 for giving me the opportunity to present. It's an honor to kick off the second season of this province-wide initiative, and I'm eager to see how it continues to grow and evolve in the upcoming years. Again, I have to acknowledge the efforts and dedication both Rafael and Fabio, who really deserve an incredible amount of recognition for bringing us together and organizing these rounds. Feedback we've received so far has been very encouraging, and we would love to continue to expand. So please email Rafael or Fabio with any suggestions regarding format or potential topics, or if you know of any other centers that would like to be included. We're going through the accreditation process at present, and hopefully will be CPD eligible by November of this year. So then at least you'll get some credits for attending as well. So I have no disclosures or competing interests, and the focus of today's lecture will be on heirs made during transesophageal echocardiography. Fabio, Rafael, and I will each present two cases in which we made heirs during our role as echocardiographers. When I speak to many of our fellows and they all share a common anxiety regarding the pressures of having to read and interpret critical echoes independently on call during their first years of practice. And I can confidently assure you that you will all inevitably make mistakes in the acquisition, interpretation, or application of your TE images. I would love to be able to tell you that the error is lessened as time goes on, but I think that experience has shown me now that I don't make fewer errors, I just make different ones. But the key is to analyze and reflect on those errors and to learn from them and be open to modifying your practice with critical self appraisal and commitment to lifelong learning. So without further ado, let's get into the first case. So for our first case, you're called to perform an emergent TE for a type E dissection who has become hemodynamically unstable during a T-VAR. The patient is a 76 year old male with no known cardiac history. He presented to the ED after experiencing one day of left-sided scapular pain which progressed to band-like chest pain. In the emergency department, he reported intermittent motor changes in the left lower leg with no sensory changes. Examination revealed an absence of a palpable pulse on the left, lower extremity. He was, sorry, he was hemodynamically stable, but reported intermittent abdominal pain concerning from out perfusion. A STAT-CTA showed a neortic dissection involving the aortic arch and descending thoracic aortic standing to the abdomen. The dissection started in the aortic arch just beyond the left carotid artery takeoff and does involve the proximal left subclavian artery. An intubal defect is seen approximately and the false lumen has a large amount of thrombus with narrowing of the true lumen. Note that what is not captured in the CTA is the arch. He was booked for emergency T-VAR and your culturally after induction before the endovascular stent is deployed. So your first images of TE show grossly normal biventricular function with an estimated LVEF of 55 to 60%. The transgastric short axis view shows hypokinesis of the inferior wall, but no other regional wall motion abnormalities. So transesophageal long axis views show thickened aortic valve leaflets, but no significant AI. The non-coronary cusp appears most calcified, but all the aortic valves appear to be opening or sorry, all the aortic valve cusps appear to be opening freely. The ascending aorta does not show any evidence of a retrograde dissection and the sinuses in the coronary arteries appear intact. Deep transgastric views perform to assess gradients through the aortic valve and Doppler interrogation yields the following measurements. So a max aortic velocity of 1.59 meters per second, a max gradient of 10, a mean gradient of five, but an AV or aortic valve area by continuity equation of 0.93 which is concerning for severe aortic stenosis or critical aortic stenosis I should say and dimensionless or Doppler velocity index of 0.24 which also suggests critical aortic stenosis. Views of the descending thoracic aorta shows a thrombus of the false lumen and a small compressed true lumen. The internal tear was identified in the arch just proximal to the left subclavian artery as was identified also on the CTA. So this brings us to our first poll and thank you to Raphael for helping to set up the polling system and the interactivity. So in the study, one or more errors was made in image interpretation. So please select as many options as you think apply and which part of the study do you think a misinterpretation occurred? I'll give you the next 30 seconds to lock in your decision. Okay, so we have kind of a mixed bag but the majority of people think that error was made interpreting the aortic valve and I agree with that. So in terms of the specific error, the aortic valve is where the misinterpretation occurred but what was the error that was made when interpreting the aortic valve gradient? And your options are incomplete AS trace, incomplete LVOT trace, inaccurate LVOT sample envelope or miscalculation. And here's the images again that you can see to make your decision if we can put up the second poll Raphael. And again, this is multiple choice you can select as many as you think apply. So inaccurate LVOT sample envelope is the most popular choice and that is the correct one. So the error made here is the placement of the pulse wave Doppler sampling envelope during measurement of the LVOT velocity. The first indication that this is the case is the extremely low velocity through the LVOT which should be closer to 0.8 to one meter per second than a patient with a normal left ventricle or at least a normal ejection fraction. Here we see that the velocity or the max velocity through the LVOT is closer to like 0.4 meters per second. The effect of an improperly placed sampling envelope is highlighted in this diagram by the British Society of Echo Guidelines on the echocardiographic assessment of the aortic stenosis from 2021. Flow acceleration occurs as the blood enters the narrow LVOT. The further away from the LVOT that the envelope is placed the slower your velocities will be and the greater the difference relative to the aortic valve velocity. This in