 Next in the agenda is Dr. Robert Burke. Dr. Burke is a practicing cardiologist in Scottsdale, Arizona. He's with the Honor Health System. He had gone to medical school in RWJ, completed his residency in internal medicine at Mayo Clinic Rochester, came back to Arizona, was chief resident down here, and did his cardiology and echo imaging fellowship down here. His interests include cardiac imaging, especially with structural heart disease. And without further ado, he will be talking to us about echocardiographia and strain imaging in cardiac amyloidosis. Thank you, Dr. Burke. Well, good morning, everybody. And thank you for having me here. Dr. Dev, Dr. BJ, thank you again. So cardiac amyloidosis and echo, I think that we've all heard about this before and we're relatively familiar with the concept. I think that echo has been viewed as the, generally the introduction and primary screening tool for amyloidosis going back for pretty much as long as we've been doing echo. We do have guidelines that actually reflect this and we'll go through this very briefly. I think this is probably the most important paper that we have to look at what we're supposed to be doing in clinical practice. So again, the algorithm here, you've actually seen this before. We're not going to go through this again. Clearly, we all understand that this is incredibly important and that we need to have echo as a primary tool to determine whether or not somebody should even be evaluated for possible amyloidosis. So recommendations again, I'm not gonna read through this. You all seen this a couple of times before. So consensus recommendations for multimodality imaging and amyloidosis. And realistically, there's gonna be a lot more than just echo, but given the fact that echo is relatively inexpensive, it's very readily available, it will still remain the primary tool from an imaging standpoint to say, is there a problem or is there not a problem? Again, I'm incredibly biased because I'm an echo guy and I anticipate that everybody's going to love the echo and start to use that as the way to really help to differentiate what's going on. So basic assessment is the LV thick. Do you have an increased LV mass and low-voltage EKG? We've already heard that that's not 100% and it's not going to be something to exclude us. Atrial enlargement, incredibly important. For those times when somebody does have a transesophageal echocardiogram, looking for evidence of left atrial stasis or smoke, particularly within the left atrium, that should definitely elevate your pretest probability or suspicion for possible amylidosis, particularly in the absence of mitral stenosis. Somebody has mitral stenosis, that's a different creature altogether and they shouldn't be overlapped and it's pretty easy to take a look at. Valvular thickening, we can comment on that somewhat, but again, valvular thickening in the absence of a reason for it is incredibly important and that's actually been hit on already. Atrial septal thickening and pericardial effusion, as was noted again by Dr. Vijay, a pericardial effusion with no reason, well you might need to start thinking about amyloid as the etiology. So again, standardized acquisition, interpretation, reporting for echo with amyloid, these are the things that we're expected to talk about. Now, for those of you who are practicing cardiologists, now you have to realize at least in part why I'm such a pain in the butt when it comes to structured reporting. All of this is supposed to be on an echo report per IAC. None of this is unusual. This is all inherently there. One comment that I'll have here is myocardial echogenicity and saying that sparkling or starry night appearance to the myocardium. There's a caveat to that one and unfortunately a lot of what we have historically relates to fundamental imaging. So now that we use harmonics in the vast majority of our studies, we get more of that sparkly or hyper refractile texturing to the myocardium and it doesn't always relate to amyloidosis. So we need to just sort of take a little step back there. I know that I've got a colleague of mine who likes to sting starry night every time that he thinks that something's going on with amyloid but that's not always the case, particularly with types of imaging that we use from a technology standpoint. Atrial size, septum, effusion, we talked about that stuff. Again, anytime that you're starting to see diastolic dysfunction in the absence of a reason, this is not a hypertensive heart, they don't have a history of terrible hypertension. You really should perk up your ears a little bit more to say that there might be a problem there. Again, a couple of things just from a very basic standpoint in this panel A, you can see that there's thickened myocardium. It does have a little bit of hyper refractile or starry night type appearance. You can see that there's a little pericardial effusion. You can see that there's overall thickening. So this all fits. Now, do we see this commonly? Yes, we do. Do we often blame it on things like, well, there's renal insufficiency, it's a kidney problem, they're gonna have hypertensive heart disease. Don't worry about it too much. The overlap there is still significant and we need to be mindful that just because somebody has hypertension and kidney problems doesn't necessarily get them off the hook and the underlying etiology could still be amyloid. So again, thickening here, as you can see with the white arrow, thickening of that anterior mitral leaflet. We see that and we see it quite a bit. Again, there's a caveat with this one that I would say the more we're going with harmonic imaging, the more we're going with lower dynamic range or compression, the more likely you are to end up with thickening of structures that's somewhat spurious. So just be mindful of that as an etiology. The yellow cursor here, what that's looking at is thickening of the interatrial septum and that's what we had spoken about before. So echo assessment, functional assessment, elevated filming pressures, restrictive physiology and decreased strain. So tissue Doppler, the 555 sign out, I don't know if you guys are familiar with that or if it's just an echo geek thing, but all the tissue Doppler velocities being less than five centimeters per second, that's very abnormal and that tends to correlate very well with restrictive type inflow patterns because your ratio tends to be with your EE prime in that 20 plus range and you start getting it 25 or more, that really pushes toward, this is restrictive physiology, Dr. Steadley knows this better than I do and it's just one of those things that as soon as you see those numbers, something's wrong and you really want to have a reason for that and it's just, well, they got high blood pressure and they've got a bad valve. There's probably something else happening. Strain, now, the interesting thing here is that when we talk about GLS or global longitudinal strain, we talk about values less than negative 15, that's a little bit dependent upon the vendor. You don't have to worry about that too much. If it's low and oftentimes these are in the 10 to 12 range, you've got a real problem. That deserves an evaluation. The cherry on top sign is not always perfect but if it's there, it's a wonderful thing. So again, this is our 555 sign. I'm not gonna go into all the echo intervals and when we talk about looking at the cherry on top sign and strain, here you can see that really the apex is spared. It has normal strain parameters and then that falls off as you get through the mid to the base. That is entirely a non-coronary distribution for a problem. Okay, so that's incredibly important. Just keep that in mind. It's not always this pretty. We saw another example of strain where there's gonna be some more heterogeneity and there may be a little bit of basal normal strain. That's not uncommon. Strain imaging is still somewhat technically challenging and it does depend upon whether or not you've got good imaging up front. So there are times when strain, I really can't give you a good strain number and I can't give you a great pattern because you've got intercostal spaces that are incredibly small, we lose segments, that kind of stuff. So you don't have to go and say, well, we couldn't tell it on the strain or the strain looked okay. You still have to keep an open mind. Again, same stuff through here, this section looking at the left atrium and looking at left atrial strain. And again, if you have infiltration of the left atrium, that's gonna set you up for atrial fibrillation. Those values will be lower. Your mechanical function of the left atrium actually drops off. So reporting all this stuff, as far as whether or not we should say, is there any question of amyloidosis? Things that are gonna be very suggestive. Increased LV wall thickness, we talked about that with the relative wall thickness already increased LV mass and mass index, typical strain patterns, the 555 thing on tissue Doppler, atrial enlargement, particularly by atrial enlargement and loss of A wave. So the atrial contraction, the left atrium's not contributing much to filling. That's incredibly important because that is infiltration of the left atrium, goes along with potential for atrial fibrillation as well. That's small to trivial pericardial effusion and pleural effusions that we can't explain.