Eur J Cardiothorac Surg 2000;18:550-556
© 2000 Elsevier Science NL
Mid-term results of partial left ventriculectomy in end-stage heart disease
Kerem M. Vural,
O
uz Ta
dem
r
Cardiovascular Surgery Department, Türkiye Yüksek 
htisas Hospital, Ankara, Turkey
Received 12 May 2000;
received in revised form 14 July 2000;
accepted 22 August 2000.
Corresponding author. N. Tandogan cad. 5/6 Kavaklidere 06540, Ankara, Turkey. Tel.: +90-312-426-7574; fax: +90-312-426-6181
e-mail: kvural{at}tr.net
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Abstract
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Objective: Immediate and mid-term effectiveness of partial left ventriculectomy (PLV) is assessed in 27 idiopathic dilated cardiomyopathy patients. Methods: All patients were in New York Heart Association (NYHA) class III (17) or IV (ten). The average left ventricular ejection fraction (LVEF) was 19±4% by MUGA, and 23±4% by digital echocardiography. The mean end-systolic volume (LVESV) was 259±66 ml and the mean end-diastolic volume (LVEDV) was 342±83 ml. Mitral valve replacement was a routine part of the procedure. Results: Operative mortality was 18.5%, a LVEDP>25 mmHg, left atrial diameter>55 mm, pulmonary artery systolic pressure>40 mmHg, congestive hepatomegaly and NYHA class IV being the mortality predictors. Three-year Kaplan–Meier survival was 64±10%, including operative mortality; freedom from congestive heart failure was 65±11%. Functional status improved from 3.2±0.4 to 1.5±0.6 (P=0.0003). The mean LVEF was dramatically increased after PLV (to 40±4%, P=0.0001); LVESV was decreased to 90±30 ml (P<0.0001) and LVEDV to 160±49ml (P<0.0001). This improvement was sustained during the first 30 months. Conclusions: PLV is a reasonable approach for end-stage patients, providing sustained dramatic changes in ventricular geometry and functional capacity, especially in the absence of compromised right and diastolic left heart functions. Routine replacement of the mitral valve allows a more liberal ventriculectomy and eliminates mitral regurgitation, and this may help minimize ventricular distention.
Key Words: Batista • Ventriculectomy • Cardiomyopathy • Congestive • Mitral • Heart failure
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1. Introduction
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End-stage heart disease is prevalent and expected to steadily increase. Although advances in medical therapy have improved survival in patients with end-stage heart failure, heart transplantation, as the definitive treatment modality, is severely limited by donor availability, which is never expected to meet the overwhelming demand. Approximately 20% of the candidates die while waiting for a donor heart, 20% die during the first year after transplantation, and mortality is 5% per year thereafter [1,2]. In addition, the cost of transplantation and the considerable morbidity of immunosupression and other medications have to be considered. In an attempt to seek alternative approaches to the patients with terminal heart disease, various surgical methods other than cardiac transplantation have been proposed.
Partial left ventriculectomy (PLV), introduced by Batista and coworkers [3] is a novel surgical treatment for severe heart failure consisting of resection of a large wedge of myocardium to reduce wall stress and restore the normal mass-volume ratio. Candidates for this operation are patients awaiting cardiac transplantation due to end-stage dilated cardiomyopathy and those unsuitable for transplantation because of age, physical or economical reasons. This procedure directly and rapidly reverses detrimental remodeling associated with dilated cardiomyopathy by acute removal of a portion of the lateral wall [4–6]. Although left ventricular ejection fraction (LVEF) has been shown to improve after PLV, few other data describing its mid-term effects on left ventricular performance are available. In addition, determining the patient group expected to have the maximum benefit after the procedure has been a major concern in many clinical and experimental studies. In this study, we reviewed our patient population in regard to the immediate and mid-term outcomes such as survival, functional capacity improvement, and certain left ventricular indices.
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2. Materials and methods
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Between November 1996 and May 1999, 27 consecutive adult patients with idiopathic dilated cardiomyopathy underwent PLV in our institution. Patient demographics and preoperative hemodynamic data are summarized in Table 1. Our inclusion criteria were refractory heart failure with New York Heart Association (NYHA) class III or IV symptoms despite optimal medical therapy (a combination of digitalis, diuretics and converting enzyme inhibitors) for at least 2 months and documented dilated cardiomyopathy. Preoperative evaluation included NYHA class determination, right and left cardiac catheterization with coronary angiography, MUGA (for LVEF determination) and transthoracic echocardiography (TTE). All patients were re-evaluated by means of clinical and echocardiographic parameters at discharge and then at 6-month intervals during follow-up. Mean follow-up was 27±3 months (sum: 594 months; range: 2–39 months).
