2009 Heart Valve Summit: When to Use a VAD in the Patient With Valve Disease
So, I am just going to go through different applications of ventricular assist devices in patients having valve disease. You can use it as a backup for high-risk surgery; you can use it preemptively for postcardiotomy as an alternative to high-risk surgery and some other novel applications. So, by ventricular assist devices, we generally mean temporary assist devices, such as this. This is as Thoratec CentriMag pump which is probably the most frequently used short-term device in the United States now. There are other devices like the Abiomed device, which some of you might have in your centers. Some centers use ECMO, extracorporeal membrane oxygenation, some use the TandemHeart, and there also are the older Thoratec devices.
So, the first application is a back up for high-risk surgery. Basically, these are patients who are going to have conventional heart surgery but are very high risk of developing post cardiotomy shock. Patients with very low ejection fractions having a very long ischemic time, a long cross-clamp time, and you do surgery with a plan to place an assist device if you cannot come off the heart-lung machine. Once you plan preemptively it is much better than doing it in an emergency when the patient is very sick.
This is an example of such a case. This was a 50 year-old male patient who was an immigrant from West Africa, did not have insurance, so he was not a transplant candidate. He has got a lot of aortic regurgitation, a lot of mitral regurgitation, an EF of about 10%, very dilated ventricle; 8.5 mm, severe pulmonary hypertension, PA pressure of 75. This is a patient that ordinarily you would refer for transplantation, but because he cannot have a transplant, we decided to offer him triple valve surgery. So, in such a case, you do the surgery, you have the ventricular assist device in the room, if you cannot come off the heart lung machine you put the patient straight on the device. He actually did well and he did not need a device and his ventricular function actually improved marginally and the size of his ventricle came down 6 to 7. He eventually died about 20 months later of multiorgan failure. He came into hospital in cardiogenic shock and died but he did get about 18 months of good quality of life.
The second use is preemptively. So this is going a step forward. We have a patient like this and we say we are not going to try and come off the heart lung machine, we are just going to put in an assist device. The patients that we do this in, is essentially the same as the first group; people with severe ventricular dysfunction having conventional surgery. So, you decide before how you are going to put a VAD and then you take it out in a planned fashion either days or weeks later, and the rationale for doing that is that the alternative for all these patients as you see in your hospital is they come out of the operating room on high doses of epinephrine, norepinephrine, Milrinone, balloon pumps. They are on so much medication they get vasoconstricted, sometimes they get ischemic guts, they get ischemic limbs, they go into kidney failure and as an alternative to that you can switch off all those ionotropes and just put in a ventricular assist device. It will give you good flow, good perfusion, you do not have to go on high-dose pressors and ionotropes. So, in the immediate post-op phase you have good tissue perfusion and you can rest the heart. So the heart is off-loaded, it rests, and it can recover from whatever the trauma of the operation was.
The type of device you put in depends on how long you think the recovery will take and the likelihood of recovery. If you think that the heart is going to recover within days you can use a CentriMag, or a TandemHeart; simple devices you take out within a week of surgery. If you think it is going to take several weeks then there are other devices you can use like the old Thoratec devices that you can leave in for weeks or months, but importantly if you think that this is a patient that you are not sure; 50/50, he may fly, he may not fly, then put a device that you can leave in for ever, like a HeartMate device, an implantable device. So, if you cannot wean them then you do not need to do any more surgery. Just leave them with a device either as a long-term, lifetime device or you can bridge them to cardiac transplantation.
Here is an example of such a patient. He is 65 years old. He has two previous bypass operations, very poor biventricular function with severe mitral regurgitation. So, we offered him a mitral valve repair but in that case we decided electively we would put in an assist device. So, he had a TandemHeart placed and we placed this through the axillary artery. He has had his surgery through a thoracotomy. This is the head of the patient. This is his abdomen here and you can see the tubes from the device coming from his right shoulder. This is the surgical incision to replace the valve and this is the pump, which is a centrifugal pump, and we left that in him for four days. The advantage of that is that the patients can actually sit up in the bed with this. It is not like when you have the TandemHeart in the groin there, sort of have to lie down. This is the patient getting ready to have the device taken out and it is just taken out under local anesthetic. So, he does not need to be put to sleep to take this out. We just open this small incision here; control the vessels and take it out. The patient did very well and was back to work as an accountant within three weeks. We published just recently; had this accepted for publication; this technique and we have done it in about four patients so far.
The postcardiotomy shock is the use that most of you would have seen in valve surgery and it is probably the one we should discourage the most, but basically it is people who cannot wean off the heart lung condition, if you have had a cardiac arrest in ICU and if you are in shock, so the shock is your hypotensive low index; and you are not responding to ionotropes and you have to exclude things you can treat; like if a bypass graft has gone down or cardiac tamponade. Those are things that you should treat first but most importantly you have to exclude irreversible causes. So, if the patient suffered some major catastrophe in the operating room, the heart is not working, there is a stone heart, the heart will never ever, ever, ever recover. You can put in as many LVAD's and BiVAD's and ECMOs as you like, they are not going to get better. It is a futile exercise and it is important to exclude those patients, putting in a VAD for postcardiotomy shock. And the patient should otherwise be salvageable. So, it should not be a patient who has got terminal cancer, 85 years old. You have to do it in someone who you think there is a chance, who will succeed, but most importantly the prognosis is poor. This is data published from Medicare; data a few months ago which showed that patients in postcardiotomy shock at one year; only about 27% were alive. So, three and four patients will die and of those alive many of them have severely impaired quality of life and it costs a lot of money. So, it is something that we question whether we should do. Ideally you would want to put in the VAD's preemptively in these patients before they deteriorate so significantly and go into multiorgan failure and in that way you might be able to save some of these patients.
The fourth application is an alternative to high-risk surgery and this comes about because we now have better ventricular assist devices. This is a paper published in the New England Journal last year about a HeartMate II device which is an implantable device, put in the abdomen, connected to the heart. It is a continuous flow device, a second generation device and this device can be put in with very low mortality and indeed very good outcome. Six months after implant in this study, this was the FDA study, 85% were either alive or had transplants. So, this device has revolutionized ventricular assist device therapy and the question then arises; if you have a patient that is very sick who is going to have conventional surgery, you do a very good operation, they survive, many of them do not live that long, or they do not have a good quality of life, the question is whether you should just put an assist device as an alternative to doing surgery because often you fix the valve you do not fix the ventricle, they still spend the rest of their life with a 15% ventricle, they will still have symptoms, they still will not be able to do a lot of what they want to do and there is an example of a patient we operated on just last week.
He is a 64 year old with severe aortic stenosis and moderate mitral regurgitation, ejection fraction 15%, very dilated ventricle, severe RV dysfunction. So, we could repair his mitral valve, replace aortic valve, repair tricuspid valve but he is not going to go very far. The best thing for him would be to put an assist device, which is what we did. We put an assist device. He is doing fine. He is going to go home on Monday and he will have a good quality of life and since he is 64 he can be considered for heart transplant and at the end of the day you probably save more patients by doing this then embarking on heroic operations, and we all sort of feel good that the patients survived, they left hospital but really it means nothing, I mean surviving is not the key in this kind of patient. It is your quality of life and how long you live in the long term, not whether you survive surgery.
So, the fifth indication is not one we have done much but is popularized by the group at Texas Heart. Basically, if you have patients in cardiogenic shock, they come to the cath lab or emergency room; let us say they have a ruptured papillary muscle or post infarct VSD. Rather than rushing them to surgery to do salvage operation just put in an assist device and see how they do. So, they put in an assist device through the groin in the cath lab like a TandemHeart or put them on ECMO, give them a few days, let them wake up, let their liver get better, kidneys get better and if they look salvageable then go and do the major surgery. It is something that can save a lot of resources ultimately because it saves you having to invest in a lot of surgery and saving people that cannot be saved. Then at the end you are left with those that recover and then you can go ahead and operate on them.
The sixth I will not dwell on; this is just dealing with complications of surgery and sometimes when there are some complications it is better to rest the heart for a few days and you can use an assist device for that.
So, I will just say very little about the postoperative care which is that these patients are different from other heart surgery patients once they have an assist device and it becomes very important to maintain their volume quite tightly, if they come out on just a single ventricular assist. If you overload the body, the other ventricle can struggle. The afterload is very important because you need tissue perfusion, and if it's too high, because the pumps have to pump against the afterload. So, if you have a left ventricular assist device and you are hypertensive with a systolic blood pressure of 140, the flow of the device would be low. You have to maintain that. You will have to support the unassisted ventricle with ionotropes, give nitric oxide for the lungs, and optimize the heart rate but most importantly; bleeding. You have to reexplore them if they bleed. You do not watch this kind of bleeding because they go into tamponade very quickly and the tamponade affects the fitting of the ventricular assist device and affects the other ventricle.
In terms of weaning, we wean the patients when there is no organ dysfunction. So, the kidneys are working, liver is working, brain is working, lungs are working. There has to be good tissue perfusion so the patient is well perfused, in that they do not have black legs, ischemic legs, they do not have ischemic gut. There should be no acidosis. They should be passing urine. You turn the VAD flow down, you do an echo. The echo should show at least moderate ventricular function. You cannot be perfect on everyone because many of these patients are very sick. So, you are not looking for a 50% ejection fraction, 30% you'd take. Then once you see that, you start weaning down the VAD over a period of usually 24 to 48 hours, sometimes longer, you heparinize the patient fully to reduce the chances of thrombus and then if that is all successful you explant the patient.
Often, I must say though that a lot of the patients, quite a few that we have seen, we explant them successfully but some of them will still go and then die of low output syndrome or multiorgan failure. So, the salvage rate is not always high. If you cannot wean them, they'll usually die and you would have to speak to the families and involve palliative care and discuss end of life. It is often traumatic because unlike other forms of death this is one form of death where it can only happen if you actively do something; which is switch off the machine. So, it is very difficulty for families to take, which is another reason why it is important not to put these devices in patients that you think have no hope at all because it is just making a more difficult situation even more difficult for the families. Some patients, if you cannot wean them, can be transplanted, but that is a minority, and then some patients can be converted to long-term devices but that is even a smaller minority for the reason that most patients who cannot wean are also in multiorgan failure and very sick patients.
So, in summary, something useful for high risk valve surgery but it is really a niche intervention, it is something that is probably less than 1%; 1 in a thousand patients should get, but where we use it, we should consider using it early. For postcardiotomy shock its use should generally be discouraged because the results are universally poor. In my institution we do about 40 to 50 ventricular assist devices a year, so it is a sizable program, and in the last three years, we probably had 20% of patients survive postcardiotomy shock, and that is with an experienced team, so it is not something we should be doing too often. Thank you.
