MonteHeart Cath Conf W/Dr. Matthew Ryan: Revascularization in Ischemic Left Ventricular Dysfunction

Hinzugefügt: 2026-05-27

[00:00:00]Let's see have the control. Okay, there it is.

[00:00:05]>> We're recording on both. Yeah.

[00:00:07]>> Yes.

[00:00:09]>> Okay. Good morning to everyone and welcome to another Monty heart.

[00:00:14]The topic of today is revascularization in eskeemic left ventricular dysfunction and we are very glad to have here Dr. Matt Ryan uh a worldly owned expert on uh coronary heart disease physiology complex PCI uh and this is a very interesting topic so we are very looking forward to hear from you. Thank you.

[00:00:35]>> Thank you Andre and thank you very much to all the organizers for the invite.

[00:00:38]I'm uh I'm honored to come and speak to you all today. Um I'm just going to provide an overview on revascularization eskeemic LV dysfunction probably about 25 minutes or so and then plenty of time for for discussion and things at the end. Um, so I'm a consultant interventional cardiologist. I'm an academic working at Guys and St. Thomas's and King's College London with Dvaraka Pereira and the rest of the group. Uh, and uh, you know, St. Thomas's uh, is a hospital uh, which I'm fortunate to say today we're just talking about the the fair weather we're fortunate to have in London and we sit just across from uh, from the Houses of Parliament in London. Uh, it's a very busy center. It's an academic center. Uh it's also I thought worth just explaining a little bit about our clinical program and how it sort of feeds into this because we run a complex PCI program which serves a a decent part of the population of South London which is a city of 12 million people but we also look after a essentially with a the sort of tertiary and quturnary center for a large population of of Kent. Uh and Kent is a a big area about two million people with a lot of deprivation and a lot of patients with sort of complex coronary artery disease. um we provide the the surgical services and therefore also the the sort of uh the surgical turndown service and the complex high-risisk PCI program for for this area. So covering a population all in all of about 4 million people. uh and the invite today was very kindly I think based around this article uh which uh Dvarker and I uh wrote along with a real panel of experts from around the world looking at uh the topic of revascularization eskeemic left ventricular dysfunction how we go about doing it but there's some other work I've been involved in in the chip besis 3 trial which I think it now uh definitely merits discussion and is is probably of an interesting topical bit to this as well so why are we talking about es schemic leftricular dysfunction we do a lot of PCI we do a lot of high-risisk PCI I you know what what is it about this condition? Well, as far as I'm concerned, es schemic left ventricular dysfunction is one of the most advanced and most severe states.

[00:02:30]You know, in the acute coronary syndrome setting, we deal with cardiogenic shock.

[00:02:33]That's been a big area. But in the stable coronary artery disease setting, this is about as bad as it can get. You have coronary artery disease reaching a point where you start to develop heart failure and deteriorate. And we know this is from J&J's heart recovery. Uh you know, but we know across all of the data around that the mortality rate for this condition is high. You look at those big trials recently. You look at revive, you look at stitch, you look at chip, you're looking at a mortality rate over five years for people with stable eskeemic left ventricular dysfunction somewhere in the rate of 50 to 75% 5-year mortality. And that is much much worse than many cancers. Again our institute provides a big you know oncology service big cardiooncology service and with the advent of imunotherapy there are many many cancers with fiveyear survival rates much better than 50 to 70 uh sorry 5 year mortality rates much better than 50 75% we're dealing with probably you know tens to you know reaching almost to 100 million people in the next few years living worldwide with with heart failure and one in four people will go on to develop some form of heart failure with coronary artery disease being the most uh frequent eeology ology and so that's a massive problem and despite that you know we don't have a consensus criteria definition for this we don't have a an internationally agreed definition of what is eskeemic left ventricular dysfunction is and to me that's surprising you know if you look at marodarditis you look at hyp hypertrophic cardiamopathy there is a clear international consensus but what is es schemic left ventricular dysfunction and in our paper that's really the first thing that we discuss you can define it based on extent of coronary artery disease you can define it based on some imaging evidence which shows a likely eological link, but we don't have a single gold standard test that establishes an eskeemic ideology.

[00:04:12]We still don't have answers to really fundamentally important questions. Why do certain patients with horrendous coronary artery disease develop eskeemic left ventricular dysfunction when plenty of others don't? We can all think of hundreds of patients if you sit back and think about it, you know, left main critical block right and a completely normal left and tricky ejection fraction. So why do a certain proportion of patients develop left and trickle dysfunction? And you can argue everything through, you know, a particular genetic predisposition, they've got physiologically worse disease all the way through to some who argue that this is all just bystander cardiammyopathy, which I think, you know, the the basic science evidence suggests not. And we put plenty of data into the paper about that. But we really do have to have a think about these really fundamental questions which we still don't have answers to. And that's why I think this condition is very important alongside the mortality on the shop floor. On a practical basis, I I you know, I just put up a case. This was from uh my Monday cathab list last week.

[00:05:05]Uh and this is the sort of thing we see all the time and I think here we're pretty happy. This is es schemic left ventricular dysfunction. This is someone with extensive coronary artis blocked very calcified right coronary artery.