turn causes an overestimation of the degree of stenosis or an underestimation of the aortic valve area when calculated by the continuity equation. Although one of the benefits of using the Doppler velocity or the dimensionless index is a non-reliance on the accuracy of your LVOT measurement. As we see in this case it is still susceptible to air if the pulse wave sample envelope is misplaced. So here this just highlights the distance. Sorry, my error doesn't show up on the presenting screen but as you can see on the left side of the screen that the PW sample envelope is quite far away from the aortic valve. To avoid this error, the guidelines recommend placing the pulse wave Doppler sample envelope initially right on the aortic valve which usually results in aliasing as seen in slides A and B here. The envelope should then be slowly moved apically. And as you move away from the valve you'll see a trace with a wide area of density at the apex which represents blood flow through the zone of acceleration immediately proximal to the valve. Sampling here will cause an underestimation of the degree of stenosis. So you don't want to sample here yet. But as you continue to move away the wide area of density resolves and the PW trace takes on its normal empty appearance. And the earliest appearance of this characteristic trace is the correct site for sampling. As we see from our study the pulse wave trace is full and low velocity suggesting the sample envelope is outside of the LDOT which drastically reduces the measured velocity. The patient was stabilized with general measures such as volume, transfusion and pressers and this erroneous finding was reported to the vascular surgery team who did their due diligence in order to follow up echo postoperatively. As we have already deduced the finding of AS was a misinterpretation and the valve was normal on repeat interrogation with low gradients and a normal valve area or at least only moderately reduced valve area. Okay, so that's the first case onto the second and we're gonna be talking about a mitral valve repair. So case two involves a 62 year old female with severe symptomatic mitral regurgitation and atrial fibrillation. She has a history of a long-standing murmur and has progressive fatigue and shortness of breath on exertion for the last year. She's noticed that she has now difficulties with activities of daily living. Her echo showed thickened mitral valve leaflets eccentric MR due to severe P2 prolapse and flail, dilated LV with normal biventricular function, moderate TR, no flow limiting coronary artery disease and a past medical history which is significant for BMI of 42. She stands 5'3 and 250 pounds, atrial fibrillation on the relto and she's had a jaw injury after motor vehicle accident in the past. So initial images show a dilated LV with preserved function as well as a grossly dilated LA which explains the associated atrial fibrillation. There are no regional wall motion abnormalities seen in the trans-gastric short axis view. An examination of the mitral leaflets show thickened interior and posterior mitral valve leaflets characteristic of myxomines disease. There is clear flail of the P2 leaflets seen with an eccentric interiorly directed jet of severe MR. Here's the same valve in the bi-commercial view with them without color and the 90 degrees and 3D images which show the expected P2 flail and this was reported as the mechanism for the MR to the surgeon. Whenever we're doing mitral valve repair, we always look for both predictors of SAM and predictors of post mitral valve or persistent mitral valve regurgitation after the repair. So these static measurements include an interior leaflet length of 3.44 centimeters and they are at a mitral angle of 120 degrees and a CCEP distance of 36 millimeters. So this patient was deemed relatively low risk for SAM post repair and the surgeons chose an angioplasty ring using a physio-sizer meaning that they didn't upgrade or downgrade the size of the mitral ring. So poll number three is what feature of the mitral valve was missed during the assessment and the options are AML tethering, A2 prolapse, P1 prolapse, a P2 cleft, P3 prolapse or mitral stenosis. And while the poll goes up, I will show you the images and a little bit bigger. So a little bit of a mixed bag here. So nothing clear and I think that represents well actually or kind of goes along with the ambiguity that was involved in this case, right? Okay, so having identified the prolapsing P2 as the likely culprit, we proceeded with a straightforward PML repair. Three neocords were placed in each of the enteral lateral and posterior papillary muscles and attached directly to the posterior mitral valve leaflet. All the neocords were attached specifically to the prolapsing P2 segment. There's a size 36 millimeter physio ring and there was good co-optation on water tests. They also performed the tricuspid valve repair, left and right atrial maze and the left atrial appendage exclusion. So we discontinued bypass and we met with the following images. There's at least mild MR with a vina contract that measured anywhere between three and five millimeters on serial measurements. And although we considered accepting this result, the surgeons were not happy and returned to bypass to re-arrest the heart before a complete inspection of the valve could be performed. As we arrested the surgeons asked specific questions about the native valve morphology, including whether there were any prolapse of the A2 or P3 segments. We examined the valve closely and felt that there could potentially be billowing above the annular plane, but no evidence of Frank prolapsed. However, we could not rule out a small cleft between P1 and P2. The surgeons repaired the cleft which was easily identified on closer inspection. So we felt that we identified the culprit and then repeat he showed the following. Clearly things have gotten worse and we hadn't fixed the problem. So now we did what we should have done the first time. I spent a considerable amount of time inspecting the valve while kicking ourselves for going back on in the first place. And here I'll take you through the various views. Mitra valve at zero and 60, which you can see the clear, regurgitated jet. Couldn't really appreciate it very much at 90 or 120 degrees. And then at around 150 degrees, what became obvious was the large co-aptation gap that was the source of the worsening mitra regurgitation. So this was actually like a defect where the anterior and posterior mitra valve leaflets weren't meeting. And this was likely because of this severity of the restriction of the posterior mitra valve leaflet. 