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Ann Thorac Surg 2001;72:91-95
© 2001 The Society of Thoracic Surgeons

Original article: cardiovascular

Evaluation of predictors of clinical outcome after partial left ventriculectomy

Geetha Bhat, MD, PhDa, Robert D. Dowling, MDb a Department of Medicine, University of Louisville, Louisville, Kentucky, USA
b Department of Surgery, University of Louisville, Louisville, Kentucky, USA

Accepted for publication April 13, 2001.

Address reprint requests to Dr Bhat, Jewish Hospital, Heart Failure/Cardiac Transplant Center, 3rd Floor, 217 East Chestnut St, Louisville, KY 40202
e-mail: g0bhat01{at}gwise.louisville.edu


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 References
 
Background. Outcome after partial left ventriculectomy (PLV) is difficult to predict. Our goal was to determine if clinical measurements including exercise testing could predict outcome after PLV.

Methods. Sixteen patients with dilated cardiomyopathy had left ventricular ejection fraction, left ventricular end-diastolic diameter, amount of mitral regurgitation (MR), New York Heart Association (NYHA) functional class, and cardiopulmonary exercise testing measurements measured before PLV and 3 months after PLV. Eleven patients who remained stable after PLV (group 1) were compared with 5 patients who deteriorated after PLV (group 2).

Results. Similar significant improvements were seen in both groups 3 months post-PLV with respect to left ventricular ejection fraction (group 1: 0.136 ± 0.037 to 0.212 ± 0.046; group 2: 0.139 ± 0.042 to 0.179 ± 0.073) and left ventricular end-diastolic diameter (group 1: 8.5 ± 0.7 to 7.0 ± 0.6 cm; group 2: 7.6 ± 0.6 to 6.5 ± 0.6 cm). The MR grade (1.0 ± 0.6 versus 2.5 ± 0.6), NYHA functional class (1.5 ± 0.31 versus 2.5 ± 0.6), and peak oxygen consumption (17.8 ± 1.1 versus 12.2 ± 2.0) were significantly different in the two groups 3 months after PLV (p < 0.05, analysis of variance).

Conclusions. Patients that do not show significant improvement in peak oxygen consumption, NYHA class and significant decrease in the amount of MR 3 months after PLV, compared with pre-PLV, are at increased risk of clinically deteriorating.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 References
 
Partial left ventriculectomy (PLV) has been recently introduced as a surgical treatment for patients with dilated left ventricles and severe heart failure [1–3]. The operation consists of resection of a wedge of myocardium from the posterior wall and is often accompanied by mitral valve replacement or repair [4, 5]. Heart transplantation has become accepted therapy for patients with severe heart failure on maximal medical therapy. Unfortunately, donor shortages and selection criteria limit heart transplantation and surgical procedures such as PLV have been proposed as alternative approaches to patients with end-stage dilated cardiomyopathy. Although several short-term studies have shown improvement in left ventricular function, there has been a high incidence of progressive heart failure and ventricular arrhythmia after PLV leading to significant morbidity and mortality [6]. Clinical outcome after PLV is variable and minimal information is available on determining outcome after PLV. One report has shown that midterm survival the first 7 months after PLV was significantly affected only by myocardial cell diameter [6].

The aim of this study was to determine if clinical measurements including cardiopulmonary exercise testing variables could predict short-term outcome after PLV.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 References
 
Patient selection
Patients considered as candidates for PLV had idiopathic dilated cardiomyopathy, left ventricular end-diastolic diameter (LVEDD) greater than 7 cm, refractory New York Heart Association (NYHA) class IV symptoms, and severely impaired exercise oxygen consumption (less than 14 mL O2 · kg-1 · min-1). Patients were not excluded from PLV based on right ventricular dysfunction, elevated transpulmonary gradient, or need for inotropic therapy or need for an intraaortic balloon pump. All patients underwent a complete heart transplant evaluation. Patients found to be candidates for both cardiac transplantation and PLV were given both options. Two patients who were not candidates for transplantation were given the option of PLV or continued medical management.

The study group consisted of 16 consecutive patients with idiopathic dilated cardiomyopathy who underwent PLV from April 1996 to April 1998. All patients had NYHA class IV symptoms despite maximal medical therapy. There were 14 men and 2 women with a mean age of 49 ± 10 years (range 30 to 67 years). Values for various measurements were as follows: mean preoperative left ventricular ejection fraction (LVEF) 0.139 ± 0.056, mean LVEDD 8.2 ± 1.1 cm (range 6.7 to 10.2 cm), and mean peak oxygen consumption 13.5 ± 3.0 mL O2 · kg-1 · min-1. Fifteen patients had mitral regurgitation with a mean grade of 3.3 ± 0.7. Six patients (37%) were on the cardiac transplant recipient list, United Network for Organ Sharing status I.

