ARTICLE IN PRESS doi:10.1510/icvts.2005.121590
Interactive CardioVascular and Thoracic Surgery 5 (2006) 356–361 www.icvts.org
Institutional report - Valves
Results of mitral valve repair in rheumatic mitral regurgitation夞 Arkalgud Sampath Kumara,*, Sachin Talwarb, Anita Saxenab, Rajvir Singhc, Devagourou Velayoudamb Department of Cardiothoracic & Vascular Surgery, Cardiothoracic Centre, All India Institute of Medical Sciences, Ansari Nagar, New Delhi – 110 029, India b Cardiothoracic Centre, All India Institute of Medical Sciences, New Delhi, India c Department of Biostatistics, All India Institute of Medical Sciences, New Delhi, India
a
Received 6 October 2005; received in revised form 14 February 2006; accepted 1 March 2006
Abstract Between January 1988 and December 2003, 898 patients with rheumatic heart disease (mean age 22.4"10.1 years) underwent mitral valve (MV) repair. Five hundred and sixty-five patients (63%) had pre-operative atrial fibrillation. Six hundred and ten (68%) patients were in NYHA class III or IV. Four hundred and twelve (45.9%) had pure mitral regurgitation (MR) and 486 (54.1%) had mixed mitral stenosis and MR. The pathology was leaflet prolapse (ns270, 30%), annular dilatation (ns717, 79.8%) and calcification (ns39, 4.3%). Reparative procedures included annuloplasty (ns793, 88%), commissurotomy (ns530, 59%), chordal shortening (ns225, 25%), cusp excisionyplication (ns41, 4.5%), cuspal thinning (ns325, 36%), cleft suture (ns142, 16%), decalcification (ns30, 3.3%), chordal transfer (ns13, 1.4%), and neo chordae construction (ns3, 0.3%). Early mortality was 32 (3.6%). Follow-up ranged from 6 to 180 months (mean 62.7"31.8 months) and was 96% complete. Six hundred and twenty-one patients (69%) had no, or trivial, or mild MV. Two hundred and seventy-seven of the 866 survivors had MR which was moderate in 153 (18%) and severe in 124 (14%) patients. Thirty-five patients underwent re-operation. There were 21 late deaths (2.4%). Actuarial and re-operation-free survival at 10 years were 92"1.1% and 81"5.2%, respectively. Freedom from moderate or severe MR was 32"3.9%. MV repair in the rheumatic population is feasible with acceptable long-term results. 䊚 2006 Published by European Association for Cardio-Thoracic Surgery. All rights reserved. Keywords: Mitral valve repair; Rheumatic heart disease; Regurgitation
1. Introduction Rheumatic heart disease (RHD) is the leading cause of mitral valve (MV) disease in the developing world. Mechanical MV replacement has its attendant complications w1x. MV repair avoids these complications, permits growth and preserves left ventricular geometry and function. MV repair in RHD is technically demanding w2–4x. However, current techniques permit surgery to be carried out with acceptable late outcome w5–8x. This study analyses the results of MV repair for RHD performed at our institution over the last 15 years. 2. Materials and methods Between January 1988 and December 2003, 2718 MV procedures were performed by the author (ASK) including isolated MV (ns882), combined aortic and MV replacement (ns452), open mitral commissurotomy (ns362) and MV repair (ns1022, 37.6%). Of the 1022 patients who underwent MV repair, 898 (88%) had pure mitral regurgitation (MR) or a combination of mitral stenosis (MS) due to RHD. Patients with pure MS are not included as many of them undergo closed mitral valvotomy or open mitral commissur夞 Presented at the joint 19th Annual Meeting of the European Association for Cardio-thoracic Surgery and the 13th Annual Meeting of the European Society of Thoracic Surgeons, Barcelona, Spain, September 25–28, 2005. *Corresponding author. Tel.yfax: q91-11-26588889. E-mail address:
[email protected] (A. Sampath Kumar).
