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Ann Thorac Surg 2004;77:1272-1276
© 2004 The Society of Thoracic Surgeons


Original article: cardiovascular

Midterm results of aortic valve repair with the pericardial cusp extension technique in rheumatic valve disease

Nilgün Bozbuga, MDa*, Vedat Erentug, MDa, Kaan Kirali, MDa, Esat Akinci, MDa, Ömer Isik, MDa, Cevat Yakut, MDa

a Department of Cardiovascular Surgery, Kosuyolu Heart and Research Hospital, Istanbul, Turkey

Accepted for publication September 10, 2003.

* Address reprint requests to Dr Bozbuga, Kosuyolu Heart and Research Hospital, Department of Cardiovascular Surgery, 81020 Istanbul, Turkey
e-mail: nbozbuga{at}kosuyolu.gov.tr


    Abstract
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
BACKGROUND: The encouraging results of valve repair in the atrioventricular valves have influenced a decision about aortic valve (AV) reconstruction. We report our experience with pericardial cusp extension to repair rheumatic AV disease.

METHODS: From 1993 to 1998, 46 patients (25 women, 21 men) with a mean age of 31.5 ± 12.2 years (range, 15 to 58 years) underwent AV repair. Twenty-two (47.8%) patients had moderate and 24 (52.2%) had severe aortic insufficiency (AI). Severe cusp retraction was repaired with glutaraldehyde-treated autologous pericardium. Twenty-one patients had more than one maneuver (mean, 1.8) to attain competence besides augmentation, which consisted of the release of stenotic commissures (in 11 cases), thinning of the AV cusps (in 10 cases), and resuspension of the cusps (in 17 cases). Simultaneous mitral valve repair was performed on 17 patients. Eight patients received triple valve reconstruction.

RESULTS: There was no early mortality. Thirty patients no longer had AI with any significant transvalvular gradients. Five patients were followed with mild residual AI, and 2 patients with moderate AI not requiring reoperation. Nine patients developing severe AI required AV replacement with a reoperation rate 19.6% (4.26%/patient-year). The mean interval between repair and reoperation was 28.2 ± 18.3 months (range, 3 to 58 months). The mean observation time was 4.6 ± 3 years (211.6 patient-years). Late mortality rate was 2.2% with 1 patient. The significant negative predictors of aortic reoperation determined by univariate analysis were preoperative New York Heart Association class (p = 0.002) and postoperative severe AI (p < 0.001). Cox hazard studies identified that all risk factors were insignificant for aortic reoperation. The actuarial rate of freedom from aortic reoperation was 76.1% ± 7% at 7.5 years.

CONCLUSIONS: Although AV repair by extension with pericardium is worth considering with an acceptable solution to achieve a good geometry from unequal cusps, especially in young rheumatic patients for preservation of the native AV, the patients should be followed periodically for reoperation risk.


    Introduction
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
The first surgical attempts to treat aortic insufficiency (AI) were performed using reconstructive techniques on the aortic valve (AV) [1]. Advances in valve repair and the preoperative predictive accuracy of valve repair versus replacement suggest a favorable risk-benefit ratio for early surgical intervention. The encouraging results of valvuloplasty in the atrioventricular valves have influenced a resurgence of AV reconstruction that otherwise would have been a replacement procedure [2].

The competence of the AV depends on the integrity of its two components, the annulus and the aortic cusps. The length of the free margin of each cusp should be equal to the diameter of the aortic annulus at the level of the sinotubular junction for a normal AV anatomy. Organized structure of the native AV leaflets can be created by remodeling of the diseased AV components.

This study was undertaken to determine the durability of AV reconstruction in rheumatic disease. We have reported on our experience with reparative pericardial patch technique of aortic cusp extension for rheumatic AV disease.


    Material and methods
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
From January 1993 to September 1998, 46 patients underwent aortic valve repair using glutaraldehyde-treated autologous pericardium for cusp extension. There were 25 women (54.3%) and 21 men (45.7%) with a mean age of 31.5 ± 12.2 years (range, 15 to 58 years). Twenty-four patients (52.2%) had isolated AV disease and 22 patients (47.8%) had combined AV and mitral valve disease, with significant tricuspid valve disease in 8 patients. At the time of operation, 18 patients (39.1%) were in New York Heart Association (NYHA) functional class II, 26 patients (56.5%) were in NYHA class III, and 2 patients (4.4%) were in NYHA class IV. Thirty (65.2%) patients were in sinus rhythm and 16 (34.8%) were in atrial fibrillation.

