JTCS Speed Up Your Browser
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 Author home page(s):
José M. Bernal
José M. Revuelta
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 Bernal, J. M.
Right arrow Articles by Revuelta, J. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bernal, J. M.
Right arrow Articles by Revuelta, J. M.

J Thorac Cardiovasc Surg 1998;115:1130-1135
© 1998 Mosby, Inc.

SURGERY FOR ACQUIRED HEART DISEASE

Repair of nonsevere rheumatic aortic valve disease during other valvular procedures: Is it safe?

José M. Bernal, MD, Mónica Fernández-Vals, MD, José M. Rabasa, MD, Francisco Gutiérrez-García, MD, Carlos Morales, MD, José M. Revuelta, MD

From the Department of Cardiovascular Surgery, Hospital Universitario Valdecilla, Universidad de Cantabria, Santander, Spain.

Received for publication April 17, 1997. Revisions requested June 18, 1997; revisions received Dec. 8, 1997. Accepted for publication Dec. 9, 1997. Address for reprints: José M. Bernal, MD, Department of Cardiovascular Surgery, Hospital Universitario Valdecilla, E-39008 Santander, Spain.

Abstract

Objective: To investigate the long-term performance of aortic valve repair, we analyzed the results obtained in a 22-year period in patients who underwent repair of nonsevere rheumatic aortic valve disease during other valvular procedures.
Methods: Fifty-three patients (mean 40 ± 11.6 years of age) with predominant rheumatic mitral valve disease had concomitant aortic valve disease in association with serious tricuspid valve disease in 25 of them. Preoperatively, aortic valve disease was considered moderate in 47.2% of the patients and mild in 52.8%. All patients underwent reparative techniques of the aortic valve (free edge unrolling, 44; subcommissural annuloplasty, 40; commissurotomy, 36) at the time of mitral or mitrotricuspid valve surgery. The completeness of follow-up during the closing interval was 100%, with a mean follow-up of 18.8 years (range 8 to 22.5 years).
Results: Hospital mortality rate was 7.5%. Of 49 surviving patients, 26 (53.1%) died during late follow-up. The actuarial survival curve including hospital mortality was 35.4% ± 8.7% at 22 years. For patients who underwent mitral and aortic valve surgery, the actuarial survival curve at 22 years was 32.3% ± 13%, whereas for patients who had a triple-valve operation the survival was 37.0% ± 10.1% (p = 0.07). Twenty-five patients underwent an aortic prosthetic valve replacement. Actuarial free from aortic structural deterioration and valve-related complications at 22 years was 25.3% ± 9.3% and 12.7% ± 4.8%, respectively.
Conclusions: Long-term functional results of reparative procedures of nonsevere aortic valve disease in patients with predominant rheumatic mitral valve disease have been inadequate at 22 years of follow-up. According to these data, conservative operations for rheumatic aortic valve disease do not seem appropriate.

Reconstructive surgery for aortic valve disease is an attractive idea in the light of the excellent long-term results of mitral and tricuspid valve repair.Go Go 1-3 Under a historical perspective, aortic surgery started with conservative procedures that fell into disuse when reliable valve prostheses became available. Aortic valve repair has recently elicited a renewed interest as a result of encouraging data published in the past few years.Go Go 4-6 The lack of long-term results, however, limits the same level of general application witnessed for prosthetic valve replacement.

To investigate the long-term performance of aortic valve repair, this report retrospectively analyzes the results obtained in a 22-year period in patients with nonsevere aortic valve disease and predominant mitral valve disease of a rheumatic cause, who underwent classical reparative techniques of the aortic valve at the time of mitral valve operation.

Materials and methods

Between June 1974 and December 1988, 53 patients with rheumatic mitral or mitrotricuspid valvulopathy in association with nonsevere aortic valve disease underwent concomitant two-valve or triple-valve operations. The study population was made up of 41 women (77.3%) and 12 men (22.6%), with a mean age of 40.8 ± 11.6 years (range 17 to 69 years). Two (3.8%) patients had a previous repair of the mitral, aortic, or both valves with cardiopulmonary bypass, and seven (13.2%) had a closed mitral commissurotomy. At the time of operation, 9 (17.1%) patients were in New York Heart Association functional class II, 40 (75.5%) in class III, and 4 (7.5%) in class IV. Cardiac rhythm was in atrial fibrillation in 32 (60.4%) patients and in sinus rhythm in the remaining 21 (39.6%) patients.

