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Ann Thorac Surg 2006;82:1349-1355
© 2006 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Left Ventricle Volume Affects the Result of Mitral Valve Surgery for Idiopathic Dilated Cardiomyopathy to Treat Congestive Heart Failure

Taiko Horii, MDb,*, Hisayoshi Suma, MDc, Tadashi Isomura, MDa, Fumikazu Nomura, MDa, Joji Hoshino, MDa

a Hayama Heart Center, Hayama, Japan
b Kagawa University, Kagawa, Japan
c The Cardiovascular Institute Japan, Tokyo, Japan

Accepted for publication April 27, 2006.

* Address correspondence to Dr Horii, 1750-1 Ikenobe, Miki-cho, Kita-gun, Kagawa, 761-0793 Japan (Email: thorii{at}med.kagawa-u.ac.jp).

Presented at the Forty-second Annual Meeting of The Society of Thoracic Surgeons, Chicago, IL, Jan 30–Feb 1, 2006.


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 Southern Thoracic Surgical...
 Discussion
 References
 
BACKGROUND: Mitral valve surgery is a recommended treatment for congestive heart failure; however, its effect for idiopathic dilated cardiomyopathy (DCM) with an extremely enlarged left ventricle (LV) is not well documented. We examined our long-term results of mitral valve surgery for idiopathic dilated cardiomyopathy.

METHODS: Fifty-five patients of idiopathic dilated cardiomyopathy have undergone mitral valve surgery to treat intractable congestive heart failure since 1998. Forty-two patients were male with an average age of 55. Preoperative New York Heart Association functional class was III in 25, IV in 30, and 19 were dependent on inotropic infusion. The mitral valve was repaired in 37 patients and replaced in 18. The tricuspid valve was repaired in 35 patients and replaced in 3. We divided 46 elective cases into two groups by LV end-systolic volume index.

RESULTS: Postoperatively, an intraaortic balloon pump was required in 2 patients and a left ventricular assist device in 1; both were emergent cases. Hospital mortality was noted 4.3% in elective cases (2 of 46) and 14.5% in overall cases (8 of 55). One-year, 3-year, and 5-year survival rate of elective cases was 73.3%, 58.2%, and 51.7%, respectively. Left ventricle size has decreased and LV contractility has increased in a small LV group year by year, but those in a large LV volume group have not changed subsequently after surgery. There was a significant difference noted in the survival rate of the two groups divided by LV end-systolic volume index.

CONCLUSIONS: Mitral valve surgery for idiopathic dilated cardiomyopathy to treat end-stage heart failure is relatively safe and effective in elective status. However, isolated mitral reconstruction without any other type of surgery may not suffice for an extremely enlarged LV.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Comment
 Southern Thoracic Surgical...
 Discussion
 References
 
Bolling and colleagues [1, 2] reported that mitral reconstruction could restore left ventricle (LV) function in cardiomyopathy to treat heart failure with severe mitral regurgitation. Mitral ring annuloplasty is a feasible technique and one of the most common practices in our surgical community. The idea that the fixation of mitral regurgitation by means of mitral ring annuloplasty restores LV function seems to be acceptable as nontransplant surgery, especially for intractable heart failure patients. Soon mitral reconstruction has been recognized as one of the most important choices to treat congestive heart failure with severe mitral regurgitation. Since then several reports have followed [3–6].

Last year a Michigan group also published a controversial report that there was no impact on long-term mortality in patients with mitral regurgitation that were surgically corrected [7]. Although there is still a big concern as to how the study was constructed and the reason why the study concluded, we also have encountered diverse outcomes in our practice. Mitral reconstruction worked very well and restored LV dramatically in some patients, but it did not work so well in others. We wondered why such a simple operation as mitral reconstruction ended up with such diverse results.

In our experience, larger hearts seemed not to respond well to only mitral reconstruction. We retrospectively examined our long-term results of mitral reconstruction for idiopathic dilated cardiomyopathy (DCM).


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 Southern Thoracic Surgical...
 Discussion
 References
 
From 1998 to 2005, we performed mitral valve surgery for idiopathic DCM to treat end-stage heart failure in 55 patients at Hayama Heart Center, Japan. This study was not submitted for institutional review board approval because this was a retrospective study with no individual patient identifiers used, and patient consent was waived. Written informed consent for the procedure was obtained from all patients before surgery. There were fifty-five patients in total (42 men and 13 women). The average age was 55 years old, varying from 17 to 77. The cause in this study is exclusively idiopathic dilated cardiomyopathy and does not include any other type of cardiomyopathy.

