Host with very few skills other than hosting, Dave Shulman. I will introduce our guests in a moment, but I appreciate your kind attendance. We are once again live streaming to our friends out in internet land. The internet tubes seem to be working at the moment, so good morning, everyone. I will ask the panel to be cognizant of the fact that we are live streaming, and please not do anything inappropriate that you would regret later, although, Dr. Farber, knowing you very well, there's very little that you would regret later. Before we pardon the introduction, I'd like to go ahead and, sorry, pardon the interruption. Let's pardon the introductions, if we can. Here we go. First up, the devil from the City of Angels, the guest with the most from the westernmost coast, hailing from Cedars-Sinai Medical Center, ladies and gentlemen, I give you Dr. Vic. That's a load of Tapsin. Oh, my God. That was his picture of choice, and we, of course, honor him with that. Great looking audience, by the way. Great to see all of you. Brilliant, great looking audience. If I could take a point away already, I would, but the game has not started yet. The audience will be able to grant points, but you can't suck up too early. Coming up next, the cardiologist with heart, the frantic romantic from the mid-Atlantic, the un-PCMD from D.C., hailing from George Washington University School of Medicine. Doctor, you've got to fight for your right to Marty Gomberg-Maitland. Please welcome Dr. Gomberg. I just want to say that we all understand why I'm up here, and there's no other female up here. I'm wondering if I should ask for clarification, but I probably do not want to ask for clarification of that. Well, I know who the man next to you is all too well, the crass doc who sits in Massachusetts, the beat-down of Beantown, hailing from Tufts University School of Medicine. Ladies and gentlemen, I give you Dr. Hap of Bridge 2 Farber. Hap, welcome to the octagon, as they say. All right, so whatever. That sounds about right. Let's have Hap. I learned from him 30 years ago, and that's pretty much all I learned right there is whatever. So just rules of engagement for the audience. We have done this before, but for those of you who may be new to the octagon, we're going to have about 14 topics listed. We're going to get to all of them that we can. For most topics, I'm going to select speakers in a random order. I will introduce my color commentator on the far end in just a moment. I'm going to ask my panelists to keep their comments under one minute. I will move on if I get bored. If you hear this sound, you've bored me. We're moving on. Volume, humor, and accuracy are encouraged in that order. I cut speakers off if need be. But more importantly, you should cut each other off if need be, because you will hear your opponent say silly things, and you need to correct them. Four points are available for topic per contestant, two for data, two for just being entertaining to the group. And I can take away points if somebody comes at you. You are welcome to come at me. I will warn you, Hap, since I was a fellow, I've gotten a little stronger and better at this game. So if you come at me, bring your A game. Audience, you have some panels. Hold up your panels or your pedal paddles for me if you've got one. If you don't have one, they're back in the back of the room. Feel free to go grab one. If you hear something you like, feel free to give them a thumbs up. They can get points for that. If you hear something that sounds stupid, give them a thumbs down. They can lose points for that. So you are in charge. If you're interested in hearing more on a specific topic, I'm going to ask you to tweet at the hashtag ChessPTI. That's true for those of you out in the internet land as well. The gentleman to my far left, your far right, Dr. Victor Tess, round of applause for Victor Tess real quick, please. Dr. Tess hails from the Texas Tech University, and Victor will keep them honest with a little bit of a debrief at the end. So he is not an active participant, although, Victor, if you do hear something you want to hear more about, you are invited to jump in and poke the bear. I will. Thank you. I think Marty has a comment that she would like to make. Yes, ma'am. Is that okay? Of course. If I interrupt. So for those of you who have been around for a while, you know that my colleague here always has limericks that outshine everybody. So I thought, you know, I'm the youngest on the panel. I am the best looking. Shit, that's too easy. I know. But I thought I should come prepared so that, you know, we set the stage. So here's a hippie PH doc named Hap who's so old he needs his daily nap. A daredevil off-site, he skis and rides his bike. Does his coffee have added schnapps? Hap's dress at work is unsuitable. Confused with the riffraff is quite usual. Despite his looking gruff, he really knows his stuff. But thinking he'll win today is delusional. Nice. All right. We're going to do one more verse just in the interest of time. Okay. Let's speed it along. Here's the famous PH MD Vic. In his day, he was a top-notch slick. He'll fool you with charm, thinking he'll do no harm. Look in his eyes. You'll see his true schtick. Vic is now working for the dark side after years as a star doc bedside. He's focused on clots, PH skills gone for naught. And then... Lose he will, says Yoda, but he tries. I will say, Dr. Gomberg has done her homework. Round of applause. Unfortunately, she did not remember that until the game starts, you cannot gain points for any of that. So that's good. I want you to give a minus points to the audience. You do not boo me here. That's never going to work. All right. So, folks, again, if you want to chat at us, Dr. Chess, we'll keep an eye on the Twitters and we'll come back later. But that's the hashtag ChessPTI for you out in the real world as well. Here are the first eight topics. Ladies and gentlemen, it's go time. First topic, echo chamber. Should echocardiography and ultrasound be performed on every patient with pulmonary embolism? Dr. Farber, let's start with you on this one. It probably depends on how good your radiologists are, okay? Because if you have really good radiologists who can give you a decent CTA and show you a RV to LV ratio, probably not. And most cardiologists hate like hell to be woken up at three o'clock in the morning and come in and do an echo. At some point down the road, yes, but not right up front, not necessary. Do your own echo? No? Huh? Your own echo? Well, unofficial, you know, critical care docs, we do this. No, I thought you meant like a real echo. So you're saying what the audience does is not a real echo. Okay. Just wondering. Dr. Gomberg. Wow. So, I appreciate that he doesn't want to wake us up. And I also appreciate that our intensivists can do a nice floor chamber and tell me that the RV is really atrocious. And I think that that says a lot more than that CAT scan. The CAT scan is not moving. You don't have any idea of chronicity. You just get a ratio. So it really depends on what you're trying to decide. Where are you in the scheme of the QPE? So should every patient have an echo ultrasound? Yes. Dr. Tapson. Yes, absolutely. The reason is two reasons. One, ultrasound, you want to know what's in the legs, right? David Jimenez showed, 2010, published one of my favorite journals, Chest, that if you're – Point for sucking up. I've got to give it to him. But don't go to that well too often. Hazard ratio of 4.2. You have acute P and concomitant DBT hazard ratio for death of 4.2. So second reason is you don't want someone to get up and walk with iliofemoral DBT. You want to go to the bath and the kitchen. You don't want them walking around. It's kind of like when this creek in my neighborhood overflows during big rain season, you see logs going down the river. You decrease cardiac output, big iliofemoral DBT, it goes to your lungs. You want an ultrasound. You want to know what's there. Tell people walk a little bit, but don't walk a lot yet. Number two, the RV, you want to do the echo. Not just for RV-LV ratio, not just like Hap said, get a CT. You want that echo so you can see if there's clot in transit. Now if there's clot in transit, about 5% to 