otomy. Also, only patients with successful MV repair in the operating room were included. Pre-operative transthoracic echocardiography was performed in all. Cardiac catheterization and cineangiography was performed on suspicion of associated aortic valve disease or coronary artery disease. MR was graded by Doppler echocardiography or angiography or both w9,10x. After January 1994, intra-operative trans-oesophageal echocardiography (TEE) was performed in all. Echocardiographic assessment included mitral annulus, leaflet thickness and mobility, commissural and chordal fusion, calcification, regurgitant jet, thickness of chordae tendineae, left atrial thrombus and other valvular lesions. 2.1. Surgical techniques Surgical approach was via a mid-sternotomy (ns735) or a right anterolateral throacotomy in young females (ns163) for cosmetic reasons. Aorto-bicaval cannulation was used in all. Before 1996 moderately hypothermic (32 8C) cardiopulmonary bypass was used. Since 1996 normothermic perfusion was used in all. Cold blood cardioplegia and topical ice slush was used for myocardial protection. MV was exposed through an incision behind the interatrial groove. In patients with associated atrial septal defect the approach was through the right atrium. Depending on the valve morphology, a combination of techniques was used including annuloplasty, commissurotomy, chordal shortening, cusp excisionyplication, cuspal thinning, cleft suture,
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decalcification, chordal transfer and neo chordae construction. Annuloplasty was performed using a C-shaped ring cut out of a piece of polytetrafluoroethylene felt. These procedures were developed by us and are detailed in our prior publications w5–7x. No commercially available rings or bands were used. At completion of repair, MV was tested by injecting cold saline into the left ventricular cavity to observe co-aptation of leaflets. Since TEE became available, we used this modality in addition after discontinuation of cardiopulmonary bypass. The left atrial appendage was routinely ligated in all patients. Prior to discharge from the hospital, transthoracic echocardiography was carried out in all patients and was repeated at six-monthly intervals. Prior to 1998, all patients who underwent annuloplasty were prescribed acenocoumarin for six weeks and dipyridamole for six months. Since April 1998 this was discontinued. Currently anticoagulation with warfarin is prescribed only to patients having associated mechanical aortic valve replacement. All patients were seen at six-monthly intervals and underwent clinical examination and echocardiography. Between January 2004 and December 2004, the records of 831 of the 866 survivors were obtained and their last follow-up during this period was taken for reporting the results. 2.2. Statistical analysis Mean"standard deviation have been calculated for continuous variables. Simple percentages were used to express categorical variables. Actuarial estimates were calculated and compared using the Kaplan–Meier analysis with Mantel– Cox log-rank tests. MR was considered to be significant if it was moderate or severe. Factors analysed as predictors of early and late mortality and development of significant MR are listed in Appendix A. These were subjected to multiple logistic regression analysis. A valve related event was defined as per standard criteria w11x. Linearised rates for these events are reported. Cox’s proportional hazard model was used to analyse factors associated with a higher early and late mortality and the development of significant MS or MR.
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Table 2 Profile of patients undergoing mitral valve repair Symptoms: Dyspnoea Palpitations Chest pain CHF NYHA I II III IV Clinical diagnosis Pure MR MSqMR Associated AS Associated AR Associated ASqAR Associated TS Associated TRyTSqTR Atrial fibrillation Severe PAH LV dysfunction
832 657 32 144
(92.6%) (73.2%) (3.6%) (16%)
32 256 466 144
(3.6%) (28.5%) (51.9%) (16%)
412 486 96 30 9 6 12 565 265 64
(45.9%) (54.1%) (10.7%) (3.3%) (1%) (2%) (4%) (62.9%) (29.5%) (7%)
CHFsCongestive heart failure, MSsmitral stenosis, MRsmitral regurgitation, ASsaortic stenosis, ARsaortic regurgitation, TSstricuspid stenosis, TRstricuspid regurgitation, PAHspulmonary arterial hypertension, LVsleft ventricle.
Leaflet prolapse was present in 111 (26.9%) patients with pure MR (Table 3). Associated valvular involvement is listed in Table 2. In addition, seventeen patients had atrial septal defect, three patients had coronary artery disease and six patients had infective endocarditis. Surgical procedures are listed in Table 4. Tricuspid valve repair was accomplished by a combination of commissurotomy and suture annuloplasty. No additional surgical procedure was performed for AF. 3.1. In-hospital mortality There were 32 (3.6%) deaths (Table 3). None had significant residual MR. Logistic regression analysis identified preoperative left ventricular dysfunction and CHF as predictors of early mortality. Average postoperative stay in survivors was 6.2"1.9 days (range 5–23 days).
