 Thank you Emerson and Let's start because it's a little long presentation, but I think is worthy. He's a very unusual Discussion of a subject that probably has not come to the attention of most of the audience So we need to start from basic and go gradually to full-blown Comprehensive discussion of the condition that came to the literature in the last 20 years Maybe and it's still very confused and very Interesting intriguing It was a color on the background today after seeing the weather. It's great Tending to blue because tomorrow is going to be beautiful, but today is a good day to be in a conference This is a picture that will give you a basic idea of what we are going to discuss today it's a noon compaction left ventricle which is basically a condition identified by the presence of a lot of bundles or muscles or presume muscles inside the Normal compact myocardium Outside, this is something that obviously has been present all the time But until recently nobody they did give a name and no one understood what it meant I had any interest in Dealing with it because it seemed to be quite irrelevant for the majority of the province They are not really inside them main cavity, but in the wall itself Well, let's see if we can advance the discussion in view of important Discoveries that we have Published last year in the final form After seven years of collecting data in a large study that we did by cardiac MRI In the Houston community in the public school in Houston By using MRI to identify risk factors for high risk cardiovascular condition for sudden cardiac death in atlas one of the surprises of the studies is Exactly the incredibly high incidence of or prevalence of high Non-compaction cardiomyopathy or non-compaction left ventricle that is a more proper main We're going to touch several points both The basic data from this study that we Referred to and then we'll go to non-compaction as it shows in the Embryology of the heart in normal and in animal We're going to discuss the spectrum of presentation in nature of this condition because many animals have predominantly hyper-turbiculated ventricle and not compact muscle in the heart We're going to eventually come up with a major Discussion in the Refine analysis by MRI of what is non-compaction in its entity or lack of entity in the muscle of the main Pumping chamber of the heart the left ventricle Eventually we're going to this Discuss specifically the prognosis and the clinical implication of this condition and Try to come up with the final theory on what is really this condition Should it be called cardiomyopathy a disease entity or just be a Unusual variety of normal anatomy because This is basically what Arts study NIH promoted Called the Mesa trial started introducing in the literature some 10 years ago 15 years ago eventually in 2012 they came up with a new Report that in the general population of people studied at 65 years of age they were looking for factors promoting Events in cardiovascular disease of the atherosclerotic kind They described this and described that that if you assume two segments of the heart to have high Neutrulations 6% of the general population in the population of about 1,000 persons Had non-compaction and they call it non-compaction cardiomyopathy and that was a little Douthful if it was a cardiomyopathy They describe it as Peterson this is a name they were recurring in many slides Peterson criteria to identify non-compaction by a ratio between the compact and non-compact Myocardium if the non-compact thickness is more than 2.3 times the normal Compact myocardium we call the condition as a non-compaction Also as a secondary feature They discovered and is a main point of our discussion That when there is a non-compaction the compact myocardium underlining the non-compaction is thinner than normal As an average many reports were given none so precise and extensive as in our study But it's basically half of the normal thickness in other segments of the heart So it's something that could lead to eventually cardiomyopathies by hyperplasia of the compact function in myocardium but this is pretty much the result Inclusion of our study 5,169 kids age 11 to 18 years of age We are dividing here in two in two groups to see if there is a progression with aging but basically the news and the main news that they want to get from this presentation that 1.47 of The patients at these ages have High risk cardiovascular conditions and we did not call non-compaction cardiomyopathy as a high risk but after coronary anomalies cardiomyopathies EKG and normality is leading to a high risk of sudden death There is a condition here non-compaction live ventricle. That is amazingly frequent 959 cases in the 5,000 kids is totally unexpected and reported previously This is something that we are going to see in different category and different subgroups of our Paper but is by itself something that requires some attention Here is an interesting sub-analysis if you look at the total number of 5142 they had diagnostics Value of MRI the males had 21 percent While the female had 16 percent prevalence of non-compaction cardiomyopathy in different subsets of the ethnic or racial Courts you can see that the ratio difference Between male and female is confirmed Both in half for American the mean is still 18 18.2 But in female only 14 percent had non-compaction like 21.5 percent of the males had it So this is also true for Asians Hispanics have the lowest Probability having no actually the highest probability of having non-compaction Cardiomyopathy 23.7 male the 20.4 The white people Are something like 30 percent in the used to schools have also a significant amount with the same difference So between male and female with aging the incident the prevalence of this condition is basically the