Keynote du Professeur Gilles Dreyfus à la 59ème conférence annuelle de la société cardiaque d’Israël, 16-17 avril 2012
First of all, thank you very much for your kind invitation, and also for these very kind words.
I was given this topic « Advanced Mitral Valve Repair », and I said to myself « What can I talk about? » Should I talk again and again like many surgeons about how skillful we are, treating anterior leaflet, bileaflet prolapse, using whatever bands or rings, and I know that I am probably in front of a majority of cardiologists, and I thought it was rather boring to talk about surgery. So I think for advanced mitral valve surgery, I will keep following what Sarano just said, which is, « should we treat asymptomatic patients?”. I will share with you our personal data.
Then there is another problem which arises, and it’s a problem to all cardiologists and surgeons, which is the annular calcifications going along with mitral regurgitation. I will show you an example.
There is another one which is very important also, the more the people are elderly, the more we have calcification not only on the aortic valve, but also on the mitral valve. Should we leave these mitral valves alone? What should we do? Because they are very dangerous to treat.
And finally there is an entity which I think is interesting, and could be just a keynote, is, what should we do with MR and hypertrophic-obstructive cardiomyopathy? This is an entity which we see now more and more, and these patients are very sick.
Let’s start with asymptomatic MR. The optimal timing for surgery still is controversial. I personally fully agree with what Sarano has said, that is, first of all, quantification is the key method. If you have severe MR, then you probably need to think about surgery. I would like to make a plea for removing from the guidelines of the cardiologist whether mitral valve repair is feasible are not. I always found that, it’s a bit of a joke that someone who has never seen a mitral valve repair tells whether it is feasible or not. I think it is not the feasibility of the repair which is the problem. I think it is the surgeon which is the problem. Either the surgeon can do the repair, or he cannot do the repair. I think most of the cardiologists, in the end, think that something is not repairable because they do not have a surgeon who can repair the valve. If you have a surgeon who can repair a valve – I will show you the data – most of the valves, about 98-99% are repairable, and you can plan a repair which is good and long-lasting.
Indications, I am not gonna go through that. Left ventricular end-systolic, it is a mistake, end-systolic may be greater than 40, some society say 45, I didn’t think that we could go below 40. Ejection fraction, of course, below 60, you are already too late. Atrial fibrillation, you are already too late. Pulmonary hypertension, you are already too late, because you have an impact on the right side. So basically, the recognized guidelines are late. I think there is a crucial issue which is the LA size, independently from the size of the left ventricle, along with the amount of regurgitation.
This paper shows there is a significant difference in outcome according to the size of the left atrium, this is one study of many others, and I really think and you would agree with me, that we are now paying attention more and more to atrial fibrillation and the impacts on the quality of life, and secondary problems. This is our own series of about 500 patients, we have another cohort of merely 500, but we are still on the way of assessing these patients. But the question you have to ask yourself when you see an MR: first of all, is the mortality low enough to take someone who is asymptomatic and bring him to surgery? First question you need to answer. Is valve repair always feasible? The feasibility should approach 100%. Of course if you take a 45 year-old gentleman who’s got no symptoms, and guess the mechanical valve, or fail repair, it’s a disaster. This is the big problem.
Will the valve repair be long-lasting? We need a freedom of re-operation greater than 90% on 10/15 years, otherwise it’s not worth it. Will it improve survival? This has been showed by the Mayo clinic, but if you take the patient at an early stage, they have a similar survival than a matched population who doesn’t have mitral regurgitation. Whereas if you take patients at a later stage, survival rate is lower. Is it better when performed early compared to late, in regards to hospital mortality, functional class, end systolic, atrial fibrillation, and all other questions.
So basically there are definitive end points: Operative mortality, re-operation rates, survival. And there are surrogate end points, like symptoms, MR, LV dimensions and functions, and BNP.
So over a cohort of 530 patients, we had 70% who had degenerative mitral valve disease, and I think we should concentrate on these. When you look at this, you see there were patients that I would say asymptomatic, let’s take I and II, and symptomatic, III and IV. These are all, let me remind you, degenerative diseases. When you look at the first message that I think we need to convey, it’s not because a patient is asymptomatic that the mitral valve lesions are simple. They can be complex. As you see, there are some isolated, for 18% anterior leaflet prolapse, half were nearly posterior prolapse, but 1/3 were bi-leaflet prolapse. Being asymptomatic doesn’t mean that you have a simple lesion.
