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Video Transcript:

My charge this morning is to show you the pictures from the operating room of both the mitral and the tricuspid valve and by way of disclosure I am the inventor of a couple of different rings which I am sure I will get ribbing from Randy about later but they do not have much to do with what I am going to show you here.

We will start with a question, a 64 year-old man presents with gradual onset of dyspnea. He smokes a pack of cigarettes daily, has a history of PCI for coronary disease. Examination reveals a loud systolic murmur and I am showing you his echocardiogram. We are going to use the audience response here. So have a look, a) Degenerative disease with anterior chordal rupture, b) Degenerative disease with posterior chordal rupture. c) Ischemic mitral regurgitation with ruptured papillary muscle, d) Ischemic mitral regurgitation with severe leaflet tethering, e) Ischemic mitral regurgitation with papillary muscle elongation.

So here is the echo, and now let us go to the questions again, degenerative disease with anterior chordal rupture, degenerative disease with posterior chordal, ischemic MR with ruptured papillary muscle, ischemic MR with severe leaflet tethering, ischemic MR with papillary muscle elongation. Okay, use your response, pick one, for those of you that have them us: Can you show us the answer back there. So, a) very good. So about half the group has it right. Let us look at this. Okay, you can go to the next slide and there is the answer.

So, history is just one thing, recognizing lesions is another because of course ischemic MR, and we will talk about that later. It is not very complicated, it is annuloplasty and anterior leaflet prolapse actually can be more complicated to fix. So history is one thing, recognizing lesions is the other. The message I have for you in the next 10 minutes showing you these pictures is that we all have to know the lesions and Craig is right if we are going to move into this era of percutaneous therapy, we are going to have to a nomenclature that unified and we are going to have to all understand exactly what the lesions are because this is not aortic stenosis. Aortic stenosis is calcified leaflets. The spectrum of mitral valve disease actually is very complex and that is why I want to show you how we sort of put that together and what we have learned along the way looking in a lot of different valves. If you look at the mitral valve, you should think about it as an interventionalist or a surgeon in five components: the annulus, leaflets, commissures, chordae, and then papillary muscles and left ventricle together. Papillary muscle pathology is actually pretty uncommon. Most of the time, it is part of the ventricular complex. The other thing that is very useful and it is a very old concept introduced by Carpentier a long time ago but it is still very useful in terms of broadly classifying the dysfunction that results from a lesion is this type 1, type 2, type 3a and type 3b and what type 1 means is that your leaflets move normally in the annular plane. You could still have still MR. The two ways you get that of are from perforations or from annular dilatation. Type 2 is excess motion so almost always that is chordal elongation or chordal rupture, and then 3a is where your subvalvular apparatus is fibrosed or frozen that will restrict your leaflet motion in both systole and diastole and 3b is the typical dilated cardiomyopathy or ischemic MR case where you have a restricted leaflet motion in systole and that is useful to sort of also start to look for etiology or the disease and the lesion because they are all intertwined or linked.