10% of patients, clot in transit imparts a death rate of 12% to 45%, and you want to be aggressive. AHA condones being aggressive with clot in transit. That's my short answer. But I'm trying to think of something funny. Well, look at me. Look at him. He just threw so much data all over you. You're buried. Hey, look. I just bought a 66 Toyota from the guy. It was a nice Corolla. The only issue I would say is that a clot in transit isn't often seen by the- By the CT, right. By the bedside guys. Or by the bedside guys. So then if you have any question of that, then you should be getting- Sure. You got to wake Marty up at 3 o'clock in the morning. You got to get the echo. You got to get the echo. You do. We love our patients. I was trying to be nice to Marty. That was so nice of you. Don't be nice to people. In real life, you're not here. They're paying for blood. They want to see some aggressive. I know you're capable of it. I've seen it. All right. Let's move on. Topic number two. Number, please. Is the diagnostic threshold for mean pulmonary artery pressure appropriate at 20 millimeters of mercury? What about a pulmonary vascular resistance at three units? Dr. Gomberg. Yeah. So, I mean, I think this is kind of outrageous that we finally went back to what we did, I don't know, when I was a young'un and just kind of gave a- Last week. Yeah. A mean threshold. Wow. I think I was in kindergarten when that thing happened. But, you know, guys, you can't now start to use the standard deviation and do it properly because the reason why you guys said it was so that you wouldn't over-treat. So I think that it's just gone a little nutty because now we're relying on the science, but none of our clinical data relates to a mean PA of 20. So I think we should have just left it as it is. If you disagree, go at her. So, no, but the craziest thing about this, if you actually use these numbers, I'll give you a quick case. So you got a person who's hypertensive, dyslipidemic, and diabetic. They're 5'6". That's HFPEF. That's HFPEF. Yeah. Yeah. We don't need that. We don't need the diagnostic. Hang on. Hang on though. So they have a... And they're 80. No. They have a PBR of 42. Okay? They have a decent cardiologist who diuresis the hell out of them, you cath them. Their wedge is 13. Okay? Their mean PA is 22. Okay? And their cardiac output is 4.4. That gives them a PBR of 2.2. Okay? Their wedge is still high though. So you're going to tell me that this person has PA. In addition, if you actually do the math, this person has a cardiac index of less than 2, and you're going to put this person on systemic therapy? The question is just, is the diagnostic threshold 20? That's the question. COVAX 2009, European Respiratory Journal, right? 1,187 patients, 47 sites, 13 countries, PA pressure, mean PA pressure of 14, right? PA pressure of 14. Two standard deviations above is 20. That's the diagnostic threshold. That's the question, right? But the issue is that the people who have that lower, if you will, mean pulmonary pressure or the lower PBR, almost invariably, are going to have either group 2 or group 3. But the way the new guidelines are set, they now have true PAH. So are you saying the diagnostic threshold shouldn't be 20? Or should it be? No, the bottom line is, I don't really know what it is. Okay? Thank you. Thank you. Yeah. Ladies and gentlemen, Dr. Farber has just said, editing carefully, the bottom line is, I just don't know. This is not nice. This is not nice. Okay. We understand. We understand physiology versus clinical shit. All right. No cursing. All right. Watch the language, Dr. Farber. I'm sorry. When you tell all these people that it's okay to treat with a mean of 20, that's just not okay. That's nonsense. Plus, as pointed out, none of the studies have ever been done on these patients. And you're going to now tell me about all the patients, there's only 2% that changed their diagnostic when they presented at 2018 World Symposium. So what's the diagnostic threshold? What's the answer to the question? The other point, Vic, is nobody... What is the best answer? It's 20, COVAX. All right. And Mario Super wrote a nice commentary along with that paper, right? Hang on. There's a difference between what your physiologic pressure is and what clinically you actually have and what you treat. Yeah, exactly. Sure. Hey! But what's the diagnostic threshold? Well, hang on. That's the question. I'm going to call 20 seconds on this topic. I grew weary. There's a difference between whatever you want to use as your diagnostic number and whatever you're going to treat. Yes. And the thing I have is with these new guidelines, there are people out there in the real world who are going to start treating these people with no data. Yeah. You know that. You know that. When you treat a patient and their mean PA pressure goes to 30 from 50, you're pretty damn happy. But that's not the question. The question is the diagnostic... So wait. So wait. Yes or no? That's not, would you treat them? Would you not treat them? So yes or no, Hap? Yes or no? Is this mean diagnostic... So are these change of guidelines or are these data appropriate as written? By the world pH guidelines in the last meeting in Niche, what did they say? Yes. Just because people say it's true doesn't mean it's true. You can't thumbs up yourself, Dr. Tapson. So Nick, under that scenario I gave you, are you going to treat that person? I might. It depends on the patient. Oh, give me a break. Okay. All right. So I've got a 40-year-old woman with dyspnea and a mean PA pressure of 22 PVR4. But you realize then you need to do the PVR of 2.2 if you're going to use all the data and that says three. So is that the argument it's the PVR? Is that the argument? Well, you just said the diagnostic threshold. Well, PVR3, I mean, we know the... What about PVR3? Are you going to use the PVR of 2? If you're going to use the data, you have to use the data throughout the whole thing. The question is what's the best answer. No, no, no. The question is what's the best answer to the question. That's the official answer by the world pH guidelines. Audience, hot take. Thumbs up, thumbs down. You're good with that argument. Come on, you guys. Thanks. Love you all. Love you all. All right. It's about 50-50. All right, I'm going to leave the score as is. We can come back to this if time allows. We have things to get to. Liverly dilate is our next category. Should all patients undergo vasodilator testing at initial evaluation? Dr. Tapson. I would say no. Nowadays... Hold on. Let him answer. I love the original data by Stuart Rich. Are we going to use calcium channel blockers? I mean, when's the last time you used diltiazem and someone? I think we've got really good drugs now. Way more data on our other three categories of drugs than we do for calcium channel blockers. So I would say no, not everyone. Not everyone. Should all patients? No, not everyone. Should a portal pulmonary patient? No. You don't want to give them a vasodilator, a portal pulmonary at their cath? No, you're not going to do that. So should all patients? Absolutely not. Dr. Gomberg. So I unfortunately agree with him. I might have to take a point away for agreeing with him. But I will say that you do need to do it more often than people are. Because if you miss it, you're really putting that patient in a very different circumstance. And there are tons of patients that you get that are on oral therapies that are actually calcium channel blocker responses. So you agree that not all do. We agree, Marty. I agree. I agree. I'm on your side this time. Thank you. But it's a rarity. Farber, do you agree on this? You don't agree on anything. Unfortunately, I have to agree with the two of them. Because I'm notorious for not doing it. You're notorious for not doing it, but you agree? No, no, no. So the vasodilator studies are basically, in my mind, are people who clearly you're not going to put on systemic therapy to start with. People who fit certain categories. Or the people you, unless you're doing this all for research, fine. But in general, are you going to do somebody, you're not going to do a vasodilator trial on somebody you cast as a wedgie? Cardiac index is 1.5. Are you going