All patients were routinely investigated by transthoracic and transesophageal echocardiographic technique. Twenty-two (47.8%) patients in the series had moderate and 24 (52.2%) had severe AI owing to aortic cusp retraction resulting in central triangular coaptation defect on echocardiography (Table 1). Fourteen patients received catheterization for measurement of heart chamber pressures. Coronary angiography was performed to rule out coronary artery disease in older patients (>40 years for men and >45 years for women). Left ventricular function was normal in 29 cases (63%) with the ejection fraction being more than 0.60, and mildly impaired in 17 cases (37%) with the mean ejection fraction being 0.421 ± 0.096.


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Table 1. Preoperative Valve Disease

 
Surgical technique
The operation was performed under cardiopulmonary bypass with the ascending aorta, single or bicaval venous cannulation and moderate systemic hypothermia (28°C). Myocardial protection was achieved with isothermic retrograde blood cardioplegia.

To make a decision to repair, preoperative echocardiographic criteria and intraoperative observations were used to determine the feasibility and durability of reconstruction. However, the intraoperative findings helped to make the final decision for valve repair. Repair was attempted if the valve was pliable and free of severe calcification. The AV was inspected through a standard J-shaped aortotomy incision. The pliability of leaflets, the amount of the calcification, and the valve involvement led to patient selection. The AV findings determined the type of aortic repair procedures. At operation all AVs had a characteristic appearance: leaflets were retracted and failed to coapt, producing central incompetence. In our series we found that the most attacked and retracted cusps owing to rheumatic disease were right and noncoronary cusps.

Severe cusp retraction was repaired with glutaraldehyde-treated autologous pericardium. The patch was harvested from pericardium, then trimmed and stabilized with 0.62% glutaraldehyde solution for 5 minutes [3]. We preferred to shorten the stabilization period to obtain more-pliable patch material. The retracted cusp or cusps were incised on the base of the Valsalva sinus 1 mm away from the annulus between the commissures (Fig 1). A semicircular pericardial patch was sutured from the annulus to the mobilized leaflet edge with a 4-0 polypropylene continuous suture. The base of the semicircular patch was sutured to the annular edge of the incision. The dimension of the semicircular patch depended on the size of the native leaflet. The radius of the patch was 2 mm smaller than the annular radius of the treated cusp. The enlargement procedure of the cusp provided optimal depth of the Valsalva sinus for coaptation. Monocusp extension was performed on 29 patients, double-cusp extension on 15 patients, and triple-cusp extension on 2 patients. The mean number of extended aortic cusps was 1.41 ± 0.47 (Table 2).



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Fig 1. Schematic drawing of cusp extension pre (left) and post (right) procedure.

 

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Table 2. Operative Procedures

 
Twenty-one patients (45.7%) had more than one maneuver (mean, 1.8) to attain competence besides augmentation. Associated AV repair techniques consisted of release of stenotic commissures (in 11 cases), thinning of the edge of the cusps (in 10 cases), and resuspension of cusps (in 17 cases; Table 2). Fused commissures were incised back to within 1 mm of the aortic annulus. If the free edge of the cusps was fibrotic or thickened, the edges were unrolled or shaved. This maneuver led to a slight increase in the depth of the cusp, with a larger surface for coaptation of the adjacent cusps. In repairing stenotic valves the hypertrophied nodules were debrided. The resuspension technique involving the horizontal mattress suture with polytetrafluoroethylene (Teflon) felt pledget was placed through the prolapsed side of the commissure and the aortic wall. This technique was preferred for increasing the Valsalva sinus depth without interfering with the range of cusp motion.

The presence and the type of concomitant mitral valve surgery had a considerable influence on the type of aortic surgery. First, the associated mitral valve lesions were corrected. Simultaneous mitral valve repair was performed in 22 patients, with mitral repair in 17 patients and mitral valve replacement in 5 patients in whom 4 received bioprosthetic and 1 mechanical valves. Eight patients had triple-valve disease treated by triple-valve reconstruction.

