ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Radovanovic, N.
Right arrow Articles by Jonjev, Z. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Radovanovic, N.
Right arrow Articles by Jonjev, Z. S.
Related Collections
Right arrow Lung - cancer

Ann Thorac Surg 2002;73:751-755
© 2002 The Society of Thoracic Surgeons

Original article: cardiovascular

Reductive annuloplasty of double orifices in patients with primary dilated cardiomyopathy

Ninoslav Radovanovi, MDa, Bogoljub Mihajlovi, MDa, Jan Selestiansk, MDa, Vladimir Torbica, MDa, Milan Mijatov, MDa, Miroslava Popov, MDa, ivojin S. Jonjev, MD*a,b

a Clinic of Cardiovascular Surgery, University of Novi Sad, Novi Sad, Yugoslavia
b Department of Physiology and Biophysics, University of Illinois at Chicago, Chicago, Illinois, USA

Accepted for publication October 19, 2001.

* Address reprint requests to Dr Jonjev, Department of Physiology and Biophysics, University of Illinois at Chicago, MC 901, 835 S Wolcott Ave, Chicago, IL 60612-7342, USA
e-mail: jonjevz{at}uic.edu


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 
Background. Patients with primary dilated cardiomyopathy exhibit extensive remodeling of the left ventricle, mitral and tricuspid annular dilation and both mitral and tricuspid regurgitation. These factors significantly contribute to heart failure, and are predictors of early lethal outcome. The aim of this study is to show hemodynamic and clinical improvement after reductive annuloplasty of both mitral and tricuspid orifices in primary dilated cardiomyopathy.

Methods. There were 76 patients with primary dilated cardiomyopathy. Mitral annuloplasty using a Carpentier-Edwards sizer was performed on 9 patients, and posterior semicircular reductive annuloplasty was performed on 67 patients. Modified De Vega’s tricuspid annuloplasty was performed on all patients.

Results. Immediate and long-term results showed significant improvement in hemodynamic values and myocardial contractility after operation.

Conclusions. Reductive annuloplasty of both mitral and tricuspid orifices corrects remodeling of the left ventricle of the heart, changes sphericity and geometry of the left ventricle, improves hemodynamic action of the left and right ventricle, and slows down progression of heart failure. We recommend reductive annuloplasty of both mitral and tricuspid orifices before or soon after the first decompensation.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 Acknowledgments
 References
 
Primary dilated cardiomyopathy has been defined by the World Health Organization as dilation of the left, right, or both ventricles, with impaired systolic function of an unknown cause [1]. Patients with primary dilated cardiomyopathy (PDCM), particularly in the end-stage, present an enormous clinical problem because of refractoriness to medical treatment. Even with aggressive medical therapy, heart failure in the terminal stage of PDCM is associated with high mortality and poor prognosis [2]. The occurrence of significant mitral valve regurgitation is generally categorized as either functional or volume dependent [3]. It has also been reported that double orifice insufficiency is an unavoidable complication of end-stage PDCM, contributes significantly to cardiac failure, and is a predictor of early lethal outcome [3, 4]. This poor prognosis has led to an increasing interest in treatment of heart failure using different surgical procedures: conventional heart transplantation, cardiomyoplasty [5], partial left ventriculectomy (Batista’s procedure) [6], and mitral and tricuspid valve repair [7–10].

Heart transplantation provides good short-term and long-term results, but a limited donor heart pool, high costs, and contraindications for heart transplantation stimulate interests for alternative surgical options [11]. Pressed by great political and economical difficulties after the breakup of former Yugoslavia in 1991, our Heart Transplantation Program was stopped. Many patients have been affected by these unfavorable events. Patients in end-stage PDCM with the highest risk for poor outcome were placed on a long waiting list for heart transplantation. Encouraged by our experience with patients with ischemic dilative cardiomyopathy (IsDCM) and an ejection fraction (EF) less than 30%, in July 1991 we began correction of mitral and tricuspid regurgitation to improve hemodynamic status in patients with PDCM. Reductive annuloplasty of double (mitral and tricuspid) orifices (RADO) quickly became an acceptable solution as a bridge to heart transplantation for patients with PDCM. The present study reports our early experience with surgical treatment of PDCM in which RADO was used as a method for correction of mitral and tricuspid regurgitation.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 Acknowledgments
 References
 