All patients had normal coronary arteries and were treated with maximal medical therapy including angiotensin-converting enzyme inhibitors, digoxin, and diuretic agents. Mean follow-up after PLV was 11.1 months. Nine patients required inotropic support, 3 of whom were also treated with an intraaortic balloon pump.

All patients underwent evaluation for heart transplantation that included cardiopulmonary exercise testing, echocardiography, and NYHA functional class assessment. Cardiopulmonary exercise testing was performed using the Naughton protocol with upright exercise treadmill testing. The evaluation was repeated at 3 months after PLV. The study was approved by the institutional review board and all subjects gave informed consent.

The surgical procedure in these 16 patients has been described in detail previously [2]. Echocardiographic assessment of LVEDD was determined before operation with a transgastric short axis view for assessment of the interpapillary muscle distance to determine whether resection of the lateral wall between the papillary muscles would be adequate to decrease the LVEDD to approximately 6.0 cm or less. If resection of the interpapillary muscle would not result in an adequate decrease in LVEDD, a decision was made to proceed with either mitral valve replacement or mitral valve repair with reimplantation of the papillary muscle. There were no strict guidelines to differentiate the need for repair or replacement. However, if it was planned that more than 3 cm posterior to the posterior papillary muscle was to be resected, mitral valve replacement was performed. Doppler echocardiography and color flow Doppler were used for the detection of mitral regurgitation. The severity of mitral regurgitation was graded on a scale of 1 to 4, with 1 as mild and 4 as severe and 2 and 3 being intermediate grades.

Twelve patients underwent a mitral annuloplasty with placement of a physio-ring (Baxter Carpenter-Edwards, Baxter Health Care Corp, Irvine, CA) through a standard left atriotomy. One patient with mild mitral regurgitation had an Alfieri mitral repair. One patient without mitral regurgitation underwent PLV without a mitral valve procedure. Four patients had resection of the posterior papillary muscle to allow for adequate resection of the left ventricle. Two of these 4 patients had mitral valve replacement, and 2 patients had mitral valve repair with reimplantation of the posterior papillary muscle. Tricuspid valve repair was performed in 6 patients for significant regurgitation (rated higher than 2) with a physio-ring in 3 and a DeVega annuloplasty in 3.

Eleven patients who remained clinically stable after PLV (group 1), were compared with 5 patients who deteriorated after PLV (group 2) who were relisted for transplantation or died. Table 1 shows preoperative demographics and comorbid information in the two groups. Five of 11 (45%) in group 1 and 4 of 5 (80%) in group 2 were on inotropic therapy before PLV. Among these patients on inotropic therapy, 2 in group 1 and 1 in group 2 were also on preoperative intraaortic balloon pump support. Nine patients (82%) in group 1 underwent mitral valve repair with 5 patients also undergoing tricuspid valve repair; the remaining 2 patients in group 1 had mitral valve replacement. In group 2, 4 patients (80%) underwent mitral valve repair with 1 patient also undergoing tricuspid valve repair. Table 2 lists valve procedures and immediate postoperative variables in the two groups. In all 16 patients, preoperative to postoperative mean left ventricular end-diastolic pressure increased from 11.9 ± 2.0 to 17.0 ± 2.5 mm Hg (p < 0.05), mean cardiac output from 2.4 ± 0.3 to 3.5 ± 0.3 L/min (p < 0.05), and mean stroke volume from 29.9 ± 5.3 to 35.4 ± 4.7 mL. There was no significant difference in the preoperative to postoperative hemodynamic changes between the two groups within 24 hours after PLV.


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  		Table 1. Preoperative Demographics and Comorbid Conditions

 

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  		Table 2. Postoperative Variables and Valve Procedures

 
Statistical analysis
Data in Tables 3 and 4 are presented as mean ± standard error. The measurements were compared in the two groups by using the repeated measures analysis of variance. A p value less than 0.05 was considered significant.


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  		Table 3. Pre-PLV and Post-PLV Variables

 

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  		Table 4. Cardiopulmonary Exercise Variables Pre- and Post-PLV

 

   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 References
 
Clinical data were monitored for a mean of 11.1 months. Eleven patients (group 1) remained stable after PLV. Five of the 16 patients deteriorated after PLV (group 2). Three patients had progressive heart failure and were listed for cardiac transplantation, 2 of whom required left ventricular assist device (LVAD) placement on postoperative days 246 and 445. One patient on LVAD underwent cardiac transplantation at 344 days post-PLV and the other patient on LVAD died after a cerebrovascular accident at 612 days post-PLV. One of the patients not on LVAD was transplanted at 483 days post-PLV. Two other patients died at a mean of 3.5 months after PLV, 1 from possible sepsis and the other from refractory heart failure. The 12-month Kaplan–Meier freedom from death was 86%. Table 3 shows the comparison of pre-PLV and 3-month post-PLV variables between groups 1 and 2. Table 4 shows the comparison of pre-PLV and 3-month post-PLV cardiopulmonary exercise test measurements between the two groups.