Preoperative Clinical Status
All patients suffered from congestive heart failure and were treated by thorough medical treatment, including several cardioprotective agents with temporary convalescence. Most of the patients with intractable heart failure, in spite of optimal medical treatment, were referred to our hospital for further treatment. The duration of heart failure in these patients was an average of 5.5 years, varying from 5 months to 9 years. As cardioprotective agents, all but 4 patients took angiotensin converting enzyme inhibitor or angiotensin receptor blocker. Beta-blockade therapy was introduced to 44 patients, but 19 of these patients were unable to tolerate the agents after several attempts, because of the negative inotropic effects of the beta-blocker.

After optimal medical treatment, including the temporary use of drip infusion of catecholamine, the preoperative New York Heart Association (NYHA) functional class and LV function was measured at the stable condition if possible. The preoperative NYHA functional class was class III in 25 patients and class IV in 30 patients. Nineteen patients were intractably dependent on inotropic drip infusion and were unable to be weaned from intravenous administration of catecholamine in spite of optimal medical treatment. Nine of these patients were on pre-shock status and 2 were on intraaortic balloon pump. Subsequently, 9 patients underwent emergent operations. Serum brain natriuretic peptide (BNP) varied widely, even after optimal medical treatment, and the preoperative BNP level just before surgery in an elective 46 patients was 628 ± 420, from 140 to 1440 pg/mL.

Serial echocardiography is mandatory for all to calculate LV diameter and ejection fraction (EF). Left ventricle volume was measured by biplane, not single plane, with the LV angiogram primarily if the condition of patients allowed or quantitative gated scintigram at rest was subsidiary. Cardiopulmonary exercise examination was carried out to measure oxygen consumption for the relatively stable condition of 12 patients, and maximal oxygen consumption rate was 13.8 ± 1.8 mL/kg/m2.

Surgical Technique
The surgical procedure was performed through a median sternotomy in all, and tepid warm blood cardioplegia was delivered through an antegrade route in all, and a retrograde route in addition if needed. The mitral valve was repaired in 37 patients (67%) with a 2 to 4 mm downsized semirigid, full annuloplasty ring, with a mean size of 26 mm, and a supplemental technique such as an artificial chordae implantation or Alfieri stitch in 6 patients. The mitral valve was replaced by a bioprosthesis in 18 patients (33%) with a preserving subapparatus continuity technique. In the very beginning of our experience for extremely enlarged and depressed hearts, we managed to shorten cardiac arrest time and avoid second pump run as much as possible. At first we adopted the replacement often, even for simple annular dilatation without any organic disorder, and then the technique, which has gradually shifted toward a complex one.

Surgical correction of tricuspid valve was required in 38 patients (69%). The tricuspid valve was repaired by a DeVega type of annuloplasty in 23 patients, by the Carpentier's classic ring annuloplasty in 12 patients, and it was replaced in 3 patients with a bioprosthesis. The Maze procedure was added in 8 patients for supraventricular tachyarrhythmia. Since 2001, biventricular resynchronization pacing was installed in 5 patients when the intraventricular conduction disturbance was noted preoperatively.

Follow-up
Most of the survivors returned back to our hospital for routine follow-up of the LV function every 6 months to 1 year. Four patients of survivors were distant from our hospital and were unable to show up routinely, and were therefore telephone interviewed with referring cardiologists. Patients were followed-up for a total 106 patient years, with a mean follow-up among survivors of 29 ± 23 months.

Statistical Analyses
Calculated data of variables were expressed as mean with standard deviation. Variables of two groups were compared by the unpaired t test. Correlation between the two groups was calculated by the Spearman's test and patient survival was calculated using the Kaplan-Meier method. For the survival results reported here, all deaths related or unrelated to the cardiac event were regarded as the end points. Differences between the survival rates to groups were assessed by the log-rank test. The p value less than 0.05 was considered as statistically significant. Data were analyzed using Statistica 6.1 (StatSoft, Tulsa, OK).


