15. HF part 4: LVAD 101 with Dr. Steve Hsu​

Worldwide cardiovascular disease affects the lives of hundreds of millions. Dedicated cardio nerds everywhere are working hard to fight this global epidemic. These are their stories. Hi, everyone. Dan and Corrine here. We are so excited to continue our heart failure series with an interview with Dr. Stephen Su.

But before we jump in, remember, this podcast is not meant to be used for medical advice. The views expressed here do not necessarily reflect the opinions or policies of our employers. The goal is simply to enjoy learning more about cardiology directly from expert cardio nerds.

Hi, guys. Dan and Karine here. We are so excited to be joined by one of our wonderful heart failure faculty, Dr. Stephen Su. Dr. Su received his medical degree from the Johns Hopkins University School of Medicine. and he did his medical training on the Osler Medicine Service, during which he also served as an assistant chief of service. He then completed cardiology and advanced cardiomyopathy training at Hopkins. Dr. Sue takes care of patients with advanced cardiomyopathies.

LVADs and heart transplants. He serves as the medical director of the mechanical circulatory support program. He's also funded by an NIH NHLBI K23 and leads a translational research effort studying the physiologic and molecular characteristics of right ventricular failure in the setting of pulmonary hypertension. He is a true physician scientist and a master educator, and we are so thrilled to have him join us. That's right. And I actually will add, speaking of the master educator.

When I was going through my training, as I got to intern year, I was really confused about my future career. not even sure if I chose the right specialty as internal medicine. I was just having a real panic breakdown. And then there was one weekend where I was in the CCU and CCU happened to be rotating through that day, you know, just covering the weekend. And he gave this phenomenal,

phenomenal talk on EKGs and hemodynamics all tied into one with these like brilliant simple diagrams and I realized at that point that this is why I went into IM and this is why I'm going to go into cardiology this is just a to understand the hemodynamics and to also be able to use it as an educational tool to teach trainees on all levels was just something that totally inspired me and I never looked back. Well, you guys are too nice.

First off, I think I stole that from Harrison's. And really, it's just an honor to come to work every day and have the privilege to work with house staff and fellows like you guys. You really make taking care of patients a privilege and a blessing. I really appreciate you guys having me on the show.

So with that, we would love to continue our series in honor of Heart Failure Awareness Week. So today we're going to discuss with you the management of the post-LVAD patient. And we'd love to get your input on how you approach the post-LVAD patient.

patient and the specific complications that we commonly encounter among these patients. So with that, we'll start with our first question, which I think it would be great to get your overview of sort of the nuts and bolts of the LVAD and how it works. Yeah, so, you know, LVADs are a really exciting frontier in cardiology these days. LVAD stands for Left Ventricular Assist Device. And basically, it is a mechanical pump that takes blood out of the left ventricle.

and pumps it back up into the aorta. It's used for primarily failing left ventricles. And I know the indications and placement of LVADs are covered in another talk in this series, so we won't get into that. But suffice to say, LVADs essentially create a parallel circuit. So remember that you still have your right heart, your pulmonary circulation, you still have your rhythm, and blood does enter the left atrium.

And then it's at this point that blood will preferentially get pumped out of the LVAD and up into the aorta. But the LV and the aortic valve and the LV's intrinsic ability to contract is still there. And we'll come back to some of those points.

So once someone gets an LVAD, what are the main goals of medical management? Great question. This is really what we do over the months after the LVAD surgery, but we really want to... to rethink how the advanced heart failure patient has to live with their LVAD. And so if you think about it, the biggest thing that you just went through is you put in an LVAD, and an LVAD is essentially the ultimate medicine for the LV.

It is continuously pumping out blood and unloading that left ventricle. And so the speed of the LVAD that you set is really the dose of your new medication, your LVAD. You really want to find the speed that effectively unloads the LV without overdoing it. So you want to provide adequate blood flow to the body, but you don't want to set the speed so high that you're basically sucking down and drying out the LV.

So we look at a balance between how much the pump is pumping, and then we also try to look at the echo, and then more importantly, often with a right heart catheterization. to make sure that we're not taking out too much fluid and essentially sucking the LV dry. Next things we do are we want to make sure that the patient's afterload and preload are optimized as well in conjunction with the LVAD.

