Dr. Michael De Bakey
Dr. Mahaffey, Distinguished Guests, Ladies and Gentlemen:
First, I want to express my very grateful appreciation for the opportunity of being with you on this occasion. I know this is your annual Founderís Day meeting, and I am delighted that I can be associated with you on this day. I always enjoy coming to Louisville. Of course, I need not comment about your legendary hospitality, that is well known, and it has always been so gracious and charming when I have been here. It is always a great pleasure to come.
Of course, I am especially delighted to come on this occasion, too, because Dan and Herman Mahaffey are both former residents of mine, and I take great pride in having had something to do with their training and surgery.
I am going to speak to you about a subject which has interested us as it has others and discuss the topic of Cardiac Replacement. Now, our experience with cardiac replacement has been somewhat limited but I think of sufficient extent in terms of its intensity to give us some observations that can clarify its role as a method of treatment. What I will do is talk about this along with our experiences experimentally because I think they both have a bearing on the subject. I am going to do this with a series of slides, and then if there is time, perhaps I will show you a strip of movie that also bears upon this whole area. In trying to give a better perspective of he place of this particular method of therapy and possibly experimental therapy, too.
Now, If I may have the first slide I will start with this series of slides, and I think you can follow me with the slides a little better. And I hope you can see these at the other end of the room, because it seems to me that the screen is rather small. But I will try to tell you what you are supposed to be seeing on it if you canít see at that end.
First, let me say that as far as the indications for cardiac replacements are concerned, and particularly for cardiac support, mechanical support of the circulation, the great majority of cases will fall in the category of coronary artery disease. And, of course, the instage disease is what we are talking about. Now this is well illustrated by this particular patient who is about a 51 or 52 year old woman who, when we first saw her had very moderate angina and the arteriograms that you see at the top of the screen represent the nature of the disease that she has. You can see that she has got arteriole sclerotic disease of the corneal arteries, but it seems to be a rather moderate disease at that point. And so she was put on a medical program of treatment to try to control the angina. She then returned a year later with much more severe symptoms of her angina and you can see the coronary arteriogram which is shown in the middle of the screen indicates that there has been considerable progression of he disease, with now complete failure of the coronary and much more severe involvement of the circumplex and anterior descending. Well, at this point we decided that we might be able to help her with the Lindbergh procedure and did a double internam memory implant. She seemed to do better for the first five or six months and then began to have more trouble and much more severe symptoms, and returned, as you see, about a year after that, a year and a half: and at this point, she was virtually bedridden. She was in , she was having severe symptoms, she could hardly get around her own room. And it was sort of incredible to see this kind of very severe arteriole sclerotic disease take place over this short period of time. But we do this happening, and this is not really an unusual pattern. And at this point there was really nothing else that could be done for this poor lady except to replace her heart. So this is the picture that you do see from time to time.
Iíll comment about other aspects, other patterns of this disease a little later, but I wanted you do see this particular pattern which, of course, leaves no other method of therapy available. Here is a woman who was in her early 50ís, who otherwise was in good general condition but whose body really was virtually unable to function because the heart was in such a bad state.
So in the experience that we have with cardiac replacement, clinical replacement, there were 12 patients, and as you can see, ten of these were patients with this type of instage coronary artery disease. There was one with cardiomyopathy, and one with a congenital form of heart disease that was irreparable, and for which nothing could be done. I will discuss him a little bit more in a moment.
So of the 12 cases, thatís what we had. Now, here you see example of still another type of late stage coronary disease, and this particular patient we did operate upon, did replace, but today if we evaluated this patient, and I will show you again a little later, we would consider him today a candidate for coronary surgery, which I will point out, too, a little later. But it merely indicates how indications can change, indications for doing a particular procedure.
This man, these are pre and postoperative arteriograms, the preoperative are up above. And is the preoperative arteriograms of one of the first patients that we successfully performed cardiac replacement on a heart transplant. The postoperative arteriograms are shown below. Now, it is interesting, and Iíll comment about this patient a little bit later , but he was a man of about fifty who was an engineer, and who was very active until his coronary disease made him completely disabled. He too had not only severe angina but was in partial failure. Youíll see his heart, I think in one of the slides a little later. It is interesting to contrast the heart transplant coronaries with his own preoperative coronary. You can see the quite normal ones below.