[00:05:14]And this just speaks to the sort of the disease we're dealing with and some of the technical challenges of interventionist we then face alongside the other the mortality. You know you've got a an L which is heavily calcified critically diseased at the oium. The left main itself is okay. the big intermediate that's got some proximal disease and a circumlex which is sort of relatively undesized through its course but blocked at the end before it really feeds any distal branches. So this is exactly the sort of patient we're generally thinking about and we're treating uh you know really calcified disease a reasonable amount of complexity to treat certainly far from the the worst disease we come across treating but you know what's the nuance how are we going to manage this patient and this you know is this the heart of the same patient if you saw this anatomy in a patient with normal leftricular function you'd be thinking okay you have a think about it this is a relatively complex PCI but something we're going to be planning pretty routinely with the cat lab staff not really thinking you know making a plan, having a thought about the contingencies, the prep for complications that we always have, but not thinking this is going to be the hard case of the day and not thinking this is someone who's going to be at really high risk of cardiovascular collapse, which I think is the thing that affects us all the most. This patient, you know, however, has very severely impaired left ventricular function and we know from retrospective data from registries done in the US, in the UK and Europe that these are the patients who are most likely to experience a cardiovascular collapse and early mortality. For a patient with a similar outward anatomy, the risk of uh of early early mortality, first 30 days or so, is probably four to sevenfold higher if you got severely impaired left ventricular function compared to a patient with normal left ventricular function. And so this is a group of patients who need particular and special attention. And this is what brought us forward to write the article. I think it's worth just very briefly revisiting the the pathophysiology because actually I think here it's really critical to understanding the patients and perhaps some of the outcomes of the studies and why they behave differently. We've known this for some time. You've got a patient who starts with coronary artery disease and they get eskeemic. They get an eskeemic hit and they have a transient period of stunning. You know they transiently drop their left ventricular function after flow's normalized. So they they walk up a flight of stairs their LV function drops transient and they perusion normalized and the LV catches up a short time afterwards. And that's stunning. And we also see stunning of course in acute micardal inffection. That's one of the big things in N STEMI or STEMI. Those ACF patients have a transient drop in left ventricular function but it's very very recoverable. The problem over time with those repeated hits is you start to get into myioardial hibernation. And again the paper talks a bit about the genetic basis of that uh actually some really interesting allegorories and parallels to to hibernation in nature. You know in in animals that go to sleep in the winter because they're starved of of resource. Well, the you know there are similar genetic signals in some ways in the hearts of patients with hibernation as in hibernating mammals. But over time you start to get this reduction in left ventricular function which stays more persistent. And hibernation is characterized by cellular degiation expansion of the extracellular volume fibrosis and eventually irreversible change and that's been demonstrated in animal models and also in clinical models. But I think this is really key that hibernation is not something that's just one thing. Hibernation is in itself a spectrum from the very early almost stunninges-esque hibernation in that early phase to really advanced irreversible hibernation. That's something that I think is probably more difficult to reverse than we always thought and in this slightly old-fashioned model perhaps where we just thought revascularization switches off hibernation and off you go.

[00:08:36]Um I just want to touch very briefly on something that I think is important early on in the paper and and speaks to how we go about investigating because as I'll come on to and many will be aware the evidence base for routine revascularization in es schemic left ventricular dysfunction is not as strong as it was perhaps thought at one point to be or you know the observational evidence suggests it was before trials like revived and stitch and one of the big questions comes about investigating patients with uh heart failure new left ventricular dysfunction for coronary artery disease should we be doing And again, the paper touches on this your choice from a non-invasive test to an invas an invasive catheter based angagram to look and try and determine what's going to benefit patients. And that's not all about revascularization.

[00:09:16]We know that an eskeemic eeology is associated with more symptoms, more quality of life, a worse outcome than a non-eskeemic eeology of heart failure.

[00:09:24]And we know that there are disease specific therapies we can offer statins, antiplatlet therapies plus revascularization in certain patients.

[00:09:32]And I think this is a really fundamental question again we still don't have the answer to. Should these patients be having routine investigation for the coronaries? This is the crotchf trial which is run by someone called Peter Suaboda uh in leads in the UK and this is a trial that's in flight at the moment and I think will provide a really useful answer. And this is taking 3,000 patients with new diagnosis of heart failure which can be hep but is going to be predominantly he ref uh and they're randomized to either a CT coronary and which has some of its additional value in looking at back characterization looking at uh you know um uh at uh sort of extra plaque features good evidence in primary prevention of course um stress fusion cardiac MRI with the value of other morphological things about the ventricle scar and the like or a catheter angagram uh per usual care to look and try and see which of these strategies would benefit patients overall. I think there will be some really useful work to come through.

[00:10:24]I just want to talk about this because I think this is the really key randomized data to date in terms of how we manage patients with leftricular dysfunction.

[00:10:32]should they be having a coronary androgram uh and you know revascularization or not and stitch and revived widely discussed lots of talks about patients with es schemic left ventricular dysfunction extensive coronary art disease and impaired left ventricular function with a question of does routine revascularization help these patients. stitch obviously run in the US uh uh published first in 2012 run by Eric Velasquez and the team and this uh was a trial looking at medical therapy versus coronary artery bypass surgery in a quite a young population median age of 60 uh but otherwise outwardly a very usual left dysfunction population ejection fraction of 27% on average and in the initial trial phase of 5 years there wasn't a benefit and there was an early harm to coronary artery bypass surgery so after you know the first 30 days still about one in 11 patients had either died or was still in hospital after having their bypass surgery. So a real early hit and we know these are high-risisk patients for revascularization but over time some evidence of benefit in in mortality in particular cardiovascular mortality seemed to be reduced. So they ran longer they ran to 10 years and after 10 years showed a substantial improvement in survival of about 18 months in these patients. So a real benefit but in a young group of patients and I'll talk in a second to why I think that's particularly important. We then re revived BISS 2 Devar is the chief investigator here and this was a UK trial randomizing patients uh with extensive coronary disease uh and LV dysfunction and viability as additional criteria to try and enrich the population to either PCI or medical therapy. So answering the same sort of question and looking to see if there was any benefit and as is widely known and revived we showed absolutely no benefit whatsoever. We did get around the early harm. We didn't have that early uh rate of complications but no benefit emerging over time. I think lots of questions have come from there as to why why do we think that's why did that happen? Why did stitch seem to show benefit when revived didn't? Well, I think within the paper we really deep dive into that and what could the reasons be? The simple most straightforward one people like to throw out is you know well it's just a different mechanism of revascularization. Bypass surgery gives you new grafts. It prevents infart all of those sort of things. But actually I think that's does an undisservice to understanding the differences. The rate of death from myocardial infaction in this population is actually relatively lower compared to the death from sudden arrhythmias from pump failure other things that I don't think bypass surgery would necessarily be helping with but there are these key differences and I think age is fundamentally the most important one. Stitch recruit patients in their 60s. Now if you take your norm your average 60-year-old with es schemic left ventricch dysfunction they're not as likely to be as extensively comorbid.

