 Thank you, Boel. And thank you, Nat, for a wonderful talk. It's always a great opening session for the conference. And we'll touch on some of the themes that Nat raised as well with these two cases here. So as often happens with aortic insufficiency cases, the primary indication for surgery is not necessarily that related to the direct severity of the AI as is measured instantaneously, but to some of the related pathology or secondary morphologic changes that happen as a result, such as ventricular dilation or aortic aneurysms. And these two cases kind of further illustrate that as well. I have no competing interests with respect to this presentation. So our first case is a young patient with Marfan syndrome, chemopinetic differential diagnosis that Nat put up for aortic aneurysms. She was diagnosed as a young child after her mother passed away quite suddenly, unfortunately, in her 30s from aortic rupture. And she'd been followed since then. And she was known to have an aortic aneurysm that was followed with serial imaging. And about three years before coming to us, it had reached 46 millimeters. And she was taken to the OR for an attempted valve sparing repair. Unfortunately, this had to be abandoned because she had pretty severe Pectis and the exposure was very limited for the surgeons. So they basically closed everything up and consulted the surgeons here. The recommendation was to actually send her for a ravage procedure, which is a modified version of the NUS procedure, which you may be more familiar with. But the ravages, from what I understand, use more commonly in adult patients because for the NUS it works best when it's done on young patients who are not, whose bones aren't fully developed yet. So she had the ravage procedure done and had the bars in for a few months before coming to us. And the bars had just been removed a few weeks prior to her OR. Otherwise, her prostate was significant for some of the common comorbidities of Marfan syndrome, including mild asthma. So her pre-op evaluation included some CT, ECHO, and angiogram. She was asymptomatic from a cardiac functional perspective. And her aortic root now was at 55 millimeters. And looking at the trend of her size measurements over time. So starting from when she went for the first OR three years ago to when she came to us, to the OR here, you can see why 50 millimeters is often the criteria that threshold for operating on these patients. Because you can see how the growth of the aneurysm goes from a fairly linear trend to suddenly becoming looking much more exponential after that. So not all patients obviously follow this exact trend, but she was a good illustration of why that number is there. The other finding we had in her pre-op imaging, which I'll some of which I'll review, is that she had annual dilation and prolapse of the mitral valve with only mild MR. So the question was whether we should fix this or leave it. She's a young patient. You don't want to replace the valve, but it may be repairable. And obviously the reentry arrest for a restronomy in this patient will be very high if we leave it. And she has to come back to the OR a few years and a few years time. Her LB function was preserved and there was no CAD on the angiogram. We had some of her external transoracic images on our system, so I'm just going to go through some of those. She has some atrial enlargement related to the possible for the elevated pressures of the AI because she didn't have a lot of MR. Her ventricle was definitely dilated. Here the diastolic diameter is measured at 5.4 in the peristernal long axis view. Looking at her function in the OR, she had a fairly typical sort of bulb or globular LV. Now our image is a bit foreshortened as well. And as I pointed out in her talk, you kind of get a fourth chamber where the fourth chamber is the aortic root. And you kind of see that here as well on the left. And her RV function was reasonably normal. And her LV function was probably well preserved, but you can definitely see that thinning and dilation of the ventricle in this transgastric short axis view. And note that we're imaging at a depth of 10 centimeters. So that sort of clues you in that if it takes that much space to fit the ventricle in. Looking at the aortic valve, this is a aortic valve short axis view in the middle itself, I guess. Notice the leaflets are fairly normal. You have a nice clover leaf shape. You do see a bit of a co-optation defect in the center. And if you look at the edge of the right coronary cusp, you may sort of see a double line in a few frames. So there may be some prolapse there. That double line is a pretty sort of telltale sign. This is actually the best long axis view we had was from her thoracic thoracic, which shows a little bit of prolapse on what is the left or the non on the right hand side. To this image, these leaflets would be reversed from what you're used to from the trans salvageal echo, because the right cusp is at the top here. And we're seeing