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Interact CardioVasc Thorac Surg 2009;9:471-475. doi:10.1510/icvts.2008.200592
© 2009 European Association of Cardio-Thoracic Surgery

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Institutional report - Valves

Early and mid-term functional and survival benefits in ischaemic versus degenerative mitral valve repair using Duran flexible ring: a single surgeon series

Zeena Makhija* and Jatin Desai

Department of Cardiothoracic Surgery, Kings College Hospital, Denmark Hill, London, SE5 9RS, UK

Received 12 December 2008; received in revised form 3 June 2009; accepted 4 June 2009

*Corresponding author. Tel.: +44 7853304079; fax: +44 2032993433.

E-mail address: profknow171{at}yahoo.com (Z. Makhija).


    Abstract
 Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 References
 
The late results of ischaemic mitral valve (MV) repair have been less than satisfying. We compared echocardiographically, the changes in LV function, mid-term durability and survival between MV repair caused by ischaemic cardiomyopathy (n=60) with degenerative MV disease (n=73) over a period of 15 years. The duration of mean follow-up was 3.7±4.1 years in the ischaemic group and 3.9±2.9 years in the degenerative group. Freedom from reoperation at seven years was 98.3%±1.5% and 98.9%±2.1%, respectively (P=0.889). At the last follow-up, NYHA functional class I or II was present in 78.4% of patients in the ischaemic group and 80.9% patients in the degenerative group (P=0.347). An improvement in LVEF was noted in both the groups: ischaemic – 41.3±12.7 (pre-op LVEF: 38.8±14.1) and degenerative – 46.5±11.1 (pre-op LVEF: 45.7±11.7) (P=0.014). At seven years, freedom from a cardiac cause of death was statistically similar in the two groups: 93.3%±1.3% and 92.2%±0.6% (P=0.967). In conclusion, the mid-term results of ischaemic MV repair are similar to those obtained for degenerative MV repair. Surgical correction of ischaemic MR results in long-term improved LVEF and comparable outcomes in terms of freedom from reoperation and survival.

Key Words: Ischaemic; Mitral valve; Repair


    1. Introduction
 Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 References
 
The functioning of mitral valve (MV), besides its valvular structure is governed by the subvalvular apparatus of papillary muscles and the chordae. The left ventricular (LV) function (measured as ejection fraction – EF) therefore assumes importance besides the degree of mitral regurgitation (MR) when considering a patient for surgical repair [1]. Coronary artery disease (CAD) leading to myocardial infarction is a common pathology which, by affecting the leaflet mobility or subvalvular structure, can cause MR [2, 3].

The asymmetric deformation of the mitral valvular apparatus in ischaemic MR has been shown by Kwan and colleagues using 3-D echocardiography which makes repair in such cases more challenging. With the increasing incidence of CAD, the incidence of related ischaemic MR has grown [4]. Clear benefits of operating on such patients are yet to be shown in randomized controlled trials.


    2. Materials and methods
 Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 References
 
One hundred and sixty patients underwent MV repair in our institution from 1992 to December 2007 under a single surgeon. These were all prospectively entered into the hospital database. For the purpose of this study, only patients with either ischaemic or degenerative MR were selected. Therefore, 27 patients were excluded from the statistical analysis based on one or more of the following criteria:

  1. Aetiology of MR other than ischaemic or degenerative,
  2. Associated aortic disease,
  3. Associated aortic or tricuspid repair or replacement.

Of the 133 selected patients, 60 had ischaemic and 73 had degenerative MR. There was no significant difference in the preoperative characteristics of the two groups (Table 1).


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Table 1 Preoperative data

 
2.1. Surgical technique

The valve repairs were preformed through median sternotomy with cardiopulmonary bypass. Moderate hypothermia (32–36 °C) was used with blood cardioplegia. The MV was exposed through trans-left atrial approach. An initial inspection of the valve was done to assess annular dilatation and/or disproportionately elongated segments. Traction sutures were placed in the annulus, if required at commissures to elevate valve and facilitate exposure. The repair was appropriated towards correcting ruptured, elongated, or sclerosed chordae; and/or redundant or defective leaflet tissue. Duran flexible ring was used for the MV repair. Annular debridement and commissurotomy were required in 8 (2.6%) and 14 (4.5%) cases, respectively. We found that the posterior MV leaflet (pmvl) pathology was responsible for the MR in most cases irrespective of the two groups. Leaflet restriction and prolapse were responsible in the majority of cases for ischaemic and degenerative MR in the respective cohorts.

