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Ann Thorac Surg 1995;60:1044-1047
© 1995 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Results of Mitral Valve Reconstruction in Children With Rheumatic Heart Disease

Department of Cardiothoracic and Vascular Surgery, Cardiothoracic Sciences Centre, All India Institute of Medical Sciences, New Delhi, India

Accepted for publication April 27, 1995.

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Background. Between January 1988 and November 1994, we developed techniques of reconstructing diseased mitral valves in patients with rheumatic heart disease. Four hundred thirteen patients underwent mitral valve repair using these techniques. Of these, 125 children and adolescents less than 15 years of age form the study group.

Methods. The mean age was 8.9 ± 4.3 years (range, 5 to 15 years). One hundred seventeen patients (93.6%) had rheumatic heart disease. There were 72 boys (57.6%) and 53 girls (42.4%). All of these patients were symptomatic: New York Heart Association class III or IV. Mitral regurgitation alone was present in 49 patients (39.2%), and combined mitral stenosis and regurgitation were present in 76 patients (60.8%). Surgical techniques included commissurotomy (n = 70; 56%), annuloplasty (n = 122; 97.6%), chordal shortening (n = 46; 36.8%), cusp thinning (n = 27; 5.6%), and associated procedures for tricuspid valve disease (6 patients) and aortic valve disease (2 patients).

Results. The operative mortality rate was 4.8% (6 patients), and late deaths occurred in 1.6% (2 patients). Follow-up was 378.25 patient-years. In 15 patients, severe mitral regurgitation developed after a mean follow-up of 37.14 ± 20.47 months (seven reoperations). At 6 years, actuarial and event-free survival rates were 92.1% ± 3.19% and 75% ± 8.18%, respectively. One patient (0.15%/patient-year) had transient right hemiparesis. None had anticoagulation-related bleeding.

Conclusion. Mitral valve reconstruction in children and adolescents with rheumatic mitral regurgitation provides satisfactory early results. Progression of disease is the most important risk factor for reoperation. The technique described provided stable repair in the majority of patients.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Valve replacement in children is associated with higher early and late mortality rates than in adults [1–4]. Further, problems related to the prosthetic valve and to life-long anticoagulation remain substantial. The safety and the long-term stability of mitral valve reconstruction are well established [5–8]. Emerging evidence indicates that the cause of disease [6, 9–12] and young age [6, 7, 12, 13] play important roles in the results of mitral valve repair. We report our experience in children and adolescents (less than 15 years) with predominantly rheumatic cause.

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Patients
Between January 1988 and November 1994, 413 patients underwent mitral valve repair at our institution. Of these, 125 patients, age range 5 to 15 years (mean age 8.9 ± 4.3 years), form the study group. Thirty-two patients (25.6%) were less than 10 years of age. There were 72 boys (57.6%) and 53 girls (42.4%). The cause was rheumatic in 117 patients (93.6%) and congenital (secundum atrial septal defect with mitral valve prolapse) in 8 patients (6.4%). Mitral regurgitation (MR) alone was present in 49 patients (39.2%), and combined stenotic and regurgitant lesions were present in 76 patients (60.8%). All patients were in New York Heart Association class III or IV preoperatively. Forty-three patients underwent cardiac catheterization. In the others, left atrial and pulmonary artery pressures were recorded at operation. Left atrial pressure was mild (12 to 19 mm Hg) in 36 patients, moderate (20 to 25 mm Hg) in 40, and severe (greater than 25 mm Hg) in 27. Pulmonary artery pressure was mild (20 to 29 mm Hg) in 24, moderate (30 to 49 mm Hg) in 38, and severe (greater than 50 mm Hg) in 24. Patients with isolated mitral valve lesions were accepted for operation on the basis of echocardiographic diagnosis alone.

Preoperative Assessment
Preoperative transthoracic echocardiography was performed in all patients using an ATL Ultramark 9 or HP Sonos 1500 echocardiographic machine. In addition, patients who were operated on after January 1994 (17 patients) had transesophageal echocardiography using a Hewlett-Packard Sonos 1500 ultrasound system (Hewlett-Packard Co, Andover, MA) intraoperatively.

We performed a systematic examination of the mitral annulus, leaflets, thickness and mobility, commissural fusion, presence and localization of calcific nodules, areas of prolapse and billowing, direction of the regurgitant jet, and thickness and length of chordae.

Indications for Reconstruction
Keeping in mind the age of the patients, valve repair was attempted in all. Because no patient had extensive calcification, all patients underwent mitral valve repair at the primary operation. Four patients underwent mitral valve replacement at reoperation.