In all patients the diagnosis was based on results of cardiac hemodynamics. Mean left ventricular ejection fraction was 55.9% ± 9.4% (range 37% to 87%), mean cardiac index 2.4 ± 0.7 L/min/m2 (range 1.2 to 4.3 L/min/m2), mean systolic pulmonary artery pressure 42.9 ± 13 mm Hg (range 22 to 84 mm Hg), and mean pulmonary capillary pressure was 20.9 ± 6.2 mm Hg (range 8 to 35 mm Hg). The aortic valve disease consisted of pure stenosis in 8 (15.1%) patients, with a mean aortic valve gradient of 21.8 ± 15.2 mm Hg, mixed lesion in 10 (18.9%), and pure aortic insufficiency in 35 (66.1%). Aortic regurgitation was mild (grade I/III) in 24 (45.3%) patients and moderate (grade II/III) in 21 (39.6%) patients. Overall, 28 (52.8%) patients had a mild aortic valve disease, and the remaining 25 (47.2%) patients had a moderate aortic valve disease. In all patients, however, rheumatic mitral valve disease was the predominant lesion. Twenty-five (47.2%) patients had an associated serious tricuspid valve disease.

All operations were performed with standard cardiopulmonary bypass. Myocardial protection was achieved with systemic hypothermia to 25° C and local hypothermia with cold saline until 1977 and by cardioplegic arrest thereafter.

The aortic valve disease was initially evaluated through a J-shaped aortotomy incision. The mitral valve was repaired first followed by reconstruction of the aortic valve and tricuspid valve repair. The type of technique used for mitral and tricuspid valve repair is shown in Table I.


View this table:
[in this window]
[in a new window]
  		Table I. Operative techniques in 53 patients with rheumatic mitral and tricuspid valve disease
 
Mitral valve reparative procedures were done in 41 (77.3%) patients. In the 25 patients with associated tricuspid valve disease, reparative procedures were done in 24 (96%). Aortic valve findings are described in Table II, and reconstructive procedures for aortic valve disease are shown in Table III. The technique most frequently used was free edge unrolling followed by subcommissural annuloplasty and commissurotomy. An average of 2.4 reconstructive procedures per patient was required. The mean time of myocardial ischemia was 64.9 ± 16.3 minutes (range 43 to 140 minutes), and the mean time of cardiopulmonary bypass was 104.6 ± 27.7 minutes (range 49 to 175 minutes). Intraoperative testing was only made by direct observation of the repaired aortic valve.


View this table:
[in this window]
[in a new window]
  		Table II. Anatomic lesions in the aortic valve
 

View this table:
[in this window]
[in a new window]
  		Table III. Reconstructive procedures for aortic valve disease
 
All surviving patients were evaluated before discharge or during the first postoperative year by means of left cardiac catheterization, left ventriculography and aortography in 24 patients, and echocardiography in the remaining 25 patients. Surviving patients in atrial fibrillation were treated with acenocoumarol for 3 months or permanently in patients with a giant left atrium or massive atrial thrombus. All other patients received antiplatelet drugs for at least 3 months after operation. Thromboembolic prophylaxis was modified according to the patient's requirements during follow-up.

Follow-up of all surviving patients was done at regular intervals of 3, 6, and 12 months after operation and then annually. Salient information was stored in a database for outpatient clinical consultations of the Spanish Ministry of Health. Follow-up was completed from October to December 1996. All patients had a Doppler echocardiographic study during the closing interval. The completeness of follow-up during the closing interval was 100%, with a mean follow-up of 18.8 years (range 8 to 22.5 years). Cumulative duration of follow-up was 925.76 patient-years.

Actuarial curves were obtained by the life-table method.

Results

Hospital mortality occurred in four (7.5%) patients. The cause of death was heart failure in three patients and cerebrovascular accident in one. In the 49 surviving patients echocardiographic or hemodynamic assessment over the first 12 months after operation demonstrated a normal functioning aortic valve in 10 (20.4%) patients and mild residual lesions in 30 (61.2%) patients (regurgitation, 25; double lesion, 4; stenosis, 1). Moderate residual lesions were documented in nine (18.4%) patients (regurgitation, 5; double lesion, 4).

