[MUSIC PLAYING]

KUNJAN BHATT: So Kunjan Bhatt again. I am a heart failure specialist with Austin Heart. I work alongside my partners, Dr. Morris and Dr. Thomas. And it's a privilege to be here today. I appreciate you all and Molly asking me to speak.

I thought that this lecture I had given previously for the inpatient service line for heart failure was very apropos to what's happening both in the hospital but also in our practice. And it really is, if we are considering a patient for advanced therapies, what do we do? So I've written here, "So you want to get an LVAD-- the workup and the evaluation process and the patient experience." It really is more just the advanced therapy process, as there's a lot of overlap with transplant.

Housekeeping rules. I really can't-- it's going to be hard through this product to do a Q&A live. So what I would ask is perhaps through the chat if you can send your questions. And Alisha and Shelly are here with me, so they can certainly keep a list of questions. And if there's some time at the end, I'm happy to answer them.

And of course, as you know, if you have questions and we don't get to them, just-- you can always text me or call me offline, and we can address them. So thank you.

That being said, we have an epidemic of heart failure. I know we have a pandemic of corona, but we have an epidemic of heart failure, and it's been there. So if you estimate the US population as 300 million Americans, estimates of 2% to 3% of the population have heart failure. So we would say 2.5% or 2.6%. About 6 to 7 million Americans have heart failure.

And then the division of reduced EF versus preserved EF-- so EFs above 40%, EFs less than 40%. So if you think of the preserved EF population, it's about half. And then by default, then the other half are reduced EF.

The patients that we really kind of consider advanced therapies for are those who have, as the name implies, advanced heart failure. And that's about 10% to 12% of that HFrEF population. And that roughly estimates to about 150,000 to 250,000 patients-- a lot of patients. That's not a small sum of patients.

The problem is that if you look at transplants over time, transplants being the gold standard therapy for decades, the transplant volume is pretty small. These are pretty modest numbers. If you think of there's a 200,000 patient in need and only about 2,000 to 3,000 patients getting advanced therapies [INAUDIBLE] family heart transplant, big gap in therapy.

And that's where kind of the advent of the LVAD came in to begin with. We have a big patient population, large wait times. A lot of patients don't do well and expire because they expire on the wait list. And so to really get patients better therapies, and potentially advanced therapies for those who aren't eligible for transplant, that really was the gap which-- the LVAD has to some degree met that unmet need, or that unmet niche.

So about 5,000 patients who get LVADs per year, and we'll go over those numbers in a few slides. So about 3,000 with transplants, about 5,000 with VADs. Doing the math, that's still a big gap in therapy.

It's estimated that about 16,000 patients with advanced heart failure actually present to a heart failure specialist. So 200,000 patients with advanced heart failure, 16,000 that see physicians like myself and Dr. Thomas. So then there's still a large population of patients that don't see us and don't get considered for advanced therapies. Humbling statistics.

So LVAD volumes over the last several years, still pretty modest. If you go back to 2014 to 2019, though the pumps have changed, and the pumps have I think unarguably improved in quality, the number of implants themselves have been pretty steady.

And then the type of LVADs-- you may have heard names like HeartMate 2, HeartMate 3, HVAD. Two companies kind of have the lion's share of the market. Abbott makes the HeartMate 2 and HeartMate 3, and then Medtronic makes the HeartWare. If you look at the black bar graph, that is the HeartMate 2, an older pump that was really the workhorse for the late 2008, 2009, up until the mid 2000 and teens.

HeartMate 3, because of the MOMENTUM 3 trial, really took off. And that's this, I guess this light purple color. And that really from 2017 has essentially replaced the HeartMate 2, and really, to some degree, the HVAD. So the HeartMate 3 we do feel as a community is an excellent pump and really has probably the best hemodynamic profile.

And interestingly, looking at the kinds of implants we're doing, we are picking patients who are older, perhaps sicker, and in that realm perhaps those patients are better suited not for transplant, maybe not to get a VAD as a bridge to transplant, but maybe they just get a destination therapy VAD. Does that mean the pump is different? No. The pump is the same. The HeartMate 3 doesn't taste, look, or smell any different in a patient who is at bridge to transplant or a destination therapy VAD.

It's just nomenclature. Destination therapy means that's a standalone therapy. Bridge to transplant means that they deserve a heart transplant if they can get one, we need to kind of get them there, and the VAD kind of serves as that niche.

So we get this question a lot. When's the right time to refer to a heart failure specialist? And we always appreciate early referrals, because when patients are referred early, we can start having those critical conversations about what is life like with advanced heart failure therapies? What is life like without advanced heart failure therapies?