3. Results
3.2. Follow-up
Patient profile is presented in Tables 1 and 2. Mean age was 22.4"10.1 years (age range 4–70 years). Six hundred and ten (68%) patients were in NYHA class III or IV. Majority had mixed MS and MR. Leaflet prolapse was seen in 270 patients (30%), annular dilatation was seen in 717 patients (79.8%) and calcification in 39 patients (4.3%).
The follow-up data (96% complete) ranged from 6 to 180 months (mean 62.7"31.8 months) and totaled 4341.9
Table 1 Age and sex distribution of patients Age (years)
Male
Female
Total (%)
0–10 11–20 21–30 31–40 )40
40 195 107 23 25
21 189 192 76 30
61 384 299 99 55
Total
390 (43.4)
508 (56.6)
898 (100)
(6.8) (42.8) (33.3) (11) (6.1)
Table 3 Profile of patients with early deaths (ns32) Patient characteristics Age Sex (M:F) Pre-operative LV dysfunction Pre-operative severe PAH Pre-operative CHF Cause of death Persistent low cardiac output Acute renal failure Septicemia Malignant ventricular arrythmias Cerebrovascular accidents CHFscongestive heart failure.
9 to 60 years (mean 25"11 years) 20:12 28 (87.5%) 20 (67%) 16 (50%) 19 3 4 4 2
(59.3%) (9.4%) (12.5%) (12.5%) (6.3%)
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Table 4 Surgical procedures Surgery
No (%)
Annuloplasty Commissurotomy Chordal shortening Cusp excisionyplacation Cuspal thinning Cleft suture Decalcification Chordal transfer Neo chordae construction Associated procedures AVR (Mechanical valve) AVR (Homograft) Aortic valve repair TV Repair ASD Closure CABG
793 530 225 41 325 142 30 13 30
(88%) ( 59%) (25%) (4.5%) (36%) (16%) (3.3%) (1.4%) (3.3%)
73 (8.1%) 30 (3.3%) 32 (3.6%) 18 (1.9%) 17 (1.8%) 3 (0.3%)
AVRsAortic valve replacement, TVstricuspid valve, ASDsatrial septal defect, CABGscoronary artery bypass grafting.
patient-years. Among survivors, 37 (4.5%) were followed up for G10 years, 141 (17%) were followed for G8 years, 252 (30%) G5 years, 586 (71%) G3 years, and 752 (90%) G2 years. 3.2.1. Thromboembolism Twenty-five patients had a thromboembolic complication (0.58 events per 100 patient-years). Seventeen (68%) of these were in AF. Eight of these had concomitant aortic valve replacement and were receiving oral anticoagulants. One patient had undergone associated coronary artery bypass grafting and was on oral aspirin. Four of these died. Seven patients recovered with residual weakness, and the remainder recovered completely.
required re-operation between 25 and 175 months. Pathology at re-operation was typical of recurrent RHD with reappearance of leaflet thickening, commissural and subvalvular fusion. Twenty-four patients underwent MV replacement with a mechanical valve, nine patients underwent re-repair and two underwent homograft MV replacement. Three patients died because of persistent low output syndrome following re-operation. Freedom from re-operation at 10 years was 81"5.2% (Fig. 1). 3.2.5. Valve function Of the 898 patients, 621 operative survivors (69%) had no, or trivial, or mild MR at last follow-up. Two hundred and seventy-seven of the 866 survivors (32%) had MR which was moderate in 153 (18%) and severe in 124 (14%) patients; 35 (4%) of these underwent re-operation. Seventeen died as a result of persistent CHF. Freedom from development of moderate or severe MR was 32"3.9% at 10 years of follow-up (Fig. 2). Multi-variate analysis of risk factors for significant MR showed a high probability in patients with mixed (regurgitant and stenotic) lesions (hazard ratio 1.93, 95% confidence interval 1.29–2.6, Ps0.004) and in patients with significant left ventricular dysfunction (hazard ratio 5.2, 95% confidence interval 1.99–8.7, Ps0.003). 3.2.6. Functional class and rhythm Patients with no or trivial to mild MR are in NYHA class I. Of the 153 patients with moderate MR, 136 are free of any symptoms, 10 patients are in NYHA class II–III due to development of aortic valve disease, seven are in NYHA class III due to left ventricular dysfunction. Of the 124 patients with severe MR, 73 were in NYHA class III or IV, 35 of these underwent re-operation (three died at re-opera-
3.2.2. Hemolysis Hemolysis was seen in 35 patients (0.8 events per 100 patient-years). All had undergone annuloplasty. They presented with anaemia and evidence of intravascular hemolysis. Twenty-six of these had significant MR. Twenty of these underwent reoperation, four died without further operative intervention and two are awaiting reoperation. In nine patients with mild or moderate MR, hemolysis gradually subsided. 3.2.3. Infective endocarditis Twelve patients had infective endocarditis (0.3 events per 100 patient-years). All were successfully treated conservatively. 3.2.4. Re-operation Thirty-five patients underwent re-operation (0.8 events per 100 patient-years) for valve dysfunction after a mean period of 57"29.3 months (range 1–175 months). In four patients, re-operation was required within one month due to dehiscence of the repair. Fourteen patients required reoperation within 2–24 months. These patients had moderate MR at the time of hospital discharge and were found to have suture dehiscence (ns8) or suboptimal initial repair (ns6) at re-operation. The remaining 17 patients
Fig. 1. Reoperation free survival.
