|
|
||||||||
J Thorac Cardiovasc Surg 1996;111:211-217
© 1996 Mosby, Inc.
SURGERY FOR ACQUIRED HEART DISEASE |
Santander, Spain
From the Department of Cardiovascular Surgery, Hospital Universitario Valdecilla, Universidad de Cantabria, Santander, Spain.
Received for publication Nov. 28, 1994. Accepted for publication Feb. 9, 1995. Address for reprints: José M. Bernal, MD, Department of Cardiovascular Surgery, Hospital Universitario Valdecilla, 39008 Santander, Spain.
Abstract
Sixty-two patients with rheumatic mitral valve disease (mean age 42.2 ± 10.2 years) underwent repair of chordae tendineae between June 1974 and May 1994. Chordal shortening was done in 38 patients, fenestration in 17, resection of secondary chordae in 3, replacement in 2, and transposition in 2. In 41 patients, mitral commissurotomy was also done. Ring annuloplasty was done in all patients. The mean follow-up was 10.2 years (range 2 months to 20 years). The completeness of follow-up during the closing interval (January to July 1994) was 100%. Hospital mortality occurred in four patients (6.5%) and nine patients died during the late follow-up. The actuarial survival curve at 20 years was 65.8% ± 10%. Six patients with mitral valve dysfunction (restenosis 4, insufficiency 2) and one with aortic valve dysfunction (structural deterioration of bioprosthesis) underwent reoperation. The actuarial curve of freedom from reoperation at 20 years for mitral valve dysfunction was 73.1% ± 10.5%. In the 49 surviving patients, a Doppler echographic study during the closing interval showed a mean mitral valve area of 1.9 ± 0.3 cm2. In the 43 patients with a repaired native valve, absent or trivial mitral regurgitation was documented in 35 and mild or moderate regurgitation in 8. In conclusion, repair of chordae tendineae in rheumatic mitral valve disease when feasible is a stable and safe procedure with a low prevalence of reoperation. However, the type of reconstructive operation and experience of the surgical team are major considerations in successful repair of the mitral valve. (J THORAC CARDIOVASC SURG 1996;111:211-7)
Although mitral valve reconstruction has been shown to provide better results than valve replacement,
1-3 there is a paucity of proper comparisons as to the long-term stability of the results obtained with different reparative operations. Technical difficulties in the repair of the subvalvular apparatus and the limited experience with this type of complex operation have been major impediments to the widespread repair, rather than replacement, of the incompetent mitral valve. On the other hand, most of the reports tend to describe the results of repair in a mixed population with different causes of the valve disease.
4,5 This report retrospectively analyzes the results obtained in a 20-year period in patients with rheumatic valvular disease who underwent repair of chordae tendineae.
Patients and methods
Between June 1974 and May 1994, 354 patients with rheumatic mitral valve disease, excluding those with pure mitral stenosis treated by isolated open mitral commissurotomy, papillary muscle split, or both, underwent an operation for mitral valve reconstruction with a ring annuloplasty at our institution. Repair of chordae tendineae in association with mitral valve annuloplasty was done in 62 (17.5%) of 354 patients. The patient selection criteria were based exclusively on intraoperative findings and feasibility of repairing the subvalvular apparatus. Data in these 62 patients constitute the basis for this report.
There were 14 men and 48 women with a mean age of 42.2 ± 10.2 years (range 18 to 73 years). At the time of operation, 19 (30.6%) patients were in New York Heart Association functional class II, 34 (54.8%) in class III, and 9 (14.5%) in class IV. Before operation, 14 (22.6%) patients were in sinus rhythm and 48 (77.4%) in atrial fibrillation. Forty-two (67.7%) patients had an isolated mitral valve lesion, 17 (27.4%) an associated tricuspid valve lesion, 1 (1.6%) an associated aortic valve lesion, and 2 (3.2%) triple valve disease.
The mitral valve disease consisted of combined stenosis and insufficiency in 25 (40.3%) patients and mixed lesions with predominant insufficiency in 37 (59.7%). Preoperative evaluation included cardiac catheterization in 30 (48.4%) patients, echocardiography in 15 (24.2%), or both in 17 (27.4%). In 47 patients mean systolic pulmonary artery pressure was 41.4 ± 12.1 mm Hg and mean mitral transvalvular gradient was 8.4 ± 5.3 mm Hg.