[00:13:10]they're like ultimately going to have less competing risk. We know that as you get older, your risk of uh non-cardiovascular mortality rises very quickly. That's why if you look at a hep population, their risk of mortality, non-cardiac mortality is much higher. If you look at your average 60-y old with eskeemic leftric dysfunction, the vast majority of mortality is going to be cardiovascular mortality. And so you're just giving yourself more room to modify and more room to make changes. And I think that is quite fundamental. A lot's been said about functional class. So I think that is that is true. I think the revived population were very much stable eskeemic left ventricular dysfunction stitch you know gen there were a lot of those patients represented but you were allowed to have had a myocardal infaction even up to seven days earlier as long as you'd stabilized. So it is a slightly sort of hotter population from a coronary perspective. Um different things to note though so you know the quality of life was really impaired at baseline in both. Now I think there's a difference between angina associated impairment of quality of life and overall impaired quality of life but certainly quality of life came up in both trials equally over time. So we did seem to see some difference in quality of life between the two groups. And then there comes down to difference in medical treatment fund the fundamental difference between revive and stitch was the implantation of ICDs. Uh now how does bypass surgery affect arhythmic risk? I think we're not really desperately clear on that. Some of the subsequent work we've done in revive suggests it's predominantly SCAR that um that looks at arhythmia uh sorry that that you know modifies your risk of arhythmia rather than eskeemia and so I think there is some uh you know some signal there that the ICD rates fundamentally different otherwise actually the medical therapy was pretty balanced between groups you know we looked at differences in medical therapy we we wrote in EHJ comparison of the two trial looking between them there may have been subtle differences in medication titration obviously systems for titration RAS inhibitors or beta blockers getting people onto different RAS inhibitors like scrol balsam probably have been beneficial but ultimately I think fundamentally that younger population would have made the difference and much lower competing risk of non-c cardiovascular mortality I think is the biggest difference now what does that mean in practice it still means I think that your average patient with leftricia dysfunction will not benefit from PCI if they are stable if they have a stable heart failure phenotype the average age of diagnosis with heart failure in the UK is about So your 60-year-old toss the the more the less routine and I think overall the benefit is you know I do believe there is still a benefit but I believe in those stable patients is very much going to be isolated to a small population of the younger more symptomatic patients and your routine uh you know average average should never be the word I guess for a patient but your your average patient who comes along with leftric function diagnosed at 75 coronary disease there's probably going to be no benefit to PCI because of that risk of competing cardiovascular mortality.

[00:15:53]think and this is just one of the the the forest plots from the initial revive paper that I think shows a little bit the same. These are all obviously completely hypothesis generating. These are small shifts. None of them are statistically significant. But if you look down this chart at the signals for benefit with PCI better to the left and medical therapy be better to the right.

[00:16:11]You see a little trend towards younger patients under 70 having a marginal benefit from PCI. You see those with a more extensive Jeopardy score besis Jeopardy score. you know a bis shephy score can only go up to 12 10 was the median here. So, you know, 10 or 10 or higher, a little signal of benefit. And again, those with more impaired left ventricular dysfunction, left ventricular function seem to benefit more. And if you look at uh the stitch trial, there's a really nice paper looking at the the uh the who benefited more from bypass surgery. And those signals were all the same within their secondary analysis. More extensive coronary disease, more uh impaired LV function, and age were really the three drivers of greater benefit from bypass surgery. And I think there's going to be some interesting data coming in the future. uh hopefully looking at those those aspects a bit more deeply in in the revived population.

[00:16:59]That said, what can we do? So, we're going to we're going to talk about our routine, you know, patient who's come through eskeemic left ventricular dysfunction. There's a feeling sometimes if we're not going to revascularize, we're not doing anything. Well, that's just fundamentally untrue and there is so much to do in medical therapy and this is where we should focus a lot of our attention. And one of the key messages of the paper is if we're working a patient up for revascularization, we decide they're not for, there is lots and lots we should be doing to try and treat them. anti anti-thrombotic therapy, anti-coagulation for atrial fibrillation and the like, careful titration of the heart failure meds in combination with with those teams and really aggressive device therapy. I'm a big believer in device therapy in this population. The eskeemics, they do get lots of arrhythmias. We've seen I've you know there's too many 24-hour tapes get done that show a ventricular arhythmia and sometimes a fatal ventricular arhythmia along the way. Really important to pick those patients up and get ICDs in risk stratify appropriately. statins. The evidence base for lipid lowering therapy is not fantastic in this population again because life expectancy is relatively short. How much time does the statin have to benefit? But I do think you know the the really powerful lipid lowering therapy particularly with PCSQ9s these days really do need investigating these populations because I think there probably is a big benefit if we get lipid levels low enough and I work very hard on lipid levels in these patients. And then diet, exercise, cardiac rehab. Again, heart failure patients coronary. Often people are uneen to get them into cardiac rehab.

[00:18:19]Get them exercising. You know, they think our diet, you know, is the life expecty that long? Is it worth it? I think it's somewhere really important to focus.

[00:18:27]Um, but what about those we do get to PCI? You know, ultimately this chat, we did end up doing PCI in this. Why did we end up doing PCI? Well, this because he was an acute coronary syndrome presentation. So, he'd come in as an N STEMI. uh he had you know a wellins looking ECG or have trickier function here I think it's inarguable and I think one of the really key things about revived and I've had you know conversations with colleagues of late one of the challenges for us as interventionists has been the conflation of the results of revived with all patients with es schemic left ventricular dysfunction revive stitch they are stable patients who seem to predominantly follow a heart failure phenotype they've walked in off the street they've come for some outpatient diagnostics a patient who comes in with acute coronary syndrome is totally different. A patient who had limiting angina despite medical therapy is totally different. And these are patients in whom revascularization is going to be substantially beneficial.

[00:19:15]They're at much higher risk. And we we know it's going to help. We know it's going to reduce mortality. We know it's going to reduce reinction. We know it's going to help symptoms. And we've got a real responsibility to not allow those messages about revived and that population to creep into the ACS and and angina space because I get you know I see these patients sometimes who've been managed medically for an NT STI based on revived who've got limiting angina managed medically based on revived. I think we do really need to push back against that when we are doing those cases though you know we need to think about uh what we are doing. So these are our our high-risisk patients. They're patients who've been uh you know uh more unstable. They're the patients where things get really really tricky and I think cardiovascular collapse on the table is one of the worst. You know we we all know the feeling of having a patient who often walks onto a cath lab or slides across the cath lab table. You have a chat with them in the case beforehand. We operate on patients who are fundamentally awake. You know a lot of the time we we've got very limited access to to general anesthesia anesthetic support even at times. uh you know we we don't routinely have an anist in the kath lab in the NHS uh and so we're we're managing all of that and is that patient who you've spoken to who's walked in has a cardiovascular collapse and arrest and dies it's it's one of the worst days in interventional cardiologists and I can name the names of all the patients that's happened to and you know that I think those those stories and those experiences stay with us for a long time so how do we prevent that happening how do we keep these cases safe uh and you can see there's an you know an impeller in and that's that's always sort of been the been the thought recently impella that's the way to keep these patients safe but is it is it the right way and the second half of this article really then covers in a patient who's going to have PCI how do we keep them safe and I've got to say a big thanks to Alex Trudel uh who was a major part of writing this section together with I we we shared a lot of experiences and discussions as we were doing it we came in the end to thinking about these three main aspects and this is the bit that's sort of come into chip and some of the discussions afterwards no one feature can really tell you I think a lot of the algorithms that came out for chip a lot of the stuff that came out from J&J was all about single factors or you know scoring systems but where one or two scoring points could quite easily get you into the point that you got LV unloading uh left and trigger performance so high LVDP systolic dysfunction valvular heart disease and association I've got to say still terrifies me so if someone's got severe aorticosis poor LV bad coronary disease those I think are the you know the highest of high-risisk cases um but then there's also that complexity you can be you can have a bad heart but you can be doing a simple type A lesion and those cas is yes they worry me yes I take them seriously but they don't have that really high-risisk feature about them it's when you've got that ventricle and you're doing a retrograde CTO you're calcium modifying in the left main you're doing multi vessel calcium modification people often worry about rotationalctomy but experience from my perspective shockwave type therapies awesome cause a lot of eskemia with a shock wave balloon you're often keeping it up for a long time and those are the patients where LV performance can really really drop and they can go off quite quite quickly uh I think you got to be really cautious particularly in final patient conduit because that's a complexity feature and then again complex left main fine and paper contract high mioardial jeopardy you know if you've got final pavement vessel the other two are CTO's that I think is high risk and it's a combination of those things together I don't think we've codified it I think it's a feel thing but those are the patients who can deteriorate acutely so what can we do to keep them safer putting impeller in at one point was was thought to be the answer and the device based things you know we're very device based in interventional cardiology and having a device you know gives you as gave you as an operator a feeling security. You know, you saw that loss in pulse pressure, but MAP stayed normal, patient stayed awake. That felt very reassuring.