And I think like anyone else, patients deserve to have an informed discussion. And having an informed discussion when someone's in intensive care, such as someone we have right now on VA-ECMO, it's hard to talk to them. They're intubated. They're critically ill. Their family members are flustered. It's hard to make kind of informed decisions when things are crashing and burning.

So here we have the INTERMACS scoring system of how critical is an advanced heart failure patient. So advanced heart failure patient INTERMACS 7 is kind of a placeholder, a patient who is a functional class III. We see them in clinic every three to six months, and they're doing OK. They're kind of percolating along.

And as your number goes down, so say INTERMACS 4, for example, that's a patient who has been admitted for decompensated heart failure. They're not on inotropes. They're on medical therapy, but perhaps they are starting to become the revolving door. They're starting to get admitted over and over again. Those are folks we definitely want to be seeing if that's, in fact, what the patients may consider and what the referring team may consider.

But really, the sweet spot for where we find patients to get LVADs would be at INTERMACS 3. And INTERMACS 3 represents someone who presented to Heart Hospital or to Round Rock or to Georgetown, South Austin, somewhere in our network, who came in with reduced EF heart failure. They needed an inotrope because it was felt that they were shocky, and their inotropic support seemed to help them.

And we sometimes prove that they're inotrope dependent either in the hospital or as an outpatient by weaning the inotrope and then showing that they felt worse or they objectively did worse on some kind of a functional assessment. And then we put them back on the inotrope, and we call them inotrope dependent because on the inotrope they're better. Off the inotrope, they're worse. And some of this is subjective. Some of this can be objective.

But those are stable patients who then are on an IV drip with a PICC line, and they're home. And we see those kinds of patients on a weekly basis. Those are the sort of folks I would almost think if you have a general surgeon taking out a gallbladder, or an orthopedic surgeon operating on a knee, you don't want your general surgeon operating on the gallbladder when the gallbladder has perforated and the patient's in septic shock. You don't want your orthopedic surgeon operating on a knee when the patient's bed bound from such bad DJD.

So likewise, you don't want your heart failure surgeon to operate on your patient when they're crashing and burning on four drips, intubated on VA-ECMO. You want them to go in electively on their own two feet with a PICC line on an inotrope so that they have the biggest chance of success.

And I know this is intuitive, but the sicker you are going in, the sicker you are coming out. The healthier you are going in, the healthier you are coming out. And it's all about outcomes. And so as we start our LVAD program literally in a few weeks, which we're very excited about, we want to be choosing patients who are in this risk category, INTERMACS 3s and 4s, and not so much the 1s and 2s, as we know their outcomes are not great.

So when we look at our patients, we want to use our yardstick of what's our clinical gut tell us about this patient, how sick are they, but there's also some objective scoring systems. And there's two that I want to discuss with you. There's the Heart Failure Survival Score and the Seattle Heart Failure Model score.

If you look at the left sided graph, the Seattle Heart Failure Model looks at survival based on numerous clinical parameters-- demographic information, such as age, gender, functional class, weight, ejection fraction, systolic blood pressure; looking at medication profile, such as diuretics, guideline-directed medical therapy; looking at lab data, such as hemoglobin, other markers of the CBC. Also, uric acid levels and serum sodium, and then device support, such as ICD or CRT or CRT-D.

And those are all kind of put into the system. And on that website you see there, SeattleHeartFailureModel.org, that's available. And then you can get a one, two, three, and five-year predictive estimate of survival for these patients with HFrEF at baseline and then if they actually get an intervention. And you can see that survival curve kind of to the top right of the table.

The Heart Failure Survival Score uses seven variables listed here-- coronary disease, bundle branch block, LV function, heart rate, sodium, MAP, and VO2 max as measured on a cardiopulmonary stress test. There are some peculiar fudge factors that we use, and then you summate those and you get a Heart Failure Survival Score. And at the bottom of that screen, you'll see that the high-risk patients have a certain delineation, medium risk, and low risk. And of course, we want to be favoring low-risk patients, as they seem to do the best.

So you've identified your patient who needs advanced therapies. Who is this individual?

Is this individual someone who just took their COVID-19 Healthstream quiz? Finding out that Santa Claus doesn't exist? Cardiologist who ordered Golytley on a patient with C. diff colitis? Anyone who's seen Office Space hopefully understands that fourth reference. Or we just triggered the workup for an LVAD?

And of course, the correct answer is number 5. LVAD workups are extensive. And they include this.