So from an Afterload perspective... LVADs are very afterload sensitive, especially the centrifugal pumps. As a result, we really want to make sure that afterload is set at around 80 millimeters of mercury. The goals will say 70 to 90. for heart made and 70 to 85 for heart wear. But the closer you can get to 80, the better. And to clarify, we're talking about a map? Yes, that's a map. And so that's the mean arterial pressure that you're trying to get after.

LVAD patients essentially don't have a pulse, and they essentially lose their pulse pressure. So it becomes very hard and unreliable to get blood pressures using a regular blood pressure cuff. So we also measure this MAP using a Doppler. But we want that map to be right around 80, and 80 is basically the potential energy against which that LVAD has to pump. So if your afterload is too high, it's essentially like a higher hill.

Imagine you just kind of have a basic little kiddie bike and you're trying to bike up this hill. The higher or the taller the hill, the harder it is for that bike to overcome that hill and get past the hill and into the systemic circulation. As a result, we really want to make sure that afterload is optimized because the LBAD can only do so much. Last thing I think about is a preload, and so you want to make sure that the patient is euvolemic.

There are some patients on LVAD who can come off of their diuretic requirements, and whenever possible, we try to strive for that. But there are patients who still need some diuretic requirement, whether that be because of...

very profound intrinsic LV dysfunction, or maybe some concomitant right heart failure. And so you want to optimize preload in conjunction with afterload so that the LVAD is working at its best. What would happen if preload was too low? Yeah, so if preload is too low, then... You know, the LVAD is unfortunately not as smart as our intrinsic. And so if preload is too low, the LVAD is set to a certain speed and will constantly try to churn along at its speed. When the preload drops...

It does make it harder for the LVAD to flow, and so the LVAD will naturally flow less blood from LV into aorta, but the LVAD is still going to try to churn. And so if you drop preload too low... While the LVAD is still chugging along, you can get what are called suckdown events. And so this is basically where the LVAD just continues to draw so hard from the LV that it starts to empty the LV.

and perhaps the LV walls touch upon the cannula. That can cause intermittent stoppage and flow. It can tickle the heart and cause ventricular tachycardia. And then if it really progresses, then it can cause basically suction and maybe permanent suction. which can be life-threatening for the LVAD patient. So if you don't fill your LV, like your patient comes in dehydrated, you're not supplying the pump with the...

flow that it needs, but the pump doesn't slow down. As you said, it's not a smart pump. It's just operating at a continuous speed, and so it's just going to suck down the LV. Well, let me go back to that other point for a second. I don't want to say that the LVADs are...

that dumb, they do have functions that try to dial down their speed temporarily when they detect a suckdown event. And so if the LV does... dry itself out, the LVAD does drop generally to a lower speed limit that we can set on either pump.

So one way you'd pick up a suckdown event is through, as you mentioned, perhaps a drop-in speed. What are other signals or alarms within the LVET itself that might suggest? Yeah, so this gets into LVAD alarms, but one of the biggest alarms that we can start to see that signal dehydration would be low flow. So low flow would be kind of, you know, we're there. We've gotten to the point where the LV is so dehydrated that...

flow is now compromised through the LVAD. And so in this case, flow is not equivalent to RPMs. You can set the RPMs however you want, but if there is no blood in the LV to pump, then you're really not going to be flowing much through the LV. For a second... just imagine an elevator at the mall going up from Nordstrom basement

The basement rack or whatever that thing is. I go shopping a lot with my wife. So we're going from there to the food court. The LVAD is sort of like your L escalator. And it's going to be chugging along no matter what. Whether there are three people at the bottom of the escalator or 20 people. the bottom. Ah, very good. Is this what you think about while he's shopping? I do. Amazing. Um, and so if you get to the point where the LV is that empty, then you're going to have low flow.

And so that's one big cause of low flow, that the LV is empty. Leading up to outright low flow alarms, you could have what are called, on the heartmate, PI events. These are episodes where the LVAD is really kind of... consistently having to dial down its speed because it's detecting low volume and also low pulsatility in the LV. On a heart where you can start seeing decreased pulsatility because we...

interrogate the amplitude of the hardware waveform directly. So those are some of the warning signs that we would see along the way on the LVAD. But, you know, it always boils back down to the patient, too. I think sometimes we... see somebody have an LVAD and then just focus on the LVAD itself. But I would say 90% of our evaluation of LVAD patients boils down to, you know, knowing the common complications of LVADs and then just taking our good old history and physical.

talking to the patient, touching them, assessing their vital signs. You can get the vast majority information you need from...