[00:22:49]I think it's also a simple marker of the ability of a complex PCI program. We're a complex PCI program, we can use Impella. Um, but actually a lot of the bits that I think are more important are the bits that are much harder to to sort of uh to to show uh evidence of and to to demonstrate externally, but are more critical. And these are the things that we came to talking about. And this I think is one of the key things because one of the things we've really got to do is look at optimizing these patients beforehand. This chap came in with an ACS. He you know he had a say a wellon ECG. He had a degree of primary edema.

[00:23:24]Uh he sort of you know you need to sort much of that out as you can pre-procedure. A patient who goes into lab hypotensive with high wedge pressures with wet lungs has very very little reserve and a slight hemodynamic deterioration can cause much more problem in a patient who is more stabilized. If you can get them onto a diuretic, if you can get their blood pressure a bit better, if you can get them into a slightly better space, then there's benefit. Now, you've got to balance that against the time. You know, if you spend two or three days, what's the risk of reinfection? What's the risk they deteriorate further? We don't have perfect answers to those things but where we can optimize them. I think that's better. Heart team discussions are really important and we we devote quite a bit uh of the paper to discussing a well functioning heart team because a heart team discussion is sort of the panaceia in all the guidelines these days. You know a well where there isn't specific evidence where things are high risk run it through a heart team. I think a heart team is critically important. I think from a governance perspective running things through a heart team does demonstrate that you followed an appropriate process. But we all know that there are heart teams that function well and heart teams that don't function well. and heart teams that are adversarial, heart teams where there's only one voice. Those are the heart teams that can be really problematic.

[00:24:31]And we, you know, we need to work towards heart teams. Not saying our heart team is always perfect. Uh but we need to work towards heart teams where we get, you know, real meaningful input.

[00:24:40]People have met the patients often in the NHS here. That can be a real problem because again, we've got this huge geographic area, lots of patients referred in, often being discussed before they come in because we've only got finite capacity to offer treatment.

[00:24:51]So you know having people in the room who've met the patient and who are going to follow through on plans and the like is really important and then shared decision- making uh because you then got to look at patient priorities you know lots of patients especially around those questions I think of bypass surgery versus PCI and patients who are going to have one or the other you know these ACS type presentations when it's one or the other lots of when you sit down and talk to patients you know quality of life is really really important especially with schemic left ventricular dysfunction they've often been living with poor quality of life for a while they don't want to feel things are going to get any worse. I've got a chap on the ward who, you know, I've just spent >> a week and it's my fire alarm here, but I'm hoping it's just a moment of test or something.

[00:25:34]>> Yeah. Good. Um, chap on the water. I've been spending some some time with, you know, three or four consultations. He was someone I knew from outpatients who'd had previous PCI stances had failed elsewhere, referred into me, and we were having a long discussion about PCI versus bypass surgery. His goal is to get back onto the golf course. That's what he wants to He wants to go back and play golf. He lives down in Kent. He's, you know, he's got a nice life pottering around town. He's 81. He does not want three months recovering from a bypass operation. He wants to be able to swing his golf clubs. And so for him, that was the main thing. We had lots of discussions. He fully understood the benefits and risks of each. And we decided to redo PCI uh which we're doing later on this week. So that sort of shared decision-m is really important.

[00:26:11]Procedural planning. We've learned a lot from Tavi about access uh vascular access planning. I think it can be really useful even in patients who you aren't planning upfront mechanical circulatory support from an access uh management perspective and to understand what you're going to be dealing with bailout planning discussion team and I think really key is to define your expected completeness of revascularization if we look back at that angagramram I showed at the start you know he's got a couple of bits he's got a a really complex CT of the right we're probably going to leave alone that's scarred he's got that distal circumflex occlusion with a couple of branches again there's some scar down there he's got an intermediate lesion which is tight and a big big intermediate and it's his second vessel.

[00:26:47]I would like to treat that but my goal going into that procedure was to sort his left main to midL and a bit of dist LD disease as well which I wasn't really planning to touch but I had a a plan that my you know the most important thing was to treat his left main LED the intermediate we could come back for another time and I think setting those what's the minimum I can achieve and there's someone called Elliot Smith at Bart here in London who's excellent at that you know what's the bare minimum that's acceptable here what's the stretch goal and defining that in your head beforehand so you know when to Stop surgery. More is more. If you're having an open heart operation, you've got to have everything done in one go. And in some ways, we need to get away. The trials completeness of revascularization have all driven us to feel the need to meet what the surgeons do to get to the point I can open up as many arteries. I can get as much done. I can get a Now, first off, we don't really know what the surgeons actually often get done. Our surgeons here are worldleading. The Tommy surgeons are absolutely fantastic.