possibly a little bit of prolapse as well as I think that line you're seeing. Let me see if I can get a laser pointer here. This abnormality here is probably just the edge of the cusp that we're catching. That's the line there. Putting on some color in the short axis. We see that this is both a central jet and what looks like a commercial jet as well between the right and the left cusps. And it's good to always look at your blood pressure when looking at these color droplets. And I'll show a few examples where we're comparing the pre-op trans thoracic to the interop. A trans salvageal echo and what difference the blood pressure can make. So we can go into the summit for deep trans gastric. Again, we see a fairly central jet. Obviously, the goal here would be to ideally repair this valve. And so far, there was a little bit of a concern about the leaflet prolapse, but the valve was fairly normal. And having a central AI jet is sort of a reassuring factor. But you notice that this jet is not entirely is not entirely a central jet. So you have a central component, that's the predominant component, but there does seem to be one area that's going towards the septum here. And that raises some concerns that there might be leaflet, more leaflet damage than we've seen. Looking at measurements of the route on top, we have the trans thoracic measurements from pre-op and the interop measurements from echo from TE at the bottom. And you can see they're generally in fairly good agreement. So for the sentence of El Salvador measurement, we're about three millimeters within three millimeters. And in the trans ophogil, we also were able to measure the diameter, all three diameters. And you can see the significant eccentricity. So they go up the range from as low as 4.4 to over five centimeters. The biggest difference you actually got was in the measurement of the annulus, which was about four millimeters different 2.9 on the trans ophogil. And that's significant because it looked like there was no real annular dilation previously, but the annulus is slightly dilated. Let me look on the TE. Looking at the vena contracta, and again, in this patient, the key decisions did not rely on severity of the AI. But I will go through the evaluation of the severity to illustrate the case of the comparison between the trans thoracic and trans ophogil. I have some good points. So on the trans thoracic, with the blood pressure of 162, she had a vena contracta of six millimeters, which sort of threshold for severe. And if she was coming, if her social indication was the severity of the AI, this would sort of qualify her for surgery. Whereas on the trans ophogil, with the disloct pressure now of 40 instead of 60, we're measuring about three millimeters, so half as much. Obviously, the orifice itself is not entirely circular, and these views are not directly comparable. So some of the difference has to do just with geometry. But it's very likely that this jet, especially if you compare it to the alveoterea, is smaller now under anesthetic conditions. Looking at the pressure half times, again, you see that these are sort of in a moderate range on the trans thoracic, just around 500, but in more or less the normal range on trans ophogil against comparable pressure difference. So again, it's important to, if you can, document the blood pressure at which you're taking these measurements for future interpretation, especially because in the OR, as you can see, the blood pressure can be quite labile. So if you're getting unexpected numbers, it's always good to repeat the numbers under different hemodynamic circumstances. And looking at her descending aorta, we have the pulse wave Doppler in a descending aorta long axis view, and we have some early reversal that's pretty clear, and it looks like there is some late diastolic reversal as well. A lot of times, in a lot of sort of borderline cases, you get this fuzzy signal under the line, and it's not totally clear whether that's noise or how much of it is real, but certainly it's not the very classic severe pattern, which is often fairly unmistakable, but to keep in mind that here the blood pressure was fairly low now, 80 to 90 over 35, and again that can influence the severity of the reversal that you see. So in this case, we have a bit of angular dilation in terms of mechanism, so the cause in her case, to clarify that point, would be her Marfan's syndrome and the connective tissue disorder that that includes, but the mechanism is dilation of the annulus and the aortic root. Her ascending aorta is generally intact. There was some dilation at the STJ and the proximal ascending, but their men are fiora was normal in investigation, so she fits in a sort of between the B and the C category or B and a half. So the decision was to take it to the OR for valve sparing root repair with a 28 millimeter graft and also do a mitral annulplasty and left atrial appendage ligation. Because of the very high risk of reentry, so she had a previous