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Fig. 2. Mitral regurgitation free survival.
tion) and 14 died due to persistent heart failure. Twentyone patients are awaiting re-operation. In India, no health insurance benefit exists. Therefore, the re-operations have been delayed. The remaining 51 patients are in NYHA class I and II, and there is no cardiomegaly, and the left ventricular function is not significantly deranged. Two hundred and ninety-three (52%) of the 565 patients with pre-operative AF are still in chronic AF. We do not prescribe anticoagulants in these patients unless they have associated mechanical aortic valve replacement.
issues which are adversely affected by anticoagulation. In the absence of insurance, the cost of long-term anticoagulation, need for repeated hospital visits for monitoring anticoagulation and valve function are important. Our results with MV repair in children with RHD have been encouraging w8x and have led us to choose MV repair over replacement. Our results are comparable to those of others w2,13–16x. The majority of our patients in whom significant MR developed had mixed lesions or left ventricular dysfunction and these were independent predictors of valve failure. Others have reported similar results w2,13–16x. The majority of the failures occurred within the first 2–3 years following operation indicating technical factors as a cause. It is important the adequacy of the repair by intra-operative TEE as MR early postoperatively is mainly due to technical factors. The repair is based on adequate function of the anterior mitral leaflet and if it is thick or immobile, early re-operation is required. Our experience indicates that patients with isolated MR are likely to have a better longterm result as compared to patients with mixed lesions. To prevent early re-operation, one should not accept more than mild MR in the operating room. The later peak in re-operations after 7–8 years was due to recurrent attacks of rheumatic fever and gradual degeneration of the cusps. We believe that regular penicillin prophylaxis may prevent this; therefore, all patients are prescribed regular three-weekly injections of benzathine penicillin. 4.1. Anticoagulation protocol The left atrial appendage was routinely ligated in all. Because of this and because repair achieves an acceptable MV area, the incidence of clots in the left atrium is very
3.2.7. Late death and survival There were 21 (2.4%) late deaths (0.48 events per 100 patient-years). Four patients died due to thromboembolism, three died at re-operation and 14 died due to CHF secondary to severe MR. Four of these also had persistent haemolysis. At 10 years, the event-free survival was 32"3.9% and the actuarial-survival was 92"1.1% (Fig. 3). 4. Discussion MV repair is the procedure of choice for degenerative MR w2x, but is technically more difficult in RHD and has mixed results w3–8x. Our experience with MV repair in RHD has been encouraging w5–8x and follow-up has confirmed that if the initial repair is satisfactory and patients are followed up regularly with penicillin prophylaxis, good long-term results can be expected. As demonstrated previously w1–3x, MV replacement is associated with (a) gradual decline in left ventricular function, (b) hazards of anticoagulation, (c) thromboembolism and (d) higher incidence of endocarditis. Results from a recent series w12x show a poor survival after valve replacement. This is important in RHD as the patients are younger. Growth, marriage and pregnancy are important
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Fig. 3. Actuarial survival.
