Hi, my name is Amy Dillenbeck, and I'm joined here today by Brad Meehl and Cody Fry. And welcome to Mimicromania with the advanced concepts of echocardiography for the sonographer HCM. And today we're going to show you some cases that may appear to have similar features of HCM, but we'll show you some distinguishing characteristics that may separate the two. And so hopefully you'll enjoy these cases and you'll really get a lot out of the cases and you'll be able to use this in your clinical practice every day. Good morning. Let's start with the first case study here. We had a 55 year old male. He's very active, runs triathlons, a lot of outdoor activities. He was having some chest pain while he was training, so he went in to see his primary care physician. As we look at the echo images here, we're definitely seeing some thickened walls here. We're seeing normal, appears to be normal aortic dilatation. We do not get any presence of SAM by M mode here. M mode looks pretty good. We don't see any turbulent flow going across the outflow track here that would indicate any type of outflow obstruction. As we take a look at the measurements, the wall thickness is a little bit thickened on the thickened side at 1.2, both septal and posterior wall. The micrometer did a good job not including the paraceptal structure here and just getting true septal measurement. Everything else looks pretty good in normal size and normal diameters. Short axis view, the mitral valve again looks like we're not seeing any type of SAM or outflow obstruction. Four chamber view looks like a good and nice function here. No evidence of papillary muscles being inserted incorrectly. Flow across the mitral valve looks great. For a 55-year-old, it looks like a really good heart here. Tissue Doppler is nice. We got a nice perpendicular flow, so we know we're not off angle, as we know that any type you do, some type of Doppler angles play, factor into what your gradients may show or your velocities may show. Flow five chamber here, we don't see, again, we don't see any type of outflow obstruction that would indicate any type of maybe some increased velocities across that outflow track. And of course, as we sample this, we definitely see the same thing. We don't see any type of increased flow, like daggering indication of hypertrophic obstruction. Aorta gradients are great with the mean gradient of less than four, so we know that's a bright normal flow. Going to the two chamber and three chamber here, we are looking at, or the three chamber, just looking at the normal function again, looking for any type of obstruction, any type of subaortic membrane. Again, we see a nice flow going across outflow into the aorta. There's no aliasing flow. Our color scale here is normal, so we're not too low, we're not too high. We're right where we want to be to ensure that we're getting definitely the right color flow across that outflow track. And when we perform strain on this athlete, on this patient here, we get a normal pattern clear across, normal strain pattern with a global strain of negative 22, which is really good, really normal variance. We don't have the cherry on top appearance, any type of abnormal normal findings here with the strain pattern. So this definitely is an athletic heart. It can trick you at times with, looks like it's thickened. As athletes train, their ventricles remodel and to meet the demands of the body during the activity that they are performing. So just to compare the two, we have a 2D findings, we have concentric LVH here, hypertrophic, we definitely can get some asymmetrical LVH. So just be aware of those. Usually on athletics heart, that left ventricle cavity is less than 55 millimeters, hypertrophic give a smaller cavity. So be aware of that, it's less than 45 millimeters. The reason why left ventricle cavity on athletes bigger, again, is for endurance, their left ventricles remodeling to meet the demands of the body when they're performing their sports. Normal diastolic dysfunctions, very important to look for athletics heart. On hypertrophic cardiomyopathy, you definitely can get some MR, you have SAM, and then of course your outflow obstruction. So just be aware of this mimicry as it comes into your lab. This case, we have a 64-year-old male with a history of hypertension and diabetes. The patient presented to the emergency department for syncope, and he was secondary to epistaxis, which is a nosebleed. We first noticed that the wall thickness appears increased here, and there's no obvious valvular pathology. In this zoomed in view of the mitral and aortic valve, we're looking for systolic anterior motion of the mitral apparatus by 2D, and so far there's none appreciated here. As we move on to our 2D measurements, they confirm that we do have increased wall thickness. Both the interventricular septal and the infralateral wall are measuring 1.6 centimeters, which categorizes this as severely increased wall thickness. One thing to note is that we want to look at the aortic valve in our short axis to confirm that there's no aortic stenosis, which there's not in this patient. And moving to the basal and mid sections of the short axis of the left ventricle, we can appreciate the increased thickness and also the ejection fraction. Another thing we like to look at in this view is papillary muscle morphology. As we move into our apical views, we're evaluating for mitral regurgitation, and as you can see through our color doppler, we don't appreciate any of the pulmonary vein flow appears normal, and you would