same So the first conclusion on the S2p screening to prevent study was that Unespectedly in non-compaction left ventricle is the most frequent anomaly in the human heart anomaly in the heart and This can occur in two conditions one is should be called as being frequent and benign garden variety non-compaction left ventricle and another one much less frequent non-compaction Cardiomyopathy that is less than point one percent of the cases in this context the Peterson criteria was the one that we used also in our study with two point three to one non-compaction to compaction layer And the eco criterion as you know is that two point zero to one Is observed in insistently which is as we will describe the major technical mistake But the important thing that describes a non-compaction cardiomyopathy is not so much the presence of Trabaculations, but the presence of a left ventricle ejection fraction or less than 40 percent that defines basically simply cardiomyopathy This could be associated with exercise and one of the surprises of our study is that to find out that in Houston 60% of the kids They do the did this study Basically is the general population had the free study that doesn't hurt. It's very simple and is very Potentially useful or curious to have 60% do more than six hours of running a week So it's not Definition of an athlete but could be related to the manifestation of this Condition in a little higher degree than another but most likely this is not the true Clarification of the the reason of why this Prevalence is so high. Let's start to go then to embryology. How does a non-compaction or high Trabaculation appear in in human embryo in the first week of Development we recognize the heart initial presentation as a straight heart a straight tube Where the layers of the heart are basically three an outside clean surface no a Epicardium Then a single cell layer of myocardial cells Then jelly and then an endocardial layer inside This goes on for the first week or two and eventually the Epicardium they call it also a picardial organ a layer of cells that come from the liver travels Around the coronary sinus from the back of the heart to cover the whole extension of the heart to give a Third layer or the epicardial layer. This is a very important Population of the traveling cells That comes from the liver but is destined to form especially the coronary arteries 90% of the coronary arteries Have this origin of the cellular cells So this is a population of cells covering the heart. There has a lot of the coronary bound stem cells They have also cells for the adventitia for the media Not only for the endothelial part of a coronary artery Eventually this heart monolayer muscle becomes Proliferating actively And at the end of the first month that we can see that the inside of the vessel while the outside increases by five times the number of layers of myofibers the inside of the Cavity of the primitive leth ventricle or common ventricle is Filled up with the trabeculations. They call it embryonic trabeculation Structure that is not functional It's in the middle has a capacity of acquiring energy and nutrient from the direct transference of the oxygen and but also Glucose and anything goes on in the blood for its own nutrition It keeps the viability is the logic viability But functionally there is nothing to do to be coming in the early embryo from These trabeculations is the muscle that is compact that starts beating at the end of the first month. There is also already heart beating At the end of the six week There is the most critical event that occurs in the embryo This regard which is the appearance of the aortic valve the separation of Comontrancos in two arteries so the art and pulmonary artery Leads to the formation of the aortic valve and the aortic valve is essential for the coronary circulation to appear and function properly because it gives us a high diastolic pressure otherwise before The aortic pressure is the pressure in the ventricle. There is no separation between aorta and left ventricle So this is the issue of The first month Anatomy the presence of an aortic valve a high diastolic pressure goes with a An attraction that this cell cells in the probe picardium and the picardial layer of the heart have to reach the outlet the aortic and the pulmonary outlet of the heart At that point the coronary arteries are organized in local known functional no circulation Primordial vessels or lakes that eventually touch and enter into the aortic wall and start the Circulation and in a few days Even in human that has a longer gestational period in a few days Yeah, see the appearance of coronary arteries from the art coronary veins to the coronary sinus and Capillary network around each cell. There is a system of vessels that Provides a local distribution of the nutrients So it's a very important We call it miraculous time that eventually The plex also in terms of maturations of this Trabacule embryonic Trabacule inside the main pumping chamber At this time the condition for Compaction transformation of the Trabacule into compact myocardium that exists for sure It is a normal phenomenon in embryo in human the condition for this to be cut to occur is the presence of coronary arteries You will see how amazing is the formation of the coronary arteries at the intra myocardial level It uses the intertrabacular Spaces the space where blood of the main leventical cavity Surround the Trabaculations. There is a period around the end of the first month and a half of the embryonic life in which the compaction becomes quite aggressive and quickly doubles or triples the Thickness of the compact myocardium why? Tendentially the compact compacted Trabaculation Disappeared being acquired by the compound myocardium and at the end of The first month of