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low. In our initial experience anticoagulants were prescribed but this practice was discontinued later as we observed no additional benefit. Most of our patients come from rural areas, belong to poor socio-economic strata and their compliance with medication is poor, making it difficult to monitor anticoagulation. Therefore, we do not prescribe anticoagulants unless they have aortic valve replacement with a mechanical prosthesis. 5. Conclusion MV repair for RHD is possible in a majority of patients and carries low operative mortality, acceptable re-operation rate and satisfactory long-term survival. Considering the hazards of anticoagulation in the majority of our younger patients, repair is definitely a better option than replacement and the patients can undergo safe re-operation after their initial period of growth and development. Appendix A Factors analysed as predictors of early and late mortality and development of significant mitral regurgitation
w8x Talwar S, Rajesh MR, Subramanian A, Saxena A, Kumar AS. Mitral valve repair in children with rheumatic heart disease. J Thorac Cardiovasc Surg 2005;129:875–879. w9x Helmcke F, Nanda NC, Hsiung MC, Soto B, Adey CK, Goyal RG, Gatewood RP Jr. Color Doppler assessment of mitral regurgitation with orthogonal planes. Circulation 1987;75:175–183. w10x Grossman W. Profiles in valvular heart disease. In: Baim DS, Grossman W, editors. Cardiac catheterization, angiography, and intervention.5th ed. Baltimore: Willams & Wilkins;1996. p. 742–744. w11x Edmunds LH, Clark Re, Cohn LH, Grunkemeier GL, Miller DC, Weisel RD. Guidelines for reporting morbidity and mortality after cardiac valvular operations. J Thorac Cardiovasc Surg 1996;112:708–711. w12x Gao G, Wu Y, Grunkemeier GL, Furnary AP, Starr A. Forty-years survival with the Starr-Edwards heart valve prosthesis. J Heart Valve Dis 2004;13:91–96. w13x Gillinov AM, Cosgrove DM, Lytle BW, Taylor PC, Stewart RW, McCarthy PM, Smedira NG, Muehrcke DD, Apperson-Hansen C, Loop FD. Reoperation for failure of mitral valve repair. J Thorac Cardiovasc Surg 1997;113:467–473. w14x Deloche A, Jebara VA, Relland JY, Chauvaud S, Fabiani JN, Perier P, Dreyfus G, Mihaileanu S, Carpentier A. Valve repair with Carpentier techniques. The second decade. J Thorac Cardiovasc Surg 1990;99:990– 1001. w15x Duran CM, Gometza B, Saad E. Valve repair in rheumatic mitral disease: an unsolved problem. J Card Surg 1994;9(2 Suppl):282–285. w16x Skoularigis J, Sinovich V, Joubert G, Sareli P. Evaluation of the longterm results of mitral valve repair in 254 young patients with rheumatic mitral regurgitation. Circulation 1994;90(5 Pt 2):II167–174.
Appendix. Conference discussion Age Sex Type of lesion (MR or mixed) Pre-operative NYHA class Pre-operative CHF Atrial fibrillation Valve pathology Cusp prolapse Annular dilatation Chordal elongation Chordal rupture Calcification of valve leaflets Left ventricular dysfunction Associated aortic and tricuspid valve disease Cardiopulmonary bypass time Aortic cross clamp time Various reparative techniques
References w1x Enriquez-Sarano M, Schaff HV, Orszulak TA, Tajik AJ, Bailey KR, Frye RL. Valve repair improves the outcome of surgery for mitral regurgitation. A multivariate analysis. Circulation.1995;91:1022–1028. w2x Duran CG, Revuelta JM, Gaite L, Alonso C, Fleitas MG. Stability of mitral reconstructive surgery at 10–12 years for predominantly rheumatic valvular disease. Circulation. 1988;78(3 Pt 2):I91–96. w3x Erez E, Kanter KR, Isom E, Williams WH, Tam VK. Mitral valve replacement in children. J Heart Valve Dis 2003;12:25–29. w4x Duran CM, Gometza B, De Vol EB. Valve repair in rheumatic mitral disease. Circulation. 1991;84(5 Suppl):III125–132. w5x Choudhary SK,Talwar S, Dubey B, Chopra A, Saxena A, Kumar AS. Mital valve repair in a predominantly rheumatic population. Long-term results. Tex Heart Inst J 2001;28:8–15. w6x Kumar AS, Kumar RV, Shrivastava S, Venugopal P, Sood AK, Gopinath N. Mitral valve reconstruction: early results of a modified Cooley technique. Tex Heart Inst J 1992;19:107–111. w7x Kumar AS, Rao PN. Restoration of pliability to the mitral leaflets during reconstruction. J Heart Valve Dis 1995;4:251–253.