Now Iíll talk about him a little bit later. This is his heart and you can see the heart that we removed, and you can see the extensive damage to the myocardium with fibrous replacement of much of the left ventricle. He had simply had such poor myocardial function that he was unable to have enough cardiac output to maintain normal function.
And this shows the ventricular gram and you can see the marked allotation of the left ventricle. There was extensive marked dysphenasia and as you can see quite an extensive thinning out of the muscular wall of the left ventricle.
Now, this is the boy who had the congenital heart disease. He was about 16 when we first saw him. The picture that you see of him in the operating room was snapped, just before he went into arrest. And we had to try to keep him alive until we got him transplanted. The operation itself was sort of an emergency because the cardiologist felt that they were unable to keep him alive much longer. He was deteriorating rapidly and this was on a Saturday afternoon when we got a donor as an emergency, or rather arrived ASAP, and we decided to go ahead with the operation as an emergency. Now, he was lucky. He is the only survivor we have right now. Iíll talk that a little bit later, too.
Now from a technical standpoint, the operation is cardiac replacement whether it be by means of a heart transplant or by a mechanical pump, it is a relatively simple operation from a technical standpoint. There is little to be said or needs to be said or explained in terms of the technical aspects of the operation, so I am not going to comment about that further. That really is not one of the problems is this field at all. Technically, the problems are completely solved and are relatively simple.
This simply shows the need sometimes for assistance following even a transplant. In a number of the patients whom are transplanted, the heart would sometimes take off but would not accept the full load immediately, so that we had to assist them for part of the time as this slide indicates, with the heart machine before the old heart transplant would take the full load and accept the cardiac output that was required to sustain the patient. But usually this didnít require much more than fifteen or twenty minutes.
Well, now there are several aspects of cardiac transplantation that needs to be, I think, put into proper perspective, and one of them is the donor situation, because I donít think this is thoroughly appreciated by those who have close contact with the problem and it has been so badly misunderstood in terms of the news media presentation of the problem. It is an important logistic problem and definitely a serious limiting factor for clinical heart transplantation. You have to appreciate the fact at least at the present time the donor has to be alive, I mean alive in the sense that the heart is beating, when the heart is used, and that the donor must be relatively young and healthy individual. Now there are no volunteers that we have had any experience with for this purpose, and the only donors really that can be considered donors are accidents. They are accidents by one means or another. So you are dependent upon an accident for a donor when you do need a transplant. And since they are, you see, since they have to fall into the category of being relatively healthy, young people, the only way they will be able to give up their hearts is because they are in an accident and the accident has killed them. But it has to kill them in a rather special way. They canít just be killed out right. We do a lot of killing in this country as all of you know. But we donít do the killing in just the right way for the transplant. The transplant killing or accident has to be one that doesnít damage the heart, that allows the individual to remain alive until he gets to the hospital permitting the maintenance of continued heart function until the heart can be removed. And there arenít many that fall into that category, and, unfortunately, they donít always come at the right time, so that we have often had need for a heart transplant badly, but the accident didnít occur at the right time and as a consequence, many of the patients who need a transplant, died before an accident came along to provide them with a donor. So this is an extremely important, limiting factor in the application of this method of surgery, and will always be that way even if we solve the rejection problem. Unless, of course, a method ultimately, is developed that would allow banking these hearts, you see, so that they could be used any time after that and would function adequately well at the moment there is nothing that I see on the horizon that would permit that. So, we are still dependent on the method we are using and that, will limit as I say, its application severely.
Now the other limiting factor, of course, is rejection. Now we have not solved that at all. We are still dependent upon the same method for control of the rejection mechanism. These are as you see up there mostly steroids actually, thatís the main method of control. And in our experience anyway, we have not been able to reverse the rejection, an acute rejection, once it has started, in patients with heart transplants. Now, we have been able to do this with kidney transplants. But you are dealing with a different kind of a problem, a problem of different dimensions, in terms of kidney transplants, and they are not really comparable to heart transplants. A different level of problem completely.
Now you can see from this experience, of the ten patients who died, up until just recently, ten of the twelve died, mostly from rejection, as you can see. And the others had severe infection which is the other side of the coin of rejection because if you control rejection and use enough of the drugs and particular steroids to control it, then you subject the patient to uncontrollable infection. And you are walking a tight wire between the two very often. So thatís another very limiting factor in the application of this method.