Of the 49 surviving patients, 26 (53.1%) died during the late follow-up. The causes of death were heart failure in 10 patients, reoperation in 5, prosthetic endocarditis in 2, noncardiac death in 3, and unknown in 6. The actuarial survival curve, including hospital mortality, was 35.4% ± 8.7% at 22 years (Fig. 1). For the subgroup of 28 patients who underwent mitral and aortic valve surgery, the actuarial survival curve at 22 years was 32.3% ± 13%, whereas for the 25 patients who had triple-valve operation it was 37.0% ± 10.1% (Fig. 2).



View larger version (20K):
[in this window]
[in a new window]
  		Fig. 1. Actuarial survival curve.

 


View larger version (27K):
[in this window]
[in a new window]
  		Fig. 2. Actuarial survival curve for patients undergoing mitral and aortic valve reconstructive procedures (top; M+A) and mitral, aortic, and tricuspid valve procedures (bottom; M+A+T) (p = 0.07).

 
Of the 49 surviving patients, 31 (63.3%) required a valve reoperation. The reoperation was necessary because of mitral valve dysfunction or structural deterioration of the mitral bioprosthesis in 30 patients (moderate lesions in 26.7% and severe in the remaining 73.3%), aortic valve dysfunction in 25, and tricuspid valve dysfunction in 10. Indications for operation included isolated mitral valve dysfunction in 6 patients, mitral and aortic valve dysfunction in 15, aortic and tricuspid valve dysfunction in 1, and triple valve dysfunction in 9. Predominant aortic stenosis was the cause of reoperation in 10 patients and predominant aortic regurgitation in the remaining 15. At the time of reoperation aortic valve lesions were considered mild in 3 patients, moderate in 7, and severe in 15. In the three patients with mild aortic valve lesion, prosthetic valve replacement was indicated to prevent a third operation because all 3 had a mitral valve replacement performed. In all aortic valve reoperations a prosthetic valve replacement was done. Hospital mortality for valve-related reoperation was 16.1% (5 of 31 patients). Fig. 3 shows survival free from structural deterioration of the mitral valve (21.3% ± 8.1%) and the aortic valve (25.3% ± 9.3%).



View larger version (27K):
[in this window]
[in a new window]
  		Fig. 3. Actuarial freedom from mitral or aortic structural deterioration.

 
Of the 10 patients with a normal functioning aortic valve after repair, 6 (60%) were reoperated. Reoperation was performed in 18 (60%) of the 30 patients with mild aortic valve lesions and in 7 (77.7%) of the 9 patients with moderate lesions. Actuarial curves of survival free from structural deterioration of the repaired aortic valve at 22 years was 20.0% ± 17.9% for patients with normal functioning valves, 33% ± 11.4% for those with mild aortic lesions, and 22.2% ± 13.9% for those with moderate residual lesions (Fig. 4). The comparison of patients without residual lesions with patients with mild aortic dysfunction did not reveal significant differences. However, statistically significant differences were found between patients without residual lesion and those with moderate valve dysfunction (p = 0.007), and between patients with mild versus moderate aortic dysfunction (p = 0.02).



View larger version (28K):
[in this window]
[in a new window]
  		Fig. 4. Actuarial freedom from aortic structural deterioration according to initial result of aortic valve repair; normal functioning valves versus moderate dysfunction (p = 0.007), mild versus moderate dysfunction (p = 0.02), and normal functioning versus mild dysfunction (p = not significant).

 
Of the 25 patients reoperated because of aortic structural deterioration, none had surgery within the first 2 postoperative years, four patients after 3 to 5 years, eight patients after 6 to 10 years, seven patients after 11 to 15 years, and the remaining six beyond 15 years. Actuarial freedom from structural deterioration of the aortic valve was 89.3% ± 4.5% at 5 years, 71.2% ± 6.8% at 10 years, 51.8% ± 8.0% at 15 years, and 25.3% ± 9.3% at 22 years (Fig. 3Go).