This study was approved by the scientific committee of the University Clinic of Cardiovascular Surgery, Sremska Kamenica-Novi Sad. There were 76 patients with end-stage dilated cardiomyopathy. Patients were operated on between July 1, 1991 and April 1, 1998 at the University Clinic of Cardiovascular Surgery in Novi Sad, Yugoslavia. There were 58 males (76.3%) and 18 females (23.7%), with a mean age of 49.9 years (range, 17 to 66 years). At the time of admission all patients were in New York Heart Association classes III (26%) and IV (74%). The average duration of illness was 4.25 years (1 to 20 years). Previous cardiac decompensation had occurred in 66 patients (87%), with an average period from the first signs of illness to the first decompensation of 24.5 months. The average number of decompensations was 2.8 [1–18] per patient. Patients with combined ischemic heart disease and primary valvular disease (mitral or aortic), diagnosed before cardiomyopathy, were excluded from the study. All preoperative data used for further analysis was obtained after aggressive drug treatment of at least 2 weeks duration postadmission. Preoperative medical care included digoxin (75 patients; 99%), diuretics (76 patients; 100%), ACE inhibitors (21 patients; 28%), and antiarrhythmics (57 patients; 75%). Fifteen patients (19.7%) were dependent on stimulation by inotropic agents (intravenous administration of adrenalin or dobutamine) at the time of operation.

Surgical procedures were done using standard cardiopulmonary bypass with membrane oxygenator, moderate systemic hypothermia (28° C to 30°C), and hemodilution. Myocardial protection was achieved using intermittent administration of cold crystalloid St. Thomas No. 2 cardioplegia (t = 4°C), and local topical cooling of the heart. Transseptal approach to the mitral valve was used as a routine approach in all patients. For mitral annulus reduction, a Carpentier mitral valve ring (size No. 32) (Edwards Lifesciences, Irvine, CA) was used in 9 patients, and semicircular posterior annuloplasty was performed in 67 patients. All patients underwent modified De Vega tricuspid annuloplasty. The correlation test between body surface area and mitral annulus area by two-dimensional multiplane transesophageal echocardiography in normal, healthy adults helped us to determine the dimension to which the mitral annulus area should be reduced (Fig 1). Carpentier valve gauges (Edwards Lifesciences, Irvine, CA) for mitral and tricuspid orifice measurements were routinely used to control the size of reduction at the end of the procedure.



View larger version (12K):
[in this window]
[in a new window]
  		Fig 1. Relationship (correlation test) between body surface area (BSA) and mitral annulus area (MAA). Mitral annulus area measurements were performed by two-dimensional multiplane transesophageal echocardiography in normal, healthy adults. (n = 15 patients; r = 0.847; p < 0.001; MAA = 0.59 + 2.9 x BSA.)

 
The mean aortic cross-clamp time was 40 minutes (range, 24 to 68 minutes) and the mean time of extracorporeal circulation (ECC) was 48 minutes (range, 33 to 78 minutes).

Continuous hemodynamic monitoring by flow-directed pulmonary catheter allowed the measurement of cardiac output, cardiac index, central venous pressure, mean pulmonary artery pressure, pulmonary capillary wedge pressure and pulmonary vascular resistance. Measurements of these variables began immediately after anesthetic induction, and were continued during the next 24 to 48 hours postoperatively. Left ventricular size, systolic function and results of mitral and tricuspid repair were analyzed by transesophageal echocardiography. Transesophageal echocardiography was performed using Toshiba SSH-140-A device and Omniplane 5.0 mHz sonde (Toshiba Medical Systems Co, Ltd, Tokyo, Japan), before and after ECC.

All patients were regularly contacted by telephone, and all exams were done in the University Clinic of Cardiovascular Surgery, Sremska Kamenica-Novi Sad.

Mitral annulus area was calculated according to the Goldberg formula: {pi}/4 (mitral valve annulus diameter2). Mitral valve area (MVA) was calculated according to Doppler pressure half-time method. Meridian wall stress (WALLS) was calculated using Laplace’s law according to a simplified Laplace formula P (R/Th), in which P is systolic pressure, R is radius of left ventricle, and Th is left ventricular wall thickness.