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 Southern Thoracic Surgical...
 Discussion
 References
 
Preoperative measurements are summarized in Table 1. Eight patients were unable to survive surgery in an overall 55 patients. Hospital mortality noted 2 cases (4.3%) in an elective 46 cases, and 6 (67%) in an emergent 9 patients. Survival rate in the elective 46 cases are showed in Figure 1. One-year, 3-year, and 5-year survival rate, including hospital mortality was 73.3 ± 6.9%, 58.2 ± 8.2%, and 51.7 ± 9.5%, respectively. In a long-term survival rate, there was no difference between repair and replacement (p = 0.382). Symptoms improved in most of the survivors, and the NYHA functional class changed from 3.5 ± 0.5 to 1.9 ± 0.8 after surgery.


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  		Table 1. Preoperative Measurement of Left Ventricle Factors
 

Figure 1
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  		Fig 1. Survival curve of elective 46 cases by the Kaplan-Meier method.

 
We specifically looked back at the relationship between preoperative LV contractility and LV volume. Left ventricle EF and LV end-systolic volume index (ESVI) were plotted in Figure 2. There was no correlation between LV EF and LV ESVI (r = 0.033; p = 0.82) in our patient group. Left ventricle volume varied widely with 150 mL/m2 in average of LV ESVI from 70 to 270 mL/m2. Considering the wide variance of LV volume size, we divided elective 46 patients into two groups by the average value of LV ESVI 150 mL/m2. Preoperative measurements in two groups are shown in Table 1. Left ventricle size, volume, and EF have a significant difference between the two groups. Intra-cavital pressure and systolic pulmonary artery pressure in a large LV volume group were greater than those in a small LV volume group, but those did not reach a statistical difference.


Figure 2
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  		Fig 2. Relationship between left ventricle (LV) contractility (vertical column) and left ventricle volume (horizontal column). LV volume varied widely from 70 to 270 mL/m2 of LV ESVI even though LV contractility remained in a relatively small range between 10 and 34% of LV EF. (EF = ejection fraction; ESVI = end-systolic volume index.)

 
We serially measured LV factors before and after surgery. Left ventricle end-diastolic dimension (DD) has decreased year by year in a small LV group from 66.4 ± 6.4 mm before surgery to 65.1 ± 6.1 mm at 1 month, 62.3 ± 5.8 mm at 1 year, and 60.8 ± 6.5 mm at 3 years after surgery. Left ventricle DD at 3 years after surgery is significantly smaller than that before surgery (p = 0.032). On the contrary, LV DD in a large LV group has not changed subsequently after surgery (Fig 3). Left ventricle EF in a small LV group has serially increased year by year after surgery from 24.6 ± 6.4% before surgery to 26.5 ± 4.1% at 1 month, 30.4 ± 7.2% at 1 year, and 34.0 ± 7.5% at 3 years after surgery (Fig 4). Left ventricle ESVI in a small LV group has decreased year by year from 114 ± 26 mL/m2 before surgery to 106 ± 21 mL/m2 at 1 month, 99 ± 28 mL/m2 at 1 year, and 92 ± 21 mL/m2 at 3 years after surgery (Fig 5). Left ventricle EF at 1 year and 3 years after surgery is significantly greater than that before surgery (p = 0.019 and 0.008, respectively), and LV ESVI at 1 year and 3 years after surgery is significantly smaller than that before surgery (p = 0.029 and 0.022, respectively). On the contrary, LV EF and LV ESVI in a large LV have not significantly changed after surgery.


Figure 3
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  		Fig 3. Serial change of left ventricle (LV) diastolic diameter before and after surgery in a small LV volume group (solid bar) and in a large LV volume group (open bar). (See details in the text.) (Dd = diastolic dimension; pre = preoperative.)

 

Figure 4
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  		Fig 4. Serial change of left ventricle (LV) ejection fraction before and after surgery in a small LV volume group (solid bar) and in a large LV volume group (open bar). (See details in the text.) (EF = ejection fraction; pre = preoperative.)

 

Figure 5
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  		Fig 5. Serial change of left ventricle (LV) end-systolic volume index before and after surgery in a small LV volume group (solid bar) and in a large LV volume group (open bar). (See details in the text.) (ESVI = end-systolic volume index; pre = preoperative.)

 
Mitral reconstruction could reversely remodel depressed hearts with relatively small LV volume and could restore LV function of relatively small LV. However, isolated mitral reconstruction had little effect on LV function for an extremely enlarged LV.