So when we're thinking LVAD, we're thinking we need a full body assessment to look to make sure these patients can tolerate this pretty extensive, heroic, aggressive surgery. And it really is kind of a full body scan, so to speak.

There are functional studies we do. We look at different organ systems, such as the kidneys, the GI tract, the liver, blood, the peripheral vasculature, pulmonary functions, infectious status, nutritional status, neurocognitive function, psychologic function. We look at hemodynamic parameters. So we want to make sure patients are adequately unloaded. Are they on inotropes? Are they off inotropes? We would look at resistances.

Also want to look at imaging. So imaging includes CTs, echos, Doppler. Want to make sure we pay attention to the RV. The right ventricle is-- oftentimes we call it the forgotten ventricle, and I can tell you, and anyone who practices advanced heart failure, especially the surgeons, we cannot forget the RV.

We also want to look at coronary disease to exclude any significant unrevascularized coronary disease that may need to be addressed. Arrhythmias need to be addressed as well, and of course a whole host of tests that we'll go into.

We favor these workups in the INTERMACS 3 patient to be done on the outpatient side. I think patients would appreciate not being imprisoned for elective outpatient tests. Although they're extensive, these can all be done as outpatients.

And so we can do this in our CVICs. We can do this through our outpatient Heart Hospital ARA suite for some of the CT scans. Caths can be done on INTERMACS 3 patients, which they come in to get done at Heart Hospital. They come in, they get a cath, and they leave.

So a lot of these can be done as an outpatient, but we do do some of them as an inpatient. Some of these patients have come from several hundred miles away, and if they're coming from a couple hundred miles away, I think it's only ethical and kind to not have these patients go back and forth. So we of course aren't hard and fast about the outpatient rule, but it's ideal for the patient. [INAUDIBLE].

So let's look at functional assessments. Let's look at our six-minute walk. Six-minute walk is easy. And it literally is exactly what it says it is. It's a six-minute walk.

We do these in every office that myself and Dr. Thomas go to, both at Heart and in the outreach. So if you are at Harker Heights, Georgetown, at Round Rock, in Fredericksburg, Marble Falls, in San Marcos, in La Grange, and of course at Heart Hospital, and including any of the offices I haven't mentioned, a six-minute walk is very feasible.

You want to place two cones in a straight path about 30 meters apart. And our MAs do this. And so the MAs initially measure blood pressure, heart rate, O2 sat, a perceived effort scale called a Borg scale, and then of course distance. And then without provocation or without cheerleading, you have to then have your patients walk for six minutes.

And you tell them, you know, bring your A game. Walk, but don't run. And then you basically document distance. And then so you take a pre-six-minute walk vital sign assessment and a post-six-minute walk vital sign assessment. And interesting as it sounds-- so kind of willy-nilly, but this has really been robust in terms of its predictive outcomes.

And the kind of key number to remember is 300 meters. If those who walk less than 300 meters or roughly three football field lengths in six minutes-- if they don't do that, that's roughly equivalent to functional class IV. I know people think of functional class IV as bedridden and can't do anything, but it's actually not true. It's with symptoms at rest. But symptoms of rest doesn't mean the patients can't do stuff. It just means that they're not feeling well all the time.

So functional class IV, less than 300 meters, those patients have been shown to have poor outcomes. And again, there are some limitations to the six-minute walk-- patient motivation, orthopedic issues-- so that has to be considered as well.

But we really feel for functional capacity assessment, the cardiopulmonary stress test has been quite helpful and really, for our practice, revolutionary in identifying patients who are sick. To get the patient's heart rate and get them anaerobic, we use either a treadmill or a bike.

So a bike is an option. A treadmill is perhaps a better option. If you look at bike versus treadmill, your VO2 max achieved on a treadmill is probably about 10% to 20% higher than on a bike for the same patient on the same day. So that's why we always favor treadmill.

Additionally, on the bike, for those patients who have pacemakers, if they don't swing their arms-- remember, the pacemakers respond to motion, so if your patients are moving their legs but not their arms as much, the pacemaker may not sense motion, and their heart rate response-- they may not have a chronotropic response-- so another reason that we like the treadmill. Those who do bikes and have pacemakers, we have figured out kind of a swinging arm protocol to kind of thwart that and to help us get their heart rate up.

We measure a few variables and then can do a lot of calculations. And the most robust numbers we look at are the VO2 max, the maximum consumption of oxygen. And key numbers to remember are 14 milliliters per kilogram per minute or less, or less than 50% of predicted. Whichever is lower is thought to be a predictor of poor outcomes.