[00:27:42]Um, but we don't necessarily know what grafts go on and what what you know what happens. We every trial ever has just sort of assumed that everywhere they've said a graft has gone that's effective revascularization whereas in PCI we study the andagrams afterwards we say this is complete or incomplete we lost that cyber branch there's lots more to it and I think we're trying to compete on an unlevel playing field and I think we're also not always speaking to the benefit of PCI which is that you can do a bit and then bring the patient back you can fix the culprit lesion okay and stem you're not always going to know what the culprit is but you can fix the culprit leion you can do the big stuff and then have a think and decide if they need to come back for the smaller stuff later on. Uh the higher the stuff where the balance of risk and benefit is a bit smaller. The patient symptomatic and struggling, of course, you're going to do it, but you're not necessarily going to do it routinely. And I think that's really key going to these sort of procedures. Infra procedurally, hemodynamic monitoring, the the right heart cath, which is something that sort of went away completely now obviously coming back in a big way. And I think that's that's, you know, really valuable. We found that incredibly helpful. I'll show some data from one of our fellows in a second. And dual operators is the other thing. the cognitive load of doing these sort of cases. If you've got two consultant attending level operators, even a senior fellow, uh you know, you can just find and some of these with our really really flying senior fellows, I will second operate both because they're brilliant and that's good training for them, but also because it keeps my cognitive load such that I can just keep an overview of the case, keep an eye on the humanics, manage the rest of the Kath Lab team, have the next bit of equipment coming where, you know, I don't need my hands to be so busy. So I can I can really focus my and having that adaptive strategy across what we do and then postprocedure you know it bed obviously team debriefs and and clinical governance and audit are all absolutely key to these things and all of that together I think prevents this this sort of cycle of deterioration. This is what we're ultimately trying to head off. You know, patients from previous hemodynamics. Uh I think it's useful if they're having a high-risisk PCI. We're trying to minimize the eskeemic time, short balloon inflations, you know, shock wave, things like that. Margaret McIntaget, uh who was obviously here in Glasgow for gave a fantastic talk a while ago about how she changes her strategies for many CTOs and tries to stay a lot more antigrade than she would in a patient with normal LV function because keeping antigrade is a really good way of minimizing eskeemic time. So where in as someone with normal LV function she might be thinking switch it switch switching earlier to retrograde actually in these patients an antigrade approach may be better reduce the fusion keep the blood pressure up really important and try and keep away from from cardiogenic shock where mechanical circulatory support may be important now I'm just going to touch briefly on chipsis 3 obviously very topical this was work that Dvarker and I did here together at kings as a as a randomized trial and this sort of came out from this whole story of highrisisci essentially this trial started because of one patient who was enrolled in revived who uh had uh you know had initial PCI did really well actually had it with impella support. was a complex left main, lots of calcium modification and a CTO of the right and he had his left main done and he came back for his CTO of the right because we were trying to get complete revascularization and we' done the first case with Impella but he'd done well he was much improved he was he was still symptomatic he was getting angina so he's getting a sort of breathless should I say after about 200 yards or so but he was much improved he'd been in decompensated heart failure when he' first come in and so we decided to do it without him for the second stage uh and sadly he had an onstable cardiovascular collapse and uh and that patient was what informed this whole trial. So we said well come on we really need to know would impella have helped this this chap would impella have saved this guy's life and so we wrote chip piece history uh it was funded by the NHR across 20 hospitals in the UK patients had to have extensive coronary disease and severe left ventricular dysfunction uh they were going to have scheduled complex BCI they could be elective or acute in the end about 70% were acute and they were randomized to either elective LV unloading with an impella device or to standard care and standard care here was very much with no elective mechanical circulatory or you know intraal to balloon pumpers bailout was pretty much the norm as defined by the bis one trial they all had a PCI and then they had follow-up for at least 12 months and a primary outcome of a a win ratio and this was the win ratio we used so win obviously when we designed it was a bit of a a newer thing now is pretty well established but we had this hierarchy which we worked on uh as a process with some patient reps death stroke spontaneous MI CV hospitalization and per procedural mioardial injury a biomarker based definition and at the time the initial thing we around 125 in each arm increased to 150 in each arm over time. Uh and the characteristics were similar I think to the sort of revive population. They're a little bit older uh as one would expect for a really complex high-risisk patient. We know as you get older you get your coronary disease gets more complex.

[00:32:18]You're more likely to have heart failure higher risk. Very heavily weighted to male although actually a bit of an improvement on uh that seen in uh in um stitch and revive. I think one of the features here is that we in screening for the trial we saw lots of female patients with bad coronalities with left ventricular dysfunction but with ejection fraction sort of 40 to 45%. I think you know that this is a answering these questions in a in a female population incredibly important going forward and I think we need to have a think about how women's ejection fractions are expressed differently. We know ejection fraction you know women dilate less therefore do you just get a a lower number for the ejection fraction for an equivalent level of pathology.

[00:32:56]And I think we need to have a think about some of these thresholds in women because you see lots of female patients who've just got an injection fraction of 40% and so aren't eligible for these trials. Ejection fractions here were poor. Coronary disease was extensive.

[00:33:08]The medium was 12. You know a full mioardial jeopardy and synthes were were super high 38 in both arms. About 70 to 80% were acute coronary syndromes but about sort of you know 25 30% were retrograde CTO. So across the range of really complex PCI we do and many will have seen this and this may well have been discussed in the former already but you know a win ratio which ultimately showed no benefit to routine use of the impellp uh with a 7% 6 and a half% uh difference not statistically different between arms uh favoring the the standard care uh which I think came as a big surprise and it's disappointing whenever you're on a trial you want to show that the you know your intervention carries benefit you don't want randomize something to people to something that's not going to help them.

[00:33:54]Again uh looking at the subgroups uh you know no real big difference across no statistically significant difference uh other than that it seemed in those who had you know uh higher anti-bromps that there was a trend towards uh more more harm uh a bit of harm with um with the micro microaxial flow pump and I'll talk in a second more as to why that may be and I think this was the bit that generated a lot of discussion was that you made a difference >> you're decompensated and it's better Yeah, exactly. I think you know those who are those who are more decompensated I think there's a you know a I think it's difficult I think there's there's a you know I'll show a bit of data on it in a sec which I think speaks to it. You think the decompensated would carry more benefit from microaxial flow pump but perhaps there's reasons that you that it's you might after seeing the data think otherwise. um death from any cause higher in the microaxial flow pump group but not statistically significant just bordering on death from cardiovascular causes significantly higher always challenging to know whether to include those sort of things in a manuscript you know from the Excel trial uh there was obviously massive discussion about the fact that some of the cardiovascular death stuff hadn't been prioritized enough so it's finding the balance of those two clearly it's a secondary clearly it's not the primary outcome it's a signal it's not conclusive but there's there's something there um but so why why why did this not Well, the key difference is the impella group had more revas done and I think a priori before this trial was run. That was the stated benefit. You know, everybody the the Abiomed protected PCI program said, you know, you can get more complete revascularization. This is beneficial.