3D imaging does not add much in this case, although the color 3D does show the source of the jet originating from the tip of the posterior mitra valve leaflet, which goes along with what we think so far. But complicating this case is that after two prolonged pump runs, the RV has become dilated in showing signs of a significant dysfunction. The surgeons themselves disagreed between themselves or amongst themselves about the best next possible step with one advocating for replacement and the other feeling that repair was still possible. So they turned to you for the tie-breaking vote. And at this stage, what would you recommend the surgeon do to address the residual MR? Would you downsize the ring, appreciating that the patient was a low risk for Sam? Would you release neocourts to the anterior leaflet? Would you release neocourts to the posterior leaflet? Or would you just elect for valve replacement at this stage? I'll put this up so you can take a look while you decide. So the top two answers here are release neocourts to posterior leaflets and valve replacement. And I think that's probably what the main thing that we were deciding between in this case in particular. So we felt that the co-optation gap likely resulted as discussed already from an overly restricted posterior valve leaflet. There were no neocourts to the anterior leaflet. So that was a red herring of an answer. And the idea here or what the surgeons planned to do was release two of the six neocourts, which isn't a major intervention. So we were a little bit of two minds as to whether or not this was gonna work. And we were putting the patient at significant risk, likely if it wasn't going to work only because now we'll probably leave us six or seven hours into surgery. So the idea by releasing the neocourts is you release some of the restriction of posterior leaflet in order to increase the co-optation and close the gap. This was ultimately successful and the MMR was reduced to trace and the outcome was accepted and we left the OR after an eight hour surgery. Despite the long surgery and cardiopulmonary bypass time, the patient did well postoperatively and echo on postoperative day two showed normal biventricular function and no residual regurgitation through the valve. So thank you very much for your attention. We'll pass it on to Rafael for the next two cases. Thanks, Marcos, excellent presentation. I think Fabio has already joined, there he is. You wanna go ahead and do your cases, Fabio? Sure. Hi guys, sorry I was a little bit late. Yes, let me just share my screen. You guys can see my slide? Yes. Yeah, okay. So hi everyone, thank you for being here again. Our second year doing the echo rounds together. So yeah, so just carry on with the session of imaging misinterpretation. So I have no disclosures related to this topic and my objective is actually I borrow some of those from Marcos is basically critical, like do the analysis of the case in which the TEO is used to refine diagnosis, detect new pathology and adjust the surgical plan and assess surgical results. Also do the interpretation of TEO findings in the context of surgical literature and main mostly important that the purpose is for learning improvement through blame-free discussions around improving patient safety and quality of care. So my first case is gonna be around like the main topic is gonna be around refined diagnosis. So our first patient is a 54 years old male has a past magical history of mother to severe MR. Interfibrillation, COPG, reflux and anxiety. So his pre-optic TE shows normal LV size, normal LV function, the same for the RV. Severe pulmonary hypertension, RV SPF around 80. Also a severe micro-regulation, micro-regulation secondary to severely prolapse and flay OP2 segment. The auto valve seems to be normal and the pre-op plan is mitral valve repair slash replacement and plus or minus dracoster drink. These are first image on TE that we did on that morning, the long axis view. You guys can see the mitral valve is disease. The posterior segment, actually the P2 segment of the mitral valve is prolapse slash flail. Here we have the same picture pretty much with color and although it's very clear patient has severe mitral regurgitation based on the 2G and on the color flow. We actually did the quantification which we got for a piece of radio more than one centimeter. Also the regurgitant volume more than 60 cc per bit and also an airway of more than 0.4 square centimeters which put this patient on the severe mitral regurgitation classification. Also this patient had like a systolic reversal on the pulmonary vein flow. And although the jet was eccentric, we were able to align pretty well and you got a pretty good pretty high velocity jet with a good pretty good envelope. This is the unfossed view 3G. We can see the mitral valve defect is a pretty much isolated P2 segment. We can see the P2 is kind of prolapse and flail and also between the P2 and P3 segment we can see there is a cleft in there that was not diagnosed on the T prior to the surgery. And then comes the first question. The mitral valve prolapse can be associated with what type of congenital heart disease? Oscio primum ASG, oscio secundum ASG, sinus venous ASG, peri-membranus VSG or none of those congenital heart disease? Raphael, please give you 15 seconds. Which one is more associated with mitral valve prolapse? If any, Raphael, I think you're okay now. Yeah, so we have pretty much split between oscio primum and oscio secundum ASG and also 18% of peri-membranus VSG. So the most common congenital heart disease associated with mitral valve prolapse is the oscio secundum ASG. It's associated with mitral valve prolapse and mitral regurgitation. It accounts for 70% of all atrial communications. And why I'm doing this question? Because this patient also had like a small ASG as you can see on this four chamber view with the focus on the right side and with the focus on the inter-atrial septum. Here, the ASG is confirmed