Failure Of Mitral Valve Repair Research Articles

Hemolysis after mitral valve repair: mechanisms and treatment

Background The objectives of this study were to determine the mechanisms of hemolysis after mitral valve repair and to determine outcomes after surgical treatment (mitral replacement or re-repair). Methods Between 1981 and 2002, 32 patients (mean age, 58 years) presented with hemolytic anemia after mitral valve repair for degenerative, rheumatic, or ischemic mitral regurgitation (MR). Three types of annuloplasty were used at the initial mitral valve repair: Cosgrove-Edwards, Carpentier-Edwards, and bovine pericardial (Perigard). The diagnosis and the mechanisms of hemolysis were investigated with laboratory testing and echocardiography. Results Median interval from initial mitral valve surgery to diagnosis of hemolysis was 3 months (range, 1 week to 4 years). At presentation, mean hematocrit was 27.5% ± 4.9% and 22 patients (69%) required transfusion. Echocardiographic findings varied. Twenty-four patients (77%) had grade 3 or 4 MR. Mitral regurgitant jet types included fragmentation (11 patients, 34%), acceleration (10, 31%), slow deceleration (5, 16%), collision (4, 13%), and free jet (2, 6%). Mitral valve replacement was performed in 28 patients, mitral valve re-repair in 3, and 1 patient did not undergo reoperation. At reoperation the mitral valve repair was physically intact in 25 of 31 patients (81%). There were 2 hospital deaths in patients having reoperation (6%). Actuarial survival was 95% at 1 year and 85% at 5 years. In 1 patient recurrent mechanical hemolysis developed caused by a perivalvular leak after mitral valve replacement. Conclusions Hemolysis is a mode of failure of mitral valve repair. Patients with hemolysis generally present within 3 months of mitral valve repair. Although echocardiographic features varied, most patients had high-grade MR and regurgitant jets that fragmented or accelerated. Mitral valve replacement yields favorable outcomes for patients with hemolysis after mitral valve repair.

Mitral valve replacement after late failure of mitral valve repair

M itral valve repair is the preferred surgical treatment for mitral valve dysfunction. Although the feasibility of mitral valve repair extends to 95% of patients with degenerative valvular disease and up to 75% of patients with rheumatic or ischemic valvular disease, nearly all reports describe patients who have required reoperation for recurrent mitral valve dysfunction.1-5 Late reoperation after mitral valve repair is required in 5% to 10% of patients with degenerative disease and 25% to 50% of patients with rheumatic disease.1-5 Reoperation after mitral valve repair poses specific challenges related to choice of procedure and surgical technique. Should the dysfunctional valve, which has been repaired once, be re-repaired or replaced? Except for instances of recurrent, localized degenerative disease and early technical failure (eg, suture or ring dehiscence), we favor valve replacement. How should the valve be approached? Median sternotomy with left atriotomy is our preferred approach. However, alternative strategies are useful in particular situations. Right thoracotomy may be used when patent grafts are in danger at resternotomy, and an extended transseptal incision on the heart exposes the mitral valve in the setting of a small left atrium (less than 4 cm in maximal dimension).

Pulmonary autograft: Should it be used in young patients with rheumatic disease?

Background: Although pulmonary autograft is being increasingly used to replace the diseased aortic valve with excellent long-term results, its use in the population with rheumatiic disease still needs careful evaluation. Patients and methods: From October 1993 through March 1998, 102 patients underwent aortic valve replacement with a pulmonary autograft (Ross procedure). The mean age was 27.9 ± 4.2 years (range, 0.8-56 years). The cause was rheumatic disease in 75 patients (73%), bicuspid aortic valve in 26 patients (26%), and myxomatous aortoarteritis in 1 patient (1%). The root replacement technique was used in all. In addition, 31 patients had 33 associated procedures: mitral valve repair (n = 15 patients), open mitral commissurotomy (n = 15 patients), tricuspid repair (n = 2 patients), and homograft mitral valve replacement (n = 1 patient). Results: Operative mortality was 6.9% (7 patients). Late mortality was 7.8% (8 patients). Follow-up ranged from 1 to 60 months (mean, 25.3 ± 15.4 months) and was 98% complete. Two patients required reoperation for failed mitral valve repair, and 2 other patients underwent reoperation for failure of both the autograft and mitral valve repair. Echocardiographic assessment showed moderate to severe aortic regurgitation in 13 patients, along with thickening of the autograft. All of these patients had rheumatic disease and were young (<30 years). Ten of these patients had undergone associated mitral valve procedure. Morphologic and histopathologic examination of explanted autografts showed features compatible with rheumatic valvulitis. Conclusion: Pulmonary autograft is susceptible to rheumatic involvement. Young age (<30 years) and associated mitral valve disease are significant risk factors for autograft failure in patients with rheumatic disease. Use of pulmonary autograft in this subgroup of patients requires a cautious approach. (J Thorac Cardiovasc Surg 1999;118:483-91)