All data are presented as mean ± standard deviation. Statistical analysis was performed by Student’s t test, and survival analysis was performed by the Kaplan-Meier method. A value of p less than 0.05 was considered significant.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 Acknowledgments
 References
 
Immediate postoperative results
The mean preoperative EF, evaluated by echocardiography and left ventriculography, was 23.1% ± 5.2%. There were 32 patients (42.2%) with EF less than 20%. The majority of patients (76.3%) had fourth degree mitral regurgitation and third degree tricuspid regurgitation (Table 1). Mean mitral annulus area was reduced from 8.8 cm2 to 5.0 cm2, without any significant increase of postoperative transmitral gradient.


View this table:
[in this window]
[in a new window]
  		Table 1. Preoperative Transthoracal Doppler Echocardiography

 
The mean preoperative cardiac output was 3.7 L per minute (2.1 to 6), and the mean cardiac index was 1.9 L per minute/m2 (1.2 to 3). Other preoperative hemodynamic data are summarized in Table 2. One patient died on postoperative day 8 because of a cerebrovascular accident, and the total postoperative 30-day mortality was 1.3% (1 patient). There were no major immediate postoperative complications. There were no wound infections, and all patients have remained in their preoperative cardiac rhythm.


View this table:
[in this window]
[in a new window]
  		Table 2. Hemodynamic Data

 
Significant improvements in hemodynamic variables and elimination of mitral and tricuspid regurgitation were observed in the early postoperative period after RADO (Table 3). Cardiac output increased immediately after ECC from 3.7 ± 2.1 to 7.3 ± 1.7 L per minute, and this persisted during the complete observation period. Cardiac index similarly increased from 2.0 ± 0.6 before ECC to 4.0 ± 0.6 L per minute, and was stable at a mean value of 3.4 ± 0.7 L per minute after 48 hours. All other hemodynamic variables (central venous pressure, mean pulmonary artery pressure, pulmonary capillary wedge pressure, and pulmonary vascular resistance) showed significant improvement during the first 48 hours after ECC compared with the preoperative values (Table 2).


View this table:
[in this window]
[in a new window]
  		Table 3. Echocardiographic Parameters Before and After Operation

 
Mitral and tricuspid regurgitation were both significantly reduced from averages of 3.7 ± 0.4 to 0.7 ± 0.3 and 3.4 ± 0.4 to 0.9 ± 0.2, respectively. Changes in other variables obtained by echocardiography are presented in Table 3. Medical treatment in the postoperative period consisted of inotropic stimulation with adrenaline and dopamine, or both, nitroglycerine, prostaglandin (PGI2), digoxin, and diuretics. Average length of hospitalization after the operation was 33 days (range, 13 to 35 days) versus 119 days (range, 15 to 127 days) before the operation.

Follow-up study
The closing date of the follow-up study was May 1, 1998. The follow-up study was achieved at a rate of 100%. The average time of follow-up was 20 months (1 to 83 months). All patients reported significant clinical improvements, especially regarding dyspnea. The mean New York Heart Association class of the patients before operation was 3.6, which changed to 1.9 during the mean follow-up period. Mean EF was increased from 26% preoperatively to 34% postoperatively, and remained stable during the following year at the rate of 36%. All patients were discharged with long-term therapy including digoxin, diuretics, antiarrhythmics, and angiotensin-converting enzyme inhibitors. The daily doses of medications were significantly reduced compared with the preoperative values. The digoxin dose was reduced from a mean of 0.49 ± 0.05 mg per day to 0.24 ± 0.03 mg per day, and the furosemide dose was reduced from a mean of 416 ± 17 mg per day to 74 ± 9 mg per day.

Survival rate at 3 and 7 years after operation was 48.7% and 38.15%, respectively (Fig 2). There was no indication for pacemaker implantation during the follow-up study. Freedom from decompensation at 3 years decreased to 52.63% ± 7.0% and was maintained at the same level during the following 7 years (Fig 3). The major causes of late mortality were cardiac failure (72.36%), rhythm disturbances (19.73%), and other noncardiac causes (7.91%).