Here you see an example of how severe an acute rejection can be. This patient did extremely well for the first few days, and here you see the course over a period of a week, when we suspected that he was beginning to develop rejection on about the fifth day when he was just beginning to feel a little badly, when he had been feeling good. We then started giving him more of the steroids and other drugs and went up to massive doses as you see over the next 48 hours and despite that he had an acute rejection.
Now, here is what the rejection looks like. You see, the heart, this is the donor heart what was rejected, and it looks like it is kind of inflamed. There is this surface of the looks a little inflamed, angry looking.
And here you see in this low power you see this very severe lymphasitic infiltration destruction of the myocardial fibers.
And the most dramatic thing is the extent of involvement in the coronary arteries with complete occlusion. And actually I think this is what causes the heart finally to fail, when it does fail acutely. Now of the 12 patients that we operated up until just a few days ago, in fact, Sunday night, there were two patients that survived as you can see, one for 45 months, and one for 44 months. Last Sunday night, the man whose heart I showed you, earlier, died suddenly, 45 months after the operation. So, you see, he is the second longest survivor. There is one patient who has survived one week longer, and these were the only two that we had who lived more than six months after the operation. The boy is still alive a little more than 44 months after the operation. Both of these patients did extremely well. They were very lucky. They required only a small amount of drugs to control their rejection. They had very little reaction, and they had unlimited activity. The man who just died was about 55, something like that, he was an engineer, worked every day, played golf, love to play golf, and really was quite an active person.
The boy is an active musician, he composes music, he is from Yugoslavia, going to the university there, he is quite a character there, and has made several hit records, has a little band that he plays in, too, and is quite active, still active. In fact, just recently I had word that he was in an automobile accident, not serious but bruised up a bit. But he has done extremely well.
Here you see the pre and postoperative x-ray on this boy, showing the most recent x-ray on you right, of the transplanted heart, and as you can see, it is relatively normal.
This is the man who just died last Sunday night on the golf course, he was quite active.
Well, to sum up the problem as far as cardiac transplantation is concerned, this is the only method available to us at the moment for total replacement of the heart, at least clinically. It has very, very limited clinical application. It has severe restrictions so far as its future is concerned at the moment, because of the rejection and yet, I think one has to recognize in terms to both pro and con of the problem, that at least for a few patients, it does an opportunity to extend the life a little longer, a life that can be meaningful for individuals who in their present condition have really no meaningful life. So it must be considered still a possible method of application for certain types of heart disease for which nothing else can be done and in which the patient may still have a chance to live another year or two years or three years.
But, as you can see, it does have an extremely limited applicability.
Now, let me shift to all methods of cardiac replacement or assistance, or support of circulation. These will be mechanical methods. Now, it is obvious, that if you had a mechanical method that could support the circulation indefinitely, you could use this as a means of supplementing a diseased heart that is unable to provide an adequate cardiac output. If you had a mechanical pump that would replace the heart, completely, this would solve a number of the problems, that would exist so far as cardiac transplantation is concerned. Well, where do we stand on this. Well, a no. of different methods that you see on this chart of cardiac assistance. Iíll just talk about a few of these, the ones we have experience with.
One of these is the use of the so called intra-aortic balloon which Dr. K. has popularized. In this slide you simply see the way it is used in an animal in experiments which we have conducted along with others.
You can readily see that it does have the ability to increase the mean pressure in the aorta proximal to the balloon and in the coronary arteries. There is no question about that. We have demonstrated that both experimentally and clinically. We believe that it has the capability of increasing flow in the coronary bed, too. We think we have demonstrated that experimentally, too, along with others. Now, clinical experience with it has been quite limited. We have used it, I think, in less than ten patients, all the patients we have used it in have been extremely critically ill patients, patients who were in cardiogenic shock. Some who had and we were trying to resuscitate. Some we have operated on along with to resuscitative methods, and did direct revascularization of coronary arteries.
We have been able to increase the pressure and flow in most of these patients. We have resuscitated very, very small percentage of them, and our general impression at the present time is that it is a method worthy of further study.
But we are far from being able to say that it has a considerable application or that it will provide successful application in the majority of the patients. At least, in our hands, it has not. Now it may well be that we have not yet relineated the exact indications for its use. Now, there have been using patients who are irreparable. But that is how you have to try to define its use.