2.1. Transthoracic echocardiographic assessment
Digital stress echocardiography (a Freeland Cineview device, Prism Imaging, USA) was employed for obtaining the left ventricular indices. Eight frames per cardiac cycle, triggered from the R-wave at 50 ms intervals, were recorded in a continuous loop format. Apical two and four chamber views were acquired at rest. To calculate diastolic and systolic left ventricular volumes, endocardial borders were traced digitally in diastole and systole. A commercially available software (Cine'view Version 5.05; Prism Imaging Inc., 1986) was used for the calculations of the left ventricular volumes and thus the ejection fraction, according to modified Simpson's rule [7]. The echocardiographic data is represented in Table 3.
2.2. Surgical procedure
The originally described beating heart technique with mild (33–34°C) hypothermic cardiopulmonary bypass (CPB) was used without aortic cross-clamping or cardioplegic arrest. After establishing CPB with standard aorto-bicaval cannulation, 10–20 meq KCl were injected into the aortic root using a large bore needle syringe. This provides a smoother course with a flaccid ventricle and a slow rhythm, and also increases ventricular fibrillation threshold during manipulation of the heart. The apex was elevated and a diamond-shaped excision line started at the apex of the left ventricle where it was made relatively sharp-pointed. At the base of the heart, the shape of the resection line is made relatively blunt. Transected coronary branches are immediately cauterized to avoid any coronary flow steal that may lead to distant ischemia and deterioration. Generally a slice as large as possible of the left ventricular myocardium was resected between the papillary muscles. The anterior papillary muscle may (in 11 cases) or may not (in 16 cases) be included in the resected wall mass, depending on the necessary extent of the resection. The mitral valve was replaced through the left ventriculotomy with a 29 no. St. Jude mechanical prosthesis. Ventricular wall was closed with a continuous bilayer suturing technique with a double armed 2-0 polypropylene suture. Transesophageal echocardiography was used to detect entrapped air as well as for repetitive assessment of LV function before weaning off bypass.
2.3. Statistical analysis
Statistical analysis was performed by SPSS software (release 6.0, SPSS Inc. Chicago, IL). Data were presented as mean ± standard deviation. Pairwise comparisons of TTE data obtained at 6-month intervals during the first 30 months of operation (the period which contained enough number of patients to make statistical comparisons) were performed using paired t-test. Wilcoxon matched-pairs signed-ranks test was used for pairwise comparisons of functional classes during the follow-up. Survival curves were estimated using Kaplan–Meier method and influence of certain parameters on survival compared by LogRank test. Univariate analysis for determining early mortality predictors was performed using either Chi-square, Fisher's exact or unpaired t-tests, depending on the data character. A P-value equal to or smaller than 0.05 was considered statistically significant.
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3. Results
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3.1. Immediate results
The operative mortality was 18.5% (five patients), low cardiac output being the major cause. According to univariate analysis, a left ventricular end-diastolic pressure (LVEDP) exceeding 25 mmHg (P=0.02), left atrial diameter over 55 mm (P=0.03), pulmonary artery systolic pressure exceeding 40 mmHg (P=0.02), a prominently enlarged liver on physical examination (P=0.04) and a NYHA class IV functional capacity (in comparison to Class III; P=0.04) were predictive for operative mortality. As can be seen in Table 2, no association could be shown preoperative left ventricular indices (LVEF, LVEDV, LVESV), as well as demographic factors such as age, sex, diabetes mellitus, hypertension, smoking, or the laboratory parameters namely blood urea nitrogen, creatinine, hematocrit or sodium levels. Nine patients (33.3%) required mechanical support by means of intra-aortic balloon counter pulsation. In all survivors, recovery period was uneventful except in one who necessitated emergency re-exploration for abundant hemorrhage through the chest tubes following extubation. Bleeding was from a point in the ventricular closure line and a successful repair was achieved by using a few stitches reinforced with teflon pledgets. The patient otherwise displayed an uneventful course and discharged as scheduled.