The second point is that the repairs have to take into account multiple and complex surgery. It’s not because you’re asymptomatic that the surgery is simple. You have to use choral transposition, choral shortening, papillary muscle, artificial chords, all the armentum that surgeons have to treat these patients in the same time.
Here we just see the posterior leaflet, because we all have in mind that posterior leaflet is simple, and that anterior leaflet and bi-leaflet are complex. I would like to reverse this proposal: Posterior leaflet can be very complex. Posterior leaflet can be a big issue. If you have a P2, which is more than half, or even sometimes 2/3 of the posterior leaflet, then if you have a prolapse and a huge P2, you might be in big trouble to treat this lesion if you don’t know how to do it. So a P2 repair is not always as simple as it appears to be.
What is the hospital mortality in this group? You see that of course for class I we had no mortality. Unfortunately, for class II we had 2.9, class III 1.7, class IV shows really a striking difference with 5.7. The overall mortality in this group is 2.2%. So yes we can say that mitral valve repair can be achieved with low-mortality, but mortality of 0 is quite rare in the group of 300, 400, or 500 patients. So we have to keep that in mind when we make the decision of operating a patient.
Now how successful was the repair rate? as you see, we were able to achieve the repair in 98.4% of the patients. So we’re getting close to this 99% I told you. Still there were some patients, 1 or 2%, where the repair was unacceptable, or the tissues were too fragile to achieve this kind of repair. It is rarely in young patients more in elderly patients. But the message is that, yes, high successful rates can be achieved.
What is the long-term MR grading? This is very rarely produced in publications. Well you see that we had a fairly standard rate of residual MR at 10 years: 0.5, 0.8, 0.6, 0.7. Therefore, in respective the functional class, the MR grade remained low. However, as you can see, it remained low at follow-up. So a good repair with a high coaptation surface, and properly performed, is a safe and has long-lasting result.
Now what is the freedom for re-operation? Weel we achieved a 96.7% over the 355 patients, and we had to re-operate only 3.3%, that is 12 patients. So we can say also that mitral valve repair is successful in the long run. And the freedom from re-operation at 10 years, when you compare isolated anterior leaflet at 96.6%, isolated posterior leaflet at 99.3% and bileaflet at 92%, you see there is still a little discrepancy between the type of lesion, with a posterior leaflet, which is properly repaired, you can say that most likely you will have no reccurence. With an anterior leaflet sometimes, you can have some surprise, and bileaflet repairs still convey a slight difference, although reduced drastically when compared to the figures provided by the Mayo Clinic in the nineties, where you can remember there was a discrepancy of more than 15% between anterior, posterior and bileaflet repairs.
There are also some papers that have been negative in the literature, such as this paper from Flameng where he basically has
29% of severe MR at 7 years. I don’t think you should pay attention to that, ans also you should really be very critical over the expertise of some publication: this paper reflects 180 repairs over 10 years, which is an average of 18 repairs per year. Probably, the expertise of the surgeon is a risk factor in itself.
Now the functional class at late follow-up, you see that there is a significant difference statistically: asymptomatic patients remain asymptomatic hopefully, but symptomatic patients might improve but they will never match the asymptomatic patients at long-term follow-up. If you look at the LV reverse modeling, it occurred in all groups, but it did occur, far less, in patients who had symptoms prior to surgery, as opposed to patients who were asymptomatic. At baseline, the end-systolic dimension in symptomatic patients was greater than that of asymptomatic patients at baseline.
Very importantly, atrial fibrillation, you remember I mentioned this, and I think it is a very important cut off point, there is a highly significant difference between patients who were asymptomatic and patients who were symptomatic to develop after valve repair atrial fibrillation. The incidents of AF, in symptomatic patients, was really strikingly higher. So I think this is something we should bear in mind.
The actuarial survival shows that the patients were operated being totally asymptomatic is 97% at 10 years, and is 95% at 15 years. We have 94%, it doesn’t seem to be so different between class II and III, but we know that the functional class is a very rough and very subjective classification, although we still use it. But we have a striking difference again when you go with class IV patients, or class IV intermittently. It’s very difficult to apply a functional class because we know well that it depends when you do apply: at entrance, when the patient is admitted, or when he is medically treated and stabilized, usually the functional class changes, and where is the functional class picked up.