on the 3G where you can see the jet coming from the left to the right atrium, okay? We carry on with the examination. We finish our TEE examination and eventually got the normal EF as you can see on the left on the four chamber view. Sorry, on the bike on the long axis view and also a normal RV, although the right atrium was a little bit enlarged. Carry on with the examination, we went to the deep transgastric view and when it did the continuous A to the upper on the aortic valve, we got this pretty like high velocity dense envelope and measuring the velocity and also the gradient across this valve. We got a like a velocity of 3.8, almost four meters per second and it got a mean gradient of almost 30 millimeters of mercury with according to the ASC guidelines, put this patient also on the moderate aortic stenosis range. So, but the funny thing is when this patient had the TEE done a few weeks before, the aortic valve was pretty much normal. So what we did before telling the surgeon before doing anything, so we just went back to the aortic valve, we looked at the aortic valve from the short axis view also on the long axis view and you could tell the aortic valve was opening and closing pretty well. So what was the cause of this high velocity jet and this mean, this high mean gradient? That comes with the pool number two, based on the TEE findings, what's the cause of the gradient across the aortic valve? Patient actually has moderate ASL view to obstruction, patient is hyper-dynamic or there is a micro-urgent jet interrogation. Rafael, let me stop. Okay, so 82% says is the micro-urgent jet that we are interrogating, which is true. It's really important every time we are interrogating the either the LVOT or the aortic valve in patients with especially anterior directed severe MR that we make sure that we are measuring the LVOT or the aortic valve flow. It's not unusual that when you're using the post wave doper or the continuance of doper, especially instead of measuring the flow across the LVOT or the aortic valve, we end up measuring, there's some contamination and we end up measuring the micro-urgent jet. So instead of getting like a low velocity jet, a nice and low velocity jet that is related to the normal aortic valve, we end up getting this high velocity envelope that was not related to the aortic valve, instead was related to the micro-urgent jet. So on this view on the left, we have the envelope related to the aortic valve. You can see the low velocity jet around 1.2 meters per second. And on the right, you can see the jet that is coming from the aortic from the micro-urgent jet, which is a high velocity jet around four meters per second and also a pre-dense envelope. Okay, and that comes our question number two, the answer. We're interrogating the micro-urgent jet and then comes our question number three, what are the common ecopathic features of anteriorly directed MRJET and AS aortic stenosis jet that make them easily to be mistaken? High velocity jets, they are negative, they pick in mid-systole, they lie in the same path of interrogation or all the above. What are the characteristics that make the MRJET and the in patients with aortic stenosis, ASJET that make them easily mistaken? Rafael? Yeah, so the vast majority said all the above, which is true. So all the above, the question number four, let's say the patient has aortic stenosis on top of the micro-urgentation. How can you differentiate the micro-urgent jet from the aortic stenosis jet? The onset of micro-urgentation is during isovolimic systole. The onset of aortic stenosis jet is in the mid-later portion of the QRS. They view morphology to assess the literate mobility, BNC or all the above, which one are correct? How can you differentiate the micro-urgent jet on the aortic stenosis jet? Rafael? Okay, there is a split between G and E. 63% says all the above, which is the right answer and why? So the micro-urgentant jet because the pressure for the LV to overcome and cause the regurgentant jet into the literate is way lower than the pressure that the LV needs to generate in order to open the aortic valve and equalize with the ascending aorta. So the micro-urgentant jet needs a low pressure. So the micro-urgentant jet always starts earlier in the QRS than the aortic stenosis jet. As you can see on this view, we have like the micro-urgentant jet and you compare with the ECG and compare this one with the aortic valve. You can see the aortic valve because the pressure that the ventricle needs to generate in order to eject the blood flow across the aortic valve is much higher. So it starts and peak a little bit later in the QRS. Here we can compare both. On top you can see the micro-urgentant jet. It starts a little bit earlier during the isobalemic systoline because the pressure between the left ventricle and the left atron is way lower compared with the AS jet, which starts a little bit later in systoline. So probably together with the 2G assessment with the aortic valve is the easiest way to differentiate the micro-urgentant jet from the aortic stenosis jet. So this is the true aortic valve jet on this patient. We can see the mean grade instead of being 28 or 30, something like that is way normal is 1.2 millimeters of mercury which is pretty much normal for a normal aortic valve. This patient ended up getting the ASG closure and also ended up getting a mitral valve repair with an annuloplasty ring. Patient came off by pass and did well in the ICU. So case number two, the goal of this one is how we can use TEE to detect new pathology. So case number two, patient 55 years old is female, past medical history. She has a bicoastal aortic valve with a severe aortic stenosis, hypertension, type 2 diabetes, also ulcerative colitis, OSA and elevated BMI and also asthma. She presented to another service, to another hospital in three weeks, history of low grade fever and an intentional 17 pounds weight loss over the last two weeks. So the first diagnosis was pretty much like related to a flare from the colitis but then the cultures came back positive. So she had an initial TEE which showed no evidence of a vegetation or effective endocarditis. A week later, she was deteriorating. She had another TEE that showed vegetation on the aortic valve and also on the mitral valve. Question mark regarding