2009 Heart Valve Summit: The Repaired Mitral Valve Leaks: Now What?
So the first case, a 54 year-old man presents with a 10 year history of heart murmur, gradual onset of dyspnea; and a 6-month history of increased palpitations. His echo reveals severe MR due to bileaflet prolapse. The patient is referred for elective surgery.
Here is a Barlow's case. You cannot really appreciate that with the ventricle full. You notice when the ventricle, just make one point for surgeons, when you decompress the ventricle and your clamp is on and then you fill the ventricle you do not see the same degree of prolapse. You really have to fill the ventricle because now the ventricle is relaxed, you have a lot of excess tissue so valves often will not leak, that is why when you have a little bit of AI, you can really distend the ventricle because the valves will not leak as often times when you do not have that systolic pressure. Well I did a valve sliding plasty you saw that the sliding plasty typical Carpentier type repair and this was the echo afterwards. They called me back to the room. I thought the valve looked okay and they call me back a few minutes later and they said, "come in here and look at this echo, Dave, see what you think." There is no bleeding. The pericardial well is completely dry. They want to know whether they should give protamine or what to do. So let us let the panel think about that and then I will ask the question too. So here is the question.
Q: Did you look behind the heart?
Dr. Adams: I have looked behind the heart and I do not see anything.
Q: You do not see a big hematoma.
Dr. Adams: I do not see a hematoma, and I do not see any blood.
Q: Intramural hematoma back there?
Dr. Adams: I do not see anything behind the heart. I see literally just what I have showed to you.
Q: Did you decalcify the annulus?
Dr. Adams: I did not. Straight sliding plasty. It could not have been a more routine.
Dr. Martin: Can you go back just for a second?
Dr. Adams: Sure.
Dr. Martin: So play it again, can you play the images there. Because you have clearly got MR, okay, that looks like it is coming around the side of the ring.
Dr. Adams: Yeah.
Dr. Martin: You got a lot of that. You can see the ring there. The ring looks a little funny to me, but I am you know.
Dr. Adams: Well watch again. This is tricky. See I have got, I agree that we have a systolic jet and it is at the ring.
Dr. Martin: I mean that you got.
Dr. Adams: I am trying to sort out what the heck has happened here.
Steve: Did you rupture into the coronary sinus?
Dr. Martin: That is what you are wondering about?
Dr. Adams: That is what we were thinking about. What I am thinking about is something going on.
Dr. Martin: Although when you show us the coronary sinus, the flow there is blue.
Dr. Adams: Looks pretty good.
Dr. Martin: Yeah coming toward us.
Dr. Adams: The other thing you notice is there is something odd.
Dr. Martin: What did you? You left a sickle in the left atrium there?
Steve: No, I think...
Dr. Adams: Okay guys.
Steve: I think it is the left atrium. I think the left atrium is that little thing.
Dr. Martin: Not only that the color was sort of, you had a dropout, so it is likely to.It is not now, but you have got a space there. You have got some kind of big space. If you watch the color.Turn the color on again David. See the color, it is interrupted, so you have got some kind of space-occupying lesion and the color is actually going around it. Now, looking back there posteriorly, you look like you have got a.I agreed with Steve, it looked like he had a hematoma or something posteriorly. Alright.
Howie: Dave was he instrumented with a Swan before the surgery?
Dr. Adams: Yup, all patients get a Swan.
Howie: I mean, it was obviously done blindly and typically those catheters are soft but, you know, it is very easy to miss and get into the coronary sinus and cause mischief with the catheter.
Steve: I think they are little things. That is the posterior of the LA wall push forward.
Dr. Adams He did have one in and he does have it in now. So here we go. What would you recommend next ? Re-institution of cardiac pulmonary bypass. Now we are going to vote; valve replacement; reinstitution of cardiopulmonary bypass and valve re repair; give protamine and observe carefully in the operating room; consultation with an interventionalist for possible device closure.
Steve: In the OR?
Dr. Adams: It is true para-ring leak, I might do that. Give protamine and plan on repeat echo in 24 to 48 hours. What do you guys think? I was trying to come up with 5 instead of 4.
Steve: Somehow, you got to take a look back in there again.
Dr. Adams: We are just ready to wean from bypass. He looks rock stable. When I showed you that, we had just put our clamp on and the heart is working great. Everything looks perfect. This guy looks good. He has got a funny looking echo.
Dr. Martin: Let us go ahead and vote.
Dr. Adams: Why don't we vote?
Steve: He has got to have an intramural hematoma back there. Everyone should take a look.
Dr. Martin: I like the 1% called for Howie.
Dr. Adams: Okay, well, I think the main message and you notice the title of my little 5-minute or 8-minute clips here is, you know, the valve leaks, what do you do. We have some perivalvular systolic jet. We are not completely sure to be honest with you about what is going on here but we know we are not going to leave that behind. Fortunately, it is not going outside the heart; it is inside the heart. Let me just go to the next slide. And that is what we found. And so what we had was, is we had a tear. This is the hematoma. Now that we saw an intraatrial hematoma in the left atrium, we took the repair back down, I had to literally start all over, take the ring out, redetach the leaflets that had been slid along the annuloplasty and sure enough, one of these sutures that was used to tie the ring in had torn the atriaventricular groove and instead of rupturing out, we ruptured back into our left atrium.
Dr. Martin: You know, that was the point I was making about the color. The color was, you had a significant amount of leak but it was interrupted by this shadow and that had to be a hematoma or something around it.
Dr. Adams: And so, at any rate, we took it all down, I used a couple of pledgeted sutures to repair that defect and we re-repaired the valve, put it all back together again and you can see where the X is, where now this cavity is thrombosed. The patient went home and did fine but I think it is an interesting case, certainly one we have not seen before. Of course, we have had a lot of fun kidding our chief resident about that case but I think it shows a good example of things you do not understand after valve repair, or mitral surgery, you need to look at and the reason you need to look at is because things are under systolic pressure.
Dr. Martin: So the guy did okay.
Dr. Adams: The guy did fine and again I think the key there I think from the surgeon's standpoint is it is not just re-replacement and actually it was quite a simple thing to do but to get there, you have to take it down and be thinking about looking at the annulus when you see that. I will show two other real quick ones. Again, it is a promise that they are just for interest sake. This guy is 54 years old, he has dyspnea, he has an echo. Again, this is the intraoperative TEE. The MR is downgraded a bit. You can see this QLAB analysis suggests there is some prolapse around the posterior commissure. And so, here is his valve and he is interesting for the surgeons here that you will notice that he has a, it takes me a while to figure this valve out too. He has got again a posterior commissural leaflet. So he has a freestanding posterior commissure leaflet that is not P3 that is a posterior commissure leaflet. That is what is prolapsing. I make the decision as you can see in this picture to make it, to attach it to the anterior leaflet because I do not want to leave this free standing. It just had some chordal elongation, so I have attached that to the anterior leaflet and you can see my saline test, I am pretty satisfied with that. The ventricle looks watertight. And here is the postop echo, and they called me back by the way and said it leaks some. I think everybody wants me to go to the next room. I am of course distraught because I am looking and thinking about the picture of the saline test and very happy in seeing that. So, anybody have any ideas what is happening here? Randy? I think one good point you can make Randy is that you agree that is inside the ring this time. Last case outside the ring.
Q: Yeah, that looks fairly inside the ring and David I cannot see it well enough to say.
Dr. Adams: And I know I am just showing one view but I think the message here is that there might be one case or two cases you might accept something like that, I do not know.
Dr. Martin: No, that is a lot of MR.
Dr. Adams: But not in degenerative disease. I am saying may be it is reop, it is calcified, you have done a valve replacement, you have calcium you cannot get rid of. Sometimes we accept paravalvular
Dr. Martin: By suturing them together, have you restricted the motion or have you done something to distort even though that looks like it is at the P, you know, at the posterior P1.
Dr. Adams: I was cursing myself honestly, as soon as I saw that echo because I had known the mistake that I had made because I thought about it. First of all just the question is obvious this time, reinstitution of valve replacement, valve re-repair, or protamine. I think everyone should re-repair that valve or at least go back and look at it again and the mistake I have made is right there. See when I close the septal, when I attach the commissural leaflet, in this particular case, I thought that my indentation would close and it closed with saline, but under systole I had this leak at the base of that and I needed to put two sutures in there to close that, so by going back on for literally 15 minutes, putting two interrupted sutures there and doing a careful interrogation of the rest of the valve, you see the difference in the echo. And the message is again, you just do not accept these kind of jets and always focus on those deep indentations because you do not want to close all of them, particularly in smaller rings because you will limit motion but if you see a leak like that, that is the thing to do. The last case I will show you.
Steve: Can I make a point about you know, when you come off bypass, people ask me, when you come off bypass, how much MR do you accept? Well, I sort of think of a factor of 2 so if they had 1+, they are going to walk around with 2+. If they had 2+, they are going to walk around with 4+. The amount of regurgitation you had the first time coming off was pretty analogous to what you started with so, I mean, it is pretty downgraded, so I agree with you, I would not have accepted that. And the other point is we have that same feeling that when you move something over, you may open up a cleft more than you think and you may have to put those things together.
Dr. Adams: I think that is a good point is that one thing about you and in triangular resection can be that too. You can separate an adjacent indentation so that is almost always the most common source of a recurrent or a residual leak after a valve repair is something very simple along the margin line which is why I think re-exploration in almost everyone is a right answer. I will show you one last case.
Kevin: When you go back to look at the valve it is hard because it is out of the level plane of how your used to looking at it and when you put the stitch in the ring. Is that the way you put a valve stitch in? You pull the valve up?
Dr. Adams: Yeah, I am sorry, yeah, you can see that.
Kevin: Because otherwise it is hard to evaluate it.
Dr. Adams: Yeah. Guys, what Kevin is bringing up which is an excellent point is that whenever you need to do something fine after you have done an annuloplasty, what the ring now has let the valve rotate almost flat; it is not pulled up like it was when you had your annular sutures in. So you see, the first step we always do is put a ring, we would normally used to implant the ring, an Ethibond stitch into the ring and retract it toward the drape and that rolls the valve toward us, so now we can look at the plane in the annulus again so that is an extremely important trick and it is useful not just like in a case like this but also at the end of the case when you are just not quite happy with your saline test, that is the way to roll it up and really look at your edge.