sternotomy for the attempted repair, then she had previous surgery on the sternum for the ravage to repair her pectus, so the risk of reentry was quite high, so they accounted her by the femoral artery in vein and went on bypass before opening the chest and replacing the cannulus to central cannulation for the surgery. Coming off, we have the same imaging issues that I mentioned, so you have the graft material in there and the valve has been resuspended. The leaflets on surgical inspection were found to be fairly normal with just a little bit of thickening at the tip of the red coronary cusp. And here we're seeing essentially no residual AI in this image, and we looked at other views as well, and it was comparable. You see the thickening in the space between the aortic root and the left atrium, that's the graft coming in. And we can see the leaflets fairly clearly. And it's important again, initially coming off pump, the surgeons are often obviously keen to know whether there is any significant AI, because they want to know if they need to go back on pump or not. But at that time, the blood pressure, especially labile, and it's important to repeat these measurements once the blood pressure normalizes as well, because this is reassuring now at this pressure, but we need to look at it again once the diastolic pressure is up in the 60s, 70s, 80s, as well. Looking at the morphology, here it looks fairly good. We zoom in. And this is sort of three good prognostic factors for the durability of this repair. So the first is the co-optation height, which is the actual length of the two leaflets are contacting each other. And there's a good evidence that if this is above four millimeters, the risk of residual worsening of the AI is fairly low, even if there is a trace AI immediately. The other good prognostic indicator is the fact that the co-optation point, the point where the leaflets first come together, is above the annular plane. That makes it a much more mechanically advantageous place to be, because it's not experiencing downward forces. If the leaflets are meeting down here, there would be a constant force trying to push them further down, and that would stress the attachments of the leaflets to the aortic root, and cause a stretching over time and further prolapse. So this is very positive. And the last thing is the size of the annulus itself, which was in this case about 22 millimeters, and an annulus under 25 is also a good prognostic factor. A more dilated annulus, again, typically entails more stress on the leaflet suspension, and more risk of stretching and deformation of the root over time. The mitral annuloplasty was also pretty successful. We've seen no turbulence on the inflow here in the four-chamber view. You see the fairly thickened leaflets there. We don't see any SAM or any LVOT, ex-flow acceleration. And looking at the gradients of both valves, the aortic is amena 4, peak of 10, and the mean gradient for the mitral valve is 2. And the ventricular function was well preserved here. And you can see the ventricular actually looks much smaller now, and it would be sort of convenient to think of this as the remodeling resulting from the repair, but obviously this is just due to the fluid fluctuations prioroperatively, and it would take some time for this ventricle to start returning to kind of a more normal shape. Unfortunately, we also discovered this, which we hadn't seen before, because now that the left side of pressures are slightly lower with reduced AI, this PFO, which we had missed previously, the side of the show itself. So it's always a good idea in patients where you're suspecting elevated left pressures to do a bubble study or a valsova maneuver to check for a PFO. With this kind of visibin fix, it's not going to be a big problem. It's not a very large one, but it would have been nice to fix it while they were in there. So we had tribute residual AI, a good prognostic indicators for durability of the repair, and a good mean gradient of four, and a successful multiranguloplasty. But unfortunately, we missed the PFO. So I'll talk a little bit about pressure half times. You saw the use of pressure half time in the case there. And basically, we spend a lot of time in peroperative echo worrying about the sizes of holes. And we have different tools for measuring holes. And some of them are morphologic measurements like vene contact and plenometry. But a lot of what we rely on, both for historical and technical reasons, has to do with inferences from flow velocity. And that's because historically, we were able to get good Doppler signals long before we were able to get good brightness mode images. And even now, our brightness mode images, depending on the angle and where the structure of interest is, are not high resolution enough for us to get reliable plenometry data. But as the imaging is improving, plenometry is definitely becoming more and more a part of our toolkit. So pressure half time and deceleration time, which are