It is a pleasure to be here. I am going to talk about reconstructing the left ventricle for both ischemic and idiopathic cardiomyopathy and I am going to start with a few sort of historic slides and a little bit of background before we go to the new material that we are working on. This is some information from Dr. Favalaro and it was published in 1968. He is talking about ventricular aneurysm resections. He is talking about 22 patients with extensive anterior scar, and these patients were very symptomatic, increased end-diastolic pressure. After resection of the aneurysm, the elevated EDP has come back down and the patients are clinically improved. Before the era of coronary bypass surgery, and without the benefit of mitral valve repair, we already knew from ventricular aneurysm surgery that you can change the shape of the heart and exclude an infarct and improve the ventricle. To put it in a greater perspective, there are a lot more patients now with heart failure. Four hundred thousand new cases of heart failure in the United States every year. The number of heart transplants has plateaued. It is at about 2300 per year. Therefore, we desperately need alternatives to conventional human heart transplantation. We are looking at a lot of heretofore high risk conventional operations for heart failure patients, as well as other options like permanent LVAD implant, and other different ways of doing heart transplantation like Xenografts. Today, what I am going to talk about is the ventricular reconstruction for these patients. Historically, we know that patients that have these very big, dilated hearts don't do well. This is data that came from Lynn Warner Stevenson, a heart failure cardiologist, and she stratified it. What we are looking at here are these patients with these huge dilated ventricles. Twelve month survival was only 40%. This is the type of patient that we are reconstructing, for instance, with the Battista procedure. Why these operations work partially have to do with the law of Laplas. Wall tension equals intraventricular pressure times the ventricular radius divided by two times wall thickness. If you reduce the ventricular radius, you are going to decrease the intraventricular wall tension. There are a lot of operations really in cardiac surgery that work along this line. One would be the conventional aneurysm operations. The other would be the Door procedure, or be it Cooley or whatever that you give them credit for; also, the Battista procedure that became popular a few years ago. But also, as we will see with the data, mitral valve repair because a heart remodels and reconstructs late. Also, the LVAD so-called bridge to recovery when the heart goes on support and it immediately shrinks. Why does it help the heart if you reduce wall stress? First of all, directly you decrease myocardial oxygen consumption and that should improve myocardial efficiency. You should be able to use a decreased amount of energy and create the same amount or a larger amount of work. It also probably affects the neurohormone feedback mechanism, the cytokines and all that are part of the heart failure milieu. It may reorient the myocytes and avoid slippage. There is with the LVAD data anyway indications that the fetal phenotype is reprogrammed back to normal and there is definitely myocyte and mitochondrial recovery. I am not just going to talk about the ventricle because one certainly important aspect of this is that as the ventricle dilates, the papillary muscles are displaced, and most patients will have some element of central mitral regurgitation associated with this. We have been treating that usually with an annular ring. I usually use the Cosgrove-Edwards ring, but remember that the pathology is not so much here with the annulus. The pathology is really with the ventricle. The annuloplasty will improve the mitral regurgitation, but it many times won'' eliminate it. This is Steve Bolling's approach to these patients. He recently reported on 48 patients, 71% two year survival, late improvement in ejection fraction, and as I mentioned, the ventricles are becoming smaller because they don't have that volume overload and they change from these globular ventricles to a more normal shape. There was hemodynamic benefit. This again because of this difference in ventricular changes may be partially the Law of Laplas. In addition, those valves may still be centrally incompetent. What I have been doing and many of us are doing is a so-called Elfirier repair or an edge-to-edge approximation of the anterior and posterior leaflets of the mitral valve. You create this figure eight or bow tie appearance to the mitral valve afterwards. This is not just applicable to the Battista procedure but also we have done this in about 150 patients now. This is a very useful technique. In terms of the direct operation on the left ventricle, you can really attribute to many different people, Dr. Cooley, of course, Vincent Door, Dr. Jatene, Tyrone David more recently, Dr. Fontan taught us about a stitch that creates a neck of the aneurysm and Dr. Buckberg recently has been popularizing this technique. He has been investigating the cardioplegia and the different techniques that we use for myocardial preservation. I am going to show a short video, but before I do, this is essentially what we do. This would be a typical patient with an LAD infarct. The important part of this is that the septum, the anterior septum, is also thinned and