Heart Failure and COVID-19 Crisis (Hussain, MD, Fida, MD, Trachtenberg, MD, Zainab, MD) 09/10/20

[Music] good evening everyone and welcome to the debakey cv live heart failure hour and i'm your host imad hussein just keep a couple of housekeeping items before we start and introduce our topic and panelists if you have live questions we are taking it you can either text debakey which is 37607 or you can go to polleverywhere.com so poll ev.com to send your online questions so today is a very interesting topic that we have it's basically pertaining to the current era the current crisis going on termed heart failure and the cov19 crisis as this you know this is the heart failure hour so we're going to focus a little bit more on patients that have heart failure or can develop heart failure as a result of covid19 infection um so i would like to start by introducing our panelists for today on my right is dr nadia fida she is the medical director of heart failure and cardiovascular imaging at houston methodist baytown then we have on to my left doctor asthma zanub dr zaneb is a critical care medicine and doctor she's an intensivist she bans our cv icu she's a assistant professor of medicine with will cornell and in the department of cardiovascular anesthesia and then lastly online i have dr barry trachtenberg he is the director of the cardio oncology and cardiac amyloid programs he's also the associate director of our mcs program and he is the program director of our advanced heart failure transplant cardiology program so i would like to welcome all our panelists and with that i think we should swing into it so dr feda i would like to ask you starting just so that our audience can kind of get a sense if you could go just give us some brief introduction about the sars kovit ii virus coronavirus 2 virus how it enters the cell and how it causes infection and what is the relationship between that and cardiovascular disease and if there's any data pertaining to heart failure patients in particular yes thank you and good evening everyone so i think the first introduction uh first appearing in wuhan china last year of 2019 uh covet caused by severe acute respiratory syndrome has quickly become a pandemic declared by who on march 11 2020. since uh since then uh we this is very humbling that in the united states there there are close to uh close to four million cases now and uh just to explain a mechanism of entry of the of the virus into the cell uh first of all it shares the genetic material which is similar to the uh sars pandemic in 2003 and hence uh the name was changed to sars kobe 2. it attaches to the angiotensin converting enzyme to a protein on the surface of the cell after it forms a complex it then is is endocytosed into and after that the ace2 or angiotensin converting enzyme inhibitor 2 is converting enzyme 2 is kind of downregulated after that the virus starts replicating um this is to mechanism and we will talk about it later again is very crucial in our understanding and especially pertinent to the cardiovascular population disease population where we employ a lot of these medications ace inhibitors and angiotensin receptor blockers so as you can see uh this this is the surface of the alveolar cell the cells in the lungs and the the as2 is amply available in these cells and other organs so once this complex is formed the cell goes inside starts replicating and then the formation of angiotensin ii starts increasing which can lead to further damage in the lungs and pertinent to the cardiovascular system as well the as we are talking more and more and understanding this disease process and the research studies that are coming out uh the the mechanism of injury and the biomarkers um uh in code 19 the heart failure biomarkers we have recognized a few but the susceptibility to the uh to the cardiovascular system is broad uh is broad in the terms of myocardial injury uh from stressors from systemic endless critical illness hypoxia hypotension that then starts the cascade of neurohormonal activation sympathetic biomarkers and the biomarkers of inflammation and remodeling so i think what what we know the most is the troponin levels and that we constantly measure in all our population when they are admitted for various reasons for example with chest pain and decompensated heart failure similarly in this illness we have seen that troponins are quite a bit associated with not only with the severity of the disease but also the outcomes as i'll show later the bnp is a biomarker of stretch in the heart and the volume overload and there is some data that suggests that the inflammatory biomarkers like interleukin 6 the crp the tumor necrosis factor ferritin d-dammer may be playing a role as well we have not seen much that are pertinent to the myocardial remodeling biomarkers which are st2 and galactin too as we see here i think this this is this is a very good uh state-of-the-art reviews recently published in jack by dragons at all and it shows us the relative frequency of cardiovascular risk factors and an underlying cardiovascular conditions in all the available covert 19 cohorts and what they have done is is is also if you look at the bottom the last reference which is close to 13 000 these are the patients this is the population prior to covert 19 and taken as a competitor population from china and then the the latter half the vu at all and was a large data set close to 45 000 patients that were um that were looked at and then fang at all close to 3 000 patients and they looked all these cohorts have really looked at cardiovascular disease which is mainly a composite of cardiovascular disease heart failure and cerebrovascular disease and the traditional risk factors like diabetes hypertension smoking and coronary artery disease and we can see that their prevalence