Dr. Adams: Yeah, you are right. I should have made that point. I think it was intuitive. These cases, you have got to have great intuition because your saline test is normal and I really distend ventricles, a lot of you guys have visited me before, I really let the ventricle get distended. I want to see a watertight valve repair so you do always have a little bit of consternation when you have to go back on because you do not have saline now to guide you because we normally will not close with that abnormal saline test. But this is an intuitive thing, like Steve said; just keep it in mind when you close segments together, if you have adjacent indentations or clefts, that is almost always a source of recurrent leak.
Steve: This is a good point that the saline test, David, is not foolproof, that the left ventricular pressure you get when you fill it up with a bulb syringe of saline is about 45. So unless that patient is an amphibian you know they could have possible mitral regurgitation. You just cannot get it tense enough to fill it up. So the real proof in the pudding is unfortunately the TEE. So you really have to think about how you have done that, you know, have you opened it up, you know, we do a sliding plasty sort of rob peter to pay paul , we pulled the P1, P2 cleft or P2, P3 cleft open, do we need to do something than that.
Howie: Do you guys use 3DT here to assess these things? so that, it would seem to me you would be able to tell more quickly what the problem is without having to go before you open up in a more physiologic state if you had 3D.
Dr. Adams: Yeah, I think how 3D is in my experience, 3D is best for QLAB in telling you position of leaflets in the annular plane. I think it is less precise in terms of locating the actual, you know, sort of regurgitation, I think it locates regurgitation in quadrants but I am not sure it can show you the specific.
Dr. Martin: Well, Howie, there are lots of technical problems that you have to overcome. I mean, you can make clefts appear, you can have all sorts of stuff.
Howie: We use it a lot to figure out for e-valve, mechanism of MR if you are unsure sometimes.
Dr. Martin: No, I think there is. He is saying that, I mean, he is saying that but on the fly it is a little bit more difficult.
Steve: I think that where 3D is going to be really important while we see it as an enabling technique to make people more comfortable doing mitral repair increasing the ability of everybody to do mitral repair. What we see, is, you know, I get in there,the first time I look at the valve is when the cross-clamp is on its cardioplegia and I do not really have an understanding. If somebody sends me a 3D you know, 2 weeks ahead of time, I can really think about that and see. And that is exactly what we do. I think it is a great technique to think about the valve ahead of time.
Dr. Martin: It is different than in the interventional lab where I think that the evaluation makes a difference.
Steve: Even ahead of time we use it to figure out whether we think, you know, what
Question at the mic?
Q: I just wondered how much mitral stenosis do you accept when you do these kind of repairs.
Dr. Adams: Well, in degenerative disease, it is extremely uncommon to get a gradient so that is very different than when you are downsizing in ischemic cases because in degenerative disease we are true sizing the annulus as some patients do have a size 24 or a size 26 normal size annulus in relation to the leaflet surface area but it is very uncommon to get mitral stenosis, even functional stenosis after degenerative valve repair.
Steve: Yeah, I agree in degenerative we do not really see stenosis, you know, you accept a gradient of 3 or 2 or 4, it depends on what their heart rate is and what the cardiac output is. I think it is very hard in degenerative disease to provoke mitral stenosis.
Dr. Martin: You want to go forward?
Dr. Adams: I will show one last case. So here is the last case I will show you and it looks like a simple prolapse of the posterior leaflet. Of course there are a lot of ways to fix this and, let's see, here is I just show you quickly what we did. It is sort of tall P2, a quadrangular resection is a good choice in this particular thing I thought maybe we will do a triangular resection. We had a hypoplastic P1 closure line, so far so good, and that is the postoperative echo.
Dr. Martin: So you got a little SAM?
Dr. Adams: This is really after the, and you notice we do not have a lot of MR guys. This is after, I'm sorry we didn't rotate this probe we didn't leave it on long enough. We have optimized it. You know, we are not on epinephrin. We tilt the ventricle up. We obviously do the usual hemodynamics sort of optimization and we have got a gradient in the outflow tract and minimal MR and a young patient, you know, sure, you could always give me a 90 year-old or some reason I would not do it but let us just assume it is the usual 60 year-old or 54 year-old and we have a high gradient in the outflow tract with no MR. And the question is again, what should we do.
Dr. Martin: Are you going to give us a choice?
Dr. Adams: Reinstitution of bypass and valve replacement. Reinstitution of bypass and valve re-repair. Give protamine and optimize.
You know whatever you are going to do is only going to take a couple of minutes because the other thing, almost all these reinterventions are very quick. The first case was very unusual, an annular disruption. These sort of cases are going to be quick and I would go back on and fix this because we have already done our optimization. Keep in mind that there are a lot of these that are created by our friends in anesthesia when they are trying to sort of, especially the younger the anesthesiologist and the quicker they are to go to epinephrin regardless of what is going on with the patient, you can easily create SAM in perfect valve repair. So you do have to be patient, come back to the room, make sure that all the conditions are optimized and often times, I will just give Levophed and give the beta-blocker and if it resolves then I never worry. As soon as you see an echo where it has gone, it is going to go away. I think, you know, almost variably it goes away eventually. I will still leave the room with some if I can make it perfect by filling with volume, slowing the heart rate down and raising the pressure, I am always happy it is going to be resolvable. If it looks like what I just showed you, even though there was no MR in that case, I would actually go back on as well and I will show you what the mistake I made was.
Steve: Dave, can I ask you a question?
Dr. Adams: Sure.
Steve: You think that the height of the P2 was still too high?
Dr. Adams: That was the mistake. Well you see, I made 2 mistakes here. One was the anterior leaaflet was a little bit triangular in shape; it was a little bit taller than the size of the ring and I thought I had a displacement of closure line and I was not worried but you can see what I did there, Steve, was I did a small tip triangular resection and I used a Gore-Tex cord to displace the posterior leaflet lower in the ventricle to make room for the anterior leaflet to come up so again, very simple re-repair you can see, Kevin, that suture you always correctly pointed it out, always here to help me see everything but I think that systolic anterior motion is another process that you will see occasionally when you do valve repair and it is not just in Barlow;s disease; it can be in this sort of intermediate size ring and tall leaflet segment and I think that one thing, you know, Randy, I will say in closing is that one thing what would really help us in the future, you know Carpentier has talked about closing angles of aortic mitral valve and Roberto mentioned that earlier but I wish we could get more sophisticated in preoperatively predicting which patients are sort of at higher risk versus a lower risk for this because we spent a lot of time worrying about it and sometimes you have that exact same case and you come off and for whatever reason the balance is still far away but at any rate, when you do see it, I think the best thing to do is, is take your medicine and go back on and we used to make a horizontal incision in the leaflet and shorten it; now I think leaflet displacement. That is why I never get too frozen because even though I do not do primary leaflet displacement as my first routine without some resection, I learned from Fred Moore and others that Gore-Tex displacement is extremely useful in this sort of setting when you are trying to optimize your closure line if you have left it too tall, just tying it a little bit lower so effectively, the margin in that leaflet acts like cord, is a very simple trick and takes very little time.
2009 Heart Valve Summit: The Mitral and Tricuspid Valves from the OR
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.
2009 Heart Valve Summit: Rheumatic Mitral Valve Repair
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.
2009 Heart Valve Summit: Peri-operative Care of the Patient with Mitral Valve Disease
I am talking about perioperative care of the patient with mitral valve disease, and by that, I mean the care delivered before and after surgery. I am not discussing the operative period today. These are the things I want to talk about and hope to provide an overview of the role of the nurse practitioner at Mount Sinai's Mitral Valve Repair Program. I want to discuss the nursing issues specific to mitral valve repair patients, and at the end touch upon the benefits of a physician-nurse practitioner collaboration in a specialty practice.
So this is one of our patients, status post mitral valve repair. You may think, well that does not look like a typical open heart surgery patient and that is just the point. Our patients are a little different. Dr. Adams was talking about this morning that many of our patients are asymptomatic and that can require a little more education in terms of the nurse practitioner's role in dealing with the patient, the patient who comes in asymptomatic and feels great and is active, needs a little extra education as to why surgery can be beneficial to them
Just a little bit about our program, and specifically as you can see, Dr. Adams came to Mount Sinai in 2002, and the number of mitral valve repairs has almost tripled in that time. So the program has seen steady growth over the past seven years, which again makes a nice role for a nurse practitioner to augment a practice. Our program is growing not only in numbers but in geographic reach as well, and some of you may notice this in your programs too that while most of our patients are still from the New York metro area, with greater frequency are seeing patients from out of state and from out of the country, and as a result, we need to be really efficient in order to streamline the preoperative and operative experience, so hopefully the patient only has to make one visit to Mount Sinai. We also hope that the patient feels confident that we will be able to give them a comprehensive experience even though they live a few time zones away. Just to give you an idea of our weekly patient volume, the nurse practitioners see 10 to 12 patients a week in consultation and Dr. Adams sees these patients as well, but that is about our number. We have done as many as 17 in some weeks, but on average our typical week is 10 to 12. We will see 8 to 10 postoperative patients in followup in the clinic, and in general, he does about 10 to 12 cases a week and to manage this volume we have two NPs; I am an adult health NP and one of my colleagues is an acute care NP and we also work with a clinical nurse specialist.
The initial patient contact is made when the patient calls us for an appointment for a consultation and most of the referrals are still made by cardiologists though with greater frequency we are seeing more and more self-referrals. The patient will be told that they need to see a surgeon regarding an opinion for surgery and maybe they will be given a local referral, but the patients today are often going on to the internet and doing their own research, and sometimes, the patients will find us that way. When they call us to schedule the consultation we will give them the information that we need to have before they come, and if they have not already seen the website, then at this point we will give them that information. We do like for them to go to the website because there is a lot of information available there. They can learn more about their disease process, they can learn about surgery options, and they can watch a video of Dr. Adams doing a surgical procedure. They can read papers that he has published or that his associates have published, and they can also learn more about what to expect before, during, and after surgery. In fact, on the left there is a "what to expect" that they can click on, and they can watch a video which explains to them what to expect at the consultation.
We started this just a few months ago, and I think it is working out really well. We find that patients are more prepared when they come to their consultation, they bring the list of medications, and they have questions ready. It also helps in terms when I go out to greet a patient in the morning, they will say, "Oh, I recognize you from the website" or "Oh, you look familiar," and as we were talking earlier, Dr. Osterman's nice presentation on anxiety, a lot of these patients are very anxious and anything that helps to decrease that level of anxiety is a good thing.
Our goal on the day of consultation is to provide a one-stop process. We want to be able to give the patient a definite indication for surgery on the day of consultation, and this is very important, especially with our patients who come from great distance. So in order to accomplish this, the NPs at least a week prior to the consultation, will review each incoming patient's chart to make sure that it is complete, to make sure that we have not just an echo report but a film as well. If they have been done, we need to have the cardiac cath film and report and chest CT film and report. If the patient is a reop, we would want prior operative notes, and if they have comorbid conditions and see consultants such as pulmonologists or hematologists, we would like reports from them as well.