[00:35:31]But I think this almost speaks to what I was talking about before. In cardiac surgery, more is more. And this was said by one of the discussions at ACC. You know, in cardiac surgery, more is more.

[00:35:38]The more you can do, the better. Fix everything. in PCI is more always more because we saw a higher rate of periphederal myioardial injury more revascularly index procedure and there is a possibility that we're doing more damage along the way and it's those particularly vulnerable patients who might be at risk and this is from Euro APCR that's just come out presented by Sard Aad who's our fellow who's absolutely wonderful future leader in complex intervention um so Sad uh ran his PhD his PhD was a trial called Heracles which is looking at LV unloading in uh in ECMO and that was when he was funded to study by the British Heart Foundation. Essentially on the side he ran the hemodynamic sub study of chipbasis 3. Um so he recruited a 100 patients into a sec sub study where basically we did routine uh pre and post right heart cath. Uh so the patients in the standard care arm would have a pre-ostright heart cath and then the impellar arm would have a right heart cath at baseline once the impella was in and on. Uh the same at the end of the procedure and then once the impella was taken out. uh and they were a comparably similar population or essentially the same population. There was no suggestion of a selection bias compared to the main trial and that's largely because it just ran in a set of centers rather than a picked population.

[00:36:49]Um and what he showed was that they were, you know, there were patients who were decompensated at baseline. You know, they had a slightly elevated wedge pressure. Yeah, it's not super high, but they had a a slightly elevated wedge pressure. Their cardiac indices were pretty low, though. 2.1 for patients who were, you know, stabilized, not AMI type patients. It's it's just below you 2.2 for shock. I know that it's a uh not the most accurate thing in the world, but you know, if you say 2.2 shot, they're sort of teetering on that. They're certainly sort of definitely sky and getting into sort of sky B at the start of the procedure.

[00:37:18]Um, and with the microaxial flow pump, when you put the impeller in and turned it on, you got a you got a benefit. You know, your MAP went up, your wedge came down by three, which is small but important, and your cardiac output went up a bit, only by about 500 mls a minute. you know not the 3.5 but I think the suggestion as we all know that when you start unloading with the impeller then your own intrinsic cardiac output's not you know is going basically the ventricle is going to take the opportunity to rest a bit and so it's not going up masses but it's going up a bit probably for much less myioardial work but what was important was that by the end of the procedure in all patients MAP was a bit higher wedge pressure had gone up a little but look at the drop in cardiac index okay cardiac index had dropped really quite substantially to 1.8 during these complex PCIs and we know that we cause stunning with an intervention. We know that's a part of what happens. But was there a difference between arms? Well, no. The really key thing was there was absolutely no difference in cardiac output. Now remember, there was more revascularization done. So, you know, the impeller was, you know, maybe you got more revas done to the same amount, but there was certainly no benefit. This hadn't magically prevented the stunning that we used to think happened to the ventricle. Is it possible if you did an equivalent amount of brevas with an impellerin in both arms you'd see less stunning and maybe some benefit?

[00:38:33]Absolutely. Hypothesis future study maybe. But for the moment using the strategy that before we'd have all said I think was the right thing to do. The impeller did nothing to prevent myioardial stunning in the setting of doing more angoplasty within the procedure. And I think that this is going to be one of the really key things going forward that we need to try and understand and take forward from there.

[00:38:53]So to sum up this at the end of our paper uh was sort of what we what we'd said you know case selection who are the right people to take forward or recent ACS limiting angina we have to work hard to encourage those patients to be revascularized where appropriate and that balance between PCI or surgery is really really important many patients will favor PCI from a quality of life perspective and I think that's perfectly appropriate with a patient who understands fully if they're stable they have no symptoms their phenotype is really heart failure I haven't got time to cover it today but there's lots of revised sub studies where we unpicked how these patients patients behaved and essentially the stable patients behave like they have heart failure. They don't behave like people with coronary artery disease. They have a heart failure phenotype and heart failure management is right for them. ECI planning define those minimal acceptable and ideal completeness of revascularization.

[00:39:36]Absolutely crucial. Consider myioardial viability and making a PCI plan again didn't have time to talk about but sit look through all the imaging again and again the echo the MRI. We're all getting better at looking at CT looking at MRI looking at those things. Put them all together with the androgram maker plan and a really detailed team brief.

[00:39:51]Get that second operator in where you can. Hemodynamic monitoring crucial.

[00:39:55]Right heart cath is amazing. Bailout in chip eight patients had bailout injury at balloon pumps and they work brilliantly. Again, people have have sort of thrown away the balloon pump because it wasn't useful electively in vis one. But as a bailout device, they're brilliant. You can get them in quickly and they work really really well as long as the patient's not too decompensated. So hemodic monitoring there is great informed uh evidence-based in information of the the MCS decisions and Chip will add to that.

[00:40:19]I think we do need to see the results to protect four. It's not that far away. I think that'll be fascinating data to add in and the human factors in the lab are crucial and and working correctly with that. Stitch three is uh you know is coming. That's comparison of PCI versus CABG and chip and protect for are coming through for the future. I think consensus criteria for me are really important. I think we should have a consensus definition. I think it's bizarre that we don't need to think about the mix and eskeemic non-eskeemic eeology and then perhaps think about that post-procedural eskeemic burden.

[00:40:47]What does it mean to leave things alone?

[00:40:49]Can we take a step-wise approach and and do these things in a stage manner? So, thank you very much for I know I've overrun a little bit. So, uh but thank you very much for taking the time to to hear me talk through these are the QR codes just for the state-of-the-art article from last year and uh chip history in Neim. Delighted to take any questions and and discuss anything that comes up.

[00:41:10]>> Matt, phenomenal talk and congratulations on all the work you and Jeepa are putting to uh are putting together. I met with him last week and he got to answer some of my questions. Um, but I I'll ask it again depending on actually let me just ask it now. So one of the things that struck me um when you look at the mortality curves in chibesis is how you know there's that acute difference which I think is probably related to um the vascular complications the large access potentially bleeding but then there's also a later hit the mortality keeps increasing it almost seems to happen like at one year the curve continues to separate more and when I looked at it and I went this looks exactly like we've seen in the structural heart space with u mital clip with tricuspa when you treat patients with bad LVs and heart failure the difference differences between therapies really start coming out at one year and so I was trying to think about the mechanisms and the only thing that I can come up with and tell me how wrong I am is the fact that in the microaxial pump uh group we uh maybe a little too aggressive, right? We did too many vessels. I also watch how younger tendings do rotor in a patient with a microaxial pump compared to when they do rotor when there's no pump, especially in a low EF patient. It's something I always like try and teach is you see a lot more aggression. You see a lot more runs of rotor without, you know, stopping or pauses, long pauses between letting the patient recover. When you're on a balloon pump or nothing in a low EF patient, you're so much more gentler when you when you do a rotor. You stopping immediately. You see a drop in blood pressure. You see STD changes. You pause. You try and get the the blood pressure back. You wait for the ST segment elevation to resolve. So, I mean, for me, it's something I've always suspected. Uh, but is that too much of a jump in my thinking?

