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Eur J Cardiothorac Surg 1998;13:337-343
© 1998 Elsevier Science NL

Partial left ventriculectomy and mitral valve repair for end-stage congestive heart failure¹

^a The section of Cardiac Transplantation and Mechanical Circulatory Assist Program, Department of Thoracic and Cardiovascular Surgery, Cleveland Clinic Foundation, 9500 Euclid Avenue, Desk F-25, Cleveland, OH 44195, USA
^b The section of Heart Failure, Department of Cardiology, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA
^c The Transplant Center, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA

Received 6 October 1997; received in revised form 29 December 1997; accepted 14 January 1998.

Corresponding author. Tel.: +1 216 4440648; fax: +1 216 4440777; e-mail: mccartp@cesmtp.ccf.org

	Abstract

Top Abstract Introduction Patients and methods Results Discussion Conclusions Appendix A. Conference... References

 
Objective: Partial left ventriculectomy (PLV), pioneered by Batista, has been proposed as an alternative treatment strategy in patients with refractory congestive heart failure. In order to analyze the midterm outcome of PLV and mitral valve (MV) repair and stratify patients according to risk, we prospectively studied 57 consecutive patients who underwent this procedure at the Cleveland Clinic Foundation (CCF). Methods: Patients had a mean age of 53 years and were predominantly males (74%). In 95% the etiology of heart failure was idiopathic dilated cardiomyopathy. All patients had a left ventricular end diastolic diameter of >7cm and were in New York Heart Association (NYHA) functional classes III and IV. A total of 54 patients (95%) were awaiting heart transplantation. Preoperatively, requirements included inotropes in 23 (40%), intraaortic balloon pump counterpulsation in 3 (5.3%), and left ventricular assist device placement (LVAD) in 1 (1.8%). Concomitant procedures included MV repair (55 patients), MV replacement (2), tricuspid valve repair (34 patients), coronary artery bypass graft (CABG) (5), and aortic valve repair or replacement (1 patient each). Results: Measurements preoperatively and at 3 months demonstrated improvement in left ventricular ejection fraction (14.4±7.7–23.2±10.7%, P<0.001), left ventricular end diastolic volume (254±85–179±73 ml, P<0.001) and left ventricular end diastolic diameter (8.4±1.1–6.3±0.9 cm, P<0.001). Peak oxygen consumption (MVO2) increased from 10.6±3.9 to 15.3±4.5 ml/kg per min (P<0.001). Cardiac index did not change (2.2 l/min per m²), although 40% had been on inotropes preoperatively and none were on inotropes at 3 months. NYHA functional class improved from 3.6±0.5 preoperatively to 2.2±0.9 at 3 months (P<0.001). LVAD support was required as rescue therapy in 11 patients (17%). Actuarial freedom from procedure failure, defined as death or relisting for transplant, was 58% at 1 year. Hospital mortality was 3.5% (n=2). On follow-up, there were 7 late deaths (including 3 sudden deaths) giving an actuarial survival of 82% at 1 year. Multivariate risk factor analysis revealed that age less than 40 years was associated with failure (P=0.02). Conclusions: Although PLV with MV repair is now a surgical option in the treatment of end-stage congestive heart failure, caution is advised as early failures are unpredictable and mechanical support may be required as rescue therapy. Better risk stratification and patient selection may improve outcome. Further study is required to determine the procedure's exact role in the treatment of congestive heart failure.

Key Words: Partial left ventriculectomy • Batista • Dilated cardiomyopathy

	Introduction

Top Abstract Introduction Patients and methods Results Discussion Conclusions Appendix A. Conference... References

 
Heart failure is becoming an increasing medical challenge as life expectancy continues to increase. Currently it affects 1% of people under 55 years and 9% of those over 80 [1]. Despite improvements in pharmacological treatment, approximately 50% of patients are dead within 3 years of presentation [2]. While heart transplantation has evolved to become a highly effective therapy for patients with end-stage heart failure, the limited number of donors makes it applicable only to a small percentage of patients [3].