Our initial assessment includes assessing the impact of disease as indicated by the echo, we are looking at the severity of mitral regurgitation; we are looking at their EF, and their left atrial and left ventricular dimensions. We assess impact on the patient's life as indicated by their symptoms. Are they short of breath, are they having dyspnea on exertion, are they having palpitations, has this changed their level of activity. And then also, we want to know about the existence of comorbid conditions such as diabetes or a prior surgery or renal failure, and we do use the decision tree as published, this is the 2008 update to the 2006 ACC/AHA guidelines published by Dr. Bonow and if you look at the red highlighted areas, most of our patients have severe mitral regurgitation and so the first question is do they have symptoms. If they have symptoms then as long as their EF(ejection fraction) is greater than 30% it is a class-I indication for surgery. It gets a little more complicated if the patient does not have symptoms and then we look at their LV(left ventricular) function, and if their LV function is less than 60 it is becoming compromised, then that again is a class-I indication for surgery. If they have good LV function then we want to look to see are they in atrial fibrillation or do they have pulmonary hypertension because that is a class-IIA indication for surgery.
This is just our consultation form; it is a two-page form that we use when the patient comes. We do our history and physical and we document the echo parameters. We hope to be going electronic sometime in 2010, so hopefully, we will not have these paper forms much longer. Then again back to the decision tree, we can present all of the information to Dr. Adams about what the indications for surgery are, but only he can determine whether a mitral valve repair is likely, and the way he does that is through the echocardiogram and so we have to have an echo film the day of the consultation, and he reviews the echo film with the patient so he can show them their exact disease and the likelihood that he can repair the valve. As it was mentioned earlier this morning, we see more and more asymptomatic patients, and we can kind of tell how busy we are going to be that day or how far behind we will be in the afternoon because asymptomatic patients do require more time to educate. Dr. Adams spends a lot of time with them discussing their disease process and why surgery would benefit them.
The additional goals of consultation are to assess the patient's social situation and to give the patients an idea of what to expect after surgery. It is a time for us to just talk to them about what to expect in terms of length of stay, recovery afterwards, and it is a way to almost begin discharge planning before they have even been admitted to the hospital if they are going to have issues with recovery and convalescence.
The possible outcomes of the consultation are that there is an indication for surgery and the patient schedules a date. When that happens, I would say probably 85% to 90% of our patients schedule that morning after the consultation. Another indication would be that there would be an indication for surgery, but the patient wishes to seek other opinions. We are in New York, people like to shop in New York as they do in Chicago as well I am sure, and so it is not uncommon for people to want to get a second opinion even if there is a very clear indication for surgery, but that does not happen too often. Sometimes, there might be no indication for surgery. I have to say this happens very infrequently, and I think that is because NPs do put so much time into pre-evaluating each patient's file before they come. At times, we do have patients who are very high risk and it is determined that further evaluation is needed before final determination can be made and we will bring them into the hospital, admit them, and have a multidisciplinary evaluation.
After the consultation, we give each patient a booklet. This is relatively new; we started this a few months ago and this I think is also working out well. This booklet contains information about the what to expect preoperatively, preoperative testing, and it has information, most of our patients are day admit surgery patients, and so, there are instructions about that. We give them instructions about what to expect afterwards and instructions for the families about where to wait. They can read articles published by Dr. Adams and his associates, and then, there are also blank sections in this booklet, and we give it to the patients telling them that we would like them to bring this booklet to the hospital when they come in and we will supplement the booklet with their operative notes, with their postoperative echo, with relevant lab results so that when they leave Mount Sinai they leave with full documentation of their experience there, which is a nice thing for them to have and nice for them to share with their cardiologist.
Prior to surgery, we would review any abnormal preoperative tests and results. We will report any abnormal findings to the surgical team and field questions from patients. It is not uncommon for patients to call after the consult. Again, the level of anxiety can be high during that period, and even though certain things were discussed, they may not always remember everything that was talked about so they know that they can feel comfortable calling and asking to speak to one of the NPs. So that covers everything that we do before surgery.
On the day of surgery, we might update the family on the progress or outcome of surgery. Our fellows do a lot of this, but we fill in for them sometimes. We will answer questions from the family regarding ICU care. Again, it is a very anxious time not just for the patients but for the families as well. It is often difficult to see someone you care about in the ICU and often fluid overloaded; they look very different, and so, we try to spend a little time educating them.
Then during the postoperative inpatient period, we do afternoon rounds every day on all the inpatients. So, we go up, it is for a couple of reasons: (1) we do provide clinical update to our surgical team and (2) it is a good time to do a lot of one-on-one education with our patients and families. Dr. Adams does sometimes four cases a day, so there is not a lot of time in the day and for us to be up there and talking to patients and talking to families is really a nice benefit for the patients. Not only do we do one-to-one teaching, but also twice a week we do a formal discharge teaching class on Tuesdays and Fridays. We use our visitors lounge, and we do a PowerPoint presentation and this is very, very nice. We have just found that there is a nice interaction between us and the patients and also between the patients themselves. Somebody might ask a question that someone else was uncomfortable asking and it is usually just a very nice dynamic, and we cover all the topics of what they can expect when they go home, and at this point, we will schedule their followup appointment because they are going to come back to see us in four to six weeks in the clinic, and we also let them know that they can call us anytime after they have gone home from the hospital. In this way, I feel like we have established a relationship with the patient and with the family.
We do provide continued followup after discharge from the hospital. In 24 to 48 hours, we contact each patient at home basically just to see how they are doing to assess recovery, and they know to expect this phone call because we have told that we will be calling. If they had rhythm issues in the hospital, if they were in atrial fibrillation or sinus tachycardia, we assess to see how that is going and make sure that they are having appropriate followup with their cardiologists and are on appropriate medications. Our PAs actually do a good job before the patients are discharged. If someone is going home on Coumadin then the PAs will contact the local cardiologist to follow the INR, but we do get a lot of patients who are from out of state and those patients we do ask to stay in a local hotel for at least a week so that we can keep an eye on them, and for those patients we will make arrangements to have their INR checked and we will dose the Coumadin for them. We also assess to see how their incisions are doing. If they are having any drainage or any sign of infection we bring them right into the office. We assess pain issues, pulmonary status, weight and fluid status.
Our current anticoagulation protocol for our mitral valve repair patients, if someone is in atrial fibrillation for more than two days, they will get Coumadin for three months; if someone has a MAZE procedure they get Coumadin for three months; if there is no atrial fibrillation and there has been no MAZE procedure, then they will go home on aspirin 325 mg. This is our followup phone call sheet that we use for each patient and that just really prompts us to ask about their sternum, remind them we do want them to shower every day to keep their incisions clean, we want them to walk, we remind them about their lifting restrictions and again we remind them that we want them to see their cardiologist 7 to 10 days after they have been discharged from the hospital. They should see the cardiologist at least once before they come back to see us.
We provide continued followup after discharge from the hospital. I think that we provide continued support and reassurance to patients so they continue to feel connected. We definitely triage and streamline flow of care. As I said, if a patient is having any problem either with a wound or shortness of breath we do not hesitate to bring them into the office that day, so those followup numbers I gave you using earlier of 8 to 10 followups, those are scheduled followups. We have unscheduled followups as well that we bring in during the day. I am sure we do help to prevent emergency department visits. Certainly, if there is an emergency and they need to get to a local emergency department, that is fine, but if it is a non-urgent issue we would really prefer that they come into the office and see us.
Then in four to six weeks, our patients all return for a followup clinic appointment. This is one of my other colleagues Joel, and at this time, it is continued education reminding them they still cannot lift anything for about six more weeks, or at least anything over 20 pounds. We do a physical assessment, we do an EKG, we send them to radiology for a chest x-ray, they are seen by the surgeon, and at this point, they are basically, assuming that they are doing well from a surgical standpoint, they are cleared. They will continue to follow up with their cardiologist on a regular basis. At this point too, we also have to remember that we have a lot of reporting in New York State. I am sure it is probably similar in your states as well, but we have to provide New York State with a lot of information about each case.
So, the benefits of an MD-NP collaboration in specialty practice, I do think that in a growing practice like this one has been, NPs can definitely provide an additional resource for patient education and communication. We help to improve continuity and comprehensiveness of patient care. If you are looking for an article, there is a nice article by a Dr. Herrman and Dr. Zabramski that talks about neurosurgery practice with an NP and MD and it just highlights the benefits. It is a nice article.
For me, it has just been a great experience. I love working with Dr. Adams and the entire surgical team. I think that the surgeons really respect our clinical judgment and our autonomy and yet they are always available for questions if we have them and I think the patients also feel connected. They see us as a resource that they can contact if they have questions.
Again, we bring up the ACC/AHA guidelines, and if you look at this last paragraph, it says cardiologists are strongly encouraged to refer patients who are candidates for mitral valve repair to surgical centers experienced in performing mitral valve repair. So, I think this is a definite opportunity for nurse practitioners to work in a center where you can really focus on a particular disease like mitral valve disease and become an expert in an area.
I started with a photo, so I will end with a photo. This is another one of our patients, the guy in the middle who is just touching the alligator; he is an alligator catcher down in Florida. So, again highlighting that our patients are different and it is a good thing he is not holding on to that leash because it would definitely be against rules for postoperative patients.
I hope you have enjoyed this. Thank you.
2009 Heart Valve Summit: Patient Prosthesis Mismatch: Fact or Fiction
I will start with the scenario that we see now and then. So, this is a patient, 68 years old female patient with aortic stenosis. Body surface area is 1.5. Good LV function. No comorbid factors. We have consented her, she is in an operating room. The plan is to have a stented biological valve, pericardial valve. The surgeon opens her up. The biggest valve size he can fit in is a 19 mm. He looks at the chart that comes in the insert of this valve and that would put her in so called severe mismatch with the indexed orifice area of 0.73 in the red. So, you are a surgeon or you are the cardiologist who referred this patient, what would you expect as a cardiologist and what would you do as a surgeon. So, would you proceed with a standard 19-mm stented valve, pericardial valve, would you put a 19 mm mechanical valve expecting better hemodynamics, would you expect root enlargement and a 23-mm stented valve pericardial, the subcoronary stentless valve 21 mm, or would you replace the aortic roots with a 23-mm porcine valve? So, half would enlarge the roots and put a 23-mm stented valve and about 20% would use a stentless valve either as a root or subcoronary. So, I will follow on with that question and ask why you gave the answer. What is the reason that you gave best qualifies the answer. You believe a 19-mm valve was inconsequential in most patients, you believe it's associated with reduced short and long term survival, you believe that industry charts indicate the patient has severe patient prothesis mismatch, PPM. You believe it is best to avoid 19 mm valves but we have no reproducible ways of doing so or you believe stentless valves or roots have better long-term outcome. So what is the reason you gave the answer you gave; it is inconsequential, it has reduced survival, the industry charts say it is severe, you do no have good ways of fixing it, or the stentless valves are best. Let's see the answer. So, most people believe the stentless valves or root enlargement have better long-term outcomes. A lot of people go by the charts and only 14% believe it is inconsequential.