Just our good old-fashioned H&P. It's all about talking to the patient. I want to go back to the MAP goals that you mentioned. So with regards to the MAP goal, you said about 80, and you mentioned that the centrifugal pumps or the heart wear. or HeartMate 3 are more afterload sensitive. That map goal is the same for both types of pumps. Yeah. So nowadays in the adult setting, pretty much all of our pumps are continuous flow elevates.

in contrast to pulsatile flow LVADs. So continuous flow LVADs or CFLVADs are basically constantly pumping a very steady amount of blood flow. Continuous flow LVADs come in two flavors. axial and centrifugal. And I bring up that point because the C in centrifugal and continuous can sometimes be confusing, and certainly were to me when I started. It turns out that with the axial flow pump, which is really just a heartmate 2 these days,

The axial flow pump is basically a propeller housed in kind of a tube, and this propeller and tube sit outside of the LV and pericardium. The propeller basically pumps blood in an axial fashion, and then so it takes blood in from the inflow cannula and then... pumps blood through a propeller into the outflow cannula. Centrifugal flow pumps are housed more in the intrapericardial space, and there there's basically a rotor that spins inside the pericardial space and then pumps blood out.

through the outflow graph. I'm not an engineer, and so I don't understand why, but centrifugal flow pumps are much more afterload sensitive than axial flow pumps. And so they will be much more sensitive to changes in... afterload or your map distal to the pump and also preload. Whereas axial flow pumps are a little bit more inelastic or insensitive to the preload and afterload conditions. They can keep churning along. And so they can do a little better when the patient's hypertensive.

but they might also be a little bit more prone to suck down when the patient's hypovolemic. Last thing I'll say about overall goals are, in addition to the LVET speed, afterload, and preload, we want to make sure we're managing these patients' anticoagulation. Because these pumps are prone to thrombosis if we don't anticoagulate. So all patients need aspirin, somewhere between 81 and 325 milligrams per day, and warfarin for an INR goal generally of 2 to 3. And we're at a stage now where...

Direct oral anticoagulants are... a no-go for LVAD patients for various reasons. Is that because of lack of evidence? So there was one group in Europe that actually tried to study dabigatran and found an increased pump thrombosis rate almost immediately. And so that was called off quickly. We also know from mechanical heart valves that... that direct war anticoagulants have been tested and are not quite as safe for mechanical valve. It's going to take a lot for somebody to do a trial of that.

Okay, so now we want to get into a little bit more of the complications. You know, the LVAD space has been so rapidly evolving. The devices have become smaller and much more effective. But unfortunately, what remains is... high rates of complications and there are really a variety of complications that we unfortunately have to deal with in these patients. What are the most...

common types of complications that affect LVAD patients? And are there differences in complications? We sort of touched on this already, but any other differences between the centrifugal and axial pumps? Yeah. So Karine, you bring up a great point. I think LVADs have made humongous strides in the last couple of years in terms of their near-term survival. Some of the latest LVAD trials show somewhere between 85% to almost 90% one-year survival for LVAD patients. And that's starting to rival...

the one-year survival of transplant patient. Now, that comes at a huge cost. Patients are living better and living longer, but now dealing with a lot of the adverse events that we see with LVADs. The kind of medium-term survival of LVAD patients is not where it is for transplant patients, and that has a lot to do with the adverse event profile.

that they need to face. And so broadly speaking, there are adverse events that are specific to LVADs, and then there are also just cardiovascular complications. that we can still see in LVAD patients. Specific to LVADs, a lot of the complications that we see have to do with hemo compatibility, which basically means the balance between clotting and bleeding that we struggle with in LVAD patients. Some of the biggest offenders...

are stroke, and they come in both ischemic and hemorrhagic forms. Pump thrombosis, which where we don't have enough anticoagulation and the pump is clotting. And GI bleeding, which generally arise from AVMs inside the gut. The thing I would say that's specific to LVADs are driveline infections because patients have to live with a driveline that's coming out of their abdomen that then funnels into the controller and the batteries. Driveline infection, bleeding, stroke.

and pump thrombosis are probably the four biggest LVAD-specific complications. Other things to keep an eye out for are persistent left heart failure or right heart failure in the LVAD patient, because as we know, the right heart... And the pulmonary circulation still have to function as their own in conjunction with the LV and the LVAD. You can also see arrhythmia.

including VT and V-fib, and also atrial arrhythmias. And then lastly, you can see aortic regurgitation, which can be very hard to manage in the LVAD patient. Because blood is pouring right back. It's going right into the aorta and then right back through the valve. Exactly, and that's hopefully something we don't run into. If we manage their blood pressure and LVAD speed well along the way, we can minimize the chances of aortic regurgitation settling in years out.