Left ventricular ejection fraction improved significantly (p < 0.05) 3 months after surgery from 0.136 ± 0.037 to 0.212 ± 0.046 (p < 0.05) in group 1 and from 0.139 ± 0.042 to 0.179 ± 0.073 in group 2. Left ventricular end-diastolic dimension also decreased significantly (group 1: 8.5 ± 0.7 to 7.0 ± 0.6 cm; group 2: 7.6 ± 0.6 to 6.5 ± 0.6 cm).

There was significant decrease in mitral regurgitation from preoperative echocardiographic grading of 3.4 ± 0.4 to 1.0 ± 0.6 in group 1 compared with group 2 whose mitral regurgitation did not improve significantly 3 months post-PLV (2.9 ± 0.5 to 2.5 ± 0.6).

The functional capacity of group 1 and group 2 differed significantly 3 months post-PLV, with group 1 improving from NYHA class 4 to 1.5 ± 0.3 versus group 2 improving from class 4 to 2.50 ± 0.6.

The cardiopulmonary exercise testing measurements were compared pre-PLV and 3 months post-PLV (Table 4). Anaerobic threshold and percent predicted peak oxygen consumption (PVO2) were not different at base line and did not change significantly 3 months after PLV. The PVO2 pre-PLV was similar in both groups but was significantly different in the two groups post-PLV (group 1 versus group 2: 17.8 ± 1.1 versus 12.2 ± 2.0, p < 0.05, analysis of variance).


   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
References
 
Similar to other studies, PLV improved left ventricular function and functional capacity short-term in our patients. Despite this improvement, there was significant clinical deterioration in 5 patients, 2 of whom died. Our analysis of patients with advanced heart failure undergoing PLV suggests that those patients who do not have significant changes in exercise capacity measured by peak oxygen consumption or NYHA functional classification or a decrease in the amount mitral regurgitation at 3 months post-PLV will experience worse outcomes.

In a study of 120 patients with cardiomyopathy of various etiologies undergoing PLV, short-term left ventricular performance was noted to improve, but few conclusions can be made regarding selection criteria for PLV, as the surgical techniques were variable and the follow-up was incomplete [1].

The left ventricular performance after PLV was observed to improve in 19 patients with nonischemic cardiomyopathy. In this study various mitral valve procedures were performed, with most patients undergoing mitral valve repair and 3 patients undergoing mitral valve replacements [3]. The authors concluded that an increase in LVEF correlated with a decrease in end systolic stress and left ventricular sphericity.

Early enthusiasm for the PLV procedure has greatly decreased because of the significant number of patients deteriorating after the procedure. Because some patients have done remarkably well after PLV, however, it would be valuable to know how to select these candidates. Minimal data are available on predicting who is an appropriate candidate for this procedure. The impact of concomitant mitral valve operation on the PLV procedure remains to be fully delineated. Both the reduction of mitral regurgitation and effect on the geometry of the left ventricle becoming less spherical has been postulated to result in improved left ventricular performance in 24 cardiomyopathy patients after PLV [4]. The relative contribution of these two mechanisms has not been defined.

The increase in left ventricular function has been noted to be less after PLV in a study of 22 patients with left circumflex artery dominance [5]. Examination of variables such as age, preoperative NYHA class, heart rate, atrial fibrillation, pulmonary capillary wedge pressure, LVEF, and left ventricular end-systolic volume did not identify any preoperative predictors of death after PLV [5].

Minimal data are available on preoperative risk factors that may be used to predict prognosis after PLV. Having preoperative markers for prediction of poor outcome after PLV would be useful. Unfortunately, we were not able to identify any significant predictive factors preoperatively. As shown in Tables 3 and 4, we compared several preoperative measurements such as LVEF, LVEDD, mitral regurgitation, NYHA class, anaerobic threshold, and percent predicted PVO2 and PVO2, none of which were statistically significantly different between groups 1 and 2. Preoperative peak oxygen consumption (pre-PVO2) showed a trend toward lower values in group 2 than in group 1. Perhaps if there were larger numbers of patients in group 2, pre-PVO2 differences between the two groups may have achieved statistical significance. A significant number of patients is probably required to identify individual preoperative risk factors for survival, although in a larger study the preoperative NYHA functional class and peak oxygen consumption were not associated with PLV failure [7]. In this study of 57 consecutive patients who underwent PLV, multivariate risk factor analysis of patient factors, echo measurements, and surgical measurements showed that age younger than 40 years was the only significant factor associated with failure. Analysis of factors influencing outcome in another study showed that midterm survival was significantly affected only by myocardial cell diameter [6].