very closely related, are based on the same idea. So if you have two chambers, one with a higher pressure, one with a lower pressure that are connected by some orifice, you're going to get a passive flow from the higher pressure chamber to the lower pressure chamber until the chamber pressure is equalized. And the larger the hole is, the faster that takes place. And the smaller the hole is, the slower that takes place. And again, the model assumes fairly passive chambers. So you're not nobody's actively squeezing one chamber or actively applying suction to the other chamber. And the compliance of the chambers is relatively constant. So as you have volume flowing from the higher pressure chamber to lower pressure chamber, the lower pressure chamber fills up and stretches, and the higher pressure chamber gets smaller. So pressure half time is one way of quantifying this phenomena. Pressure half time and deceleration time are basically two ways of quantifying this. And pressure half time refers to the time it takes for the pressure gradient to go from its initial value to half that value. So for a given size, holy, that's your pressure half time. Then if it's smaller, you're going to have a slower equalization of the pressures. And your pressure half time is going to be longer. So the pressure half time is inversely related to the size of the orifice. But of course, we can measure pressure gradients directly with echo, we measure velocities. And it turns out that in cases where the flow is fairly passive, and the compliance of the chambers in question isn't varying significantly, you can often get a fairly linear profile on the velocity trace. And because we know that pressure and velocity are related by the Bernoulli equation of pressure gradient is 4v squared, having the pressure works out to going from the initial velocity to 70% of the initial velocity. So 30% reduction. We don't have to worry about that this all takes place within the machine. And here's an example that we just saw from AI. And we have pretty nice clean traces. What's important to note that you again, the blood pressure does make a notable difference. So it's not a load independent measure. And you do want to try to make this measurement intraoperatively with blood pressures that are as close to patients resting blood pressures as possible. There's a difference between the trans thoracic and spontaneous ventilated measure of 500 and two measurements, 726 and 627 at the intraop T. And you can see even just on the same trace, it's very easy to get a significant variation just by where you make your click. The other big application of pressure halftime is in mitral stenosis, estimating the area of the mitral valve. And one of the key things with mitral stenosis is that often in the trace, as you get an initial diastolic, this is the mitral trans mitral continuous wave Doppler profile. So you have your e wave and your a wave. And as you get the early active relaxation of the LV, you can get this period of very brief drop, very rapid flow and very brief drop in pressure followed by secondary slope. And it's important to actually use that secondary slope for measuring for estimating the mitral valve area. And so the classical rule of thumb, this is an empirically derived equation. So it's important to remember the units, the pressure halftime is in milliseconds, the mitral valve area is in centimeters squared. And deceleration time is just another way of quantifying the same slope. And deceleration time is always, sorry, pressure halftime is always about 29% of deceleration time just by geometric definition of them. So the MVA formula is 750 over deceleration time or 220 over pressure halftime. But aside from the size, so ideally we want to find measures that vary only with the size of the hole we're trying to measure and are independent of all the other biasing factors. But nothing is perfect and pressure halftime is no exception. And pressure halftime can be affected by really anything that affects the pressure volume relationship of the receiving chamber and less so the source chamber. So that can include any kind of filling impairment such as diastolic dysfunction or enterothoracic or pericardial pressure, for example, from pericardial effusion, high ventilatory pressures, or even just positive pressure ventilation. Anything that enhances the filling, so we saw at the beginning of the from mitral valve stenosis, whether from the high gradient in the original chambers on the left atrium for mitral stenosis, or the active diastolic suction, you can get an initial higher gradients, dilation of the downstream chamber will increase the compliance of the downstream chamber, so that'll give you a longer halftime. So it's important to kind of think about each of these and think about the direction in which they would affect their pressure halftime. So filling impairment generally would lead to faster equalization. If you have a more rigid receiving chamber, the pressure in it