Reoperation for failure of mitral valve repair

Background and Objective: Mitral valve repair is the procedure of choice to correct mitral regurgitation of all types. Up to 10% of patients who undergo mitral valvuloplasty require late reoperation for recurrent mitral valve dysfunction. To determine the causes of failed mitral valve repair, we examined the surgical pathology of patients who underwent reoperation for failed mitral valve repair. Patients and Results: From 1986 to 1994, 81 patients had 86 reoperations for recurrent mitral regurgitation after mitral valve repair. Mean age was 59.2 ± 1.4 years; 55 were men. Primary valve disease was degenerative in 48 patients (59%), rheumatic in 16 (20%), ischemic in 13 (16%), endocarditic in 3 (4%), and congenital in 1 (1%). Mean time interval between initial mitral valve repair and reoperation was 15.6 ± 2.5 months. Causes of repair failure were procedure-related (50 cases, 58%), valve-related (33 cases, 38%), or unknown (3 cases, 3%). Procedure-related valve failure was caused by suture dehiscence (21 cases), rupture of previously shortened chordae (19 cases), or incomplete initial correction (10 cases). Valve-related repair failure was caused by progressive primary valve disease (27 cases), endocarditis (5 cases), or extensive leaflet retraction (1 case). Repair failure was procedure-related in 70% of patients with degenerative valvular disease versus only 13% of patients with rheumatic valvular disease ( p = 0.0001). At reoperation, mitral valve replacement was performed in 64 patients (79%) and repeat mitral valve repair in 17 (21%). Conclusion: We conclude that (1) most mitral valve repair failures are procedure-related in degenerative disease and valve-related in rheumatic disease; (2) rupture of previously shortened chordae is a common cause of late failure in patients with degenerative mitral valve disease; and (3) repeat mitral valve repair results in successful treatment for a minority of patients. (J Thorac Cardiovasc Surg 1997;113:467-75)

From aortic cusp extension to valve replacement with stentless pericardium

Between 1988 and 1994, 82 consecutive patients (median age 24 years) underwent reconstruction of the aortic valve with glutaraldehyde-treated pericardium. Simultaneously, 29 of 30 mitral valves were repaired. The first 27 patients underwent resection of the free edges and suture of a single strip of bovine pericardium. Transient ischemic changes suggested the need for a change in technique. The subsequent 55 patients underwent total valve reconstruction with an autologous pericardium fixed with glutaraldehyde in the appropriate shape and size according to the patient's aortic annulus. There were one in-hospital and three late deaths. No patient received anticoagulation, and no embolic events were detected. Nine patients required reoperation as a result of failure of mitral valve repair in 4 and severe aortic regurgitation in 5 (endocarditis [n = 2], commissural tear [n = 1], root dilation [n = 1], calcification of one bovine cusp [n = 1] at 58 months). There were no reoperative deaths. Complete linear echocardiographic follow-up of these patients showed low gradients, valve competence, and no progressive deterioration. No difference between techniques was detected.

910-21 Ross Procedure: Is It Really the Ideal Solution?