Now, the heart-lung machine is used daily by cardiovascular surgeons and has been found by most experienced cardiovascular surgeons to be a definitely helpful as an assist device. We are using it with greater frequency as an assist device. And here is just a few examples of cases in whom it was used for cardiac assistance or relatively short periods. In this patient who required valve replacement, when we tried to get off, this is a very thick heart, with extremely low cardiac output, less than two beats per minute, once we got the valve replaced, and we tried to get him off the pump too quickly, you can readily see that there was a significant rise in it. Atrial pressure, and a decrease or drop in the mean arterial pressure. So we had to go back on the pump. We tried to come off the pump this time not quite as rapidly but still fairly quickly, within ten minutes, again the same thing happened. The mean arterial pressure dropped and the left ventricle pressure rose, heart ran into obvious failure and was unable to maintain an adequate cardiac output that quickly. So we then went back on the pump again. As you see over the next hour, hour and a half, we gradually came off of the pump and you can see how at the end of that time of an hour or so assistance, the heart was able to take over. Now we have had this experience many times.
And here you see another patient in whom we repeated this experience a couple of times merely to demonstrate that the heart was unable to take over, and then to demonstrate by a more prolonged period of assistance that the heart was able. In other words, with a longer period of assistance, the heart was able to come back and take over and provide an adequate cardiac output.
Now as far as the heart-lung machine, there is no question about the fact that if you simply need assistance for a matter of a few hours, it is the best method we have available and we are using it that way. But there are situations where it requires longer than a few hours. Sometimes a few days or even a week or for longer. And this is an example of such a case, and here you see is why we developed a method that would provide the same kind of assistance to the heart and maintain support for a longer period of time. After a week of this, it was possible, then, for the heart to take over.
Well, one of the methods we use for this purpose is what we call the left ventricular by-pass pump. Now, this was developed in the laboratory, in our experimental laboratory first, as a method of assisting the left ventricle. In this diagram you see how this pump acts an auxiliary to the left ventricle. It takes blood from the left atrium just the way the left ventricle does by a tube that we attach to the left atrium that acts as the inlet tube for the pump. And the outlet tube is then connected to one of the major systemic arteries. In experimental animals, we usually attach this tube to the aorta. The pump can be triggered from the of the electrocardiogram so as to synchronize the pumping cycle with the left ventricle. In this way one can use the pump to really support the left ventricle, take the load off the left ventricle and increase the total cardiac output.
Now, experimentally, we try then to develop a no. of different kinds of pumps and finally settled upon the diaphragm type of pump because we can control it better, and it is just easier to work with. And you see here different models of this type of pump. The diaphragm pump consists of a rigid outer housing and an inner double chamber separated by mobile diaphragm, that can be moved up and down to act as a mean of moving the flow of blood within the inner chamber. So that you can compress that inner chamber by this mobile diaphragm and this can be done either by air pressure, or by hydraulic pressure. Then you use valves to act as a means of unilateral, provide any directional flow through the pump.
Well, material constitutes a very important factor. By material, I mean the material you use to make the pump out of, the material that will act as the blood interface. We have used all kinds of materials for this purpose, but we work mostly with plastic materials, because in the laboratory, it is easier for us to work with plastic materials because we make all these in our own laboratory. But we have tried many other kinds of materials and all of them have add varying degrees of trauma to the blood, the blood interface. This material that you see here is inside one of the pump chambers and its made out of a plastic material called polypropylene, but it doesnít matter, it can be made out of vinyl or anything else and it will effect the blood. Here you see one aspect of the affected blood which is clotting. Unless you use anticoagulants, you will get this affect. And, of course, if you do use anticoagulants, then of course, you do run into other complications.
But we wanted to get away from anticoagulants, and we wanted to develop a blood interface that was compatible. We drew upon our experience with the use of Dacron graphs, which had provided us with long experience with the development of (atolagous) tissue lining the graphs. We thought that by means of material such as this, Dacron, that we could develop an lining which then would be very compatible with the blood and would act as a good blood interface. We tried this first using the same kind of material that we use with our graph, but there is a difference in the graphs and the a lining of a pump with Dacron. The graph the arterial graph when it is put in, has tissue on both sides, that is tissue all around the sides of it, live tissue that grows into the graph. The pump has to be made out of material that is impervious to bloods and no tissue can get into the lining. The only thing it comes in contact with is blood. So we decided that possibly with the use of a velour surface that the fiber that would come from the blood would become more closely enmeshed, wouldnít flake off, and would act as a good blood interface. And ultimately that one might become organized. In the last aspect of it, we failed. Now first, we were successful.