The result of the surgery is summarized in Table 2. Both groups have 1 hospital mortality each, without intraaortic balloon pump support or a left ventricular assist device postoperatively. Late mortality was 5 in a small LV group and 10 in a large LV volume group. Six of 10 late deaths in a large LV group suffered from recurrence of heart failure after surgery.


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  		Table 2. Surgical Outcome of Elective 46 Cases
 
Mitral reconstruction ameliorated symptoms in most of small LV group, but did not do so in large LV group. In small LV group, preoperative NYHA functional class was III in 16 patients and IV in 9 patients. Twenty of these 25 patients survived 1 year after surgery, 16 of these patients (80%) remained in NYHA functional class I or II. Eleven of 13 patients survived (85%) at 3 years after surgery who remained in NYHA functional class I or II, and all 3 patients who survived at 5 years after surgery remained in NYHA functional class I or II. In large LV group, those who survived were in the preoperative NYHA functional class III (10 patients) and IV (11 patients). Eleven of 21 patients survived 1 year after surgery; and 4 of these patients (36%) remained in NYHA functional class I or II, 2 of 5 patients (40%) survived at 3 years and stayed in NYHA class I or II; and none of them survived at 5 years after surgery.

Survival curve in both groups are shown in Figure 6. In the small LV group, 1 year survival rate was 83.7%, and 3-year and 5-year survival rates were 67.1%. In the large LV group, 1-year survival rate was 59.7%, and 3-year survival rate was 42.0%. There was a significant difference in the survival rate between two groups (p = 0.0299).


Figure 6
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  		Fig 6. Survival curve after mitral valve surgery in a small left ventricle (LV) volume group (solid line) and in a large LV volume group (dashed line) by the Kaplan-Meier method. There was a significant difference between the two groups (p = 0.0299; log-rank test). (ESVI = end-systolic volume index.)

 

   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
Southern Thoracic Surgical...
 Discussion
 References
 
The concept introduced by Bolling and colleagues [1, 2] that mitral reconstruction could restore LV function of cardiomyopathy had a big impact on the treatment of heart failure. Mitral ring annuloplasty is a feasible technique and can be reproduced all around the world. Several reports have been published since then, and a short-term to intermediate-term result was fairly good. We also started a program of treating heart failure with mitral valve surgery for idiopathic DCM accordingly. In some instances, LV function improved dramatically, immediately after surgery, but not in others. We wondered why such a simple operation as mitral reconstruction ended up with diverse results and noticed several factors. Factors that should be taken into consideration are as follows: the cause of the diseases, the condition of the patient, and the status of the heart function.

In all previous reports there were various types of cardiomyopathy and the majority of cases were ischemic in cause [2–6]. We need to consider each cause separately, because each cause has different patterns of myocardial insult to the ventricle. Idiopathic DCM is a progressive disease. Left ventricle dilates time by time for some reasons, and mitral regurgitation advances presumably due to the dilatation of LV [8]. Considering that consequence, the effect of mitral reconstruction may have limitations. The fixation of mitral regurgitation can restore LV function of moderately dilated LV. Once LV extremely dilates, surgical manipulation of atrioventricular valves may not suffice. We have no real tools to measure the amount of myocardial damage in the ventricle before surgery, and we can not prove that extremely enlarged hearts have more damage in the ventricle than do small hearts.

Idiopathic DCM is difficult not only to treat, but also to understand. The disease itself is not uniform and exhibits various features. Left ventricle size, LV wall motion, and the extent of myocardial damage in LV vary widely from small to large in size, from moderate to severe in function, and from homogeneous to heterogeneous in damage. All are mixed up under the same diagnosis as idiopathic DCM. We need to treat this disease according to its status. A homogeneously and globally damaged heart needs to be replaced by either a sophisticated assist device or a transplanted donor heart. As several reports point out, idiopathic DCM often reveals regional and localized damage [9–11]. In our practice, we count on intraoperative echocardiography [12] and apply LV restoration surgery in conjunction with or without mitral reconstruction once we find regional and focal damage in the LV [13, 14]. Heterogeneously damaged hearts can be restored by LV restoration surgery with careful selection [15, 16].