In an effort to address this problem, alternative surgical strategies have evolved including mechanical circulatory assist devices [4] [5], cardiomyoplasty [6] and the use of xenografts [7]. More recently, partial left ventriculectomy (PLV), a new surgical option has been introduced by a Brazilian surgeon, Randas Batista, and became popular as the ‘Batista operation’. The procedure involves resection of a large segment of the posterolateral wall of the left ventricle [8]. The result of this ventricular remodeling is a left ventricular cavity which has a significantly smaller diameter, and consequently, improved function as a result of the reduction in ventricular wall tension according to the Law of Laplace [9]. Considerable interest has been generated by reports of patient improvement after surgery [10]. However, these initial reports lacked significant information on the safety and efficacy of the procedure, presence of preoperative risk factors, and on quality-of-life issues pertaining to the procedure. Furthermore, intermediate and long-term follow-up data have been relatively scant. While the Brazilian experience has been primarily with patients who had dilated cardiomyopathy from Chagas disease, reports of experiences with the procedure for the management of cardiac myopathies from other etiologies has been sparse.

In an attempt to address these issues, a prospective study of PLV and mitral valve (MV) repair was initiated at the Cleveland Clinic Foundation (CCF) in May of 1996 [11]. This report outlines the midterm results of this procedure with particular emphasis on the pre and postoperative status of the patients and on freedom from death or relisting for transplantation.

	Patients and methods

Top Abstract Introduction Patients and methods Results Discussion Conclusions Appendix A. Conference... References

 
Between May 1, 1996 and August 15, 1997, 57 patients underwent PLV at the CCF. These patients consisted of 42 males (72%) and 15 females (28%), with a mean age of 53 years (range 17–72); 35 patients (61%) were in New York Heart Association (NYHA) functional class IV (61.4%), 21 (37%) were in NYHA class III, and 1 (1.8%) was in NYHA class I bridged-to-transplant on an implantable left ventricular assist device (HeartMate LVAD, Thermo Cardiosystems, Woburn, MA). The etiology of heart failure was idiopathic dilated cardiomyopathy in 54 patients (95%), ischemic, familial and valvular cardiomyopathy in the remaining (1 patient each); 54 patients (95%) were awaiting cardiac transplantation of whom 23 (40%) were listed status I on the United Network for Organ Sharing (UNOS) allocation list, and 31 were listed status II.

Candidate selection was based on a left ventricular end-diastolic diameter (LVEDD) greater than 7 cm on echocardiography coupled with standard heart transplant listing criteria in all but 3 patients [12]. Emphasis was placed on an integrated approach to patient care and all patients were reviewed by the heart failure/transplant team. All patients gave informed consent and were advised of the surgical risks and the possibility of postoperative salvage bridging on an implantable assist device and transplantation. Patient enrollment protocols were approved by the CCF Institutional Review Board.

Serial measurements were carried out in all patients. The principal timepoints were at baseline (when deemed suitable for PLV, usually within 4 weeks of surgery), preoperatively, immediately postoperatively (in the operating room), at 1 week and at 3 months. Intraoperative transesophageal echocardiography was carried out in all patients. Standard esophageal and transgastric views were obtained using HP sonos 5.0/3.7 Mhz probe with HP sonos 1500/2500 echocardiography machine. Left ventricular dimensions and volumes were calculated using the method of discs from the apical four-chamber view. Valvular regurgitation was assessed by standard color flow Doppler. Forward stroke volume, derived using the velocity time integral from pulsed wave Doppler of the left ventricular outflow tract, is divided by the LVEDV (left ventricular end diastolic volume) to obtain the forward ejection fraction. Right-sided heart pressures were measured at cardiac catheterization with a strain gauge transducer. Cardiac output was derived with the thermodilution technique. Procedure failure was defined as death or relisting for transplant, and thus included all patients requiring rescue LVAD support postoperatively.

Surgical technique
The surgical technique has been previously described and is a modification of that described by Batista [8] [11]. Briefly, the procedure is carried out on cardiopulmonary bypass at normothermia with bicaval cannulation. Myocardial protection is achieved with antegrade and retrograde cold blood cardioplegia. It was initially carried out on a beating heart but resection and reconstruction of the heart were deemed easier with cardioplegia. The ventriculectomy involves resecting a wedge-shaped portion of left ventricle in the circumflex coronary artery distribution ( Fig. 1 ). This begins lateral to the left anterior descending artery (LAD) near the apex and extends between the papillary muscles to 2 cm from the mitral annulus. Typically one or two obtuse marginal branches of the circumflex coronary artery are divided and oversewn. If enough muscle can be removed between the papillary muscles to reduce the LVEDD to normal or near normal, the papillary muscles are left in situ. However if there is not enough left ventricular wall between the papillary muscles to achieve this aim, as calculated from echocardiography, one or both papillary muscles are resected and transferred to an adjoining site on the ventricular wall [11]. The ventriculotomy is closed in three layers using 3-0 polypropylene suture passed through felt or bovine pericardial strips. The first layer of horizontal mattress suture distributes tension evenly along the ventricular wall, while the two ‘over and over’ layers complete hemostasis. The papillary muscles are then seen to lie side by side on cross-section.