to do it? No, you're not going to give someone a vasodilator. You're not going to do it. Absolutely not. So should all patients? No. Actually, I hate to agree with Marty's point. Stop manhandling the other contestants, Dr. Farber. Marty's point is actually well taken. And people who have like idiopathic PAH, or heritable, or drug and toxin, you know, every once in a while, if you don't do it, you're going to miss somebody who actually is calcium channel blocker. And the case I always used to bring up to do some of the patients you wouldn't think of doing, is I have a guy who has truly sickle cell PAH. No question. He's had it for 22 years. And back then, we were doing vasodilator trials on everybody. And he dropped his mean pulmonary pressure from 50 to 22. And he has been on a calcium channel blocker for 22 years. But should all patients undergo vasodilator testing? No. All right. We're done. We spent a long time coming to a full agreement on this topic. Moving on. CTEF Curry is the next one. Is ventilation perfusion scanning still the best test for CTEF? Dr. Farber. It depends if you're a radiologist or not. That's the second time you've gone to that. Yeah. Yes. Yes. That's all you have. Okay. Dr. Gomberg? Just to be the contrarian, I'm going to say no. And I'm going to say that because most places don't have EQ scans. And through all of COVID, I couldn't get one. Because nobody was doing the ventilation. Yeah. But that's a special instance. Wait, wait, wait. I want to do an audience poll. The assertion on the table is most places agree or disagree. Most places do not, is this assertion. Oh, okay. Wait, wait. During COVID. Okay. During COVID? Did that flip you around? You went from a grossly negative to a grossly positive response. You did. You did. And do we think that it prevented the diagnosis of CTEF? No. The answer is no. We didn't. It's the best screening test. But then you need a CT scan. You can't determine operability or whether someone gets BPA based on the VQ. So the VQ is the best screening test. You've got to do a CT. And ultimately, some agree you've still got to do a PA gram. Most surgeons would agree. So I think a PA gram is the best. I think it's the best initial screening test because if it's normal, you're done. It's not CTEF, right? It's not CTEF if it's normal. So do that. Save the patients more tests. So aren't these patients getting CAT scans anyway at some point in their workup generally? Exactly. So then in that context, what's the point of a screening test if you're going to go on to the second test? Then you get two points for that right there. Thank you. No, no. But they get- And what happens in the ER? They get a CTPA the minute they walk into the ER. Right. Well, not for CTEF. That's for PE, but not for CTEF. Oh, my God. His hormone is a little bit positive. The D-dimer is 51. You're getting a CTEF. So back to the question, everyone has said you're getting a CTPA in that context. Should we be doing VQ? It's the best screening test, but it's not the best test, as the question's worth. Fair enough. Wait, wait, wait. Screen? Someone's got PE, so they have CTEFs. Let's do a VQ. So you agree with me. It's not the best test. You can walk into an ER and get a VQ scan. I agree. It's not the best test. It's the best initial screening test. We have a VQ scan to the wellness center if you go over and look, I think. We do not. We do not. For those in attendance, we do not have VQ scans. Okay, moving on. Next topic, take a walk. Is a six-minute walk a useful diagnostic test or an utter waste of time? Dr. Gomberg. This is, to me— Oh, I heard some groans from the audience. I apologize. I've disturbed the audience with this question. You know, one of the first things that I did was a six-minute walk test versus the treadmill test. Now, I know that I have an audience of pulmonologists, and why would we do a treadmill test where we only go to the gym and have our home Pelotons that are telling us how many mats we go. And it's because—and now it's even more real that the six-minute walk has its limitations. You can only walk so far. And we see that, and now we don't even often have a cutoff for the entry into our trials. I think we need to move away from that six-minute walk test finally and move on to something that's truly a max test, not a sub-max test. Dr. Farber. I think it's a waste of time. Yeah. My turn? Yeah. Okay. Forget it. Rick. Somebody who— Hey, you lost your turn. It's fine. Sorry. So, the six-minute walk is a useful test, and it's not a total waste of time. It's a useful test. It's not the best test in the whole world. Maybe everybody doesn't need it. I mean, I don't need one right now. It doesn't say anything about who needs it. But, you know, for pH patients, it's a good test. It's a useful test done correctly in the clinic, good hallway, good sats, your personnel doing it the correct way. It's a useful test. It's not the best test in the whole world. What does it add? What does it add? So, it's a useful test. It implies that you're collecting some data. You're using it for something. What's its role? What it adds is the distance someone can walk in six minutes. Yes. Okay. And so— Is that more sensitive, specific, useful, additive? I would argue that you're one with a cardiac index of 1.5 can still walk 400-something meters. Well, I mean— So, then what does that do? Well, it doesn't mean everyone needs the test, right? Everyone might—but there's some people. I think it's very helpful. You want to follow how they're doing. You follow these patients. You want to see how they're doing. I want to know how they're doing. It's one part of your assessment. It's not everything. But it's a useful test. It's not a total waste of time. If you're waiting for him to stop, you're going to be waiting a long time. Jump in. I know. This guy's selling mattresses now. He says, look, Michael and Bill, the pillow guy. You got points the first time you went there. You're not going to keep winning points every time you call him a salesman. As a person who wrote the paper about the six-minute walk improvement sucks, but if you fall 15%, that's really good. That's the way I believe it should be used. The problem is, if you're going to be a salesman, you're going to be a salesman A six-minute walk is really unreliable because they have so many other reasons that they can't walk. So it's a total waste of time, you're saying? Or is it a useful diagnostic test? It depends on the patient. You would have said every question depends. Not for everyone. Not for everyone. Also, I mean, I can tell you there are certain places where it's done poorly. Yeah. Are you going to tell me that you can't tell looking at the patient? I mean, I know a place, not to name it, but in Boston, where the six-minute walk ends where the cafeteria lets out. No, so they go, right. No, so I think overall, and it's time it was a useful test. It now has become less useful as things have moved on to other things that are clinically more important, like hospitalization, things like that. Do you think you should be walking these people with canes and walkers? No. I mean, because that's what's happening. I know, it's ridiculous. So it's not a required test, so it sounds like there's a general consensus it's useful, but in the right case. There's another two points for Dave. Thank you. It's lost its usefulness. Audience, thumbs up, useful diagnostic test, thumbs down, waste of time. Well, that's what I'm calling it here. So not a diagnostic test. The audience is actually learning and watching the reading the question. So half, I'm going to give you a yellow card. You didn't know, but there is a rule that we had to put into play after Atul Malhotra was up here referencing his own manuscripts multiple times that we yellow card you the first time. If you keep doing it, you will red card. So that's okay. It's good to be self-referential. It's good to know. Yeah. So that's why I'm warning you all. Nobody loses points the first go-round. Well, I might end up coming up with the rules later. You lose a point. I'm allowed to change the rules. That's the beauty of being chess president. Let's move on. I'm going to be a millionaire. That's fine. Feel free. All right. Next