The mean cardiopulmonary bypass time was 106.3 ± 38.9 minutes, and the mean cross-clamping time was 49.2 ± 25.8 minutes. Transesophageal echocardiography was used to assess the adequacy of repair intraoperatively in 35 patients. Coaptation of the three cusps, leaving no triangular defect in the center, was achieved. A diastolic arterial pressure of more than 60 mm Hg was maintained after AV repair.

Follow-up
Follow-up data were collected by echocardiography on a monthly basis during the first 6 months and annually thereafter. Three patients were lost 2, 2.5, and 4 years after the follow-up. The mean observation time was 4.6 ± 3 years (211.6 patient-years).

Statistics
A commercial statistical software package (SPSS for Windows, version 10.0, SPSS Inc, Chicago, IL) was used for data analysis. Results are presented as mean ± standard deviation. Postoperative cardiovascular events were further classified as early (<=30 days) or late (>30 days). Ten variables were analyzed: age, sex, NYHA class, rhythm, cardiomegaly, type of AV disease, the degree of AI, mitral valve disease, the number of extended cusps, associated aortic valve procedures, and concomitant valve procedures. Differences between continuous variables were tested using the paired Student's t test. Univariate analysis was used to assess the risk factors as independent predictors of late mortality and reoperation. The analysis of reoperation focused on AV replacement after AV repair. Cox proportional hazard regression analysis was used to assess the risk factors for late mortality and aortic reoperation. Survival curve was constructed using the Kaplan-Meier method, and the result was presented as mean ± standard error of the mean. Results were considered to be statistically significant when the p value was less than 0.05.


    Results
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
We did not encounter early mortality. Three of the 16 patients with atrial fibrillation returned to sinus rhythm after surgery. No patient received anticoagulation therapy except 1 patient who had undergone mitral valve replacement with a mechanical valve.

Postoperative transesophageal echocardiographic at hospital discharge showed statistically significant reduction of AV insufficiency. The diastolic pressure increased significantly after repair. Doppler echocardiographic study at the last follow-up showed a mean gradient of 13.1 ± 5.6 mm Hg and mean regurgitation on a scale from grade 0 to 4 of 0.98 ± 0.47 (Table 3). Left ventricular function was improved in 15 of 17 cases that had been mildly impaired. Left ventricular ejection fraction was increased from 0.421 ± 0.096 to 0.473 ± 0.066 (p > 0.05), and left ventricular end-diastolic diameter was decreased from 5.6 ± 2.5 cm to 5.1 ± 1.8 cm in this subgroup of patients (p > 0.05).


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Table 3. Echocardiographic Studies

 
All the patients were in NYHA class I or class II with improved functional capacity. No thromboembolic event has occurred during follow-up. Late mortality was 2.2% in 1 patient after 53 months during the reoperation for double-valve replacement. Actuarial survival was 97.8% ± 2.1% at 8.6 years. The significant negative predictors of late survival determined by univariate analysis were reoperation (p = 0.026) and postoperative mitral regurgitation (p = 0.015). Multivariate analysis demonstrated that there was no significant negative predictor of late-term mortality.

Reoperation and risk factors
Thirty patients no longer had AI with any significant transvalvular gradients. Five patients were followed with mild (grade 1) residual AI, and 2 patients were followed with moderate (grade 2) aortic insufficiency not requiring reoperation. Nine patients developed severe (grade >= 3) AI after the first operation and reoperation for required AV replacement with a mechanical prosthesis. The reoperation rate was 19.6% (4.26%/patient-year). Eight patients (17.4%) received double-valve replacement for recurrent mitral regurgitation. Early failure occurred in 1 patient owing to insufficient patch enlargement. Explanted valves with pericardial extension demonstrated significant progression of rheumatic disease with dense fibrosis causing deformation and restriction of optimum closing mechanism. Patch dehiscence or tear was not detected in any of the cases. Calcification of pericardial patch was not seen at macroscopic investigation. The mean interval between repair and reoperation was 28.2 ± 18.3 months (range, 3 to 58 months).