Intraoperative testing of mitral valve competence and surgical procedures used for valve repair have already been described,
6-9 and recently the use of transesophageal Doppler echocardiographic study has been reported. Mitral valve findings are described in
Table I. The mitral anulus was found to be dilated in 41.9% of patients, the mitral leaflets were affected in 61.3% of patients, and the commissures were fused in 48.4% of patients. Rheumatic lesions of chordae tendineae were found in all patients. These involved marginal chordae in 59 (95.2%) patients and medial (secondary) chordae in the remaining 3 (4.8%). Chordal elongation was present in 61.3% of cases, severe fusion in 30.6%, and rupture in 8.1%.
|
|
Follow-up of all surviving patients was done at regular intervals of 3, 6, and 12 months after operation and then annually. Follow-up was completed from January to July 1994. The completeness of follow-up during the closing interval was 100%. All patients were seen at our outpatient clinic and had a Doppler echographic study during the closing interval. The mean follow-up was 10.2 years, with a range from 2 months to 20 years.
The values are expressed as means of the average and standard deviation. The
2 test was used to analyze the significance between variables. Actuarial curves were obtained by the life-table method.
Results
Hospital mortality occurred in four (6.4%) patients. The causes of death were heart failure in two patients and massive hemorrhage in two. Hospital mortality for patients undergoing isolated mitral valve operation was 4.8% (2/42) and for patients having polyvalvular operations 10% (2/20) (p = not significant).
Of the 58 surviving patients, nine died during the late follow-up (15.5%). The causes of death were heart failure in three patients, thromboembolism in one, noncardiac death in one, and unknown in four. The actuarial survival curve at 20 years was 65.8% ± 10% (Fig. 1). For the group of 42 patients who underwent isolated mitral valve repair, the actuarial survival curve at 20 years was 75.3% ± 13.3%, whereas for the 20 patients who had polyvalvular operation it was 52.1% ± 18.6% (p = not significant) (Fig. 2).
|
|
|
|
|
Discussion
Although data from different reports have confirmed the predictability and stability of the results achieved with reconstructive procedures of the mitral valve,
1,11,12 repair of chordae tendineae is done occasionally and only by some surgical teams. In most patients, valve replacement continues to be a widely accepted approach for rheumatic disease because of inadequacy of the valve anatomy to be repaired. Repair of chordae tendineae is conditioned by the limited surgical experience, the variety of operations used, and the lack of terminology to classify both subvalvular abnormalities and types of valvular procedures, as well as by the absence of long-term results with this kind of complex operation.
On the other hand, conservative surgery of the mitral valve often implies repair of the leaflets, the anulus, and each structure of the subvalvular apparatus. In our study, an average of 2.7 procedures per patient was required to complete valve reconstruction successfully. The presence of abnormalities of the chordae is frequently a major impediment to the repair of incompetent mitral valves by means of mitral valve annuloplasty alone.
Although different attempts to repair chordae tendineae have been made in the United States as early as 1960,
13,14 chordal repair was eventually abandoned as a result of its unpredictable efficacy. The principles of mitral valve repair introduced by Carpentier and coworkers
15,16 renewed interest in mitral valve reconstruction and encouraged various European and North American groups to use conservative operations regularly.
1,17-21 Newer techniques were evolved and others were used with indications different from those originally intended.
Mitral valve repair in rheumatic mitral valve disease is technically more difficult and less stable than repair in ischemic and degenerative lesions because of the progressive nature of the pathologic condition and the type of patient population affected.
4,22,23 This confirms the importance of reporting the results in patients with a homogeneous cause of the disease.
24-26
Although our study, like others,
24,25 has shown the necessity to repair the subvalvular apparatus in most patients with rheumatic heart disease, the degree and extent of chordal involvement are primary determinants of the likelihood of successful repair. Leaflet retraction is a most common finding in rheumatic mitral valve disease that frequently represents a major impediment for mitral valve repair. In our experience, only four patients with mild leaflet retraction were successfully treated by means of ring annuloplasty to increase leaflet coaptation. Chordal elongation, a less common finding in these patients, is more suitable for repair. Intraoperative two-dimensional and Doppler echocardiography done before cardiac operations provides a reliable assessment of the feasibility of valve repair versus replacement.
27 However, partial homograft replacement of the mitral valve is an alternative for patients with extensive rupture or elongation of marginal chordae, commissural involvement, and anterior leaflet disease that cannot be repaired by standard techniques.