Twelve patients had a thromboembolic episode during the follow-up (six central with permanent neurologic impairment). The actuarial survival curve for freedom from thromboembolic events at 22 years was 65.9% ± 8.7% (Fig. 5). Survival free from valve-related complications at 22 years was 12.7% ± 4.8% (Fig. 5Go).



View larger version (25K):
[in this window]
[in a new window]
  		Fig. 5. Actuarial freedom from thromboembolism (top) and valve-related complications (bottom).

 
At the closing interval of follow-up, 9 (16.9%) of the 53 patients were alive and had the repaired native aortic valve. Eight of them were in New York Heart Association functional class I or II, and one in was in functional class III. Echocardiographic evaluation during the closing interval showed mild aortic valve disease in four patients and moderate to severe aortic valve disease in the remaining five patients who are pending candidates for cardiac operation.

Discussion

It is generally accepted that reconstructive operation for mitral valve disease offers better immediate and long-term results than prosthetic valve replacement,Go 1 even in patients with rheumatic heart disease.Go Go 2,3 Mitral valve reconstruction has become a routine procedure for many operative teams with satisfactory results. In contrast operative experience with reconstructive surgery of the aortic valve is limited. Although a number of authors have recently reported acceptable short-term results,Go Go 4-8 the long-term stability of aortic valve repair in terms of the future development of aortic regurgitation or stenosis is currently unpredictable.

A separate but related problem is whether aortic valve repair should be performed in patients referred for other cardiac operations who have associated aortic valve disease that is not severe enough to warrant valve replacement but may progress further in subsequent years, necessitating cardiac reoperation.Go Go 9-11 Although polyvalvular involvement is common in patients with rheumatic heart disease, the decreasing prevalence of the rheumatic cause has been an impediment to know the natural history of nonsevere aortic valve disease. On the other hand, results of two-valve operations are worse than isolated repair of the mitral valve. In this group of patients with mild to moderate aortic valve lesions operated on 8 to 22 years ago in whom mitral valve disease was predominantly repaired, a number of previously described techniquesGo 12 were used for reconstructive operation of the aortic valve. Immediate results were not as favorable as expected. These initial discouraging results may be explained by the method used to test aortic valve competence, directed observation, which is obviously less reliable than transesophageal echocardiography or visualization of the aortic valve before unclamping the aorta with an endoscopic instrument,Go 13 or by inadequacy of the techniques used for aortic repair to obtain a normal functioning valve. Interestingly, initial results (within a year of operation) of aortic valve operation have a predictive value over the next years in terms of the need for subsequent surgery. A significantly higher incidence of reoperation caused by aortic structural deterioration was found in repaired aortic valves with moderate residual lesions compared with normal functioning valves or valves with mild dysfunction.

With a completeness of follow-up during the closing interval of 100%, late mortality was high. This finding indicates the poor prognosis of patients with rheumatic heart disease and polyvalvular involvement as shown by a substantially better long-term survival in patients with two-valve operations than in those with triple-valve operations. The analysis of the actuarial survival curve showed a continuous mortality throughout the follow-up period, with a linearized rate of 3.0% patient-years exposed to death.

Because all patients underwent mitral valve repair or bioprosthetic valve replacement, there was a reasonable expected need to undergo reoperation in the future. Of the 49 surviving patients, 31 required a valve reoperation. In 25 of the 31 reoperated patients the repaired aortic valve was replaced by a prosthesis because of evidence of severe or moderate residual aortic valve disease (88%, 22 of 25). Survival free from valvular reoperation showed a linearized rate of 3.4% patient-years exposed to reoperation. The results obtained in relation to thromboembolism with a linearized incidence of 1.4% patient-years are noticeably worse than those expected in patients with rheumatic heart disease undergoing isolated mitral valve repair.Go Go 1,3

It should be noted that in the very long follow-up (at 22 years), 22 of the 41 patients who underwent mitral valve repair required reoperation because of structural deterioration of the repaired valve (48.9%), suggesting that valve repair procedures are not going to last forever even in the mitral position.