The significant negative predictors of aortic reoperation determined by univariate analysis were preoperative NYHA class (>=class III; p = 0.002) and postoperative severe AI (p < 0.001; Table 4). However, the number of extended cusps was insignificant for aortic reoperation (p = 0.625). Cox hazard studies identified that all risk factors were insignificant for aortic reoperation. The actuarial rate of freedom from aortic reoperation was 76.1% ± 7.0% at 7.5 years (Fig 2).


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Table 4. Univariant Analysis for Aortic Reoperation

 


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Fig 2. Actuarial freedom from aortic reoperation (AR).

 

    Comment
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 
Rheumatic valvular disease is a progressive inflammatory process involving the leaflets with inflammatory cells, scarring, and calcification. Rheumatic AI is associated with cusp thickening and retraction, in which decreasing pliability and shrinkage of the cusp tissue results in a lack of coaptation in diastole with the cusp free edge being too short for the annular diameter.

Mitral valve repair feasibility has been well demonstrated in patients with rheumatic valve disease in young ages [4]. However, the AV repair for acquired valve disease is still controversial, and its indication should be restricted to selected cases. The degree of AV disease and the type of adjunct procedure make interpretation of the results and conclusions difficult. The presence of moderate AV disease associated with other disorders that require surgery presents a clinical problem. Vaturi and associates [5] detected among their patients with rheumatic heart disease that a considerable number of the patients have mild AV disease at the time of mitral valve surgery, and AV replacement is rarely needed after a long follow-up period. This conclusion was supported by other studies [6]. Prophylactic AV replacement is not indicated in these cases. Aortic valve repair under these circumstances can be a feasible option [7, 8]. The results of reparative techniques, particularly in young patients with stenotic congenital valves, aortic regurgitation associated with acute aortic dissection, or ventricular septal defects, have been encouraging [911].

The important factor of AV repair is the pliability of the leaflets. Reconstructive valve surgery is considered for patients with the appropriate techniques applied in accordance with the intraoperative findings. A careful analysis of the anatomic and functional valvular lesions is completed to ensure that each valve is suitable for repair. We attempted reconstruction if restoration of cusp mobility, shape, and central apposition was deemed feasible. But the repair of AV lesions has yielded mixed results. The repair procedures in rheumatic valvular disease are technically more difficult and less stable than in degenerative lesions as the complex nature of the rheumatic valve disease involves all parts of the valve structures. Rheumatic valve disease poses special problems owing to deformity of the valve, presence of combined lesions, and restricted valve mobility. Persistence or recurrence of the rheumatic activity distorts the valve structures, resulting in regurgitation. Multiple techniques are required in repairing the AV. No single technique can be expected to achieve satisfactory results [7].

Patch enlargement provides an alternative in rheumatic valves. Mitral dysfunction in rheumatic patients because of the restricted motion of the posterior leaflet can be corrected by extension with a crescent-shape pericardial patch of the posterior leaflet. Pericardial patch enlargement in patients with severe retraction of the posterior leaflet allows effective leaflet enlargement and surface for coaptation [12]. Adaptation of this technique in rheumatic AV insufficiency owing to central regurgitation resulting from cusp retraction increases the depth of the sinus together with the area of leaflet coaptation to achieve a good geometry from unequal cusps.

Fused commissures can be divided, and thickened leaflets can be thinned or debrided of calcium to increase mobility and pliability [13]. It has been reported that ultrasonic debridement of calcific valves caused AI to develop in a large number of patients [14]. Shapira and colleagues [15] reported on their experience with lunular hypertrophy managed by shaving, with a 6-year actuarial freedom from valve-related morbidity of 92%.

There are a few reports in the literature describing the long-term results of AV extension technique for rheumatic disease. Al Fagih and colleagues [16] reported on 20 patients followed up to 2 years with no complication. Duran and associates [17] reviewed 107 patients and concluded that cusp extension techniques using pericardium were superior to AV repair without addition of extravalvular tissue. Grinda and colleagues [18] reported their midterm results in 89 patients with rheumatic AV disease.