life of the first month and a half of life Most of the Trabacule are already part of the compact myocardium and normally this embryonic Early Trabacule disappear from the mature heart Give an idea. What is this Trabaculations? This is a state 17 This is a picture from the Carnegie collation of human embryos at this stage as you see there is already a Almost compact myocardium in the septum a compland myocardium of four or five cells The myocardial fibers in the outside of the main cavity This is the left ventricle separated by a primitive ventricular septum. This is the right ventricle and These are not functional functional myofibers. They are actually cells primitive cells but not functional myocardial cells The myocardial cells my myofibers are here in the outside But this is a dramatic picture of a day or two in the life of an embryo that for some reason Inspire a lot of people and you see it Frequently in YouTube in Google and nobody knows where it comes from But it's an incredible picture to show how compacted myocardium occurs by while coalescence of this Trabricular embryonic structure inside the muscle and The organization of these white lines are the early intramural Vessels artery veins and capillaries There are obviously the transformation of the intertrabricular spaces into vessels So the endocardium Layer the inside the endocardial Layer is transformed into a vessel. This is amazing, but this is well described and confirmed Recently with the dramatic increase in in Sophistication of astrology This is basically the work that is done not only but mainly by these people are led by Dr. Christie Red Horse Stanford University This shows that the heart of the end of a month and a half of life In human but is in embryo is eight days of life in this is a mice and It shows in red what is the Pro-epicardial layer Originating coronary arteries and the part of the heart that the anterior and the septum comes from the Vessels from the endocardium intertrabricular spaces and here you see exactly the magic moment where a Picardial this is the outside of the muscle and this is the inside of the muscle where the compacting of the trabeculae becomes a Compa myocardium and the intertrabricular spaces become the lumen of vessels that separates heart muscles from Vascular space But this is definitely something that is confirmed to occur with very sophisticated Cellular and molecular Astrology Later in life the ventricle walls normally increase in thickness by Multiplication of the cells existing there besides acquiring compact a non-compact Myocardium these trabeculations into the outside wall in a normal human being at the end of the fetal period at birth the Ventricular anatomy basically is established the left side of the left ventricle or The ventricular septum is smooth and clear of the trabeculation The rest that may have minor Trabeculations, but not the compact a Consistent layer of non trabeculation non compact myocardium as we see in this 20% of the normal population in in the school from analyzing the histologic molecular and Gross anatomy of Development in embryo and in early Development after birth we can say definitively that two myths there are in the literature about the possibility that non-compaction left ventricle Appears and disappears cannot exist you cannot expect compact myocardium to lose the complex intrinsic Population of cells Vessels cannot become endocardial layer these two possibilities that Compaction and the compaction occurs and disappears and recurs in relation to a pregnancy typically hyperthyroidism typically athletes under severe stress and Exercise conditions cannot make their heart develop and then D Decompact the left ventricle. This is on genital occurs before birth is a Genital defect not necessarily a genetic and we will talk about the genetics of non-compaction in The presence or absence of cardiomyopathy now we call for the animals General to show what they can do in the absence of compact myocardium This is a group led by dr. Jensen Danish the lives in England and is a friend of dr. Peterson So they did the MRI histology and gross anatomy of embryos and adult mammals and fishes or sort of animals Where the heart is fairly large and at different dimensions and you can see how frequent plus is the presence of Non-compaction myocardium both in human both during development and at the end of development There is a certain probability of having non-compaction Here it says the ship and see it doesn't have developmental Non-compaction. I'm not sure but in general we can prove from this Summary of the situation in the animals in total that the mice is a good example of similar Panel pattern of Organization of the left ventricle in both in development and in embryonic development and in adults They have a certain probability of non-compaction. They are simple animals like Fishes that have a very highly Traboculated myocardium 90% of the muscle is there and only 10% is compact myocardium And they work pretty well is the way they measure as Peterson was advising the Part of the ventricle that they call non-compaction with respect to compact myocardium. This is a normal heart the space between the popular muscles and the wall of the Heart is not really known compact myocardium Compact layer of the left ventricle, but this is obviously different in animals or human they have Multiple trabeculation inside the compact myocardium. So this is the most extreme case of the pig where there is no absolute any Trabaculation inside the main pumping chamber of a normal adult pig in sheep and see is frequently and normal to have Half a 50% of the muscle to be highly Trabaculated but in zebrafish is the redfish there are plenty of of Trabaculations you see there is a progression with the evolution of the species They