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Okay, so I will start with a question so, you can use the audience response. You have a 39-year-old female. She is NYHA class II. She has atrial fibrillation. She has got an echo, which shows a valve area of 1.4, Wilkins score 13, immobile, calcified leaflets, PA pressure is 54. So the recommended management should be: 1, balloon valvuloplasty; 2, mechanical mitral valve; 3, bioprosthetic mitral valve with a Maze; 4, 1. repeat clinic assessment in 6 to 12 months; 5, surgical commissurotomy and a Maze procedure. So if you can vote please. Okay, could we see the response? Okay, so the majority would favor bioprosthesis, so about 60% feel she should have a mitral valve replacement, 7% want a repeat assessment and 7% want a valvuloplasty which means they were not listening to Dr. Herman's presentation because he said quite categorically if the Wilkins score is more than 12 he would not do a valvuloplasty.

If you look at the AHA guidelines, and if I could have my slides again. the AHA and ACC guidelines state in a class II patient there is actually no indication for surgery except if they have severe pulmonary hypertension and that is a class IIA indication. So the AHA guidelines would say that if you have a valve morphology that is not suitable for valvuloplasty, your PA pressures are low, then you should be on regular surveillance. So the recommendation should be you see the patient every 6 to 12 months and then if the PA pressure goes up or if she becomes more symptomatic and moves into the class III or IV, then you can consider surgery and this actually is the main crux of my talk today which is why rheumatic disease is different from other diseases, why there is a reluctance to do surgery. Well let us say this lady says, "Look, I am 39 years old, these symptoms are too bad, I can't work, I want to be normal, I want to run marathons again, I want to have surgery" and we decide to have surgery. So if you vote again you are counseling her on the options. Which of these options is the most true: 1, with the valve repair she could expect 15% to 20% chance of reoperation in 10 years; 2, with a mechanical valve she can expect a 90% to 95% chance of survival for 10 years; 3, this valve is not reparable; 4, a mitral valve homograft if available has better long-term outcomes than stented bioprosthesis; 5, bioprosthetic valve is contraindicated because of atrial fibrillation. So if you vote, so either a repair as of 15% to 20% reoperation, mechanical valve has a 90% 10-year survival, the valve is not repairable, homograft is better than bioprosthesis, all bioprosthesis is contraindicated because of atrial fibrillation. Okay, it is funny being a surgeon and standing up here. So most people feel a valve repair would have a 42% chance of succeeding at 10%. I will say the correct answer here is C. This valve is not repairable. Obviously because I am talking to you about mitral valve repair, you feel otherwise, but if I could have slides now, so really a valve for mitral stenosis that is not suitable for valvuloplasty is effectively not suitable for repair surgery because what we do at surgery for mitral stenosis is what Dr. Herman does with a balloon except we do it with a knife. So it is practically inconceivable that you would have a valve with such a high Wilkin's score, the leaflets calcified that can be repaired and the mechanical valves certainly do not have a 95% survival and the valve repair of this nature even if you could execute it would not have a 20% reoperation rate. And essentially that is the problem with rheumatic repair and that is why the guidelines are trying to push people away from surgery rather than towards surgery because in practice these valves are not frequently repaired, they are less frequently repairable, the durability is not predictable and there are no good valve replacement solutions. And indeed, if you go back to the guidelines, the only class I indication for surgery for mitral stenosis is if you have class III or IV symptoms you are a good candidate for surgery and you are not favorable for balloon valvuloplasty. So everything is trying to push you away from surgery and that is because there is no good surgical solution for this disease in terms of valve replacement, and repair is unpredictable. Repair obviously is mainly for regurgitant disease. The problem with mechanical valves is that they shorten patients' lives. It is not 90%. If you look at this series of population of almost 300 patients aged 15 to 40, the 10-year survival in this cohort was about 85% at 10 years and these are 15-year-olds. So if you take a teenager, 16-year-old, you put a mechanical valve, you are talking 1 in 5 of them, is not going to live the next 10 years. That is how bad it is. And look at the normal life expectancy. So all other people in this age group over 95% will live 25 years if you have a valve replacement, the chances of death are almost 30% at 25 years. So that is how bad a mechanical valve is. How