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Ann Thorac Surg 1998;66:1585-1591
© 1998 The Society of Thoracic Surgeons

Determinants of midterm outcome of partial left ventriculectomy in dilated cardiomyopathy

Noedir A.G. Stolf, MDa, Luiz Felipe P. Moreira, MDa, Edimar A. Bocchi, MDa, Maria de Lourdes Higuchi, MDa, Fernando Bacal, MDa, Giovanni Bellotti, MDa, Adib D. Jatene, MDa

a Instituto do Coração da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil

Address reprint requests to Dr Stolf, Instituto do Coração, Av. Dr. Enéas Carvalho Aguiar, 44. São Paulo, SP, Brazil. CEP: 05403-000

Presented at the Thirty-fourth Annual Meeting of The Society of Thoracic Surgeons, New Orleans, LA, Jan 26–28, 1998.


    Abstract
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 
Background. Partial left ventriculectomy has been proposed for treatment of severe cardiomyopathies. This study reports midterm results of this procedure in 37 patients with dilated cardiomyopathy.

Methods. All patients were in New York Heart Association class III (16) or IV (21). Partial ventriculectomy was associated with mitral annuloplasty in 27 patients and with mitral replacement in 2.

Results. There were seven operative deaths (18.9%). During a mean follow-up of 18.2 ± 9.3 months, 9 more patients died. Actuarial survival was 56.7% ± 8.1% at 6 and 24 months. Analysis of factors influencing outcome showed that midterm survival was significantly affected only by myocardial cell diameter. Otherwise, functional class improved from 3.5 ± 0.5 to 1.8 ± 0.9 in the survivors (p < 0.001). Furthermore, left ventricular diastolic volume decreased from 523 ± 207 to 380 ± 148 mL (p < 0.001), and left ventricular ejection fraction increased from 17.1% ± 4.6% to 23% ± 8% (p < 0.001), whereas significant changes in cardiac index, stroke index, and pulmonary pressures were found at 1 month of follow-up. Although left ventricular diastolic volume tended to increase in the late postoperative period, left ventricular ejection fraction and hemodynamic variables did not change significantly.

Conclusions. Partial ventriculectomy improves left ventricular function and congestive heart failure in patients with dilated cardiomyopathy for up to 24 months of follow-up. Nevertheless, this procedure’s clinical application is limited by the high mortality observed in the first postoperative months. Otherwise, new perspectives may be advised by the identification that partial ventriculectomy results seem to be influenced by compromised myocardial cells.


    Introduction
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 
Surgical reduction of left ventricular (LV) volume has been proposed as an alternative treatment of severe cardiomyopathies. The primary objective of this procedure is to decrease LV wall tension by the reduction of the chamber volume to mass relationship, resulting in partial restoration of myocardial contractility and slowing progression of the underlying disease.

Since the pioneering efforts of Batista and coworkers [1], partial left ventriculectomy has been evaluated by several authors throughout the world [28]. Initial results of this surgical technique demonstrated the improvement of LV function and reversal of congestive heart failure in patients with dilated cardiomyopathies [36, 8]. Nevertheless, high incidences of heart failure progression and arrhythmia-related deaths have been reported in the early postoperative period in most of those series [24, 7, 8]. Furthermore, no documentation is found yet regarding long-term survival and prolonged benefits after this procedure.

The purpose of this report is to outline the clinical and LV function effects of partial left ventriculectomy, associated when necessary with mitral insufficiency correction, for up to 2 years of follow-up in patients with advanced heart failure caused by idiopathic dilated cardiomyopathy. The influence of preoperative and surgical factors on patients’ outcomes is also analyzed.


    Patients and methods
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 
Study population
Patients selected for partial left ventriculectomy by the Heart Failure and Heart Transplantation Program of the Heart Institute, University of São Paulo Medical School, were those with significant functional limitation despite attempts to optimize medical therapy with maximal doses of diuretics and angiotensin-converting enzyme inhibitors or vasodilators. They also had reduced LV function characterized by radioisotopic ejection fraction less than or equal to 25% and persistently high filling pressures. Medical or psychosocial contraindications to heart transplantation were present or this procedure was refused by the patients, and they signed a special informed consent form according to our Ethical and Scientific Review Board.