Surgical Technique
The heart was approached in the majority (98 patients) through a standard midsternotomy incision. However, in 27 patients a right anterolateral thoracotomy was chosen for cosmetic reasons. Cardiopulmonary bypass was established by ascending aortic and bicaval cannulation (even in patients undergoing right thoracotomy). Systemic hypothermia, antegrade cold blood cardioplegia, and topical ice slush were used for myocardial protection. The mean aortic cross-clamp time was 44.2 ± 10.17 minutes (range, 30 to 71 minutes) for isolated mitral valve repair.

The left atrium was opened behind the interatrial groove. Any thrombus was removed. Careful evaluation of the mitral apparatus was performed using a pair of curved hooks. A variety of surgical techniques were required to restore function of the mitral valve [14]. Chordal shortening was performed at the cusp level by plicating the thickened and elongated chordae by the appropriate length, as described previously [15]. Restoration of pliability of the anterior and posterior mitral leaflets required peeling of the fibrous layer encasing the valve leaflets. Various other techniques used are listed in Table 1.

All patients received oral anticoagulant agents (Acenocoumarin) for 6 weeks. A prothrombin time ratio of 1.5 to 2.0 was maintained over control values during the 6 weeks of anticoagulation. The international normalized ratio was not followed in our series.

Follow-Up
Patients were followed up in the outpatient clinic by one of us (A.S.K.). In addition to the clinical examination, patients underwent regular transthoracic two-dimensional echocardiography with Doppler color flow mapping at discharge, within the first 3 months, and at 6 monthly intervals thereafter. Those patients who did not attend the outpatient clinic replied to a written questionnaire sent to them enquiring about clinical, echocardiographic, and medication details. Assessment of MR made at the last visit was included in the results. Follow-up was complete (100%), ranging from 1 month to 72 months (mean follow-up, 37.83 ± 18.37 months).

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Mortality
There were six early deaths (4.8%). Five deaths (4.0%) were due to low output syndrome. One of these deaths occurred at reoperation, and one patient (0.8%) died of cerebral infarction. There were two late deaths (1.6%), one due to hepatitis 2 months after repair and the other due to congestive heart failure at 4 months, while the patient was awaiting reoperation.

Reoperation
Reoperation was performed in 7 patients. The mean interval between primary repair and reoperation was 36.29 ± 22.38 months (range, 1 to 53 months). In 2 patients, reoperation was performed within the first month (24 and 27 days). In both patients, some of the sutures holding the teflon felt had given way. In one patient, the valve was replaced on request, and in the other the valve was repaired using the same technique. These 2 patients were in the early part of our experience.

In 5 patients, the reoperation was done at 48 months or later (mean, 50.4 ± 2.06 months). These patients demonstrated evidence of recurrence of rheumatic heart disease: fusion of the cusps and chordae and new thickening and contraction of the cusps noted at operation. In these patients, two of the valves were considered fit for a second attempt at repair performed by the same technique. In the remaining three, the valve was replaced.

One patient died after reoperation. All the remaining patients who underwent reoperation have been followed up for a mean of 24 months. They returned to New York Heart Association class I, and the 2 patients who had a revision of repair had no more than trivial to mild MR at follow-up echocardiographic examination.

Complications
One patient (0.15%/patient-year) had transient right hemiparesis with complete recovery. No patient had hemorrhagic complications related to anticoagulation.

Residual Mitral Regurgitation
Seven (5.83%) of the operative survivors developed severe MR after a mean follow-up period of 37.14 ± 20.47 months (range, 4 to 69 months). One patient died of congestive heart failure 4 months after repair, while awaiting surgical correction. All of the remaining 6 patients are awaiting reoperation.

In 9 other patients (7.5%), moderate MR developed after a mean follow-up of 24 ± 14.7 months (range, 11 to 54 months), but the patients were asymptomatic. In these patients, MR was not considered serious enough to warrant reoperation. Mitral regurgitation was absent in 47 patients, trivial in 18, and mild in 37 (together equaling 87% of patients).

Valve Failure
Valve failure is defined as either valve-related mortality or morbidity, including reoperations and severe valvular dysfunction (grade IV MR) or severe mitral stenosis (mitral valve area less than 1.0 cm²) after repair.

Valve failure occurred in 20 patients (16%) during a mean follow-up of 36.7 ± 21.43 months. This included 7 valve-related deaths (one patient died awaiting reoperation), seven reoperations (one hospital death), and 6 other cases of severe valve dysfunction (grade IV MR in 5 and severe mitral stenosis in 1 patient). Mitral valve areas measuring greater than 3.1, 2.6 to 3.0, 2.0 to 2.5, and less than 2.0 cm² occurred in 15, 21, 34, and 13 patients, respectively.