want to angle through because systolic anterior motion in MR can be at different levels of the mitral apparatus, so I wouldn't rely on just one view to appreciate that. As we go into our five-chamber view, we use color here to interrogate the left ventricular outflow tract for turbulent flow, which would indicate an obstruction, and it appears to be laminar here, and there's no spectral doppler evidence of obstruction as well. And again, looking at our two-chamber and three-chamber view, we can appreciate the wall thickness and ejection fraction, and with color doppler, again, over the LVOT, we confirm that there is no increased flow through the LVOT. And we would use these optimized images here to perform strain, which could help us differentiate between HCM and just one of our mimickers here. So we also can look at the EF and appreciate that the wall thickness is consistent around the heart, which would lead us to consider what other etiologies we might have for this increased thickness. So we have severe LVH with an IVS thickness of 1.6 centimeters, an EF of 59 percent, and the RV is normal in size and has normal function. So this is a hypertensive case, and it can be really difficult to differentiate hypertensive heart disease versus HCM, and in this case, it would have been helpful to try and provoke a latent valsalva gradient by use of, I mean, latent gradient by use of valsalva, exercise, or amyl nitrate. If at all possible, we also want to perform strain, like I mentioned earlier, to help us further differentiate the hypertension versus HCM. This is a case of a 55-year-old male, history of carpal tunnel syndrome and chronic kidney disease. And so this carpal tunnel syndrome should give you a key, I think already, of what we may be seeing coming up. Admitted in cardiogenic shock, blood pressure is low, 88 over 55, so hypotensive, pulse is a little bit high, 98, no murmurs, gallops, or rubs. As we can see, even just in parasternal long image, this should give us some keys of what may be going on. We can see there's a small pericardial effusion here, and next to the posterior wall. We also can see that the walls look a little different than possibly what we may normally see. They may, what you may see is some speckled appearance here or some infiltrative disease, so that may be a key for us of what we may be finding in the future in some other images. The sonographer measures the walls, and they do get a thickened heart, so this would be severely thickened. They get a 17 millimeters and 16 millimeters for the walls. The LV looks like it is small. As we get a closer look at the function of the mitral valve and the color flow, which is really helpful when we're looking for any sort of obstruction in the LVOT, we see there is laminar flow through that LVOT, so there is not any sort of aliasing or what appears to be any sort of obstruction right now in the LVOT, which is great. Mitral valve, there is a little bit of mitral regurgitation and a little bit of kind of an unusual AI, but nothing as far as LVOT that we can see with mitral valve SAM or increased flow velocities with the color flow Doppler. There is higher TR velocities, as we can see, 2.8 is the TRV max at this point. I think it gets a little bit higher as we proceed with the exam. As we get an important short axis of this mitral valve, this can also prove if there's mitral valve leaflet SAM. It's a nice view as well to be able to show that, and here we can prove that there is not mitral valve leaflet SAM. There is some MR again, as proven with this view, along with a parasternal long axis view. As we move on to our apical four chamber, we can see that that LV does still look thickened. The LA looks dilated just visually from looking at it compared to the LV, and it has again that speckled look to the LV. As we look at the MR again, consistently with what we've been seeing, the MR appears to be about mild or so. No surprise, because of the LV and how it appears with the dilated LA, there's going to be some diastolic dysfunction. Here we see that the mitral valve D cell time is very short, a very high E to A ratio of 5.2, and then we can see that this is probably indicative of some sort of restrictive pathology, which is consistent with an infiltrated disease. The sonographer had some really nice E prime velocities, very low E prime velocities, so a high E to E prime ratio of 18, again, consistent with restrictive filling pattern. As we look through at the LVOT, consistent with what we saw in the parasternal long, nice laminar flow through that LVOT area, so confirming there is no obstructive LVOT pattern at this time. The MRV does show that there is some more TR when you put the CW through that TR. We're getting a higher Vmax now of 3.4. The RVSP is going to be probably somewhere near 60 or so. We're also getting some flows through that LVOT, the pulse wave and continuous wave. Continuous wave, I'd probably optimize this a little bit better, but it does show that it's still laminar flow confirmed with our spectral Doppler as well as our color Doppler. Our two-chamber, again, confirms what we're looking at with the speckled myocardium, and LV function looks like it's maybe mildly down. IVC looks very dilated. We're measuring 2.7, and then we also get our final strain pattern, which I think we're all probably familiar with now, what we call that cherry-on-top strain pattern where the apex is preserved with our strain pattern, but we have those lower strain values in the mid and base. This is what we would, stereotypically, this