akinetic. The old data with linear aneurysm repairs would simply be attacking that part of the free wall of the left ventricle, but they weren't doing much for the septum. It was really more the techniques in the 80s that understood the importance of the septum. The Fontan stitch is to open the ventricle, and then place this purse string suture which is placed through the border zone between the infarcted and the normal myocardium. After you tie that down you create this sort of neck or small opening. Dr. Door's procedure has been to then take a patch and to do the endoventricular circular patchplasty, and to close this with a patch. More recently, what I have been doing is to simply take additional sutures and Dr. Door says that we are doing an internal Jatene or a modification of the Jatene, and simply reconstructing with additional sutures instead of leaving an akinetic patch. Otherwise, you have a large akinetic area with a smaller akinetic patch. If you don't use a patch after reconstruction, you have this situation where a normal ventricle is being closed back to normal ventricle on the other side. The entire infarcted area is now excluded. This is a video I made within the last few weeks of two patients that we recently operated on. The first patient was about 55, and this is a classic true LV aneurysm. He also had mitral regurgitation, and he had coronary artery disease as well. This shows the typical adhesions to the pericardium. Again, this is sort of a classic aneurysm with a very thin-walled area of the left ventricle, and the overlying adhesions to the pericardium. This is similar to the operations we have been doing for ventricular aneurysms now of course for 30 or 40 years. This is a huge aneurysm. There was a very proximal LAD occlusion involving also the first septal. We did a radial artery graft to the right coronary artery, and then he had 3+ mitral regurgitation and so we put in a ring. One of the things that Dr. Buckberg has been having us look at is that cardioplegia may not protect these ventricles well. After that portion, I removed the cross clamp, and this is now done on the beating heart, open through the aneurysm and extend this up proximally. As you can see, of course, the heart is beating and there is an improvement in the rhythm and the patient is already coming back to sinus rhythm. A large amount of clot within this wall. This is an Alfieri repair that we are doing and sewing the anterior and posterior leaflets together right there. The exposure through the ventricle is great. It is a little harder to do through the left atrium, but we have also done that. With the heart beating, it is easy to palpate, as I showed there. This one was very simple. This was a very straightforward demarcation between scar and no scar, but sometimes with more akinetic areas, they are not clearly demarcated. The palpation helps you determine that. That was the Fontan purse string suture that I placed, and we are tying this down to exclude the infarct. You can see that we are creating a nice neck to this aneurysm. There was a huge amount of septum that was involved in this patient that is now also being excluded. Usually, I will put a second purse string suture in like that. Occasionally, I will just use a third suture, and be able to completely close that. We use a horizontal mattress suture. These sutures are going right through the area where the purse string suture was so that you are taking tension off of those purse string sutures and, in addition, it is able to completely reapproximate the normal areas of myocardium. This simply shows that we are going to close this up with a mattress suture, and then we'll oversew that after this is complete. After this type of reconstruction, there is, in fact, what appears to be a sort of a new LV apex down here, and the heart is changing from its globular appearance after this type reconstruction. This is kind of an unusual patient in that he had such a huge aneurysm. Most of the patients that we have been operating on have not had that amount of infarction. Usually, we may trim some access tissue here before we close that up. One thing that was not shown here is 3-D echo which gives us excellent information regarding ventricular volumes and dimensions, and has become routine in these patients. We are studying it with MRI and ventriculograms and 2-D echo to determine the best way to really assess these patients. Here he is after the completed aneurysm. This is about three weeks ago, and the patient was discharged after a week. That was not too surprising. This is the second patient, and she was 70 years old and opposed to the dyskinetic aneurysm, this is now an akinetic area. This is the new part that Dr. Door has had us looking at. The patient also had mitral regurgitation and coronary disease and she was already listed for a heart transplant elsewhere. You can see now there are no adhesions to the pericardium and instead of an aneurysm, we have an akinetic area in this LAD infarction. She had simply an LAD infarction, no circumflex or right coronary disease. She had been hospitalized multiple times for inotropes requiring dobutamine. She had 2-3+ mitral regurgitation, and this is the completed ring. The video I didn't have a chance to re-edit. The coronary bypass was shown there out of sequence. The cross clamp is off. We are opening through the akinetic area, and extending it more medially. This is more typical, I would say, of the kind of patients that we