loosen accredited by the American Medical Association for Continuing Medical education. Um Dr Bloomberg doctor brings field I think I would first like to say how happy I have been to be brought here to Atlanta, particularly in honor of giving this lecture and I'm so pleased to have met Mrs Stacey worried I thank you all for your kindness and particularly Mrs Stacey White and the members of the Department of Pediatrics for offering me this opportunity. I hope you feel in the Department of Pediatrics that I an ordinary cardiologist and not a pediatrician and worthy of the honor that you give me an inviting me to your course and to give this very special and first lecture, thank you. Now congenital heart disease has advanced in the last 20 years so that we now have a complete change of philosophy. Through these years, bedside diagnosis has become more precise, human dynamics, more sophisticated and all really. Thanks to our Sergent whose degree an expert of expertise and success has brought audience to their feet and the pediatricians and cardiologists out of their therapeutic nihilism, we owe them very much and thus our philosophy has changed. We have a new set of people to look after the survivors. Now eyes a cardiologist have the opportunity to see these same diseases From the age of 0 to 80 and one cannot help but be impressed that the heart also has a say in the matter of the patients changing symptom metrology and their way of life. The heart has a fantastic ability to change its structure with or without the help of surgery. The credit for my bearing down and studying more carefully, my own clinical views should go to a pathologist. Dr Lewis baku, chief of pathology in the Children's Hospital in Buenos Aires, who in asking me to speak at his session on morpho genesis in the world. Congress made me against my own will and with much reluctance study the matter of changes in structure and function. And I owe him a great debt for having the pathology slides and the teaching which has helped me understand much that many of the diseases that I am studying and looking after. Uh huh. Now, in order to illustrate post natal changes and by post natal, I mean after birth, to the age of 80 I'm not concerned with the instant changes of the fetal to the living circulation. It is the next 10 2030 years of life I am concerned with. Let us look first at ventricular septal defect. Next slide, please. That gives us the very best example of how the heart structure may change and alter the patient's way of life. I took a series of patients with large ventricular septal defects under eight months underweight with thriving difficulties, high heart rates and respiratory rates. Large hearts and plethora. These were not the extremely ill dying ones that deserved instant surgery because they had their surgery. These are the ones that we just managed to hold onto or who refuse surgery. But they all were retreated for heart failure. Now, what happened to these patients next? Please. Now, here the signs, if you like of these 73 patients, all inference, in so called failure or thriving difficulties. Only 15% stayed the same. 6%. The pommery vascular resistance rose. That's the pommery hypertension took over, but they improved. That was a lung change. Not a heart change. 8% turned into fallows. But look at this 59%. The ventricular septal defect became smaller, either to have just a pan systolic murmur left, or a funny little late, early, early systolic or late systolic or even a little systolic murmur and a click And 12% the signs completely disappeared and catheterization confirmed the defect had gone next. Please. Thus, we can immediately say that in these large ventricular septal defects, 80 to 85 altered as a result of changing structure within the heart. This influences physical signs, symptoms, and natural history. That is the theme of my talk today. Next piece Here you see the infant with the large heart, the plethora thriving difficulties Here you see the patient, 10 years later, there just was a little pan systolic murmur, an unmeasurable shunt on catheterization, although that we assume there was a little VSD. But you notice the heart is slightly larger than normal. Next, please. This is the sort of thing. Here is the left ventricle A. VSD once absolutely huge clinically in a failing infant. This child died from non cardiac causes and you see the fibrous ring around the defect, that is a defect that is going to get smaller. Next please. Now, in a number of these investigations in the intermediary phase. As you are watching, you may actually see the fibrous tissue or the septal cost for the tri casted valve coming across to divide the streams of the VSD. Here actually is trick a speed septal cusp tissue. And here is the jet once this defect was this size. Next, please. And here you see the so called aneurysm of the member in a septum which is in fact spontaneous closure or neo closure of a ventricular septal defect caused by the central cusp of the tri casted valve coming across, just leaving a tiny hole in the middle. Such patients on Oscar rotations may just be left with tiny late systolic clicks and a little murmur no longer the florid signs of a ventricular septal defect. Next now, which are the V. S. Ds. We are not quite certain. Here is the electrocardiograph IQ evidence that goes for the clinician here is the one month old child in heart failure, right ventricular hypertrophy. Some left Here. You see that three months with a 3-1 shunt by ventricular