topic. Exercising your demons. Does exercise-induced pH exist? Is this a real thing? And if so, how would you define it? The groan from Dr. Farber tells me I need to go to him first. So I believe it exists as an entity. How to define it has defied definition. Okay. The current definition that was put forth in the guidelines is horrible, okay, because it's based on a single study of which it's all people with left heart disease. Okay. So I don't know that it actually has any relevance to true PAH patients. How you actually define it, just to define it with a change in mean pulmonary pressure is not sufficient. In my mind, if you really do have exercise-induced PAH, you will raise your pressure, but the main thing is what happens to your PBR when you exercise. If it stays the same or certainly if it goes up, that's evidence of pulmonary vascular disease. Okay. And if you wedge doesn't go up with it, there are people, especially some of the scleroderma patients that you catch really early who have what looks like exercise-induced PAHs. Colleagues? So I would argue that it's just part of the continuum. Yeah. I mean, as you age, your resistance goes up, right, in the body, systemic. But your resistance still go down when you exercise. Yes, understood. But why can't it just be that some people have abnormal reserve in the pulmonary circulation versus others? I mean, as a cardiologist, and I know that's going to get me a negative. No, it did not, yet. You know, we've done this. We know the microvasculature plays a role. Does it warrant a PAH diagnosis? Do we know that our drugs treat it? No. So I think to give it its own entity- Can I talk? No. Let her finish. You can always jump in, but I like what I'm hearing. To give it its own definition as this, you have exercise PAH. I think that if you see what's happening, it was with the cath, are we looking at the blood pressure? Are we looking at the heart rate? Everyone has exercise PAH on their way to getting PAH. And then some people, and some people, and some people, they stop. You have to. You have to. It's kind of like you can't have PE without DVT, except from a few other places. But I mean, bottom line is, if you have exercise PAH on the way to getting PAH, you have to bump with exercise. You can get resting PAH without ever getting it with exercise. You walk 10 feet, you don't- So then you should just test everybody. You're going to get it on the way to get, and then some people stop, and they're functional class too. And they're treated and never get worse. No offense, but that's freaking nuts. No, it's not. No, it's not. Continue. So any data? Do you have exercise PAH? No, I don't. But if I'm going to get... I'm saying not everyone has it. Everyone that gets PAH has it on the way to getting their resting PAH. Yes, you can. How can you not? How can you not? There's no evidence on the mean PAH meter. There's no evidence. The freaking world is round, you guys. Come on. No, it isn't. On the way to getting resting PAH, you have to get exercise PAH. Some people stop there and never get rest PAH. Some people keep going and get class, functional class for resting PAH. It's a continuum. It's a continuum. I'm going to put a whole audience. What's your take on that? Is it likely that people have exercise-induced PAH on the way to getting regular PAH? How can you not? Thumbs up, thumbs down. Now you guys are looking into his eyes. You have to. Don't look into his eyes. They're looking into his eyes. I gave about 60% thumbs up on that. So why is the audience wrong? Well, the problem is you may or may not be right, but there's absolutely no way to... No proof of it. There's no way to prove it. You're not going to cath every human in the world and say, okay, we're going to wait around for five years. But do you think he's right? The doctor of PAH, they call HAP, could cure your PAH in a snap. When it comes to debate, he's good, but I'm great. And he knows that I'm not full of crap. Wow. And I don't think he came prepared with that. I don't know. I don't want to know. I prefer thinking you didn't. So you can't prove it. Do you believe it? That's the question. Do you believe it? No, I don't. No. How physiologically is that not likely to be true? I'm not a... How can it not be true? Vasculologist. But teach me. This is the same thing as if you actually look back and you look at autopsies of people who don't have PAH, okay? People like, especially scleroderma people who don't have PAH. A lot of them have vascular changes that look like they have PAH and they never develop anything. Well, then they don't have resting PAH. They don't have exercise PAH. You can't get to the resting point without going through exercise. You bump your pressure with exercise before you bump it with rest. Sorry. So they can have the histology that looks like PAH, but they never develop it. So I have no idea what you're talking about. Actually neither do you. But the thing is, we don't diagnose it on the way. We miss it. He does. He says it with authority. We don't diagnose it on the way to resting PAH because we don't. Patients get resting PAH too quickly. We don't always say, oh, you've got resting PAH now. We don't diagnose it, but they have to have it. What you would do well is the movie Back to the Future, and you would go back and cast all these people that show up and prove it. It doesn't help to do that. It doesn't help to do that. We don't need to do that. We just know it's true. It doesn't matter. I'm sure we're coming back to this topic later, Dr. Schatz. Fair to say? Oh, he nods. Yeah. Sorry. Let's move on to ejection day. How should we diagnose pulmonary hypertension in the context of heart failure with preserved ejection fraction? The second time we're hitting HF today. Dr. Gomberg. Yeah. So I would say that that's definitely, if we're really looking for pulmonary vascular disease in a mixed component, then you need to do the cath. I don't see how to go about it. We can add up all the echo criteria and diagnostic phenotypes. It's very commonly a phenotype, but yeah, you've got to have a cath, sure. But here's the thing. Again, although Vic doesn't care about treating patients, he just cares about the definitions. If, since we actually will likely have medicines for this, then you want to make sure you're treating the right people. Do I cath 80-year-olds with diabetes and hypertension and a BMI of 50? No, because I know what the answer is. But if you have stuff, like if you really want to know what it is, then- So you need a cath most of the time, but sometimes you don't need a cath. Is that what you're saying, Mari? I agree with that. That makes sense. It's a phenotype. You look at the phenotype. That's probably a HF, and then you do an echo. Oh, the EF 70%. It's really probably HF, and then you decide to do the cath or not, depending on the phenotype. We all agreed. We all agreed. I haven't heard from Dr. Farber yet. Well, I was just going to answer that. I think the problem here is severalfold. One is, you have no idea of the HF-PEF is just too many phenotypes all rolled into one. That's part of the problem, is we have not defined the phenotypes, for one. You can't definitely- I don't know if that's the case. There's a nice- Obesity, diabetes, hypertension are pretty good phenotypes. No, no, but you can't tell me that somebody like with scleroderma who's really thin and all this is the same phenotype as somebody who's in the BMI of 40 or whatever. The second thing is, if, in fact, you diarese somebody really well, I can make them look like they don't have HF-PEF. That's pretty mean to do that, because you don't want to make them look like they don't have HF-PEF. You want to get the right answer. No, no, no. What I'm saying is, in the real world, a lot of the patients you get referred in on treatment are people who've been well diarese, and they've been started on meds, even though you- And so what are you going to do? You're going to cap them. Right. So we diagnose it by looking at the phenotype, looking at the echo, making decisions and considering a cap. I think the one point that Marty made that's really good is, unfortunately, you can use any echo criteria you want. You can use any of the scores, but when push comes