in this population is much higher that is infected by covert 19. cbd about 10.5 percent diabetes 7.3 percent hypertension 6.5 which is much much higher than the case fidelity rate of 2.3 percent and this further sub classifies according to the outcomes and the patients who had these risk factors more likely to be admitted to either icu or die so i think this paints a picture of how cardiovascular disease has a very important measure of how patients with kubern19 are going to do when we talk about a little bit more on the incidence of myocardial injury in covert 19 here we can see all the cohorts that have done it and as the level of or the incidence of injury increases so does the mortality this is just another example this is by by stratified by the level of troponin t so higher the level higher the mortality and if we see outcomes like ards mechanical ventilation fatal arrhythmias like vt and ventricular fibrillation and even death more so in patients with higher levels of troponin positivity so troponin as as i mentioned earlier remains a very robust biomarker not only for diagnosis but also for prognostication of of this population and and serially measuring it may have a potential value in further risk ratification of these patients who is going to do well and versus who is not and needs a further or higher level of management when we go to a little bit of imaging data in these patients this is another um review that came out recently um and this this clearly shows that the patients uh in the cohort of patients that were taken for spectrum of cardiac manifestations in the covert 19 population and the systematically done echocardiograms a 32 percent of population did not have 32 percent of population and normal echocardiograms and the most manifestation that we see in quiver 19 population is rv dilatation and rv dysfunction close to 40 percent left ventricular systolic dysfunction was a small cohort only 10 percent of cases and if we go and further the authors look at what is the association with outcomes if if you look at the death the the parameters out of the echocardiogram that correlated with this were low lvef the e to a ratio which is a ratio of how much is the filling pressures inside the heart or how decompensated a person is and the rv and diastolic area and the myocardial performance index also known as t index this is a nice uh study that was done that came out of frankfurt uh germany that looked at a prospective cohort of people who were initially hospitalized but then have recovered from covert 19 illness and they have done mris and then matched it to a normal control population and in this uh if we just uh see it through the other two panels show um histopathological slides from patients who were severely ill but now have recovered so this is at the bottom panels through the mri in the recovered patients but as you can see the green lines that mark the native t1 and t2 times on cardiac mri that are related that identify the edema or ongoing inflammation are much higher in this population the median time to scan from the recovery from the diagnosis was 67 days in this population so these patients have already recovered and are at home so this is concerning uh that this information goes on and the authors actually rightfully suggested that maybe there should be serial evaluation so so so dolly i think for our audience it sounds like what we're saying is that even when you talk about the cardiovascular disease as being a predisposing risk factor for developing more severe coving 19 infection and higher mortality the studies do not reflect per se heart failure patients they are very vague about defining cardiovascular disease is that is that correct that is correct there are actually very few studies that have actually stratified patients by lvef and yes if the patients and i think the comorbidity just drives the um outcomes here right in the setting of code 19. and and and i guess troponin we can use justice for the audience to summarize as a prognostic marker primarily because troponin could be a marked or myocardial injury but we don't know if that's true infection from microbitis or if there's some ischemia going on or what is the cause of it absolutely absolutely and i think more and more that studies that are coming and we are realizing uh this there are several mechanisms of injury and it it's it could be direct myocardial injury versus from the stress or type 2 mi but the troponin as a prognostication in patients with underlying cardiovascular disease and and how much does it rise also uh gives us prognostication and also um the as we have realized scuba 19 is also a very pro-thrombotic disease as well so that is also another cause for troponin elevation all right well i mean that gives us a very good set way into i would like to uh reach out to our um colleague dr trachtenberg and then barry tell us is there i mean for the audience do you can you get my is there mycarditis with kobe 19 or this troponin is a bystander yeah no that's a great question i mean so the truth is probably we don't there there's not been clear evidence of myocarditis in the sense that you have everything coming together including um biopsy data that that really puts the positive dallas criteria which we have for lymphocytic infiltration and myocardial necrosis with a viral positivity but certainly you know as dr feda mentioned the troponin is a non-specific marker of mild side injury and it could be due to you know sepsis or um you know and endothelial dysfunction and and hypercoagulability um you know myocardial infarction in these patients and pes there's so many causes and myocarditis as well so the troponin is we definitely see that that's commonly positive in hospitalized patients uh but that doesn't mean myocarditis similarly we have a lot