Pulmonary autografts have shown promise in the intermediate and long-term results as being an ideal valve substitute for diseased aortic valve. We have adopted this procedure as an option for aortic valve replacement, especially in the young, growing patients who are difficult to anticoagulate. In the period between Jan 1990 and Aug 1994, we have performed this procedure on 79 patients (pts), 57 (72%) males and 22 128%) females. Their age ranged from 1 – 41 years (yrs) (mean, 18.6 ± 7.36 yrs). The etiology was rheumatic in 62 (79.5%) pts and regurgitation was present in 60 (76.9%). stenosis in 5 (6.4%) and both in 13 (16.7%). Five pts had undergone previous surgery for aortic valve (3 repairs, 2 replacements). Associated mitral surgery was performed in 22 (28.2%) pts all of them undergoing repairs. The mean bypass time for isolated Ross procedure was 117.9 ± 36.6 minutes (mins) (74 – 243 mins) and mean ischemic time 79.8 ± 25.1 mins (46 – 155 mins). The right ventricular to pulmonary artery connection was established in all but one case with homografts. There has been no hospital deaths or documented thromboembolisms to date. There have been 2 (2.2%) late deaths, 1 unrelated and 1 due to systemic sepsis and renal shutdown in a pt with T-cell abnormality and congenital immune deficiency at 12 and 36 months (mos). respectively. Four pts (5%) have been reoperated: 1for mitral valve repair failure and suture line leak with false aneurysm (6 mas) and 3 for autograft failure with progressive regurgitation (20 – 26 mos). One reported valve showed histology compatible with rheumatic valvulitis. Even though the left ventricular dimensions and function show immediate recovery and are maintained in the short follow-up, there is a small but definite progression of the autograft regurgitation followed beyond 6 mos. The effect of sizing: surgical distortion, recurrence of rheumatic activity of these transplanted valves and of the repaired mitral valves remain to be evaluated in the long-term. In conclusion: the Ross procedure, while being a safe and excellent option in the young, growing pts with aortic valve disease, should be moderated by the concerns expressed above.

Valve-related events and valve-related mortality in 340 mitral valve repairs *1A late phase follow-up study

To assess the early and late valve-related events, 340 consecutive patients undergoing mitral valve repair from 1969 to 1988 were evaluated. Follow-up was complete, with a mean of 7.5% years and range from 2 to 22 years (cumulative 2456 patient-years). There were 221 (65%) female patients. Rheumatic valvular disease was present in 246 (68%) patients. The remaining patients had ischemic or congenital valve disease, floppy valve or infective endocarditis. At surgery, 47% of the patients had pure mitral incompetence, 43% had mixed mitral stenosis and incompetence and 10% had predominant mitral stenosis. Seventy-three percent of the patients were in functional class III or IV. Twelve percent had had prior heart surgery. Concomitant valve procedures including coronary revascularization were performed in 62.3%. There were 23 hospital deaths (6.8%) but only 3 of these (0.8%) were valve-related in patients who died at reoperation for valve repair failure. There were 4 other early repair failures who survived early reoperation. Of the 317 hospital survivors, there were 127 late deaths, and an actuarial survival of 44 +/- 3.7% (70% CL) at 14 years. Of these, 13 were valve-related or 0.5% patient-year. Late events included thromboembolism (TE) 1% patient-year, anticoagulant bleeding 0.4% patient-year, infective endocarditis (IE) 0.2% patient-year and late reoperation for mitral valve repair failure in 63 patients or 2.8% patient-year. At the late follow-up, 88% of the hospital survivors were in functional class I or II.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanisms of failure of mitral valve repair: An echocardiographic study

Surgical valve repair for mitral regurgitation has significant advantages over valve replacement, but little is known about the mechanisms of its failure. This echocardiographic study examined abnormalities leading to falled mitral valve repair in two populations: “immediate failure” of the valve repair in the operating room requiring a second run of cardiopulmonary bypass and “late failure” of valve repair necessitating reoperation on another occasion. Intraoperative echocardiography (IOE) after cardiopulmonary bypass was performed in 309 patients undergoing valve repair for mitral regurgitation over a 3-year period. Twenty-six (8%) of these patients had immediate failure of the repair demonstrated by IOE, requiring further repair or replacement during the same thoracotomy. The causes of immediate failure were left ventricular outflow tract obstruction (10 patients), incomplete correction (10 patients), and suture dehiscence (six patients). Echocardiography was performed on 17 patients requiring reoperation for recurrent mitral regurgitation who had undergone previous primary valve repair. These late failures resulted from progressive degenerative leaflet or chordal disease ( n = 9) or suture dehiscence of the annular ring or the leaflet resection site ( n = 6). In only two patients early in the series did the problem originate from inadequate initial surgery. IOE is an effective marker for unsuccessful mitral valve repair, and affords an understanding of the mechanism of the persistent dysfunction. Immediate failure of mitral repair may be reduced by greater attention to the mechanism of valve dysfunction and by changes in valvuloplasty technique to avoid outflow tract obstruction. Late failure after mitral repair occurs predominantly due to progression of disease, particularly in patients with severe myxomatous or annular abnormalities that are prone to progress.