Dr R. Dion (Leiden, The Netherlands): I would like to congratulate you on your work because repair of the mitral valve in rheumatic heart disease is usually a difficult operation. Of course we do not have so many patients in Leiden although the number is increasing since a few years. I was surprised not to see in the array of your techniques the patch augmentation of the anterior or posterior leaflet. Indeed, in rheumatic valve disease, the anterior leaflet is still pliable but too short: we augment it with autologous pericardium with usually excellent results. Also in the presence of a calcified or rigid posterior leaflet, we just preserve the free edge with the attachment of the chordae and we replace the whole leaflet with a patch of autologous pericardium again with very encouraging results. Would you comment on it? Dr Kumar: Yes. The technique I mentioned of cusp thinning is an extraordinary technique which makes the mitral valve more pliable, and particularly in the posterior leaflet, after thinning the posterior leaflet, we get nearly 5 to 6 mm of the posterior leaflet, which is imprisoned by this fibrous tissue. I will be showing a video tomorrow morning about this particular technique, and it is dramatic how it improves the appearance of the leaflet and its motion as well. So we have not used any augmentation for either the anterior or the posterior leaflets. Dr P. Kolh (Liege, Belgium): It is really a tremendous achievement for your population. Thank you for sharing your results with us. I just would like to ask you what is your policy concerning anticoagulation in the short term, for example, the first three months, and how compliant is the young Indian population towards anticoagulation after cardiac surgery? Dr Kumar: In this population of young patients, we did this repair to avoid anticoagulation altogether. We don’t give them any anticoagulants. Dr Kolh: Not even for two months or six weeks? Dr Kumar: In the beginning we used to give them for six weeks but that was insufficient anticoagulation just for preventing any thromboembolic complications, but when we followed up and found that there was no difference in the patients who were anticoagulated or not anticoagulated, we stopped using it. Dr T. Chotivatanaponk (Nonthaburi, Thailand): In rheumatic heart disease, frequently we found that the subvalvular aorta has some shortened fused chordae in such a way that sometimes we cannot find appropriate native chordae to replace that shortened chordae. So in that situation what is your approach in order to repair the valve? What is the role of PTFE surgery in these particular cases? Dr Kumar: In such patients who have combined mitral stenosis with severe subvalvular fusion, we use a technique of fenestration, which was originally described by Professor Carpentier’s group, and we remove all the fibrous tissue and try and return the appearance of the subvalvular apparatus
ARTICLE IN PRESS A. Sampath Kumar et al. / Interactive CardioVascular and Thoracic Surgery 5 (2006) 356–361 to normal, which many times is possible. And once we have done that, we split the papillary muscles down to its base, and that helps improve the movement of the anterior and posterior leaflet. We have not used artificial chordae in these patients except in one or two, and in those patients it was quite satisfactory, but we have not used it in a large number of patients to comment on that. Dr G. Sami (Cairo, Egypt): We see a lot of those cases back home. I don’t know if I missed it or not, but if you have 100 of those cases you are going to do or you are planning to do mitral valve repair, what is the percentage in whom you are going to replace the valve that you find the repair will not be feasible? Dr Kumar: I did not mention that in this particular presentation because of time, but it doesn’t exceed 3% in whom we have made an attempt despite the fact that some of these valves are really not repairable, because in patients who have noncalcific mitral stenosis or mitral stenosis and regurgitation, we attempt this repair. In patients with calcific regurgitation, it is practically impossible to repair them. Dr Sami: You see the disease at an early stage of its development in order to repair like 97% of those cases and replace only 3%? Dr Kumar: Not likely. In India the patients don’t present early and they come very late. They come in a moribund state. And as you have seen,
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many of these patients require surgery for other comorbid lesions, particularly of the aortic valve and tricuspid valve, and many of them have huge hearts. So it is not that they come early. It is just that our ability to repair is not 100%.
ICVTS on-line discussion A Author: Mohammad Ali Yousefnia, Farideh Roshanali, M.H. Mandegar, Day Hospital, Tehran 19389, Iran doi:10.1510/icvts.2005.121590A eComment: Are the techniques you used w1x enough for all forms of pathology in rheumatismal mitral valve? If you had tissue loss, what technique would you use? References w1x Kumar AS, Talwar S, Saxena A, Singh R, Velayoudam D. Results of mitral valve repair in rheumatic mitral regurgitation. Interact CardioVasc and Thorac Surg. doi:10.1510/icvts.2005.121590.