Once the status of patients with extremely enlarged hearts has profoundly deteriorated, in our experience, emergent mitral reconstruction could not save patients. In urgent status, extremely enlarged hearts need to be replaced by either sophisticated assist devices or with the transplantation of a donor heart.

Mitral reconstruction can restore LV function with the cut-off value of 65 mm in LV DD for an ischemic cause [17]. In our study, the average was 150 mL/m2 in LV ESVI and 70 mm in LV DD. There is a big difference in the amount and the extent of solid fibrosis in the ventricle between an ischemic cause and a nonischemic cause. In idiopathic DCM with LV ESVI exceeding 150 mL/m2 or LV DD exceeding 70 mm, isolate mitral reconstruction may fail to restore LV function effectively.

As nontransplant surgeries to treat congestive heart failure, there are several new therapies such as passive cardiac containment [18] or cell transplantation [19]. Any other type of surgery such as LV containment surgery, regenerative therapy, or LV restoration surgery, in conjunction with mitral reconstruction may be a choice to treat end-stage heart failure as nontransplant surgery, even if the LV extremely dilates.

In conclusion, mitral valve surgery for idiopathic DCM to treat en-stage heart failure is relatively safe and effective in an elective status. Isolated mitral reconstruction without any other surgical modality, however, may not suffice for extremely enlarged LV.


   Southern Thoracic Surgical Association: Fifty-Third Annual Meeting
Top
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 Introduction
 Patients and Methods
 Results
 Comment
 Southern Thoracic Surgical...
Discussion
 References
 
The Fifty-Third Annual Meeting of the Southern Thoracic Surgical Association (STSA) will be held November 8–11, 2006, in Tucson, Arizona. The meeting will include Surgical Motion Pictures, the STSA Post-Graduate Program, an ethics session, a coding workshop, and the STSA Scientific Sessions. In addition, there will be a special program Saturday morning, "Strategies and Vision for the Future of Cardiothoracic Surgery," presented by William Baumgartner, MD, and Michael Stahl, PhD. This year's Presidential Invited Speaker is Edward L. Bove, MD, who will address attendees on Friday morning just prior to the STSA Presidential Address to be given by Ross Ungerleider, MD. Physician attendees can earn up to 23.75 category 1 credits toward the AMA Physician's Recognition Award. Registration is available at www.stsa.org through October 13. On-site registrations will be accepted.


Please visit the STSA (http://www.stsa.org) or CTSNet (http://www.ctsnet.org) websites for detailed information regarding the meeting.

 


   Discussion
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 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Southern Thoracic Surgical...
 Discussion
References
 
DR ROBERT A. E. DION (Leiden, the Netherlands): I rise to congratulate the work of Hisayoshi Suma and his group, and your presentation was excellent. I just want to know which technique you used to perform the mitral valve repair, how much are you undersizing? And in the best group, below 150 mL/m2, how many of these patients had no recurrence of mitral regurgitation at follow-up? The reason why I ask you this is that, our experience in Leiden, we have been able to define a preoperative cutoff value of 65 mm end-diastolic diameter to predict whether the left ventricle (LV) is going to "reverse remodel" or not. Therefore my last question: In the best group of patients, less than 150 mL/m2, how many did reverse remodel? Thank you.

DR HORII: Thank you for your question, Professor Dion. At first we used full ring annuloplasty and we undersized it, as you say, restrictive mitral annuloplasty. When preoperative LV volume is below 150 mL/m2 of LV ESVI, most patients had no recurrence of mitral regurgitation. I don't have the exact number of recurrence of mitral regurgitation in all. Could you repeat the last question?

DR DION: How many patients did "reverse remodel" in the best group?

DR HORII: Roughly 70% of small left ventricle patients had reverse remodeling.

DR GERALD D. BUCKBERG (Los Angeles, CA): Congratulations, Dr. Horii, on a lovely paper. You have shown that it is not just the base of the heart, but it is the whole volume that is important. I have several questions. The first is, have you had any patients that you have operated on where you just fixed the base of the heart, that is, did an annuloplasty, and then had to later re-operate to then do a restoration? Your echocardiographic (echo) studies show more dynamic contraction occurs when the procedure reduces the global ventricular size. This implies a second procedure may be in store in patients who have not done well, due to increased size after [they have] left the hospital following only a mitral procedure.

DR HORII: No, we didn't do that, a second operation.