So some patients, going back to our preload ideas, you definitely need an adequate preload in order to load the pump so that it can actually perfuse the body. But there are patients that can't handle excessive amounts of preload, especially if they have right side of failure.

or if the pump can't handle that excessive reload in the ventricle, those patients will have manifestations of heart failure. Yeah. So let's start with some of those cardiovascular complications. So first thing I think of, so... If you have an LVAD patient who is coming in with heart failure, one thing to think about is essentially whether your LVAD and blood pressure and preload...

are adequately managed. And it may be that a person with a bad LV plus an LVAD who is still in left-sided heart failure, and so they have all the historical and physical exam findings of orthopnea, bendopnea, you know. Parachysms of nocturnal dyspnea. For that patient who still has some degree of left-sided heart failure, I think about, number one, if their LVAD is at the right speed.

If they're adequately diuresed and if their blood pressure is well managed. Because again, if their afterload is too high, everything else may be just peachy keen, but their LVAD may not be able to pump well enough. whereas it maybe can pump well enough at a good blood pressure. So that would maybe be the most benign explanation for heart failure in an LVAD patient. When I see left-sided heart failure in an LVAD patient who is otherwise doing fine, let's say you meet...

Somebody who, for two years, they've just been awesome and living their life. And then now they develop left-sided heart failure all of a sudden. And their blood pressure is fine. Their preload is fine. Their speed hasn't been touched. Then I start thinking about more worrisome. things that can cause left-sided heart failure in an LVAD patient. Things include cannula, malpositioning, pump thrombosis, anything that could be jeopardizing the proper function of the LVAD could be giving you LVAD.

dysfunction, and left-sided heart failure when you didn't have it before. Other causes include inflow cannula obstruction. Let's say you have a panace that's starting to grow over the inflow cannula or outflow cannula obstruction. Sometimes you can have extrinsic compression of the outflow graft.

That could then start causing heart failure. And then sometimes you have patients who might have been fine, but are now dealing with some other insult in their body that's just putting a strain on their LV and LVED. So people who are newly hypo or hyperthyroid. or dealing with infections, or maybe they're at home on IV antibiotics and getting a lot more saline than they're used to getting, those patients may now get...

left-sided heart failure symptoms when they didn't have it before. I see. The other thing you alluded to was right heart failure, which unfortunately, sometimes when we place LVADs, although we try and optimize patients the best we can, you can often unmask. RV dysfunction? How does that usually present and how do you manage that? Yeah, that's a great question. And that's one of the big bugaboos of left ventricular assist devices. And so we try our...

to figure out pre-op if somebody's RV is going to be at risk. There are dozens of right heart failure risk scores nowadays. But I think what it really boils down to is the sicker the patient is going in, the more dysfunctional their right heart looks like, whether by right heart catheterization. or echocardiographic features. And then the longer the operation takes, the more they're going to be at risk of right heart failure postoperatively.

We encounter right heart failure in its most severe forms in the immediate post-op period. A lot of times that has to do with underlying right heart dysfunction, perhaps from the underlying primary cardiomyopathy, or maybe long-standing. heart failure with reduced ejection fraction that already had enough time to adversely affect the pulmonary circulation in the right heart. For whatever reason, the right heart may come out of the operation struggling, struggling in terms of contractility.

struggling in terms of having to handle the new preload that it's seeing from the left heart. Postoperatively, you also might see shifts in basically pericardial restraint and the septal positioning that may really adversely affect right heart contractility.

contraction depends on a lot more than just contractility of that free wall. It depends on your rhythm, depends on the deceptal positioning, depends on LV contractility, and also depends on this little pericardial cummerbund that just kind of wraps around the whole heart. If you impact some of those things post-op, then you can really deal with a vulnerable right heart immediately post-op. Add to that just the humongous stress of having to deal with a cardiac surgery.