View larger version (99K): [in this window] [in a new window]   Fig. 1. PLV involves resecting a wedge-shaped portion of left ventricle in the circumflex coronary artery distribution.

View larger version (125K): [in this window] [in a new window]   Fig. 2. A suture is used to approximate the central portion of the free edge of the anterior and posterior mitral leaflets to reduce MR (Alfieri repair).

	Results

Top Abstract Introduction Patients and methods Results Discussion Conclusions Appendix A. Conference... References

Data obtained by echocardiography are listed in Fig. 3 Fig. 4 Fig. 5 . Mean LVEF increased from 14.4±7.7% preoperatively to 23.2±10.7% at 3 months (P<0.001). Similarly LVEDV and LVEDD improved at the three postoperative timepoints. Mean LVEDV decreased from 254±85 ml preoperatively to 179±73 ml at 3 months (P<0.001), while mean LVEDD decreased from 8.4±1.1 to 6.3±0.9 cm at these timepoints (P<0.001). Mean MR (scale 0–4) decreased from 2.8±1.1 preoperatively to 0.65±0.8 at 3 months (P<0.001). Mean cardiac index preoperatively was 2.2 l/min per m² and did not change at 3 months (2.2 l/min per m²), although 40% of patients were on inotropes preoperatively and none were at 3 months. MVO2 increased from a mean of 10.6±3.9 ml/kg per min at baseline to 15.3±4.5 ml/kg per min at 3 months (P<0.001).

View larger version (40K): [in this window] [in a new window]   Fig. 3. Left ventricular ejection fraction trends.

View larger version (38K): [in this window] [in a new window]   Fig. 4. Left ventricular end diastolic volume trends.

View larger version (45K): [in this window] [in a new window]   Fig. 5. Left ventricular end diastolic diameter trends.

Follow-up is complete at a mean of 9±4 months. Mean NYHA functional class has decreased from 3.6±0.5 preoperatively to 2.2±0.9 at 3 months (P<0.001). Apart from the LVAD group, 6 other patients deteriorated and were relisted for transplantation; 5 have subsequently been transplanted and 1 is waiting. There were 7 late mortalities; 3 were sudden and unexpected and occurred between 3 and 9 months postoperatively and may have been due to arrhythmias, while 2 were related to progression of heart failure, 1 was due to multiorgan failure after late LVAD placement, and 1 was due to right ventricular failure posttransplant. Actuarial survival is 82.1±5.5% at 1 year ( Fig. 6 ).

View larger version (7K): [in this window] [in a new window]   Fig. 6. Actuarial survival after PLV.

View larger version (11K): [in this window] [in a new window]   Fig. 7. Actuarial freedom from failure (death or relisting for transplant) in those greater and less than 40 years of age.

	Discussion

Top Abstract Introduction Patients and methods Results Discussion Conclusions Appendix A. Conference... References

Actuarial survival in this prospective study was 82.1±5.5% at 1 year which compares with a 1-year survival after dynamic cardiomyoplasty and heart transplantation of 86 and 83%, respectively [16] [3]. This is gratifying when one considers that this is our earliest experience, and the group mainly included patients at high risk of dying within 1 year [12]. However to achieve this survival, aggressive management was required with 11 patients having LVADs placed as rescue therapy when deteriorating. Accordingly we felt that a more meaningful marker of success or failure than actuarial survival would be to analyze the failure rate of the procedure, i.e. those who died or were relisted for transplant. The actuarial freedom from failure (relisting free survival) was 58±7% at 1 year. Because of this considerable failure rate, risk stratification assumes increasing importance.