would be what we'd want to see for our amyloid case. This is the echo findings for this case, moderate LVH, EF, they called mild, 48 percent, grade 3 diastolic dysfunction, that restrictive filling pattern. RV size was normal, it was mildly down. There was some mild thickening of the mitral valve and the aortic valve, and we found that mild mRNAi. RVSP was high, we had in the 60s or so for pulmonary hypertension. So when we compare findings for amyloid and hypertrophic cardiomyopathy, a lot of times those can be similar and can be confused. So the big thing is to look at the LVH versus increased wall thickness, so when we want to compare and we want to do our reporting, we want to call amyloid increased wall thickness as opposed to LVH. So just make sure you're aware of that when you're reporting those. The myocardium does look speckled when you're looking at your myocardium for amyloid as opposed to HCM. You will have thickened valves for both. The pericardial fusion is also a key when you're looking at amyloid patients, that can be helpful as well. And you can have LVOT obstruction sometimes with amyloid cases, but the other big thing to look for is that amyloid cherry on top when you're doing your strain pattern. So it really shows the importance of strain and the patterns you'll see with strain that's going to be really helpful when you're trying to diagnose some of these cases and to try to figure out what's going on with these patients. In this next case, we have a patient history of known Fabry's disease. This patient has a kidney transplant, they have a history of a PCI. The patient presents today with shortness of breath, blood pressure is 141 over 81, slightly elevated, pulse of 53, and grade 2 systolic murmur at the left sternal border. And as we look here into the images, I was first taking a look at these pictures here, we're definitely seeing some thickened walls, which also should grab your attention as a sonographer. Look at the valves, the valves seem to be opening just fine, no significant stenosis or reduction in valve openings here. The walls do measure thick, which would put into at least a hyper terrific category of 1.5 to 1.8. As we continue to do our 2D measurements, we do notice that the aortic sinus does measure large at 4.5 centimeters, sonographer did a great job of measuring this by the AOC guidelines from leading edge to leading edge in the cardiac cycle, which is very important for consistency. As we look here, moving forward into our color Doppler, we do get a little bit of much regurgitation here at the peristal long view. We do not see any outflow obstruction going into the aortic valve. We cannot appreciate any SAM by 2D here. Our short axis definitely shows the same thing we saw in the peristal long thickened walls. Look at the papillary muscle inserts, make sure they look correctly, make sure not misaligned. Our four chamber views here, oops, let me back up. Epico four, we appreciate the same thing. We definitely had some thickened walls, maybe a little bit thicker here in the lateral side. Definitely not see anything concerning a nice ejection fraction here. The flow across the outflow track is laminar coming out the outflow track. No indication of increased velocity coming across that LVOT by color Doppler. Looking into our three chamber view here, similar to the peristal long, we're definitely getting a look at a thick heart, thickened walls. Again, looking at the anterior leaflet of the mitral valve here, does not appear to be any SAM by 2D. Our color flow across our three chamber is like the five. We do not see substantial increase flow here, does look laminar. We'll put the Doppler across the outflow track and we get a nice laminar flow like we saw in the other reviews here. So no increased velocities here from the LVOT velocity, nice laminar, no increased velocity in our aortic valve either. So definitely no outflow obstruction in this patient. So what is going on with this patient? As we do our Doppler, we are definitely getting grade two diastolic dysfunction by all of our measurements that we have performed here, left atrium dilator, tissue Doppler, and EDA ratios all indicate that it is a grade two diastolic dysfunction. One thing that's very important to get is a good subcostal view in our patients. We know this can be challenging at a time if you see a thick heart. We definitely want to know, does it include the right ventricle as well? And the right ventricle looks prominent. I wouldn't say it's excessively thick, but definitely looks a little bit thicker than on what we would consider on a normal patient. As we perform our strain pattern, we do get this abnormal pattern here. We have this hypobasal posterior lateral segment here on our strain. This pattern as we know, strain patterns are just as important as the numbers. And so this is a kind of indication of what's going on with the patient with the dilated aorta. So our findings here on this echo is there's moderate concentric LVH, the EF is 60%, grade two diastolic dysfunction, RV is normal size, normal function, there's mild thickening of the mitral valve and aortic valve, mild MR, RVSP at 30 millimeters of mercury. So this patient has Fabry disease, and why does this mimic close to hypertrophic cardiomyopathy? Increased wall thickness, definitely we know are in both Fabry and hypertrophic. A thin basal posterior wall in advanced Fabry is indication here that you can usually point towards Fabry versus hypertrophic cardiomyopathy. Aortic dilatation is also indication for Fabry's, is