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J Thorac Cardiovasc Surg 2008;135:274-282
© 2008 The American Association for Thoracic Surgery
Surgery for Acquired Cardiovascular Disease |
a Cardiac Surgery, Department of Cardiovascular Diseases, Katholieke Universiteit Leuven, Leuven, Belgium
b Cardiology, Department of Cardiovascular Diseases, Katholieke Universiteit Leuven, Leuven, Belgium
Received for publication February 2, 2007; revisions received June 12, 2007; accepted for publication June 14, 2007. * Address for reprints: Willem Flameng, MD, PhD, Cardiac Surgery, University Clinic Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium. (Email: willem.flameng{at}med.kuleuven.ac.be).
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Abstract |
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Methods and Results: In 348 patients having undergone mitral valve repair for degenerative valve incompetence, clinical outcome was excellent: 10 years after repair, survival was 80.1% and freedom from reoperation 94.4%. However, freedom from mitral regurgitation (>2/4), 98.7% at 1 month, decreased to 82.2% at 5 years and 64.9% at 10 years. The linearized recurrence rate of mitral regurgitation (>2/4) was 3.2% per year. Recurrence rate was higher in patients with Barlow disease (6.0%) and lower in those with fibroelastic deficiency (2.6%) (P = .01). Performing chordal shortening, the nonuse of sliding plasty and the nonuse of an annuloplasty ring were determined to be factors predicting recurrence of mitral regurgitation. In reconstructions avoiding these risk factors, recurrence rate decreased to 2.4%. There was no difference between Barlow disease and fibroelastic deficiency: 2.9% versus 2.2% (P > .05). Recurrent regurgitation is characterized by leaflet prolapse, thickening, and calcification.
Conclusion: When optimal surgical techniques are used, the residual recurrence rate of mitral valve regurgitation remains between 2% and 3% per year and is related to progressive degeneration of the chordae and the leaflets. Long-term results of mitral valve repair in Barlow disease are essentially the same as in fibroelastic deficiency.
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Introduction |
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demonstrated that the linearized recurrence rate of recurrent mitral regurgitation greater than 2/4 after surgical repair was 3.7% per year in patients with degenerative valve disease. Inadequate surgical techniques could only partially explain this recurrence of regurgitation. In patients receiving optimal repair techniques, the recurrence rate of regurgitation dropped to 2.5% per year. We suggested that the progression of the degenerative disease of the valve was responsible for this small but constant recurrence rate. Recurrence rates of regurgitation were not previously reported because most studies so far were focusing on survival and reoperation rates, which were found to be excellent.2-9 In our study, survival was also high (80.1% at 10 years), as was freedom from reoperation (94% at 10 years). Diseased valves can be successfully repaired by a variety of surgical techniques, and our results confirmed this high immediate operative success: 98.3% of the patients was free of significant (>2/4) regurgitation 1 month postoperatively as defined by echocardiography.1 However, as recent studies have demonstrated, myxomatous valve leaflets are structurally, biochemically, physically, and mechanically abnormal10 and a certain progression of the disease can be expected after repair. Therefore, we were not surprised to find that 7 years postoperatively only 71% of the patients were still free of greater than 2/4 regurgitation.1 This finding was confirmed by David and associates9 in a more recent study. They found that 12 years postoperatively, only 73% of the patients were free from moderate or severe mitral insufficiency of more than 3/4, a result is even worse than that of our study.
In patients with degenerative mitral valve disease, Carpentier and colleagues11 distinguished two different forms: Barlow disease and fibroelastic degeneration. These two diseases may not have the same outcome, because Barlow disease is a more generalized degeneration of the valve.
The goal of the present study was to analyze the recurrence of mitral regurgitation in terms of incidence and degree in a series of patients undergoing mitral valve repair for degenerative disease, with special reference to Barlow disease. All patients were operated on in the same institution, by the same surgeon, with standard repair techniques.
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Materials and Methods |
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Mitral Valve Characteristics
On the basis of the preoperative echocardiogram and a detailed drawing of the operative findings, valve pathologic status was identified and coded at the end of the operation. We differentiated between Barlow disease and fibroelastic deficiency on the basis of gross appearance of the valve, according to Carpentier,11 Fornes,12 and their associates. The following criteria were used to classify the patients into these two groups:
Eighty-three patients were classified as having Barlow disease (24%) and 265 (76%) as having fibroelastic deficiency. Demographic data and mitral valve characteristics are listed in
Table 1.