for the body. And so you may... basically turn a left heart failure patient into a right heart failure patient post-op. You mentioned hemodynamic parameters, echo parameters that could guide you or help you in your assessment of RV failure. What are some of those that you find most useful? Yeah, so immediately post-op, we very much rely on a swan-gans catheter post-operatively to help manage these patients. So on the right heart cath, if we see a central venous pressure that's...

upwards of 15 or more and not really coming down. A CVP to wedge ratio that's kind of approaching the 1.0 ratio. Hypotension systemically. or low cardiac index and low PA saturation, those are all signs of right heart failure manifesting in cardiogenic shock. And then if we start seeing signs of end-organ malperfusion, so abnormalities in the transaminase levels or rising creatinine, worsening urine output, poor mental status, those are basically all the...

features of cardiogenic shock, but with a right heart flavor to them. That basically starts to signal a right heart failure post-operatively. Depending on the severity of the situation... And depending on the chronicity, we grade right heart failure post-op as mild, moderate, severe, or severe acute.

The thing that we are scared most about is severe acute, because severe acute is basically defined by either death from your right heart failure or need for a mechanical bailout for the right heart, whether that be percutaneous or surgical. right ventricular assist devices. How do you decide who might benefit from additional RV support in the immediate post-op setting? Yeah, I think the more we learn about this, the more we realize...

that the earlier you intervene with mechanical options when necessary, then the better off you will be. If you end up delaying your mechanical circulatory support for the RV, then you may... find yourself in a situation a day or two later where you've already suffered. Yeah, exactly. You've already started to suffer some of the systemic complications. And then it becomes harder to put...

Kind of Humpty Dumpty back together. Yeah. As long as you're not in that severe acute territory, then for the most part, the right heart should be able to recover. If you give it enough time, you know, it can't take that joke up front, but eventually it'll kind of come back around. Right. And so up front, if we can really aggressively manage, preload, support the patient with inotropy.

so that that intrinsic right heart keeps chugging along. Minimize your LVAD speed so that you don't flood the right side, so you don't suck over the septum too hard. And then maintain sinus rhythm. I think those are kind of the big keys to managing.

Anything less than severe acute right heart failure. Post-op. So moving on to a next unfortunate common complication, pump thrombosis. We sort of have already touched on this, but possible signs and symptoms of pump thrombosis and how is this usually managed? Yeah, so pump thrombosis is essentially either the early workings of a clot or a full-blown clot. inside the pump rotor itself. When this happens, then you can start having intermittent or continuous signs of left-sided heart failure.

because the LV is not working that well. Because you have pump thrombus inside the pump, that starts to really impede on blood flow through a very narrow space. And so you can start having very... overt and dangerous hemolysis. And that we pick up, that we can pick up on. Exactly. And so the way that we pick these things up is patients try to stay very in tune to their power and flow and RPMs.

RPMs shouldn't change on a given day. And, you know, there's an equation that relates power to flow, and that is power equals flow times resistance inside the pump. Ah, the old V equals IR. So actually, no, V equals IR. Don't worry, you can edit that out. V equals IR. You probably won't. V equals IR is actually pressure, relates pressure, flow, and resistance.

So I'm actually talking about power, flow, and resistance. And I think you bring up an important point. This is not an often used equation when we think about patients hemodynamically. But here we're talking about power. And so power is equal to flow. through the pump times the resistance inside the pump. Ah, I see. So, the LVET companies don't...

have flow meters inside their LVADs. What they do is they can calculate for you the amount of power that the LVAD is consuming, assuming that resistance inside the pump is negligible, close to zero. Power and flow are very intimately related, and they will track with one another in lockstep. The one situation where that is not true is a pump thrombosis. And so all of a sudden in a pump thrombosis...

you start having astronomical resistance inside the pump. Flow may actually be decreased in a pump thrombosis, which makes sense because that pump, which is having trouble pumping, is not going to be flowing as well. However, the LVAD is going to be spending gobs of power because it's going to have to churn through that pump thrombus. And now it's going to give you a flow. And so the LVADs don't have a flow meter, but they have a power meter. And so they estimate the flow for you.

In the situation of a pump thrombosis, patients will have a marked increase in their power, and then they will have a false increase in their flow. And that's because they are... incorrectly surmising that their flow has increased just because the power has increased. Whereas the flow is actually not increased. Power is increasing really because resistance is increasing inside the pump. So we've had patients call and say, Hey, doc.