28,29
Advanced morphologic changes in the subvalvular apparatus, progression of native valve disease, and lack of experience have been considered important risk factors for failed mitral valve repair.
4,23,30 One of the arguments against this kind of operation is that chordal repair is time consuming and results in a much longer ischemic time and significantly higher hospital mortality than straight replacement. In the present study, however, the hospital mortality rate was lower than that for mitral valve replacement.
31Long-term survival at 20 years has been lower in patients with polyvalvular disease than in patients with isolated mitral valve lesions (52.1% ± 18.6% versus 75.3% ± 13.3%).
Thromboembolism has been the most common late postoperative complication in this group of patients. However, given that a substantial number of patients had polyvalvular disease with a high rate of preoperative risk factors, such as atrial fibrillation, giant left atrium, previous thromboembolism, and left atrial thrombosis, the prevalence of postoperative thromboembolic events has not been higher than that reported for bioprosthetic valve replacement.
31
Only seven patients in this series underwent reoperation because of mitral valve dysfunction. When valve insufficiency was the cause of failure, reoperation was done early in comparison with the timing of reoperation for restenosis (51 ± 33.7 months versus 194 ± 33.2 months). These findings may indicate that in most cases residual insufficiency is a result of incorrect indication for repair, technical errors, or incomplete repair causing early valvular incompetence. Restenosis of the repaired mitral valve is usually a result of progression of rheumatic disease. A Doppler echographic study done during the closing interval showed, in 81.4% of patients, a normal functioning mitral valve, a mean valvular area of 1.9 ± 0.3 cm2, and no evidence of valve incompetence.
In conclusion, repair of chordae tendineae in unselected patients with rheumatic mitral valve disease when feasible has been shown to be a stable and safe procedure with acceptable long-term results, in particular with regard to a low prevalence of reoperation. There are, however, insufficient data about the long-term results of this procedure in young populations with rheumatic disease. The type of reconstructive operation and experience of the surgical team are major considerations in the successful repair of the mitral valve.
We are indebted to Carlos G. Durán, MD, for his valuable active surgical participation in the early series of patients. We thank Mrs. Charo Sánchez for secretarial help and Marta Pulido, MD, for editing the manuscript and editorial assistance.
References
This article has been cited by other articles:
![]() |
J. M. Bernal, A. Ponton, B. Diaz, J. Llorca, I. Garcia, A. Sarralde, C. Diago, and J. M. Revuelta Surgery for rheumatic tricuspid valve disease: a 30-year experience. J. Thorac. Cardiovasc. Surg., August 1, 2008; 136(2): 476 - 481. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. M. Bernal, J. Gutierrez-Morlote, J. Llorca, J. M. San Jose, D. Morales, and J. M. Revuelta Tricuspid Valve Repair: An Old Disease, a Modern Experience Ann. Thorac. Surg., December 1, 2004; 78(6): 2069 - 2074. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. A. Timek, S. L. Nielsen, G. R. Green, P. Dagum, A. F. Bolger, G. T. Daughters, J. M. Hasenkam, N. B. Ingels Jr, and D. C. Miller Influence of anterior mitral leaflet second-order chordae on leaflet dynamics and valve competence Ann. Thorac. Surg., August 1, 2001; 72(2): 535 - 540. [Abstract] [Full Text] [PDF] |
||||
![]() |
C.-K. Ng, C. Punzengruber, O. Pachinger, J. Nesser, H. Auer, H. Franke, and P. Hartl Valve repair in mitral regurgitation complicated by severe annulus calcification Ann. Thorac. Surg., July 1, 2000; 70(1): 53 - 58. [Abstract] [Full Text] [PDF] |
||||
![]() |
F. Gregori Jr, C. O. Cordeiro, U. A. Croti, S. S. Hayashi, S. S. da Silva, and T. E.F. Gregori Partial tricuspid valve transfer for repair of mitral insufficiency due to ruptured chordae tendineae Ann. Thorac. Surg., November 1, 1999; 68(5): 1686 - 1690. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. M. Bernal, M. Fernandez-Vals, J. M. Rabasa, F. Gutierrez-Garcia, C. Morales, and J. M. Revuelta Repair of nonsevere rheumatic aortic valve disease during other valvular procedures: Is it safe? J. Thorac. Cardiovasc. Surg., May 1, 1998; 115(5): 1130 - 1135. [Abstract] [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| 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 |