiac binding was beneficial in the setting of progressive cardiac dilatation. Serial studies showed attenuation of the increase in left ventricular end-diastolic pressure and the decrease in left ventricular end-diastolic volume. The procedure appeared to avoid severe constrictive effects. These data suggest that composite cardiac binding achieves a sustained girdling effect without exacerbating left ventricular dysfunction.

Survival was significantly prolonged in the composite cardiac binding group, as compared to the untreated heart failure group. The difference in survival rate can be attributed to the limitation of left ventricular dilatation and to the lower left ventricular end-diastolic pressure. Composite cardiac binding, therefore, offers the potential of delaying heart failure progression. Survival improvement and prevention of ventricular enlargement is accomplished with a relatively simple and short lasting procedure, which could be tolerated by chronic heart failure patients. Hence, a skeletal muscle wrap may not be needed because an equivalent result could be achieved by wrapping the heart with a synthetic membrane. Prevention of ventricular dilatation could make composite cardiac binding an effective addition to reduction ventriculoplasty.

Further studies will investigate the optimal amount of pericardial interposition and the effectiveness of composite cardiac binding in established heart failure. The potential clinical application of composite cardiac binding include the treatment of early-stage left ventricular dysfunction and the prevention of recurrent dilatation following reduction ventriculoplasty for end-stage heart failure.


   Acknowledgments
 
We thank the Adria Laboratories of Columbus, OH, for graciously providing our laboratory with doxorubicin, and W. L. Gore and Associates, Inc, Flagstaff, AZ, for providing our laboratory with a generous supply of surgical membrane. This study was supported by The Foundation for Surgical Education and Investigation, Inc, SUNY-Health Science Center at Brooklyn, and the Maimonides Research and Development Foundation.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

  1. Kannel W.B. Epidemiological aspects of heart failure. Cardiol Clinl 1989;7:1-9.
  2. Mudge G., Goldstein S., Addonizio L., et al. 24th Bethesda Conference Task force 3. Recipient guidelines/prioritization. J Am Coll Cardiol 1993;22:21-31.[Medline]
  3. Griffith B.P., Kormos R.L., Hardesty R.L., et al. The artificial heart. Ann Thorac Surg 1988;45:409-414.[Abstract]
  4. Batista R.J.V., Verde J., Nery P., et al. Partial left ventriculectomy to treat end-stage heart disease. Ann Thorac Surg 1997;64:634-638.[Abstract/Free Full Text]
  5. Carpentier A., Chachques J.C. Myocardial substitution with a stimulated skeletal muscle. Lancet 1985;8440:1267.
  6. Chachques J.C., Grandjean P., Schwartz K., et al. Effect of latissimus dorsi dynamic cardiomyoplasty on ventricular function. Circulation 1988;78(Suppl):III203-III216.
  7. Capouya E.R., Gerber R.S., Drinkwater D.C., et al. Girdling effect of nonstimulated cardiomyoplasty on left ventricular function. Ann Thorac Surg 1993;56:867-871.[Abstract]
  8. Patel H.J., Lankford E.B., Polidori D.J., et al. Dynamic cardiomyoplasty. J Thorac Cardiovasc Surg 1997;114:169-178.[Abstract/Free Full Text]
  9. Mott B.D., Austin L.L., Chiu R.C.-J. Dynamic cardiomyoplasty. In: Cooper D.K.C., ed. The transplantation and replacement of thoracic organs. Lancaster: Kluwer Academic Publishers, 1996:767-773.
  10. Vaynblat M., Chiavarelli M., Shah H.R., et al. Cardiac binding in experimental heart failure. Ann Thorac Surg 1997;64:81-85.[Abstract/Free Full Text]
  11. Shah H.R., Vaynblat M., Ramdev G., et al. Experimental cardiomyopathy as a model of chronic heart failure. J Invest Surg 1997;10:387-396.[Medline]
  12. Singal P.K., Iliskovic N. Doxorubicin-induced cardiomyopathy. N Engl J Med 1998;339:900-905.[Free Full Text]
  13. McCarthy P.M., Starling R.C., Wong J., et al. Early results with partial left ventriculectomy. J Thorac Cardiovasc Surg 1997;114:755-765.[Abstract/Free Full Text]
  14. Misawa Y., Mott B.D., Lough J.O., et al. Pathologic findings of latissimus dorsi muscle graft in dynamic cardiomyoplasty. J Heart Lung Transplant 1997;16:585-595.[Medline]
  15. Grandjean P.A., Austin L., Chan S., et al. Dynamic cardiomyoplasty. J Card Surg 1991;6:80-88.[Medline]
  16. Moreira L.F., Seferian P.J., Bocchi E.A., et al. Survival improvement in patients with dilated cardiomyopathy. Circulation 1991;84(Suppl):III296-III302.
  17. Magovern G.J., Simpson K.A. Clinical cardiomyoplasty. Ann Thorac Surg 1996;61:413-419.[Abstract/Free Full Text]
  18. Jondeau G., Dorent R., Bors V., et al. Dynamic cardiomyoplasty. J Am Coll Cardiol 1995;26:129-134.[Abstract]
  19. EI Oakley R.M., Jarvis J.C. Cardiomyoplasty a critical review of experimental and clinical results. Circulation 1994;90:2085-2089.[Free Full Text]
  20. Soltero E.R., Glaeser D.H., Micheal L.H., et al. Hemodynamic effects of different pacing ratios in chronic dynamic double cardiomyoplasty. Ann Thorac Surg 1996;62:1380-1387.[Abstract/Free Full Text]
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Accepted for publication July 6, 1999.


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