The common diseases that we all see; annular degeneration particularly in atrial fibrillation, fibroelastic deficiency, Barlow's disease which Craig mentioned, endocarditis, rheumatic disease, ischemic or dilated cardiomyopathy, related mitral regurgitation, and then congenital valve disease which is less common but you will see some cases of partial AV canal and things like that in adults. That is the etiologies and the lesions that I will show you are annular dilatation and calcification; leaflet distention, calcification, or perforation; commisural prolapse or fusion; chordal elongation or rupture; fibrosis; and papillary muscle calcification or displacement, and these things happen in combination, so again learning how to recognize those and maybe working backwards seeing them from the OR and going back and thinking about an echo is a good idea. So here is the annulus, the aortic valve is here, the fibrous skeleton of the heart does not continue posteriorly so this part of the heart really is not supported the same way, so the most common lesion that you see in things like atrial fibrillation is just an increase in the circumference of the posterior part of your annulus, so this part of the heart is less likely to dilate. This part of the heart dilates more and you can see the gap that you create and I will not show you any surgery today except a couple of pictures because for the cardiologist here you should at least see an annuloplasty ring and how that works. You can see how this annuloplasty ring now restored the normal shape of the valve compared to the anatomy of the anterior leaflets and now you have this coaptation. That is all it required was an annuloplasty ring and that is actually not very common in nonischemic cases but that is how that works. You can see the annular calcification here, so here is annular calcification and you do see that or will see that a lot on echocardiography and you can see various degrees of annular calcification and that is important because if you want to do valve reconstruction in patients that have severe annular calcification and that can be a very complex operation where you have to get into a plane between the atrioventricular groove and perform a resection of that and then either close this with a sliding atrialplasty or a patch, so this is something that you want to recognize particularly in young people if you are talking to them and they are asymptomatic to look for that because it is common in endstage Barlow's disease. Leaflets are segmented according to Carpentier's nomenclature which I think is useful. The posterior leaflet has normal clefts or indentations sometimes that are clefts, so you have P1, P2, and P3 and then the corresponding anterior leaflet which is not normally segmented and it is just named by a relationship to the posterior leaflet and then you have two commissures that are like the corner of your lip, the anterior commissure toward the aortic valve and the posterior commissure, so that is the best way to talk about them when you are in an echo lab or in an operative note when you are talking about what you did. You have simple prolapse of the posterior leaflet. You can see it is not very tall and not very complicated. The other thing you can see in surgery of course is the jet lesions, so keep your eye on the atrial wall when you are looking to try and understand directions of jets; sometimes that is useful in planning. Then the fun starts and this is where the challenge of thing is like e-valve is. You cannot just talk about prolapse. You got to think about the anatomy of the posterior leaflet, so here is P2 prolapse that is a little bit different than the first one I showed you broad-based and very wide and here is a P2 prolapse. It is almost 5 cm tall. It covers the top of the valve so P2 Prolapse is not just P2 prolapse.

These are less common types of P2 prolapse but you have to recognize that I think particularly if you are planning interventional strategies and then you have the multisegmented valve, so not all valves just have nice little indentations like the pictures show. You will open and find a cauliflower type valve like this, that can be tricky and then this is a partial AV, the patient had an undiagnosed partial AV canal and you can see the cleft in the middle of A2 or the anterior leaflet, and then perforation you can have this case is a healed case of endocarditis you can see that with the windsock deformity and acute endocarditis. Then you also have this issue of hypoplastic segment, so here you can see that you have a very small, very thin P1 segment next to a prolapsed and distended P2 segment, so that can pose some issues for surgeons trying to sew two leaflets like that back together and then you can have these clefts or indentations that now become clefts and they go all the way to the annulus. So, now if you try and close these sort of things, you can actually restrict that. You need to think about what you are going to do with these chords if you are trying to reconstruct one surface of coaptation and fortunately with 3D echo a lot of these anatomical findings are all being shown now to us beforehand so we can really think about them and it does matter because as you look at your planning as a surgeon, the location of indentations helps guide where you may do resections or which segments you may want to put back together again. So, it is important.

The next structure I will show you briefly is the commissure. The commissure is about a 5-mm piece of tissue normally that is between the annulus and the anterior and the posterior leaflet and it is important and actually I would say move up a little bit in terms of degrees of complexity. It is interesting that endocarditis often affects the commisural tissue when you see complex jets in patients that have endocarditis and you are thinking leaflet perforation, put commisural prolapse into your equation because for some reason we do not know why commissures tend to rupture in acute endocarditis. This is a true commisural leaflet, so when you open up and you are counting the leaflet segments and you count four instead of three or you count four areas, and you are not sure whether this P3 or what it is. What it is, is a true commisural leaflet. It is about in 5% of patients who will actually have a commisural leaflet. That is important and we will show later in the video session because you really should connect that to the anterior and posterior leaflet, make a decision and not leave that hanging but try and make that part of one of your leaflets and then rheumatic disease affects the commissure, so when you open up in any rheumatic patient you are going to see varying degrees of commisural fusion and that has to be addressed in any reconstructive procedure and then finally you will see in degenerative patients occasionally patients that have ruptured chordae to a commisural segment, so again this is not a posterior leaflet prolapse but really commisural prolapse and shows you again why it would be important to identify that if you are thinking about trying to do for instance a percutaneous therapy because there is really not an adjacent segment to attach that to that would correct that prolapse. The chordae tendineae I told you either rupture or they elongate. I will just show you a few examples of that. They can also restrict. Here is the simple fibroelastic deficiency type or thin chord Carpentier describe with a normal segment and a simple rupture of a two chord apparatus to the posterior leaflet.