And here you see the surface of a diaphragm lines with this Dacron velour that had been pumped for about ten days, and you can see that this lining is very intimately adherent to the fibrous lining, very intimately adherent to the Dacron velour surface. It is smooth and glistening, and is quite acceptable to blood. It doesnít produce any destruction to the blood. Now unfortunately, it doesnít become organized either. It just continuously gets a little larger and a little larger, thicker and will ultimately block the outflow track after about six weeks to three months. So that, of course, does not solve the problem for indefinite pumping. It did solve the problem for the left ventricular by-pass pump because we rarely needed that for more than a week, ten days, to two weeks.
Clinically, we applied it in small series of patients and here you see the way we applied it to simplify its application. These are all patients that have operated upon, they are all patients that require valvular replacement, with very sick hearts and weak cardiac output. So we applied it in the manner shown here.
And here you see one of the patients in whom it was applied. You can see the tubes coming out of the chest, and the way the pump is used. And this is on about the sixth or seventh day. This patient is still doing fine. She was in for a checkup just the other day. You can see her x-ray six years later.
Now, here you see just a few physiologic, hebodynamic observations of the use of the pump. You can see, and this is quite typical, and we did this to illustrate what the pump does so far as left ventricle pressure is concerned. And you can see that by increasing the pump flow, you can very rapidly affect the left atrium pressure. And increasing flow, increasing or decreasing, will cause the left atrial pressure to drop or to rise. And we can control this very easily, so there is no question about its physiologic affect. Now what about is clinical effect here you see an example of its clinical effect upon renal function. This patient, now this was on about the seventh day or so, and you can see that the renal function has decreased significantly the left atrial pressure has started to rise slowly, and we give the patient a lot of diuretics with no response. And then immediately just increase the flow, and you see what happens to the kidney function. Urine output has significantly increased rather dramatically after the pump flow was increased increasingly total cardiac output.
One of the most dramatic observations is shown in this slide in which the left atrial pressure, we are monitoring the left atrial pressure continuously. And you can see that it rather suddenly went up even though it was rising rather slowly. Meantime the patient was beginning to get a little restless saying that she was having a little difficulty breathing but we werenít particularly anxious at that point until she suddenly went into very severe acute pulmonary edema and was having great difficulty breathing, and coughing up frothy pink and looked like she was about to die. We simply increased the pump flow as you can see from about 800 to around 1400 per minute, 400 I mean to about 1400 per minute, and within a few moments the left atrial pressure dropped from about 45 millimeters of mercury when she was in severe acute pulmonary edema to more normal level, and the acute pulmonary edema just disappeared in a matter of minutes. Now, this is not an isolated observation. We saw this happen on a number of occasions, so that there is no doubt in the minds of all of us who made these observations that the pump, an increase in pump flow, the decrease in left atrial pressure can effect the hemodynamics of the heart so as to eliminate failure in just a moment.
This shows her picture about six months after operation. We removed the two tubes under local by just separating the sin from the edges of the tube and then cutting the tubes off just under the sewing and leaving the rest of them in. They do no damage. They are completely surrounded by a fibrous tissue and.
And here she is you see six years approximately after operation, she is still have of course what seems to be a large heart. Actually that is mostly left atrium. She is doing very well. She is working regularly. She was an extremely sick lady when we first saw her. So we feel we carried here through solely because we had a method by which she could get support for nearly ten days after operation.
Well, what about replacing both ventricles. It was an easy step from the auxiliary support of one ventricle to the development of two ventricles putting the two together and here you see a model of how this was done.
These are made out of plastics just like the other. And we just attached to the two ventricles atrial connections and aortic and pulmonary artery connections. The tubes, of course, are the same coming out of the chamber ventricle to move the diaphragm.
Another view of it showing the atrial attachments now, and the two tubes connected to the aorta and the pulmonary artery.
And this is an atrial view looking into the atrial chambers of this artificial heart, Here you see still another more recent model of the same thing, the same kind of the artificial heart that we are using now in the experimental laboratory.
Another view of that same type of more recently devised pump, but it is the same concept. This simply shows how we power the two pumps in much the same way we power one of them. The power, of course, is all outside the body in the driving both mechanism.
Here you see how the attachment is made to provide replacement for the left and the right ventricle.