View larger version (13K):
[in this window]
[in a new window]
  		Fig 2. Survival rate in patients with primary dilated cardiomyopathy after reductive annuloplasty of double orifices procedure. The straight lines represent cumulative survival rate, and the dashed lines represent confidence limits equivalent to one standard error (± SE) of cumulative survival rate. (N = the number of patients at risk at each time point.) Mean follow up was 20 months (range, 1 to 83 months). The follow up rate was 100% (n = 76 patients).

 


View larger version (14K):
[in this window]
[in a new window]
  		Fig 3. Decompensation free rate in patients with primary dilated cardiomyopathy after reductive annuloplasty of double orifices procedure. The straight lines represent cumulative decompensation free rate, and the dashed lines represent confidence limits equivalent to one standard error (± SE). (N = the number of patients at risk at each time point.) Mean follow up was 20 months (1 to 83 months). The follow up rate was 100% (n = 76 patients).

 

   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
Acknowledgments
 References
 
The importance of mitral valve regurgitation in chronic PCDM has been underestimated for years. In many institutions, patients with cardiomyopathy, severe mitral regurgitation, and reduced left ventricular function (EF <= 30%) are not usually considered for mitral valve operation. However, low biventricular systolic function, presence of significant mitral and tricuspid insufficiency, and increased sphericity of the heart (diameter/length) are usually accepted as predictors of the poor outcome [8]. Our experience in the surgical treatment of IsDCM helped us not only to understand the importance of the mitral valve insufficiency, but also to recognize significant differences between IsDCM and PDCM. Similarity of structural remodeling of the left ventricle in IsDCM and PDCM can explain the similar decrease in EF and increase in end-diastolic volume observed. These two conditions contribute to lengthening of myocytes, myocyte hypertrophy, cell dropout, slippage of muscle bundles and alteration in cardiac interstitium [12]. Gerdes and associates [13] reported in 1995 that there were no differences in cellular dimensions (shape and length of individual myocites), between IsDCM and PDCM. Aside from similarities at the cellular level, IsDCM and PDCM are two very different diseases and should be evaluated separately.

According to Borer and colleagues [14], mitral regurgitation is a disease of both ventricles. Left ventricular failure usually starts first, causing enlargement and remodeling of the left ventricle. A very important part of this process is remodeling of the sulcal connective tissue and fibrous skeleton of the heart. The mitral valve annulus becomes so dilated that mitral leaflets can no longer be effective in coaptation, and mitral insufficiency occurs [3, 15]. Prolonged mitral valve regurgitation causes pulmonary hypertension followed by right ventricle dilation [12]. Further progression of the PDCM is a direct cause of global heart insufficiency, which is responsible for frequent episodes of cardiac decompensation.

From analyzing recent publications [15–18] concerning Batista’s [6] operation (partial left ventriculectomy), we found the best results in a group of patients in which mitral valve repair was combined with partial left ventriculectomy. This indicates that the reduction of mitral annulus is of significant importance for improvement of left ventricular function. Bolling and associates [15] describe mitral annuloplasty as a "slow auto-remodeling of left ventricle" contrasting this procedure to the more "acute Batista remodeling."

This short review of the pathophysiology of PDCM emphasizes the significance not only of mitral annulus diameter, but also of tricuspid annulus diameter as well. According to our experience, tricuspid annuloplasty is a mandatory procedure for patients with PDCM.

Recent publications about the natural evolution of PDCM and life expectancy for patients in end-stage PDCM recommend early and aggressive treatment of PDCM because of the high risk of poor early outcome [2, 11]. At the beginning of our work we were of the opinion that only early elimination of mitral and tricuspid regurgitation could improve the function of the heart. Mitral annulus area reduction is of essential importance in this operation. Its goal is not merely the elimination of mitral regurgitation, but also the change of left ventricular geometry. We consider that severe remodeling of the left ventricle with dilation of the mitral annulus area larger than 7 cm2 is an independent factor causing heart failure.

Limitations of this study might include the lack of a control group and the lack of volunteers for control catheterization to be obtained at least 6 months after the operation. These important measurements could be important in the assessment of mitral valve competence and left ventricular function. However, both of these limitations are very difficult to overcome and they are usually present in this type of investigation.