The one subgroup that was significantly associated with adverse outcome on risk factor analysis was age <40 years. However this may be related to disease severity in this subgroup of patients and not age. When measuring severity of disease, no single factor became significant on risk factor analysis, but the combination of factors in those <40 years did. This is probably a reflection of the limited number of patients in this study and risk factor analysis may be more meaningful in larger studies.

While the vast majority of patients had idiopathic dilated cardiomyopathy as a primary diagnosis and appeared similar, some clearly responded well postsurgery while others did not. According to the definition, idiopathic dilated cardiomyopathy is a disease of unknown origin. However it may be that it is a collection of different entities with different responses to this surgical intervention. Therefore other aspects such as the quantity of scar tissue and the quality of the myocardium may be important determinants of outcome. All patients are now being studied with dobutamine echocardiography as it is our clinical impression that preoperative patients who respond to inotropes do clinically better after surgery than those who respond poorly to inotropes. The collagen content of resected specimens is currently being analyzed to quantitate fibrosis. Positron emission tomography (PET) and magnetic resonance imaging (MRI) scans are now carried out to assess myocardial scarring. These markers may however prove to be too crude and the answer may lie at the cellular level. Myocyte studies are currently underway, and differentiation of apoptotic myocytes from those that can recover function after ‘surgical unloading’ will be essential.

Evaluation at 1 week reveals a slight increase in LVEDD and a slight decrease in LVEF compared with intraoperative measurements. However the difference is probably related to the ideal loading conditions seen intraoperatively. More importantly, the measurements at 1 week are significantly better than at baseline. Furthermore these improvements appear to be sustained at 3 months. This significant improvement in left ventricular function is not unlike that seen after dynamic cardiomyoplasty [6] [16]. Here the skeletal-muscle-synchronized contraction increases left ventricular systolic function and decreases ventricular wall stress which improves myocardial oxygen utilization and thus ventricular function. The fact that ventricular function remains improved at 3 months and that MVO2 is also significantly increased is encouraging and may indicate halting or slowing of heart failure progression. However, further studies and longer follow-up are required to prove this hypothesis.

When analyzing these results it is also important to consider the effect of MV repair on outcome. Bolling and coauthors have demonstrated clinical improvement in patients with end-stage cardiomyopathy after MV repair alone and report an actuarial 1-year survival of 75% [17]. All but 2 patients in our series had MV repair. This leads to the valid question of whether our results are due to the MV repair. However 27% of patients had only 0–2+ MR and yet they showed significant clinical improvement which is unlikely to be due to the mitral repair alone. This leads us to believe that the beneficial effects of PLV and mitral repair are complimentary.

Interpretation of reports of PLV for both ischemic and dilated cardiomyopathy may be confusing, as it is comparing two different disease entities which may respond differently to this operation [18]. For ischemic cardiomyopathy we already know that the Dor procedure improves function in the left ventricle [19] [11]. We use the Dor procedure in suitable patients with ischemic cardiomyopathy with associated left ventricular dilation. It is our opinion that the true contribution of Batista is the application of the Law of Laplace to patients with idiopathic dilated cardiomyopathy.

This study has many limitations. Being from a single center, patient numbers are small and meaningful risk stratification is difficult to attain. While it is prospective, it is not randomized. Ideally, a prospective randomized trial comparing medical treatment with a variety of surgical treatments, including isolated mitral repair, would be carried out. This would have to be a multicenter trial, ideally undertaken in centers with experience in transplantation and mechanical circulatory support. However, that being said, this study is the largest to date with total patient follow-up and represents a realistic marker of current results with PLV. It also represents our earliest ‘learning curve’ and may not reflect the eventual potential of this operation after patient selection has been refined.

	Conclusions

Top Abstract Introduction Patients and methods Results Discussion Conclusions Appendix A. Conference... References

 
PLV with MV repair is now a surgical option in the treatment of end-stage congestive heart failure. However, caution is advised as early failures are unpredictable and mechanical support may be required as rescue therapy. Improved results will depend on better risk stratification and patient selection. Further study is required to determine the procedure's exact role in the treatment of congestive heart failure.

	Footnotes

 
Presented at the 11th Annual Meeting of the European Association for Cardio-thoracic Surgery, Copenhagen, Denmark, 28 September–October 1, 1997.