The idea of conservative operations for acquired aortic valve disease is very attractive, but caution should be exerted because ultrasonic debridement of the aortic valve,Go Go 14,15 with promising initial hemodynamic results, has recently been shown to be associated with early recurrence of severe and progressive aortic insufficiency. In our experience the surgical techniques used for aortic valve repair were not changed since the beginning of the study in 1974. Results at 20 years in this group of patients are inadequate given the high incidence of reoperations and valve-related complications. On the other hand, a lower incidence of structural deterioration of the aortic valve compared with replacement with the Hancock I porcine bioprosthesis was not achieved.Go 16 Operative management of nonsevere aortic valve lesions in young patients with a predominant mitral valve disease should be individualized, and, in our opinion, if an adequate mitral valve repair is achieved, an attitude toward ignoring the aortic lesion may be adopted, which, in turn, would initially decrease the risk of time-related valve complications.

Other authors, however, have recently introduced new aortic valve reparative proceduresGo Go Go Go 6,8,17-20 to repair nonrheumatic aortic valve lesions, including cusp extension with bovine pericardium,Go 18 triangular resection of the free edge of the prolapsing leaflet,Go 6 and aortic valve reimplantation inside a collagen-impregnated tubular Dacron graft for patients with aortic incompetence and aneurysm of the ascending aorta,Go 17 with encouraging short-term results, particularly in cases of predominant valve insufficiency.Go Go 6,19

In conclusion, early and long-term functional results of reparative procedures of nonsevere aortic valve disease in patients with predominant rheumatic mitral valve disease have been inadequate at 22 years of follow-up. According to these data, conservative operations for rheumatic aortic valve disease do not seem appropriate.

Acknowledgments

We are indebted to Marta Pulido, MD, for editing the manuscript and editorial assistance.

References

  1. Deloche A, Jebara VA, Relland JYM, et al. Valve repair with Carpentier techniques: the second decade. J Thorac Cardiovasc Surg 1990;99:990-1002.[Abstract]
  2. Bernal JM, Rabasa JM, Vilchez FG, Cagigas JC, Revuelta JM. Mitral valve repair in rheumatic disease. The flexible solution. Circulation 1993;88:1746-53.[Abstract/Free Full Text]
  3. Bernal JM, Rabasa JM, Olalla JJ, Carrión MF, Alonso A, Revuelta JM. Repair of chordae tendineae for rheumatic mitral valve disease: a twenty-year experience. J Thorac Cardiovasc Surg 1996;111:211-7.[Abstract/Free Full Text]
  4. Waller DA, Essop AR, Scott PJ, Nair RU. Repair of asymptomatic aortic valve disease during other cardiac surgery. Int J Cardiol 1992;36:309-14.[Medline]
  5. Duran C, Kumar N, Gometza B, Al Halees Z. Indications and limitations of aortic valve reconstruction. Ann Thorac Surg 1991;52:447-54.[Abstract]
  6. Cosgrove DM, Rosenkranz ER, Hendren WG, Bartlett JC, Stewart WJ. Valvuloplasty for aortic insufficiency. J Thorac Cardiovasc Surg 1991;102:571-7.[Abstract]
  7. Shapira N, Lemole GM, Fernandez J, et al. Aortic valve repair for aortic stenosis in adults. Ann Thorac Surg 1990;50:110-20.[Abstract]
  8. Okita Y, Miki S, Kusuhara K, et al. Long-term results of aortic valvuloplasty for aortic regurgitation associated with ventricular septal defect. J Thorac Cardiovasc Surg 1988;96:769-74.[Abstract]
  9. Chizner MA, Pearly DL, De Leon AC. The natural history of aortic stenosis in adults. Am Heart J 1980;99:419-24.[Medline]
  10. Cheitlin MD, Gertz EW, Brundage BH, Carlson CJ, Quash JA, Bode RS. Rate of progression of severity of valvular aortic stenosis in adults. Am Heart J 1979;98:689-700.[Medline]
  11. Wagner S, Selzer A. Patterns of progression of aortic stenosis: a longitudinal hemodynamic study. Circulation 1982;65:709-12.[Free Full Text]
  12. Duran CMG, Alonso J, Gaite L, et al. Long-term results of conservative repair of rheumatic aortic valve insufficiency. Eur J  Cardiothorac Surg 1988;2:217-23.[Abstract]
  13. Ghandour A, Al Halees Z, Duran C. A simple method for intraoperative visualization of the repaired aortic valve [letter]. J Thorac Cardiovasc Surg 1994;107:632-4.
  14. Cosgrove DM, Ratliff NB, Schaff HV, Edwards WD. Aortic valve decalcification: history repeated with a new results. Ann Thorac Surg 1990;49:689-90.[Medline]
  15. Craver JM. Aortic valve debridement by ultrasonic surgical aspirator: a word of caution. Ann Thorac Surg 1990;49:746-53.[Abstract]
  16. Bernal JM, Rabasa JM, Cagigas JC, Echevarria JR, Carrion MF, Revuelta JM. Valve-related complications with the Hancock I porcine bioprosthesis: a twelve- to fourteen-year follow-up study. J  Thorac Cardiovasc Surg 1991;101:871-80.[Abstract]
  17. David TE, Feindel CM. An aortic valve–sparing operation for patients with aortic incompetence and aneurysm of the ascending aorta. J Thorac Cardiovasc Surg 1992;103:617-22.[Abstract]
  18. Al Fagih MR, Al Kasab SM, Ashmeg A. Aortic valve repair using bovine pericardium for cusp extension. J Thorac Cardiovasc Surg 1988;96:760-4.[Abstract]
  19. Fraser CD Jr, Wang N, Mee RBB, et al. Repair of insufficient bicuspid aortic valves. Ann Thorac Surg 1994;58:386-90.[Abstract]
  20. Moidl R, Moritz A, Simon P, Kupilik N, Wolner E, Mohl W. Echocardiographic results after repair of incompetent bicuspid aortic valves. Ann Thorac Surg 1995;60:669-72.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 J. Thorac. Cardiovasc. Surg.Home page
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]