show that the more evolved the animals have more frequently only partially Trabaculated heart in the majority of the heart is compact myocardium and eventually simple animals they will have mainly non-trabaculated myocardium business histology finally something solid to show what is the In animal with high level of the known compaction This is the shark and the trout if you look at the compact myocardium a lot of inter muscular vessels if you look at the Very high percent of the left ventricle is full with the fine Trabaculations the tabiculations are Disorganized are like in a sponge not in a muscle that has to have some structure to produce if there is contraction a systolic production of blood pressure Here there are some fibers But it's not clear if it is functional muscle in the absence of the functional result of the Muscular effect. This is a another Mention of this group Dr. Jensen and collaborator that came with the a general theory of what is a normal embryo and a Normal adult especially in human, but especially they looked at the purkinje fibers because one of the Utilizations that is given by people that started talking about non-compaction cardio myopathy is that arrhythmias are more frequent sudden death it's more frequent and They are talking about the need to put in plant of a defibrillator in people with non-compaction Reality it's important to see where the purkinje system is subtle in a normal anatomy in human compact myocardium is Below the small tabiculation the residual there is are present at birth and the Purkinje fibers comes from the AV node artery on top of the muscle organized muscle compact myocardium and it's Endocardial structure when you have as it is a non-compaction Leventric or a lot of tabiculations a lot of tabiculations the purkinje fibers appear and Disorganized rare and probably non-functional this muscle doesn't have Coordinated activity if it has any active obviously in totally Non-compacted muscle like in the simple ectoderm Animals there is no purkinje fibers system now in animals specifically In mice it's easy to do experimentation Changing the genes so this is what they have done in an incredibly popular theory philosophy The basic embryologist experimental embryologist started affecting deleting basically genes that affect the normal development of the heart and it has been Now 20 years since these experiments were started and we'll see the list of the experiments Well, there's something like 30 different gene deletion that lead to non-compaction most of the time non-compaction comes by application of these deletion Techniques affecting some genes applied in the first few days of life of the mice not in the late age of the embryonic Development or feet of development the conclusion by all these studies is that it's easy to see Non-compaction as a side product of any genetic influence in the heart but Only one study has Produced the human what we saw in the MRI study Example of non-compaction of ventricle with the normal function of the heart and that was Described later on by John. This is a first part of a list of 26 different studies that a year and a half ago were Reported by this group in Indianapolis all sort of different genes deletion applied by viruses will lead to this kind of an incredible Pathology this is a normal animal and this is the animal given this Intervention in this case. It might be one mutant Where you basically affect the notch? Organizing system of the human embryo heart in in this case After applying this deletion the heart to cannot Basically form a compact myocardium even the ventricular septum is quite incomplete and It's a very thin Free wall of the left ventricle compact layer. This is the normal aspected and eventually The mortality in in this experiment is something like 25% spontaneous abortion but at the end who has Survived in this series Has Trabeculated are free in the ventricle and don't really make any action For the function of the heart as a pump the conclusion of this studies seen from a Functional or clinical eye from as mine Is that you can indeed cause easily non-compaction? malformation of the heart, but usually they come with other important and anomalies like the ventricular septal defects Like cardiomyopathy also hypertrophic cardiomyopathy. It's a different disease state Then the benign non-compaction that we're seeing human. This is another idea of what is histologically the non-compacted Ventricle in human. This is a best anatomic study. I found in the in the literature this is Bill Roberts a famous pathologist from Washington and eventually now in Dallas that does Describe the correct way for pathologists to find Non-compaction cardiomyopathy or non-compactual a ventricle in in autopsies What you need to do is a cross-section of the heart if you don't do this you will describe that Network of the trabeculae but don't understand the importance of this if you do cross-sections you will see With some frequency the presence of a layer of non-compaction inside a muscle that is Frequently or usually thinner than at sites where there is no non-compaction like in this This is the septum no non-compaction and this is the free wall with Non-compaction and thinner wall You know we did the study simultaneous with the MRI study in the forensic center in Houston and reviewed the reports of The autopsy in 7,000 autopsies in three years in Houston Not even one Diagnosis of non-compactual ventric pathologist don't know what it is or don't think that is Severe enough or significant enough as to recognize it or even with the name. This is our pathology in Heart to usually come to our observation at the time of transplantation the extreme degrees of Non-compaction with cardiomyopathy. So these are very proliferative hyper-trophic Trabeculae disorganized