hypertrophy, obvious here at 3.5 years. The VSD was clinically and categorized closed. He has lost his left ventricular hypertrophy and his right but residual right bundle, branch block and left axis deviation remain. Next, please. I shall speak about this in a minute. Now, here you see a child in whom we documented a large VSD. In infancy and it has closed. This is from the left ventricular side. The patient in fact died as a result of surgical of postoperative mismanagement after mitral valve surgery. And here we found the closed VSD. That we had documented in early infancy. Next, please. And here is a bigger VSD. Closed by exactly the same mechanism. And this is Kordell tissue of the septal cusp of the tri casted valve. Next, please. And here from the right side is here's the trick a spit valve. Here is the papillary muscle of the Conus. And here is the so called aneurysm of the membrane is septum made up of fibrous tissue. And trick a speed septal tissue. Now, as far as we can see, it is a question of where the VSD is in part as to whether or not it will close. And those patients that we can document who have closed and looked at the specimen because you don't have the opportunity very often, it appears to be these defects that extend behind the papillary muscle of the Conus. Next please. So one can say from our studies that in infancy 59% becomes a smaller. 12% close spontaneously. The mechanism is variable. It maybe fibrosis or platelet deposition around the whole. It may gave tri casted valve, cast tissue or later. it may actually close from prolapse of aortic tissue. Next please. Now, is closure of the VSD. Always beneficial in the patient's natural history. You might initially think so, but there are just a few patients who still have problems firstly. The infant tubular obstruction, which I may speak of later. If the crystal bands are abnormal, may progress after the VSD is closed and leave the patient with severe in funding Bulus stenosis, severe pommery stenosis and severe R. V. H. And the surgeon dealing with loan in funding bill A stenosis if he looks may often find the pit of the closed VSD. That is once there. Yeah, try crossfit regurgitation may occur, leaving a tiny BSD and try to speed regurgitation. And the patient appear in middle age with early april fibrillation, a tiny VSD. And try to spit regurgitation. We have documented this on three occasions and we assume this is a late natural history of closing VSD in some cases. Another adverse thing is if aortic regurgitation occurs this time, it tends to be, but not always in the ventricular septal defect that is round the corner in front of the crystal, but it can also occur in other large V. S. Ds. The customers come down, shut off the defect but leave aortic regurgitation, which is progressive loss of a ventricular septal defect, therefore is not necessarily beneficial. Next please. Now, another interesting thing. Looking at this critically here is a patient age two weeks in heart failure with paroxysmal tachycardia with a wolf Parkinson white. Also had a large ventricular septal defect at three months, 2 - one shunt and high pommery artery pressure documented left ventricular angiography showed quite a large defect. Now, interestingly enough, at six years we saw the patient again, no sign of A VSD patient of E. C. G. Now near normal except the partial sort of wolf Parkinson white. But look at the pulmonary artery pressure Immediately. one must ask oneself do some of these patients who then present in adolescent or early life. Adult life have they had V. S. Ds closed and not left their pommery vessels completely normal. Next please we don't know but it opens up a whole vista of thought about many of the diseases we treat in later life here you see is that patient with a documented VSD. And failure at three months here the VSD is closed by all the methods you can tell. And the pulmonary artery pressure is 60/25. Next please. Yeah I would therefore put to you and this is entirely armchair thinking with no proof. But it might make you think and do more research. Could some of the sexually a spontaneous closure of the VSD possibly cause fibrosis affecting the conducting tissue later to produce the so called idiopathic heart block of middle age. Are there ever residual abnormalities of the pulmonary arterials causing so called primary primary hypertension. At a later age. And what is the effect on the tri casted valve? I don't know. You perhaps may answer the question. Next mm. Now the adverse effects of a ventricular septal defect in congenital heart disease becoming smaller may also alter the knife history of a number of other complex conditions In tree custody atresia. As I'll show you, it diminishes the pulmonary blood flow in certain cases of double outflow right ventricle, it may cause left ventricular obstruction where the whole getting smaller. In common ventricle. The the inter ventricular for Raman or Balbo ventricular for Raman. Make get smaller from the same fibrosis cause sub pommery stenosis or severe aortic stenosis. Let us look at the examples in these complex conditions. Next place here is a common ventricle, rudimentary sub aortic chamber. A v valves emptying into this hole into this chamber and all the blood into the aorta has to pass through this foramen. Next, please, here is such a child who was entered the hospital as an infant. In gross heart failure. You notice no gradient between the oughta symbiotic or common ventricle. Next, please, now, as we follow this