So the conclusion of this part is that early mitral valve repair in asymptomatic patients is safe and has a very low operative risk, it can be achieved in most cases, its long lasting, but you need to have someone who can deal with this repair to have such repairs. Outcome is better with mitral repairs performed early I would say rather than late, because its difficult to talk about really asymptomatic patients. Because the operative mortality is lower, the functional class is preserved, there’s an improved survival, there’s an improved reverse LV remodeling and less incidence of atrial fibrillation.
This has been confirmed by the Cleveland Clinic as you see according to the function of class the survival is quite strikingly different, and it has been proved with also an incidence of residual mitral grades over time according to the symptoms – I’m not completely in agreement with this but lets skip that.
Second topic quickly, extensive annular calcification. I think we have to really make a clear distinction between myxomatous valves, so called barlow’s, we’re not sure what barlow is really, and degenerative disease. One occurs in younger patients, calcification occurs secondary to MR, and I think there is something we should perhaps bear in mind, is the longer you wait in these patients the more you will develop calcification, and therefore the repair will become problematic. So I think that we have to be aware of this incidence of calcification perhaps related to time, we have to wait. There is always a dissection plane between the calcium and the micardium. You always have to decalcify the annulus otherwise you cannot achieve a repair, you cannot put the ring, and you cannot achieve the principal of mitral repair which is to restore the pliability and full opening of the mitral valve.
In degenerative disease, it occurs in older patients, the calcification are due to aging process similar to aortic stenosis, and I think there are no planes of dissection, I would be very careful to not decalcify this because there is a risk of failed rupture. So in Barlow, that’s what we do here, you have a prolapse with a ruptured chordae. You can see here on the 3D echo which is not playing, but you can see clearly the ruptured chordae and some calcification. Now you see here this case you have a flail leaflet of the posterior leaflet and you have some calcium here at the hinge of the posterior leaflet and the annulus, it goes deep down into the ventricle. The echo does not truly reflect the reality, you have severe MR. If you think this a simple P2 prolapse, I’m going to show you this movie to show you how this plays.
Ok this is the same patient, you do recognize the echo, you do recognize the quantification of the MR. You have here the 3D echo with the prolapse. We have here the P2; we have shortened P2 at the upper level because it was very high, all the ruptured chordae have been removed. You have P3 here, P1 is under there. So what we need to do is decalcify here because you cannot put a ring here, and you cannot achieve pliability and the result will not be good if you dont do that. Now you know, or you don’t know, but if you go and tackle this, thats where I said that there is a striking difference in young patients and myxomatous disease as opposed to elderly patients, is that, here there is a plane of dissection, but you are going right into the ventiricular muslce, so if you do that you have to be well aware of what you’re doing, because you can also have a ventricular rupture, which is a very highly fatal complication of mitral valve surgery.
But you will see once the decalcification will be achieved, the amount of calcium that is here, and that is not only stiffening the valve. So we are detaching now P2 from the annulus completely, because we need to restore the annular pliability in order to implant a ring. So you see now we have to find the plane of dissection of the calcium. We are below the plane of the annulus, the annulus is here, but the calcium is here down there- you have calcium here, you have calcium here, you have calcium everywhere.
This patient was known to have a mitral regurgitation for the last 20 years, he was seen even 9 months before turning into heart failure and AF, and he was told, “Oh you’ve got no problem, you have a good heart, you have a mitral regurgitation, don’t worry.” He had 400ml left atrium, he had a severe TR, he had this complex mitral valve. So this was a very very complex case. Although the guy I presented earlier if you look at the echo with a simple P2. And he turned into AF, so he had a maze procedure, he had a left reduction of his atrium, he had a complex mitral valve repair, then he had a decalcification of the annulus, he had a tricuspid annuloplasty, and thankfully he’s okay.
Now exactly as Maurice has said before, his objection fraction looked very good prior to surgery- he had a big heart and he was about 70% after surgery he’s 55%. Let’s hope that he will come up, but I mean this patient has been operated a bit late. Now you see this a piece of calcium that has been removed, and you can see the muscle here, and we keep going on because we need to remove this calcium, otherwise the repair is not complete.
You see we are well below the annular plane here, we have to remove this calcium completely, because otherwise you are not doing a good job, and also we need to remove it because once we’ve started we need to reconstruct the annulus. You see there is no more annulus here, the annulus is gone with the calcium, so we need to reconstruct the annulus, which will be done just after this piece of calcium will be removed. But you see there is a plane. Even with a knife you can find the plane, but you go into the muscle, you see the muscle behind here. Okay this is another piece of calcium that is removed. This can take very long. It’s a little bit like aortic stenosis. There we go, second piece of calcium. Now reconstructing the annulus by re-approximating the endocardium of the atrium with the endocardium of the ventricle. And there’s no pledget, nothing it is very solid, provided you have decalcified.