According to our results, the RADO in patients with primary dilated cardiomyopathy resulted in significant hemodynamic and clinical improvement in patients with end-stage heart failure. This procedure was safe with low perioperative risk. In our series of 76 patients, 30-day postoperative mortality was 1.3% (1 patient), and is significantly lower compared with the alternative surgical options [6, 16, 18, 19]. All variables of the left ventricular function based on hemodynamic and transesophageal echocardiography studies showed significant improvement. We are even more enthusiastic about the results combined with the follow-up study. Survival rates at 3 and 7 years after RADO were 48.7% and 38.15%, respectively, which correlates with some other recently published data [20]. Freedom from decompensation (52.63% ± 7.0% after 7 years), and significant decrease of medication postoperatively encourage us to continue with this approach. However, further investigation should be done to analyze social and economic impact, and quality of life after RADO procedure.

Our data demonstrate that RADO eliminates mitral and tricuspid regurgitation, changes sphericity of the left ventricle, reverses remodeling of the left ventricle, improves hemodynamic action of the left and right ventricle, slows down the progression of myocardial insufficiency, and prolongs life. We propose RADO before or just after the first episode of decompensation. Reductive annuloplasty of double (mitral and tricuspid) orifices may serve as a bridge to heart transplantation, but in the patients in which cardiac transplantation is impossible, we believe that RADO is a new strategy and the best alternative.


   Acknowledgments
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
References
 
This work was supported by funds from the University Clinic of Cardiovascular Surgery Sremska Kamenica-Novi Sad, Yugoslavia. Dr ivojin S. Jonjev thanks the Department of Physiology and Biophysics at the University of Illinois at Chicago, Chicago, Illinois, and especially the staff at the laboratory of Professor William R. Law, PhD, for their assistance in preparing this article.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Richardson P., McKenna W., Bristow M., et al. Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the Definition and Classification of Cardiomyopathies. Circulation 1996;93:841-842.[Free Full Text]
  2. Kao W., Surjancev B.P. Management of acute heart failure exacerbation. Crit Care Clin 2001;17:321-335.[Medline]
  3. Starling R.C., Young J.B. Surgical therapy for dilated cardiomyopathy. Card Clin 1998;16:727-737.
  4. Kamp D., Castello R., Jennison S. Mitral regurgitation by echocardiography predicts 18 months survival in dilated cardiomyopathy. J Am Coll Cardiol 1995:841-844.
  5. Mordeira L.F., Stolf N.A., Bocchi E.A. Latissimus dorsi cardiomyoplasty in the treatment of patients with dilated cardiomyopathy. Circulation 1990;82:IV257-IV263.
  6. Batista R.J.V., Santos J.L.V., Takeshita N. Ventriculectomy to improve left ventricular function in end-stage heart disease. J Card Surg 1996;11:97.
  7. Bolling S.F., Deeb M., Brunsting A.L. Early outcome of mitral valve reconstruction in patients with end-stage cardiomyopathy. J Thorac Cardiovasc Surg 1995;109:676-682.[Abstract/Free Full Text]
  8. Juilliere Y., Danchin N., Briancon S., et al. Dilated cardiomyopathy: long-term follow-up and predictors of survival. Int J Cardiol 1988;21:269-277.[Medline]
  9. Kameda Y., Kitamura S., Kawachi K., Kawata T. Annuloplasty for severe mitral regurgitation due to dilated cardiomyopathy. Ann Thorac Surg 1996;61:1829-1832.[Abstract/Free Full Text]
  10. Bach S.D., Armstrong F.W., Bolling S.F. Early improvement in congestive heart failure following correction of secondary mitral regurgitation in end-stage cardiomyopathy. J Am Coll Cardiol 1995:901-975.
  11. Rockville M.D., Richmond V.A. 2000 Annual Report of the U.S. Scientific Registry of Transplant Recipients and the Organ Procurement and Transplantation Network: Transplant Data 1990–1999.
  12. Francis G.S., McDonald K., Chu C., Cohn J.N. Pathophysiologic aspects of end-stage heart failure. Am J Cardiol 1995;75:11A-16A.[Medline]
  13. Gerdes A.M., Kellerman S.E., Shocken D.D. Implications of cardiomyocyte remodeling in heart dysfunction. Philadelphia: Lippincott-Raven, 1995:197-206.
  14. Borer J.S., Hochreiter C., Rosen S. Right ventricular function in severe non-ischaemic mitral insufficiency. Eur Heart J 1991;12:22-25.
  15. Bolling S.F., Pagani F.D., Deeb G.M., Bach S.D. Intermediate-term outcome of mitral reconstruction in cardiomyopathy. J Thorac Cardiovasc Surg 1998;115:381-386.[Abstract/Free Full Text]
  16. Batista R.J.V. Partial left ventriculectomy to treat end-stage heart disease. Ann Thorac Surg 1997;64:634-638.[Abstract/Free Full Text]
  17. McCarthy P.M., Starling R.C., Wong J. Early results with partial left ventriculectomy. J Thorac Cardiovasc Surg 1997;114:755-763.[Abstract/Free Full Text]
  18. Suma H., Isomura T., Horii T. Early result of volume reduction left ventriculoplasty (Batista operation) for dilated cardiomyopathy. J Cardiol 1998;31:83-90.[Medline]
  19. Bridges C.R., Bogen D. The Batista procedure. Theoretical analysis and clinical implications. J Cardiovasc Surg 2001;42:175-185.[Medline]
  20. Bolling S.F. Mitral valve reconstruction in the patient with heart failure. Heart Fail Rev 2001;6:177-185.[Medline]