3.2. Survival and follow-up
Four additional deaths occurred in the follow-up period, on the 56th, 288th, 378th, and 568th postoperative days. Three-year Kaplan–Meier survival was 64±10%, including operative mortality (Fig. 1)
. All the late deaths were following a congestive heart failure episode necessitating hospitalization and thus the result of the end-stage heart failure. Postoperative freedom from congestive heart failure was 65±11% at 3 years (Fig. 2) . Of the 22 early survivors, 7 (32%) were readmitted to the hospital a total of 11 times (0.41 re-hospitalization per patient year). Congestive heart failure was the principal cause of hospitalization. Five of 15 patients presenting congestive hepatomegaly as a sign of right heart failure were lost in the early postoperative period, and three of ten survivors of these patients died during the follow-up while only one died from those without congestive hepatomegaly. As we reported previously [8], one patient underwent emergency reoperation due to mechanical valve thrombosis 3 months after the initial operation. The stuck valve was replaced with a new one and the patient was counseled on the importance of routine anticoagulation. This represented a unique case who survived a cardiac reoperation after a partial left ventriculectomy demonstrating that the hemodynamic recovery achieved after such an operation could enable a patient to tolerate reoperation on cardiopulmonary bypass, even in the presence of acute pulmonary edema and cardiogenic shock.
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Fig. 1. The 3-year Kaplan–Meier survival curve including operative mortality. * Number of patients available at each time period.
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Fig. 2. The 3-year freedom from congestive heart failure curve in survivors of operation. * Number of patients available at each time period.
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3.3. Postoperative trends in left ventricular dimensions
LVEF was increased to 40±4% at discharge (P<0.0001), and remained significantly elevated in comparison to the baseline (23±4%) at the 6th (36±6%; P=0.0004), 12th (32±8%; P=0.004), 18th (35±9%; P=0.008), 24th (LVEF=35±6%, P=0.008) and the 30th (LVEF=37±5%, P=0.008) postoperative months (Table 3, Fig. 3)
. The average LVESV was reduced from 259±66 to 94±30 ml after the operation (P<0.0001). This reduction was also maintained during the follow-up period at the 6th (105±37 ml, P<0.0001), 12th (128±42 ml, P<0.0001), 18th (136±50 ml, P<0.0001), 24th (109±40 ml, P=0.002) and the 30th (110±14 ml, P=0.008) postoperative months. Similarly, the average LVEDV was decreased from the preoperative value of 342±83 to 160±49 ml postoperatively (P<0.0001, Fig. 4)
, and maintained this reduction during the follow-up period (172±60 ml at the 6th month, P<0.0001; 184±53 ml at the 12th month, P<0.0001; 204±45 ml at the 18th month, P=0.008; 169±53 ml at the 24th month, P=0.006; 180±28 at the 30th month, P=0.008). Briefly, the effects of the operation on ventricular geometry were still evident even 30 months after the operation.
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Fig. 3. Trend of left ventricular ejection fraction after the operation. * Number of patients available at each time period.
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Fig. 4. Trend of left ventricular end-diastolic diameter after the operation. * Number of patients available at each time period.
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3.4. Functional status
All surviving patients except one displayed substantial improvement in functional capacity in comparison to their preoperative status. Mean NYHA Class regressed from 3.2±0.4 preoperatively to 1.5±0.6 at their most recent follow-up (P=0.0003, Fig. 5)
. This improvement sustained during the follow-up period. One patient remained in class III despite the operation and four patients died subsequently in the follow-up period (three in class III and one in class IV, preoperatively).
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Fig. 5. The change in the New York Heart Association Functional class (based on patient symptomatology) after the operation.
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4. Discussion
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The concept of reducing LV volume to improve function of the remaining LV muscle is not new. LV aneurysmectomy reduces LV cavity to treat heart failure [9,10]. Partial left ventriculectomy differs from aneurysmectomy in that the LV scar is not removed; instead, viable but over distended LV muscle is resected. The mechanism of action is thought to relate to improvement in wall tension and myocardial efficiency resulting from effects engendered by the law of Laplace. Hence the principal mechanism responsible for the beneficial effect of the procedure may be the increase in cardiac effectiveness instead of directly augmenting forward flow. That may explain the controversy between the reports concerning the effects on stroke volume and cardiac index. Some reports point that despite the substantial improvements in LVEF, LVESV, LVEDV and functional capacity, cardiac index remains relatively constant after the operation [11], while others report augmentation in stroke volume and cardiac index as well [6].