to shove, if you're not sure, you need to know the answer. I feel like he's giving me compliments again. No, I'm not. I don't know. I feel like you're all taking the same journey, and the two of you on the far side get right there and Hap sort of wanders around for a while. He's a wanderer. And then comes back around and meets you at the end. That's just the drugs kicking in. He's a wanderer. There's a point, self-deferential's worth a point. Let's move on, the clot thickens. How important is clot burden in stratifying pulmonary embolism, Dr. Tapson? I think it's important, it's one feature, right? I mean, if you have extensive clot burden, if you block every PA in the lung, you're gonna die or code or something. So I think there's a nice paper by our colleagues in the Netherlands, Vandermeer 2005, and Mena Weesman was on that paper too. And they found if you have acute P and your clot burden is more, your obstruction addicts more than 40%, your mortality is 11.2 fold increased over the next three months. And that's PE related mortality. So clot burden does matter. It's not the only thing. RV function matters, vital sign matter. Clot left in the leg matters. A lot of things matter, but it's important. We always look at it. You can make decisions sometimes about a patient with clot burden, just a few other parameters. It definitely matters. Dr. Farber. Okay, Anari Barath. I'm still at Cedars. I was on PERT last week, by the way. I think the major thing about clot burden, there's no way that if you obstruct the vessel, the burden of what you obstruct isn't important, okay? But the thing that's important. So we agree, we agree. No, hang on. Oh, you don't wanna agree. Calm down. So the more important thing to the clot, the thing that's equally important to clot burden is how well or not your right ventricle can handle that clot burden. Of course, yeah. Okay? Yeah, that's true and false because if you've had multiple PEs and your RV's already compensated. Then you can handle it. You can have a high clot burden. No, I agree. And your RV's compensated. So I think that what you're trying to say is clot burden matters. It does. It matters. If you have a sub-segmental clot versus extensive bilateral PE, there's a difference. All right, Dr. Chapson, we have a minute, let's go. Dr. Gomberg, you're with Dr. Martin. Yeah, I just think the problem is that we don't, I look at a CT and I go, oh, there's a high clot burden. But how are we actually measuring it and how is that factoring in? Miller index or Canali score, or just your gestalt, is it gestalt? There's no really good way. I mean, even our interventional radiologists will say, geez, there's a lot of clot in there. They're not gonna say, you know, that looks like about 42% of my clot. No, they say, geez, there's a lot of clot in there and it's important. Wait, but sometimes the CT doesn't show a lot of clot and there's actually a lot of clot. And it also depends if it's proximal versus distal, because you can have a ton of distal clot and not see it. Well, what was the question? Does clot burden matter? That was the correct. It matters. It matters. It eventually matters. It matters. It matters, period. It matters, we agreed. You keep getting pulled over. He went around. He got there, all right. No, no, you just get there in a different room. Intermedial lytics is the next topic. Should intermediate risk PE undergo intrapulmonary lytics and extraction? Dr. Farber, let's start with you. Should intermediate risk PE undergo lytics or extraction? So this is the one that has people who do PERT teams ripping their hair out, okay. The data suggests, although the data aren't good, there's only one controlled study that suggests that if you have intermediate clots with any kind of evidence of, or if you have an intermediate status, the people who are high risk or low risk are easy, okay. The people, this is sort of like PAH, the people in the middle are the hardest, okay. So my gestalt actually is that they do, you do need to be more aggressive, especially if they have evidence of right ventricular dysfunction. So are you doing intrapulmonary lytics on your intermediate risk teams? We actually do thrombectomies, okay. Because, no, no, no, but for a reason. Because our radiologists and me, okay, are much, I think that the age of lytics is like the six minute walk, is headed out the door and down the road. I agree. Because there's no reason, if you have a better system potentially, to expose somebody to the risk of lytics, even though it's smaller if you do it intravascularly than systemically, why do it? Yeah, so what I'm gonna say is that I don't understand why folks don't treat this like a heart attack. Because if you don't get all the clot. So then you pull it out. Whether it's intrapulmonary lytics versus extraction, I think it's gonna depend on the center. So yes, I would use intrapulmonary lytics for intermediate patients, and I do. And I don't base it on like, oh, but their oxygen sets are fine and they look fine. It's like, if this were my family member, I want it out. So regardless, you're taking it out regardless of any clinical center. I'm taking it out, I don't care which way it is. Whatever the IR is willing to do. I think in centers where the interventional cardiologists are doing it, you're getting, there's more aggressive. I think that patients get back to work. I see them all post. And they get back to work faster. You wouldn't do a thrombectomy in a low risk person. I didn't say low risk, we're talking intermediate risk. I know, but we know that the low risk has a good outcome and that we can treat it with our current therapies. So. Well, I agree with my colleagues here. I think we should be aggressive here. If you look at the data out there, look at the mortality of intermediate risk patients. We divide them, by the way, into intermediate, high, and low, right? Intermediate low risk means your trope or your RB is abnormal. Intermediate high means both are abnormal. If your intermediate high risk data show your mortality is 10 times higher, 10 times higher than if you're low risk. And that's PE-related mortality. That's Cecilia Beccatini's study where she went through. And intermediate low risk patients, by the way, had a mortality four times higher than low risk patients. So these patients need to be looked at. They need a conversation. And I agree with half and Marty that most of them should be considered for aggressive therapy. And we published the FLASH 800 data. 800 patients, large board thrombectomy, mortality less than 1%. So you gotta look at the data. But it's not controlled. Did you say we published? Yeah, we, sort of. Me and my partner. Is that the royal we or you? Royal team. Royal team. Is that the yellow card? I may yellow card him. I meant we as a group. We as a group. Okay. Not me, not me. I think there's another point to keep in mind too. So what we have mostly is we're basing decisions or we used to base decisions on data that was old. Okay, and technology that was old. And as the technology has improved as far as getting the clots out, I think most of us would agree. Great point, great point. What's it gonna take to make it so that the PERT team is like the acute MI team? No, that it's time to getting it out because that's where I'm at. That's where we're headed. But I don't feel like. Well, our hardest thing at the beginning was to get IR on the same page of let's get these things out. And then I would argue that quality of life is making a huge difference. And we're not looking at it. So I wanna go to the audience here. What, again. Well, wait, there's one other point. Some need contractions, some don't, some don't. Aside from what we're talking about initially, the real question is, is down the road, do we do something that prevents people from going on to develop CTEP? We do not know the answer to that. We don't know. Yeah, I think it's irrelevant. But we do know that RPVO predicts increased mortality and increased recurrence rates. Residual pulmonary vascular obstruction, even without CTEP. And that's our bona fide data. All the European data suggests that leaving clot that persists in the lung is bad. But we don't know yet whether getting it up, getting it out