Home page
 Ann. Thorac. Surg.Home page
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]

Home page
 Ann. Thorac. Surg.Home page
N. Bozbuga, V. Erentug, K. Kirali, E. Akinci, O. Isik, and C. Yakut
Midterm results of aortic valve repair with the pericardial cusp extension technique in rheumatic valve disease
Ann. Thorac. Surg., April 1, 2004; 77(4): 1272 - 1276.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
S. Chauvaud, J.-F. Fuzellier, A. Berrebi, A. Deloche, J.-N. Fabiani, and A. Carpentier
Long-Term (29 Years) Results of Reconstructive Surgery in Rheumatic Mitral Valve Insufficiency
Circulation, September 18, 2001; 104 (2009): I-12 - I-15.
[Abstract] [Full Text] [PDF]

Home page
 Eur. J. Cardiothorac. Surg.Home page
Z. Al Halees, B. Gometza, A. Al Sanei, and C. Duran
Repair of moderate aortic valve lesions associated with other pathology: an 11-year follow-up
Eur. J. Cardiothorac. Surg., August 1, 2001; 20(2): 247 - 251.
[Abstract] [Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
A. M. Gillinov, E. H. Blackstone, J. White, M. Howard, R. Ahkrass, A. Marullo, and D. M. Cosgrove
Durability of combined aortic and mitral valve repair
Ann. Thorac. Surg., July 1, 2001; 72(1): 20 - 27.
[Abstract] [Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
R. C. Millar, J. M. Arcidi Jr, and P. J.M. Alison
The maze III procedure for atrial fibrillation: should the indications be expanded?
Ann. Thorac. Surg., November 1, 2000; 70(5): 1580 - 1586.
[Abstract] [Full Text] [PDF]

Home page
 J. Thorac. Cardiovasc. Surg.Home page
T. M. Yau, Y. A. F. El-Ghoneimi, S. Armstrong, J. Ivanov, and T. E. David
MITRAL VALVE REPAIR AND REPLACEMENT FOR RHEUMATIC DISEASE
J. Thorac. Cardiovasc. Surg., January 1, 2000; 119(1): 53 - 61.
[Abstract] [Full Text] [PDF]

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 Author home page(s):
José M. Bernal
José M. Revuelta
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 Bernal, J. M.
Right arrow Articles by Revuelta, J. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bernal, J. M.
Right arrow Articles by Revuelta, J. M.

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