of mri data showing inflammation um and and certainly there was a concerning article that came out of gemma showing that you know 60 of patients and these were predominantly patients that were had coveted and were not hospitalized uh two-thirds of them were not hospitalized and 60 percent of them had what we would consider myocardial inflammation or myocarditis by mri now we don't know any knowledge on the outcomes of those patients most of these were not hospitalized they probably will have a good outcome and we don't have any tissue data on those patients so we have a lot of mri data what we don't have is a lot of tissue data it's been very hard to get autopsy or endomyocardial biopsy data on patients that are suspected of having acute copin myocarditis due to the concern of spreading the covalent to the cath lab or pathology etc so we do have now probably about a dozen or more case reports that are suggested of myocarditis and if you look at the data if you look at the slide here you can see that that you know we have certainly um you know patients that have what we would consider myocarditis the case report by sila at all which is the fourth from the left it was a patient that that had clinical myocarditis mri myocarditis and had a classic lymphocytic infiltration that you would see with with a viral myocarditis now there was no sars kobe to replication in the myocardium which is not a requirement for the diagnosis of myocarditis i would say it's a that that patient clearly had myocarditis and we also have evidence that that patients may have viral replication without without in the true inflammatory response of myocarditis um so there was one uh study in jama that looked at 39 patients who died of covet now these are predominantly septogenarians and octogenarians and out of those 39 24 of them did have sarge kov2 replication and 16 of those had a really a significant what was considered a significant viral world which is somewhat arbitrary and they looked at cytokine panels and that they were pro-inflammatory in those 16 patients um compared to those that didn't have viral replication however none of those patients had a true you know my definition of myocarditis according to the taoist criteria um showing you know lymphocytic infiltration in the heart um so we know you can have viral replication you can have lymphocytic infiltration um but but we haven't really seen the two go hand in hand we have seen uh patients that are case reports of patients with suspected myocarditis who undergo biopsy do have viral replication and then they have sort of this low-level inflammation including macrophages but really no t cell infiltration so it's a bit mysterious in terms of having hard definitive evidence from a large population of having classic myocarditis but we are seeing certainly a lot of patients with suspected myocarditis a lot of mris that are highly suggestive of myocarditis but which isn't surprising we know that viruses cause myocarditis if you look at the sars outbreak in 2002 there's autopsy data that had 35 percent of patients who died did have the presence of viral rna in their myocardium we haven't seen it as much with with uh with this virus but i just want to kind of you know preface all this with the fact that we're still learning a tremendous amount there's a lot we don't know um you know and it's a very humbling disease um and and we've had a lot of case supports a lot of small reports and uh i i think we'll know a lot more several months down the road okay so i mean um it looks like that currently the myocarditis cases we have are limited to small case reports a case reports a small case series there was an autopsy study like you mentioned um with show so one thing that was i was uh was wanted to ask you for and especially for the audience was so when they looked at the um the viral copies of rna and when they looked at where they were staining i it sounds like it came in the interstitium in the macrophages and one thought that would come to mind as a question would be that it's possible that this is just a manifestation of systemic inflammation and even if you were to look in the kidneys you would find some macrophages with some um you know sars cove to cov2 or if you were to look in the liver you might find some so it still could be a bystander but then i agree in your with your point that like the pro-inflammatory um panels they were they were positive so they were suggesting inflammation so uh do you think it's a bystander or do you really think that there is a viral cytopathic effect going on here so i mean i guess it depends on the so the study that you know that we're talking about this is an autopsy study from germany 39 patients predominantly older that are less likely to have a robust inflammatory response and in that in those patients um you know most of those patients buy it from pneumonia so i think as to your point i think that the macrophage presence and the intercession i think that's probably you know that could be you know from the lungs or from from just systemic inflammation and i don't think that is a proof of uh inflammatory myocarditis and by the daoist criteria definition which is probably um you know it's an outdated definition to be fair of myocarditis it's probably not going to be the gold standard forever but that's what we have and by that the gold standard those patients didn't meet criteria so i think in that study aside i think it's a bystander but i do think that certainly there is i mean you would expect there to be patients that do have myoparditis in the classic form from this disease we haven't seen we've only seen a couple cases that seem to suggest it which is surprising but on the other hand we're not biopsying a lot of these patients so i think if we you know there are some states that