child, two things happened here. She was in infancy. The big murmur, loud aortic second sound. She developed angina. We couldn't understand it. But when you look at our clinical features, two things happened. She lost the noise of her loud aortic valve closure? The murmur became longer and her karate pulse developed a slow upstroke. So she clinically had the symptoms and added features of symbiotic stenosis. Next, please. What had happened is obvious to you here is the catheter tracing now the same as I showed you before, but now as a gradient to the water and the common ventricle. Next please. Now, what had happened? Excuse the pictures of my thumbs, you're supposed to be looking at that area. Here is the common ventricle. Here is the inter ventricular for Raman and there is a red bead in it. You see the fibrosis around it obviously creating an obstruction. Next, please. Now, in order to get to the aorta which is here, all the blood had to come through the common ventricle through the way of the red bead is. And up here this child had developed acquired symbiotic obstruction and we should have predicted this would occur by her original anatomy where you could see the foramen was surrounded by muscle and thereby there would be turbulence fibrosis. Next, please. Here is another example, a rather shadowy X ray. The one you always want to show is a bad uh angio but never mind. Here is the left ventricle VSD. The aorta is up here and the pulmonary artery. This is a double outflow, right ventricle at this stage. Nobody took any notice of the fact that there was an indentation here around the defect. Here you are. You see the left ventricle looks all right. The aorta is stuck up here. Nobody took any notice that there was narrowing. Nobody did anything about it as the child wasn't doing too bad. Next, please. However, following that child who did not improve her electrocardiogram, watch V. Six. Here she is with right ventricular hypertrophy as you'd expect. But look by the age of six years she has left ventricular hypertrophy and she had developed obstruction of this VSD. By fibrosis forming around it. And in fact the condition had become inoperable and she died not only with her double outlet but acquired symbiotic obstruction. Now, we, as clinicians should have recognized from the morphology we saw on the first ngos that this potential was possible. Next please. Another condition of common ventricle where the inter ventricular foramen leaves into the rudimentary chamber and up into the pommery artery. If this closes or get smaller, the patient will get sub pulmonary obstruction. Next, please, here is a patient who presented in heart failure as an infant with heavy lungs. Thought to have a VSD. She then became SIA nosed. And when you look at what the problem is, here is her rudimentary chamber. Here here is a large pulmonary artery depicting that once she had a large pommery blood flow. But look there is a hole here and that whole has the potential to get smaller. Next, please. Here you see the patient when she was first seen at four months. A cyanotic with a huge murmur here. You see it 10 months. She has developed cyanosis allowed a to a pan systolic murmur like a small VSD. Next please. And here when investigated later you see that there is the whole here you can't actually see the size of it but it was small. And here there is fibrous tissue indentation here where the inter ventricular for Raymond is closing and is the cause of sub pommery obstruction and diminished pulmonary flow. An ideal example of morpho genesis. The change in structure and function. Next. Please try custody Atresia and in disease because there's a new operation. Let us look at it for a minute. The blood in tricastin. Patrizia passed from right atrium to left atrium to left ventricle. It gets out into the pulmonary artery through the ventricular septal defect. two things happen to make these patients blue. Either they increase the pulmonary stenosis. If they've got bands or pulmonary valve stenosis or the VSD gets smaller. How often does this change in morphology influence the natural history Next please. Well, I took from the hospital for sick Children and the National Heart Hospital. All the cases I could find of trick a speed atresia without transposition. And I put down the age at which the patients were blue enough to require surgical help. Mhm. Now you see that under six months and under a one year we often found associated pommery atresia or pommery vows to nurses. But after this period there was no obstruction in the pulmonary valve or in funding bill. Um the problem the obstruction lay in the VSD. Next. So the size of the VSD. In trick custody. Atresia is by far the most critical factor dictating its natural history. Here is a child with tri casted Atresia presenting at the age of five weeks in heart failure where the VSD was large. Here is that child at one year with ali gimmick, lungs and cyanotic. What has happened? Not primaries two nurses. It's the VSD has started to get smaller. Next please. And this change occurs at various rates. Here is a large VSD in tri casted Atresia. Next please. And here is the same patient. The VSD is absolutely minute and very little uh die can get through into the outflow tract. It's not the permanent stenosis dictating in this patient. It is the size of the VSD. Next. Please. And what dictates the size of the VSD will be in tricastin. Atresia is anatomy. And if you watch your patient, your clinicians, you must observe carefully