So, I have got a task here and I am going to be very controversial because I am going to try and convince you, I will try to convince you and we will see what you get convinced about. So, I am going to go through several myths about patient-prosthesis mismatch. I am going to deliberately challenge the data. The first is that it is a clearly defined entity. So, where does this all come from. This comes from Rahimtoola a seminal paper 31 years ago and what did he say. He said mismatch can be considered present when the effective valve area of a prosthesis is less than that of a normal human valve. That is what Rahimtoola said. Although, he did say it is often of no clinical significance which is interesting, but then he goes on to confound himself saying while the area of almost all types of prosthesis is less than that of a normal human valve. So does that mean that patient prosthesis mismatch is a necessary part of prosthetic valve replacement. He went on to have a nice graph like this and he indexed the valve area to the body surface area and defined an area of mismatch. So, that introduced the concept which we have carried until today which is indexing body surface area but where does it come from. I mean if you have a sort of BSA of 1.8 as a nice young patient and then you put on a weight you go up to 110 kg your body surface goes up, does it mean your valve now becomes stenotic, the same valve. I mean is it mathematical invention or is it a true phenomenon. Indeed if you look at the theory this is a lot of that comes from Pibarot's group and if you look at the theory for the same valve orifice here, as the body surface area goes up the gradient should go up but what happens in practice, so the valve area is going down, the gradient is all over the place. So, a lot of patients even with an indexed valve area of 0.7, 0.6 have little gradient across the valve. I mean the only thing that is true is that you do not get mismatch with a big valve. That is certain. So, if your indexed orifice area is 1.6 you do not get mismatch. I mean what is quite strange they have patients with indexed areas of 2.6, 3.0, I mean the only way you could do that is if you pull like an elephant's valve into a child well otherwise how could you possibly have an indexed area of 2.6 in an adult. This is amazing. But anyway what if you look here for the patients with a mismatch less than 0.85 indexed, the gradient could be anyway from very little to very much with all types of valves and that is the reality. The third myth I would like to point out is that we as surgeons cannot predict the likelihood of PPM. So, we use these charts but the reality is that the charts have nothing to do with what happens. The gradients are all over the place; whatever size valve we pick we see that unless you are going to put 25 valves in everyone you will see this dispersion. The fourth myth is that we get higher mortality with patient-prosthesis mismatch both early and late. You will see a lot of data in the literature that compares mortality with mismatch and without mismatch and as always you will see this was with mismatch. So, if we go back to Rahimtoola because he is the one that created this 30 years ago and now it has become an animal of his own and what does he say. He says to correctly address the issue, prosthetic valve area should be calculated from echo or Doppler studies six or twelve months after implantation, not in the operating room, not with these kinds of charts. He is saying that you have to do echo and workouts on echo. Look at all these studies, all of them are using the manufacturer charts, none of them have to find a mismatch based on real hemodynamics, real gradients, and real valve area. So, how then can they define the outcome and the reality is as we have seen you cannot use valve size to predict the postoperative orifice area. The correlation, as you can see, is very weak. So, we if we look again at the data this is data from Angelini's group published a few months ago and they looked at all the 19-mm valves. Based on the manufacturer's data, the orifice area should be 0.6 but actually measured on stress echo what the true area was and the average area was 0.8. So, what the manufacturer's say and the reality are not necessarily the same. So, it is true that you would rarely see patient-prosthesis mismatch a lot sizes that are concieded but the size of the valve alone does not explain mismatch. Many patients who you expect to have mismatch based on the industry data will not if you measure it in the clinic with echo and we do not know how to predict those patients who do have small valves that will transform to clinically relevant patient-prosthesis mismatch. So, the data that supports the adverse effect of patient-prosthesis mismatch are weak in the long term. So, let us look at some of the data. This is data from Dr. David's group published about nine years ago. So, although it is titled "Effect Survival", if you look at the 12-year survival whether you had mismatch or no mismatch, it was the same. There was a higher instance of cardiac related deaths in the mismatch group but overall survival was the same and when on multivariant analyses valve area was not a predictor of long-term survival; this is 12 years out and this is substantial, over 2000 patients. Although, it is important to know that about 30% of patients were dropped from the study because they did not have data on body surface area so it could be that with those patients the results could be different but it is difficult to see how a patient cannot have a body surface area given that every patient has a height and every patient has a weight, so how that data can be missing is a bit puzzling but anyway that's the data. This is a more recent paper published from Vienna and they found the same thing. No difference in long-term survival, so the axis starts at 65, probably a tendency towards high rate of mortality but the curves stay the same. The fifth myth is that as surgeons we can actually eliminate patient-prosthesis mismatch, so we can design better valves, stentless valves, we can sew the valve in the annulus, outside the annulus, enlarge the roots and then we can do this without risk but let us first look at what happens in practice. These are recent papers now. So, this was just published a few months ago in the American Journal of Cardiology. This is from Brisbane. They have 156 patients and 58% by definition had patient-prosthesis mismatch. This is the real world. In Vienna, the same thing, 54% of patients had patient-prosthesis mismatch. So, we have been talking about this for the last 20 years, but in practice as surgeons we are still putting in these small valves and indeed if you go through where the source started with Dr. David's group who over the last 30 years has led the field in terms of ways we can prevent this. Look at their data and they say that almost 30% of patients received valves with a ratio of less than 0.9. So, even with all attempts to fix the problem in Dr. David's hands there was still about 30% instance of mismatch. So, even with the techniques we have available it is not certain that we can actually fix the problem in all patients. We can certainly fix it in some but not all. So, let us assume for argument sake that we can reduce the incidents of patient-prosthesis mismatch, so the stentless valves work, the root enlargements work, is there a cost to this? And if we go back to Dr. David's data, I'll just concentrate on this period 1995 to 2000. The mortality for root enlargement was 7.5% and this is in 360 patients, so this is isn't a learning curve. This is a very experienced team who have led the field in this specialty and in the recent time had a 7% mortality. Now the mortality is down but if this is what David's group achieves what would I achieve if I do this only once every three years. So, for the patient I presented to you I have never done a root enlargement in maybe three years and I do that today, would I expect to be even in this 7.5% for a surgeon that has done 360 or will I be much higher? Chances are is that most of us will in reality be much higher. I mean some people do report even better results and you can see here the 30-day mortality if you have a root enlargement is 1%, 0.9%, which is even better than Dr. David's but is even better than a valve replacement, you can see in valve there is 4%. So, we might as well replace everyone's root and we will lower the mortality so you can choose what you want to believe. So, the other alternative is a freestyle valve. So, a lot of patients when were driven by the bandwagon of patient-prosthesis mismatch in the 1990s and received freestyle valves and it was said to be the best thing. It was even better than root enlargement. So, this is from Quebec again, Pibarot's group and 419 freestyle valves and of those 68 had the size 19 or 21. The operative mortality was 6% in this group. The five-year survival if you had a 19 was 58% and 82% for 21, which isn't very good and indeed the other observation is, that we all think a root replacement solves the problem and if you look; these patients had a freestyle valve, some are subcoronary and some are roots and if those that had a 19 still had a 100% instance of patient-prosthesis mismatch, 21 had a 70% instance of patient-prosthesis mismatch and this is real mismatch measured with echo. So this is not manufacturer areas, these are Doppler measured orifice areas and if you had a 23 freestyle there was almost a 50% incidence of patient-prosthesis mismatch. So, this led the office to conclude that an AVL with a freestyle subcoronaries associated with a high instance of patient-prosthesis mismatch and this is interesting to put this in perspective under high mortality because it then means that a lot of patients in the 1990s actually suffered because of our belief in patient-prosthesis mismatch and I believe that we had a solution, i.e. freestyle valve replacement.
This is another paper about stentless valves, now this is a randomized trial. So, stentless valves are supposed to do the trick and in a randomized trial they found no difference in the orifice area in patients randomized to either Perimount valve or a Toronto stentless valve. So, the sixth myth I would like to dispel is that these strategies to eliminate patient-prosthesis mismatch result in better long-term outcomes. There are really no good comparative data and even if there are late gains there might be offset by the higher early mortality that I have alluded to, but I think more important to consider is that patient-prosthesis mismatch might actually just be a confounding factor and the worst outcomes may have nothing to do with the valve area but to do with whatever factors make that patient have patient-prosthesis mismatch in the first place. This is a paper from the Vienna group again which I've shown earlier and they have looked at patients with mismatch and those without them and compared various characteristics. It does not matter what the details are but you can see a lot of P-values, a lot of differences; their older like seven years older than the people with mismatch there are more females who have a higher euro score and indeed on multivariant analyses the only thing that has predicted the outcome in these patients was not prosthesis mismatch but the euroscore and diabetes. So, a lot of these patients that we say do badly because the valves we put in are too small may be they were going to do badly anyway because of other factors within the patient and they said that the result shows that patient-prosthesis mismatch is stronger, I should say that with unfavorable preoperative conditions. So those unfavorable conditions probably put them at disadvantage at the time of surgery. So, the last myth I would like to dispel is the one of low-grade intra-aortic stenosis. So, we say that if the gradient is low there is no EF. That is the one that you really must, must, must avoid patient-prosthesis mismatch and indeed there are data to show that. So, here you have data from Ruel and colleagues and you find that if you have an impaired ventricle and patient-prosthesis mismatch your survival is worse and it is good to read the papers because when the study is not looking for what you are looking for you find other things that they were looking for. So, if you look here at the top of the graph you see that patients with normal LV with no mismatch and patient with impaired LV with no mismatch seem to have the same survival and that does not make sense because we all know that impaired LV function is a predictor of survival and obviously if they were writing a paper about impaired LV they would have not published this but anyway, what's important here is that they defined a poor LV function as less than 50% which probably isn't what most of us in this room and certainly not what Dr. Carabello would regard as low EF aortic stenosis. So, really if you torture the numbers they will tell you whatever you want to tell them, they will confess to anything and that is what statistics do. So, many of you would have seen this picture before. This is what tells you that if you have a low EF you must not mismatch the patients because if you have a low EF here and severe mismatch you are 70 times more likely to die than anyone else which is interesting because how is it possible anything in biology that your odds ratio is 80, it is not possible. So fine, what it reveals is interesting but there is something that is hidden which has to be vital and the answer is if you read between the lines. So, as I said you torture the numbers they will tell you anything. So, you have 1000 patients. This was published in Circulation. So, Circulation, the editors like the 1000 patients but they did not realize what was concealed by the bikini which is that in this group on which they base their entire study there was three patients. So, there were three patients with poor LV function and mismatch. Of course, they all died and they wrote a paper in which they say that 1000 patients published in Circulation, the best journal in our specialty, to say that you should not mismatch patients. So, I will tell you what the facts are that I see. The first is that the definition is unclear. The second is that most cases are of no clinical significance; I agree some are but most are not. The problem is we cannot predict those cases like the case we saw this morning, I think it was Lisa that presented the echo this morning. So, sometimes it is significant but the valve area is a poor surrogate and indeed there may be confounding factors rather than the valve area that explained this and those are approaches that we favored like 50% in the audience wanted to enlarge the root, 20% wanted to do stentless valves. They do not yield consistent results even in the hands of the experts, so I would implore that the cases should be considered on a case to case basis and we still need research to be able to predict who actually develops clinically relevant patient-prosthesis mismatch and the fiction is really everything else.