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In every patient, the specific surgical repair techniques used were identified and coded at the end of the operation: intervention at the leaflet (none, quadrangular resection, triangular resection, plication, cleft closure), intervention at the annulus (none, sliding plasty, plication, decalcification), at the chordae (none, shortening, transposition, artificial chordae), at the papillary muscles (none, shortening), and the placement of an annuloplasty ring (yes or no). The frequency with which these different techniques were used is listed in
Table 2.
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Statistical Analysis
The Cox proportional hazards methods were used to analyze the data on recurrence of mitral regurgitation in time. For survival and follow-up of events, Kaplan–Meier techniques were used with log–rank testing. For recurrence of mitral regurgitation, a classic Kaplan–Meier technique was used with the first echocardiographic follow-up date demonstrating the recurrence of regurgitation as date of the event. Since the mitral regurgitation did in fact recur between the last echocardiogram without regurgitation (or the date of the operation if the echocardiogram before hospital discharge showed mitral regurgitation) and the first echocardiogram with regurgitation, an interval-censored survival curve using the Turnbull algorithm was constructed additionally. For plotting the nonparametric maximum likelihood estimate on the basis of interval-censored data, the mass was always placed at the at rightmost limit of the interval.
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Results |
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Figure 1, A). Survival was identical between patients having Barlow disease and patients having fibroelastic deficiency (P > .05). Survival did not differ significantly between patients with or without associated coronary artery bypass graft procedures (P > .05). Freedom from reoperation at 5 years was 95.4% ± 1.4% and 94.4% ± 1.6% at 10 years for all patients (Figure 1, B). Freedom from reoperation for fibroelastic deficiency was better (96.6% at 10 years) than for Barlow disease (86.1% at 10 years) (P = .002).
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During the most recent postoperative follow-up period, NYHA class was recorded. Corresponding to the mean follow-up time of the entire population, 91.3% of the patients improved by at least one NYHA functional class. Seventy-five percent of the patients were in class I, 19% in class II, 5% in class III, and 1% in class IV. Postoperatively, 71% of the patients had sinus rhythm, 22% had atrial fibrillation, and 7% had a pacemaker. Anticoagulation therapy using coumarin was given during the follow-up period in 35% of the patients. Freedom from thromboembolic events and/or major anticoagulant-related bleeding was 93.5% ± 1.5% at 5 years and 86.7% ± 2.7% at 10 years for the whole group.
Immediate Surgical Result of Mitral Valve Repair
Operative success of the mitral valve repair was assessed by the echocardiographic examination of mitral valve function within the first 4 weeks postoperatively. At 1 month postoperatively, 98.7% of all patients had no or trivial mitral regurgitation (0/4 or 1/4). In patients having fibroelastic degeneration, this was 99.8% and in Barlow disease 97.1%. Suture dehiscence of the ring annuloplasty was encountered in 2 patients. Endocarditis of the repaired valve did not occur in this series.
Recurrence of Mitral Regurgitation
Postoperative echocardiography was performed serially at 6-month intervals. According to the classic Kaplan–Meier approach, freedom from failing repair (regurgitation > 2/4) was 98.7% ± 1.2% at 1 month, 82.2% ± 3.7% at 5 years, and 64.9% ± 5.6% at 10 years (
Figure 2). When the interval-censored Turnbull approach is used to calculate the freedom from recurrence of mitral incompetence, similar results are obtained. Freedom from failing repair is better in fibroelastic deficiency and worse in Barlow disease (P = .01). Remarkable is the constant rate of recurrence of mitral regurgitation after the first 6 months postoperatively. When the classic Kaplan–Meier curves are restricted to the period from 6 months until 7 years postoperatively, a linear regression can be made, allowing calculation of recurrence rates per year. Recurrence of mitral regurgitation of greater than 2/4 occurs at a constant rate of 3.2% per year for the whole patient group (
Table 3). The linearized curves are shown for the patients with fibroelastic disease and Barlow disease separately in
Figure 3, A and B.