We encountered ruptured and elongated chords from the middle section of the posterior leaflet in 82% (n=60) patients in the degenerative group. Pmvl repair was done before implanting the annuloplasty ring in these cases. Amvl repair was performed in 17.8% (n=13) cases, with 6.8% (n=5) requiring bileaflet repair in the degenerative group. After repair of the primary valvular lesion, the valve was tested for competence with instillation of saline in left ventricle. The characteristics of the leaflet coaptation were carefully analysed. We identified eccentric regurgitation jets in 18.3% (n=11) cases in the ischaemic group associated with a failure of coaptation along only a limited part of leaflets' free edge. In these cases a partial posterior reduction annuloplasty was done.

CABG was done in 28.7% (n=21) patients in the degenerative group and 45% (n=27) in the ischaemic group. The number of single-vessel, two-vessel and three-vessel grafts in the degenerative group was 12.3% (n=9), 6.8% (n=5), and 9.6% (n=7), respectively. The number of single-vessel, two-vessel and three-vessel grafts in the ischaemic group was significantly higher at 5% (n=3), 15% (n=9), and 25% (n=15), respectively.

There was no significant difference in the bypass or cross-clamp times between the two groups (Table 2).


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Table 2 Intra-operative data

 
2.2. Follow-up

All the patients were regularly seen at six weeks, six months and yearly thereafter. Our follow-up was 100% complete. An echocardiographic examination report was available for all patients at six months and in 96% at one year. Mean follow-up was 3.7±4.1 years in the ischaemic group and 3.9±2.9 years in the degenerative group. Echocardiographic data were available for 56.1% (n=41) patients in the degenerative group and 78.3% (n=47) patients in the ischaemic group at the last follow-up.

2.3. Statistical analysis

Data analysis was done using SPSS version 16.0 for the Windows software package.


    3. Results
 Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 References
 
3.1. Postoperative morbidity

See Table 3.


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Table 3 Postoperative outcomes

 
3.2. Post-repair TOE findings

All patients had trans-oesophageal echocardiogram (TOE) intra-operatively. These findings are tabulated in Tables 4 and 5. Residual 1+MR was present in 3 (5%) patients in the ischaemic group and 11 (15.1%) in the degenerative group (P=0.131). Residual 2+MR was present in 1 (1.7%) patient in the ischaemic group and 2 (2.7%) in the degenerative group (P=0.149).


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Table 4 Comparison of degree of MR

 

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Table 5 Functional status evaluation

 
3.3. Echocardiographic and functional status

All patients were examined with a transthoracic echocardiogram prior to discharge and serially on follow-up in the outpatient department (Tables 4 and 6). At the last follow-up, in the ischaemic group MR was absent or mild in 95% patients. The mean and peak mitral gradients were 3.1±1.6 and 8.4±3.8, respectively. In the degenerative group, MR was absent or mild in 95.9% patients. The mean and peak mitral gradients in this group were 2.6±1.3 and 7.5±3.6, respectively. An improvement in LVEF was noted in both the groups: ischaemic – 41.3±12.7 and degenerative – 46.5±11.1 (P=0.014). NYHA functional class I or II was present in 78.4% of patients in the ischaemic group and 80.9% patients in the degenerative group (P=0.347) (Table 5). In symptomatic NYHA grade III or IV patients, it was noted that they had poor preoperative LVEF and/or chronic atrial fibrillation. It was not correlated with the degree of postoperative mitral valvular dysfunction.


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Table 6 Comparison of LVEF

 
3.4. Atrial fibrillation

Preoperative atrial fibrillation was present in 42.4% (n=31) vs. 35% (n=21) in the degenerative and ischaemic groups (P=0.412). The incidence reduced at discharge to 31.5% (n=23) in the degenerative group vs. 25% (n=15) in the ischaemic group (P=0.362). At follow-up, this had further reduced to 23.2% (n=17) in the degenerative group as compared to 23.3% (n=14) in the ischaemic group (P=0.98).

3.5. Reoperation

One (1.7%) patient in the ischaemic group and one patient (1.4%) in the degenerative group underwent reoperation for significant residual MR between 1–84 months after the first repair. Successful MV replacement was performed on these two patients. Freedom from reoperation at seven years was 93.3%±1.3% and 92.2%±0.6% (P=0.967).