This is great. My flows are so much better these days. And that's when we get an interrogation and maybe bring them in to treat a threatening pump thrombosis. So increases in power and then... False increases in flow are some of the earliest warning signs of a pump thrombosis. Other things that can pop up are increases in LDH. This is a blood test that we get very routinely on our outpatients to try to catch pump thrombosis before they happen.

Oftentimes LDH will rise well before the pump thrombosis is at its worst form. If we're catching things a little late... or let's say things happen suddenly, the LVAD ingested a pump rhombus, then you might start having more overt manifestations of a hemolysis. So LDH will be our earliest manifestation of hemolysis.

If patients start having cold-colored urine, hemoglobin pigments in their urine, that's kind of a really bad warning sign. And so those things plus symptoms of left-sided heart failure are kind of all our warning signs of pump thrombosis. If we can catch them very early, then there are some antiplatelet agents and heparin type agents that we can use to try to avert the pump thrombosis. But oftentimes we are stuck having to replace the pump.

Because earlier, pump exchange can be life-saving in these patients before they develop all the complications of hemolysis. The dreaded pump exchange. Yeah, but you know... Nowadays, if you do it earlier in the course of the disease, you can get away with it better. So you'll usually try it. You actually are not...

You don't hesitate to go towards pump exchange. Correct. In previous years, I think we tried to anticoagulate a lot and then reach for pump exchange a little later. Nowadays, it's clear that we probably want to reach for it sooner. So we're looking carefully at... the severity, and then also the pace of disease in a pump thrombosis to see if we can give it a trial with medical management or quickly switch to pump exchange. Fascinating.

I actually remember a case when I was a junior resident where a gentleman came in with that classic, you know, co-colored urine and then LDH was sky high. I took him in. There was tons of thrombi in the pump. Life save. So... Let's talk a little bit about strokes in these patients. So you mentioned that we see actually both hemorrhagic and ischemic strokes. How do you tackle strokes in these patients? Are there ways to avoid it and particularly the different...

ideologies of stroke. Yeah, I think this is always kind of a bummer if we run into it. Fortunately, a lot of the strokes that do happen are minor. They rang kind of on the order of... TIAs or very minor strokes with minor residual deficits that recover in time.

If we are dealing with major strokes, then we're working with our NCCU colleagues to try to manage the stroke with more extreme measures. But hopefully we don't get that far. I think the real keys to treatment are to try to prevent strokes. We know from great work in recent years that basically there are risk factors to stroke and that if we can keep those tightly managed, then we can try to avoid those. And so risk factors for ischemic stroke are... You taught me this.

It was aspirin and atrial fibrillation. Excellent. Yeah. So if you're not on enough aspirin or you have atrial fibrillation... then that increases your risk for ischemic stroke. INR impacts more hemorrhagic strokes. So if you're dealing with insufficient aspirin or high INR, greater than 3, or a high MAP, especially in HVAD patients,

of greater than 90, then those are the risk factors for hemorrhagic strokes. And so we really try to keep that well controlled at around 80 millimeters of mercury. And in particular, for anyone with a heart wear LVAD or an HVAD, The goal should be 70 to 85 for your map, very strictly. And then everybody should be on aspirin, and then we really try to avoid and treat AFib.

if present. You mentioned initially the 81 to 325 milligrams of aspirin. Is there a different requirement based on the device? There used to be more nuances between different devices. The HVADs in their instructions for use manual mandated 325 at first, but they've recently dropped down to 81 as a bare minimum. And so we should be on at least 81 in all our patients. And different centers actually...

have quite different goals in terms of their aspirin use. I think where this gets gray is when you're balancing clotting and bleeding issues. So if you have somebody... who is a bit of a bleeder, whether that be GI bleed or nose bleeds or various other types of bleeding issues, then sometimes we are trying to dial down their antiplatelet and anticoagulant therapies. And so that's why you'll hear some variation.

INR goals and aspirin goals. And you mentioned bleeding, which is sort of the other unfortunate complication. GI bleeds that we see a lot in these patients. You mentioned that most commonly due to AV malformations, perhaps acquired von Willebrand factor. How do you manage bleeding in these patients? when you're unfortunately sort of bound to anticoagulating them. Yeah, so bleeding is a very common complication for our LVAD patients, especially AVM-type bleeding.