Thanks for your audience.
2009 Heart Valve Summit: Degenerative Mitral Regurgitation: Who Should Operate?
My topic is about who should operate, which is always politically charged somewhat since none of us like anything to do with regulation, at least some people in Washington do but I do not. On the other hand, this field sort of requires this question to be answered and there is a lot of data that is going to show that; my disclosures really do not have anything to do with what I am going to talk about. Let us start again with a question.
An otherwise healthy 50 year-old asymptomatic man has severe MR and preserved left ventricular function. Which of the following is most relevant in deciding on whether to proceed with mitral valve surgery at this time? So let you look at the echo, and here are the possibilities; a, accessibility to a very high volume mitral valve surgery center; b, age of the patient; c, high probability of repair based on echocardiographic lesions, the patient is a potential candidate for warfarin therapy, pulmonary artery pressure documenting to be 42/28.
So, let us have the answers. Everyone, pick one.
Okay, let us see the answer. So, it is interesting, you see 58%, I think have what is the right answer, which is that you have an asymptomatic patient and the guidelines are clear that if you do not think you are going to repair the valve with a very high probability, you should continue to do followup. We could argue about exercise or we could introduce the concept now of exercise echo to see where the PA pressures go but I do not think that answer A, which is what I predicted would be the second most common, is exactly right and I will show you why in a second. Can we go back to the slides?
So the guidelines again are very, they like to talk about mitral valve repair a lot and I like to show this algorithm a lot, I show it actually to every patient that I operate on. I put this picture up to walk them through why they should be considering surgery or why they have been referred and I put a double circle around the question mitral valve repair likely and I think this is the fundamental question that we have to start taking more seriously. The days of saying, well we have got these boxes and we are going to try and do a repair and when we got there we were surprised. We should not be that surprised anymore. I think the echo lecture this morning and the imaging lectures really show us that. We are doing better. This paper was just published from Jim Gammie, it is looking at 60,000 or 70,000 patients in the STS database, a large number of patients, and you can see I have put some blue up there what I consider still is the gap. Meaning that the gap has narrowed some in terms of, and I drew the line at 90%, well just for the sake of argument use the ACC guideline that 90% repair should be a goal. Again, several centers are in the 95% to 96% repair range depending on the lesion or higher, but you can still see there is a significant practice gap. I do not think in oncology, you would accept a 20% gap in terms of class I care, so I think we do have a significant gap and we need to think about how we are going to address it and of course the thing that always comes up is volume and skill, so let us look at that. Gammie looked at it in this paper in circulation that is sort of an earlier time period in the STS database. Again, they looked at a large number of patients, this time about 14,000 patients and they made a couple of intuitive observations but they are always worth reemphasizing, that is there is a relationship to volume versus repair and that of course makes sense and this was again data sort of in the early part of 2000-2003. You can see that higher volumes centers were sort of getting in the 70% to 75% range at a time where the average repair rate was in the 30's, so it was still double. The other observation that was made, which I do not think gets enough emphasis, is the decreasing mortality rate associated with volume.
The more you do of this operation like most operations, the better you get at recognizing the 2% or 3% of catastrophes that are about to happen, so I do think that it is not just your repair rate but I do think there is going to be a safety issue when you do very few mitral operations versus when you do a lot of them. We should not be surprised by that. The other issue about volume I think was addressed in this excellent paper from Cleveland which had a lot of data in it about degenerative repair and rates and various predictors and all kinds of things, but one thing I thought that was interesting to point out was that it is not just going to the Cleveland Clinic. It mattered a lot which surgeon you got at the Cleveland Clinic and I see lots of patients that tell me we may go to the Cleveland Clinic and I say who is the surgeon and they say we do not know yet. That is true, and I am sure the cardiologists here, some of you have had that conversation, but it does matter quite a bit because some surgeons at Cleveland were predictive for more replacement and one surgeon or some surgeons now I am sure are predictive of more repair, so it is not just volume or center, it is something else. There is something else there. This concept and Craig Miller actually sent me this paper after a meeting about two to three years ago. He e-mailed it to me. I was getting ready to take off on a plane and it was a paper I thought that he had recognized and I have since recognized was very provocative By Ben Bridgewater talking about best practice standards. It was the first time someone had actually put pen on paper and started to define this and one of the things they were saying in the United Kingdom was; surgeons should do 25 repairs a year and centers should do 50 a year, so at least we are starting the concept of volume. They were not getting into lesions yet except a little bit with Barlow's but at least they were starting to put parameters on volume and I will show you, this is data from 2008. It has just come out in the last two or three weeks and we actually were asked to write a commentary in this. It is published actually as a book. A commentary about their mitral data, so I had a look at this beforehand and I just want to point out that their experience in the United Kingdom where they track and actually unlike the STS where they do not differentiate at least yet, we will in the future be able to differentiate the type of etiology versus the operation in the STS database, those valve elements have been worked on by our committee including Steve and several people in this room and that will be coming so we will get more information. They do already, so they are not validated but they do at least ask people to check the box degenerative or non- degenerative and so this is the degenerative surgery arm and you can see that just like in the United States, repair is going up, replacement is coming down. Their repair rate now is a little over 60%, so they are looking a lot like the United States in terms of repair versus replacement for degenerative disease, but this is the figure that shows volume versus repair rate and look at the percentage of repair and the number of operations and what you can see, which you would expect, some low volume centers have very low repair rates and most of the high volume centers have high repair rates but regardless of whether you want to take the highest volume centers, you can still see there is an outlier that is very low and even when you get in this sort of middle category, I tell you there is a big swing between almost the highest repair center and one of the lower repair centers and the difference was only 20 to 30 cases. So, it is not just volume. There is something else to it obviously and of course that is going to be skill and I think what we have to do is say okay what else do we do to narrow this practice gap. One thing of course could be concentrated volume but there is certainly going to be more. This was their summary of their findings and this was an eight year study, so this is all inclusive, all patients that had mitral surgery in the United Kingdom over eight years, many patients. Another corollary by the way which I am sure we see in the United States and we do not talk a lot about, one of the reasons patients are not referred in a timely fashion to surgery and Bob will bring up in the discussion this paper just published by David Bach showing at the University of Michigan patients having indications for surgery not being referred for surgery.
One of the reasons I think globally patients are not referred is because they are worried the surgeons are not going to do a good operation, so you wait for the patient to get sicker and sicker and a lot of these patients were referred when they were class III and class IV and in fact a majority of them in the United Kingdom over that eight years were class III or class IV. Asymptomatic patients were rarely referred there. The mortality rate just like we saw in Gammie's paper was low or just one of the other elements Gammie had shown was lower for repair versus replacement. It is probably safer to do valve repair in most patients. Again repair rates crept up to 67% over the time of the study and there was a wide variation between hospitals performing repair versus replacement. So, Ani coined a phrase about postcode lottery. It should not matter within an 80-mile radius where you live as to which operation you do but today in the United Kingdom that is in fact what happens. Well, the other thing is this complexity of lesions. We talked about skill and Bob introduced that in the last set of guidelines and my partner Ani and I wrote this last year in the JTCBS and we are writing about an article that was talking about recurrence of MR and we were saying that basically complexity of the valve that you are confronted with and the type of repair you do is probably the fundamental thing we have not talked enough about to narrow this practice gap, so we are very interested in the concept of trying to differentiate degenerative disease and for you cardiologists that are here the next time you see a patient try and sort it out, is it single segment FED. This is the type of disease Craig was mentioning and these are older patient that go to Mayo Clinic and they are in their 60s and they have maybe unrelated two vessel coronary disease, but they generally have simple pathology and most of those patients by the way have simple triangular resection. They are not very complicated repairs. These are the patients Craig was saying and in a quaternary level, mitral valve referral practice in Northern California. This is what you get. You are happy the day you see P2. Most of the time you are seeing Barlow's patients, young, asymptomatic people, multisegment disease, giant leaflet segment distention, deep clefts, calcified anterior papillary muscles, you see these fissures, which is the beginning of displacement of the hinge of the valve toward the atrium and off the atrioventricular groove that leads to these micro-fissures that probably evolve into calcification. Totally different, you do not have to be a surgeon to know which one of these two valves you would like to try and repair. There are very different valves and again with imaging, it should not be a surprise anymore, which valve you are going to the operating room with. Keep in mind and I will show you in a second most repair rates in most centers were these two lesions, type I and anuloplasty, AFib the most common etiology are type II P2, a simple posterior leaflet prolapse which is about 60% of mitral valve repair and then all those pictures that I showed to you, 60% of the valves you would actually see just in a 100-case practice in a regular hospital would be this type II P2, not quite sure why that is the leaflet that actually prolapses most commonly but those valves get repaired very frequently in centers and you can read between the lines in papers if you want to understand this. So don't look at papers that are talking about what we repair. Go read the literature and read between the lines. Here is a paper that was talking about 3D echo and how 3D echo can accurately predict what the surgeon saw that they had a very high agreement between the preoperative 3D and what the surgeon saw but what they also provided not intentionally but just in the paper was the repair rates and you can see the overall repair rate was 50%, posterior leaflet was higher, bileaflet lower, anterior leaflet in this series is very low. So again, there is a clue. Posterior leaflet repairs are simpler to do, they are going to be done in maybe not a reference mitral center much more efficiently, anterior leaflet particularly in this center. There is a message there. Same thing, here is another paper, it doesn't matter what they are talking about, this one was talking about minimally invasive surgery doing side surgery incredibly safely but essentially no mortality, very high volume over 150 patients over an 18-month period published just last year, very current series. Overall repair rate is 66% but that is what you cannot tell the patient.