DR BUCKBERG: The second question relates to the brain natriuretic peptide (BNP) measurements and their relationship to volume. Dr Bolling had talked to us about the fact that annuloplasty will reduce BNP, but some of his patients did not show this reduction. Did you see a correlation between the BNP measurements of the patients who had smaller ventricles versus larger ventricles, that is, could this neuroendocrine response have a volume trigger?

DR HORII: I can tell you about the correlation between the BNP and the result of surgery. If the patient has a preoperative BNP rate that exceeds 1,000, you should stay away from some sort of nontransplant surgery procedure, but below 1,000, I can say below 800, we have some chance to fix or restore LV function by means of mitral valve surgery.

DR BUCKBERG: Did it correlate with the size of the ventricle, that is, in the smaller ventricles did you see more reduction than the larger ventricles?

DR HORII: Yes.

DR BUCKBERG: And my last question is linked to the importance of selecting the right site to remove. In this nonischemic cardiomyopathy population, you either excluded the septum or the lateral wall. Don't you think this choice also relates specifically what we do with ischemic cardiomyopathy; we find the ischemic site or scar and exclude this nonfunctional region of the ventricle? I suspect the principles you showed in nonischemic disease for site selection in nonischemic disease may be exactly mirror our choice with ischemic cardiomyopathy, where we identify the scar by echo or by angiogram.

DR HORII: We decide at the time of surgery by echocardiography, but preoperatively we don't have such a fantastic method as volume reduction test on pump and simply we cannot do that. So we do need angiogram, sophisticated magnetic resonance imaging, or something that can help us as to which site is better and which site is worse. But at the time of operation we decide by echocardiography. You mentioned the relationship between ischemic cardiomyopathy and idiopathic dilated cardiomyopathy, which are totally different types of disease. Ischemic cardiomyopathy is mostly due to anteroseptal myocardial infarction. So you have no need to worry about any other portion the LV. On the contrary to ischemic cardiomyopathy, the damage portion of LV in idiopathic dilated cardiomyopathy varies widely. Someone has just localized damage in the anteroseptal wall, others in the posterolateral wall, and sometimes diffusely affected and homogeneously damaged. That is the time we should go away from simply restoring or repairing as non-transplant surgery and just go ahead straight to the replacement, like left ventricular assist device (LVAD) implantation or heart transplantation.

DR STEVEN F. BOLLING (Ann Arbor, MI): Dr. Suma and his group should be congratulated. In support of that, our JACC paper, regarding mitral valve plasty for congestive heart failure (CHF) that came out in 2005, of our 10-year surgical experience has now been subdivided into the first and the second 5-year period. In the second 5-year period, 2000 to 2005, there is a mortality benefit for mitral valve annuloplasty versus medical therapy. In those patients, we found them to be earlier patients, who also had smaller ventricles. So this is in support of your findings and very much in correlation with what you have said. In terms of those larger ventricles, perhaps you could enlighten us in terms of is there a device we should be using? Should we use direct surgery on the myocardium? Should we use an Acorn? How do we make that decision? Thank you very much.

DR HORII: A very good question and I want to know exactly the answer. I don't have such a luxury for using LV containment therapy or any other type of regenerative therapy or some nice sophisticated LVAD machine. We are doing nontransplant surgery, doing LV restoration surgery in conjunction with mitral reconstruction. The result of mitral annuloplasty with LV restoration surgery for too much dilated LV of idiopathic dilated cardiomyopathy is fairly good. There is some hope to have space to repair and restore LV function as non-transplant surgery even for extremely enlarged LV and I will present our data in the next Western Thoracic Surgical Association meeting this year.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Southern Thoracic Surgical...
 Discussion
 References
 