Valve repair for AV disease has advantages not only because of the lack of need for anticoagulation but also the considerable low cost compared with prosthetic valve replacement in selected patients. All repair procedures carry a very low operative mortality and long-term morbidity risk, such as thromboembolism, anticoagulation-related bleeding, and endocarditis. Poor left ventricular function is not a contraindication to valve repair. In contrast, poor left ventricular function increases the risk of thromboembolism from the prosthetic valve. Pericardial extension technique provides reconstruction of the optimal leaflet coaptation mechanism and more coaptative surface with the native AV tissue without any distortion of the retracted cusp or cusps causing aortic regurgitation. Our technique allows growth of the annulus and sinotubular junction without interference of annular growth in childhood and adolescence. The pericardial patch method does not disturb the architecture of the aortic root and allows the equalization of the cusp geometry without turbulence or residual stenosis. Although aortic valvuloplasty by extension with the pericardium is worth considering as an acceptable solution for preservation of the native AV, especially in young rheumatic patients, the patients should be followed periodically for assessing the risk of aortic reoperation.


    References
 Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

  1. Taylor W.J., Thrower W.B., Black H., Harken D.E. The surgical correction of aortic insufficiency by circumclusion. J Thorac Cardiovasc Surg 1958;35:192-205.
  2. Carpentier A. Cardiac valve surgery: the French correction. J Thorac Cardiovasc Surg 1983;86:323-337.[Medline]
  3. Chauvaud S., Jebara V., Chachques J.C. Valve extension with glutaraldehyde-preserved autologous pericardium. J Thorac Cardiovasc Surg 1991;102:171-178.[Abstract]
  4. Duran C.M., Gometza B., Saad E. Valve repair in rheumatic mitral disease: unsolved problem. J Card Surg 1994;9:282-285.[Medline]
  5. Vaturi M., Porter A., Adler Y., et al. The natural history of aortic valve disease after mitral valve surgery. J Am Coll Cardiol 1999;33:1003-1008.
  6. Ha J.W., Choi S.H., Chang B.C., et al. Is prophylactic aortic valve replacement indicated during mitral valve surgery for mild to moderate aortic valve disease?. Ann Thorac Surgery 2002;74:1115-1119.[Abstract/Free Full Text]
  7. Al-Halees Z., Gometza B., Al Sanei A., Duran C. Repair of moderate aortic valve lesions associated with other pathology: an 11-year follow-up. Eur J Cardiothorac Surg 2001;20:247-251.[Abstract/Free Full Text]
  8. Bernal J.M., Fernandez-Vals M., Rabasa J.M., Gutierrez–Garcia F., Morales C., Revuelta J.M. Repair of nonsevere rheumatic aortic valve disease during other valvular procedures: is it safe?. J Thorac Cardiovasc Surg 1998;115:1130-1135.[Abstract/Free Full Text]
  9. Bozbuga N., Mansuroglu D., Isík O., et al. Aortic reconstructions. Eur J Cardiac Intervent (Cor Europeum) 1996;5:143-145.
  10. Cosgrove D.M., Rosenkranz E.R., Hendren W.G., Barlett J.C., Stewart W.J. Valvuloplasty for aortic insufficiency. J Thorac Cardiovasc Surg 1991;102:571-577.[Abstract]
  11. Fraser C.D., Wang N., Mee R.B.B., et al. Repair of insufficient bicuspid aortic valves. Ann Thorac Surg 1994;58:386-390.[Abstract]
  12. Bozbuga N., Mansuroglu D., Isík O., et al. Mitral posterior leaflet extension. Eur J Cardiac Intervent (Cor Europeum) 1997;6:78-81.
  13. Kitamura N., Uemura S., Kunimoto R., et al. A new technique for debridement in rheumatic valvular disease: the rasping procedure. Ann Thorac Surg 2000;69:121-125.[Abstract/Free Full Text]
  14. Freeman W.K., Schaff H.V., Orszulak T.A., Tajik A.J. Ultrasonic aortic valve decalcification: serial Doppler echocardiographic follow-up. J Am Coll Cardiol 1990;16:623-630.[Abstract]
  15. Shapira N., Fernandez J., Hirshfeld K.J., et al. Lunular hypertrophy and aortic valve disease. Ann Thorac Surg 1994;57:305-310.[Abstract]
  16. Al Fagih M.R., Al Kasap S.M., Ashmeg A. Aortic valve repair using bovine pericardium for cusp extension. J Thorac Cardiovasc Surg 1988;96:760-764.[Abstract]
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