up front will matter. It's a nice hypothesis. So in that context, in the audience, thumbs up, thumbs down. How many of you are currently, not maybe want to, if you're currently performing one of these procedures on your intermediate risk patients? You can get some paddles for those of you in the back. We have the thumbs up, thumbs down paddles right next to you. So it looks like about 75% are actively doing this. Does that surprise you? No, actually, over the last couple of years, it's more, since interventional, since intervention, I consider myself sort of an interventional pulmonologist, and I are a cardio. You're a frustrated cardiologist. Yeah, he is not an interventional pulmonologist, ladies and gentlemen. Because they're not hard to do, and they're. So I would say that in the 75% of folks that actually do it, do you have to push to get it, or are you like the last case of the day? Like, are you the last case of the day because you're looking okay, or you immediately open up the lab? And I bet it's that you wait till all the elective procedures are done. If you're high risk, you do it right away. If you're not high risk, if you're intermediate risk, usually you wait, and it's probably reasonable to wait. Well, the hardest part to get IR was. What are you waiting for? If you're gonna do it anyway, I mean, other than the fact that you don't wanna wake up. The IR people get it done before three in the morning. The reality of it is, the hardest part to get done is if it happens at night or over the weekend, and the IR people say, ah, they look pretty stable, we'll do it tomorrow. The cath lab opens. I'm just saying. It's usually pulmonary that says they look okay. An IR wants to do it. All right, I'm ready, move on. All right, coming around the final turn, we're in a three-way tie, folks. So we're going into triple play. Should PAH patients be on triple therapy regardless of clinical response? Dr. Gronberg-Maitland. Woo-hoo. Ha ha ha. Ha ha ha. He cackled at it, so I'll give him a point. I like the cackle. I'm gonna be honest. If we want everybody to go into debt and without the evidence, if your PVR is normal, there's no reason that on two therapies that you need to add a third just to add the pathway. It kind of reminds me of when folks were on oral locentin and they had zero objective evidence that they were responding that we just added because we were afraid to take it away. When in hypertensive disease, when things don't work, you just stop it and you move on. So to me, just starting everyone on triple therapy is just nutty. Dr. Japson. I think Marty summed it up very nicely, yeah. I mean, first of all, we don't want to start everyone at once on triple therapy. We want to make sure there's side effects of their drug, add another drug. We've got the ambition study, but we don't have the ambition study for three drugs yet. In fact, it failed, right? Yeah, exactly. It failed. Yeah, that's the zip-on paper, yeah. So not everybody, and certainly not regardless of clinical response. If you've got someone three drugs and they're not responding at all, you don't keep them on a drug they don't respond to. It takes good clinical detail, good clinical care, and you make that decision. The bottom line is there is no proven or robust evidence that starting people on three drugs at once is beneficial. Okay, we might believe it in our head that it makes scientific sense, but there's no evidence for it. We agree. We all agree on that. We should all probably get the same amount of points for that question. He's gonna find something he disagrees with. Go ahead, Al. So I think to extend Marty's point about the money is also, you have to remember that the more drugs you pile on, there's more likely to be side effects and drug-drug interactions. And especially in some of these patients that are misdiagnosed as PAH and actually have left heart disease, all of a sudden they show up and they're in Florida, left heart failure. Maybe that makes me say a PAH doctor named Marty. All right. Says PAH treatment should never be targeted. Now I know you just came prepared. She's a brilliant, great doctor, researcher who rocks. She's a PAH expert and smarty. I like it. Thank you. Should I give him a point for that? We know he wrote it yesterday or two weeks ago. I wrote it yesterday. All right, they're giving you a thumbs up. So I'm gonna give you the point back. I took it away, but let's move on. Three topics left. While IV never, are we under-utilizing intravenous therapy and PAH, Vic? I think we are. I mean, when somebody, I'm not gonna say who, published the paper, the Flolan paper in 1996, New England Journal, nice paper. I mean, we learn, we learn. Where's Abby? Abby's here. Where's Abby? Abby and I, we treat a lot of patients. Abby and I put in 600 people in IV procycline therapy. I mean, the bottom line is, yeah, Abby did. Abby gets a point. It was Abby. Abby, come on up. Abby gets a point. It was Abby. Abby gets it. That's true, it was Abby. She did all the work. I tried to get the credit. Bottom line is, this drug works well. What do we do in cancer? We don't sit around and wait for something to happen. We give them induction therapy, blast them out of the water. IV therapy works really well, and yeah, it's a little inconvenient, but it saves lives. I think we're under-utilizing. I think we should be more aggressive up front with people. Maybe we put them on, maybe we stop it in a year, but be aggressive up front with these patients. Dr. Farber. These are human lives. As somebody who probably uses more intravenous systemic therapy than anybody. It's a packed channel of IV, but it's. I think people actually, when there was only one drug around, okay, I'm convinced that people actually did better, okay, because they all got intravenous therapy, and I think the thing that's most rewarding, or more telling, is the fact you can put somebody on intravenous therapy, and within 48 hours, the difference is just unbelievable in time. So I think it's underused for several reasons. One, we've gotten into this situation where physicians don't tell people the truth, okay? They go, we'll put you on this oral drug. You'll be okay. It's inconvenient for the physician and for the patient. And they go, we're only gonna use intravenous therapy as a rescue. What's their motivation for lying? Out of curiosity. I think it's. Half the saying, you're all liars. I don't like it. I don't think you are. Yeah, I mean, nobody likes a crying patient in clinic when you're just meeting them. It's not good form, it's not good form. So what I would say is that I think that right now, we are fortunate to have other options. And that sometimes, surprisingly, and I will say that now it's been over a decade that we've been doing dual combination upfront that I've been surprised that some people do really well. But the problem is is that we're all biased because I inherited a huge IV practice that we still have patients that we started 15 years ago that are doing fine, 20 years. And so it's one of those things where we've always wanted to do sort of an induction therapy. But here's the thing, Hap. The problem is that now there's so many sites that have no idea how to use IV. Absolutely. That they don't even think about it. So we are underutilizing it. I mean, there's people out there that should be on it. We're underutilizing it. No, we all agree on that. I think the issue too is that we have been hoodwinked, some people, into believing that other modes of therapy are gonna be just as effective. Well, clearly they're not, okay? And you would love to have easier therapy, but you don't. And the one thing Vic has said, the entire thing here for the hour, it's true, is the fact that you should treat this disease like you treat heart failure. What's heart failure? Like you treat HIV, like you treat cancer. You get on top of it first, then you can back out. It's not- Thanks, Hap, thank you, Hap. No, you never wanna get behind and then try and catch up because that's almost, almost always gonna be a failure. Let's move on. I mean, how many patients have you and Guy C- I completely agree. And they are now functional, class four, in floor and right heart failure, and they should have been on IVF- I feel like we have consensus. Any closing remarks? 