Another thing we look at is ventilation capacity. And a VE/VCO2 slope of greater than 36 has been associated with poor outcomes. So we look at both those numbers in addition to a whole host of others to kind of identify who's sick and who's not sick. And US payers definitely look at this in a determining way of who they would consider payment for LVADs.

Renal function-- not my most favorite subject. As a heart failure specialist, I think my understanding of the nephron is not nearly as robust as a nephrologist. So I'll just briefly mention some pathophysiology.

And we talk about this all the time. Everyone who comes in in decompensated heart failure, cardiorenal syndrome. And it's kind of like, do you just want to sound smart? Say cardiorenal syndrome.

It's a pretty complicated process. This meds review out of JACC published a few years ago shows that when you have decompensated CHF, there are two cardinal pathophysiologies that lead to badness. One is, if you have decompensated heart failure, I think we all can appreciate that there's going to be a relative decline in cardiac output and cardiac index. If you have that, and you look at kind of the top part of that table, you'll have less flow to the body, so therefore arterial underfilling.

If you have arterial underfilling, less kind of load going to your body, then your neurohormonal cascade gets activated. We all know in heart failure that's bad. So your sympathetic nervous system, your RAS axis all gets amped up. That causes further vasoconstriction, and that decreases perfusion to the kidneys, and that can worsen acute kidney injury-- therefore one pathophysiologic mechanism for the cardiorenal syndrome.

The other one that I've appreciated more and more and more is the venous congestion-- so decompensated heart failure, hemodynamic congestion. Your wedge pressure's up, therefore the pressures to the right side go up. The right-sided pressure goes up, therefore the pressures in your abdomen, your splanchnic circulation, and your venous circuit go up.

And therefore your kidneys get congested. So if your kidneys get congested, perhaps one way to make that better is to decongest them. And so that would be the role of maybe a diuretic.

And so that's kind of the basic understanding of cardiorenal syndrome. There's actually several types. This is type 1, the most commonly spoken about. There are several other types, but that's the one that's listed here.

So renal function from my viewpoint. I look at two or three kind of variables or two or three metrics. When I see renal dysfunction, what's the CVP? What's the cardiac index? And what's the MAP?

CVP-- is the CVP high? So the idea that, is there congestion to the kidneys? Because if there's high CVP, the kidneys will be congested, and they may fail or they may malfunction. So therefore, decongesting the kidneys may make that better.

Fick cardiac index or arguably thermodilution cardiac index-- are the kidneys getting perfusion? So on one hand, they're congested. On the other hand, are they getting enough flow? And in that realm, how do you get the cardiac index better?

That's kind of a complicated question. Do you want to add an inotrope? Do you want to afterload reduce? But that's something that could be considered as well, where you could do Nipride, hydralazine, milrinone to tweak SVR or to improve cardiac output and index to get flow to the kidneys.

MAP-- is your perfusion pressure to your kidneys OK? Do you have a MAP of 50? Maybe you have to use vasoconstrictors to get better flow to your kidneys. And again, in doubt, in these complicated patients we have a pretty low threshold to get our nephrologist on board.

So of course in renal function, it's critical that we measure renal function for patients who have advanced heart failure. And the bedside exam of course is [INAUDIBLE] Meditech or even in Epic through CPL, they will do a kind of adjusted Cockcroft-Gault assessment for creatinine clearance. And I think we're all comfortable with CKD stage 2, so GFRs above about 60, to say that those patients probably aren't at significantly elevated risk.

Early CKD stage 3, which is the majority of our patients in clinic, do have some elevated risk for advanced heart failure therapies. It's those whose GFRs are less than 30 that really we kind start to take pause, saying, are we doing the right thing?

And remember, when we say a GFR of 30 or of 50, it's a rolling target. Kidney function changes all the time. So their creatinine of 2.5 on admission may be 1 on discharge because they were in cardiorenal syndrome, they were in cardiogenic shock and inotropes seemed to make that better. Or perhaps they came to the hospital, their renal function changed, and their creatinine now-- their reset hemostat is now 2 or 3, and their GFR is bad, and they have stage 5 CKD.

So anyways, advanced CKD for advanced heart failure therapies is bad, as that would imply, because the last thing you want to do is take a patient who has a GFR of 10, put a VAD in them, only for them to have to need dialysis. And we know that patients who go on dialysis with an LVAD, or are patients already on dialysis who have gotten LVADs-- not necessarily in our center, but at outside centers-- they generally don't do well. I mean, that's just not a great way to go. So really, the best assessment is a 24-hour urine collection to estimate GFR.