Accordingly, partial left ventriculectomy was performed in 37 patients with idiopathic dilated cardiomyopathy between April 1995 and August 1997. Sixteen patients were in New York Heart Association (NYHA) class III and 21 were in persistent class IV. Nine of these patients also had reversible cardiogenic shock with temporary use of intravenous inotropic drugs. Mean duration of symptoms was 3.9 years, and patients had at least two hospitalizations for heart failure treatment in the year preceding the operation. Patients’ ages ranged from 28 to 72 years (mean, 46.1 years), and 30 patients were men. Preoperative laboratory data are summarized in Table 1. Two patients had atrial fibrillation and 22 patients had nonsustained ventricular tachycardia episodes documented by Holter recordings. Absence of significant coronary artery compromise was shown in every patient. Mitral valve insufficiency was present in 31 patients, being moderate in 12 and mild in 19 patients. Seven patients also had significant tricuspid valve insufficiency, being moderate in 5 and severe in 2 patients.


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Table 1. Preoperative Laboratory Dataa

 
Surgical procedure
Partial left ventriculectomy was performed as an isolated procedure or associated with atrioventricular valves annuloplasty or replacement. The procedures were usually done during standard cardiopulmonary bypass with moderate hypothermia and on the beating heart. When mitral valve replacement was necessary, it was performed during hypothermic myocardial arrest induced by the infusion of cold-blood cardioplegia.

Left ventricular volume reduction was performed according to the technique initially described by Batista and associates [1]. A slice as large as possible of the ventricular myocardium was resected between the papillary muscles, from the apex of the heart up to 2 or 3 cm from the mitral annulus. The left ventricle was then repaired with a double 3-0 polypropylene suture anchored in bovine pericardium strips.

Mitral valve annuloplasty was done in the presence of any degree of mitral regurgitation. The mitral valve was assessed through the left atrium and the mitral annulus was reduced by plication of the posterior leaflet region with sutures anchored in a bovine pericardium strip. In patients with malposition of the papillary muscles, precluding an effective myocardial resection, these muscles were resected and the mitral valve was replaced by a bovine pericardium bioprosthesis. The De Vega tricuspid annuloplasty was performed in patients with moderate to severe tricuspid regurgitation. Endocardial automatic cardioverter-defibrillators were routinely implanted in patients who presented with episodes of sustained ventricular tachycardia or ventricular fibrillation.

Follow-up protocol
Patients were studied at the first postoperative month and every 6 months of follow-up by means of radioisotopic angiography and right heart catheterization. They continued to use diuretics and angiotensin-converting enzyme inhibitors or vasodilators. Amiodarone was routinely used at the first 2 weeks of follow-up and in patients who presented with episodes of sustained ventricular tachycardia or atrial fibrillation.

Left ventricular radioisotopic angiography was obtained after in vivo labeling of red blood cells by technetium 99m. Gated blood pool imaging was acquired in left anterior oblique view with a Siemens model LEM+ camera (Siemens, Union, NJ). The images were analyzed in a Microvax model 3300 computer (Siemens), and LV volumes and ejection fraction were calculated. Right heart catheterization was performed with a thermodilution balloon-tipped catheter positioned in the left pulmonary artery.

Statistical analysis
Cumulative mortality and event rates over time were determined by the Kaplan-Meier method, and differences between them were assessed by the log-rank test. Repeated measures analysis of variance and the Dunnet’s test were used to compare data obtained before and after the operation. Data are presented as mean ± standard deviation, whereas survival rates are presented as mean ± standard error of the mean.

The association of variables with survival was assessed by means of univariate analysis using the unpaired Student’s t test and Fisher’s exact test. Variables with a p value less than 0.10 in univariate analysis were submitted to logistic regression. For this analysis, we considered only the events that occurred during the first 7 months of follow-up, and patients undergoing urgent heart transplantation after partial ventriculectomy were included as deaths.


    Results
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 
Immediate surgical results
Eight patients underwent isolated partial left ventriculectomy, and this procedure was associated with mitral valve annuloplasty in 27 patients and mitral valve replacement in the remaining 2 patients. Seven of those patients who underwent mitral valve operation also had De Vega tricuspid valve annuloplasty.

Intraoperative transesophageal echocardiography after discontinuation of bypass revealed no mitral regurgitation in 28 patients and mild regurgitation in 9. The resected myocardial specimen measured 10.9 ± 2 cm in length and 5 ± 0.8 cm in width, corresponding to an estimated LV myocardial resection of 19.1% ± 2.5%. This parameter was assessed from the echocardiographic estimation of LV perimeter. Morphometric analysis of myocardial samples stained with hematoxylin-eosin and trichrome showed mean myocyte diameter of 21.9 ± 6.2 µm and mean percentage of fibrosis of 14.5% ± 6.3%.