is going to equalize much faster, so you get a shorter pressure halftime. And that's going to make your valve make your air deconsoficiency look more severe, but it's going to make your mitral valve stenosis look less severe, so a bigger mitral valve area. Filling enhancement will potentially shorten the early pressure halftime, which is why it's important to mitral stenosis to measure the secondary slope. And dilation of the downstream chamber, such as you will see potentially in chronic AI with LV dilation, will actually lengthen your pressure halftime and lead you to potentially underestimate the severity of the air deconsoficiency. And of course, any other source of flow into the chamber will affect this relationship. So if you're measuring the mitral valve area and you have air deconsoficiency, then you're going to get a shorter pressure halftime. Now one question is, why can we only use this for AI, MS, and less commonly for PIN, tricuspid stenosis? Why not for the other legions? Why is it, why can't we only use this to measure some or versus and not others? And that has to do with the profiles of the flow. So you notice that any situations where we're using these are where we're measuring dystallic flows, but systolic flows have systolic pressure gradients that are often parabolic. So this is the pressure gradient that drives aortic stenosis. So on top you have the ventricular pressure tracing. On the bottom you have the aortic pressure tracing. So you can see how it's the parabolic driving pressures, similar to from mitral stenosis, from mitral regurgitation, sorry, between the ventricular pressure and the atrial pressure. But for AI and MS, they have these fairly trapezoidal pressure gradients between the left atrium and the left ventricle and dystalli and the aorta and the left ventricle. So the first question is, how does significant aortic insufficiency influence assessment of mitral stenosis severity with pressure halftime? Does it lead you to overestimate it, underestimate it, or does it not make a difference because it's fairly low-independent? And again, we'll cover these with an explanation at the end. And for the second question, the evaluation of AI, is the increased enterothoracic pressure from positive pressure ventilation likely to increase pressure halftime and deceleration time, decrease them, increase PhD but decrease DT, or decrease PhD and increase DT. So moving on to the second case, again, another case where the patient presented with AI but the primary indication for surgery was not necessarily the severity of the legion itself. This patient was 65 years old and asymptomatic but hasn't been followed by a cardiologist because of the murmur and had been referred to the surgeon because he was found to have a moderate reduction in his LV function and the cardiologist was getting concerned about the dilation of the LV. His past history was otherwise significant for hypertension and a remote bout of infection undercarditis. And he really did not like the idea of having a prosthetic valve at all and being on blood thinners. So he had an angiogram that just showed moderate circumflex disease and then he had a pre-op transtheracic. And you notice that we had to depth of the image has to be 19 centimeters. And again, you see the fairly classic or globular rounded ventricle. So the apex is not pointed there, which definitely suggests ventricular dilation. And looking at measurements, we see that the internal diameter in Dastille is 5.9 and the Dastille is 4.9 with a pretty very large end diastolic volume of 283. And we'll look at the normal ranges for these in a moment. But a fairly preserved ejection fraction, although this number is so large that it raises some doubt about its accuracy. And if this number, if the EDV is overestimated and the ESV is measured fairly accurately, we might have an overestimate of the ejection fraction. So it's always very helpful with, if you have access to pre-op echoes to actually look at the images themselves and not just the reports. So comparing this, the guidelines from the chamber quantification by Zogby, the internal diameter in Dastille is 5.9. So that's just the upper limit of normal. But you can see that end diastolic volume is twice the upper limit of normal. And this is the end diastolic volume estimated just from the 2D diameter. And you can see the huge difference between that and this biplane measurement, which is why measuring three-dimensional things with a one-dimensional measurement is not great. Obviously, historically, this is all we had technology-wise, so it was quite useful. But really, we should not be relying on one-dimensional measurements as much as possible. And you can see the AI jet there hitting the anterior mitral valve leaflets, an eccentric jet, suggesting that the chances of repair may not be very high. A pressure halftime in the moderate range, 363 milliseconds. And this is some full reversal in the ascending aorta. And you can see there's definitely