Generally speaking, they either show up with melana or hematochesia, maybe some lightheadedness, dizziness, wooziness. Sometimes they will be bleeding so vigorously that they might really have trouble with preload. And so you might find episodes with overt dehydration, suck down events, VT. But those are the more rare versions of GI bleeds. I would say most people come in kind of knowing that they're feeling poorly.

Very quickly, a hemoglobin will tell you that the bleeding is there. Generally speaking, you can probably get away with just stopping their warfarin and aspirin temporarily and then supporting them with blood products and... fluid resuscitation, and then calling your GI colleagues for scopes. And so our GI colleagues have kind of...

All our health staff know that basically Tuesdays and Fridays are LVAD colonoscopy days. And that's because we have cardiac anesthesia on those days. And so we always try to line up our preps for Tuesdays and Fridays. And it's because, generally speaking, someone comes in. It's a bummer. They stopped their anticoagulation. We get them prepped. We get in there. We try to stop the bleeding and get them back on their merry way.

So that's usually the management for GI bleeding. Once somebody has a GI bleed, then we try to adjust their anticoagulation thresholds to maybe see if we can get away with less GI bleeding. So we might lower their aspirin or we might lower their warfarin goals. There are many medical therapies out there that have shown some benefit. One medication in particular that has shown benefit in multiple studies at this point is angiotensin receptor blockers.

And that is because of their potential role in mitigating the formation of AVMs in the GI tract. In addition to all their other beneficial effects in cardiology, the benefit of ARBs in reducing GI bleeds have been shown in at least three different centers. And so that is one mainstay for trying to help mitigate the ongoing propensity for GI bleeds.

Other medications out there include digoxin, done in a nice study out of Einstein. And then, you know, we do a bunch of other stuff like estrogen agents, octreotide. Though I'm not entirely sure if I've ever seen data showing that octreotide helps, but we do it a lot. Thalidomide is also an agent that some people use. Yeah, I've seen that. But it does come with a big adverse event.

a side effect profile of its own, and so it can be hard to prescribe. Those are some of the big things. And what about driveline infections? You mentioned this earlier as well, unfortunately having a tube coming out of the body. is anitis for infection in these patients. So what are some of the risk factors and preventative measures for driveline infections, and how are they treated? Yeah, driveline infections, I kind of put up there in the top four of LVAD-specific complications.

And when you're thinking about frequencies, driveline infections and GI bleeds are probably some of our more frequent complications in the first couple of years after LVAD. Whereas fortunately, pump thrombosis and stroke are very rare. So when we're thinking about driveline infections, again, prevention is key. A lot of it has to do with the patient and family teaching of driveline dressings all the way up front.

We really want to make sure that immediately post-op, we've anchored the LVAD surgically inside the body. And so our surgeons will throw in a stitch around the LVAD at its exit site to make sure. That's interesting. That the LVAD driveline really kind of internalizes inside the abdominal wall and doesn't have any traction. Because one of the biggest risk factors is if there is ongoing traction with the driveline or if the patient is not careful.

and they let the LVAD drop, and that tugs at the skin, then that kind of breaks the seal, so to speak, around the LVAD driveline and the body abdominal wall. And so there's a stitch that's in place. And patients also go out with a Hollister that anchors their driveline to their abdominal walls so that even if they drop their LVAD, it doesn't immediately yank at the skin exit site. So dressing supplies, chlorhexidine, that stitch.

Some centers use silver in their driveline dressings to help minimize the risk of driveline infections. We have found that a chlorhexidine and driveline dressing approach with a lot of rigor and good teaching up front has helped reduce our driveline infection rate significantly. And then those are probably the big things to help prevent.

the onset of driveline infections. When driveline infections settle in, then we're dealing with oral or perhaps IV antibiotics. I think it helps to be a little bit more aggressive with either IV antibiotics or debridement when necessary, because if you... If you end up staying a step behind on LVAD driveline infections, then you end up with the same bug over and over again, and then you'll end up slowly drifting towards surgical debridements and then maybe rerouting of your driveline surgically.

to eventually treat the driveline infection. So prevention is key, and then otherwise aggressive, upfront medical management. So speaking of drivelines and LVADs in general...