are looking to have more uh histology in the form of biopsies and autopsies and hopefully once all that's collected that we'll have a clearer picture of what's bystander and what's really positive and mary there was also a college study on college athletes about uh looking the patients who had coveted infection and um they had some it was an mri based study uh i don't remember recall the details i don't know if you can just rely on this stuff yeah the reason you don't recall the details it hasn't been published yet so this has been in the media um it hasn't been published in the peer-reviewed form but this has been all over the media as as colleges struggle with the decision to come back to play college sports especially you know contact sports like like football that there is a study from ohio state where among the big 12 athletes that had coveted 15 had myocarditis on mri by mri criteria now the minorities patients have symptoms these are largely asymptomatic patients with covid that have a positive mri findings now what this means isn't really clear i mean we know from you know older pediatric studies of children that have viral infections if you put an ekg on them up to two-thirds might have ekg abnormalities so there's probably a lot of asymptomatic myocarditis in in in the community from viruses as a whole that we never know about because we're not getting mris and and these probably the vast majority of myocarditis will will resolve on its own without sequelae so the significance of this isn't clear i mean really i mean we're talking about findings of inflammation it's not necessarily that they have um you know the scar or delayed gadolinium enhancement that that on repeat mri we don't have any of that data so it is concerning certainly as you talk about you know playing sports that are contact and having fans in the audience and all and that that you might have this um this rate of asymptomatic myocarditis but that study to my knowledge has not been published yet i'm looking forward to seeing that in peer-reviewed form well thank you very much barry um so what is sounding like to me from a non-expert with covid19 and heart failure is that um it sounds like there's an autopsy study that shows uh patients who die from pneumonia so they have already they already died and when you do their autopsies you have potentially maybe some evidence of myocardial involvement maybe not maybe a bystander but then when you look at the mri study um that is done where you're about 70 days out roughly on mean it was about 70 days yes 70 days median 70 days out so one would one would like to think that they're in the recovery stages and so early on you if you don't die from say respiratory failure or ards then in the natural history of covid19 there is a possibility that down the line you have some sequela that are somehow related to myocardial edema so i guess there was a sort of a dr yancy clyde yancey did write an editorial on this right basically raising caution that we might be seeing nuance at heart failure after covet 19 infection and this may be just a marker of of just like we get viral myocarditis patients that may have had it in the past and then we see them down the line with a non-ischemic cardiomyopathy so i mean there's more to get more data as we go along but um it is suggesting that there is some natural history where heart failure might be playing a role down the line i i don't know if any of the other panelists have any thoughts about that i mean typically since this is mostly the ones that come to the icu to us uh intubated are sick enough to um you know um i mean i would say like once they come to the icu basically they are the sicker one and um with hypoxemia and all that that one of the mechanism of injury as you mentioned the troponins are elevated that could be one possibility and a pro-thrombotic state and with that hypoxemia and being a very pro-thrombotic condition we have a very high incidence of thromboembolism in the lungs also not only at the microangiopathy level but also as pe even those patients who go on ecmo and are on systemic heparin they're about in one study from france about one-fifth of the patients had pe while on heparin and everything so considering all that hypoxemia and pulmonary embolism the right ventricular dysfunction is something that we do see and one of the slide that you mentioned most of those dysfunction that you saw was the right ventricular as compared to the left ventricular so i'm assuming the rv failure could be leading eventually to some other you know complications related with the heart and all so if you on that lines uh dr xena is there any role for anticoagulation in coving 19 patients to reduce the risk of outcomes or is there has that shown to improve outcomes in any way um it's one of the um you know biomarker as dr fida mentioned is d dimer that we see in these patients which is elevated um interestingly d dimer in the past we have seen in patients for the thromboembolism vte and pe although its sensitivity is high but it has poor specificity so it does if it is negative you will say okay there is no thromboembolism but if it is positive it does not confirm thromboembolism but in these patients majority of these patients come in with a high d dimer and actually some of those patients initially if the d dimer is not that high down the road the d dimer becomes very high like about four times the normal level or the initial level and it has been seen that the higher d dimer actually is associated with swear disease and higher mortality in these patients considering that um we also know that more recently um the one of the papers suggested that um the micro um the thrombotic phase in the microangiopathy in these lungs is nine times greater as compared to influenza ards okay which is significant