some early high reversal and then hold diastolic pattern. So we're probably most likely in the moderate AI range. There's no significant stenosis of the valve. And this is the aortic valve VTI ratio. So the ratio of the VTI from the aortic valve, 27.3 to the one taken from LVOT, which is the average of these about 25. So remember, in severe aortic stenosis, that ratio is about 25%. So it's a 4 to 1 ratio. Here, the ratio is 80%. And you can see the VTIs are quite close. And this is the range for pressure halftime. So 2 to 500 is medium. Less than 200 is considered severe. And under 500 is either normal or mild. So the patient is asymptomatic. He doesn't want a prosthetic valve. So what is the indication for surgery? What's the natural history of this if we leave it? And the best that we have is this one by Benota's side of the guidelines as well. And this is sort of a curve showing the percentage of patients asymptomatic with normal LV function. So this is not survival. These are patients that drop off in the asymptomatic patients. There's a couple of sudden deaths. They followed 104 patients here for 11 years. And you can see while there's sort of an early drop off around two years, people will become symptomatic or their LV function becomes visibly impaired, get another plateau, and then a gradual drop off from six years onwards. While this is not great, it's not catastrophic. If this is a survival curve, obviously, we'll be much more concerning. But the patient's LV is quite dilated. He is already having mild systolic functional impairment. And the AI is at least moderate. So after extensive discussion with a surgeon, they decided to obviously proceed to operation. Otherwise, we wouldn't have the case. Looking at the ACC guidelines on management of VHD and the criteria, this version kind of falls into three possible categories because his EF is around 50%. And by dimensions, we could sort of currently monitor this patient or we could perform an AVR. So it doesn't really help us get a strong answer. So this is in what's to proceed with surgery, with a valve sparing repair, if possible, with a bioproposthetic valve as a backup. There's some initial images. So the function is well preserved. And in fact, it looks a little bit better than the transtheraistic. So I'm going to set up a long axis view on our short axis view. Now looking at the valve itself, there are a couple of immediate concerning signs. So we have a zoom of a parasympathetic long axis view with an x plane through it. And we have this unexpected anomaly here of the non-coronary cusp until we remember that because we're actually x-planing from 120, this view is reversed. So the non-coronary cusp is actually this one. And this is just our left coronary cusp and the left main coronary artery. On most machines, you have the option of reversing this. But always whenever you're looking at x-plane images, they're quite useful. It's very useful to actually scan through and know where your short axis image is coming from in the long axis view. But just keep in mind that the image is flipped. So we see the kind of double line here on the right coronary cusp. And you can definitely see there's a prolapsing segment through the valve, which doesn't increase, looks bad for our chances of repairing this successfully. And zooming in again, you see the same thing. And obviously in the patient with a history of endocarditis, this is likely to be related. The AI jet harbor is largely central. So that's reassuring. And the other leaflets look fairly intact. So there is some hope. But in this view, we have to say that even though the jet source is central, it's fairly eccentric and it's hitting the anterior mitral valve leaflet. Looking at the dimensions, the error group dimensions are fairly normal. There's a mild dilation of the ascending aorta and pretty good agreement between the transsterotic and transophageal views. But then there's this. So this is why you should always be careful about your LVOT diameters. So on transsterotic, we had a measurement of 2.6 centimeters, which yielded an LVOT area of 5.3 square centimeters. But in transsterophageal, and both these measurements look pretty reasonable, we got an LVOT area of 2.86. So almost half. And of course by continuity equation, which one of these would yield a higher aortic valve area? Because one of the concerns with these valves that you have to assess as well as whether they're stenotic. And obviously with one of these measurements, we're much more likely to find the valve stenotic than the other. And the lower your LVOT area is the lower your AVA is going to be for the same VTI. So we're much more likely to find aortic stenosis with this LVOT area than with this one. Looking at the pressure halftimes comparing the transsterastic and transophageal, again, we see a notable difference with the moderate range on the transsterastic and kind of the normal or mild range on the transphageal. Again, both with good traces. I didn't have the