So a GI evaluation is important. We get our GI specialist [INAUDIBLE] are thinking advanced therapies to do pretty much a screening colonoscopy and endoscopy as well. Most of these patients are north of 45 years old. And if they are, then it's justified to do a colonoscopy I think as per the most recent guidelines by the American Gastro Association.

So screening colonoscopies just for malignancy rule-out. And then endoscopies simply as a source of-- you know, there are so many patients who have asymptomatic duodenitis, gastritis, esophagitis. The last thing we want to do is find out the patient had a gaping ulcer in their stomach, put them on anticoagulation because these VADs do require anticoagulation. And if they require anticoagulation, then the issue there would be that they had blood thinners on board, they have a gaping ulcer, and all of a sudden they're bleeding. So I think that's important to know.

Just as a point of reference, in the MOMENTUM 3 study, which was the HeartMate 3 study, a quarter of the patients studied over two years had GI bleeds. And so this is an important conversation up front to have with our patients, saying that if you're getting a VAD, there's a likely chance in your lifetime, if you have a VAD, that you're going to be dealing with a GI bleed. Some GI bleeds are minor, but some can require hospitalizations, repeat endoscopies. GI physicians can tell you that GI bleeds in VADs are almost commonplace, so it's important to do that.

Especially consider GI bleeding history in patients who have known AVMs. And a lot of GI doctors find AVMs and they kind of zap them. An interesting word I've listed here called Heyde's syndrome. We're going to talk about Heyde's syndrome in just a few slides. So I hope that that all makes sense, in terms of the need for a GI evaluation.

Hepatic evaluation is important too. And hepatic evaluation is not necessarily the same thing as getting scope. It's actually looking at synthetic function of the liver.

These patients are sick, and like any sick patient, the body starts to fall apart. The liver, like the kidneys, can fall apart on two different kind of pathophysiologic mechanisms. One is ischemia-- so acute liver insult because the blood is not going to the liver. And then hepatic congestion, because like the kidneys can become congested, the liver can become congested as well.

And so there actually are two separate types of hepatic injury. There's chronic and there's acute. And we'll go over that in just a moment.

But the presence of cirrhosis, patients who have synthetic dysfunction of the liver and they have either radiographic or even biopsy proven cirrhosis probably should not be getting LVADs. Those patients have a lot of other health concerns and bleeding tendencies and hematologic disorders. Putting a VAD in them may not be the best idea.

So if you think about contraindications from a liver perspective-- chronic liver injury-- so a total bili above 3, cirrhosis, or a MELD score-- and the MELD score is described for patients with liver disease. It's the bilirubin, INR, serum creatinine, and the presence or absence of dialysis. If the MELD score is elevated, those should be all considered as contraindications to VAD.

Are these absolute? I can tell you, having been around the country and collaborated with folks, these are not absolute. I think a lot of these are relative. But it's fair to say that outcomes can certainly be tied to these disease states.

And also equally important is when you see patients come to the hospital, you may see our notes in Meditech or in Epic saying this patient had acute liver injury, and they had a significant transaminitis. The acute transaminitis from cardiogenic shock behaves a little differently than chronic liver disease. What I mean by that is you may see LFTs rise into the thousands.

I don't think that any of us would be eager to put a VAD in those patients acutely, but I think it's fair to say that if that kind of peaks, and then that curve flattens, and then all of the sudden on the way out the LFTs have normalized as an outpatient, I think we would kind of look at that as an acute phase challenge and that that wouldn't necessarily be a contraindication to a VAD.

Looking at your blood and coagulation profile, it's intuitive, but it's important to make sure these patients don't have significant anemia and thrombocytopenia, because they are going to be married to Coumadin. And if they are and they have a hemoglobin of 7 or they have 50 platelets probably is not going to be a wise choice.

And it's important to also rule out or evaluate for clotting disorders, because if patients have hemophilias or they have a tendency to have blood clots, like an acquired clotting disorder-- antithrombin III, protein C, protein S deficiencies-- they are married to Coumadin for other reasons. And if they have GI bleeds, they can't stop. And they may have a clotting problem, and they could, God forbid, clot off their VAD. So both pro and hemophilia issues need to be addressed ahead of time.

Heyde's syndrome is an interesting name, but it's spelled this way. It's not Heidi as the female's name, but it's actually described by a physician from years ago. And it basically is acquired von Willebrand's disease.

It was first described in GI bleeding in severe aortic stenosis, and what it represents is it's a loss of high molecular weight fractions of von Willebrand's factors. And this occurs in high shear stress and the lack of pulsatility.