You have to look at the echo, turn the color off because this patient has posterior leaflet prolapse and in this center it's a 96% repair rate. Anterior leaflet while the numbers are really tiny but bileaflet repair, I think we can hang our head on that 20%, huge difference whether there was bileaflet or posterior leaflet prolapse, so the message there is not just volume, this is a very high volume center but we have to start thinking about lesions and there is a spectrum of disease and you go from simple prolapse, thin cord, non-distended tissue to the prolapsing segment developing some myxomatous change, relatively simple, then you have the sort of grey zone between fibroelastic deficiency and the true Barlow' disease which is the giant multi-segment valve and another way to think about that is that, that is the truth and you have an increasing repair difficulty as you move along this spectrum. You have got to respect rules and each one of these valves but there is no question that the more segments that are involved and the larger the valve is and the more calcium you may have and the more cordal elongation as opposed to broken cords you have, the more difficult the valve gets to fix. We published this last year talking about how cardiologists could increase the role of mitral valve repair, you are not doing the surgery but you could have a big impact on how we see that practice gap keep getting narrowed and the way you could do it is simply by saying FED or Barlow's. Single-segment, multi-segment, posterior leaflet versus bileaflet or anterior leaflet, because there is no question the likelihood of repair is going to go up substantially when you start matching the lesions and the etiology to the skill of the surgeon, and if you have Barlow's or bileaflet prolapse or complex anterior leaflet prolapse, unless you are with a reference mitral surgeon, these patients will have a high replacement rate and the current literature continues to support that. Again back to this paper from Bridgewater, there were a lot of other concepts in here that are worth mentioning and I like this one. Surgeons undertaking valve repair should subject their results to regular audit. I live in a state where things are audited and actually it is not very bad when you do not live there you sort of think, Gosh, what would that be like. It is not very bad at all. Frankly, it is healthy and I think that in this particular field we need to have some more careful monitoring of the results of repair rates, mortality rates, and quality of repair and audit should include residual and recurrent regurgitation after repair. That is another little buzz where cardiologists say now we are seeing more repairs but we do not like what we are seeing. We have to audit that, so we tried to define that in this article a little bit more. I just highlighted it. If your repair rate is less than 90% that probably means you need to differentiate more complex cases and get them out of your system and the other thing is early recurrence of MR and I will talk about that this afternoon, those are usually technical failure. If that is over 5% that is a problem. Sure, you are going to have some patients where you have a technical failure, we all do but it should be very small, a technical failure rate of 10% to 15%. Again, that suggests; refer more patients out. Another Bridgewater concept that he started was that some surgeons should have sort of super specialty practices and probably the subset that is for they mentioned to were the pan-prolapse they called, or Barlow's valve disease. So there is some logic to that and Bob mentioned this paper in his last talk, Kang, there are three of them now but the bottom line is we move towards asymptomatic surgery, the guess work about repair has to be off the table. I do not think that will change in the guidelines. If you are asymptomatic, these discussions with the patients are all predicated on an extremely high repair rate and that may be provocative. Craig may not agree with me but we said it, in the asymptomatic patient you need to approach 100%, not your whole series but in asymptomatic patients, you need to approach 100%. We know the mortality is going to be less than 1%, it has to be. It was in Gammie's analysis in the STS database. Move away from the argument of mortality, very few patients thankfully do not die any more from mitral valve repair. That is not a good quality indicator anymore. We have got to talk about repair rates and residual MR.
The last thing I will show you is this paper, just published this year from Fred Moore's Group in Leipzig because this is real world. These were all surgeons in the group. It is a very high volume center and Fred, I think he runs a meticulous research department and I think his honesty is well known among his peers. This is really what can happen in a real reference center. Overall, repair rate is 94%, posterior leaflet 97%, and anterior leaflet repair rate at 91% and bileaflet 90%, so this is a large series over 1000 patients. All the surgeons in that group by the way, or at least most of the surgeons, they were participating. So, it is possible in our own group. My research fellow, Javier Castillo just presented this in Berlin. Again, we have really been able to get over 95% repair in all of these 550 consecutive patients now, so it is coming. These degenerative patients can have mitral valve repair and this number of 90% is achievable and it is achievable in lots of places and it is achievable in reference centers now. Pat McCarthy wrote this paper earlier this year talking about when is your surgeon good enough, when do you need a referent surgeon, and I will recommend you for those that are interested to read it because it is an excellent summary, not only of the issue of repair versus replacement but also the issue of incisions which has come up more than once this morning already. I think Pat does an excellent job of discussing that. Craig mentioned this and so did Bob about durability of valve repair, should we repair all valves because some of them fail. Well, that is fair enough. Maybe there is 5% or 10% of these complex Barlow's that I happen to like to try and repair them and I think we have an obligation to really follow them carefully to make sure that those repairs are durable as well. There is an issue with the repair but please do not say well but this was Tyrone, so it had to be an excellent repair. Not necessarily true. I am sure it was an excellent repair for the time, and I bet Tyrone is a much better mitral surgeon today than he was in 1995 when he was doing those operations. I know I am. These were the repairs I was doing in 2004, they did not leak, cardiologists were happy. I frankly would not show that in the meeting anymore, I mean that does not look like a very pretty mitral valve repair. It looks like the posterior leaflet still has a fat lip. It has a very asymmetric closure line, not nearly aggressive enough taking out tissue to let the anterior leaflet completely coapt versus today where we are always looking for symmetry and perfect position along the posterior part of the valve and you can get there every time and one of the things we like to do is work backwards, show people bunch of pictures and then show them no matter what the pathology, you can get to that closure line, so Craig repairs are getting better and they are going to be more durable. This book is a good one. It is talking about outliers, what makes people special, and Gladwell talked about 10,000 hour rule, you know, doing the same thing over and over and over is how you really get to be perfect and it is true and this is the reality. This is not that common a disease. Mitral valve repair is not performed that widely among every single member of the society of thoracic surgery, so keep that in mind when you are looking at mitral valve disease. Some are simple, some are very complex. It is not just how much regurgitation there is but what type of regurgitation it is and what skill level do we need. This is not about Ivory Towers and send every patient there; I really do not want you guys to take that message home. The message is identify the etiologies and the lesions and fifth point is; develop local expertise through targeted referral. It is not who is on call that weekend. Every person in every private group or in every big hospital has to have someone that is interested in mitral valve repair and those are the surgeons who should be doing those operations. The question of who should operate right now I think the simplest way to think about it is; you go across the complexity of the disease, identify your city or regional or national reference surgeon.
Thank you very much.
2009 Heart Valve Summit: Acute Endocarditis, Embolic Stroke
Excerpted from the 2009 Heart Valve Summit.
Dr. Anyanwu: So, I am just going to present a case. This is a 64-year-old female who has no relevant prior history. She has got a two-week history of fever, malaise, and sweats. Her blood cultures are positive for enterococcus. She had an echocardiogram. I am going to show a very short clip, maybe Dr. Martin if you can just comment on this echo.
Dr. Martin: It is obviously a TEE and she has got a prolapsing mass that you are going to see severe two jets, probably of AI and probably has got leaflet destruction as well as vegetation. I am looking Ani, or want to look at that jet striking the anterior leaflet of the mitral valve, so I am always worried and I see it she has actually got a septic aneurysm of the anterior leaflet of the mitral valve. One of the key mistakes I think that echo guys can make from time to time is they get so entranced with looking at this veg on the aortic valve and the prolapsing leaflet that they do not look at the mitral, so the last thing you want to do is open up, go ahead and do an aortotomy and find out that you have got subvalvular mitral, So this is a big prolapsing mass and probably a secondary septic aneurysm of the anterior leaflet.
Dr. Carabello: Now, this patient is probably going to the OR anyway but is the mitral valve closing early?
Dr. Martin: Do they have acute severe AI ?
Dr. Anyanwu: Yeah, the patient has severe AI?
Dr. Martin: I can't tell boys, but you know if you had that question, obviously that is where Dr. Craig Miller's color M-mode, just the M-mode of the mitral valve with an EKG would tell you that.
Dr. Carabello: I mean that is an important point.
Dr. Martin: You know, you do raise from time to time, you do make important points.
You can even a blind hog finds an acorn every once in while.
Dr. Martin: All right, do not be distracted by us. You have to jump in this game here.
Dr. Anyanwu: So, just to add on, there was normal left ventricular size and there was normal function. Otherwise, the findings are as stated. So, she has no signs of heart failure, she has not embolized. There is no suggestion of an abscess in the heart. She has now had antibiotics for two days and her fevers have subsided. So I am going to ask the audience to vote but when you finish voting, before we see the answers, I would like to know what the experts on the panel say. So what do you recommend at this point if you vote. Do you continue antibiotic therapy; there is no need for surgery? Do you operate emergently as soon as you can? Do you operate urgently in the next few days, semi electively in two to three weeks? Do you wait for the antibiotics to be completed and operate? So if you can vote.
Dr. Martin: You know, nothing is going to get better with this valve.
Dr. Anyanwu: So just keep voting, do not show us the answers.
Dr. Martin: I mean nothing is going to get better. The mitral valve is going to blow out at some point. Now, you going to have acute severe MR in the face of acute severe AI and you are going to be bubbling over in the corner. When I see vedges, now this is not a giant vedge there on the aortic valve, but I always want to more importantly to me is to see what is happening with the end organs. So, I want to know has she had an embolic event to her brain.
Dr. Anyanwu: No.
Dr. Martin: What do her kidneys look like?
Dr. Anyanwu: Kidneys are just fine.
Dr. Martin: Did you scan her brain or did you not?
Dr. Anyanwu: She is perfectly fine. She is supposed to go on a cruise two days later and indeed she wants to leave hospital and go on her cruise.
Dr. Martin: She is going to go on a cruise?
Dr. Anyanwu: Yeah.
Dr. Martin: All right, is she is going go down the Hudson River and just circle near your hospital.
Dr. Anyanwu: No, no, she is going to Barbados.
Dr. Martin: She is going to Barbados. They have no pump programs in Barbados, they have good rum. She should drink a lot of rum.