3.6. Mortality

The peri-operative mortality was 5% (n=3) and 1.4% (n=1) in the ischaemic and degenerative groups, respectively (P=0.223). The causes of in-hospital mortality were ARDS (n=1), ischaemic colitis (n=1) and low output syndrome (n=2). The late mortality was 6.7% (n=4), 6.8% (n=5) in the two groups, respectively (P=0.967). Of these in the ischaemic group one death was cardiac related with an actuarial overall survival of 94.3%±3.06% at seven years. In the degenerative group, two deaths were due to a cardiac cause with an actuarial survival of 93%±2.9% at seven years. Freedom from a cardiac cause of death was statistically similar in the two groups: 97.3%±2.2% and 96.9%±1.6% at seven years (P=0.667) (Fig. 1). Cumulative survival was found to be statistically similar between the two groups (P=0.983).


Figure 1
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Fig. 1. Survival curves.

 

    4. Discussion
 Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 References
 
It is a common dilemma for cardiothoracic surgeons to predict the timing and success of ischaemic MV repair. It was believed that a repair would increase the preload on a poorly functioning ventricle by removing the decompression effect of MR and hence increase mortality as compared to repair for degenerative MR [5].

Braunberger and colleagues evaluated the results of MV repair for degenerative disease on 162 patients over a period of 14 years. They reported a peri-operative mortality of 2%. In their study, the reoperation rates for failed MV repair were 6% and 8%, respectively, at 10 and 20 years [6].

Another report by Gillinov et al. from the Cleveland Clinic had a 0.3% surgical mortality and 7% reoperation rate at 10 years [7].

In contrast, there are data in the literature to suggest that repair of chronic IMR has a higher operative mortality (as compared to degenerative MR) ranging from 3.0% to 29.4% and reoperation rates of up to 14.7% [8, 9]. More reports in the literature have added to this evidence [10].

Calafiore et al. showed that mild-moderate MR impairs the long-term outcome in patients with an EF between 31–40% [11].

Vaskelyte et al. studied the impact of unrepaired vs. repaired MR on functional status of patients with ischaemic cardiomyopathy at one year after CABG in patients with EF<0.30. They found that a significant reduction or elimination of MR after combined surgery was found to have a positive impact on reverse LV remodeling, regression of LV dilatation, increased LVEF, and decreased pulmonary artery pressures [12]. Bax et al. obtained excellent results on 51 patients with ischaemic LV dysfunction and severe MR who underwent CABG and restrictive annuloplasty. Residual MR was absent/minimal at 2-year follow-up, with a significant reduction in left atrial and LV dimensions [13]. MV repair can favourably alter LV geometry and effectively eliminate residual MR in such patients [4, 14]. These findings were supported in another study by Wong et al. who reviewed 351 patients undergoing CABG with 3+ischaemic MR. They found that patients with moderate ischaemic MR undergoing CABG had relatively poor long-term survival. The survival rates were significantly different when stratified according to preoperative characteristics [15].

More importantly, all these data show that a limited number of valve repairs can be done successfully per year with very good to excellent results for both degenerative and ischaemic disease [16].

This study shows that the mid-term results of repair in ischaemic MR are similar to those observed in patients undergoing a MV repair for degenerative MV. The freedom from reoperation and late mortality rates were comparable. Considering that there was a selection bias in the study which led to the exclusion of some of the most common factors which affect the longevity of a mitral repair (e.g. rheumatic cause, preoperative endocarditis, and concomitant tricuspid repair) this was explicable. In this series, patients underwent surgical repair even if they were asymptomatic (NYHA functional class I or II) but had poor LV function and/or severe MR. Greater than 95% of patients at follow-up were found to be in NYHA I or II functional class. Low and comparable reoperation rates (0.9% vs. 1%) are indicators of the success of MV repair in the ischaemic group. The cardiac related mortality rates reported in our study compare favourably with those in the literature. These also indicate the viability of performing MV repair in the ischaemic group.

We minimised the confounding bias in our study by including only adult patients who had MV repair using Duran flexible ring. Also, since it is a single surgeon series, same protocol was followed for patient management and selection for reoperation in case of postoperative residual MR.

Another corollary that we derived from the results of our single surgeon series with an average of nine mitral repairs/year is that valve repair can be performed adequately, even by surgeons with a lower caseload. Since there are no data in the literature which give an exact average number of MV repairs performed by a surgeon over the span of their careers, this conclusion may be an interesting indicator of the much feared learning curve of MV repair.

This, however, does not refute the fact that this study has limitations of a retrospective review. Since an echocardiographic examination was not available for all the patients, the repair failure rate could have been underestimated. Also, the derivation of insignificant differences in outcomes between the two groups could have resulted from smaller number of patients or insufficient number of events in the study groups like reoperation. Though favourable early outcomes have been shown in other studies, this study has the advantage of durable mid-term results. A complete follow-up, with serial echocardiographic examinations available in the majority of the patients validates the results of this study.