um now considering um those patients who um the society for hematology and thrombosis has suggested that just based on the fact that the d dimer is high we don't do systemic um therapeutic therapeutic heparin but in in patients who we have confirmed thromboembolism you can start um you know heparin uh otherwise um dvt prophylaxis should be it we do see a quite a lot of patients who go on ecmo we had and at methodist about 38 to 40 covet patients who were placed on ecmo we still have like few who are on ecmo and being on ecmo they required anticoagulation while on heparin um interestingly we know that rather even in those patients who do not have covet we require anticoagulation just because the contact activation of the cascade and it's a pro thrombotic state but also we do also know that in ecmo these patients do lose one willie brand factor and the glycoproteins from the platelets so their the risk of bleeding is also higher in these patients so although these patients are on heparin their d-dimer is elevated and in spite of that like i mentioned earlier in one of the french studies showed patients on ecmo on heparin had one one-fifth of those patients had pulmonary embolism and considering that um we also see that the bleeding risk of bleeding on these patients in spite of being a pro-thrombotic state is also high um in generally in ecmo they're about 2.5 percent risk of bleeding but in in these patients there is one reported study which said about five percent risk of bleeding in these patients and that's what we have actually been uh observing in our ics as well what has been our institutional um experience with uh thrombotic complications on ecmo and the second follow-up to that is are these predominantly v v ecmo or v a ecmo in terms of do they also have circulatory collapse so let me answer your first question um so we we are not seeing anything different than whatever the literature is telling us these patients are pro-thrombotic very high d dimers and some of them initially although may come in with the d-dimer which is mildly elevated but may lead to very high levels and um in generally if we do not have an evidence of vte we start them on dvt profile axis if they go on ecmo of course they require anticoagulation and in spite of that we had some cases that while the ptt was therapeutic we could see the fibrin threat threads in the quad rocks and there was one case actually where we um the patient um started having hemolysis with a higher heptoglobin level no um no obvious source of bleeding and all that so we um thought that it could be because we have seen these um coagulants state when they actually the thrombus actually lines the uh cannulation cannulas and leading to hemolysis and all that and we're changing the quad rocks you actually stop the hemolysis and we have patients who actually even while on ecmo and on crrt required systemic heparin and a pre-filter heparin just because of being a very pro-thrombotic state now coming to your second uh question about uh vv echo wire versus a vac most of our acmo patients are we purely respiratory failure patients but we do have we had about two ecmos who are va atmos one of them a patient who came in a very young patient who came in with an acute mi um from uh you know he had like thrombus at least in two um vessels i'm i don't remember if it was one was the led or a circle or something and uh and in a hemodynamic collapse as well requiring a vacuum while and they did the pci and all that luckily this patient survived and within three days we were able to come off of the vehicle his hemodynamics improved because his main issue was there is no previous history of coronary artery disease or any family history of early coronary artery disease no other risk factors other than just he was covet positive although he did not had any respiratory symptoms with that no fevers nothing was just incidental and another we atmo is um still in there and you're all you're probably aware of that patient who was a heart transplant patient who um required we acknow and we still don't know what led to this hemodynamic collapse but again in this particular patient uh it was not the lungs which was the main problem it was not the length that was the main problem so so we are seeing cardiogenic shock as part of the profile but not as frequently as as the respiratory failure and ards okay so i mean i i do have one set way to a question that i would like to ask you and then probably also lead to dr feda with with regards to that so we've talked about if you have cardiovascular disease you are at a higher risk for getting covered 19 infection with higher severity and a higher mortality we've established that so that's one unilateral relationship where you have underlying cardiovascular disease and you're getting kova 19. how about the other way around does covet 19 cause cardiovascular disease and in that regard we have talked about my potentially myocarditis being one of the often if you have pre-existing heart failure although we don't have our institutional experience there have been reports of va ecmo in the setting of a combined septic cartogenic shock picture but then leading to that there was a in the pediatric population there was a study where they talked about um patients with coveted 19 kids with covet 19 that then developed the hyperinflammatory response cytokine storm and presented with very classic symptoms of what we used to see in with kawasaki's disease where they had coronary artery involvement aneurysms and they had like the whole prodrome where um either it's an endothelitis that we know that the endothelium is very rich in ace2 or there is something else in terms of microthrombotic complications that is resulting in this phenomena of a sort of a heart involvement directly so in that light what