Dr. Carabello For me, that is one of the reasons I asked a question about mitral valve pre-closure, if there were, I would say B. I would vote for surgery within 12 hours. With this case, I would say C.
Dr. Martin: I would say C.
Dr. Carabello I would say I want to do it. I do not want to wait three weeks. I would want to do it in the next day or two.
Dr. Martin: I do not think you are going to gain anything by waiting. I mean the infectious disease guys, they always get involved, and gals, will say we need to do antibiotics and all that. I think you are exactly right Blaise if she had acute severe AI and you got pre-closure in this operation right now but this mitral valve is going to go at some point.
Dr. Carabello We have reasonably good data that says that the chance of reinfecting the prosthetic valve even within 48 hours of positive blood cultures as long as they are on the right antibiotics is tiny, so I am not worried about that because I am going to operate on her, Steve is.
Steve: There are two surgical series now, one published out of University of Maryland, looking at urgent within 48-hour surgery and one is going to be presented by the STS from our place, taking 140 cases urgently done. Basically, the ability to have a good outcome is much higher now than it used to be in the old Darwinian thought where we would give the patient six weeks antibiotics and then operate on the patient. For two reasons, we worry about that; one where we operating on somebody who had an embolus or something to their head and turn that from a bland stroke to a hemorrhagic stroke and actuality in the Maryland series and ours that does not occur and I think that is an old wives' tale, 25% of our patients had MRI lesions in their heads and not a single one turned hemorrhagic. The second thing is especially in the mitral position the ability to repair the mitral position or void an aortic abscess like she will have very soon is much higher if you treat her on antibiotics. So, our policy, and I think a lot of people have gone to this is sort of identify the bug, give them the most expensive antibiotics that the ID guys can think of and then take them to the operating room.
Dr. Anyanwu: Okay.
Dr. Martin: Audience, you all can join in, I mean, if you have questions or you want to just.
Dr. Carabello: Steve, do you care, or Ani do you guys care if you use an aortic homograph or does that not make any difference.
Dr. Anyanwu: We have not decided to operate yet, so I do not know. Can we see the answers.
So, most people want urgent surgery. A quarter feel we should wait until antibiotics are completed, so about half want to wait at least two to three weeks and the rest want to operate and 8% do not want to have surgery at all. I mean basically the concern here is that she is going to embolize, isn't it? That is what we are worried about. This study published a few years ago in 2005, was a registry of almost 400 patients and they looked at factors that predicted embolization and importantly if you had vegetation more than 10 mm, it was predictive of new embolization as was mobility of the vegetation. Also the organism was quite important if you had Staph aureus you are more likely to embolize and indeed that is shown by other studies if you have Staph aureus, you are more likely to embolize. So, this patient had Enterococcus faecalis. The second issue has been which Dr. Bolling hinted is whether early surgery has worse outcomes and indeed there are data of such as this study published some months ago in the Annals suggesting that early surgery has worse outcomes than late surgery but of course there is a confounding factor because of the patients who are selected for early surgery might have been the sicker patients, but that is what is driving the decision either way and I am sure that is what drove people to vote one way or the other in the audience. So, we all discuss this, the cardiologists, the surgeons, infectious disease, and decided to wait maybe a week or maybe wait two weeks and then operate.
The patient is very informed. The daughter of the patient is a physician, an attending physician in my hospital, one of my colleagues, and the husband is a dentist so they are very well informed. They know the risks, they know pros and cons. She still wants to go on her cruise at this stage actually. So, she is still in hospital. Four days later, we say we will get a CT. Let us make sure there is no abscess in the heart before we are comfortable with our decision to delay surgery and look at her coronaries anyway.
The CT suggests there might be a perforation in the anterior leaflet. Both the coronaries are normal. We repeat the echo. There is definitely no vegetation; perforation is the same but the patient is changing. At this point the patient has dyspnea when she walks to the bathroom. She has got tachycardia. She has got a gallop, so things aren't quite going fine. We move her to the CCU and we decide we are going to operate now because she now has a class I indication which is heart failure, so we decided we will operate the next day. On that evening, she had a TIA, and then she had several TIAs. We do an MRI and she has an acute infarct and also as you can see her middle cerebral artery on the left side is more or less gone. You can appreciate the thrombus in the internal carotid and if you look on the right of picture, which is our left side there are no blood vessels there. By midnight, she was hemiplegic and she lost her speech and she became incontinent. This is five days after antibiotics were started, so we had her in the CCU, we kept her blood pressure up and just watched. She is still hemiplegic. We did another MRI 20 hours later. There was no hemorrhage. The infarct is becoming more developed, still no blood going into her left hemisphere. So just to recap, we have a 64-year-old female with Enterococcus. She has got a kissing lesion on her mitral she has got mobile vegetation which has now embolized. She is 24 hours after a stroke. She is densely hemiplegic. She is aphasic. She has no mass effect and no hemorrhage and she has occlusion of her middle cerebral artery with no collateral flow and remember that she is in heart failure although that is controlled. Obviously, the considerations at this point are that is she still going to embolize further whether you operate or do not operate, whether she can transform into a hemorrhagic infarct or bleed into her brain whether you operate or do not operate and of course if you choose to operate you are operating on someone with effectively one carotid artery because there is no blood going down the rest so what happens when you put them on bypass and if you do operate you have someone who is hemiplegic that you have to rehabilitate after surgery. So what do you do at this point, so if you can vote again? So, you have got four options here. You can still continue antibiotic therapy that is still an option. Of course it's all embolized anyway, so there is no problem.
Dr. Martin: I think you need an E on there, why operate urgently the first time, could you put that down there.
Dr. Anyanwu: It is too late. That's done now.
Dr. Carabello: But seriously let me ask one question.
Dr. Anyanwu: Yes.
Dr. Carabello: At the time when she deteriorated, formulating the opinion that she should go to surgery the next day. We did not reimage her at that time and I guess my question would be if we had reimaged her, would we have seen or could we have seen something on the images that would have pressed us instead of the next day.
Dr. Anyanwu: Actually, we did reimage her. I just didn't put that information. You mean by echo. Yes, I did an echo which was unchanged.
Dr. Carabello: Unchanged, okay.
Dr. Anyanwu: Except that the left ventricle was probably mildly dilated.
Dr. Martin: I am surprised you did not blow out her mitral valve. I mean have seen so many like that anyhow, so now you want them to vote.
Dr. Anyanwu: Do you proceed to surgery now? Do you do surgery urgently but you want to wait at least one to two weeks because of the stroke? Do you do it semi-electively and wait four to six weeks? So if you vote. There is no point asking the panel what they will do because they wanted to operate yesterday so they will probably all operate.
Dr. Martin: I want to operate before she had a stroke.
Dr. Anyanwu: Oh, you would not operate anymore.
Dr. Martin: I said I wanted to operate before she had her stroke.
Dr. Anyanwu: And now she has a stroke.
Dr. Martin: Now, she has had worse than a stroke. I am not sure that. you know, you have to look at her long-term prognosis, does she need urgent surgery, we are going to see what the audience says.
Dr. Anyanwu: Well, half the audience wants to wait. So, 40% want to wait one to two weeks and 16%.
Dr. Carabello: These cases to me are a lot like quicksand. The more you flail the deeper you get and so I am just not sure. I would say I think it is very unlikely that we would operate on somebody that had this devastating stroke in the near term.
Dr. Martin: No, I wouldn't.
Dr. Carabello: I cannot give you any data to support that except to say I do not think we would.
Dr. Martin: Even though she has a daughter who is a physician. She is not a physician but her husband is a dentist, okay. What did the family want?
Dr. Anyanwu: Like you, they wished they had operated yesterday.
Dr. Martin: I mean what would they want for her now.
Dr. Anyanwu: Whatever you advised them, they will do. They will listen to you. I mean at this point in time, they are very distraught by it all. So, they are relying on you to make the decision.
Dr. Martin: So what did you do doctor.
Dr. Anyanwu: Can we go back down to the slides.
Dr. Martin: I sound like I work for the prosecution, tell me doctor, what did you do? Well, I need to go and walk around. So you mean doctor.
Dr. Anyanwu: So anyway, Dr. Bolling hinted on this in his answer to the first question. Usually you should have waited two to four weeks because we are concerned about secondary neurological injury but the reality is that more recent data suggests that that is not the case. There are quite a handful of small series in the literature, I have just picked two. Where they have operated on people early after a stroke and they found no change in neurological symptoms and as Dr: Bolling says it might be that we have overstated the risk of hemorrhagic transformation of these infarcts. And of course there is also data from the cardiology literature where they have anticoagulated patients being treated medically and they found that if you look at the survival if anything the patients anticoagulated have better survival and they only saw major cerebral hemorrhage in 3% of patients and it was not related to anticoagulation so it might be that these patients do not necessarily bleed if you anticoagulate them. So we decided to go ahead and operate, so we operated the next morning and the rationale was, regardless of what we do, she is still in heart failure. As you said, she has still got severe aortic regurgitation. Dr. Carabello says the valve is going to blow out someday. She is going to be in a bad way, so the decision now is death or surgery really because realistically, she has got nowhere to go and she cannot start rehabilitating from her stroke until we fix her heart. So, we did operate on her and the findings are as you expect, the vegetation is not there anymore. Aortic valve is destroyed, and as you can see on the mitral valve, I do not have a pointer here, but we are looking through the aortic valve of the mitral leaflet and you can see that lesion you saw on the echo.
Dr. Martin: Right there.
Dr. Anyanwu: And that is the lesion taken out. It is not perforated fully but it would have at some point, so we are not having a big defect in the mitral when looking from the atrial side of the valve, so we would reconstruct that with pericardium. Some people will question why you did not replace this I hope not, so we replaced it with pericardium from the mitral side and put a ring and then put a stented tissue valve in the aortic position.
Dr. Martin: So you did a pericardial patch of the mitral?
Dr. Anyanwu: Yes.
Dr. Martin: And then a stented valve in the aortic position?
Dr. Anyanwu: Yes that is correct. So, she continued the antibiotics for six weeks and she went through rehab. She did not bleed into her brain. Her stroke did not get any worse and she is now able to mobilize still with some hemiparesis and she is still hemiparetic on the right side. She is dysarthric and dysphasic a bit but she is getting her voice back. So, just to comment, I mean this case reflects the controversy regarding endocarditis and vegetations and I think the balance of the emerging data suggesting that we probably should have been more aggressive initially and I think that the historical data that suggests the role for delayed surgery might not necessarily be applicable to the current era and there is a question of whether it is time to review the guidelines.
Dr. Anyanwu: Thank you.
Dr. Martin: All right, good case, thank you.