If you think of critical aortic stenosis, there's a lot of shear stress. That mean gradient across that aortic valve is super high. Maybe your mean gradient's 40 or 50 or 60. And if you have that, those patients with critical AS, their blood pressure-- their pulse pressure isn't 40 or 50, but it's like 20, it's 15.

And so low pulse pressure, high shear stress-- those high molecular weight multimers of von Willebrand's get sheared and they get destroyed, and therefore you develop an acquired coagulopathy [INAUDIBLE]. That's the aortic stenosis paradigm that totally applies to LVADs.

Remember, LVADs are not pulsatile flow-- the HeartMate 2, the HeartMate 3. There's a teeny bit of pulsatility with the newer LVADs, but they're still mostly pulseless. So if you don't have pulsatile flow, and you have a high shear stress through this metal turbine, that can certainly cause this acquired coagulopathy known as Heyde's syndrome.

There's no specific cancer screen, per se, for patients who are undergoing an LVAD and an advanced heart failure workup, but arguably it's an age appropriate cancer screen. So again, colonoscopies. Most of these patients are above the age of 45. And endoscopy kind of becomes routine as part of that.

A mammogram and a prostate exam. [CHUCKLES] Do they're Not really optional [INAUDIBLE]. A CT scan, of course a pan CT. We feel that we just want the surgeons to have good anatomy good landing zones as to what's happening between the chest, abdomen, and pelvis.

And remember, for your patients being considered for advanced therapies, if they had a history of, say, metastatic melanoma three years ago, they may not be a candidate for a heart transplant because those patients need to be cancer free for five years. Your breast cancer patient needs to be cancer free for five years. Your lymphoma patient needs to be cancer free for five years before they can be listed for a heart, but they can get a VAD. And so in that realm, they probably would get a-- if the workup is appropriate-- a destination therapy VAD, and then once they hit the five-year mark, that nomenclature could be flipped to a BTT, and then they could be listed for transplant.

Peripheral vascular disease is important and perhaps something that we don't focus enough attention on. I think the surgeons can all kind of attest to this, that it's important to know what the plumbing looks like, both in the legs-- and as the legs look, so does the heart and so does the mesenteric system. It's important to make sure your patients don't have significant PAD, as when they get cannulated to go on the bypass machine to get a VAD, we're using peripheral arterioles. Whether it's axial or femoral or central, it's important to have your surgeons know what that anatomy looks like.

But equally important is, if they have significant atherosclerosis in their coronaries, in their periphery, they probably have it in their gut. And I can tell you, mesenteric ischemia in the throes of cardiogenic shock is a horrible problem, and patients really spiral quickly and don't recover. If those patients end up getting a VAD, then we find out that they have significant mesenteric ischemia in that realm, then that's just a bad setup. So it's important to do a thorough peripheral vascular screen, which would include kind of the standard exams of looking in the legs, looking in the abdomen, looking at carotids. And the pan CT scan also looks for PAD as well.

Another important thing to look at is quality of life impairment. In your patients with significant lower extremity PAD, are they claudicants or are they cardiogenic? What's limiting them? And that can be sometimes hard to know, hence the CPET. So if their CPET is done and they have significant PAD but they became anaerobic-- they got their respiratory exchange ratio, their RER above 1.1, meaning they become anaerobic, then perhaps they are cardiogenic more in nature by their limitation and less claudicant. I hope that makes sense.

Lung disease-- it's important to know that your patients have significant lung disease [INAUDIBLE] and ahead of transplant. The lung workup here, which is pretty intuitive, of course, are radiographic imaging, chest imaging, a formal pulmonary function study, and a cardiopulmonary stress test. The CPET, we focus really on the cardiac features, but we've had patients actually come to our CPET lab and their FEV1, their Forced [INAUDIBLE] Volume, is very low, less than 50%, their O2 saturation is very low, their CPET shows that they have a low VO2 max, but their breathing reserve is actually very low. That would be more reflective of a lung disease patient.

Their PFTs may reflect that as well. Their CT scans may show fibrotic changes. They may have advanced pulmonary disease like emphysema or some bullae seen.

It's important to get your lung doctors involved. Because I can tell you, a bad lung pre-advanced heart failure therapy means bad lungs post. And the last thing you want to do is put a patient on a VAD, on a vent, and then we can't wean the vent, and they go home with a trach or they don't go home at all.