10 seconds, anybody? Closing remarks on this topic. On this topic, on this topic. No, okay, moving on. Ileo killed the radio star. Should acute symptomatic ileofemoral DVT be treated aggressively? Dr. Gomberg-Mailand. Well, I mean, if you're gonna- I'm glad they started with you. I think if you're gonna treat your PEs aggressively, you should just be aggressive. But I guess, again, you know, like everything in medicine, it depends on the patient. But I would treat it aggressively because I don't want it to go all the way up into my lungs. I don't even need any tablets. I agree with Marty. I think we should be aggressive. And again, there's other things to take into account. If someone's 90 years old, ileofemoral DVT maybe shouldn't be aggressive. We have good techniques like referred to earlier, not just lytics, but clot extraction, clot treatment device. You can go in there and get this clot out easily. Even chronic clot, we're getting extracted now. It's a new era for DVT. It really is. But I think we can be aggressive now without lytics and our pace is a great favor. Okay, so by aggressive, you agree with the mechanical interventions? I do agree with mechanical interventions, not systemic lytics. So I think just to play a little bit of devil's advocate and temper. Not that I don't agree that if you're gonna- Either take one side or the other. No, no, hang on. Keep it short. He doesn't know what side he's on yet. He'll figure it out in the next minute or so. No, I can't wait. It's like an anticipatory. No, that's what I'm trying to do here. No, I think part of the issue is, although we do agree that we wanna be aggressive, unfortunately at this point, we don't have the data to back it up. But just as a little bit of a temper this down. But now because of the ease of doing this, we're all gonna do it and probably never get the data to prove that what we've done is actually beneficial. So we learned in the ATTRACT study, it was kind of a failure of a study, but we did learn the subcategory of patients with iliofemoral DVT have a lower risk of post-thrombotic syndrome. So I think it makes sense for post-thrombotic syndrome is a painful, chronic process. We don't want our patients to suffer. So I do think for that reason alone, it makes sense. But now, even since ATTRACT, we have better techniques. Clot treatment data has been published. We have better techniques. So I agree with my colleagues. We should be aggressive here. Audience, thumbs up, thumbs down. Treat aggressively in terms of mechanical extraction. Thumbs up if you have your little paddles. Those who are holding up, I would say about 80%. I would say about a 20% as a vocal minority. I'll tell you in the real world, that is a little harder to get past your interventionalist than doing clots in your lungs. It's more convincing when someone's very symptomatic. If they have phlegmasia, it's easy, but very symptomatic. Sure, yeah. Final formal topic, mistakes were made. What single mistake is made most commonly? Consulting HabFarber. Wow. I was gonna go to you first, but I'm now gonna go to HabFarber to defend himself. Letting Vic talk. Actually, I agree. Unfortunately, I agree with him. Having Vic's mic on. All right, let's get the answer. Well, everyone's gotten points on the smack, and I love it. Let's actually get to an audience and answer the audience is gonna like. Hab, what single mistake is the biggest one we're making? I think the most, I think if you just take the numbers and whatever, the most common mistake is treating people who have left heart disease with whatever pulmonary values of diarrhea you wanna come up with. Dr. Gomberg-Maitland? I would say that I think the most common mistake that we make is thinking that we understand pulmonary hypertension. I think the most common mistake is failing to make the diagnosis. These patients come in, they're told they have childhood asthma, this or that, they're obese, they're deconditioned, et cetera, and we finally make the diagnosis too late. We need to raise awareness. I wanna hear more from Dr. Gomberg-Maitland. Hang on, so Vic, that is true. Thank you, thank you. No, no, no, but wait, but remains true, but we have spent decades going out in the real world and trying to prove people's awareness of the disease and making the diagnosis, and at least in my mind, I don't think we've made a hell of a lot of progress. I think we have. I think we've made a lot of progress. Just the fact this room is full here right now, to me, is progress, that there's pulmonologists interested in care. Well, they only came to see your hair. Marty, I wanna, can you clarify your initial points? Yeah, I think that we're all arrogant to think that we understand all of this when we can't even see the vasculature real time, right? Like in cancer, when you've shrunk the tumor, you see you've shrunk the tumor. We have medications and patients feel better. We've done something, but then for us to be, I mean, I have old textbooks from my great-grandfather which talk about treatments that are just crazy, but at the time, were okay. So maybe, I fear that 20 years from now, they're gonna be like, what the heck were they thinking? Well, but I think part of the issue is the way, I think we've actually been led astray by the classifications of pH we actually use, okay? So if you look at all of that and say, well, group one pH patients- So like exercise pH, you mean? That's right, no. So group one pH patients are all the same. You cannot tell me that a scleroderma pH person and an idiopathic pH are sort of the same. But we all know that. So what's the single mistake is not making the diagnosis and not getting them to an expert like many of you out there. If every patient got diagnosed and seen by an expert like one of you, then we would conquer this disease state. It's pretty good argument. They need to see an expert. It's hard to argue against. Thank you, thank you, Dave. All right, so well, we have nine minutes left. I wanna make sure Victor gets time. So we are at Equipoise here. And fortunately, we need a way to break the tie because typically this is where we'd sort of end, but we can't. So Vic, while you're sort of queuing up and getting ready to speak on the far side on some debrief here on the post game, I need to find a way to break the tie. So here's what I'm gonna ask you to do. Each of you has a piece of paper in front. I'm gonna give out some... Who has a pen? I got a pen. All right. Back in the days when Pharma could give us- We don't have pens. We all have pens. I'm gonna give you a pen. All right. I'm already gonna give you a pen. Hold on. All right, so here's what I'm gonna ask. We can't do that. So actually, while he's doing this, I have a very funny story to tell you about him. Okay, that's fine. Oh, you're gonna lose points. No, no, he knows it. He doesn't care. So when he first left BU and moved to Atlanta- 21 years ago. He was on a show called- Who Wants to Be a Millionaire. It's true. You can Google it and find me on there. Can you do okay? I got to the hot seat. I met Reeves real quick because I got a task for you and I wanted Vic to talk. He's sucking up. He's sucking up, Dave. But that's really cool, Dave, honestly. Southeast Asia. I was too young. So who did he call to pray for the answer? I did not call him. He called me and I was tied up. I did not call you. I have a recording of it. You called me and I gave you the answer. Okay. Ladies and gentlemen, this is not true. You can pull the recording. It's on YouTube. I did not call Hap Farber. All right, moving on. I don't know. He's got to lose points for that. Alzheimer's must be kicking in. It did not happen. No, you can go on the internet. Pull the big clip. I did not call Hap Farber. That's a three-point deduction. All right, so here's the task. We can't do limericks. Let's do haiku. I need you to write me. So haiku to review is three lines, five syllables, seven syllables, five syllables. Victor, test. What topic should I have him write a haiku on, relevant to this presentation? Relevant to this? I would say clots. All right, so just clots in general or P.E.? What did he say? I would say P.E. P.E., all right. A three, a