a mitral, chiral mitral valve proliferation and also a fascial mark for the aortic valve to obsess. Because of this vegetation, she had an embolus that was thrown into the LAG and she had a known TMI in the anterior LV wall. On the 19th, 10 days after she presented to the hospital for the first time, she transferred to some mikes. She had another TEE when they saw a bicoastal, when they saw a large independently mobile mass attached to the LVOT side of the aortic valve, severe aortic stenosis with a mean gradient of 47, just mild AI and an aortic root obsess. LV was depressed, yeah, it was around 36% with a small vegetation around 1.4 centimeters in the mitral valve. And she also had mitral to moderate MR. So another 10 days of antibiotics, she was referred for surgery on the 26th and the pre-op diagnosis was endocarditis in the mitral and the aortic valve. And the aortic root obsess, she was in heart failure on that time and also a new set of AFibs. The pre-op plan was AVR plus the Breidman, the construction of the aortic root and plus or minus mitral valve replacement. So this is our first picture. We can see the aortic valve in short and long axis view. We can see the mitral, the aortic valve is pretty much destroyed. You can see this vegetation on the aortic valve and on the right image. We can see a free flow, probably a free flow cavity here that could be like, that could be an absence. With color, we can see there was no AI or maybe just trace AI. And here you can see the four chamber view and the long axis view. We can see the biventricular functions pretty much depressed as we saw on the previous GE. But also we can see on the mitral valve there is something, some sort of vegetation or some sort of mess on the anterior mitral valve leaflet. Patient was in heart failure as you can see on the left. She has some pericardial fusion and some pleural effusions on the right. Now looking at the mitral valve, we can see the mitral valve that is this like a vegetation or tumor in the anterior mitral valve leaflet that is flickering as you can see. And with color, we can see there is an abscess here on the right. We can see that it's flowing diastole. There is some MR and there is also some flow kind of wrap around the left atron, the left atron wall. And that comes the first question. What is the MR severity for this patient? Trace, mild, moderate or severe? Rafael, I think it's okay. Rafael, just for the sake of time. Yeah, so the vast majority of people said severe, 60%. And also 30% said moderate. Okay, so I'll come back to this question. I'm just gonna carry on with the images. Here we see the false view from the mitral valve. I apologize for the stitching artifacts. Here we can see the mitral valve and you can see this kind of vegetation on top of the anterior mitral valve leaflet. Here we can see the 3G from the mitral valve. And I put especially this view, which is not a good one, but just so I'm gonna slow down here the look. Just gonna start and look on this mitral valve here. Let's see if there is any mitral regurgitation. So there is pretty much none or trace mitral regurgitation. But what we see when the patient is in, when we are insisting is this jet here that is coming from the interatroceptome. Sorry, that is coming from the ascending aorta. Most likely a fistula as you can see here, which is gonna be much easier to appreciate on this view here. Here on the right, you can see the long axis view and you're able to see, to appreciate this jet, this fistula coming from the aorta to go into the left atron. The same thing here as you can see, pointing here, the jet here. Actually this patient had none of pretty much none or just trace mitral regurgitation. What you're seeing on this view was not a mitral regurgitation. On top here, you can see the jet coming from the fistula that has kind of wrapped around the left atron wall. So if not the attention, we could say this patient had like modern or severe mitral regurgitation. Eventually this patient had none. So based on all of that, this patient had a reconstruction of the aorta root. Also, she had an aortic valve replacement. They put a biological valve. Also the bribement of the aorta root and patch at the left atron wall and the closing the fistula. So this patient is surprisingly, although surprising came off bypass okay and did well in the ICU. So in summary, these two cases exemplify situations in which one area of interpretation could have led to undesired surgical results and not only a high index of suspicion but also the correlation of findings with the patient history and acquisition of multiple views in different modalities is essential for accurate information while performing the CHE. Thank you, Rafael. Thank you, Lisa. You just wanna stop sharing. Yeah. Okay. And just stop. Hope you guys can see my screen and hear me okay. Yeah. Okay. So here we go. Thanks, Fabio. Thanks, Marcos. My name is Rafael Zamper. Karja can you see the director at Western University in London, Ontario? No conflicts to disclose for the session. Just wanted to acknowledge on a side note I'm very grateful for all the time and effort that both Marcos and Fabio have been investing in this project. I'm very happy to be here. And we promise this second year will be a lot more interesting than the previous one which was already awesome. My objectives here are to present two cases, same objectives from the previous speakers. I'll also use some recommendations from relevant guidelines of ASC, applicable to both cases. So moving to my first case, it's a 73 years old patient with hypertension, zlipidemia, obesity, sleep apnea and CPAP that presented to his family physician's office with chest pain and exertion. Eventually had a stress test that came back positive and was referred to an endocrine that showed triple vessel coronary artery disease and was scheduled to a cabbage times tree with all grafts, arterial grafts coming from bilateral internal mammary arteries and from the left radio artery. And as many of our patients that come from for a cabbage, this one did not have pre-op T, just the angiogram TT, sorry, just the angiogram showing a normal LV function with no AS and no MR because that's what they can conclude from the injection of dye into the left ventricle. And so I start the case with the fellow. We perform the TE together and we confirm normal left ventricular function as you can see. And this is a medics of our four chambers dedicated to the RV where we assess RV function. And just want to remind you from the 2015 guidelines on the recommendations for chamber quantification, specifically for the RV function, the recommendations are to use at least one or a combination of the following recommended parameters and they elect six different methods. But when we look to each one of those, we will clearly understand that the topsy and fractional area change are the fastest ones. And once for, for example, for tissue Doppler S prime, you need a good alignment, which is very difficult with a TE, strain and 3D ejection traction. They are time consuming, they need a special software, MPI also either you need a good alignment for the tissue Doppler or you will be time consuming during the trans tricuspid and transpumonic valve flows. So usually we do topsy and fractional area change to assess once they are easier and faster. And that's what we did in this case. So to the left of the screen, you see the loop and below the loop you see how you calculate fractional area change. To the top right, you see the endostolic frame with the right ventricular endostolic area of 21 centimeters square. And to the bottom right, you see the endostolic loop frame with right ventricular endostolic area of 13.7, which gives us a fractional area change of 35. And when we use the same view to calculate the distance between the lateral tricuspid valve and the annulus and the apex in both endostolic and endostolic, we can calculate a topsy of 18 millimeters. And that brings me to my first pull to the audience, which is even the echo findings presented a fractional area change of 35 and the tops of 18. How would you describe the IRB size and systolic function? There you go. Okay, so here are the results and there's a mixed bag with trend to normal size and normal systolic function and normal size for their lines, systolic function. So let's review a few things here. First, in terms of size, from the image to the top right, you can clearly see that the apex of the heart is formed by the LV. And that by definition excludes moderate and severe RV dilatation. Now we have to decide if it's a normal size or mild dilatation. So you can see to the bottom left how we can measure the right ventricle and endiastaly and to the top left to see the cutoffs. So as we measure topsy, the endiastolic distance between the tricuspid valve annulus and the apex as being 81 millimeters, the distance highlighted in yellow, which is basically the length of the RV would definitely be less than 81 and this would make our RV normal size. And when it goes to function, here are the cutoffs. So we have an abnormal borderline fractional error change in a normal topsy. However, when you go to the guidelines, this guideline on RV or right heart evaluation adults from 2010 shows that from all criteria that you can use to assess echocardiographically of the RV, the fractional error change is the one that correlates better with the gold standard for right ventricle ejection fraction that's the MRI. So I would kind of trust more the fractional error change than the tops. And that's why I would say that this patient has borderline systolic function. So we just came up to the conclusion that this patient has a normal RV size with a borderline systolic function. And this is, these are other images from the same patient just showing the tricuspid valve with minimal trace tricuspid regurgitation and a very faint TR jets. Some people might even consider mild TR which would not be wrong. And when you see a CVP of 12 with a peak gradient of 16, you come to the conclusion that the RV SP is 25 to 30 and this patient doesn't have pulmonary hypertension. So I leave for a break and a few minutes later, the fellow calls me back to the OR. And at that point, they are still harvesting the right IMA. The, there's no major bleeding. And the fellow tells me that this patient has been progressively deteriorating and high-potensive. So now I see a patient in shock, pressure, blood pressure is 70 over 35 and also patient static cardiac with a heart rate of 120. CVP is high in the 2530s and the fellow tells me that the RV failed and it's now refractory to any volume or pharmacological interventions. So okay, so let's see the images. And this is what I can see in the same four chambers revealed that I presented before. The RV is clearly struggling at that time, there are inotropes by the vasopressors, everything is in high doses. And I can also see a significant TR jet that was not present there before. And when I interrogate the jet, now it's a different scenario. I can clearly see that with the CVP of 28 plus a peak gradient of 37. Now the RV SP is 6570. So something is not correct with this patient and that brings me to my second poll, which I will put it up for you right now. What is the cause of the RV dysfunction in your opinion? Is it acute pulmonary hypertension, crisis? Is it a massive B? Is it RCA schemia with RV failure? Is it an extrinsic compression of the RV? Okay, I'll end and share the results. So it's kind of splitted in between RCA schemia and extrinsic compression. Stop sharing, moving on. Okay, so I want you to pay attention to this area pointed by the red arrow, which seems to me something extrinsic to the heart, compressing the heart. And again, with a steel frame here, you can see this kind of a bulging area with a dark shadow underneath. And that's when I think about what they're doing with the surgery, what's the surgical phase? And we don't do bilateral ITAs very often. So when we do ITAs, we usually do left ITAs. And so the retractor in the chest bone, in the sternum, pushes the right side of the chest down, which compresses the right lung. But when they are harvesting the right IMA, they just flip the retractor to the other side of the chest. And now they're compressing the left chest, left border of their sternum down. And that's very close to the RV. So that's what was happening with this case. So it was not an RV failure because of acute pulmonary hypertension crisis or ischemia. It was simply the retractor compressing the right ventricle. And kindly, we request that the surgeon release the retractor and this is the image we see right away, which now has sort of a little bit more dilated because there's more volume given to the patient. But function-wise, I would say that it's back to the baseline. It's probably normal now if we repeat the measurements. So this is a cause of the hemodynamic collapse, the intrinsic RV compression by the retractor. And this is the RVSP now with an RVSP of 25 after the release of the retractor. Moving to the second case, it's, again, a very similar patient, but now 81 years old. Hypertension is epidemia type 2 diabetes. Family physician, positive stress test. Again, angiogram found to have triple vessel coronary artery disease. Scattered for cabbage times three. Now with the left IMA and two venous grafts. No pre-op TTE, but that angiogram showing normal LVEF, no AS, and no MR. So this is a senior fellow working with me now. I'm just observing. Lines are in, patient stable. I leave the OR to see other things and to let the fellow work independently. And he calls me back right away saying, hey, you know what? I think I found something in the aortic valve here. We might need to replace the valve. I'm interrogating the aortic valve on a deep transgastric, not a deep transgastric, but a transgastric long access view, as you can see at the top of your screen here. And I see this AI jet. It's a very dense jet. So it's compatible with severe AI. And also when I calculate the pressure half time, I find it's 65 milliseconds, right? So based on the previous image, what would be the severity of your AI? And this is what I'm matching right now. Severe, moderate, mild, or no AI. Let's stop it now and share the results. It's kind of a split between severe and no AI, which is very odd. It's either, we usually say mild, moderate, moderate, severe, but now it's either severe or no AI. So based on the guidelines, just taking into consideration the pressure half time, which is a qualitative method, we would see severe AI, right? We would say severe AI, but is there severe AI? Well, let's review this. I started reviewing the images and I see a patient, as you can see with a normal left ventric work function, apparently normal RV function based on the four chambers as well. And I see a 3D of the aortic valve, which attracts my attention because it's pretty solid that the cusps are coming together. And I can even see a Mercedes sign with the 3D of this aortic valve. And then when I see these views of the long axis zoomed in the aortic valve, I don't see any AI as well. I was just rushing to see if the... Because it's a cabbage, it's different surgery. If you have to replace the valve, they have to think about the cannulation and cardioplegia. So we have to answer this question very quickly. And quickly, after just reviewing this image, I said, hey, just carry on. There's nothing wrong with the aortic valve because it's clearly co-opting nicely and I don't see any AI just. So I think I look at the trans-classic long axis view and again, there's no AI. But when I see the continuous wave Doppler, this is what the fellow was considering AI. And then immediately I see a very low velocity and I know what's going on. So when I pause this loop to your left, to the left of your screen and go frame by frame, I was seeing the early diastolic phase. I see this red jet here, which is the cause of this first spike here. But because the alignment with the Doppler is not suboptimal, we cannot see very well this wave here, right? Only if you examine more detail. So this is the A wave and this is the E wave of the transmittal inflow, okay? Just want to bring. So the person in the OR was interrogating the mitral valve, the transmittal inflow and looking at the E wave as a possible AI jet, which is very interesting because Fabio just presented a case which is the other way around. It's a patient with MR that was thought to have AS. So we'll see how enclosed relation these two valves are and when some pathological jets can be confounded. So this is kind of the recommendation to assess AR severity based on the guidelines proposed for native valve regurgitation in 2017. And you can see that they take into consideration structural parameters, qualitative, semi quantitative and quantitative parameters. But when you refer to the ASE recommendations, they are very clear to recommend that you do multiple methods. And when you have conflicting data, then you go to a more quantitative approach to decide in which category of AR regurgitation your patient will be, right? So this is an example of AI pressure have time in a patient with real AR regurgitation that you can see in a bicuspid AR valve with a central jet that is not very wide but I would say clearly mild AI in my opinion. And this is an envelope of an AI jet showing a pressure half time of 400 that fits into the mild to moderate, maybe moderate grade. But look at the velocity very different than the previous one because this represents the gradient between the diastolic pressure in the aorta and the diastolic pressure in the left ventricle. And that gap is usually 60 to 70 millimeters of mercury which can only be appreciated with velocities around three to four meters per second and not one meter per second as I showed. So this is my last question and I'm just about to finish the very interesting question that I created. So based on the image below, I want to know what is the coronary artery perfusion pressure, the CPP? We'll put the pull up and you'll be able to see the possibilities. Give it just a few more seconds and I'll share the results. Majorities thinks that it's impossible to calculate without knowing the diastolic blood pressure in the aorta root. Some people think that this variable, others say is 64, so stop sharing. And this is how CPP or coronary perfusion pressure is calculated. The diastolic blood pressure in the aorta in the senoortic or the aorta root minus the left interchlorine diastolic pressure. To the left of your screen, you see a normal heart where this gradient diastolic blood pressure in the left interchlorine diastolic pressure, it's kind of constant throughout the whole diastolic. And to the right of your screen, you see what happens with patients in severe aortic insufficiency. The gradient is there just for a brief period of time because the pressures they equalize quickly. This gap here could be, of course, this is pressure, but pressure can be converted into a velocities and vice versa using Bernoulli's equation. So this is a pressure gradient here that can be easily calculated if you know the velocities. And this is what it would be like in a patient with myaotai, just the case I presented right now. So the gradient would be maximum in the early diastolic and it would slowly decrease along the diastolic period to the end of the diastolic here. So when you see what happens with our patient, you see that this shape is pretty much the same shape of this AI chat. And so here is a pressure, here is velocity. We just calculate the pressures in both yellow and green boxes here. And turns out to be around three and four meters per second which correspond to 36 and 64. And so the answer to the poll is that the CPP in this case is variable between 36 and 64 millimeters mercury. And that's the end of my presentation. And again, thank you very much for joining today. I don't see any questions on our chat so far. If anyone wants to just jump in and ask questions, please feel free. Rafael. Yes. Hi, hello, this is Hideo. How's it going? Hey, hi there, good, how are you? Good, good. So I have two questions regarding the last presentations. Yes. So the first, I'm gonna start with the one that's the last case. So concerning the bicosperotic valve, I had a case, I think it was Sunday, yesterday, during the weekend, so it was pretty much by myself for the decision making. And same story, the patient came for a cabbage, didn't have a TTE, had only the angiogram. Then with DDTE and we saw a bicosperotic valve with mild AS and mild to moderate AI. Actually it was most of the criteria that we would put her in the mild category. Just one, maybe the vinyl contractor looking a little bit further, it could be four, but it was closest to three, so probably mild. The thing that I'm asking is if it was a bicosperotic valve, I would be pretty sure that this patient did not have to have the valve replaced. But my question is, if you see a bicosperotic valve and you see there's some classification, even though the criteria for grading the valve is mild or maybe mild to moderate, does this change anything in terms of decision made from regarding changing the valve or not? Would it work? How old was your patient? Actually, there was a catch. She was pretty young, like six years old, but he had a terminal cancer, process cancer, stage four. So that also I think played a role in the decision. But my question is, if the valve is by a cospit, should I change anything in terms of the decision making? Because only for pressure criteria and velocity criteria, I would not have dealt at all. Yeah, I would not have dealt. Yeah. Pablo and Marcos can jump into help answer this question too, but I believe that the answer is no, it doesn't change anything. The only one thing in the caveat I would put on that question is that usually patients with bicosperotic valve, they present with aortic stenosis in the aortic insufficiency earlier in life. So if you see a moderate AI by cuspid aortic valve and the patient is 62, 63 years old, maybe you should address the aortic valve, which you would not if the patient, let's say it's a 75 years old, coming for a cabbage with a tracuspid aortic valve. The only one thing that I know that it's pretty clear cut off for patients with bicosperotic valve is when you're replacing the valve, take a look at the same aorta. If the same aorta is more than 45 millimeters, you should replace the ascending too, which is different criteria from cracus aortic valves too. I don't know if Pablo and Marcos have different opinions. I agree with what you're saying, Rafael. I think, you know, given just the natural history of bicospid aortic valve disease, you would not necessarily be able to predict that this AI is gonna worsen over time. And if, especially what you're saying with the patient's prognosis and other medical comedities, I would think just do the cabbage and get out. Excellent. Good, great. Yeah, yeah, I agree. And also if the patient, for example, if like in the next few years, like even with this history of cancer, he deteriorates and he needs like something on the aortic valve, they always have the option of a tavi nowadays. So I wouldn't do anything. Good. Another second question, right? The second question is about RV function. So do you routinely use RV strain for RV functional measurement prior to, you know, every surgery? And if you do, which one, global strain or RV free wall strains? Are there any differences between them? Yeah, that's a very good question. I personally don't use RV strain. I do from time to time, just for educational purposes with the fellows and trainees. That's my opinion about the RV. I think that the septal wall, it's basically LV, so I don't take it into consideration when I do strain on the RV. And I think that there are some recent papers on that saying that the free wall strain is the most important one when you're addressing the RV. And the other thing is, if you think about global strain, well, the RV wall, if you take the lateral and then the anterior and then the even Gabriel, they're different walls, right? So I think it's more important the basal RV wall than the others. And that's usually when you find the highest strain or the lowest, minus 35, minus 40. So I think that RV strain is still an uncharted chapter of echo. I'd like to see more evidence to use it and guide my decision-making. But just to answer your question, no, I don't do routinely RV strain only for educational purposes. Okay, thanks. I don't know if Fab and Marcos have different experiences. Yeah, our software here doesn't have the RV strain software, like the dedicated RV strain. When we use it, we use the LV, which is also doable, but we don't have. And like I said, we don't use very often. It's easy to use, but like you said, it's like we still have a long way to know exactly how to interpret. So we don't use it. Same situation at TGH, the machines don't have the software. Sorry, the anesthesia machines don't have the software, the cardiology machines do, but it's not readily accessible. Okay, great, thanks. Yeah, here in London, we have the LV strain in the OR and we can eventually use the cardiology software to do RV strain as well.