non-functional the muscle this functional is this one Frequently with the endocardial fibrolystosis, you see this white part of this In there part of the known to make known in compaction to recollect frequently is very dense and Very small interturbicular spaces are left. So it's a significant Restriction to dilatation so important symptoms of the constrictive Cardiomyopathy that comes also in this kind of the hyper-trophic Proliferative Cardiomyopathy this they present in this review paper by our virmani as a typical benign 14 quote benign Cardiomyopathy is not really benign. There is a severe Dilated cardiomyopathy behind but that is the spectrum of non-compaction in human pathology Frequently, and this is what was previously recognized a non-compaction cardiomyopathy Typically, this is in the context of heart failure probability of sudden death probability of requiring transplants for probability of requiring implant of a defibrillator This is a typically fibro elastosis inside the Terviculations, so let's summarize what we know now about the spectrum of presentation non-compaction in human and We call this simple frequent but benign case that we found In 20% of the normal people in Houston is the garden variety defined by a non-compact to compacted ratio The value varies in our experience between one and five Dr. Peterson decided that more than 2.3 should be called with a name But actually it occurs with less than 2.3 or up to five times Higher thickness of the non-compaction with respect to the compaction part of the left ventricle. They localized less than two Segments of the ventricle with non-compaction Is rare but exist the proliferate obstructive is less than one per thousand hypertrophic cardiomyopathy is one thousand Many cases initially reporting the literature of non-compaction was in the context of neuromuscular dystrophy Congenital heart diseases, especially Epstein malformation the mitre valve of the tricuspid valve is the most frequent association in patient with non-compaction and Congenian anomaly. This is a recent review by dr. Aboustini of the University of Pavia that has a great Genomic Center very interested in the Mutation that you can find in patients with usually dilated cardiomyopathy. This is the first of three pages Only showing six cases of the 52 different mutants that can be found in non-compaction patients so many Genes something like 70% of the patients with cardiomyopathy of the clinical importance have genetic Identification 30% or so don't have it but in our population the benign variety There is no association with any genes Defect, let's see if we can go to MRI as we have very little time left See this is the typical example of How we studied the heart By trying to quantify the level of hypertrophy of the non-compaction and the function of the heart as a pump and The function of the heart muscle in terms of thickness of the compact myocardium because it's obvious that this heart with non-compaction have adequate muscle simply have Some decoration inside the muscle that my associate dr. Uribe that the fortune today is not here Describes as la barbita. It's a sort of a beer inside the muscle that works in In the non-compaction left ventricle without cardiomyopathy But if you look at the type of analysis they went through went through something that is absolutely ridiculous in the precision Important obviously not necessary in clinical cases, but we measure by a Cmr 42 it's a special program that does this automatically in cross-section of the heart in this case this section Sorry we Created the radial thickness 97 different Degrees of the circumference and found out what it means to call The index of Peterson non-compaction to compaction thickness in It's done in the astrolite But the astrolite has this thickness here and this thickness there and the lowest is there But it's not the usual non-compacted the level the thickness of the wall But the important thing is that the insist on it. This is the inside of the non-compaction With respect to the outside of the compact muscle that can be measured with the system The thickness of the whole thing is much more than usual But this part with the compact myocardium, which is this part is the only functional part. This is a typical movie of by MRI of the Longitudinal to chamber view that is the compact the Popular muscle the anti-lateral popular muscle that you see as he comes from Mitre valve apparatus touching the trabeculae It leads to hypertrophy of the head of the popular muscle But the base is still non-compaction base of the popular muscle is on Trabeculae and that could be a diagnostic Index of non-compaction. This is by cat's cat and geography. It is much more precise Unfortunately is only taken in the astrolite so it doesn't give the full story but you see very clearly in this condition the thickness of the Compact myocardium and end astrolite the fibers nature of this Uncompacted Fibers at a regular in the fact that the popularity muscle Stop at this level eventually continuing to their vaculations. This is what we see in longitudinal views With the longitudinal views you don't see so well neither the thickness of the compact nor the Extent of the hypoplasia as you can see in cross-section. This is the best way to really evaluate quantitatively the Muscle in non-compactional adventurer. This is an interesting Finding a kid that does 18 hours of sports a week. This is major both swimming and running and football a lot of work and The question was that this cause Dilated cardiomyopathy with a thinning of the comp of myocardium and it doesn't seem to be the case This is an end astrolite on the left and then sisterly in the right You see that the comp of myocardium with all these things this Measurements is thinner in end astrolite, but it