Combined mitral and aortic valve repair in a patient with end-stage renal disease
C Özbek, U Yetkin, B Özcem, M Bademci, ? Yürekli, N Postac?, A Gürbüz
Keywords
aortic valve repair, end-stage renal disease, mitral valve repair
Citation
C Özbek, U Yetkin, B Özcem, M Bademci, ? Yürekli, N Postac?, A Gürbüz. Combined mitral and aortic valve repair in a patient with end-stage renal disease. The Internet Journal of Thoracic and Cardiovascular Surgery. 2008 Volume 13 Number 2.
Abstract
Mortality in patients with end-stage renal disease is higher than in those with normal renal function after a cardiac operation. Mitral valve repair and if possible aortic valve repair are the procedures of choice to treat valvular dysfunction.We present in this study; combined mitral and aortic valve repair in a patient with end-stage renal disease.Mitral valve reconstruction offers theoretical advantages in patients requiring dialysis.
Introduction
End-stage renal disease is known to be an important risk factor complex for cardiac operations performed with cardiopulmonary bypass[1]. The combination of chronic renal failure and cardiovascular disease is identified frequently and results in high morbidity and mortality without appropriate medical and surgical therapy. Experience during the last eighteen years has shown that cardiac operations can be undertaken in this high-risk group with acceptable morbidity and mortality and with reasonable expectation of symptomatic improvement[2].
Case Presentation
Our case was a 21-year-old woman that had been followed with a diagnosis of rheumatic mitral stenosis and aortic regurgitation diagnosis for 10 years. She was admitted to our Cardiology Outpatient Clinic for dyspnea and tachycardia. She was in New York Heart Association (NYHA) functional class III-IV at presentation. Transthoracic echocardiography(TTE) showed severe MR(MVA:1.6cm²,mean gradient was 13mmHg). Left ventricle EF was 60%. Other valves’ functions included severe aortic regurgitation and moderate tricuspid regurgitation. Her pulmonary systolic tension was 65mmHg. Her cardiac catheterization was performed. It confirmed that EF was 60%. Severe aortic regurgitation was diagnosed. He was under continuous hemodialysis program for chronic renal insufficiency for 10 years. There has been a brachiobasilic fistula created 10 years ago.
She underwent operation. She was operated under endotracheal general anesthesia and in supine position. Following a median sternotomy,pericardium was opened longitudinally. After heparinization, extra-corporeal circulation was established between the venae cavae and the ascending aorta. A cross clamp was placed on aorta and by retrograde continuous isothermic blood cardioplegia from coronary sinus,cardiac arrest was established.Hypothermia was moderate (28ºc). Insertion of a vent into right upper pulmonary vein was postponed until after left atriotomy due to proper bipolar ablation. Moreover, aortic exploration was left over since mitral repair and control with saline test were planned. Standard left atriotomy was made from interatrial junction. The entire valvular apparatus was carefully examined in order to assess the feasibility of reconstructive surgery and to plan the operative technique. The valvular apparatus was then mobilized as an entire unit with a nerve hook in order to assess tissue flexibility and to identify leaflet restriction. It could cover whole mitral orifice and there wasn't any commissural fusion(Figure 2).
The bilateral commissures were incised while leaving intact one milimeter of valvular tissue intact as in the normal anatomy (Figure 3).
After this step we performed bilateral segmental annuloplasty. This procedure may also be used to achieve better approximation of leaflet tissue with the placement of mattress stitches at the commissures(Figure 4).
We tested the valve competence after this step on observing valve closure while the left ventricular cavity was filled with saline solution. There wasn’t saline regurgitation.Valve competence and closure were excellent. Following right atriotomy, we didn’t detected a regurgitation of the tricuspid valve.
Aortotomy was made and aortic valve was identified as with 3 leaflets. Suspensory sutures were put on all of 3 commissures. There wasn’t any tissue loss in any of these 3 leaflet structures. Moreover, there wasn’t any calcification observed
Then, peak points of these 3 leaflets (Arantius’ nodules) were united temporarily with a single 4/0 polypropylene suture. It was identified that the valvular structure was optimal for coaptation . This temporarily placed suture was then removed. Left and right atriotomies and aortotomy were closed respectively.
Postoperative recovery was uncomplicated. The hospital stay was 8 days. Postoperatively an echocardiographic investigation was repeated. There was minimal mitral regurgitation identified(Figure 6).
There was a minimal aortic regurgitation identified also(Figure 7).
Our patient had good results immediately after surgical valve repair. The functional capacity of our patient improved dramatically and she was in NYHA functional class I.
Discussion
Heart valve surgery in high-risk patients is associated with considerable morbidity and mortality[3].
Abnormal calcium homeostasis in patients with end-stage renal failure results in dystrophic calcification[3]. Valvular and perivalvular involvement in end-stage renal disease (ESRD) is most commonly manifested as mitral annular calcification and aortic valve calcification. Both mitral and aortic valve calcification (MAC) occur more frequently and at younger age in those with ESRD than in those with normal renal function[5]. Altered calcium and phosphate metabolism are thought to predispose to these valvular and perivalvular abnormalities. No treatment is necessary for MAC unless severe mitral regurgitation or stenosis occur (both are rare). Mitral valve repair or replacement and aortic valve replacement are indicated for severe symptomatic valve stenosis or regurgitation[5].There is limited reported experience on mitral valve repair in patients with chronic renal failure[6].
In a small but important group of patients on long-term dialysis, premature valve calcification is severe and produces aortic stenosis, or less frequently, mitral stenosis[7].In the study of Maher et al., the frequency and aetiology of aortic valve and mitral annular calcification was studied by echocardiography in 87 patients aged 35-70 on maintenance haemodialysis for a mean of 7.5 years (range 0.5-19). Aortic valve calcification (AVC) was found in 24 patients (28%) and mitral annular calcification (MAC) was found in 31 (36%)[7].
Although accelerated calcification of the repaired mitral valve and high incidence of failure of the reconstruction had been reported in patients with end-stage renal disease, mitral valve repair when this can be safely performed, especially in patients with uremic congestive cardiomyopathy, in view of the added advantage of retaining the native valve in such patients[6].These patients have increased LV cavity size, poorer LV systolic function, higher LV filling pressures compared to patients without MAC[8].
In the study of Lewandowski et al., ten patients with end-stage renal failure and on chronic dialysis who underwent mitral valve repair were identified retrospectively and followed for clinical and echocardiographic outcome. All patients had good results immediately following surgical valve mitral repair, with no more than mild mitral regurgitation[3].
The mortality rate was high in ESRD patients, approximately 15% per year. After accounting for baseline cardiovascular disease and traditional risk factors, the presence of MAC did not confer additional risk for mortality[9].
The results of the study of Laws et al.,in this high-risk patient group provide a basis for cautious optimism and for a continued aggressive approach in patients with chronic renal disease who require cardiac operation[2]. Advantages of valve repair over valve replacement include improved long-term survival, better preservation of left ventricular function, and greater freedom from endocarditis, thromboembolism, and anticoagulant-related hemorrhage[10].