[00:43:17]>> No, I I I don't think so at all. I completely agree. Um I think the you're you're absolutely right. It's that that late separation that I think the structural space definitely has and I think the other place that's relevant here is danger shock because I think there you saw that late separation and I think it's the same thing. Danger shock at impeller saved you from the additional stunning of inotropes uh of being on itu on multiple presses and all that stuff >> and there that additional mioardial injury that probably came from the presses affect you over time. in CHIP it was the additional stunning and injury from doing more PCI and I you know one of the things that comes out in the paper that I think I'm really key with on our trainees is there is a temptation you see so many people when things start to go wrong and the patient deteriorates people want to speed up and actually when things start to go wrong and the patient starts to deteriorate it's slow down is a difficult term but you know what I mean slow your thinking take your time don't start throwing things in and throwing things in and throwing things let it breathe and I think that makes all the difference.

[00:44:19]>> Yeah, absolutely. Andrea, go ahead.

[00:44:24]>> Matt, uh, thanks again. It was like really brilliant. I just wanted to ask you a very quick question just coming from your, uh, I'm sure you do like routinely all these are team discussions on people with heart failure and then on coran geography or CT you see there is evidence of multivessel corre disease.

[00:44:41]We discuss all these patients as well in the art team. um what are the factors that are making you go towards like a complex PCI rather than just medical management? I know you cited a lot of stuff like the age um the territory of distribution um how likely you can revascularize successfully um is there any role for physiology um how is imaging included in this workflow just want to know from your experience in this >> yeah absolutely thanks so I think it's it is it is challenging we've got some answers but not all of them um my PhD was on sort of physiology in this es schemic left ventricular dysfunction space I I think the challenge with physiology is we don't know we don't know what FFR you need to have LV dysfunction. It certainly is probably much worse than8. Um I think imaging again you know we looked at all the viability stuff within revived viability didn't seem to carry huge amounts. It's useful in picking what lesions you treat and what you do but it didn't viability doesn't seem to fundamentally alter the benefit of of PCI. In my eye it's it's the patient symptoms. they're really important and I think that you know angina is a is still a really good one.

[00:45:53]I think good GDMT for heart failure is really really good as an anti-anginal but interesting there are also those who get bad heart failure and they can't walk they can't do anything and they're just breathless and overloaded and then you get them onto GDMT and their LV improves a bit and then they start getting angina it's ah and so what I what we do more and more is when they are stable I think ultimately it's only one clinician who makes the decision the heart team can inform but what we're very keen to do is you know Dvark or I will bring them into our clinic sit down with them meet them discuss see what the right thing to do is. But at at times as well, we just say to them, look, this is something we've got a little bit of time. We've not got forever, but this is not something we need to make a decision today. So, we get you on some GDMT, we get you optimized, and then you come back to our clinic, uh, maybe after a month. Limiting breathlessness, I think, is really hard, but if you've got them on good GDMT, you've got them well sorted, that, you know, everything else is sorted, and they're still very breathless, they still can't do things normally, I think that is a good indication. Um, and we've seen some benefits for that. But, I think you have to be careful, obviously.

[00:46:54]Let's quickly go around the team. I don't want to keep Matt from a beautiful day in London. Only happens once a year.

[00:47:00]So that's Go ahead. Whoever is next.

[00:47:07]>> Yeah, >> thank you so much. Uh absolutely great talk. Um just really quickly in light of the results of uh this trial you guys conducted now in clinical practice do you do you find yourself uh patients that are really niche that you're absolutely sure that will benefit and you're 100% going to do Impala on them to protect them. Is there any patient profile that you might still consider that requires absolutely this kind of microaxial flow pumps? Uh and I'm just wondering uh what's your strategy in terms of decision making? We touched we briefly touched upon it balloon pump versus uh uh micro full pump. I'm just curious about your clinical practice especially in light of these results.

[00:47:50]>> Yeah, thanks. So um so yes, I think there are there is still very much a role. Um the right heart cath for me really informs the hemodynamics. You know those who are not at the 2.1 but those with sort of baseline cardiac indices in the region of 1.5 I really worry about. They're very very brittle.

[00:48:06]Um uh as as you know we were just talking about I think you know your calcium modification strategy is interesting. I use a lot of rotablation as opposed to shock wave because I do think it's better generally from an eskeemic perspective. Um the orth stenosis are the other ones who really really worry me. Their risk of cardiac collapse if cardiovascular collapse if you have the slightest complication and most of the time this is about managing complications. If you can get through a procedure without losing a branch, without dissecting something, without getting no reflow, you can normally get through. But the aortic stenosis just go down. You can't get them back because you can't you can't pump the heart. You know, to have perusion, you got to have contraction. To have contraction, you have to have diffusion. And if you lose that balance in done, >> I got to say, I can't agree with you more. I mean, we've gone to the point now where we will do the valve even before left main. I mean, unless the left main's like 90% with Timmy 2 flow, we will get the valve out of the way.

[00:48:59]And just about anybody can do the left main afterwards. And the other thing I wanted to say just for the team is people sometimes underestimate how impactful moderate AS is. Like everybody gets like, oh, this is bad as I got to be more careful. Then they see moderate AS and they treat it as nothing. But moderate AS when you have a complication can be just as bad.

[00:49:20]>> Yeah, completely agree. Completely agree. And you can, you know, you can, you know, the challenge sometimes comes in centers where you don't have ready access to both structural and coronary.

[00:49:29]We're fortunate here to be able to do the two. You can put an impeller in through certainly moderate sources so I've never found a problem. And if that's your only option, it's a good one. Otherwise, I agree. If you can get the valve out the way, they they do much much better. The hybrid procedures had a bit of a a vogue at some point. I don't know about over there, but here we're very much we try and do it more sequentially and one the other is a bit safer. Tavi, not on dual antiplatlets and all that sort of stuff. Agree.

[00:49:52]>> Thank you, >> Lou. Uh, come on. You you've been quiet.

[00:49:56]Yumi, I see I see Yumi's camera. Yumi, you went on. Go ahead. Yes, please.