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Table 4) revealed that the subpopulation showing recurrence of regurgitation was mainly characterized by a higher incidence of Barlow disease (P = .01). Bileaflet mitral valve degeneration as such showed a trend toward higher recurrence of regurgitation (P = .06). The absence of ruptured chordae (P = .01) as well as the presence of elongated chordae (P = .003) predicts also recurrence of regurgitation. Specific surgical repair techniques had a predictive value for recurrence of regurgitation: the nonuse of a sliding annuloplasty (P = .002), the use of chordal shortening (P = .01), and the nonuse of an annuloplasty ring in general (P = .001) predict inferior outcome.
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When we divided the patient population into patients having Barlow disease and patients having fibroelastic deficiency, the risk factors became more focused (Table 4). In fibroelastic deficiency, the nonuse of a quadrangular resection predicts recurrence of regurgitation (P = .02) as well as the nonuse of an annuloplasty ring (P = .04) and the nonuse of a sliding annuloplasty (P = .01). In Barlow disease, the presence of abnormal or elongated chordae (P = .02) is the main predictor of regurgitation, as well as the use of chordal shortening (P = .04), the nonuse of polytetrafluoroethylene chordae (P = .02), and the nonuse of an annuloplasty ring (P = .004). When the two populations bear the corresponding risk factors, recurrence rates are 3.6% per year for fibroelastic deficiency and 14.9% per year for Barlow disease (P < .05) (Table 3, Figure 3, A and B). When the correction for the corresponding surgical risk factors is made for these two patient populations (Table 3), the following linearized recurrence rates are found: 2.9% per year for Barlow disease and 2.2% per year for fibroelastic deficiency. The difference between the two rates is not statistically significant (P > .05).
Echographic Characteristics of Recurrent Mitral Valve Regurgitation
The echocardiograms from the patients showing recurrence of greater than 2/4 mitral regurgitation were analyzed in an attempt to define possible mechanisms of valve incompetence. We found that 42% of these patients had a leaflet prolapse that was mostly an anterior leaflet prolapse (in 81% of cases). In the group with fibroelastic deficiency, 41% of the patients had a leaflet prolapse (80% anterior), and about the same results were seen in the group with Barlow disease: 43% showed leaflet prolapse (83% anterior). Chordal rupture or elongation was found in 24% of the patients. Leaflet thickening was diagnosed in 50% of the patients (50% with fibroelastic deficiency and 43% with Barlow disease), and leaflet calcifications were detected in 25% of the patients (29% of patients with fibroelastic deficiency and 7% of those with Barlow disease). These calcifications were pre-existent in only 4% of the patients. Left ventricular function was described as reduced in 55% of the patients, and 59% had a nonsinus rhythm.
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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made a clear distinction between Barlow disease and fibroelastic deficiency. In later work, Fornes and colleagues12 investigated the histologic differences but were unable to obtain a clear distinction between the two entities on this basis. They concluded "obviously the surgeons' diagnosis based on clinical examination, echocardiographic findings and operative macroscopical findings of the mitral valve apparatus should remain the gold standard." We followed their macroscopic criteria to separate Barlow disease from fibroelastic deficiency.
Our results are in concordance with the available clinical reports showing good clinical outcome and low reoperation rates after repair.2–9 We also found a low reoperation rate at 10 years (94.4% freedom) and an excellent clinical outcome. On the other hand, the present article confirms our previous findings that recurrence of mitral valve insufficiency based on echocardiographic studies is more frequent than the reoperation rate indicates.1 Obviously, reoperation rate is not an optimal predictor of recurrent mitral valve regurgitation and is not the best parameter to estimate durability of valve repair. However, long-term results (over 20 years) after repair for mitral valve prolapse were reported in 2001,13 and they suggest that the durability of mitral valve repair will be limited but that the therapeutic consequences remain delayed. Reoperation rate after repair constantly increases: at 5 years it is 7%, at 10 years 11%, at 15 years 16%, and at 19.5 years 20%. Survival at 19.5 years is 30%.