    References
 Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 References
 

  1. Degandt AA, Weber PA, Saber HA, Duran CMG. Mitral valve basal chordae: comparative anatomy and terminology. Ann Thorac Surg 2007;84:1250–1255.[Abstract/Free Full Text]
  2. Filsoufi F, Salzberg SP, Adams DH. Current management of ischemic mitral regurgitation. Mt Sinai J Med 2005 Mar;72:105–115.[Medline]
  3. Carpentier A. Cardiac valve surgery – The ‘French Connection’. J Thorac Cardiovasc Surg 1983;86:323–337.[Medline]
  4. Levine RA, Schwammenthal E. Ischaemic mitral regurgitation on the threshold of a solution: from paradoxes to unifying concepts. Circulation 2005;112:745–758.[Free Full Text]
  5. Kim YH, Czer LS, Soukiasian HJ, De Robertis M, Magliato KE, Blanche C, Raissi SS, Mirocha J, Siegel RJ, Kass RM, Trento A. Ischemic mitral regurgitation: revascularization alone versus revascularization and mitral valve repair. Ann Thorac Surg 2005 Jun;79:1895–1901.[Abstract/Free Full Text]
  6. Braunberger E, Deloche A, Berrebi A, Abdallah F, Celestin JA, Meimoun P, Chatellier G, Chauvaud S, Fabiani JN, Carpentier A. Very long-term results (More than 20 years) of valve repair with Carpentier's techniques in nonrheumatic mitral valve insufficiency. Circulation 2001;104:I-8–I-11.[CrossRef]
  7. Gillinov AM, Cosgrove DM, Blackstone EH, Diaz R, Arnold JH, Lytle BW, Smedira NG, Sabik JF, McCarthy PM, Loop FD. Durability of mitral valve repair for degenerative disease. J Thorac Cardiov Sur 1998;116:734–743.[CrossRef]
  8. Cohn LH. Surgical treatment of ischemic mitral regurgitation by repair and replacement. In Vetter HO, Hetzer H, Schmutzler H, Ischemic mitral incompetence. New York: Springer-Verlag; 1991:179.
  9. Oury JH, Cleveland JC, Duran CG, Angell WW. Ischemic mitral valve disease: classification and systemic approach to management. J Card Surg 1994;9(2 Suppl):262–273.[CrossRef][Medline]
  10. Gillinov AM, Wierup PN, Blackstone EH, Bishay ES, Cosgrove DM, White J, Lytle BW, McCarthy PM. Is repair preferable to replacement for ischemic mitral regurgitation? J Thorac Cardiovasc Surg 2001;122:1125.[Abstract/Free Full Text]
  11. Calafiore AM, Mazzei V, Iaco AL, Contini M, Bivona A, Gagliardi M, Bosco P, Gallina S, Di Maruo M. Impact of ischemic mitral regurgitation on long-term outcome of patients with ejection fraction above 0.30 undergoing first isolated myocardial revascularization. Ann Thorac Surg 2008;86:458–465.[Abstract/Free Full Text]
  12. Bax JJ, Braun J, Somer ST, Klautz R, Holman ER, Versteegh MI, Boersma E, Schalij MJ, van der Wall EE, Dion RA. Restrictive annuloplasty and coronary revascularization in ischemic mitral regurgitation results in reverse left ventricular remodeling. Circulation 2004 Sep 14;110(11 Suppl 1):II103–II108.[Medline]
  13. Vaskelyte J, Stoskute N, Ereminiene E, Zaliunas R, Benetis R, Sirvinskas E. The impact of unrepaired versus repaired mitral regurgitation on functional status of patients with ischemic cardiomyopathy at one year after coronary artery bypass grafting. J Heart Valve Dis 2006;15:747–754.[Medline]
  14. Glower DD, Tuttle RH, Shawl K, Orozco RE, Rankin IS. Patient survival characteristics after routine mitral valve repair for ischemic mitral regurgitation. J Thorac Cardiovasc Surg 2005;129:860–868.[Abstract/Free Full Text]
  15. Wong DR, Agnihotri AK, Hung JW, Vlahakes GJ, Akins CW, Hilgenberg AD, Madsen JC, MacGillivray TE, Picard MH, Torchiana DF. Long-term survival after surgical revascularization for moderate ischemic mitral regurgitation. Ann Thorac Surg 2005 Aug;80:570–577.[Abstract/Free Full Text]
  16. Angell WW, Oury JH. A comparison of replacement and reconstruction in patients with mitral regurgitation. J Thorac Cardiovasc Surg 1987;93(665.




This Article
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