All patients were weaned from cardiopulmonary bypass with dobutamine and sodium nitroprusside, and 13 patients also required intraaortic balloon counterpulsation. Two patients presented with refractory heart failure and required insertion of a centrifugal pump or pneumatic ventricular assist device for LV assistance on the second postoperative day. Another patient had dehiscence of the mitral valve annuloplasty and was reoperated on for mitral valve replacement 5 days after the initial operation.

Episodes of sustained ventricular tachycardia occurred in 9 patients (21.6%) at the first 2 weeks of follow-up. Transient periods of renal failure developed in 5 patients (13.5%), and pulmonary complications occurred in 7 (18.9%). The mean peak serum level of the myocardial component of the creatine kinase enzyme was 111 ± 54 IU.

Seven patients died during the hospital period (18.9%). The causes of death were cardiogenic shock in 2 patients; biventricular failure in the patient maintained with the centrifugal pump; multiple organ failure in the patient requiring pulsatile mechanical circulatory support; septicemia and cardiogenic shock in the patient reoperated on because of mitral annuloplasty dehiscence; incessant sustained ventricular tachycardia in 1 patient; and bleeding associated with disseminated intravascular coagulation in 1 patient.

Quality of life and survival
Thirty patients were discharged from the hospital and were followed up from 2 to 36 months (mean, 18.2 months). Ten of these patients had automatic cardioverter-defibrillator implantation.

Eight patients were rehospitalized during the first 6 months of follow-up because of heart failure progression and another 3 because of sustained ventricular tachycardia episodes. Five of these patients were listed for heart transplantation, and this procedure was urgently performed in 1 of them 7 months after partial ventriculectomy. On the other hand, 9 patients died during this follow-up period, and the survival curve presented in Fig 1 shows survivals of 62.1% ± 7.9% at 3 months and 56.7% ± 8.1% at 6 and at 30 months of follow-up. The cause of death was progressive heart failure in 5 patients, and 4 patients died suddenly or because of incessant ventricular tachycardia. Progressive heart failure was associated with pulmonary thromboembolism in 1 patient, and 2 of those patients who died because of arrhythmia-related events were using amiodarone; 1 had an automatic internal cardioverter-defibrillator.



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Fig 1. Kaplan-Meier survival curve after partial left ventriculectomy. Numbers in parentheses indicate patients at risk at each period. Values are presented as mean ± standard error of the mean.

 
Univariate analysis of preoperative and surgical risk factors showed that only greater myocyte diameter was significantly associated with an unfavorable outcome during the first 7 months of follow-up (Table 2). In this regard, logistic regression demonstrated that the risk of death or necessity of urgent heart transplantation in that period increased exponentially and achieved values of more than 40% when the mean myocyte diameter was greater than 22 µm (Fig 2). The survival curves according to this parameter are depicted in Fig 3 and show that the 2-year survival of patients with less marked myocardial cell hypertrophy was 73.6% ± 10.1%, whereas those patients with severe myocyte compromise had a survival rate of 31.2% ± 11.5% at the same period.


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Table 2. Unifactorial Analysis of Factors Associated With Outcomea

 


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Fig 2. Logistic regression curve of risk of death or necessity of urgent heart transplantation during the first 7 months of partial left ventriculectomy follow-up according to the mean diameter of left ventricular myocardial cells.

 


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Fig 3. Plots of survival rates free of the necessity of urgent heart transplantation for patients with mean myocardial cell diameter (MCD) in the left ventricle less than or greater than 22 µm. Values are presented as mean ± standard error of the mean.

 
Regarding the functional status, NYHA class significantly improved from 3.5 ± 0.5 to 1.8 ± 0.9 at 6 months of follow-up in the 20 long-term survivors (p < 0.001). The number of hospitalizations during the follow-up period also decreased for those patients from 2.3 to 0.2 per patient per year (p < 0.001). In addition, 9 of the surviving patients are currently in functional class I, 9 are in class II, and only 2 are in class III. Some of these patients are using fewer drugs and lower doses than they did in the preoperative period.