[00:50:00]>> Uh, thank you for this brilliant talk.

[00:50:02]It was very insightful. But I just want to ask you a little bit more about the viability because it's very gray. You know, it's the use is very difficult to see if we should do viability, what to do, and if it there's no viability, are there role to intervene? If patient has an type of thing. if you can um start.

[00:50:22]>> Yeah. So, so viability again my my PhD was was physiology and viability. So, it's something that I've really tried to get my head around. The thing to remember fundamentally is that the the way myioardial viability has been defined is a segment that is dysfunctional at baseline that will improve its contractility with revascularization. So, we've never defined viability against um clinical outcomes. It's only ever against segmental recovery of one bit of myioardium doesn't inform arhythmias and ultimately what's what's more at risk are you you know with that a a completely normal segment of baseline also doesn't count as a viable segment to help you know in many ways I think that's your potentially your most important segment the other part to it is our ability to co-register the two things together um and overall I think that we we probably need to go to looking at a whole heart model I think the viability test particularly on MRI is so useful LV thrombus, scarboard and all these other things that are that are of import. But I think this segmental agonizing over that segment versus this segment is it that or the other I don't think adds to the whole message because there's so many bigger pictures in managing the patient. So I think doing the test still useful but allowing the whole decision revascular not to hinge on an arbitrary you know cut point of certain that four segments still recover or not I think is probably isn't the answer because there's so much else that drives outcomes in the population.

[00:51:46]Thank you, >> Louie.

[00:51:52]>> Thank you for the great talk. That was Oh, can you turn your volume off? Okay.

[00:51:57]Thank you for the great talk. That was really amazing. Very informal. Um I I I agree with the the moderate severe as thing. Are there other subsets of patients that you know that you're going to have a flatline because I still have a a hard time putting everything together in chip basis three and I think the patients that really benefit from Impella are it's still extremely difficult to predict which one will benefit from from Impella support. We all have those patients that like they have a flatline mid procedure. you're doing and it's not the ones that you think uh you end up putting maybe 10 impedals for one that is really beneficial in in clinical practice and it's really hard to determine which one will benefit uh and we have flat lines even without sever it's sometimes it's not even a low ef patients there's patients that have EF 55% you do rotend or left nine and they collapse um it it's still very difficult for me to put everything together and my second question is how um how experience with the device uh do you think impact the outcomes? Uh when when I look at chip business 300 patients randomized in I think 20 something hospitals over three years uh it's not a a lot of cases per hospital per year. Do you think the volume has a big impact on the outcomes?

[00:53:22]>> Yeah. So I think I think they're great great points and great questions. the the the right selection of patients. I think it is for me it's baseline hemodynamics nails stenosis. They're my big things. The flatline on an impeller.

[00:53:34]I think we we need to get back to understanding it's a totally different thing from a flatline in a patient who's not on an impeller. And the the advantage of randomizing backwards and forwards is you get experience of both procedures. And actually, you know, we put bailout intic balloon pumps in eight patients in the whole arm. And I think you're right, one of the big challenges has always been we can't predict if this is going to happen to even though, you know, sevenfold higher risk. That sounds massive for a patient with LV dysfunction. The vast majority of our patients have normal LV function. So we will see more cardiovascular collapses overall in the in the more stable patients. Procedural volumes are really important. Um I think it's in some ways though the UK is the perfect somewhere where impellar isn't already ingrained is the perfect testing ground. So I always talk about PFO. If you look at PFO, PFO was launched everywhere and everybody could do a PFO closure and then they ran the trials of PFO closure and there didn't appear to be any benefit because all the patients who really needed a PFO closure were just getting a PFO closure. Then PFO closure had to go away completely. So you then get a level playing field where the patient who the same for Tavi tavi the the roll out of tavi is remarkable because the evidence base went before the clinical roll out and so everybody knows tav is a life-saving procedure and the problem is if you don't do it like that what you do is all the patients who are really going to benefit get the device and then you can't show a benefit in the population where no one really cares if they get it or not and I think so in the in some ways the UK is perfect because we didn't have impeller anywhere the downside is exactly as you say volumes are smaller now complex PCI volumes are high structural large access volumes are high would you know overall I don't think we'll see we'll see from protect I think that'll be the you know that'll be the big answer I don't I think with the complex PCI experience and the structure experience the fact often this was two people working together here often you know there is a bit more of a separation between tavy and coronary so sometimes it was two people coming together but I I don't think it will fundamentally change the outcomes of the trial um but I think it is it's always an important uh point to recognize as a a point of critique and I think protect for will be really informative from that perspective.

[00:55:35]>> Thank you. And maybe just like as a quick follow-up question uh from the chip basis uh study, are you working on some sort of score to kind of try to predict which patients uh would benefit from support?

[00:55:50]>> Yeah, absolutely. So S I didn't show everything from S's presentation at PCR, but he prevented presented some work on sort of risk of hemodynamic deterioration from there. um which I think will be really impactful. That sort of thing's been done before.

[00:56:02]There's also a plan I think you due course to look at a secondary analysis based on uh outcomes you know almost a simple forest plot baseline hemodynamics did you benefit or not and I think that will be really interesting when that comes through be small numbers though you know 300 in trial so it'll be it'll be an imperfect analysis but again useful in hypothesising for the future >> I think it'll be really interesting particularly also to see you know like you mentioned like someone with a a baseline cardc index of 1.5 versus someone with 2.2 too. I think those are very different patients. Um, >> you know, the other group of patients, what was your cut off for pH in the study for pulary hypertension?

[00:56:40]>> Uh, it wasn't we didn't have any routine assessment for it. So, yeah, that's yeah, >> it'll be interesting to see because that's often another reason we will default to putting an impella. We unfortunately see a lot of patients particularly diialysis patients who come in bad triple vessel disease and their pH pressures are you know 70 systolic.

[00:56:59]uh those patients tend to do poorly on the table unless you can support. Um any final questions team and then we'll let Met go. Any burning questions?

[00:57:13]>> It seems not. Uh Andrea Matt, thanks so much. Uh I think everyone really enjoyed this talk. I saw so many people connected not only interventional also many heart failure and non-invasive cardiologists. I'm sure you interested many many of our colleagues and many others will watch this again on YouTube. So just wanted to thank you again and we're looking forward to welcoming you again in the future.

[00:57:38]>> Thank you Raj. I'm hugely grateful to be inviting for everyone's time. So thank you. It's been it's been great.

[00:57:43]>> Thank you man. Enjoy the weather in London. Take care. Cheers. Thanks very much. Bye.