The surgical procedure for PLV has also been heterogeneous with a mix of left ventricular resection, left ventricular resection with mitral valve annuloplasty, and left ventricular resection with mitral and tricuspid annuloplasty. Although patients in our study were uniform with end-stage dilated cardiomyopathy on maximal medical therapy, there were slight variations in the surgical procedure. Most patients in both groups (100% in group 1 and 80% in group 2) had severe mitral regurgitation. Nine of 11 patients (82%) in group 1 and 4 of 5 (80%) in group 2 underwent mitral valve repair, and 2 patients in group 1 underwent mitral valve replacement. Only 1 patient in group 2 without mitral regurgitation underwent PLV without mitral valve procedure. There was no evidence of mitral regurgitation in both groups of patients by echocardiography immediately after valve operation, but at 3-month follow-up patients in group 2 compared with group 1 did not maintain the significant decrease in mitral regurgitation observed by intraoperative transesophageal echocardiogram.

The impact of PLV outcome by the correction of mitral regurgitation during the surgical procedure has not been fully elucidated. Mitral valve repair alone without the PLV procedure in 48 patients with severe mitral regurgitation and cardiomyopathy was shown to have favorable intermediate outcome on left ventricular function and geometry [8]. The effect of mitral valve repair on outcome was considered in another study of 57 patients undergoing PLV in which all but 2 patients had mitral valve repair [7]; 27% of their patients had mitral regurgitation ratings of only 0 to 2+ and yet showed significant clinical improvement, which led the authors to believe that the beneficial effects of PLV and mitral repair are complementary and the improvement was unlikely to have resulted from mitral valve repair alone. The authors concluded that ideally, a prospective, multicenter randomized trial comparing medical treatment with a variety of surgical treatments, including isolated mitral valve repair, would be necessary to address these issues.

The PLV procedure in most patients has involved both left ventricular reduction and mitral valve repair, resulting in decreased mitral regurgitation. The relative contribution of these two procedures still needs to be defined. Our study suggests that the residual amount of mitral regurgitation 3 months after PLV does contribute significantly to short-term clinical outcome. However, we could not determine precisely why some patients continued to develop mitral regurgitation after PLV, whereas others did not.

Operative and 12-month survival after PLV and heart transplantation were comparable in our institution [9]. However, despite the initial improvement, several patients who underwent PLV (group 2) deteriorated and 3 patients required relisting for transplantation. Although PLV was associated with acceptable operative and 12-month survival, we think that it may prove to serve better as a bridge to transplantation, rather than definitive therapy.

The clinical outcome after PLV is unpredictable and we need to learn more about the selection criteria for this procedure. This study, although limited by the small number of patients, suggests that good clinical outcome after PLV is dependent to a large extent on improvement in functional capacity and decrease in mitral regurgitation after the procedure.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

  1. Batista R.J., 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]
  2. Dowling R.D., Koenig S., Laureano M.A., et al. Results of partial left ventriculectomy in patients with end-stage idiopathic dilated cardiomyopathy. J Heart Lung Transplant 1998;17:1208-1212.[Medline]
  3. Popovic Z., Miric M., Gradinac S., et al. Effects of partial left ventriculectomy on left ventricular performance in patients with nonischemic dilated cardiomyopathy. J Am Coll Cardiol 1998;32:1801-1808.[Abstract/Free Full Text]
  4. Bocchi E.A., Bellotti G., deMoraes A.V., et al. Clinical outcome after left ventricular surgical remodeling in patients with idiopathic dilated cardiomyopathy referred for heart transplantation short-term results. Circulation 1997;96(Suppl II):II165-II172.
  5. Gradinac S., Miric M., Popovic Z., et al. Partial left ventriculectomy for idiopathic dilated cardiomyopathy: early results and six-month follow-up. Ann Thorac Surg 1998;66:1963-1968.[Abstract/Free Full Text]
  6. Stolf N.A., Moreira L.F., Bocchi E.A., et al. Determinants of midterm outcome of partial left ventriculectomy in dilated cardiomyopathy. Ann Thorac Surg 1998;66:1585-1591.[Abstract/Free Full Text]
  7. 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 Cardiothoracic Surg 1998;13:337-343.[Abstract/Free Full Text]
  8. Bolling F.S., Pagani F.D., Deeb G.M., et al. Intermediate-term outcome of mitral reconstruction in cardiomyopathy. J Thorac Cardiovasc Surg 1998;115:381-388.[Abstract/Free Full Text]
  9. Etoch S.W., Koenig S.C., Laureano M.A., et al. Results after partial left ventriculectomy versus heart transplantation for idiopathic cardiomyopathy. J Thorac Cardiovasc Surg 1999;117:952-959.[Abstract/Free Full Text]




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