Circulatory function evaluation
Data obtained by radioisotopic angiography in 30 patients showed that significant improvement of LV ejection fraction (from 17.1% ± 4.6% to 23% ± 8%, p < 0.001) was found at the first postoperative month associated with significant decrease in LV diastolic volume (from 523 ± 207 to 380 ± 148 mL, p < 0.001). Figure 4 shows that these modifications were maintained during the first year of follow-up in the 20 patients who survived long-term. Otherwise, LV diastolic volume tended to increase, whereas LV ejection fraction maintained the recorded improvement for up to 2 years after partial left ventriculectomy in the 10 patients with complete follow-up.



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Fig 4. Plots of left ventricular ejection fraction (A) and diastolic volume (B) values obtained by radioisotopic angiography in the preoperative period and up to 24 months after partial left ventriculectomy. Values are presented as mean ± standard deviation. *p < 0.05 compared with preoperative data of matched patients.

 
Hemodynamic evaluation showed that significant increases of cardiac and stroke indexes were associated with a significant decrease in pulmonary wedge pressure immediately after the operation (Table 3). At 6 months of follow-up, these modifications were maintained in the 20 patients who survived long term. This study additionally demonstrated that the improvement of those indexes persisted for up to 2 years of follow-up, whereas pulmonary wedge pressure values tended to increase after the first 6 months.


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Table 3. Sequential Hemodynamic Dataa

 

    Comment
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 
The present investigation showed that the midterm course of patients with dilated cardiomyopathy who underwent partial left ventriculectomy, associated when necessary with mitral insufficiency correction, was characterized by the maintenance of clinical and hemodynamic benefits documented early after the operation. This fact occurred despite the tendency of LV redilatation observed after the first year of follow-up.

Otherwise, high incidences of heart failure progression and arrhythmia-related deaths occurred in the early postoperative period in this series, precluding an optimistic conclusion about partial left ventriculectomy in clinical application. The identification of the influence of compromised intrinsic myocardial cells on this procedure’s outcome, however, opens the possibility of refining patient selection criteria, helping to establish its exact role in the treatment of dilated cardiomyopathies.

Ventricular function changes
Improvement of LV ejection fraction after partial left ventriculectomy has been demonstrated by several authors [2, 46, 8]. However, this modification occurs based on geometric rearrangement and may not theoretically represent an improvement in stroke volume or an increase in myocardial contractility [9]. On the other hand, hemodynamic benefits have also been reported after this surgical procedure in some clinical series. More precisely, significant increments in stroke volume and cardiac output were demonstrated in the presence of decreased pulmonary pressures [2, 4, 6]. Although partial ventriculectomy was associated with different procedures and performed in patients with different causes of heart failure in one of these studies [2], hemodynamic changes were also detected in our series, which included only patients with idiopathic dilated cardiomyopathy.

Several issues exist regarding partial left ventriculectomy technical aspects. The impact of its association with mitral insufficiency correction remains uncertain. Significant modifications in LV function were reported after isolated mitral annuloplasty in patients with severe mitral regurgitation [10]. On the other hand, patients in the present series had only mild or moderate mitral valve dysfunction, and similar modifications in LV function were documented whether or not partial ventriculectomy was associated with mitral valve operation [4].

Some authors advocate a more aggressive approach regarding myocardial resection, with the necessity of associated mitral valve replacement or papillary muscle translocation in more than 30% of cases [3, 8]. Otherwise, similar results have been described in those series in relation to LV function modifications documented in the current investigation. Furthermore, we previously reported the absence of correlation between LV ejection fraction changes and the level of LV diastolic diameter reduction [4].

Although in theory the reduction of LV volume could result in a secondary impairment of diastolic function [9], pressure-volume loops obtained immediately after partial left ventriculectomy in 11 patients of the present population demonstrated that this operation was responsible for significant decreases in LV systolic and diastolic wall stresses [11]. That study also showed the significant increase of maximal elastance and decreases in end-diastolic pressure and in stress-strain loops after the operation.

Because the LV wall stress is an important determinant of myocardial oxygen consumption, its reduction can reduce myocardial oxygen demand. Therefore, in a dilated, failing left ventricle, besides the partial restoration of afterload matching and myocardial contractility, slow progression of the underlying cardiomyopathy could result from LV wall stress modifications. The maintenance of LV ejection fraction values and of hemodynamic improvement for up to 2 years of follow-up in this report indicates that this fact may occur clinically. Nevertheless, the tendency of LV redilatation observed after the first year of follow-up anticipates the possibility that this procedures may become more a biologic bridge than a real alternative to heart transplantation.