As mentioned earlier, our immediate postoperative echocardiographic results were excellent: 98.7% of the patients had no or trivial (0/4 or 1/4) mitral valve regurgitation. In fibroelastic deficiency this was 99.8% and in Barlow disease 97.1%. However, despite such highly successful repair, recurrence of mitral valve incompetence occurs at a constant rate during the following years. Causes of recurrence of regurgitation after mitral valve repair may be classified as procedure-related or valve-related.
Concerning procedure-related or surgical factors, our study revealed nothing new: the nonuse of an annuloplasty ring, nonuse of a sliding plasty, and the use of chordal shortening instead of transposition or artificial chordae were factors of recurrence of mitral valve incompetence, as already shown by others.6 In a larger study, Gillinov and coworkers5 demonstrated that the instantaneous risk of reoperation consists of two hazard phases: a peaking early hazard phase in the first year after the operation followed by a slow-rising late hazard phase of reoperation. They showed that patients with an isolated anterior leaflet prolapse had an increased early risk of reoperation. Also, chordal shortening increased the risk of early repair failure and the use of ring annuloplasty and leaflet resection decreased the risk of reoperation in the late hazard phase. Nevertheless, most of these surgical factors are indirectly related to the process of valve degeneration, mainly in the chordae, which are severely structurally altered by the degenerative process. Therefore, besides overall progression of the valve disease, specific repair techniques may influence recurrence of regurgitation. For example, quadrangular resection of the billowing and degenerated portion of a posterior leaflet may fully exclude the diseased part of the valve and can be expected to be more durable than shortening of elongated and severely affected chordae, which are shortened but left in place. Obviously, the degeneration of the chordae progresses after repair, which is shown by the postoperative echocardiographic studies. More than 40% of the patients showing significant recurrence of regurgitation have a new leaflet prolapse, mainly from the anterior leaflet. This may originate either from progressive degeneration of the valve or from retraction of the repaired posterior leaflet segment, resulting in relative prolapse. The high incidence of chordal rupture or elongation suggests the first mechanism. Furthermore, half of these valves have leaflet thickening and one third have new calcifications. These findings suggest that the chordae elongate and the leaflet degenerates further. This explains also why implantation of artificial chordae is associated with superior results.14 Maybe the use of artificial chordae should be promoted and even used as a standard technique in every repair as a prevention of recurrence of regurgitation. Regarding the risk for SAM, the use of large annuloplasty rings (sizes 36 to 40) has recently been advocated instead of avoiding the use of an annuloplasty ring.15
Myxomatous degeneration of the valve affects the leaflets as well as the subvalvular apparatus, and the extent of structural and mechanical changes differs between them.10 Although histologic alterations in myxomatous valves have been well described in the past,16-20 only recently have the mechanical properties of myxomatous mitral valves been extensively studied,10 and it is shown that myxoid leaflets are more extensible and less stiff than normal valves. It is also demonstrated16 that cells of the chordae of myxomatous valves produce more glycoaminoglycans, giving them their characteristic thickening and gelatinous nature, which may account for their mechanical weakness.21 All these pathophysiologic findings may help to explain why a progressive incidence of mitral valve incompetence is found after initial adequate repair. When patients bearing the surgical risks (ie, use of chordal shortening, nonuse of an annuloplasty ring, and nonuse of sliding plasty) are excluded from the analysis, recurrence rate drops from 3.2% per year to 2.4% per year. This residual rate of 2.4% per year can be attributed to the phenomenon of valve degeneration. However, two distinct forms of valve degeneration were described: fibroelastic deficiency and Barlow disease.11,12 Because Barlow disease is a more generalized form of valve degeneration, the progression of the degenerative process in these valves can be expected to be more pronounced and reflected in the recurrence rates of mitral regurgitation. At first glance this is correct: the recurrence rate in Barlow disease is 6.0% per year and in fibroelastic deficiency 2.6% per year. However, the impact of the surgical risk factors is so high that after correction for these techniques, the residual recurrence rate decreases to almost that of fibroelastic deficiency (2.9 vs 2.2% per year).
It can be concluded that the long-term result of mitral valve repair in Barlow disease is essentially the same as in fibroelastic deficiency provided optimal surgical techniques are used. A constant recurrence rate of regurgitation (2%–3% per year) remains present owing to progression of the degenerative process in the native valve.
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Footnotes |
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