i'm saying is what i'm trying to get it and set way to my question for you dr zanub is if you have pre-existing cardiovascular disease you may not have yet manifested as having structural heart disease you may not have known heart failure but then you get this covid19 infection and all the milieu that goes with it systemic inflammation pro-thrombotic state endothelitis endothelial dysfunction you could develop manifest not necessarily half ref but maybe acute diastolic heart failure especially in the setting of cova 19 patients where we're giving iv fluids you know we're treating them like sepsis so my question to you is if a patient does develop ards and pneumonia how do we differentiate they truly have ards or they don't have true cardiogenic pulmonary edema and is there any role for using pa catheter to in these patients to specifically tailor therapy i guess there is a role especially when when we are seeing more cases of right ventricular dysfunction and whether also plus whether you want to know like you know because at one stage the x-rays become the same yes they are all like whited out bilateral infiltrates day by day have the same thing although we do keep them on the dryer side and all that then the next thing you see is like their creatinines start going up and all that so you're trying to keep balance between keeping them on the dryer side and diuresing them to keep the you know and and then at the other side you want to protect the kidneys as well to have the second organ failure and i unfortunately because the way the disease is like we try not to do too many procedures on these patients so far we have not tried um you know pulmonary artery catheter in these patients most of the time the hemodynamics are measured mostly we have an art line and we use the cbp and the non-invasive methods of going out by the cardiac output and all that so maybe there is a role um i guess we all have to brace for going a little bit more aggressive with these patients to know like what's going on and then accordingly treat these patients and so something prospectively that can be we can see if you know at a hospital institutional level in terms of a protocol or moving forward perhaps yeah i do want to add something to it um actually you know in the the the difference of practices in an academic center versus community hospital right uh what we have seen in baytown and uh we have not looked at it in a in a in a systematic way but just recalling the cases especially the patients though we have not discussed this particularly here but morbidly obese population that were stable younger morbidly obese population males and females who don't have a lot of underlying other diagnosed risk factors came in with mild to moderate disease but did not recover ended up in icus and then oxygenation becomes a problem at that stage we have actually done a lot of swan cans catheters and they have quite a bit of manifestation of pulmonary hypertension and which in uh leads to all this the rv dysfunction that we see and kidney injury then starts because we can't direct them adequately what is what is also notable again we haven't looked at into it in detail is that they respond very nicely to uh maximum strengths of inhaled floor land then we cannot do any other systemic therapies for them it makes a lot of sense makes a lot of sense um so i think that that that's a very thorough discussion about the critical care aspects of um covid19 and heart failure patients or cardiovascular disease patients nadia there's this thing out there the people um you know several of our patients we receive phone calls in clinic about um they're on like cinepril or they're on losartan they're on arbs or ace inhibitors and they're very worried because they read all these things in the press about whether they should be continuing these medications and you as you know it's a ubiquitous use it's not only used for heart failure but it's also used treatment widely for hypertension and chronic kidney disease um what what is the data out there what does the data tell us yeah absolutely and that's that's that's a great question um and i think uh to understand it a little bit uh better we're going to come into the detail of this a little bit more so as uh dr hussain has said uh the ace inhibitors or angiotensin converting enzyme inhibitors and angiotensin receptor blockers are um bread and butter of cardiovascular disease risk modification and treatment and especially for heart failure patients hypertensive diabetic patients chronic kidney disease patients and these are one of the very first medications that that showed that they start the reversing the fibrosis and reverse remodel the myocardium in heart failure so the the there is a lot of data out there and the data is conflicting uh till about now there is a data that says that since the virus uses the angiotensin converting enzyme to uh to form a complex and with that aids into entry into the cell is that the reason that more that once we have patients on these medications uh that that the the virus is using being on these medications up regulates these receptors and then there are more receptors available for this virus to cause harm and is that the reason that the patients are having bad outcomes because many of the cardiovascular disease patients are having bad outcomes are also on these medications sure versus this there is a hypothesis that if you take the patients off on when they are stable on these medical therapies for their chronic conditions now you take them off and you start down regulating the mechanisms that were beneficial and you you you up the more production of angiotensin ii that leads to more injury of the lungs and a cardiovascular system is that the reason so till now now we uh in the esc recently there was a late breaking