not an indication for hypertrophic. Thickened valves can be for both so that you can't use that alone. Right heart hypertension of the right heart can be both in Fabry's and sometimes a hypertrophic, depends on what kind of hypertrophic cardiomyopathy you're dealing with. Typical Doppler findings, both diastolic dysfunction are both in Fabry's and hypertrophic cardiomyopathy, so it's not a way to grade this. Outflow obstruction, possibly you get a thicker heart in Fabry's, you could get some outflow obstruction, definitely with hypertrophic cardiomyopathy. And of course, strain pattern, this is kind of what will differentiate the two. You have a global reduction, lower strain in the basal posterior wall, and of course, hypertrophic just reduces values in the septal segments. So strain is very important to use when you see your LV that is thickened. The next case that can mimic HCM is a 53-year-old female. She has palpitations, normal blood pressure, normal pulse, but she does have a systolic murmur that's found in her right upper sternal border. So let's start with these parasternal long images. They are a little bit lower, but I'm sure it's the best that we could get here. We're looking at the mitral valve. It looks like it's in a pretty neutral position during systole, so there's not a systolic interior motion that I can see here. When you look at the right-hand side, the measurements look pretty good. They're normal size of the LV and of the septal wall and the posterior wall. And as we get it zoomed in, look at that LVOT, a really important look that I think most people sometimes take for granted is to get a good look at not just the mitral valve, but also that LVOT area. You know, we always think about the mitral valve and SAM and picking that up, or maybe aortic stenosis, but in between the two valves can be a really critical spot to look for any sort of obstruction. So as we get a closer look at this area, we can actually see that there's a little tiny subvalvular membrane there that's going to be the source of what we're going to find is going to be some accelerated flow through that area. So really get a good look at that area. We want to use pre-processing zoom to get really good temporal resolution, to get really good spatial resolution for that area. So really critical part as well is to use that color flow Doppler to be able to detect that aliasing flow and that high accelerated flow and where it starts. And we can see it starts right at that at subvalvular membrane. So it's really helpful to use that color flow Doppler to be able to detect where that accelerated flow begins. And then also to use some unusual kind of off-axis view. So it may be a little difficult to see here, but the sonographer did a short axis kind of LVOT view. And so it's really nice to use this in biplane too, if you have the parasternal long axis and then you can at the same time put your cursor through that subvalvular membrane and get a short axis of it. And it's really just showing it multiple views. So that's a really nice view here. And then they did a good job here also just showing the aortic valve is opening. So the aortic valve is not the source of the accelerated flow that we're about to see with the continuous wave Doppler. Moving on to the apical four chamber, just trying to get some more views of that subvalvular membrane from as many views as we can. This time we can go off axis and try to pull in as much as we can. And we can see a little bit of it right here in the five chamber view. And then of course, as we would expect, the color flow Doppler is showing that accelerated flow in that area. Again, not from any sort of mitral valve SAM, but because of that subvalvular membrane. Now, the one thing that is gonna differentiate, it may be a sign for you if you're not sure if there's HCM and the high flows are from that or from the subvalvular membrane is what we call fixed gradient. That's different from a late systolic peaking gradient. So the difference is we have this triangular shape. It begins at aortic ejection and they usually have lower velocities than you would have with your LVOT SAM velocity. So just keep that in mind. The shape of your spectral Doppler is gonna be really critical with these patients. You should see this fixed gradient where it has this triangular shape as opposed to what you see with HCM gradients, which are gonna be that late systolic peaking spectral Doppler shape. Again, just confirming that same spot. We wanna show that as many views as possible. And so we're doing the same thing here. I think you probably would see it nicest here in the three chamber showing it here with the color flow again. So confirming for the reading physician in as many views as possible what we're seeing as you probably would expect, pretty normal strain pattern, nothing really with the myocardium that we're gonna see that is unusual. The echo findings were normal wall thickness, normal EF, normal RV size and function. And they stated there is a subvalvular membrane with flow acceleration at the level of the membrane. And then you would give your peak amine gradients of that membrane. So you would trace your continuous wave Doppler and report your peak amine gradients. So some of the differences between your 2D findings is of course you would have a subaortic membrane in your LVOT where you wouldn't have that with your HCM patients. You may or may not have LVH. Sometimes you have both. You might have a subaortic membrane and HCM. So it could be a little tricky sometimes. The