So remember that advanced COPD, although difficult sometimes to know who's moderate, who's advanced-- that's why we get the pulmonary people on board if that's ever a question. So again, we want to be cautious in patients who have a low FEV1, diffusion abnormalities described as less than 50%. If you have your patients who have COPD who are in that purported 50-50 club-- their PaO2 and their VCO2 are both equal-- those are problems. And of course, in patients who have advanced lung disease, they may have pulmonary hypertension which may even be mixed. And if they have significant pulmonary hypertension, those patients are at higher risk for RV failure post VAD.

Infections-- all makes sense. We want to make sure that this metal device with tubing and turbines and externalized drive lines are at lowest risk of infection possible. So those patients who tend to be septic, those patients who have been septic, who have had endocarditis, they've had device leads infected, they've had open sores, diabetic foot ulcers, sacral decubiti, recurrent bouts of septicemia, like UTIs and pneumonias, really have to be thoroughly evaluated. If they have leukocytosis, if they have a dirty urine, we don't VAD them.

We need to kind of make sure that those patients have been thoroughly treated for infections before the consideration of LVAD. And if patients have unknown fevers and leukocytosis, that really needs to be thoroughly evaluated by the heart failure team and the consulting internal medicine team to ensure that these patients are not infected.

Again, high risk for infections-- poorly controlled diabetics, patients who are malnourished, patients who are immunocompromised, such as HIV or even patients on steroids, patients who are getting active mechanical ventilation-- so those patients, we're not hot to put an LVAD in them while they're intubated. And of course those who are in multiorgan system failure. Again, those are probably the INTERMACS 1s and 2s that we're not looking to necessarily VAD right away.

Nutrition is huge. I can tell you that when we see patients as late referrals, they do, as this cartoon on the bottom, tongue in cheek, placed here, they sometimes do look like death warmed over. When we see a patient who looks cachectic and frail, and their BMI is 18, their albumin is 2, they have a low cholesterol, they have a low lymphocyte count, they're functional class IV, they have an ambulatory elevated lactate when we draw a lactate in the cath lab, that's a bad sign.

And again, it's important that they're-- it's nice for them to be thin, but not thin on account of cachexia. It's also important for them not to be morbidly obese. So I think there is a sweet spot of maybe a BMI of somewhere between 25 and maybe the low 30s to say that they have enough reserve but they're not cachectic and they're not morbidly obese.

Nutritional status needs to be addressed before LVAD because if they go in malnourished and cachectic, they will not do well. And it is fair to say on those INTERMACS 3s who are malnourished, we would have them visit with nutrition, we would get them a structured kind of nutrition routine to beef up their stores before the consideration of an LVAD implant.

And it's just an important note. I kind of addressed this. But of note here, BMIs above 40 were excluded in some of the heart failure DT-VAD trials. So BMI above 40 was excluded. Does that mean that a BMI of 40 will be excluded [INAUDIBLE] now? No, necessarily. But I think it would take pause.

And everyone wears their weight differently. Some people are very top heavy. Some people are very pear shaped and bottom heavy. As long as we feel, from a heart failure team and the surgeons, that a cannula can go in with relatively little hindrance and the patients wear that weight in a way that's conducive to the implant, that that would be OK.

We've already discussed this, so I'll keep going.

So in terms of neurocognitive function and neurologic assessment, this is all intuitive stuff, but we have to image their head. We want to make sure that CT of the head gets a good landmarks of no old strokes we weren't aware of, no tumors, no bleeds. And I'll tell you, post VAD, it's common, such as the patient who had advanced heart failure this morning who was on VA-ECMO-- not a VAD, per se-- but we get head imaging [INAUDIBLE]. It's always good to have a baseline.

Equally important-- when they're on the bypass machine, getting the VAD to look at the carotid arteries to ensure that they don't have significant carotid stenosis. In terms of cannulation technique, one of our imaging paradigms is chest, abdomen, pelvis. We would definitely want our surgeons to know, does the patient have a porcelain aorta? Are they full of calcium or not?

And then, in patients who have cognitive impairment, we do have patients who-- and I think all of us have been fooled by sometimes our 70- and our 80-year-old patients and even our nonagenarians who really seem with it, but then all of a sudden they come to the hospital and they fall apart. And whether it's sundowning or it's dementia unfolded, formal neurocognitive assessments can be helpful in teasing this out.

And having collaborated with centers, it's been interesting to kind of see them tease this out. And at a higher executive level of function, these patients fall apart. Remember, they have to be able to have some manual dexterity, some higher order of thinking to manage these alarms that can happen in the middle of the night. And that's of course important with caregiver support as well.

So significant dementia-- they may have the greatest body habitus, the greatest body for a VAD, but if their brain is not operating properly because of significant dementia, it really is not a good idea. And this can really unmask post LVAD, so we take pause there.