are operating on now, instead of the true aneurysms. After ace inhibitors and drugs like that, we are seeing less patients with aneurysms. This is the exclusion of the scar that the patient has. We have had a moderate number of patients that we have also done cryoablation. That biopsy I took of the lateral wall was for research purposes, and that is the Alfieri repair again of the mitral valve. This is during placement of the purse string suture, and then again we are creating the neck of this infarcted area. You can see that when you tie that purse string suture down, you can really create a very small opening, only about 2 cm there. Then we close this the same way. I think we can stop the video because now we just close it the same way. That patient also did very well, and was discharged in about eight days. This is the 48 patients, we are up to 50 some now, and this has been over about a year and a half. Average age is 60 years old. About half of these patients were urgent or emergent. This is a very heterogeneous patient population. The patients I am going to report out of this include acute infarct patients, and some patients with contained free wall rupture and postinfarct VSD-type problems. 40% as you can see had akinetic, not aneurysmal areas. A third had a combination of angina and heart failure. 40% had only heart failure, and most were class 3 or 4. I really gave up using the patch about six months ago. The majority now have no patch. The earlier patients we were using the patch. Almost half get a mitral valve repair usually I will also add the Alfieri repair, and we also have started doing it on the beating heart instead of the cross clamp. These are the intraop changes and ejection fraction by 2-D echo, and what it shows is no difference in ejection fraction, patch or no patch. Interestingly, at 30 patients, not 48, did reach significance and again at 30 patients this had been significant that there was a lower time on cardiopulmonary bypass if we did this on the beating heart. If you do it on the beating heart, the rhythm returns to normal, and once you complete the repair, you just drop that into the pericardium and the patient comes off bypass. There have been three hospital deaths for an operative mortality of 6% as opposed to the Battista. These are the only three early failures and so it is not at all like the Battista for idiopathic cardiomyopathy. Two late deaths were not cardiac related, and there has actually been two readmissions for heart failure. In general, the perioperative care has been much easier and these patients are going home and doing well. This is the 3-D echo data showing the decrease in end-diastolic volumes. No change in stroke volume despite the repair of the mitral regurgitation in most of these patients. The new 3-D echo data shows an increase in ejection fraction from 28 to 40% intraoperatively. There is a lot of data from Dr. Door's group looking at this, and this I think is one of the most important aspects of this operation. You improve the myocardial performance, not simply the area where the scar is but most importantly also the circumflex and right coronary distributions. Those areas of the heart are stretched out and after you have done this type of operation, those areas can contract better. There is a good body of literature about this coming from Monoco. I am going to change now to talk about the Battista procedure. This is Rondus and his cardiologist. As I said before here, what we did know about this was that some patients such as this one continued to do well in long-term follow-up. Of course, in Brazil he was losing patients in follow-up and it just wasn't ideal to get the science and so we embarked on this not really knowing how long it was going to last or who it was really best in. The surgical technique we have described before. It is typically a resection between the papillary muscles of the lateral ventricle for idiopathic dilated cardiomyopathy. About half of the time I would disconnect one or the other papillary muscles and then reinsert those into the suture line. We are at 62 patients now, mean age 54, mostly males, almost all idiopathic dilated cardiomyopathy. A third or over about 40% were in the hospital, status 1, on inotropes, some on balloon pumps, and most had had heart failure for five years beforehand. This is intraop 3-D echo recently showing a huge change in end-diastolic volume. Again, no change in stroke volume despite the mitral valve repair, and in increase in ejection fraction generally from 13% to 26%. At 12 month follow-up, and we are now just over two years, this is the improvement in functional class from 3.8 before surgery down to an average of about 2. This is the slide that we have been waiting for all these years. It is our longer term follow-up. The first line up here is survival. There were only two deaths perioperatively, but that was because we were using LVADs and such as needed to support patients. This is freedom from any failure which would be relisting for transplant or need for an LVAD or the patient returning to Class 4 heart failure. What you see is in the first three months is a very steep drop. There were a lot of patients that failed early on and those patients would be relisted for transplant and so on. It tends to level off, and it has been running about 10% per year after that. Total now, and we are at two and a half years, 40% of the patients were free of any failure. There is an interesting body