  1. Bolling SF, Deeb GM, Brunsting LA, Bach DS. Early outcome of mitral valve reconstruction in patients with end-stage cardiomyopathy J Thorac Cardiovasc Surg 1995;109:676-682.[Abstract/Free Full Text]
  2. Bolling SF, Pagani FD, Deeb GM, Bach DS. Intermediate-term outcome of mitral reconstruction in cardiomyopathy J Thorac Cardiovasc Surg 1998;115:381-386.[Abstract/Free Full Text]
  3. Bishay ES, McCarthy PM, Cosgrove DM, et al. Mitral valve surgery in patients with severe left ventricular dysfunction Eur J Cardiothorac Surg 2000;17:213-221.[Abstract/Free Full Text]
  4. Calafiore AM, Gallina S, Di Mauro M, et al. Mitral valve procedure in dilated cardiomyopathy: repair or replacement? Ann Thorac Surg 2001;71:1146-1152.[Abstract/Free Full Text]
  5. Gummert JF, Rahmel A, Bucerius J, et al. Mitral valve repair in patients with end stage cardiomyopathy: who benefits? Eur J Cardiothorac Surg 2003;23:1017-1022.[Abstract/Free Full Text]
  6. Shah AS, Hannish SA, Milano CA, Glower DD. Isolated mitral valve repair in patients with depressed left ventricular function Ann Thorac Surg 2005;80:1309-1314.[Abstract/Free Full Text]
  7. Wu AH, Aaronson KD, Bolling SF, Pagani FD, Welch K, Koelling TM. Impact of mitral valve annuloplasty on mortality risk in patients with mitral regurgitation and left ventricular systolic dysfunction J Am Coll Cardiol 2005;45:381-387.[Abstract/Free Full Text]
  8. Hueb AC, Jatene FB, Moreira LF, Pomerantzeff PM, Kallas E, de Oliveira SA. Ventricular remodeling and mitral valve modifications in dilated cardiomyopathy: new insights from anatomic study J Thorac Cardiovasc Surg 2002;124:1216-1224.[Abstract/Free Full Text]
  9. Young AA, Dokos S, Powell KA, et al. Regional heterogeneity of function in nonischemic dilated cardiomyopathy Cardiovasc Res 2001;49:308-318.[Abstract/Free Full Text]
  10. Yanagida R, Sugawara M, Kawai A, Koyanagi H. Regional differences in myocardial work of the left ventricle in patients with idiopathic dilated cardiomyopathy: implications for the surgical technique used for left ventriculoplasty J Thorac Cardiovasc Surg 2001;122:600-607.[Abstract/Free Full Text]
  11. Bach DS, Beanlands RS, Schwaiger M, Armstrong WF. Heterogeneity of ventricular function and myocardial oxidative metabolism in nonischemic dilated cardiomyopathy J Am Coll Cardiol 1995;25:1258-1262.[Abstract]
  12. Isomura T, Suma H, Horii T, Sato T, Kikuchi N. Partial left ventriculectomy, ventriculoplasty or valvular surgery for idiopathic dilated cardiomyopathy–the role of intra-operative echocardiography Eur J Cardiothorac Surg 2000;17:239-245.[Abstract/Free Full Text]
  13. Suma H, Isomura T, Horii T, Buckberg GD, RESTORE Group Role of site selection for left ventriculoplasty to treat idiopathic dilated cardiomyopathy Heart Fail Rev 2004;9:329-336.[Medline]
  14. Suma H, Isomura T, Horii T, et al. Nontransplant cardiac surgery for end-stage cardiomyopathy J Thorac Cardiovasc Surg 2000;119:1233-1244.[Abstract/Free Full Text]
  15. Isomura T, Suma H, Horii T, et al. Left ventricle restoration in patients with non-ischemic dilated cardiomyopathy: risk factors and predictors of outcome and change of mid-term ventricular function Eur J Cardiothorac Surg 2001;19:684-689.[Abstract/Free Full Text]
  16. Horii T, Isomura T, Komeda M, Suma H. Left ventriculoplasty for nonischemic dilated cardiomyopathy J Card Surg 2003;18:121-124.[Medline]
  17. Braun J, Bax JJ, Versteegh MIM, Voigt PG, et al. Preoperative left ventricular dimensions predict reverse remodeling following restrictive mitral annuloplasty in ischemic mitral regurgitation Eur J Cardiothorac Surg 2005;27:847-853.[Abstract/Free Full Text]
  18. Oz MC, Konertz WF, Kleber FX, et al. Global surgical experience with the Acorn cardiac support device J Thorac Cardiovasc Surg 2003;126:983-991.[Abstract/Free Full Text]
  19. Patel AN, Geffner L, Vina RF, et al. Surgical treatment for congestive heart failure with autologous adult stem cell transplantation: a prospective randomized study J Thorac Cardiovasc Surg 2005;130:1631-1638.[Abstract/Free Full Text]



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