Here you see an anterior leaflet rupture in a Barlow's case, giant multi-valve prolapse and you can see this complex rupture of most of the support of the anterior leaflet and actually the more complex I think chordal pathology is chordal elongation where you have a long segment, in this case the anterior leaflet and diffuse chordal elongation. That takes actually a little more thought, I think the one that rupture actually directs you exactly to where the pathology is and then rheumatic patients tend to get scarring and thickening of their chordal apparatus and in this case you can see the typical findings of a rheumatic patient with a 4 or 5 mm now scarring of the chord to the margin of the anterior leaflet, which also has migrated away from the true margin of the leaflet and towards the middle of the body, so chords are things that are actually again simple chordal rupture we all recognize there are lot of variations and then finally the papillary muscles in the ventricle are little bit simpler. In Barlow's disease, you will see calcification of the papillary muscles. Typically, it is the anterior papillary muscle and here you can see into the sort of P1 segment. This is actually pretty common and in this case it is important because then you need to think about the anterior commissure. It is almost always restricted here so keep an eye out for that in young patients with Barlow's disease that is not rheumatic or some inflammation it is just part of that syndrome and then finally it is hard to show 3B lesions or papillary displacement on the arrested heart, that truly is an echo diagnosis. If you are not sure about 3B or 3A you really need to look at the dysfunction on the beating heart but at any rate this is the case of 3B dysfunction and here is a more diffuse sort of tethering of the leaflets and the ventricle again it is a little bit harder to sort out without actually lifting up with a hook against the reference leaflet to sort out what is restricted and what is not. The adjacent structures I thought I would just point out to the mitral valve, here you can see the aortic valve. Here, the circumflex coming around, coronary sinus here, keep in mind the position of the coronary sinus, it sort of tails up and does not get up into this area. The trigones here where the aortic and mitral valve share this fibrotic curtain and all rings or sort of even partial rings are implanted up here, so that is another sort of potential anatomical issue for some types of percutaneous therapies and then when you are looking at postop echoes keep in mind that sutures here can affect the leaflet bases of the left or the noncoronary leaflet so that is why we as surgeons have to keep our needle pointed toward the ventricle here instead of toward the aortic leaflet, but keep that in mind if you see an aortic valve regurgitation that was not there before it could be distortion by a ring or from a suture and then of course sometimes a too aggressive bite here starts to head toward the conduction system on the other side of the membranous septum, so those are the main structures around the mitral valve.

I will just finish by showing you the tricuspid valve. This is the valve. Here you can see that the most important thing I will show more clearly on the next slide is the conduction system as well as the sinus, the noncoronary sinus. This is the typical picture of a relatively normal tricuspid valve and you can see they have three leaflets, anterior leaflet, a posterior leaflet which really is right here and the septal leaflet here and this is the membranous septum. Again, coronary sinus would be here, triangle of Koch would be here. This is where you're going to find your AV node and the bundle so that is where we need to be careful.

Carpentier showed this a long time ago, but I like this paper from Judy Hung's lab that used 3D echo to really define functional tricuspid regurgitation, which is the most common; now it is sort of like aortic stenosis, again we are back to 95% of patients with tricuspid regurgitation have this. They have dilatation of the annulus and it usually starts about the midpoint of the anterior leaflet and continues around just past the coronary sinus toward the first part of the septum, so you get this free wall dilatation and that is what causes most secondary or functional tricuspid regurgitation, and that is why this area that dilates is, and you can see sort of versus the normal size of a ring matched to the anterior surface area where the dilatation occurs and sort of why that is the target for most rings or plications of the tricuspid annulus to try and narrow that. So, I think the message is that, you know, we are moving into an era where we need to repair every heart valve and we need to think about percutaneous strategies and atrioventricular valves and to do that, we are going to have to really all come together and start talking about a phrase that Roberto coined, which I like, which is surgical echocardiography.

Thank you very much.

David H. Adams, MD

Cardiac Surgeon-in-Chief Mount Sinai Health System Marie-Josée and Henry R. Kravis Professor and System Chairman Department of Cardiovascular Surgery Icahn School of Medicine at Mount Sinai President, Mitral Foundation


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