Our immediate results were similar to those reported by other institutions. The operative mortality was 18.5%, which has been previously reported to be between 3.5% [12], and 28% [13]. Low cardiac output in the immediate postoperative period, and congestive heart failure episodes during the follow-up were the leading causes of mortality in our experience. Despite the common occurrence of malignant ventricular tachiarrhythmias in other reports [6,14], we did not encounter such a problem as a principal cause of death. Our overall three-year Kaplan–Meier survival rate was 64±10%, including operative mortality. One-year survival was reported as 63% by Bocchi [6], 87% by McCarthy [11], and 2-year survival as 45% by Batista and associates [5]. This variability in both early and late mortality rates from different centers may reflect the necessity to define optimal patient selection criteria and surgical strategy. Nevertheless, the survival rate obtained by PLV is generally better than what to be expected by medical therapy alone and most patients experience substantial improvement in their quality of life. Freedom from relisting for transplantation was reported as 72% by McCarthy and associates [11]. Freedom from a congestive failure episode was 65±11% at 3 years in our experience.
Certainly, proper guidelines for patient selection are critically important to achieve a successful outcome. An analysis for mortality predictors may provide some background on which a patient selection criterion may depend. Increased LVEDP results from the need for higher filling pressures in the early period of dilated cardiomyopathy and, later in the course, it may reflect the decreased compliance of the ventricle due to compensatory hypertrophy. Similarly, a substantial enlargement in left atrial diameter, resulted from constant elevation of LVEDP, may indicate a decreased left ventricular compliance preoperatively, which is expected to worsen after PLV [15,16]. An elevated pulmonary artery pressure to a point generally precedes right heart failure and expresses the load on the right, probably being a milestone in the progressive course of the disease. From this point of view, all these three predictors of early mortality (increased LVEDP, enlarged left atrium and pulmonary hypertension) may be thought as pointing at the same direction: a decreased ventricular compliance and the deterioration of diastolic functions. PLV basically targets the left ventricular geometry and is consequently expected to relieve the load on the right ventricle posed by its left counterpart. However, it does not address to an irreversible and/or intrinsic right-sided failure, which may negatively affect the outcome after a technically successful operation. This may explain why a preoperative finding of prominently enlarged liver on physical examination, one well-recognized sign indicating right-sided heart failure, was found to increase the operative mortality. On the other hand, compromised LVEF, LVESV, LVEDV, did not appear to have an adverse influence on the either immediate or mid-term results. Based on that fact, it can be concluded that the seemingly unfavorable systolic parameters should not mitigate against the surgical approach, and PLV can still be considered in patients presenting very low ejection fractions and grossly enlarged ventricles, especially in the absence of irreversible right or diastolic left ventricular compromise. Stolf et al. pointed out the importance of histological changes as an important predictor of outcome, and demonstrated that mid-term survival was significantly affected by myocardial cell diameter. The left ventricular myocardial cell diameter was 21±2.1 µm in survivors versus 23.3±2.8 µm in deaths/transplants; this difference was statistically significant (P=0.023) [17].
The stability of hemodynamical parameters over 30 postoperative months might be a selection bias; because of death of patients with worse parameters, the mean might stay stable. Immediate improvement following PLV is well observed in the majority of previous studies [5,6,11,13]. However, there is a paucity of data addressing the persistence of these effects during longer follow-up. We found that the beneficial effects on ventricular geometry may sustain at least 30 months after the operation. However, as pointed out in the histological studies of myocardial tissue after PLV, cellular derangement and myofibril slippage [18] as a result of prolonged ventricular loading is generally not expected to totally disappear after PLV. Therefore, a gradual but incessant deterioration after a period of well-being is anticipated. Although the PLV is not considered a curative means of therapy, it provides a good starting point for continued medical care for heart failure. It may help reverse remodeling, an important initiative step, but needs to be supported by strictly applied conventional medical regimen. Although there is a tendency to repair and preserve the mitral valve in the recent publications [12,14], replacement of the mitral valve allows a more liberal ventriculectomy, without having the fear of distorting papillary muscle orientation. It also eliminates mitral regurgitation, and this may help minimize ventricular distention and wall stress. This may be of benefit in decreasing the ventricular arrhythmias. Preservation of the posterior subvalvar apparatus may be attempted in an effort to augment left ventricular performance. The objective value of these speculations should be assessed by controlled randomized studies.
In conclusion, PLV may become an alternative resort for patients ineligible for transplantation or it might be considered as a bridge to heart transplantation. Hemodynamic effects and functional capacity improvement, primarily resulted from the dramatic change in the ventricular geometry, sustains for a considerable duration. Optimized supportive medical treatment is essential in reverse remodeling as an integral part of the continuous therapy. However, irreversible right heart failure or distorted left ventricular diastolic functions may put an unfavorable impact on the results. From this point of view, cardiac transplantation may be a better therapeutic approach for this subset of patients.
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References
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Abstract
1. Introduction