This is the only part where I am showing you surgery, I am sorry for the cardiologists it might be boring, but for the surgeons might be interesting. Although I’m sure that not many cardiologists have ever seen what a classification of the mitral valve means. You’ve seen an echo, but you don’t understand really what are the implications for surgeons, so perhaps its good for you to see a little bit of it.
Alright, so you see we are, as I said, we are reconstructing the mitral annulus. With a simple 4.0 suture interlock, going into the ventricle to pick up the endocardium, and as you can see the entire annulus is reconstructed. Here it is, you have some cord here which is spare cord. Now we need to reattach this P2 remnant, otherwise the repair would not be achieved. So we’re going to reattach the P2, you see its a little bit of an excess issue. We’re going to transfer secondary cord to the free edge, and we’ll put a ring and the repair will be achieved. But it looked initially very simple, it is not very simple.
Okay we are reattaching chordae here at the free edge. You see because you need to support this, you can do that with either artificial chords such as Gore-Tex chords or native chords.
Did I stop it? Okay, lets go. I’m sorry, but…
Extensive calcification in elderly. Well, calcification usually involves the entire posterior annulus, and the aim is to achieve leaflet coaptation, and you should not as I said, decalcify the annulus because you can have a real trouble. You can see here, the calcium going all around the posterior annulus in a patient of 75 years old. If you tackle this issue you can find yourself in a big trouble. Look at this leaflet- the anterior leaflet is rigid, the posterior leaflet is a massive calcium piece. If you remove that, you will find yourself in a strikingly different position as if you had the previous case. In this case, I think it’s a very elegant way to detach the anterior leaflet from one commissure to the other, put a pericardial patch, don’t even put a ring because the posterior ring is completely calcified, its not going to expand further. And this is the size of the patch. You see, this is the result. You have the patch here which you can see, you have no regurgitation what so ever. The posterior leaflet is completely stiff and calcified, the anterior leaflet is now coapting with the posterior leaflet with no ring. It’s an elegant option in elderly patients, not to put a ring, not to decalcify the patient.
M.R. and aortic stenosis. This is something which I thought was undermined for a long time because we are now operating more and more old patients, an you with the TAVI, you will be exposed to that. Of course I don’t think you’re going to have to indicate a TAVI procedure in patients who also have a mitral valve disease. But when should it be considered? Well we know that—
INTERRUPTION: Gilles we need to cut it a little short
I’m going to make it short, very short. Well, you know, if its compensated aortic stenosis, mild MR, you don’t do anything. If its decompensated aortic stenosis, then you have to probably consider whether you have an organic MR. This patient has a functional MR, we shouldn’t treat it. This patient has an organic MR, it should be treated with aortic stenosis.
And now I finish with this HOCM and atypical SAM.This is a very interesting disease. In a normal valve you have a closure which is not impaired by the septum and the position of the anterior leaflet and the height of the posterior leaflet. As you see here the HOCM surgery is a myomectomy, an increase of the anterior leaflet, and a decrease of the height of the posterior leaflet.
Okay the changes, you have a hypertrophic septum, you have a short and restricted anterior leaflet, you have a high posterior leaflet, and you have an abnormal papillary muscle position. The goal of surgery here is to displace coaptation point away from LV outflow tract posteriorly. So you decrease posterior leaflet height by neo-chordae or by ressecting the leaflet, you can augment the anterior leaflet by pericardial patch, and you oversize the annulus.
This is the echo. You see this type of patient is very very critical for you cardiologists, as well as for us surgeons. You see the height of the posterior leaflet by 3D echo is extremely high and goes right in the middle of the outflow tracks. The MRI shows exactly the same features, there is a kissing of anterior and posterior wall. And here you have the image which is a striking image of this anterior leaflet going into the outflow track, pushed by the posterior leaflet, along with this hypertrophic septum. Well if you do the surgery that I’ve just told you, which is to reset your restricted posterior leaflet, extend the anterior leaflet, put a big ring, and remove septum, you have this result, which is a good result and the patient is asymptomatic.
Well there are many other complex issues rather than Gore-Tex and bands, I thank you, and I hope next time I’ll have more time to tell you about the complex issues. Thank you very much.