This article has been cited by other articles:


Home page
 Card Surg AdultHome page
M. T. Spoor and S. F. Bolling
Nontransplant Surgical Options for Heart Failure
Card. Surg. Adult, January 1, 2008; 3(2008): 1639 - 1648.
[Full Text]

Home page
 Eur Heart JHome page
M. Di Mauro, A. M. Calafiore, M. Penco, S. Romano, G. Di Giammarco, and S. Gallina
Mitral valve repair for dilated cardiomyopathy: predictive role of right ventricular dysfunction
Eur. Heart J., October 2, 2007; 28(20): 2510 - 2516.
[Abstract] [Full Text] [PDF]

Home page
 Asian Cardiovasc. Thorac. Ann.Home page
P. Fundaro, P. M Tartara, E. Villa, P. Fratto, S. Campisi, and E. O Vitali
Mitral Valve Repair: Is There Still a Place for Suture Annuloplasty?
Asian Cardiovasc Thorac Ann, August 1, 2007; 15(4): 351 - 358.
[Abstract] [Full Text] [PDF]

Home page
 MMCTSHome page
A. M. Calafiore, M. Di Mauro, M. Contini, L. Weltert, and A. Bivona
Mitral valve repair in ischemic mitral regurgitation
MMCTS, March 24, 2005; 2005(0324): 521.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
F. A. Tibayan, F. Rodriguez, F. Langer, D. Liang, G. T. Daughters, N. B. Ingels Jr, and D. C. Miller
Undersized Mitral Annuloplasty Alters Left Ventricular Shape During Acute Ischemic Mitral Regurgitation
Circulation, September 14, 2004; 110(11_suppl_1): II-98 - II-102.
[Abstract] [Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
A. M. Calafiore, M. Di Mauro, S. Gallina, G. Di Giammarco, A. L. Iaco, G. Teodori, and I. Tavarozzi
Mitral valve surgery for chronic ischemic mitral regurgitation
Ann. Thorac. Surg., June 1, 2004; 77(6): 1989 - 1997.
[Abstract] [Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
P. Fundaro, M. Pocar, A. Moneta, F. Donatelli, and A. Grossi
Posterior mitral valve restoration for ischemic regurgitation
Ann. Thorac. Surg., February 1, 2004; 77(2): 729 - 730.
[Abstract] [Full Text] [PDF]

Home page
 J. Thorac. Cardiovasc. Surg.Home page
A. Kollar, V. Kekesi, P. Soos, and A. Juhasz-Nagy
Left ventricular external subannular plication: an indirect off-pump mitral annuloplasty method in a canine model
J. Thorac. Cardiovasc. Surg., October 1, 2003; 126(4): 977 - 982.
[Abstract] [Full Text] [PDF]

Home page
 Card Surg AdultHome page
V. Badhwar and S. F. Bolling
Nontransplant Surgical Options for Heart Failure
Card. Surg. Adult, January 1, 2003; 2(2003): 1515 - 1526.
[Full Text]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Radovanovic, N.
Right arrow Articles by Jonjev, Z. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Radovanovic, N.
Right arrow Articles by Jonjev, Z. S.
Related Collections
Right arrow Lung - cancer

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS