So, our session title is Pulmonary Vascular and Right Heart Imaging. So, we're going to talk about specific imaging modalities for the right side of the heart and the pulmonary vasculature, not keeping it specific to one particular disease. So, we're going to talk about the imaging modalities, and our goal is not to make everyone an expert in each of these imaging modalities in the next hour, but just to let you know what's available and how can we assess the RV better. So, I'm Navita Ramesh. I'm a pulmonary critical care physician and a critical care program director at UPMC Harrisburg, Pennsylvania. With me today is Dr. Parth Raleigh, who is from Temple. He will be talking about CT modalities and nuclear medicine imaging. Dr. Katie Fidden, she will be talking about, again, CT modalities, PET-CT imaging. And bringing it all together at the end of our session is Dr. Bindu Akkanti. She'll be talking about the future of right heart and pulmonary vascular imaging. Okay, so with that, we'll get started. So, again, as I introduced, I'm Navita Ramesh, and I'll be talking about the transthoracic echo, and I do not have any disclosures pertaining to this presentation. The objectives for my session in the next about 10 to 15 minutes is to go over a brief overview of the RV anatomy, assessment of the right heart on transthoracic echo. We'll talk a little bit about what is basic transthoracic echo, what can you get about the RV with the basic views, and then go up a little bit more to advanced transthoracic echo. And I'll end with the limitations of RV echocardiogram. We will not be talking about this, okay? So that's beyond the scope of our talk today. Okay, so we do have some audience response questions. So this is the first question. Please look at the image, all of you, because the next, when I advance the slide, the image will not be there. So which of the following is the recommended apical four-chamber view with focus on the right ventricle? Is it line one, line two, line three, or I'm not sure? Okay, just gonna give you one second here to look at the image. Okay, good. We have a good number of votes. Very good. Okay, line two. So we'll come back to that. Okay, very good. I like the engagement, 37 votes there. So let's go to this question here. The LV is a neglected chamber of the RV, neighbor of the RV. The importance of RV function was first described in 1616. LV function is more interesting than RV function and none of the above are true. Very good. We have a good number of votes there. None of the above are true. Okay, so we will discuss about that as well. Okay, the answer is actually the importance of RV was first described in 1616. So briefly, the RV is a thin-walled chamber. We all know that. It's behind the sternum. There are separate inflow and outflow portions of the RV. It's very asymmetric, and that's why there's so much confusion with assessing the RV's function and the structure. It's crescent-shaped. It's wrapped around the LV, and there are various changes in the shapes with the loading conditions of the RV. It's heavily trabeculated as well, and that interferes with our interpretation of RV imaging. So this slide just gives you an idea of what the RV actually looks like. It has this unique crescent shape, and this makes the calculation of the RV ejection fraction very challenging. And I think that for the context here, we all are very familiar with RV failure or right heart failure. So that's RV dysfunction with acute onset of hypotension resulting in end-organ dysfunction. It's important to understand acute core pulmonale because RV changes can happen in chronic diseases as well. Acute core pulmonale refers to acute right heart failure in the setting of acutely elevated PBR due to pulmonary disease. Briefly about the background, this is Sir William Harvey. He first described the importance of RV function way back in 1616. So this is what he said. He said, the right ventricle may be said to be made for transmitting blood through the lung, not for nourishing them. So there was a purpose to transmit blood, not just to nourish your lungs. However, despite this being described in 1616, everybody kept talking about the LV and focused on the LV, like, you know, even now that's happening. But it's changing as the awareness or the importance of RV is becoming more prominent now. We are recognizing it more, especially after MI and valvular heart diseases, in certain pulmonary disorders. And now in our ICU patients, why is the RV important, right? So I have this slide here. It's very crowded, but I just want you to focus on some important things here, which is ARDS, right? Hypoxic vasoconstriction can cause RV changes. There is acute RV dysfunction in about 32% in patients with sepsis admitted to our ICUs. And we do see a lot of pre-existing pulmonary hypertension patients getting admitted to the units for some other reason. So yeah, so paying attention to the right ventricle is very important. So with that, I'd like to switch to this slide just to go over what our expert societies are recommending. So this guideline is from 2009, okay? So that's when it was first updated. This is a collaboration between American College of Chest Physicians and the French Society. They came up with some guidelines or statements to talk about competence in critical care ultrasonography. They divided this into two domains, which is general critical care ultrasound that had thoracic ultrasound, abdominal and vascular recommendations, and then echocardiography, which in turn was divided into basic echo and then advanced critical care echo. So for competence in basic critical care echo, the recommendation for cognitive skills was you should understand the global RV size and systolic function. This is basic echo. And to take it further, recognizing RV failure on transthoracic echo is considered a basic competency. Acute or chronic RV dysfunction needs to be, we need to distinguish these two by basic transthoracic echo. And when we move on to advanced critical care echocardiography, the competencies for that include specific indications for RV, such as identifying RV infarction, especially as a complication of myocardial infarction. And when we look at the comprehensive hemodynamic evaluation, we need to understand the heart-lung interactions and how the RV changes based on changes with mechanical ventilation and influence of the positive pressure ventilation on the lungs. Same thing goes to recognizing RV systolic dysfunction in shock states and also looking at cardiac tamponade and seeing what RV changes happen in tamponade situations. They have a specific separate table for RV size and function as part of the competence in advanced critical care echo that includes evaluation of RV size, looking at the paradoxical septal motion, RV outflow imaging, pulmonary pressures, and abnormal RV outflow Doppler patterns. Okay, so this is the critical care chest and critical care society's recommendation. So what are the key questions related to RV that are answered or addressed with this advanced critical care echo? So you have to ask yourself, what is the RV systolic function? Is this acute core pulmonary? Is the RV cavity dilated? Is there a paradoxical septal motion? Is the RV systolic function impaired by the ventilator settings? And what are the pulmonary pressures? So when you do advanced critical care echo, looking at the RV, you should be able to answer all these questions. So I'm going to go over some basic point-of-care echocardiography views. So this is the peristunnel long axis with the cardiac preset, the probe pointers towards the right shoulder, and this is what the view looks like. And here when you focus on the RV, you're able to see only the RV outflow track. And then you rotate perpendicular 90 degrees where the probe pointer is towards the left shoulder. This is the peristunnel short axis. You see the RV, a tiny crescent on top of your LV. The next view is the apical four chamber where you see all the four chambers. And that's where the RV is pointed out there. The subcostal view, everyone's familiar with the subcostal or the subdiaphragmatic view. That's another view to assess the RV size and function as well. So now when you look at the American Society of Echocardiography, when they look at comprehensive right heart evaluation by trans thoracic echo, they take it a little bit further and they want to talk about RV size, right atrial size, RV systolic function with at least one of these parameters. Fractional area change. How much is the area changing? The S prime, we'll go over this in a little bit, and TAPSE or tricuspid annular plane systolic excursion. So look at the RA size, RV size, and then any one of these parameters to assess the RV function. They push it further and say this could be with or without other indices of global RV systolic function. Which include RIMP or RV index of myocardial perfusion and then looking at the systolic pulmonary artery pressures as well. So based on that paper from the cardiologists and the echocardiography society, they make some modifications to our critical care echo that we do. So this is the same peristunnel long axis where the axis is towards the right shoulder probe pointer. So you have the regular peristunnel long axis So this is a peristunnel long axis and you can see the RV outflow track here. And these are some modifications of the peristunnel long axis. The second one is the peristunnel long axis of the RV outflow track, looking at the PA. The third one is peristunnel long axis of the RV inflow. So just with a peristunnel long axis, you can make slight modifications. Can look at the other views of the RV as well. So this is a regular peristunnel long axis where you can see the RV up here. So for the intensivist and pulmonologist, this view should be considered basic critical care echo. You should be able to evaluate the RV outflow. So this is the same peristunnel long axis and you can see how much of the RV is visible. RV outflow is visible here compared to the previous image. So we should be able to pick up all these, the size of the RV, just by looking at the peristunnel long axis, even if we are not able to push it further like the cardiologist. The peristunnel short axis where the probe pointer is towards the left shoulder, that's this image here. That's the mid ventricular level or the papillary muscle level. That's the basic critical care echo that's being taught. Slight modifications on peristunnel long axis. You can look at the other sites of the RV as well. So the first one up here is the peristunnel short axis of the basal RV. The second one is peristunnel short axis of the bifurcation of the pulmonary artery. And then peristunnel RV short axis at the mitral valve level. So just being at the peristunnel short axis, very slight modification of your ultrasound probe can give you the idea of the peristunnel long axis. Slight modification of your ultrasound probe can give you the other views to assess the RV better. So this is what a normal mid ventricular peristunnel short axis at the papillary muscle would look like. So that's a normal heart. The RV is small. The LV is big. But as an RV gets more dysfunctional in the peristunnel short axis, you can see that the RV is larger and there is pressure and volume overload. Because it's compressing the LV. So this is what they call a D-shaped septum. Just a diagram to show that when the RV dilates, it compresses on the LV. And the D-shaped septum is basically a D-shaped LV. So to push it further, so once you know how to do the peristunnel short axis, you could do M-mode through that. And with M-mode, you will be able to look in real time, looking at the paradoxical motion of the septum to assess for RV dysfunction. So the next view, the basic cardiac view we spoke about was apical 4-chamber. Where you look at all the 4-chambers. This is the classic apical 4-chamber. When we focus on the basal segment of the RV, that's the RV-focused apical 4-chamber. So it's a slight modification. You can see the difference between these two. Then in the 4-chamber, we can again do another RV-modified apical 4-chamber where you're not seeing too much of the LV, but you're seeing a little bit more of the right ventricle in this view. So again, knowing basic critical care echo and getting better on that, finessing your skills, you can get better RV views. So this is the regular apical 4-chamber. And when the RV dilates, it could look like this. And the fourth view that I spoke about briefly was the subcostal or the subdiaphragmatic view. The first image here is a regular RV subcostal where the RV is the most superficial chamber up here. Making, again, very slight modifications there. You can get the subcostal short axis and get the basal RV view here. So that's knowing the basics and pushing ourselves a little bit further to get more advanced views. So that's knowing the basics and pushing ourselves a little bit further to get more advanced views. From there, calculations. I promise I won't spend too much time here. I'm going to go over this very quickly. The one formula you need to know is this. Delta P is 4V squared. So you know that any of the velocities across a valve, you'll be able to calculate the pressure there. Using this formula, you will be able to, assuming the right atrial pressure is measured by the IVC, you are able to calculate the RV pressures, RV systolic, RV diastolic, as well as your pulmonary systolic and pulmonary diastolic pressures. So again, getting your basics right, pushing yourselves further, and then just keep building on what you already know. Again, if you know that, you push yourselves a little bit further and calculate the cardiac output of the RV by looking at the velocity time integral of the RV outflow tract as opposed to the LVOT times the area of the RVOT times the heart rate. So the stroke volume is by RVOT VTI in the area of the RVOT, and you multiply the heart rate, you get the cardiac output. So the next one or two minutes, I'm going to spend on what the cardiologists are saying. So this is from a recent cardiology paper looking at the echocardiography guidelines. And they, again, push it further, and they talk about the RIMP, which is RV index of myocardial perfusion, basically looking at the lateral annulus of the tricuspid valve, looking at the pulse wave Doppler and tissue Doppler, and coming up with the global RV function data. So if the RIMP is greater than 0.4 with pulse wave or greater than 0.55 by tissue Doppler, it indicates RV dysfunction. So there are specific criteria for that. And the fractional area change, which the cardiologists like to talk about, and now us too, since we know what this is. So looking at the fractional area change of the RV, FAC less than 35% will indicate systolic dysfunction of the RV. But for FAC, you have to remember you need to put the entire RV in view. And you have to exclude the trabeculations in this view. So that's very important. The next one is... That was just your shit up when you were doing the POCUS. That's what happens all the time. The POCUS, yeah, yeah. Thank you. That's a reality. So TAP-C is next. Everyone's familiar, should be familiar with TAP-C by now. So it's easily obtainable. TAP-C less than 16 indicates RV dysfunction. And cardiologists, as you know, they keep pushing it further. They talk about S prime. That's looking at the... Again, looking at the RV function by pulsed tissue Doppler or colored tissue Doppler of the S prime. It's, again, easy to measure, reliable, reproducible. If the velocity... So this is measuring the velocity. If it's less than 10, that indicates RV systolic dysfunction. And again, this is an evaluation of global RV systolic function. The last one is GLS. That's the longitudinal strain. It's a little bit more advanced. Dr. Akanti will be talking about that in a little bit. So it's looking at speckled tracking of the... Looking at at least three segments of the RV free wall and commenting on the RV function based off of that. This is something we think about but not too much, which is the RV diastolic function. So RV, just like the LV, has systolic and diastolic function. And that's assessed by looking at the tricuspid valve E to A ratio. Again, there are different parameters for that. Like I said, we're not here to make everyone an expert with RV echo. But understanding that similar to LV, RV has similar parameters. So we have to keep pushing ourselves further to know more about the RV. The last point about the RV is looking at the RV wall thickness, which is very important to distinguish between acute and chronic diseases. Again, subcostal view is the preferred view. It's easier to get the RV free wall. And you measure the RV free wall thickness. And that's, again, cardiologists recommend this as well, looking at the RV free wall thickness. Less than 0.5 would indicate if there's an RV dysfunction with RV free wall less than 0.5 centimeters would indicate an acute dysfunction. More than that, there could be some chronicity to it. So this slide is just to go over what are the limitations. So now we know so much about the RV. So what are the limitations of assessing the RV function by echo? There are different complex contraction relaxation mechanisms of the different segments of the RV. So it's not all doing, everything coming together, going out just like the LV. There are complexities that happen within the RV. And then when you look at the evaluation methods, image acquisition is difficult because of the retrosternal location. There are too many trabeculations. So defining the border is difficult. And also, as I mentioned, there are several images you need, you need to look at properly in order to get an assessment of the RV size and function. And it's difficult to image the entire RV in a single window. Estimating the volumes of the RV is also difficult because of the chrysantic shape. It does not conform to a geometric pattern. And we have to look at separate inflow and outflow views of the RV as well. And working with our patients in the ICU, we've all seen there is changes with the preload, afterload, and LV function, and all those affect the RV in different ways. So understanding that is also important. So now, what are the pros of doing transthoracic echo for all of us in this room? To look at the RV function is it's a bedside procedure, understanding the basic critical care echo, and then pushing yourself to do the advanced, and then pushing further to do the more advanced stuff. It's doable. We can learn it and we can all do it. And it's dynamic so we can, any changes with interventions, we can go back and image the RV and see if our interventions worked or not. And we could do multiple assessments in one day or one shift. Cons, as I mentioned, challenging anatomy and also the experience and expertise of the ultrasonographer that plays a role in this. So we can't end the talk without talking about AI. AI is everywhere. Everybody's talking about it. So this paper came out in 2019, just looking at AI in echocardiography. They looked at detection, function evaluation, disease diagnoses. Basically they used AI to look at LV function and they said AI did a good job. I did not specifically see a paper on AI and RV function but it is coming. They're going to look at the RV soon. So with that, for our pulmonary critical care purposes, trans thoracic echo RV assessment, it's important to recognize the RV is not merely a conduit. RV has a specific purpose and function and we have to pay due diligence to the RV. Examine the right heart using multiple acoustic windows, assess the RV size and function, and also assess the chronicity of RV dysfunction. With that, I want to say thank you and that's my email. Thank you very much everyone. Okay, I would like to introduce Dr. Parth Raleigh next to talk about CTPA modalities and nuclear medicine imaging for pulmonary vasculature. He's the associate professor at Temple University. Thank you Navita for excellent talk. We're going to change the gears. I'm a pulmonary artist. That's the only introduction that you need. But I'm going to talk about CTPA and some of the interesting concept of nuclear medicine that may help us as a RV logist, right? That's what we are calling nowadays ourselves, RV logist. Mike, is that right? Yes. How many of you, just out of curiosity, have taken... Sorry, go ahead. You're saying something? Yeah, how many of you have taken the echo boards, by the way? I mean the critical care echo boards. I see a few hands. Good. Navita, Bindu, myself. So I think we are growing. I think we can understand RV. We can image it and we can make the bedside implication. Given that bias, in the next few minutes I'm going to convince you that there is a lot of stuff that you can learn from CTPA and the nuclear medicine, which is non-invasive, dark room, and reading from the corner where nobody knows where you are, okay? So these are my some disclosures, nothing pertaining to today. And then the objectives over next 10 minutes, what I'm going to talk about is that looking at the different measures of RV assessment, acute or chronic. A lot of us do acute, but there is a lot of chronicity that overlaps with the disease state wise. Pitfalls of some of the imaging that we think, or at least I thought was I was good at. Then we'll look over some nuclear medicine imaging and clinical workflow. And then finally, we'll end with the same thing, AI in VTE space, which is growing day by day. Lord, I have a very easy question compared to my colleague, so it's true or false. There's a 50% chance of being right, so can't go wrong, right? Only two words, come on, I need some more words, come on. Everybody has a phone, even my kids back there have phones, so okay, fair enough. Okay, we got 18, we'll move on. So half of, oh wow, 67%. So that's smart people, so bad question, I'll take that back. Yes, we can use the CTPA as a PE, the stratification as an alternate to echo. So and let's talk about it. This is a dual energy CTPA. This is a new kid in the block, not many for not many institutions, but a lot of people are adopting it. What I learned and what I know is that it's not only the dual energy has seven subtypes of it, so your institution may be doing it. It could be a single source, dual source. Basically what happens is basically you're looking at two levels of energy and what it allows is that it reduces the signal to noise ratio. It increases the diagnostic accuracy and it goes beyond the anatomical classification and it actually goes into a functional assessment. So it's, you can actually see perfusion mapping. As you can see the images here, this is a PE which is a layering thrombus, but there is a whole area of hypoperfuse area. So you are an anatomical insult and now you can see what the changes in perfusion happen simultaneously. It can also reduce the artifacts that can create it from the bone and the hardware, so that's why you get a lot of, you get very less false negative. Your diagnostic yield increases because you can diagnose the PEs or CTEF at least at segmental or sub-segmental levels. So those are some of the advantages of the new modalities. For me, I think it's very important because a lot of patients get a lot of CTPAs anyways, right? I don't order that, our ER colleagues order that, I hope for the right reasons, but somebody has a PE, they always got a follow-up CTPA. I think you can take those advantages to see the perfusion track changes. The color images that you see is iodine mapping that's always post-processing. Previously that I showed you a simple iodine map, but you can see how patient's journey evolves, their clot journey evolves, whether they're improving, staying the same, it's the same patient a few months later, and you can see how their perfusion is starting to return normal, but still remaining so abnormal at some places in the image on the right. Next one, RV chamber assessment, right? So I think that is my question. I think I'm just bringing back, I don't think given the audience is well aware, but based on current PE classification, you can use, to define RV dysfunction, you can use echo or CTPAs alternate. Why it's important in clinical practice? Because unless you are a POCUS enthusiast like Bindu and Navita are holding the probe 24-7, there are places where you order an echo, and then a lot of times I get frustrated in old days where my cardiologist will say, oh let's get an echo, and we'll talk, and not anymore, right? I think you can use this classification, you can use POCUS, you can be at the same term, so I think it's a very humbling experience to take the echo boards, but more than that, I think it's reason it's in the classification because there is an evidence behind that that CT markers are RV dysfunction associated adverse short-term outcome in patients with pulmonary embolism, all right? Where do you measure it? That's always a million dollar question, so you can measure it in a four chamber view. Ideally you can go up and down in images. You want to identify your tricuspid groove, so right around there you'll be a tricuspid groove. You go a centimeter above and you do inner wall to inner wall, so you exclude the trabecula and outside wall, so inner wall to inner wall, and RV and LV assessment don't have to be at the same slide, so you can go up and down and find the maximal basal diameter, right? That's where you measure it, and the reason why it's important, because look at the view on the right side, that actual view. This is the same view you will get it. If somebody has a PE and they have an RV dysfunction on CTPA, echo will show you exactly the same thing at that point of time, right? If you advance the journey 12 hours later, it may be different. If you tell me you want to give a bolus of liter of fluid, sure, you need an echo for that. If you're telling me that somebody's a PFO or not, yes, you definitely need an echo for that. If you tell me somebody's a clot in transit, they definitely need echo for that, but just for risk stratification purposes, you're right there making a diagnosis and prognosticating. Picking up the chronicity of the RV wall thickness is doable, right? It's a little hard compared to the echo. Echo, you go to sub-costal view and look at that, and if you start seeing the wall, it's definitely more than four millimeters, right? The CTPA is a little harder. You may need a little help with your radiologist, because it's very easy to get off, right? When you start measuring, you're talking about millimeters of acute versus chronicity definition. So again, can be done, a little hard here. PA diameter. So this is evolving. I mean, those of you who work in the pH world already know that we use that as a screening criteria. For pH, you can do it in non-contrast CT scan, but I think there's a good data, and I think we looked at our own data also where PA diameter correlated with the markers of RV dysfunction, right? Only TAPC did not correlate, but most of the markers of RV dysfunction correlated with the acute PE with a PA diameter of less than 30 or more than 30. Area is better. So if you start getting a puristic form, think about this. CTPAs are not gated, so you don't have an EKG algorithm with that. So some may argue that 30 or whatever cut off you're using could be different in systole or diastole versus area measurement, which may remain constant, is a better marker. So again, there is some literature suggesting PA area may be better than diameter, but at least for general purposes, CTPA is there. Use it to your advantage. Obstructiveness, we can spend an hour discussing whether it helps or not. All that, I'll tell you that it's usually post-processing all the papers, but the higher the cloud burden, along with other markers of PE severity, should help your patient, right? It's not the only marker you can use it to determine the treatment algorithm. LA volume. I think this is something that I've been paying more and more attention. So if you get a high intermediate high risk or a high risk PE, you start focusing the LA, and look at the size of the LA. If it's small and you reperfuse that patient, and if they get a follow-up scan, you will see that LA volume will open up. So what it shows you, that is a proximal obstruction, there's a reduced flow back to the LA, there is a reduced LVOT VTI. It has been shown in one paper and multiple papers showing the same thing. So you don't need to map the area, but if you start paying attention what LA volume would look like, I think it's a growing evidence. It's a very easy thing to do. Just eyeball it while you're scanning through images and see what the LA volume will look like. Sometimes you won't even see a contrast in LA side. That just shows you that there is nothing coming from right to left, and this is a sign of an obstructive shock. So something that I pay attention a lot lately. IVC reflux of CTPA. How many of you feel with a razor fan, feel confident measuring, seeing IVC reflux on the CAT scan? Who has seen that? All of us, right? I thought the same, but this is the most bogus interpretation that pulmonologist can do of an IVC reflux, right? There are a lot of positives that you see that can happen, but there are also false positives. So depending on injection from the groin, right? If you are injecting from a central line from the groin, you will see more contrast reflux. It's not a true reflux, it's a passage of contrast. If you have an IJ line, the contrast transit time is much faster and you will get false positive reflux. Sometimes the only technician will tell you that what was the rate of your machines are set up. So sometimes the auto injectors are set up at 3 ml per second or sometimes it could be 5 ml per second, and you may get a little bit positive ratio from that. So talk to your radiologist, particularly if you see an IVC reflux. Sometimes it's evident, right? If you see an evident contrast reflux, which is the bottom right image, it's going into the liver, that's probably true. But if you're just seeing the grade 1 or grade 2, which is right at the beginning in the IVC, talk to somebody. I've been proven wrong 10 out of 10 times when I say I see a clot in the IVC. So I'm still looking for my first one, but I diagnosis and radiologists don't. Clot chronicity, right? So I think this is where CTP is really helpful, right? Again, you will have a markedly dilated RA, you will see a layering thrombus, contrast, I mean, eccentric clot calcification. My belief is I think 10 to 12 percent of acute PE have an overlapping chronic component of the disease, whether they have acute or chronic or only chronic, that's always up for debate, but a lot of them could have an acute and chronic disease, and there is nothing wrong, that's patient's journey. And then something that I always find hard as a pulmonologist to find it is a bronchial artery hypertrophy. How many times we have that hemoptysis patient we send to the IR and say, hey, block it, and they could not find the bleeding vessel, because it takes some time to find a bronchial hypertrophy or bronchial circulation hypertrophy on CTP as a pulmonologist in CTEP patient, but again, something that your eyes needs to be trained. So I struggle with that component. I'm usually good at finding the webs and bends that you see here. I mean, if you pay attention that can happen. Clot versus tumor, I think we have a whole publication in chest. I think it's beyond the scope. It's a topic of its own beyond the clots and pulmonary circulation, so I can't go in detail, but always a clinical differential that I want to bring attention that you should always think about. And finally, all that I said, we can do it. We proved it. Our fellow, Sam Pettigrew, led this paper. We had 10 fellows. We blinded them to read CTPA-based RB distribution. We published in ATS Scholars. So all of us in this room, I'm not sure you can be a cardiologist and doing an echo, but can be definitely a radiologist and prognosticating your PH or PE patients. We proved that and it's published. Growing role of nuclear medicine, I think SPECT VQ scan, that's what I'm gonna spend next couple of minutes in, is because it allows single photon emission perfusion scan. It's different from planar in a way because the false positive rate or intermediate findings that you get, that intermediate risk of PE, doesn't happen with SPECT VQ scan. It's either positive or negative, so that increases the diagnostic yield. I use it on a lot of my post-PE follow patient to see that perfusion tracking and how they are evolving. The reason why it's easy and reason why I like it, because we combine a low-dose CT scan, which a lot of big centers have the protocol combining SPECT with a low-dose CT scan. I did not grow up in an era where there was planar VQ scan, so nobody trained me, so I still struggle. That's my full disclosure, but if I have a low-dose CT scan and perfusion mapping matched to that, I can go head-in-hand with my nuclear radiologist and actually able to have some meaningful conversation because sometimes you get a positive results and you say, hey there's emphysema here because you have an associated low-dose CT scan. It works in my favor also because a lot of our PE patients or PH patients would have a lot of comorbid conditions, so it serves as my low-dose CT scan. We pick up lung nodules on that, so I think there are multiple benefits of combining a low-dose with SPECT together. This is just one case that we had with the SPECT where we have patient and ECOS, and this is my patient, and see like planar VQ, sure, some of you are experts and definitely can pick up that, but if somebody is like little intellectual disabled like me, you can see that this area is not perfused, right? This area is not perfused, and I have two VQ scans, and you can see if the perfusion is normal, this is how it looks like. So this patient has a chronic PE in the right upper lobe which has not been perfused at all, and this is two months. She can sing, she can run, she can bike. Mike, maybe I'll send it to you, her to do a... Mike does a lot of exercise, ride hard cats, so I have not done that yet. She's scared of needles, but this patient is doing well, so I think this is the powerful imaging technologies, right? Last couple of minutes, AI and pulmonary vascular imaging. This is a paper from Europe. I mean, they always do better studies than us, but this is exactly what happens in my hospital. By the time you are at 2 p.m., 3 p.m., 4 p.m., ER or inpatient, the number of CT scans that get ordered is exponential, and what happens between 2 to 6, I mean 4 to 7, signouts, right? And that's where the backlog happens, and I think that's where the AI is really helpful, that as the scans are happening, they get prioritized, right? So at least for our PERT path, we have three FDA-approved apps. We use one of those. All of them are kind of the same, so no disclosures here, but what it allows that as soon as the patient comes off the table, you get a notification about the positive results. I mean, you can look at the entire scan. You can look at their heart, lung, parenchyma, effusion, pericardium, tamponade, everything in the palm of hand, so I think it is powerful. It's actually changing how we think, and you can see this is exactly how the images you can get. I mean, literally, you get a PERT alert, and you're scanning through which one you're gonna drop everything and go or which one you can wait and can be seen, so I think it is prioritized in the field, and you can change it with lung windows. A lot of our cardiologists don't look at that, but I change it with lung windows, and there's a big pleural effusion or pericardial effusion, and then you stop there, so I think it has its own role. I think it's evolving. Initially, I didn't believe that CTPA could be, I mean, the apps are that good, so I reached out to one of those companies. They gave us some funding, so we are doing a new certificate-initiated research. I said, I'm gonna give you my scans. I'm gonna blind you, and you guys give me the results that I want to see, and so far, we have interim data that we presented at PERT last week, and it's 91% census and 100% specific, and RV to LV ratio had a very good positive correlation, so I think this is powerful. This is changing. I think clot burden indexes and all this stuff, maybe LA volumes, everything that I showed you is within the scope of AI. I think we just need to keep pushing for that. I had to thank Dr. Kumaran, who is my partner in crime. He's helping me become this new title that I'm trying to establish, PVRologist, which is pulmonary vascular radiologist. I'm working on it, but he's my partner in crime, so I had to say thank you to him for a lot of stuff that he shared with me, and thank you. Don't forget to read the session, and if you're not bored, now we have the best talk of the day, which is Katie. She's gonna talk about PET scan and MRIs that I had no idea about, so Katie, it's all you. He's being far too humble. It is quite the honor to get to follow these folks, so I'm gonna talk to you today about right ventricular imaging, PET CT scan, and cardiac MRI in particular. My name is Dr. Katie Fitton. I come from Corwell Health South. We've changed our names about 10 times in the past year, so don't be upset if you don't recognize it. I've got nothing to disclose, and so our learning objectives today, we're gonna try to understand how FDG PET and cardiac MRI can estimate pulmonary hypertension prognosis by looking at the right ventricle, look at some normal, abnormal of both imaging, and then understand some of the variables of cardiac MRI that have been associated with risk progression and pulmonary hypertension, and name some pros and cons to each imaging modality, and I should point out too that this is a talk, like Dr. Ramesh said, on the right ventricle, not any specific disease in particular, but a lot of these imaging modalities have been tested on pulmonary hypertension patients, so you're gonna be hearing a lot about pulmonary hypertension in this portion of the talk as well. So we're just gonna go to a quick warm-up for you all. So true or false, the updated ERS guidelines from 2022 include cardiac MRI in the three strata model for comprehensive risk assessment of pulmonary arterial hypertension. And the majority got it right, perfect. We have one more. FDG PET and cardiac MRI can be used together and separately to assess and prognosticate pulmonary arterial hypertension and right ventricular RV dysfunction. Awesome. So just to get everybody warmed up, like I said, and just remind you what is in the three strata model, we can see here that they did add cardiac MRI recently. And we'll come back and we'll talk about this a little bit more later on in the talk. So first and foremost, I'm not sure if anybody else is thinking this in the back of their head, but my first question was, why in the world would FDG PET be able to visualize pulmonary hypertension? And it has to do with basic changes in metabolism with pulmonary hypertension. Evidence from models show that glycolysis-related genes and proteins, such as glucose transporter and pyruvate dehydrogenase kinase, were upregulated in the RB. And expression of genes from the fatty acid oxidation pathway is suppressed in your failing right ventricle. So basically, more glycolysis, more glucose update, and more FDG PET AVID on your scan. And this utilizes, just in case anybody was curious, something called the Warburg effect, where in the 1930s, they found that tumors were taking up large amounts of glucose compared to the surrounding tissue. So then this was later named the Warburg effect in the 1970s, which is a fun fact for your day. So it was proven in a proof of principle study done in 2011 by Hagen et al, which showed that you could see this increase in glycolysis from a failing RB and right heart as uptake on a PET scan. You can also follow it and look at the severity of mild, moderate, and severe pulmonary hypertension. This was O'Hara et al. And the other thing I want you to notice too in this is that they're looking at the difference in uptake. Let's see if I can get this to work. The difference in uptake from our LV and our RB too, which we're going to look at again as we get to some more complex imaging modalities. This one's following the prognosis or the treatment in a patient with RB, and you can see how you have less uptake as the patient was given sildenafil and improving. And since this is an imaging talk, I just thought this was a really lovely image looking at the difference between a healthy control and their lack of uptake and a PAH patient and their progression over a course of a year. So let's shift gears a little bit to something we're a little bit more familiar with as pulmonologists, cardiac MRI, which has been shown to have a plethora of data to it over the past five to 10 years. It's most specifically useful in non-diagnostic echoes where you have unclear size or function. So like Dr. Ramesh had mentioned earlier, when you're looking for those volumes of the RB and RA and you don't get a great acoustic window, you can then substitute a cardiac MRI to help you out with that. It's also very helpful in complex congenital heart disease, phenotyping, left versus right heart disease, and in complex diagnoses where you have an overlap of issues such as sarcoidosis or arrhythmogenic right ventricular cardiomyopathy. And in our case, practically speaking, it can help with risk assessment. It uses no radiation, however, you clearly can't use it in certain patients who have implants or pacers, and probably the biggest thing for community hospitals is that it's not available in all locations. So it's really helpful to know and to understand where you can use this and how you can use it to your advantage. So specifically speaking in the pulmonary hypertension patients, this is really important because the ERS made a very bold statement of quoting a study, which I'll show in a second, saying that risk assessment at one year follow-up based on cardiac MRI was at least equal to risk assessment based on right heart cath. So they quoted a study by Vanderbergen et al. looking at the value of hemodynamic measurements in cardiac MRI. Predictive models with only hemodynamic data, right atrial pressure, mixed venous oxygen saturation, or imaging parameters, your right ventricular ejection fraction at one year performed similarly, making them make the statement that they seem to be at least equal to risk assessment to right heart catheterization. The ERS recommends following your right ventricular end systolic volume index, your right ventricular ejection fraction, and your stroke volume index to help you risk assess which patients you're going to need to increase their treatments. How do they calculate this? I know we're pulmonologists, we're not radiologists. So I'm going to try to break this down as easily as possible. There are three main types of clinical cardiac MR. They use steady state free procession imaging, or SSFP, and they'll use that to evaluate left and right ventricular cavity sizes, function, ventricular mass, intracardiac shunts, valvular functions, and also to detect intracardiac masses. This is the sequence choice for synacardiac MR imaging, and probably the one you'll see most often repeated in different studies. They also can use spin echo imaging, which is something called a black blood approach, and I'll show an example of this as well. They'll use it for anatomic imaging and for identifying fatty infiltration on the right ventricular free wall, so looking at things like AVRC like we were talking about earlier, and pulmonary flow abnormalities. And lastly, flow velocity encoding used directly to measure blood flow and quantify the severity of valvular regurgitation, stenosis, and intracardiac size. So this is that very first imaging technique that I mentioned, SSFP, looking at the heart through the whole cycle from diastole to systole. And you can see, too, it's very similar to the cuts that Dr. Rabush had showed earlier with the echocardiogram and the short axis view. They'll use standard MRI protocol to calculate measurements such as end diastolic volume, ejection fraction, and stroke volume, as well as mass for both ventricles. Lewis et al. utilized this concept of SSFP and synacardiac cycling imaging to calculate and then follow patients with pulmonary arterial hypertension and their right ventricular ejection fraction, which clearly makes a lot of sense in our head. The worse that your right ventricular ejection fraction starts as, the worse the prognosis over time. In this study by Swift et al. in 2016, it showed the patient's right ventricular encystolic volume index calculated using the area between the diastolic images and the encystolic images as a measure of mortality. And again, these were all of the studies that the ERS pulled out to make their recommendations in the most recent guidelines. The next imaging technique that I'll talk about briefly is cardiac gated black blood imaging, looking at pulmonary flow abnormalities. And this is just really interesting. You can clearly see in a patient with no pulmonary hypertension, they don't have that blood flow slowing. And in patients with severe pulmonary hypertension, they do. The closer and more proximal to the pulmonary artery, the worse the prognosis. And then because I'm doing both cardiac MRI and PET scan, I found this really interesting study combining the two, looking at, like we talked about earlier, that SUVRV versus SUVLV ratio uptake. And then what they did was they combined it with the right ventricular ejection fraction and were able to prognosticate their patients using this. So the Fleschner Society put out a really great position paper in 2021 looking at pros and cons of imaging modality. And I think Bindu will go over some of this as well here in her talk. Pros, you can look at, like I said, functional, structural assessment, looking at the volumes of the RV. And then cons, you have your traditional MRI contraindications, and again, it's not always available readily for your patients in the community hospital setting. And then last but not least, since we're talking about future and we are mentioning our artificial intelligence as well, this was a study done by Dawes et al showing an analysis of that CNA cardiac MR images in patients with pulmonary hypertension. They then used supervised machine learning of the patterns of cardiac motion that looked at survival in patients with pulmonary hypertension. And then they could predict based on that. So just really interesting things that are up and coming. Thank you all. Thank you. Thank you, Katie. I think you all can agree that we have such a comprehensive review so far and that the RV is complex. So one thing that we wanted to take a few minutes to kind of wrap it up because there's a lot of key points that we discussed. And one of the things that I think most of my panelists were referring to is we, the pulmonologist. I know that there's a multidisciplinary team in the audience, but I also know that we come from the place of being a patient advocate. Just like we would not read the radiology report, we, I think, the panelists, and I think you all will agree, that we have to be just as comfortable with echocardiogram because the patient in front of us is trusting us that we are going to use this technology whether it is an echo, a CT, an MRI, a PET scan. And when all of those don't give us the answers that we need, we leave no stone unturned. Because at the end of the day, they came to a specialist and God forbid, we said nothing is wrong with you and there was, right? So with that, thank you, Dr. Ramesh, for inviting me to be part of this panel. I am a pH pulmonologist. I am also an ECMO intensivist. And the thing that combines my pH interest with my ECMO interest is, in fact, the right ventricle. And I think a lot of you here are viologists, otherwise you wouldn't be in this talk this early in the morning, right? So we talked about the echo, we talked about CT, we talked about nuclear imaging, and we talked about cardiac MR. But how do we put this together? We put this together starting with the patient. Because all of these imaging modalities that are multi-parametric are only useful if we go back to the basics, preload, squeeze, afterload, pericardial constraint, RVLV interdependence, and the rhythm. Because all of these put together, right, matter. For instance, if you're doing an echocardiogram on a patient that is on epi of 10 micrograms, it definitely matters compared to the patient that is at baseline, right? So how do we look at this big span? Dr. Sudarshan's group from Duke put out a really nice review article talking about the novel imaging techniques that are available and what is up and coming. I like this image because you look at the right atrium and the right ventricle, and we cannot be agnostic about everything else. I think we are great pulmonary artery clinicians. I think we are great RV physicians. And we are great alveologists, right? But then putting it together on the individual patient, discussing what is the role of echo? And I know there's some senior attendings in this room that may say, really, I don't need no speckle tracing, right? But what if it's obvious, like, you don't need to get the repeat right RCAT five years from now, because it really talks about that kind of tracing involves both radial and longitudinal strain. Then the cardiac MR, studies are coming over and over. RV and LV ejection fraction assessments are just as good. Okay, let's go. I'm ready. Then the chest CT, right, exactly, the dual energy CT with the impressive perfusion imaging here. VQ scans, and I think we're just touching the surface of nuclear medicine in the role of pulmonary hypertension. There is a new study looking at adrenomodulin and expression in CAT scans in nuclear imaging. And in PAH patients in severe, there's near absent adrenomodulin expression. This is a PET CT, PET CT, right? So with imaging, potentially, we can actually see if the medications are working in these patients. Are there strengths, limitations, advantages? Absolutely. Dr. Ramesh started out talking to you all about the echocardiogram. She started talking to you about the imaging, easy feasibility of tricuspid valve assessment, right? V square times four gives you RVSP, plus right atrial pressure. That's it. It's easy. It's widely available. Unfortunately, it doesn't tell you about the etiology. Chest CT, all of us, favorite. RV is seeable, PA. Dr. Raleigh talked to you about LA. LA is, I think, the soul of that ventricle right now, the right ventricle and the LA. The LA is small, RV is big. The patient is not going to do well, right? So the radiation and the contrast used, especially if you wanted to do gated CT, PA, I mean, we need to consider that. Medical energy, we still lack validation studies on that. CMR, great for the heart, still not quite there for the lung parenchyma. MRI and perfusion MRI, again, it's in combination, not alone. VQ scan, no question about it. CTEF, boom, great. But I think we are getting to begin to understand, can we use that to understand quantification further? The latest is Xenon MRI, which is in very few programs, probably like five in the country. But I really do think that as we use it, especially in PAH patients, we'll probably have greater use. I told you about the PET scan. I think the PET is probably, Dr. Fitton's talk about, we are barely scratching the surface of using it. But let's take it back to the patient. These are all great. How do you use it in your individual patient? Let me walk you through a case, pretty straightforward. 40-year-old women, recurrent pulmonary emboli, multiple spontaneous as well as therapeutic abortions, C-section times two, breast cancer, the whole host of comorbidities, former spoker as well. Symptoms was long-standing dyspnea, intermittent chest pain, and heavy menstrual bleeding. Multiple hospitalizations. You know where this case is going, right? So we're a pulmonary team that is evaluating. Along with the cardiologist, we do a multidisciplinary assessment. FEV1 over FBC, simple basic spirometry. Let's start there. Not really helpful. Then we looked at the RV over TLC again. Not quite helpful. DLCO, like, okay, maybe the exertional dyspnea gives us answers, these, you know, PEs. 69%. Not really helpful, but the patient is still quite dyspneic. So we go to the ECHO. The ESC ERS, simple. This is gold. It goes through. This is, you can take an intern as well as a fellow through this. You know, Dr. Ramesh went through all the views. What are the things that you want to look at? I want you to focus on the limitations of this. If you look at S prime, if you look at TAPC, you're only looking at the lateral free wall of the right ventricle. I want you guys to recognize that limitation, right? Because you want the radial contraction along with the longitudinal to be measured. But it's a good start. Let's start with TAPC. Let's start with S prime. Let's really look at it. But then you combine it with other modalities. So let's see what happened in our patient. The left panel right there, tricuspid regurgitant jet, gave us about PA estimate along with IVC about 60. The middle panel, beautiful four chamber view, eyeball test, which we are all good at. RV was the size of LV. RV was a little hypertrophied. The next panel is TAPC, 17 millimeters, right? That's not really grossly abnormal. Patient is still dyspneic. So where do we go from there? We look, right? So we are a big PH program now. We are seeing a lot more patients. What is this role of speckle tracking and why do we need it? I just told you that the echo by in itself only looks at one side most of the time for us. Yes, there's a lot of post-processing that can be done that can help you. So the speckle tracking of the RV, it really helps you understand what is the strain each side of the RV is experiencing throughout the systolic cycle. It actually is able to give you each individual segment. For instance, if you just looked at the basal lateral, that may be moving, but when you put it together, maybe the septum is also not moving. And that kind of strain imaging. Strain is how much the easier way I look at it is how you go to the bedside and you go, let me get a NIF, right? Take a deep breath. Negative 30. That's good. Negative 40. Man, you can get the tube out. That's strain imaging. The more negative, you're able to squeeze. So if you're less, it is really not squeezing as much. So is it useful in patients? Is there a validation? The Hopkins group, led by Dr. Ted Ford, before he moved, they looked at it and they looked at it in scleroderma patients at rest versus in exertion. Kind of like my patient that I have at the bedside. Six minute walk test, no nasal cannula improvement. But when they looked at it, you can see the red part is not moving as much when the patient exercised, but the apical and the mid parts were moving. So clearly, an echo by itself would not have helped, but in this patient, basically, especially when they looked at, and coming back to the Ted Ford paper, they looked at scleroderma patients with exertion, they could see that they can detect that the RV was not as functional whereas it was at baseline. Maybe that's something I can use in the future. But right now, I have an easier method, right? Like I can have other methods. So we look at the CT. VQ scan in the CT confirmed near total obstruction, no perfusion on the other side, which is visible. Great. So we're gonna take the patient to CTEF surgery, patient is gonna get better, great, right? And then we started looking at the CT imaging, it's like, you know, yeah, there's no perfusion, but let's, you know, this lady has the cardiac index is nearly like about 2.1. Is there any other explanation that can explain her shortness of breath? So an RAOU cranial, you can see coming from the circumflex, the entire right pulmonary artery was being fed. Do you all see that, right? So clearly, it was so bad that the heart, the lung was stealing blood from the heart quite literally. Yeah. Is that novel? Is that new? Yeah, it's highly described. CTEF patients can have malformations and collaterals, and this can be pretty, pretty devastating in some cases, but also called dyspnea. These are cases where their cardiac index is out of proportionally low, because you're literally against stealing blood, right? So the patient undergoes surgery, and the patient is recovering well, immediately after there's good perfusion to the right side. So bringing it back to our original discussion, you have multiple parametric methods, and how do you combine them to understand what's wrong with your patient? So the thought that I leave is it's not one thing that you want to do. It's what you have available, but when you don't have that available, at least let's not do premature closure. Go after the dyspnea, and I think I would argue that the best field to be in is cardiopulmonary physiology, regardless of which way you attack that from. I think we can improve patients' lives. Thank you. We hope you enjoyed our session. Thank you, everyone, for sitting through our presentation. So we'll take questions. If anyone has any questions, please come forward, or we'll be here. You can come talk to us. Thank you again. I have a question for Dr. Fitton, Rex Young from Baltimore. So my focus is actually not only on the right heart or vasculature, but from thoracic oncology. So your presentation on PET is extremely interesting, because, you know, more bang for the buck, right? Usually when FDG, or FDG, because there's FLT, there's different PET scans. With FDG PET, usually it's like, what lights up, are the nodal stations lightening up? But if we infer the ability to have a certain amount of prediction, maybe still early on, because very often now with early detection, it's all about getting the cure early, which may mean resection, versus non-resectional curative therapies attempted. So how good are you at being able to estimate the PPO, the predicted post-op function? Because so far, the usual old-time algorithm is to go through PFTs, and then if equivocal, you do a CPET, cardiopulmonary exercise testing, look for the V.02 max, and et cetera, et cetera. And then hopefully you can segment out, taking out this function, but, you know, that's predicated on good lung, bad lung distributions. So theoretically, with the application of perfusion flow, you would be able to predict much more accurately, without yet involving a lot additional studies that's expensive. CPET, I don't know how many medical centers in the U.S. still does CPET, you know, how many teachers, you know. So I'll leave it there as a beginning of the discussion. Yeah, no, that's a great question. I must admit, I didn't look at that in particular when I was doing my literature review, because I was focusing a little bit more on how the uptake might present in the right ventricle, but that's a great thought. I mean, if we're following how you have uptake and that shift in metabolism, maybe that would be a possibility in the future. There may be some studies out about it, but I'm not sure. Yeah, in fact, the other thing is, of course, sometimes we look at cardiac uptake as a bit of an annoyance. It's like, darn it, the patient did not fast like we told him or her to do. And you have a sort of confounding uptake that may steal some, plus, you know, if it's a nodule that's close to the heart. So the other thing is, how standard is an algorithm for, maybe as the radiology mind of you guys, you go to RSNA, and maybe also in terms of saying, how much would it take, because it's more reading time, to get radiologists to think about when they're doing an FDG PET for cancer? Yeah, to go back and look at what the heart is doing with it. To get additional, right. Yeah, I think it's all about, my guess is it's all about asking the right radiologist and asking the right post-processing questions. You know, say you have a patient that's getting worked up for their pulmonary hypertension, and they just happen to have a PET CT scan in the past. Calling up the radiologist and say, hey, can you comment on what that looks like? Or I'm thinking the other way around. Most PET scans, most FDG PET scans are ordered for oncologic staging at this juncture. And to say that, also comment on, because it's like the old CT, rule out P in the ED, now they're reconstructing it in one, one and a half, two millimeter slices. It used to be, you know, Dr. Sussnuts, who does interventional bronchoscopy, have to go back, the data is wiped off, we cannot do 3D reconstructions and so forth. Yeah. So it has to be at the get-go. Yeah. I think it's really, and I think this goes back to what Benji was saying, that we have multiple things in our toolbox, and learning the pros and cons as to which one we can use for our right ventricular imaging. So, good thought.