compacts to a good thickness in sisterly This is what we tend to summarize in this table the compares the risk of using the Peterson criteria to identify non-compaction cardiomyopathy the Table that compares the Efficiency of four different observers of the our population and the consistency Goal standard being the study done with cross-section. There is much more precise and quantitative it's consistent with the aware doctors for non-compaction None aware cardio radiologists have a consistency of the diagnosis of non-compaction the ventricle of 18 to 58 percent of of the cases it's a very inefficient and Inconsistent diagnosis. Let's go to something more dramatic. This is summarizing in two cases The essence of what is non-compaction of the benign kind the garden variety two cases in Dastoli and in sisterly showing the non-compaction in those 97 segments of measurements by Peterson criteria. This would be a very severe non-compaction left ventricle with the ratio of Basically five to one or actually three point zero six to one that Incisterly actually goes to a normal Leventicola thickness all through the myocardial circumference, so the functional behavior of the residual muscle is not bad at all and in this hypertrophic or Super train the athletes and this was hypertrophy the typical athlete's heart occurs also in non-compaction, so there is something to explain why thinning in the astrolite eventually leads to systolic normal thickness and Excellent function. This is the most extreme kind of dilated cardiomyopathy with non-compaction. You see a fairly Thick non-compaction and very thin outer layer This is in cross-section much more precise But confirming the fact that there is too little compact myocardium to make it a functional Heart, this is an important conclusive slides where we compare the normal Leventicola mass only the compact myocardium in a normal heart and in the heart with non-compaction and you see This is the muscle. These are numbers of the grants They are very much similar to the normal for these ages. This is the studied at 11 to 16 years of age This is in non-compaction. It's very similar to the normal heart Doesn't seem like non-compaction of the garden variety is affecting the function of the heart and This is basically the same concept in the global not only transverse Sections, what are the potential clinical complication on compaction as a lady non-compaction can eventually potentially lead to dilated cardiomyopathy because of exercise hypertension or pregnancy or Athletic exercise This is not something that we could study in our population, but it seems like even in athletes for that age You don't see manifestation of dilated cardiomyopathy Rhythmias we obviously did only an EKG addressed in these people and We never saw a single PVC. I'm not sure that is correct because probably when there was a PVC they eliminated that tracing and put another one without pvcs, but This type of benign clinically number nine And non-compaction Leventrico is not accompanied by significant arrhythmias systemic embolism is Frequent in the bed dilated cardiomyopathy but not in the usual GV type of non-compaction Aneurysm formation is an interesting question and We saw several kids with less than one millimeter of thickness of the wall of the left ventricle some parts of the ventricle and never saw bulging like in In aneurysm a dilated cardiomyopathy we didn't see But this phenomenon in our population if you look at the younger with the older Comparing with the older kids 10% more of the kids have ejection fraction between 40 and 50 percent But none less than 40 percent Let's go to a final point that is quite important because we need to explain why there is this Dramatic incidents of non-compaction in a general population And this can be the reason these are experiments done with Mice but using food or medicine. This is retinoic acid of vitamin A given in excessive dosage in an embryo the normal comparison and the Effect of the vitamins either too low or too high in the body It causes it affects the compacted the compaction of the left ventricle look our severe Non-compact the left ventricle case it is possible that if the administration of excessive amount of vitamin A but potentially many other environmental insults can cause a late fetal type of disturbance in the compact and compacting process and cause the Non-compaction of the benign variety. Let's see if we can conclude with these projects that we have now active. It is about Presence of non-compaction cardiomyopathy late after a benign presentation initiative by Doing a studies at the higher age, and it will be down there to clarify Hypoplasia of the coronary artery is the cause of fibro-lastosis. This is a study done by pathologist especially dr. Massimilia and Booyah and Anna Segura in our hospital or in the Texas Art Institute We need to find out better histologically and Molecularly the presence of the prokinzy fiber The potential is that non-compaction affects the utilization of left ventricular cyst devices as the sucking Effect of this cannula the apex can suck in Tabaculate and cause the obstruction of the inflow of the machine in Euclid our nuclear cardiologist has disappeared but the nuclear Medicine is affected by this localized especially but also diffuse high pull development of the compact can cause false scars in pet scans or similar studies of left ventricular perfusion the last Mention here is of a study that we are developing at this time with the military people to see definitively if at a higher age and in the presence of aggressive exercise Could non-compacted the myocardium lead to Acquired the later cardiomyopathy a more dynamic cardiomyopathy So this is left for you to discuss if you have any more patience and time and interest, please. Thank you