of knowledge about why this is really working, and this is a paper from Columbia and what they did was they used sort of a computer model idea of why this should improve cardiac function. These are pressure volume loops derived from the computer at 0, 25, 50, and 75 grams of resected muscle. We were averaging 96 grams of resected muscle. What the curves tell you is that as you get here, there is an improvement in systolic function after the operation, and the computer estimated that there would unfortunately be a decrease in diastolic compliance after the operation. Also, recently in this paper came out a finite element analysis looking at the Battista operation, and similarly, what they found was an improvement in systolic function, but a decrease in diastolic function. Importantly, with a balance of those two, with a 20% lateral reduction, there was 17% reduction in energy expenditure. So the net effect was that the heart was more effective. Those are interesting theoretical papers, and this is what we actually found in our patients. This is before surgery, immediately after, three months, and at one year. What we see here is an improvement in contractility which is what they would have expected. We also see as they had predicted an improvement in efficiency, and it is approximately 17% stays at one year. What we also saw was a change in diastolic function and a loss of compliance so that these hearts became more stiff after surgery. In our patients retrospectively, they fell into two groups. The patients that had diastolic dysfunction before surgery didn't do well. They fell into this poor group whereas patients who had normal compliance did well. The Battista procedure, the concept works sometimes somewhat, not always. It is very unpredictable. We still do not have good criteria that we can predict whether it will work. There have been and are excellent long-term results. Why does it fail? We think probably collagen and interstitial processes and they are doing the collagen analysis right now on the samples, probably pre-existing diastolic dysfunction. If you operate too late, when the patient is in end-stage cardiogenic shock, this probably won't work. If there is a huge amount of myocardial infarction, the example of a left main occlusion, then I don't think that you are going to have anything to gain with an infarct exclusion-type operation. There are limits to how well that will work. So where are we with this? Here is a glass and it has water in it. Then, of course, is it half full, is it half empty. Did the Battista procedure help; did it hurt. 40% of patients now two and a half years out are actually alive and well that otherwise would have been transplanted. I show these two patients briefly as examples of success and failure. This is a woman with familial cardiomyopathy. I chose familial because some people said, and it is true, that about 25% of patients with idiopathic cardiomyopathy will get better on their own. This is familial. They don't get better on their own. The problem is still there. Preoperatively, no mitral regurgitation so the debate has always come up, are the patients getting better because we repaired the valve or because we did the resection. This patient had a bad heart, no mitral regurgitation, spent ten days in the hospital, at one year follow-up had a 40% ejection fraction, near normal heart size, much improved oxygen consumption, still no MR, and she is now two years out. She continues to be functional Class 2. Clearly for her, the Laplas concept seemed to help. Here is an example of a failure. A young woman with idiopathic myopathy on a balloon pump and on three inotropes. Essentially, there were two options for her. One was an LVAD bridge to transplant, or the other was to try this new operation that we really didn't know how well it would work or not. She did have severe MR, 5% EF, 11 cm heart, and she was hospitalized for 31 days after surgery, but went home without inotropes, and clearly improved. But three months later, she did get worse, and she went back on and she was relisted as status 1, and then was transplanted. We do count that as a failure, but if you want to look at that glass as half empty, half full, another spin on it would have been that the other option would have been an LVAD. Then you have the other issues, of course, that you have with LVAD bridge to transplant. Out of this entire ventricular reconstruction idea, I think what we are learning is that the Laplas concept will work in many patients. The mitral valve repair and CABG we think is an important adjunct to this. We don't think that it is one or the other. We think that you should do these all together. Diastolic dysfunction before surgery is probably going to get worse, and therefore may limit the success. We are investigating with Dr. Buckberg whether you should do this on the beating heart, whether that is better. There are concepts for a new device, a company called Myocor for instance, that has come up with a device that should simulate the Battista operation but without going on cardiopulmonary bypass, and without discarding 96 grams of heart muscle. In summary, the way I feel about it is that the Vineberg operation in itself went by
and I think the Battista operation will go by, and we really do many less of these than we
used to do. The concept, I think, is going to continue and is going to become refined.
Thank you very much. |
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