about bioprosthetic valves? The same problem. They degenerate quickly and they also shorten patients' lives. This is a series of Hancock vavles. The mean age is 49 years old and two-thirds are rheumatic. At 10 years, half of them were dead, and that is the reality. We all think we have a solution but we do not have a solution. And that is really what drives mitral valve repair. Mitral valve repair as opposed to replacement and repair has in almost all series consistently a better survival than replacement and this paper by Tyrone David and colleagues suggests that rheumatic valve should be repaired when technically feasible and you accept the risk of reoperation because your survival even with reoperation, the survival of a valve repair is better than a valve replacement. So I just go through three aspects of rheumatic valve repair, patient selection, repair methods, and durability. For patient selection, the first is the patient. Things that push you towards valve repair are patients in whom you want to avoid warfarin. So it is usually young patients, children, females in childbearing age, and if for any reason, for example in lots of parts of the developing world, or people who are poorly compliant in the developed world, you will usually want to avoid warfarin therapy. The echo features are crucial and the things that you see on echo that would make repair more feasible if it is purely regurgitant or purely stenotic but if it is purely stenotic they should go for valvuloplasty. If the anulus is dilated, so if you have a big valve, chances are you have more leaflet to play around with. The leaflets are crucial. You want a mobile anterior leaflet. Professor Kumar, who has one of the biggest experiences in the world, from India, uses a criteria of the anterior mitral leaflet length of greater than 19 mm. There should be limited tethering of the posterior leaflet if possible but that is not critical and ideally you do not want any calcification but if it is there you want it to be limited in nature. The surgeon is probably more important. I asked a colleague in India who does about 50 to 60 of these a year, what he felt was the most critical aspect of selection for repair and his answer was the surgeon that is willing to repair and who actually attempts to repair and that is important because if you send one of these patients to an operating room and they come out with a mechanical heart valve you look at the operative report that says a cross-clamp time of 50 minutes, that surgeon had no intention of repairing the valve. So the surgeon has to attempt to repair all valves, even those that looks irreparable. You spend the first half hour to 45 minutes trying to repair and then you replace. Sometimes you will replace, sometimes you will not replace, and that is critical, because these operations need more expertise which can only be built by doing it over and over again. They are longer operations. They are more complex operations. The results are unpredictable. So it takes a surgeon with dedicated interest to do these procedures. So the classical repair methods of all the mitral valve diseases, rheumatic disease is the one that lends itself most of the philosophy that you have to have the lesion-based approach to managing it. You cannot fix this with a ring, you cannot fix it with an Alfieri, you cannot fix it with just Gore-Tex, you have to deal with the lesions you have. Usually, there is some degree of stenosis you have to do a commissurotomy. If the leaflets are non-pliable you have to do something to make them more pliable, you could shave the leaflets, you can do limited resections. The subvalvular structures if they are fused have to be either resected or split. You can resect, you should resect all restrictive chordae whether they are primary or secondary. If they are primary you replace them with something else. Anterior leaflet prolapse often occurs and classically Carpentier treated it with chordal shortening but we prefer now to use Gore-Tex cords but you could also use a chordal transfer if you find suitable chords. Pericardial patch augmentation is critical to improve the coaptation surface of the new valve and we always reinforce it with an annuloplasty. Some people have gone a step further. This is a paper published just in the last month or two months by El Khoury's group from Brussels and his philosophy is you have to treat this disease like endocarditis. You have to resect all diseased tissue and see what you have left behind and then what you have left behind he reconstructs with various materials and this illustration here he is using a tricuspid valve, he actually takes the posterior leaflet of the tricuspid valve as an autograft and transposes it to the mitral valve to use to reconstruct the commissures if he has to reconstruct the calcified commissures. Otherwise, he uses pericardium, he uses homograft to reconstruct whatever you resect and using these techniques he has achieved excellent long-term results that I will show you later.