	Appendix A. Conference discussion

Top Abstract Introduction Patients and methods Results Discussion Conclusions Appendix A. Conference... References

 
Dr C. Santoli (Milan, Italy): I have two questions. First, I would like to know, from your patients that you presented, how many patients had ischemic myocardiopathy and how many had idiopathic myocardiopathy? Because in our center we have a large experience of ischemic myocardiopathy, but from your pictures you take off the lateral part of the left ventricle. But if you have an ischemic dilated myocardiopathy, the big problem is the septum, because the septum is so fibrotic. What do you do, if you operate on those patients, what do you do with the septum?

Dr Alfieri: The experience of Dr McCarthy doesn’t involve ischemic patients, except 1.

Dr J. McCarthy: In this study there was just 1 patient with ischemic cardiomyopathy which we diagnosed at operation. The primary indication is idiopathic dilated cardiomyopathy. Dr Batista is operating on patients with ischemic cardiomyopathy.

Dr S. Westaby (Oxford, UK): Could you comment on your incidence of late redilatation and have you seen malignant ventricular dysrhythmias in association with redilatation? This has certainly happened in ischemic cardiomyopathy patients that I’ve operated on myself.

Dr J. McCarthy: Our left ventricular end diastolic diameter, the mean diameter, hasn’t changed from 1 week to 3 months. We have seen a degree of redilatation in 2 patients. They are currently functional classes 2 to 3, and we’re keeping a close eye on them. As regards malignant arrhythmias, we are concerned about it, as everybody else is. We put the patients empirically on amiodarone. Despite this, 3 of our late deaths were sudden in patients who were doing very well. This may well have been due to arrhythmias, we’re not sure, but we worry about that. Consequently all patients now have an AICD placed perioperatively.

Dr F. Brauer (Carlsbad, USA): Would you please describe the problems and management of intraoperative and postoperative bleeding associated with PLV.

Dr J. McCarthy: Intraoperatively we had 3 or 4 patients who required extra sutures in the suture line, which were spotted intraoperatively. Our postoperative incidence of bleeding requiring reexploration was 2 of the 57 patients. One was a suture line bleed, one was due to a coagulopathy. Both patients did fine. But we are very careful, we close the ventriculotomy in three layers with felt, as I stated.

Dr R. Cesnjevar (Erlangen, Germany): How do you insure that the effect you achieved is just done by a partial left ventriculotomy if you do in all the MV repair and you had a 2- or 3-plus regurgitation before?

Dr J. McCarthy: I suppose the definitive answer to that would have to be answered with a randomized trial, but I don’t see that coming very early because I’m not sure who is going to pay for that trial. But I would state that 27% of our patients had only 1–2-plus MR. Most of these patients improved significantly. I think it’s unlikely that this improvement is due totally to the MV repair.

Dr J.-E. Kim (Inchon, South Korea): During postoperative course, we had a quite peculiar experience. We operated on about 11 patients, 6 of them had renal and hepatic insufficiency. Bilirubin went up. Some patients went up to 47 mg percent, and creatinine went up to 8 mg percent. Among these 6 patients, 1 patient survived and 5 patients ended up as mortalities. But these patients, cardiac outputwise, were no different than other uncomplicated patients. Did you have any similar experience?

Dr J. McCarthy: Yes. The patients tend to have a lower blood pressure during the first postoperative night than they had preoperatively. Most of their creatinines rise in the first 24–48 h. This is a problem, but it generally tends to settle out after that. We had 2 patients with transient hepatic dysfunction. We had 2 patients after the operation who needed to go on temporary dialysis. We had 2 further patients who went on dialysis late, but this was really due to multiorgan failure after LVAD. So transient end-organ dysfunction occurred early in 4 patients.

	References

Top Abstract Introduction Patients and methods Results Discussion Conclusions Appendix A. Conference... References

 

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6. Carpentier A, Chachques JC, Carteaux JP Dynamic cardiomyoplasty at eleven years. In: Carpentier A, Chachques JC, Grandjean PA, eds. Cardiac Bioassist. Armonk, NY: Futura, 1997:3-23.
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16. Moreira LFP, Stolf NAG, Bocchi EA, Bacal F, Pego-Fernandes PM, Abensur H, Meneghetti HC, Jatene AD Clinical and left ventricular function outcomes up to five years after dynamic cardiomyoplasty. J Thorac Cardiovasc Surg 1995;109:353-363.[Abstract/Free Full Text]
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