Functional status and survival
Besides the improvement of LV function, partial left ventriculectomy was responsible for the amelioration of patients’ functional class in this series, which agrees with the overall clinical experience with this procedure [26, 8]. Most of our surviving patients are in NYHA class I or II for more than 2 years of follow-up, and a significant decrease in the number of hospitalizations per patient per year was found. The functional benefits of partial ventriculectomy in our surviving patients additionally included the improvement of physical capacity and other parameters, as assessed by a quality-of-life questionnaire [12].

Nevertheless, clinical and LV function improvements occurred only in a percentage of patients undergoing partial left ventriculectomy in this experience. Immediate and early mortalities after the procedure were high and occurred because of heart failure progression or arrhythmia-related events, being responsible for a survival rate of only 56.7% at 6 months of follow-up. McCarthy and associates [8] also described that only 58% of their 57 patients with dilated cardiomyopathy were free from procedure failure, defined as death or relisting for transplantation, at 1 year of follow-up. Similar results have been reported by other authors [2, 3, 7], although the existence of different causes of heart failure and other associated procedures in some series makes comparison less accurate.

On the other hand, no mortality or important heart failure decompensation occurred after the first 6 months of follow-up in this study. This finding, associated with the documentation that the underlying disease stopped progressing for up to 2 years, could justify partial left ventriculectomy indication as an alternative treatment of severe cardiomyopathies, if it was possible to demonstrate whether a given patient had a higher probability of benefiting from ventricular reduction.

In this regard, the existence of a significant relationship between myocardial cell diameter and partial left ventriculectomy results in our experience demonstrated that this procedure’s outcome depends on the severity of myocardial cell damage. Therefore, the identification of irreversible structural remodeling of the heart because of reactive growth processes in myocytes may contribute to a decrease in the number of partial ventriculectomy failures and to improving its clinical outcomes. Patients operated on with a mean diameter of LV myocardial cells of less than 22 µm in this series had a survival without urgent heart transplantation of 73% at 30 months of follow-up. These values contrast positively with a recent report about target heart failure populations for newer therapies [13], which showed a survival probability without heart transplantation of only 53% in 2 years for patients with initial NYHA class III or IV symptoms.

Some authors previously documented that the severity of myocardial cell hypertrophy is related to a worse clinical status in patients with heart failure [14, 15]. This parameter was used to monitor the outcomes of some medications in heart failure treatment [16]. Therefore, evaluation of myocardial specimens obtained by preoperative endomyocardial biopsies using refined histologic and histochemical examinations may potentially contribute to separating out patients with higher probability of partial ventriculectomy failure. In this regard, an absence of a large difference between the degree of myocardial cell hypertrophy on both sides of the ventricular septum was observed in patients with dilated cardiomyopathy [15], indicating that similar results may be achieved with use of either right ventricular or LV approaches.

Besides the myocardial findings, however, an absence of correlation between partial left ventriculectomy results and other risk factors was observed in the current series. This fact occurred despite other surgical interventions performed for treatment of severe cardiomyopathies, such as coronary artery bypass grafting [17] and dynamic cardiomyoplasty [18, 19], which seem to be strongly influenced by the patient’s preoperative condition and degree of LV function compromise.

Conclusions
Interpretation of current clinical experience with partial left ventriculectomy is limited. Nevertheless, we can conclude that this surgical procedure, associated when necessary with mitral insufficiency correction, improves LV function and ameliorates congestive heart failure in patients with idiopathic dilated cardiomyopathy. Furthermore, the midterm course of the surviving patients seems to be characterized by the stabilization of the underlying disease for up to 2 years of follow-up.

On the other hand, although early survival after this operation appears to be limited by high incidences of heart failure progression and arrhythmia-related deaths, these events seem to be influenced by compromised intrinsic myocardial cells. Therefore, the preoperative identification of patients with predominant anatomic remodeling instead of patients with severe intrinsic myocardial damage could improve partial left ventriculectomy outcomes and contribute to consideration of this procedure as a real alternative in the spectrum of the surgical treatment of cardiac failure.