Psychosocial-- this perhaps cannot be stressed enough. If patients don't have adequate caregiver support or adequate psychosocial support at home, this is not going to get better post VAD.

We've been fooled-- "we" being not just myself and Dr. Thomas and Dr. Morris, but "we" being the heart failure community have been fooled many times in patients who come to the hospital, feel sick, cry wolf, saying I'll do anything and everything, and the family comes in town from out of town. And all of a sudden, once they leave and they go home, not necessarily with a VAD, everything stops.

So the idea that they're going to check their vital signs stops. They're going to have caregiver support, that just stops happening. We see them in heart failure follow-up, and then sometimes they don't show up. And it's not because of the pandemic. They just don't show up because they don't show up.

Sometimes they don't have caregiver support at follow-up. So they're on milrinone, for example, and we see those patients, again, every one to two weeks. They don't get their labs. They don't know their meds. This happens all the time.

And this is not to point fingers at patients. We ask a lot of them. And asking patients to go home on an inotrope, get weekly labs, come in, do six-minute walks, document their vital signs, follow a 2-gram sodium diet, food restrictions is asking a lot. I don't know if a lot of us on this call could do that.

So when we ask them to do that when they're on their inotrope challenge/trial, that kind of is a test drive for can they handle a VAD. It's not the same thing, but if they can handle the inotrope regimen, then perhaps the idea of an LVAD may be suitable. And their wife shows up, their kids show up, and all hands are on deck.

Because I can tell you, pathologic noncompliance does not get better post VAD. I've written at the bottom here, "LVADs don't fix crazy." It actually may exacerbate this. It's happened.

And I regrettably have recommended LVAD for patients in whom, post VAD, the caregiver support stopped. The patient's I wouldn't say psychosis, but their just noncompliance was so obvious, it really-- it hurt them in the end, and it was unfortunate. So it's important to exclude those red flags. And that's why we get our social workers and our palliative care service line at Heart Hospital on board early to make sure that they can tease this out as well.

Our psychosocial evaluation is exactly what you think it is. Do they understand what an LVAD is? Do they know what it looks like?

Who's the caregiver? Who's going to be taking patients to and from visits? Who's going to be doing dressing changes? These patients need to have dressing changes done with aseptic technique. Do they have the dexterity? Do they have the cognitive skills?

Do they have coping mechanisms? I know this sounds kind of fluffy, but it's really important. I mean, we're asking more of our patients than perhaps we ask of ourselves.

So is their compliance reasonably good? It doesn't have to be perfect, but it's got to be near perfect. I don't know that anyone's 100% compliant, but it's got to be pretty darn close.

Mental health history-- I don't know that patients who have a history of bipolar disorder necessarily are contraindicated to an LVAD, but if they're bipolar and they've been hospitalized at Shoal Creek and their compliance is suspect, probably not a good idea.

Substance abuse-- this is interesting. So is tobacco a contradiction to an LVAD? The answer is no, but I think it kind of-- it sheds light on decision-making by the patient. I think we all know that tobacco definitely impairs wound healing, so I think from a wound healing perspective and from a life choice perspective, we would kind of raise an eyebrow, saying, maybe this is not the best choice for them. But it's not a contraindication to an LVAD. It is a contraindication to transplant.

I know we're running a little short on time, but this kind of gets to the nuts and bolts of hemodynamics. We want to make sure that-- when you see patients with decompensated heart failure who are being considered for advanced heart failure therapies, you want to make sure there are two things happening. Adequately unload the patient, and make sure the patient's load to their body is adequate.

So unloading-- make sure hemodynamic congestion is improved. Hemodynamic congestion is your wedge and your CVP. And that could be your bedside exam because you hear an S3 and you see elevated JVP. And that can certainly be your Swan.

So I'm sure that all of you feel similar to this, but I can tell you from our perspective, we want to be aggressive. So when you see drips happening, when you see Bumex, when you see Lasix at high octane doses, we're monitoring equally closely. So we're getting BMPs maybe, say, once, twice, three times a day.

There really is no magic to treat volume overload. I think the importance here is be aggressive. Because we know that if you don't treat volume adequately the first time that those patients will come back.

We get a nephrologist involved when we are having a hard time, and they're on 40 Lasix an hour. They're on two of Bumex hour. They're on high octane diuretics and we still can't move the needle. Then we ask our favorite nephron to come and ultrafiltrate our patients, and that can be helpful too. But again, if that's happening, that can sometimes be a marker of poor outcomes on patients who might be eligible for VADs.