when the pants systolic murmur disappears. Next please. Here is an 18 year old girl who required no surgery but just beginning to get a little blue here, you see the evidence that she has had a good pulmonary flow for a long period in her life. She's got a nice ring and a nice pulmonary artery. And here is the VSD. You can already imagine the fibrous flaps in there. And this may progress quite quickly and I must be prepared to help her at some time, even though she is now 18, 1 must watch her carefully because this will close down next. Please. Here you see a patient with ventricular settled with tri casted atresia. The fibrous tissue flaps around the VSD. Just as you would expect in that patient whose angio you have just seen next, please. And here you see another VSD. With the fibrous flap here coming down from above and here you see the massive left ventricular hypertrophy associated with tri casted Atresia. But this VSD is getting smaller and will reduce the powdery blood flow next. Please. Not all ventricular septal defects in trick us today trees as close and it all depends on where it is, what is around it and what is its morphology. And here you see is quite a large VSD in a two year old child showing no evidence of closure in tri casted Atresia. Next, please. So what have we learned by studying morphology that in 43 patients with tri casted atresia, 80 to 90% showed evidence of the VSD getting smaller. It tends to be a progressive change. It may not necessarily occur quickly, although it may do. It also occurs in association with transposition. It of course influences the size of the right ventricular outflow and it causes increasing cyanosis. It is not my role today to tell you the significance in terms of surgery. But this has very important connotation in when surgery and what surgery is advised next. Please. This closing of A VSD can also take place in transposition. Here is a child, the left ventricular angio. A large VSD. There's it's pulmonary artery. Next please. There is this same child angio two years later. No sign of A VSD. But look, the aneurysm of the member and a septum has gone the other way because this is transposition and is now obstructing the left ventricular outflow and creating sub pulmonary stenosis. Next please. Now we have spoken about changing morphology on natural history. We have discussed closing of the VSD. What else can fibrosis and platelet deposition due within the heart? Well, it can invade the conducting tissue as it does in this. These diseases may cause jet lesions. Subsequently the source of infection may cause late duct closure. One doesn't know what effect it has on congenital valve lesions. Next, please, let us look at one or two examples here is an Austrian premium. This is how the surgeon views it or rather how the physician thinks he views it slightly different. Possibly there is the coronary sinus and there is the conducting tissue lying behind the defect. Now, when we look at the natural history. Next fees of austin prime and defect. In this slide. I have plotted the incidence of spontaneous arrhythmias. Nothing to do with the poor surgeons. This is natural history against age of the patients. You know that atrial fibrillation comes on in middle life in atrial septal defects, that is probably due to distention of the atria. But this defect that lies so close to the node and conducting tissue also has an incidence of modal rhythms and heart block. And here I have plotted the incidence of heart block and nodal spontaneous nodal rhythms age wise and you notice that do come on occasionally in the first decade, in the second decade, in the third decade and in the fourth decade. In other words with age and turbulence, the conducting tissue behind the defect will be affected. Next please, here is an atrial ventricular canal or here is the trick a speed valve removed from the right here is the region of the node and conducting tissue. Next, please lifting up this specimen from a patient who died of complete heart block. You see under the tri casted valve is fibrous and cast tissue. Is it any wonder that the conducting tissue got involved? This is a change in structure and pathology that influences the patient's life history. Next, please, another example of what can happen with turbulence here is a simple condition, fixed symbiotic member Ernest nurses. Only 20% of these patients are actually born with abnormal aortic valves. But what happens to the aortic valve If you have a jet lesion on it. Next place. Next. Well, if you graph the instance of aortic regurgitation to age in patients with fixed sub aortic stenosis. You see that by five most of them have aortic regurgitation, which is not necessarily congenital, we don't know. But then there is an increase in the incidents over the first decade. Now this I believe is a morphological change due to jet lesions on what starts to be a normal aortic valve in at least 75% of the cases. Its importance. Next please. Its importance is that through life here is an aortic valve. The jet lesion that occurs on these cuffs maybe a site of infection. As in this patient here is the sub aortic stenosis here above. It was an aortic valve that was once normal, but it got fibrous jet lesions and platelets subsequent to be a source of bacterial endocarditis. Thus, you understand your morphology. The surgeon does a perfect removal of the sub aortic stenosis. He may leave a competent valve if it has a jet lesion on, it may at any time through life become infected next