blood pressures for these, unfortunately. And the floraversal that we commented on previously, but in the OR we're actually not seeing the floraversal. So we're just seeing some early floraversal and this is but no prolonged floraversal. So also important to note that this is in the ascending aorta and this one was in a descending aorta. So the further downstream you see floraversal, the more likely that is to represent severe disease. So in this patient we have some prolapse that we saw and an inspection of the valve there's actually also a perforation of the leaflet. So we have a combination of sort of 1D and type 2 here. And surgeon described the valve in the left the non-coronary cuts were fairly normal, which was the same as we saw, but the right cuts had a large perforation with loss of substance. A patch would be needed to reconstruct this valve and they deemed that a hangover valve would be more durable for this patient who was her early 60s. A delta-decoronary bypass graft to distal circumflex and ended up putting in a hand clock size 27 bioprosthetic, which is the one on the right there. And coming off we have a pretty good function of the valve. There's maybe a couple of pixels at 12 o'clock, but nothing significant. Let's proceed to look around and again looks probably good in the long axis view. A little bit of acceleration on the inflow, which is not unexpected, but we'll measure the gradient. The gradient's fairly reasonable. Now with gradients again oftentimes immediately coming off pump. Ionotropes have been given in the patient's hyperdynamic. So you may have gradients that are higher than they would be under normal conditions. So if you're getting very high gradients initially, but everything else looks normal with the valve, it's good to come back when the blood pressure is more normal and reassess that. But the patient was quite unstable and requires estimating doses of ionotropes. And they found on ECHO that this is actually without any pacing that there was some echinacea of the inferior wall and hypokinesis of the inferior wall. So they put in this device, which is an enteriotic balloon pump. And there was not any significant improvement immediately. So the patient, they dopper the graft. The graft was intact and the patient was taken to the intensive care unit. The enteriotic balloon pump was removed after two days and unfortunately there was no significant improvement in the LV function. So he had a trans-rassic echo at pulse update 5 and it was discharged at pulse update 10. The pulse update 5 echo showed a EF of 38% and pre-op we were up to 50%. Obviously the POD5 is still fairly early, but this is definitely concerning. And of course, first of all, he was really keen not to have a mechanical development beyond lifelong anticoagulation, but he ended up leaving the hospital with atrial fibrillation and warfarin. So in some cases, we clearly make people better. In other cases, the results are much more ambiguous and we have to wonder. But wonder is the thing put the images side-by-side of the trans-rassic echo pre-op and post-op. So the one that was reported as 51% ejection fraction and the one that was reported as 38%. I'm sorry, this loop is not working properly. But it turns out that they actually don't look that dramatically different. There is definitely some abnormality here in the inferior wall that wasn't there before. This is not both off inotropic support. So it may be that the ejection fraction initially was actually worse than we'd appreciated, although in the interop images, the function was quite reasonable. So some key points. Basically, measure and calculate with humility. Always remember that assessment of severity is quite limited in the operating room because of all the hemodynamic changes. But fortunately, in most cases, decisions we have to make in the OR are related to mechanism and much less so to severity. Try to document the blood pressure and measurements on your gradient measurements and any severity measurements when you can. And again, be mindful of how these change with all the hemodynamics, especially coming off pump at the end. Review the pre-op imaging if you have access to it. It's very educational and I definitely learned a lot by going through them in detail with this case. And the center operate on asymptomatic patients is often quite challenging, even if they're meeting all of your evidence-based guidelines. Thank you very much. That's a fantastic presentation and the standard is absolutely amazing today to start off this morning. I hope it stays that way. And does anyone have any questions? I'm just going to open up the Q&A. So Andre Dino, again, is asking, in situations when we observe discrepancy in AI between pre-op TTE and intra-op TEE, are there any rule for dynamic testing, i.e. increasing the blood pressure like we can do for MR? Derek, definitely, I wasn't able to actually find multiple images of the same measurement being taken at different blood pressures