clinical trial brace corona that came uh that came out that has actually done a randomized uh randomized control trial so uh brace corona is a pragmatic trial continuing versus suspending angiotensin converting enzyme inhibitors and angiotensin receptor blockers and their impact on advice outcomes in hospitalized patients with coronavirus so it's a national registry unsuspected and confirmed cases of covet 19 and it's a one-ton one-on-one randomization they have enrolled about 659 patients when they presented in an esc and the patients were either taken off of ace inhibitors and arbs for 30 days or they were left on it and then the patients who were included in the trial were all um adults hospitalized with the confirmed case of covetous 19 and the patient the exclu the patients were excluded were either too sick or decompensated in the last 12 months they were requiring a lot of medications for their blood pressure management uh the succubuture wall saturn or entrestop patients were not included in this trial patients who are on mechanical ventilation or and hemodynamically unstable or pregnant patients were not in this trial so the the primary outcome of the study was number of days alive and out of the hospital through 30 days was no different so 21.9 in this patients who had suspended treatment um and they compared with 22.9 in the continuing uh group and the secondary outcome of all cause death at 30 days 2.7 percent in the suspended group versus 2.8 percent in the continuing group so the i i guess the take home message that we can at least take that it's a randomized trial uh in a large academic center um and we have seen that among patients who are hospitalized with qubit 19 infection receiving chronic ace inhibitors and arbs is uh versus suspending them is not beneficial so suspending the therapy compared with continuing them did not improve the days alive or out of the hospital i think that the main limitation of the trial is it still does not answer the question of this mechanism that the virus binds to as2 what about the patients um who who are hypertensive on it but do not have covert 19 what should they do so i guess there is a limitation of the trial but this is the first randomized trial so in a lot of other court studies that have said the same thing that discontinuing the therapy is probably more uh harmful than beneficial sure i mean so it looks like nadia this randomized trial is basically consolidating what the retrospective data is showing that whether you're on asymmetry or not does not increase your risk of viral infection number one number two it does not increase the risk of death nor does it increase your length of stay correct um so the retrospective data is clear on that but then now we have a randomized control trial showing you whether you suspend it or not the question i have is could it be beneficial because um someone is say someone is not on ace inhibitor or they will have unopposed angiotensin ii as a result of covid19 infection and they could have a more pro-inflammatory state so i think there are some trials undergoing that are currently not out as to whether there may be a beneficial role of of of asynchronous or arbs in this population one question i did want to ask you regarding that so that is like if they're outpatient they're on asynchronous arbs they have mild infection they get admitted okay with mild symptoms you get you continue ace numbers arbs but what happens when like day seven or ten they get sicker there's a cytokine storm that hits they're now getting a little hypotensive they're an ards they're not developed rds but they're getting hypoxic they're getting respiratory failure they're getting worsening pneumonia now it's a matter of time before they get hypertensive you start having renal failure is that would that be a reasonable time to maybe consider stopping ace inhibitors or arbs well and that's a that's a great question i i think if the patient is a borderline um at the verge of you know hemodynamic collapse then we don't have an option but patients who are kind of maintaining their blood pressure should we just lower the dose and watch or switch them over to a shorter acting is um inhibitor are to have a closer monitoring could be a way to go but yes i mean we don't have data to back it up or not at this stage okay interestingly there was like a study that was done like years ago before covet came in and that was an ards basically it's a still a bench study not gone to the bedside yet but they found um that actually uh mice with ards when they induced ards and the mice and they were given ace inhibitors it reduced the fibrosis fibrotic state of erds so um i don't know like if it has a role in ards patients to prevent fibrosis as well yeah i mean because one thing that we do know that acembers do even clinically is that they present with dry cough and one of the mechanisms and so brady increased bradykinin can cause bronchial hyper reactivity and i and it may be that that that is actually um not good in a setting when you have pneumonia respiratory failure you're having difficulty oxidating but yeah i think it remains controversial in that setting whether one should continue or not most definitely if someone became hypotensive and still started developing acute kidney injury at that time i think it will all be discontinuing these medications but it's very interesting thing as to how to pursue this for the more sicker patients that have copic 19. um you know i in the likes last few minutes we had before we take some questions i wanted to reach out to dr trachtenberg and i want to switch the little gears to patients because heart failure is a spectrum we have advanced we have our advanced heart failure patients we have patients that are listed for heart transplant and then we have patients that