haiku, five syllables, seven syllables, five syllables on the topic of pulmonary embolism. Vic, I'm gonna let you present and I'm gonna let the audience vote on them. Dr. Tess, a round of applause for Vic Tess who's joining us now. Actually, wait, a round of applause for all of our competitors because we don't know who's gonna win yet. It was fantastic. All right. I don't even know what a haiku is. Five, if you don't know what a haiku is, you may not win. I'm gonna let you answer. I'll help him out. Vic, you wanna hop up? You gotta help me here. Hop up, please. Just like I helped you. All right. All right. Well, then I'm not helping at all. I won't listen to you either. So, three lines. Again? Yep. Five syllables in the first line, three syllables in the second, five syllables in the third. Just three lines. Okay. Well, so while they're trying to break this tie, which I don't remember there ever being a tie at PTI before. Okay, I'm ready. But. Shh, shh, shh. Go ahead. So, I mean, I'm just gonna run through a few of these things and I wanna say how much I really admire and respect these three. That's one of the reasons I suggested them to David. But one of my favorite phrases from today was the, you know, there's no data, but this is right. Okay? You know, like it came up yesterday in the ARDS talk. You know, there's the right way, the wrong way, and there's the way I do it. So, I think we've gotten a full dose of that today. In terms of, you know, topics. So, should intermediate risk P undergo intrapulmonary lytics and extraction? And, of course, the data there is, shall we say, not there. But we've all seen pictures of these extraction devices pulling out these enormous clots and the reports of, oh, the pulmonary pressure is immediately better. And we've also seen, you know, imaging from thrombolysis, both systemic and catheter-directed. We've been studying this for 50 years. The first trial in catheter-directed thrombolysis was in 1972, it was the UPET trial. It was a catheter-directed thrombolytic study which showed rapid improvement at 24 hours, but no difference at seven days compared to anticoagulation. We know that anticoagulation works. There's no question about that. The catheter-directed therapy, including ultrasound-directed therapy, have all been done for many, many years. Catheter-directed thrombolysis without ultrasound-assisted assistance has not dissimilar bleeding rates to standard systemic thrombolysis. Ultrasound-assisted thrombolysis, while it's been proven to be safe and effective on average in a meta-analysis study, showed only an eight millimeter mercury improvement in mean pulmonary vascular pressure. Or, pardon me, systemic pulmonary vascular pressure. Or, systolic, good gravy, I can't talk. And a .3 liters per minute per meter squared improvement in cardiac index, which is not insignificant, but at the same time, is that worth not seeing a mortality benefit? And there's no mortality benefit data for any of this. And we await those trials, hopefully with clot extraction, because we'd all like to see a better way in treating this. Also, one of the arguments for that was that if we want to prevent long-term morbidity, the Pythos study with its extension trial, which was a two-year study of the largest thrombolytic trial performed yet to date, showed no difference in treatment for submassive PE with thrombolysis compared to anticoagulation in CTEF, persistent dyspnea, and long-term RV dysfunction. So I'm gonna move on from that. That was, but the, you know, I think it's argument. Two minute clock if I can, Vic, sorry. Two minute clock on your part. Okay, okay, I just got excited. I got excited. Okay. So in terms of nitric oxide challenge test, or vasodilator challenging testing, I just want to throw out that while it is not necessary, I agree it's not necessary for everyone, and I think the data backs that up, it is often necessary to get your patient medication. So in that sense, it probably is actually required, but it's a different spin than the medical indication. The next thing I would like to add is the six-minute walk. So one of the things that came up, and actually, Marty, I want to congratulate you for bringing up on at least one of the topics that this isn't available to everybody. That's true, actually, by the way, for catheter-directed thrombolysis and clot extraction, but in the six-minute walk, one of the benefits of the six-minute walk is it is a semi-objective way of measuring someone's exercise capacity, which is available to everyone. We don't all have submaximal cardiopulmonary exercise testing. We don't all have the ability to do shuttle walk, which is probably a better test in terms of grading someone's upper limits of exercise capacity. And so the six-minute walk, I think, still has utilization. It's a terrible diagnostic test, and it shouldn't be used that way, okay? Lastly, with iliofemoral data, and I thank you, Vic, I want to, you outlined the data pretty good, as always. I'm always nervous when I get to talk data with you because you're so much better than me. But on the other hand. You're VT1, I'm VT2, believe me. On the other hand, you said it well, that in the study, which was a negative trial, the subset analysis suggested people with iliofemoral thrombosis did better. And again, with newer and better ways to approach this, I suspect that this will change. But the current data doesn't suggest that they need to be treated more aggressively unless they have significant symptoms involving the limb that's involved. Okay? I think that's pretty much what I want to say. Thank you, Dr. Chapman. A round of applause real quick for Vic. All right, lastly, we have one more task, folks. I had tried to get them to anonymize, but they've all written these about each other. So good luck trying to, despite my best efforts, I will have a difficult time to anonymize them. So I will ask the audience to grade. You can thumbs up, thumbs down, or you don't have to vote. One to five points, depending on my perspective, plus that of the audience. So here's the first one. It's the only one that you may not be able to figure out who it is. A clot in the lungs, hard to breathe, and RV fails. Treat fast and quickly. It's a perfect haiku. Thumbs up, thumbs down. A clot in the lungs, hard to breathe, and RV fails. Treat fast and quickly. Lots of hands up on that one. That's at least a four, if not a five pointer. Strong work. I'm not going to disclose who that was yet. Next. Good luck figuring out this one. Vic has clots, they say. But he evidently left for better pay, maybe referencing a little pharma slap, all right. Point deduction, point deduction. Wow, what can he say? There's actually an extra syllable in the middle line, so I have to deduct a point for that. But Vic loves clots, so they say, but he evidently left for better pay. Wow, what can he say? Thumbs up, thumbs down. Oh, audience is split on that. So that's like a two or three pointer. Last one. Last person wrote two stanzas, so you have to judge them both. If either of them is bad, you can just torpedo it. Again, it won't be hard to figure out this one. PE sucks really bad. Lets everyone do better. I'm not a pharmacist, so I can't read the handwriting of a doctor. Lets everyone do better. Let's conquer this, please. Technically, that is 575. The second verse is, pH is tough. Only four, okay. Hap and Marty treat it. I don't know who wrote this one. I do better honest. All right, so average. Give me some thumbs up, thumbs down on that. Wow, wow, the audience has turned against it. Well, on that note, I'm gonna have to give two points to Dr. Tapson. I'm gonna have to give two points to Dr. Farber and our winner, ladies and gentlemen, Dr. Marty Gomberg, Maitland. Wait, wait, wait, wait. Hold on, may I? Oh, nice. May I? Okay. Nice. Hey, you look like Flavor Flav. One more round of applause for all of our panelists and Dr. Tests, please. Let's do it again next year. Please drop your panels in the back. Thanks for coming. Enjoy the rest of CHESS 2022, everybody. Thank you.

pulmonary hypertension

echocardiography

pulmonary embolism

mean pulmonary artery pressure

vasodilator testing

CTEPH

six-minute walk test

HFpEF

intravenous therapy

thrombolysis

PH