Actuarial and Event-Free Survival
Actuarial survival (including early and late deaths) was 92.1% ± 3.19% at 6 years by Kaplan-Meier survival analysis (Fig 1). After the initial operation, 20 patients (16%) suffered one or more valve-related events, defined as either valve-related death, reoperation, infective endocarditis, or thromboembolism. Event-free survival was 75% at 6 years (Fig 2).

View larger version (16K): [in this window] [in a new window]   Fig 1. . Actuarial survival.

View larger version (16K): [in this window] [in a new window]   Fig 2. . Event-free survival.

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

The functional results of mitral valve repair in adults have been excellent [5–8, 10]. Mitral valve repair offers the advantages of avoiding life-long anticoagulation and preserving chordal and ventricular function. Recent evidence indicates that the cause of disease plays an important role in the results of mitral valve repair. The repair is technically more difficult, with a higher failure rate, in the rheumatic group, and the reoperation rate is reported to be 4.8% to 27% [9, 11, 13, 18]. This reoperation rate increases inversely with age [6, 11]. The causes of failure in rheumatic patients are as follows: (1) the error in judgment, (2) the inherent complexity of the disease process, and (3) recurrence or progression of rheumatic carditis [11, 13].

Our experience with mitral valve repairs in the rheumatic population has been encouraging [8]. The early and late mortality rates are comparable to those of Deloche and associates [5] and Duran and co-workers [6].

The reoperation rate of 5.98% in our patients is much lower than that reported by Duran and associates [6] or Skoulargis and colleagues [11]. The causes of failure of repair were technical failures in 2 patients and recurrence of rheumatic activity in the remaining 5 patients. The presence of new thickening of the leaflets, commissural fusion, and fusion of the subvalvular apparatus along with severe annular dilatation (anterior part of the annulus) despite an intact annuloplasty, and the development of organic tricuspid valve disease in 1 patient, clearly indicate that the cause of late valve failure was recurrence or progression of rheumatic activity.

Seven patients are symptomatic, in New York Heart Association class II, with evidence of severe MR on echocardiography. In these patients, serial echocardiographic examination revealed progression of MR from mild to severe, and 3 of the 7 showed a reduction in mitral valve area. In another patient, isolated severe mitral stenosis developed (mitral valve area less than 1.0 cm²). These findings suggest recurrence of rheumatic activity; the young age of these patients and the observations noted at reoperation, as mentioned above, support this view.

Moderate MR was found in 9 patients (7.5%). This MR did not appear to progress in the last few serial echocardiographic examinations. These patients were symptomatically improved and were not considered to require reoperation.

We conclude that mitral valve repair in children is safe, with acceptable early and late mortality rates. The need for reoperation is low, and the procedure allows growth of the mitral annulus, preserves chordal and ventricular function, and is free of anticoagulation-related problems. When possible, mitral valve repair is the procedure of choice for correction of MR in children.

	Acknowledgments

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
We are grateful to senior residents and consultants in cardiology for the echocardiographic studies.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Address reprint requests to Dr Kumar, Department of Cardiothoracic and Vascular Surgery, Cardiothoracic Sciences Centre, All India Institute of Medical Sciences, Ansari Nagar, New Delhi-110029, India.

	References

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 

1. Sand ME, Naftel DC, Blackstone EH, Kirklin JW, Karp RB. A comparison of repair and replacement for mitral valve incompetence. J Thorac Cardiovasc Surg 1987;94:208–19.[Abstract]
2. Perier P, Deloche A, Chauvaud S, et al. Comparative evaluation of mitral valve repair and replacement with Starr, Bjork and porcine valve prosthesis. Circulation 1984;70(Suppl 1): 187–92.
3. Schaff HV, Danielson GK, DiDonota RM, Puga FJ, Mair DD, McGoon DC. Late results after Starr-Edwards valve replacement in children. J Thorac Cardiovasc Surg 1984;88:583–9.[Abstract]
4. Bradey LM, Midgley FM, Watson DC, et al. Anticoagulation therapy in children with mechanical prosthetic cardiac valves. Am J Cardiol 1985;56:533–5.[Medline]
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7. Antunes MJ, Magalhaes MP, Colsen PR, Kinsley RH. Valvuloplasty for rheumatic mitral valve disease. A surgical challenge. J Thorac Cardiovasc Surg 1987;94:44–56.[Abstract]
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