So just to show you a few cases. So I said on echo what you are looking for is pliability of the anterior leaflets. So you can see here the anterior leaflet does have some restriction but is pliable, it is not thickened. Posterior leaflet is restricted, that is fine, and you could deal with that. And in terms of the surgical findings, this is a typical rheumatic valve with a thickening of the subchordal structures and thickening of the leaflets, so the principles of this repair, you can see the posterior commissure is fused that has to be cut. We have to resect all those thickened restrictive chordae. We have to resect any aspects of the leaflets that are abnormal, so you can see some calcification in A3 which is being gently debrided with a biter. These are restrictive chordae to A2 which we had divided and that is a marginal chord. So you just divide everything and then you see what you have left behind. Then the posterior leaflet you can see is very retracted, less than a centimeter tall, you can see at the bottom of the screen, so that you have to deal with by augmenting it. So that is a good secondary chord being divided which you could transpose if you have residual prolapse. Just take your time, divide all the chords, all the chords are restricted and then you see at this point in time you are not committed to valve repair or valve replacement. You can only make the decision as to whether this valve has to be replaced when you have dealt with all the lesions you can see. So now you have a pericardial patch and augmented the posterior leaflet and you now have a probably 1.5-cm tall leaflet. Place some Gore-Tex chords now for resuspension of the anterior leaflet. And you see as the repair progresses it is looking more and more like a valve that can be salvaged; on first sight it would be very easy to cut the valve out. So it is a reasonably sized valve and we tend to use a classic Carpentier ring because with the classic rings you can feed them to shape and you got good echo results.

The second case you can see the same thing on echo. The anterior leaflet is long, probably about 2 cm long so that would be very favorable, there is posterior leaflet calcification which on its own, if that is all you have, can usually be dealt with and the echo findings are similar to the previous case; a short posterior leaflet. So we almost always augment the posterior leaflet now. Some surgeons prefer to augment the anterior leaflet and leave the posterior leaflet as a shelf, which is also an acceptable option and some surgeons augment both leaflets. So here again dividing the restrictive chordae. There is not much commissural fusion in this case as opposed to the prior case. You can see at the bottom left hand corner that a left atrial appendage has been sutured closed with a suture because this patient was in atrial fibrillation. So to do a pericardial patch we place Prolene stay sutures at the marginal chords just to hold up the tip of the posterior leaflet and then we make a horizontal incision in the base of the posterior leaflet. So this posterior leaflet is not as calcified as the prior one and we take it from commissure to commissure and then we get the pericardial patch treated with glutaraldehyde we shape it in a way that there is some redundancy but not too much redundancy so you do not get like a funnel. And remember the main essence of the posterior leaflet patch is just to provide a surface of coaptation for the anterior leaflet. So the repair itself is based mainly on the anterior leaflet but you still need it to coapt with something. So that is it shaped and that is the patch placed. Once the patch is placed and we place our ring, then we would see whether there is a need for resuspension of either the posterior or the anterior leaflet. This posterior leaflet we have not taken any marginal chord, so it would not need resuspending and again we have got a size 30 and we use a classic Carpentier ring and there probably is a tendency to prolapse there is some thickened tissue we have shaven off A2 and then we will place a Gore-Tex chord to A2 and also a good echo result.

The last case has a bit more calcification in the posterior leaflet but again key, the anterior leaflet although there is some retraction, is moving and is long. So this valve should almost always be repairable no matter how daunting it might look. You can see here that the anterior papillary muscle is retracting the anterior commissure greatly and again the thing to do will be to divide and resect all the retracted tissue. Sometimes we can fenestrate the chords and particularly in the anterior commissure you should make an attempt to separate the chords, going to A1 to those going to P1. So it is again the same principle but here we have some calcium. So we have to excise all that calcified tissue and replace it with more pliable pericardium and then we will place a pericardial patch here too and the echo results are usually good immediately and we will talk about the long-term in a second which I am sure is a question most of you ask is how durable are these repairs.

The most long-term data come from Carpentier's group and he has reported an almost a thousand of these repairs and his freedom from reoperation at 10 years was 82% which is quite good and comparable to bioprosthesis and almost comparable to mechanical prosthesis which have about 1% to 1.5% of reoperation per year. For these, Carpentier found a 2% reoperation rate per year and the reasons for reoperation in 83% were progressive fibrosis or calcification of the mitral valve, 17% of reoperations are due to technical reasons. But if you look at El Khoury's results, he just published using this aggressive resective strategy; his reoperation rate at 10 years was almost 94%. His overall survival was not that good, in the 80% but certainly you cannot get good freedom from reoperation and if you look at other population series you find that at 10 years basically at least 80% of these valves should be functioning and I think that is a reasonable figure to quote your patient. Obviously the case I presented is not repairable in the first place. So there is no way you could get any repair that will last 10 years.

So in summary a repair is preferred if the valve shows favorable echo features and if you have a surgeon committed to the practice of rheumatic repair. The long-term results are probably better than prosthetic valves, but if the valve is not repairable we must remember that valve replacement therapy is not for the mitral valve, it is not a good option for younger patients, and for those patients you should probably reserve it to those that are very symptomatic.

Thank you.


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