big thing that's gonna be different as well is the typical Doppler findings for fixed obstruction for subaortic membrane. You don't have a fixed obstruction or that triangular shape for continuous wave when you have an HCM patient. So just trying to keep that in mind. That's gonna be a really big difference there is the dynamic obstruction versus the fixed obstruction with your continuous wave Doppler. Finally, your strain pattern is gonna be normal essentially for your subaortic membrane unless there's other pathologies happening. Your HCM pattern, we're gonna see those reduced segments in that septal area for your basal septal area for your HCM patients. Our next case is a 67 year old female with a history of hypertension, sleeve gastrectomy in 2015, chronic kidney disease, heart transplant in 2016. And she presents today to the ED with a week of diarrhea as well as ongoing nausea, vomiting and weight loss as well as a right lower quadrant pain. Her heart rate is 122. So she's kind of tachycardic and blood pressure of 103 over 71. And as you can see from this first few images here, we have hyperdynamic function as well as our beat capture is only two. So it makes it a little bit difficult to be able to evaluate some of these things by 2D. And I'm not exactly sure if she is in sinus rhythm or not but it's hard to tell with that tachycardia. But we're hyperdynamic and our wall thickness measures 1.6. The IVS measures 1.6 by 2D. And I just wanna ask you, do you agree with this measurement? I may consider excluding a little bit more of the RV in this measurement, but still we're going to come up with a little bit of increased wall thickness here. And then also wanna note that in our left ventricular internal dimension during the asthma is 3.3. So that is also rather small. Again, we're zooming in here to determine if there's systolic anterior motion of the mitral apparatus. There is maybe somewhat increased flow across the LVOT and it is kind of difficult to determine if there's systolic anterior motion because we have such a short clip here. But I would like to see that increase a little bit. But it does look like there could be some anterior motion there. And again, showing the aortic valve to confirm that there's no aortic stenosis and then looking at the LV from the short axis to look at our function. And here, our four chamber, we're looking at the, it looks like there's increased turbulence throughout the LV, which would indicate hyperdynamic functioning. You can see that in the 2D here that it's sort of obliterating there from time to time. As we look at our LVOT, here's where it gets tricky because we begin to see that we have a late peaking gradient. And so that might steer us to believe that we might have an obstruction here. So this is where we wanna pulse down and identify where that obstruction is and also how high of a gradient we have, how high of a velocity we have there. So again, we're doing this in three chamber and it doesn't appear to come over two meters per second. And we are just appreciating that we have hyperdynamic function and it appears that that's the cause of it. So we have severe septal hypertrophy if we like those measurements. And then the EF is greater than 70. Visually, it's difficult to do biplane on that type of patient because of the obliteration in systole. There's no MR, there's no SAM. And here are echo findings. We have hyperdynamic function. LVH, we might find in hyperdynamic function and in HCM. And so all of these things, if you go down the list here, are possible in our hyperdynamic function versus HCM. So we want to be able to produce strain if we can. And oftentimes with hyperdynamic function, we have increased heart rate, which would be an exclusionary criteria for strain. So we want to use Valsalva and anything else that we have at our disposal to differentiate these two. And then decreased mitral annular velocity. The thing about our diastolic function here is if we do have increased heart rate, we're not going to really be able to evaluate our diastolic function because of EA fusion if that's there. So at the bottom here, it says often hyperdynamic function accompanies tachycardia and that limits, like I said earlier, our ability to create that function and strain. All right, this last case study is really showing and highlighting the importance of our sonographers to recognize patients that have potential HCM and provoking that. So let's get through this case. It's 53-year-old female, palpitations and a pacemaker. Normal blood pressure and a pulse and has a right sternal border systolic murmur. So when we look at the first image, the parasternal long image, we see the aortic valve is slightly calcified, maybe a little thickened. We look at the LV and the measurements for the LV look pretty normal, maybe slightly thickened septum, but nothing that's really going to be eye-opening. Otherwise, posterior wall looks pretty good. And the mitral valve looks pretty normal as well. It doesn't look like it has any type of systolic anterior motion too much. The mitral valve leaflets might look a little bit long, but nothing that's going to be worrisome at this time. As we put color doppler on here, this does draw a little bit of attention as I would be scanning this patient. It does look like there is a little bit of aliasing through the LVOT. Nothing that's too worrisome, but it does draw my attention, doesn't look quite laminar. So I would definitely keep an eye on that and try to see what's going on here. I do also see a little bit through that