These patients, obviously, when they get them, they're incredibly sick, and these are life-saving strategies to really give them another chance at life, whether it's a bridge to transplant or a destination. But, you know, when the dust settles and the patients are discharged, you... notice that they kind of have this, like, change in their mood or just, like, this realization that all of a sudden they're now going to be...

dependent on this mechanical device that's coming out of them constantly? That's a great question. You know, in sitting and listening to our patients at their support group meetings, I think one of the biggest things that LVAD patients now have to deal with is just the fact that...

they have a constant reminder that they have this elvet. The driveline and the controller and the batteries are just something that they have to constantly deal with. So imagine just wanting to get up and then just pop over to your refrigerator to get a drink of water.

You know, for an LVAD patient, even something as simple as that becomes something to think about. Every time you want to move, every time you want to get out of bed. And so I hear from patients that constant reminder of having that LVAD there is a big adjustment.

And everyone deals with it a little bit differently. I think depending on how sick people were going into their LVAD, how much they were dealing with heart failure pre-LVAD can influence their ability to adapt afterwards. For most people who get an LVAD... you know, the heart failure is way worse. And so people are dealing with terrible exertional capacity, quality of life, repeated hospitalizations prior to all that. And so afterwards, you know, having a driveline.

And dealing with a battery and a controller is not as bad as what they were dealing with before. Yeah. So when actually you ask LVAD patients, most people would rate their quality of life as significantly improved after LVAD. If you look at KCCQ scores pre-op. Dan learned what that was recently. Yeah. They made fun of me on the show.

Okay, so, you know, named after our recent Super Bowl chief. Kansas City cardiomyopathy questionnaire. Most people rate their quality of life at around the 20 to 30 range. And... Post-LVAD would rate their quality of life somewhere between the 70% to 80% range in our center. And that's as soon as three to six months post-LVAD. Right, wow. So LVADs really give people a whole new lease on life. They're able to get up.

do all the stuff that they want to do, not live in heart failure, not be tired all the time, get back to driving, working, exercising at mild to moderate amounts. So for most people, I think they have a whole new lease on life. But it does come with the price that you mentioned of these things to consider. And of course, the adverse events that pop up. On average, LVAD patients do have more hospitalizations for adverse event issues post-op as they would have compared to pre-op.

Is there anything that you do to help your patients adapt from an emotional perspective? Well, there's like support groups. Yeah, we have great social workers and palliative care doctors. I mean... that are part of our pre-LVAD transplant evaluation process, but also follow our patients postoperatively. And so they really help patients adapt to the situation. I think LVAD patients end up leaning a lot on their caregiver support.

And there's a lot of evidence to show that LVAD patients do better, the better caregivers they have. And so that team on their end really helps them to cope. We help them as much as we can as well. with the medical stuff, of course, but also with the coping stuff. And so we have patient support groups and ways to help our LVAD patients network with one another so that they can kind of be each other's strengths as well.

So we would like to end our interview with what makes your heart flutter about heart failure? That is a great question. I think there are so many things I can think of. I think what makes my heart flutter is whenever... You see a patient fighting for their lives. I think we as a society underestimate the impact and mortality that heart failure can have on patients.

They have mortality rates that are upwards of some cancers. And so when they get a diagnosis of cardiomyopathy, they're in a fight for their lives. And so I really love it when I can be a part of their team. Whatever it takes, if we can get their hearts better and they get a new lease on life, then I love it every time. And that can really just be guideline-directed medical therapy. I have a lady who was on the transplant list whom I just...

made a status seven, but for good reasons. Because with Secure Patrol Valsartan and Carvedalol, her ejection fraction has kind of made a comeback from 15 to 40. And she's loving life and just not needing a transplant anymore. And so she was brought to tears when she heard how well the medical management was working.

That is a huge win for some of our patients who get really sick and maybe do need something surgical like this. To see them sick going in and then seeing them afterwards and a few months later with a new lease on life, that also makes my heart fluttered.

Every time we can get one of those wins, no matter how we get there, I think it's always wonderful. Oh, that's awesome. Inspiring. I've got goosebumps. I know. That's why I love heart failure. Gets me every time. I know. I'm almost jealous of you. Well, I'm going to cry. Well, thank you. That was amazing. Well, that brings us to the end of our show. So it's time to make like an S2 and split.

You can follow us on Twitter at CardioNerds and please share what made your heart flutter this week. Send us a clip to CardioNerds at gmail.com. If you enjoyed the show, be a nerd and spread the word.