    References
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 

  1. Batista R.J.V., Santos J.L.V., Takeshita N., Bocchino L., Lima P.N., Cunha M.A. Partial left ventriculectomy to improve left ventricular function in end-stage heart disease. J Card Surg 1996;11:96-97.[Medline]
  2. Angelini G.D., Pryn S., Mehta D., et al. Left ventricular volume reduction for end-stage heart failure. Lancet 1997;350:489.[Medline]
  3. Batista R.J.V., Santos J.L.V., Nery P., et al. Partial left ventriculectomy to treat end-stage heart disease. Ann Thorac Surg 1997;64:634-638.[Abstract/Free Full Text]
  4. Bocchi E.A., Bellotti G., Moraes A.V., et al. Clinical outcome after left ventricular surgical remodeling in patients with idiopathic dilated cardiomyopathy referred for heart transplantation. Circulation 1997;96(Suppl 2):II-165-II-172.
  5. Bombonato R., Bestetti R.B., Sgarbieri R., et al. Initial experience with partial left ventriculectomy in the treatment of terminal cardiac insufficiency. Arq Bras Cardiol 1996;66:189-192.[Medline]
  6. Dreifus G., Al Ayle W., Leroy G., et al. Left ventricular reduction (Batista): a new surgical option in dilated cardiomyopathy. Arch Mal Coeur 1997;90:1521-1525.
  7. Katsumata T., Westaby S. Left ventricular reduction operation in ischemic cardiomyopathy: a note of caution. Ann Thorac Surg 1997;64:1154-1156.[Abstract/Free Full Text]
  8. McCarthy J.F., McCarthy P.M., Starling R.C., et al. Partial left ventriculectomy and mitral valve repair for end-stage congestive heart failure. Eur J Cardiothorac Surg 1998;13:337-343.
  9. Dickstein M.L., Spotnitz H.M., Rose E.A., Burkhoff D. Heart reduction surgery: an analysis of the impact on cardiac function. J Thorac Cardiovasc Surg 1997;113:1032-1040.[Abstract/Free Full Text]
  10. Bolling S.F., Deeb G.M., Brunsting L.A., Bach D.S. Early outcome of mitral valve reconstruction in patients with end-stage cardiomyopathy. J Thorac Cardiovasc Surg 1995;109:676-683.[Abstract/Free Full Text]
  11. Bellotti G., Moraes A., Bocchi E.A., et al. Effects of partial ventriculectomy on left ventricular mechanical properties, shape and geometry in patients with dilated cardiomyopathy. Arq Bras Cardiol 1996;67:395-400.[Medline]
  12. Carrara D., Bocchi E.A., Bacal F., et al. Quality of life after partial left ventriculectomy for treatment of heart failure. Eur Heart J 1997;18(Suppl):223.
  13. Stevenson L.W., Couper G., Natterson B., et al. Target heart failure populations for newer therapies. Circulation 1995;92(Suppl 2):II-174-II-181.
  14. Beltrami C.A., Finato N., Rocco M., et al. The cellular basis of dilated cardiomyopathy in humans. J Mol Cell Cardiol 1995;27:291-305.[Medline]
  15. Unverferth D.V., Baker P.B., Swift S.E., et al. Extent of myocardial fibrosis and cellular hypertrophy in dilated cardiomyopathy. Am J Cardiol 1986;57:816-820.[Medline]
  16. Unverferth D.V., Mehegan J.P., Magorien R.D., Unverferth B.J., Leier C.V. Regression of myocardial cellular hypertrophy with vasodilator therapy in chronic congestive heart failure associated with idiopathic dilated cardiomyopathy. Am J Cardiol 1983;51:1392-1398.[Medline]
  17. Alfieri O. Coronary artery bypass grafting for left ventricular dysfunction. Curr Opin Cardiol 1994;9:658-663.[Medline]
  18. Furnary A.P., Chachques J.C., Moreira L.F.P., et al. Long-term outcome, survival analysis and risk stratification of dynamic cardiomyoplasty. J Thorac Cardiovasc Surg 1996;112:1640-1650.[Abstract/Free Full Text]
  19. Moreira L.F.P., Stolf N.A.G., Braile D.M., Jatene A.D. Dynamic cardiomyoplasty in South America. Ann Thorac Surg 1996;61:408-412.[Abstract/Free Full Text]



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Ann. Thorac. Surg., May 1, 1999; 67(5): 1541 - 1542.
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L. F. P. Moreira and N. A.G. Stolf
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Ann. Thorac. Surg., May 1, 1999; 67(5): 1542 - 1542.
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