are in the hospital on the contemporary mechanical circuited sport i mean they the cove in 19 hit but they're still waiting for their hearts what is our institutional experience or what what what has been our policy around our listed patients in terms of transplantation and what was our experience with heart transplants um in this cove in 19 era very yeah no so it's a great question i mean i think you know we did i'm sure many programs across the country have struggled with this this question and um i think we kind of tailored our um decisions to the the what the the percent case rate was the positivity rate in the in the community at the time and which wave of the pandemic we were in so when we were at the the first what we call the peak although it turned out to be kind of the hill compared to the second real peak that we had subsequently uh we really you know we would patients that are listed said it's one or two that are hospitalized on uh temporary mechanical support or anatrops we never stopped transplanting those patients that are already in the hospital we did um you know try to avoid bringing patients in from home for a transplant during the two peaks unless they were someone that was really struggling at home or was someone that was you know that was really hard to get a match for example a patient on a nail bed that was blood type o or a highly sensitized patient where um you know that they may not get another opportunity so we have to we really had to weigh the risk of the patient coming into the hospital during the peak of the pandemic and getting covet which has happened and uh with the risk of missing their opportunity for transplant and dying from heart failure which is also a real possibility because these are sick patients so we um we did back down a little bit on the transplant volume during the two peaks um but you know in between we opened it back up to the weightless population at large but we did end up doing a fair number of transplants during during these waves and uh with good success we have had a couple uh patients that had a transplant uh recently um get covered uh fortunately no one um had died from that but they they did have copay we have had an lvad patient who got colluded on his index lvad hospitalization but thankfully did well and that's consistent with the literature so for mount sinai aditi singhvi and colleagues published their experience where they had um out of 400 patients that had a heart transplant in their program during during new york and during their pandemic they had 20 um i think they had 23 patients that uh that had covet and so these are all patients that um you know that have been transplanted in the past x number of years it's not necessarily acutely and out of those 22 patients that had the covid um in a prior heart transplant five of them died so 23 of them died and four out of those five that died were at another hospital not in their institution perhaps they managed the patient differently at the non-transplant centers and they looked at numbers for other hospitalized patients and it was similar to 18 fatalities so overall there's no evidence that transplant patients are more likely to die with covet if they're hospitalized compared to non-transplant patients so that's encouraging and we've certainly seen that here as well we've had as high as 15 patients all organ transplant um have coveted or patients that were tested um have killed it uh during the worst peak and overall the survival was fairly comparable to other hospitalized patients um in in in the mount sinai experience they also proceeded to be transplanted they had five transplants at a time of their publication and one of them did get covered and had just the mild uh manifestations from coalition so i think you can the bottom line is you know patients do need to have end organ interventions and you can't put your program on hold for a pandemic but certainly if you're careful about it and you try to choose the sickest patients that really need an intervention um and do your best that you can to have in the void kovid then that was our strategy and and even with that you know you're going to have some patients that do get coded um after index hospitalization but they are overall um with comparable survival to the population at large okay well thank you very much and um i think that uh we only have a few minutes left uh first of all i would like to thank the panel for an excellent discussion but i would like to open it up for any online questions at this time if there are any um or any comments from the audience all right so please there's no questions it looks like at this point okay well uh thank you guys for joining us today this evening for the heart failure hour um again i would really like to thank our my esteemed colleagues and panelists for being here and then um just to announce that the next session so the heart failure hour is the second thursday of every every month and so the next time we're going to have our the topic will be updates on heart failure with preserved ejection fraction so thank you for your time and good evening to all and have a nice evening thank you thank you [Music] you

Channel: Houston Methodist DeBakey CV Education

Views: 1,648

Rating: 5 out of 5

Keywords: DeBakey Heart & Vascular Center, Houston Methodist, Grand Rounds Conference, Dr. Alan Lumsden MD, DeBakey CV Education, Cardiology, cardiovascular, Heart Failure, Heart Disease, DeBakey CV Live, Live, Vascular Surgery, Multi-Modality Imaging, DICET, Dr. William Zoghbi MD, Cardiology Training, texas medical center, MITIE, Cardiovascular Training, Cardiac Surgery, Transplant Cardiology, COVID-19, Imad Hussain, Nadia Fida MD, Barry H. Trachtenberg MD, Asma Zainab MD

Id: xFkeB9alri8

Length: 55min 12sec (3312 seconds)

Published: Fri Sep 11 2020