intraoperatively, but certainly being able to achieve at least blood pressures that are comparable to the awake state will give us a better indication. It's not perfect because there's are so other changes, such as changes in ventricular compliance related to positive pressure ventilation, for example, that we can't compensate for. But at least anecdotally, it does seem to be helpful to increase the blood pressures. There's a question from the House and not the Senate. I think, was there a conduction defect in this patient? A conduction defect in this operation? So in the second patient, the patient went on to develop azure fibrillation after two or three days in the ICU, although it was proxiesmal because on the day five post op echo, the patient was on sinus. There was an interventricular conduction defect. We have a number of ex fellows in with a few questions. So we've got Floren from Quebec saying, to be considered significant hollow diastolic floraversal, does it need to reach 20 centimeters per second at end diastole? Actually, I can't remember the answer to that. Yeah, I don't know either. My sense is there's a lot of variability in terms of the velocities that you measure in the descending order. And I wouldn't be surprised if you won't achieve 20 centimeters and still have significant AI. I'm not sure if it's more relevant to the proximal descending order with trans thoracic where you're probably going to be a little bit robust and get a 20 centimeter change. We've got a question from Yanis, who's our ex fellow who's in Kingston. Hello Azad, would you, how would you troubleshoot the LVOT measurements 3D MPR? So certainly, if you're able to do a 3D MPR, that would be the best option if you have good enough images and the time to actually do that, because then you can actually measure the LVOT cross sectional area directly by plenometry and account for the fact that it's not circular, instead of having to estimate the area just based on a diameter and the assumption that's often false, that it's a circular cross section. There is some interesting discussion about where to measure the LVOT diameter as well. And I didn't have time to dig into this in more detail. I've typically measured it at the narrowest part of the LVOT within a centimeter of the valve and tried to get it sort of to be as close to the point where I'm measuring my pulse wave Doppler on the argument that if that's where I'm measuring the pulse wave VTI, I want to be measuring the diameter at that point. But there seems to be better correlation with trans thoracic echoes under spontaneous ventilation, if you measure the LVOT diameter right at the level of the valve itself, which mechanistically doesn't make much sense to me, but in terms of the numbers correlating, that seems to correlate better. And now we've heard, we're hearing from the legend, really, Nair Yusuf over in Hamilton in here. So he's saying, hi Azad, thanks for a great presentation. What views do you use to measure for LV dotitation? So in the trans thoracic, they use the apical four chamber view and two chamber view and use the biplane. So the same views you would use to measure ejection fraction. You do anybody using biplane, you can measure the endostolic volume, if you're doing it with a Simpson's method. If you're measuring it just linearly, that classic as he's a parasternal short axis, and that on T, I would say the most reliable measurements would be from your four chamber view and two chamber view again, similar to where you would measure your EF. And obviously, if you can use X plane to make sure that your four chambers really going through the apex that would improve the accuracy of your image. Hopefully soon we'll have automated tracing of the cavity, so that a lot of these things will be much faster for us to do in both in biplane and in 3D. And Marcin Wasiewicz is asking, does velocity of AI need to reach four meters per second to apply the pressure halftime method? Not that I'm aware of. I will again call a friend on that one. Does anyone else aware of any low-rend limitation on that? Any of the panelists? Yeah, I think four meters is sort of the minimum requirement. It also speaks to alignment, because a lot of times with trans esophageal, it's very difficult to get good alignment and we take suboptimal tracings. So I think if you can get good alignment, you should be able to get a reasonable four meters per second. But the other thing to remember is there's so many factors you should correctly point out that will influence the pressure difference between the left ventricle and the order. So you may not be able to get four meters per second all the time, but I gather I think it's supposed to be where you're supposed to try to get it. And one point with the alignment is that you want to really align it with the jet itself. And if the jet is eccentric, ideally you want to get it aligned with the main body of the jet and not necessarily the long axis of the order itself for an eccentric jet.