please. Now, other post natal changes that one can perhaps imagine or recognize is that we've dealt with turbulence. Fibrosis is the problem of hypertrophy of abnormal muscular bands. Let us look at what they have on effect on natural history. Next please. You may remember in the first slide of ventricular septal defect that we spoke that some turned into fellows to trilogy here is a child in gross failure in infancy. Here is this child. I apologize for the bad slide and you can see something has changed even allowing for the bad slide. This is at the age of one. Next, please. And here is that boy at three. He now looks like a mild fellow which V. S. Ds will turn into fellows Next please. This is very important to know. Well, the first thing of course is to look and see if P two is getting late or being delayed. This is why phono choreography and careful Oscar rotation may be of help to you. The murmur itself will not next please. What one can say from one study of these cases and we've all had quite a large number That if you have slight delay in p. two that you recognize early on which increases that the right axis deviation is persisting in the VSD. That's been in failure. That the pan systolic murmur develops mid accentuation, that you have a small gradient across the RV outflow even at a time, the patient is in apparent failure and you may recognize that case. It has also trivial pulmonary valves to nurses. But what is more important when you investigate these patients, you should recognize the displaced crystal bands on the angio cardia graham. It's a matter of what is the basic morphology next? Please? This is from netters book. There is the huge VSD and in order to become a fellow, you have to have your crystal bands arranged like this next. Please. You may recognize this slight indentation on the angio at a time when the patient still has a high pommery blood flow. Now this patient if left, will turn into a fellow. So one thing you must not do is ban the patient however serious his clinical state. Next please, here is an infant who died at the stage where he had a high pulmonary blood flow. You are looking in the inside of the right ventricle. Here is the large defect in the fellow position anterior. You notice to the papillary muscle of the Conus. And look there is the potential to form in fund irregular obstruction. It has not yet there's no turbulence fibrosis. There's no extra hypertrophy. But had that child lived, I'm sure he would have become a fellow. Next. Please Here you see on the ngos. nine months earlier this infant was just in borderline failure. Their thickening of the christa. Here it is a year later and you see you've got much narrowing there and the patient has become a fellow. But you have to have your band's arrange like that at birth. Next please the sort of thing the surgeon. And if you have a nice surgeon and I work with a super surgeon. Donald ross kindly removed me the whole christa and the christa if you like that obstructing part is made up of muscle and this is secondary result of turbulence fibrosis. Next. Please. The fact that muscle goes all the way around in this obstruction is shown when you trans illuminate that circular piece of tissue that he removed. This is congenital it high purchase of his after birth. This is acquired and causes a fixed obstruction. Next please. So the VSD. Which becomes a fellow is interesting but it raises a few problems. What happens if the ventricular septal defect is closed surgically and the wide in fondi belem is left alone? Will the infant tubular obstruction progress? What is the best time to deal with this recognition of the type of VSD. Or dealing with means that you should warn the parents that cyanotic attacks could occur as the child improves. And you might ask yourself does digitalis and china tropic drugs increase and accelerate the development of this in fantabulous shutdown next. Please. Now this post natal potential for increasing right ventricular outflow obstruction does not only occur in fallow. It occurs in other conditions and as I've said, depends on the displacement of the colonel bland's at birth. Next, please. Or in the fetus. Here is a double outflow right ventricle age 10 months in heart failure. Here is the child at seven years having classic cyanotic attacks. Next, please, Here is a patient in failure at four months. It had a double outflow right ventricle. You can see the order is high. You had a big pulmonary blood flow. The patient was banded but that could only increase the infant tubular obstruction that was to become severe and require a section at 2.5 years. Banding was not the right treatment. Next, please. Although it brought the patient out of heart failure and the same thing can occur in association with tri casted atresia. This child, you have to take my word had try custody atresia. It had a huge VSD but was having cyanotic attacks. No wonder it was having cyanotic attacks. It had a huge fellow bands in its outflow that were shutting intermittently. Next, please. Now, other things. There isn't too much time and I hope I'm slowly wetting your appetite for this study. We've dealt with thickening of muscular bands and turbulence, fibrosis, a word about secondary ring dilatation that involves valves, valves may become incompetent as a result of turbulence or increased blood flow. Next, please let us look at a few examples. For instance, aortic regurgitation may occur in certain V. S. Ds, sub aortic stenosis, elderly fallow and pommery