And this is just another drawing show we attach it after removing the heart. You see, it is very much like cardiac replacement transplantation.
And here is an illustration of the use of another method of support. But before I get there, let me just summarize about the ventricle, the artificial double ventricle or the artificial heart by simply saying that we at the moment of course are limited to applying this in animals because about the best that we have been able to do is to keep these animals alive about a week or ten days. And we can now pretty regularly replace the hear in an animal a calf for example, and keep the animal alive about a week or ten days. Thatís about as long as we can go. The interesting thing is that we run into a phenomenon that we donít quite understand now and that is why these animals die at the end of a week or so. But they seem to go into a shock like state. And then rapid deterioration takes place in terms of organ functions such as the lungs, the kidneys and the brain. The P02 goes down very rapidly and even though you can continue to pump so to speak and keep the heart pumping, they will die as the organs die in that kind of a shock like state.
Why that happens we are not quite sure. We do know that there is certain amount of trauma to the blood that takes place in that period of time. The exact explanation for it is not quite clear to us, and so we are working on that right now. But in addition to that we also know that even were it not for that taking place we would still be limited in the time because we know that the materials we are using in terms of their blood compatibility will produce a sort of cumulative blood damage. This effects both the cellular aspects of the blood as well as the chemical aspects. So we still have that problem to solve, too. But, there is no question in our minds that this is a feasible concept and it is merely a question of trying to solve these various limiting problems to long term pumping. Now, in addition to support by the heart-lung machine, more recently we have also been interested in the use of the membrane oxygenator as a method of support, using the heart-lung machine we can support the heart for a matter of hours. With the membrane oxygenator we can support the heart and body for a much longer period of time and have done this now for as long as a week. In one patient that we tried it in we had to replace the membrane oxygenator on two occasions during that period of time. But thirty six-forty eight hours of pumping is not unusual with this, with relatively small damage to the blood. Plasma hemoglobins rarely will exceed 25, for example, even after 24 hours. So that this has proved to be a very useful method of more prolonged assistance than we can use with the heart-lung machine.
Now, one of the reasons that the indications for cardiac support and cardiac replacement change is the changing developments that take place in medicine and in surgery, and one of the most dramatic changes that has taken place over the past several years has been the direct approach to coronary arteries, which has definitely change the implications for the need for cardiac transplantation and even the need for assistance. We are more and more inclined to think that we are going to need more mechanical assistance to the heart & less replacement as we find better ways of repairing the heart. And here you see an example of the effects of this method of treatment, this modality of therapy. You see here a patient who has been followed now for over seven years who has sever lesions, coronary disease, I guess this is two years, actually three years. I think the arteriogram there shows two years, I canít be sure of that figure. You can see that he has a very severe disease in his right coronary which is the dominant coronary. And we were able to do a complete and this patient has done extremely well, even though he is extremely limited in his ability to.
Now some of these patients have been followed for fairly long periods now, still doing well. This is why this man was followed for seven years. Following endolecertony.
And here is another patient, probably the first successful coronary bypass that was done. We did this patient almost eight years ago. It was done in 1964. And the arteriogram you see here shows the vein bypass functioning well a little over seven years after operation. The arteriogram was done a little over seven years after the operation.
So we now know that these patients will do well over long periods of time, depending upon the pattern of the disease.
And here you see a longer type of vein bypass also functioning well. It is now well over four years since he was operated on. That arteriogram was made three years after operation. He is still doing well.
Now, these can be extended to bypass all the major arteries, both the right and the two major branches of the left coronary artery as you see here in this postoperative arteriogram. So that even an extensive disease, even when it is associated with valvular disease such as mitral insufficiency and this man was in sever failure this man would have been considered four years ago as a candidate for cardiac transplantation. Yet by means of bypass to his coronary and a valve replacement this man has been completely rehabilitated. He is perfectly well now, working every day, having no symptoms at all. His heart has come back to normal size.
Hereís another example with severe disease, aortic disease, valvular disease. Just about two weeks ago I did a patient who had to have a double aortic valve the aortic and mitral valve and three bypasses. One to his right coronary and two to the remaining main vessels the circumplex and the left anterior descending. He just left the hospital just a day or so ago. A patient who would have been considered a heart transplant.
Hereís another example, this patient would have been considered for heart transplant four years ago. He was in severe failure as you can see from his coronary arteriograms. He has severe coronary disease. He has endynastola pressure of over 35. We didnít really