color doppler that the papillary muscles and the cords are sort of making an appearance here that maybe weren't before. So I'm going to keep an eye on those as well. The aortic valve short axis shows a nice opening. There's no stenosis that could be causing any sort of accelerated flow. So they do a good job of showing that. Moving into our apical four-chamber view, I really see now that this cord looks different. This papillary muscle looks like it may just look a little bit different than what we may normally see. And I think the sonographer who scanned this patient saw the same thing. So it was someone who was really aware and was really astute and did a good job at recognizing that there was something that just looked a little different here. So the papillary muscle actually just had a little bit of an insertion and difference. And because of that, it was causing some problems for this patient, which we'll see in a moment. As we look through and did our pulse wave and continuous wave through our LVOT, the pulse wave looked normal, but the continuous wave did have a little bit of a late systolic peaking along with our normal fixed gradient. So that was a little bit of a sign that maybe we need to do more than that. So we talk about provoking and try to provoke any sort of obstruction. So a lot of our patients may not have any sort of obstruction at rest, but it's really important for those who may have a family history, that may have symptoms, that definitely have LVH, that we need to try to provoke any sort of symptoms or any sort of obstruction. That can be with a simple Valsalva move, and that can be with stress and some other maneuvers. So this sonographer did a good job at recognizing that this would be a candidate that would be a good candidate to try to provoke some sort of obstruction. So they went ahead and did that. So their velocity here at rest was 2.4 meters per second. This was a resting flow as well with the color of velocity. And you can see again, it looks like it's aliasing a little bit. Right now, it doesn't look like there appears to be much same at all here. So now as they go in the Valsalva, you see a huge difference. So we can see now the leaflets of the mitral valve, especially the anterior leaflet, now tends to wanna go during systole towards that septum. There's not quite systolic anterior motion with septal contact, but it looks pretty close. And you can see now where it was 2 point, I think it was two, let's see what that gradient or that velocity was. It was 2.4 at rest meters per second. Now with Valsalva, we have that typical look we have with HCM patients with LVOT obstruction, that dagger shape late systolic peaking, and now goes to 4.6, it almost doubles. So great job provoking and showing that there is an obstruction there. And this is not because there's a thickened LV, but it's because there's subvalvular apparatus. There's an issue with that. So the sonographer again did a great job. Same thing in the three chamber view. So at rest, there's only a velocity of 2.6, but when we do Valsalva, you can again see that late systolic peaking look to the velocity and it goes up to 4.7. And as you look at this 2D image, as we slow it down and we freeze it and go frame by frame, we can see here, this is the SAM and this is that anterior motion that we look for. So again, critical that the sonographer plays a role in these cases and recognizes this. So if the sonographer did not do Valsalva for this patient, they would have just been reported as a normal echo and would have gone about their day. But because they were able to recognize that there was a potential for SAM or was a candidate for somebody that we could Valsalva, it really changed the difference in their diagnosis. So a huge praise for the sonographer to recognize that. There was no LVH, EF was normal, normal RV size and function. There was SAM at rest, very slight SAM at rest with peak LVOT gradient of 23, which led to severe obstruction with Valsalva maneuver. The peak LVOT gradient went all the way up to 87 with that Valsalva maneuver. So overall, it was called a non-hypertrophic variant with hypermobile anterolateral papillary muscle and an abnormally long anterior mitral valve leaflet. So again, emphasizes the point that not all HCM patients have thickened hearts. And to make sure that you're really paying attention to that and anyone with any symptoms that you may think of that are HCM patients, so syncope, shortness of breath, family history, if they have that thickened heart, you wanna go ahead and at least Valsalva them, if not do more provocation to make sure that we're not missing anything. And then just to do the comparison between the two, we call this latent HCM. So it's HCM that's sort of hiding unless we've tried to bring it out. They may or may not have some LVH at rest. And then you really need to try to provoke that obstruction. You may not see anything at rest, but once you try some sort of a provocable maneuver, you can bring out that HCM or that obstruction. You may or may not get a high gradient at rest compared to with provocation. And then that same thing with that turbulent color Doppler, you may not see that until after you do that provocation. So just something to be really aware of. I think a lot of people overlook these kinds of cases, but I feel like we see them more and more every day. And so just be aware of those. Thank you.

Hypertrophic cardiomyopathy

Athletic heart

Hypertensive heart disease

Amyloidosis

Latent HCM

Ventricular remodeling

LVOT obstruction