athletics. Aortic regurgitation is quite common in adult fellows. My actual regurgitation the same thing can occur. The slightly abnormal valve or misplaced valve in a funny ventricle may become regurgitating as age creeps on. So it is with dry caspit regurgitation in an atrial septal defect and the pulmonary valve in the atrial septal defect and abduct next please. These are all secondary acquired changes. If you look at drinkers. A simple pediatric disease. And you you graph the instance of trunk or regurgitation against the age of the patients. When you examine them, there's the high incidence in the neonatal because of abnormal valves. Then, as age creeps on in those who survive, it becomes an age related problem from chronic stress and dilatation. Next please. The same occurs in mitral regurgitation in the austin premium only about a third in the early period have actual mitral regurgitation, even though the valve is always abnormal. Next please. Okay, here you see in transposition, this child had mild promise nurses in the VSD. And transposition. We kept it going very well for a long time and then suddenly it arrived in the ward at the age of five in sinus rhythm and gross failure. The trick a spit valve Cordy had ruptured. But if you look at the trick, a spit valve in transposition. It's no surprise that it may upset the natural history with or without surgery. Next please, A simple morphological change. Now, before I finish, a word about valve degeneration and calcification here is an aortic bicuspid valve. My really star nosed not causing embarrassment to the patients left venture. As you see there's a wide hole through it. But you can visualize as age goes on and this gets thickened and calcified. This will become a rigid mass that will obstruct that is the very condition we were talking about this morning. Again, a morphological change taking place slowly into middle life. Next, please. Much more common is what the surgeon sees in congenital aortic stenosis is not a bicuspid valve. It has a central rafei. It's a trick. A spit valve with a central raffi here, it's turned into a bicuspid valve. And very often you see a little nubbin of mixer metis tissue. Now, if this is not causing much obstruction, nobody will operate on it. But this will appear next. Please had later life looking exactly like this In Middle Life 35 depending on the severity of the stresses to which it has been subjected calcification, a very important change in morphology that will influence function. Next, please, Here one forgets the pulmonary valve. This is a pulmonary valve stenosis, Chicken, a 45 year old woman. And these valves also calcify interestingly enough in pommery vows to nurses in the elderly. The tri casted valve also calcify eyes and is worth looking for next, please Here you see the pommery valve removed from a 26 year old fellow calcified and so these elderly fallows. You may have to replace the valve. The poor surgeon may not be able to make a good result of a pulmonary valve artemis because of the secondary changes that have been allowed to occur. Next, please here you see pulmonary valves to nurses in transfer in corrected transposition here. The pommery valve lies posterior and if you are faced with an adult cyanotic. To diagnose, it is always worth looking to see if you can see calcification in the pommery valve. It may help you in your diagnosis. If it's not in the correct place, the normal pommery vows should lie. They're not back here. And this immediately gave the diagnosis of some form of transposition. Next, please. What is the onset of calcification due to pulmonary stenosis? Well, it adds to the signs of pommery stenosis. Pulmonary regurgitation. Here is the late P. Two. Here is the pulmonary regurgitation murmur which comes in the presence of old calcified pulmonary statistics. So the clinician can recognize the change that is going on under his eyes next please. So I would say that there is an effect of changing cardiac morphology in congenital heart disease. I have described to you the changes in form and function which of course relates to the basic morphology in each congenital heart disease. The symptoms and the clinical signs of course are influenced by the changes. You should be able to predict spontaneous natural change that may occur in your patient because it affects importance in management, timing and effect as surgery. I would also suggest to you that in the textbooks congenital heart disease is described as a static condition. You look up tri casted atresia. There it is the movement, the dynamic nature of the heart. Whether diseased or not diseased is not described to you. I would suggest we have to change our views and when we learn about a disease, we must know these changes that can occur. We must recognize their potential as well as the label of the diagnosis. And I believe the clinician must know the whole spectrum that can occur in the disease if he is to cope with this problem of survival, which of course we must do as our science advances. And I believe that in forward looking hospitals last slide, no longer should you see such a sign. As I saw on the fourth floor as I got out of a lift in one of your largest hospitals in this country dealing with the most heart disease, both surgically and medically, I was struck the pediatric cardiology to the left, adult cardiology to the right. And I believe, from our knowledge of changing structure and function, the arrows should point in the same way. Thank you. Mhm. Yeah.