IPC for PAD: A Proven Technology, Revitalized

This session will discuss the current understanding of PAD, including its epidemiology, risk factors, pathophysiology, clinical presentation, and diagnosis. Dr. Evans will review the latest AHA/ACC PAD Guidelines, emphasizing the critical role podiatry plays in identifying and managing patients with this progressive vascular disease. In addition, this webinar will introduce ARTAIRA®️, a new, cost-effective intermittent pneumatic compression (IPC) device designed for patients battling PAD and diabetic foot ulcers. ARTAIRA®️ is Medicare-reimbursed and VA-available, offering practices a noninvasive therapy option for both clinical and home-based care. This program is designed to equip podiatrists with the clinical knowledge and practical tools needed to improve vascular outcomes and expand treatment pathways for complex lower-extremity patients.

Darren Behuniak: Hi, everyone. My name is Darren Behuniak. I'm a founding partner, owner, and chief operating officer of AIROS Medical. We welcome you to this session. A lot to cover here from a clinical standpoint around an older technology that's now revitalized and is available again: intermittent pneumatic compression for peripheral arterial disease, or IPC for PAD. 

AIROS Medical has been around for 10 years. We are primarily focused in engineering medical technology, focused in pneumatic compression specifically for lymphedema and venous insufficiency treatment. We sell to durable medical equipment suppliers all over the country. And as we developed our company and our technology, we started to see a lot more patients with arterial insufficiency and peripheral arterial disease. So the next evolution of our product line is this Artaira device, which is an arterial compression device that treats a number of the symptoms of PAD. 

Our original business model, where we wanted to try to help patients, was in the cash pay space because it hadn't been covered by insurance—and we'll get into the fact that it is, again, covered now—and also to the Veterans Affairs. So that was really our approach to try to help some more of these patients. Now, with Medicare covering the device again, we are trying to educate the podiatry community, especially podiatrists that own their own PADs, the wound care community, and the vascular community, that there is a piece of non-invasive at-home technology that can be used to help potentially save feet and toes and legs. 

Today's session that we'll get to, I'll give a quick overview of where we're headed. So Dr John Evans, our medical advisor who I’ll introduce, will cover all the clinical aspects related to the diseases, the symptoms, the risks, and then we'll also get into some of the studies around pneumatic compression and how it's helped arterial patients with insufficiency. I'll come back in and talk a little bit about our specific device, but then also get into the reimbursement trends. And again, Medicare is covering this device. They used to, then they didn't. Now they are again. 

So with that, I will introduce our medical advisor, Dr John Evans, a gentleman most of you probably know. 

Dr John Evans: Thank you, Darren. It's a pleasure to be with all of you today. And thank you for joining for this informative session. I'm John Evans. I'm a podiatrist in Michigan. I've been practicing for over 40 years and have been very involved in a number of different aspects within our profession during that time. I've been active with the American Podiatric Medical Association, my state association, the American Board of Foot and Ankle Surgery, and the American College of Foot and Ankle Surgeons. Over the last 15 years, I've been doing a lot of work in the vascular community, working with the American Heart Association, American College of Cardiology, the Society of Vascular Medicine, different limb preservation groups within our profession, ALPS, MCLI, really looking at vascular aspects that I think podiatry needs to be aware of. 

I was working with the American Heart Association and American College of Cardiology 6 years ago when they were writing their guidelines for treatment of PAD. And one of the treatment options I came across was intermittent pneumatic compression therapy. This is something I was not aware of, even though I thought I had a pretty good feel for all the different options for treatment of it. So this is a form of compression therapy, which you're all probably familiar with when it comes to venous or lymphatic disease. 

But this has a different profile of pneumatic control. The goal is to increase blood flow into the arterial system. So it was quite unique, although it had been around for over 50 years and had been quite popular back around the early part of the century. But at that point, Medicare stopped paying for it, and so utilization dropped. And really, unless you've been in practice for over 20 years or so, you may not be familiar with this therapy. But in looking at the research out there, it found that it was a helpful ancillary and adjunctive treatment along with guidelines-directed medical therapy and interventions, but something that can be utilized for our patients in all stages of PAD to improve arterial supply. 

So I met Darren and the AIROS company almost 4 years ago now at a, really just a focus group, and realized this is something that at least our profession should be aware of. So I'd like to talk to you about that today. 

But first, I'd like to talk to you about the reasons why we want to use devices like this. Peripheral arterial disease today is a real problem. It's part of the atherosclerotic disease along with coronary disease, cerebrovascular disease, and peripheral artery disease. Now, they all involve atherosclerosis of different arterial beds of the body. There are 3 vascular beds that are affected this way: the heart, the brain, and the legs. But this is the leading killer on Earth today, diseases of this type. For PAD, over 200 million adults on Earth have this disease. And in the U.S., over 20 million of us suffer from this. 

The most severe stage is chronic limb-threatening ischemia (CLTI). We used to call it critical limb ischemia, but this is the new name, even though it's the same entity. And it affects a little over 10% of all patients who have PAD. The costs are staggering, well over $21 billion a year spent on this. And unfortunately, it leads to about 150,000 amputations every year. 

The risk factors of all of the atherosclerotic diseases are basically the same. The biggest ones are smoking and diabetes. But the numbers increase for every decade after 50. If people have reduced renal capacity, they're more likely to have this and also to have it in a more severe fashion. And the different diseases that have to do with coronary disease, such as lipid disease, high blood pressure, all of these are also factors we look at. We also see that it's related to inflammation, as are all of these other atherosclerotic diseases. So as you can see from looking at this list, a lot of our patients fall into these categories. And we need to be aware that PAD may be present even if we don't see it clinically. 

When we look at the vascular system, one way of breaking it down is by looking at the size of the arteries. So we talk about the large arteries, which is the typical peripheral arterial disease that we think about. We call that the macrovascular system. These are the arteries that have names. They are visible. And we have endovascular treatments that are amazing to be able to help open these arteries up. But on the other side, we have the microvascular component. Now, this is really on the cellular level. These are really, really tiny. And we don't really talk about microvascular as much because up until recently, we really couldn't measure it. But it's where the real work of oxygen transfer occurs, in the capillaries. 

But the disease is often overlooked until you start looking at that 1 out of 6 below-knee amputations have microvascular disease alone without PAD. Microvascular disease isn't directly related to the atherosclerotic disease process, but it's extremely important for certain diseases such as retinopathy, neuropathy, and nephropathy, which certainly neuropathy is something we come in quite frequently in the podiatric community. And also when we talk about wound healing, because if the blood can't get to the tissue, even if all of the arteries are open, these wounds aren't going to heal, and tissue's not going to be gangrenous. 

But when we look at microvascular and macrovascular disease effect on the body, we see a difference in the amputation risk. If someone has microvascular disease alone, they have a 7 times greater risk of having an amputation. If they have macrovascular disease alone, they have a 20 times greater risk of having an amputation. But if they have both microvascular and macrovascular disease, the risk of amputation goes up to almost 60 times. When we're looking at patients with PAD, it would be nice to have something that affects both the micro and macrovascular system. And the therapy we talk about today does just that. 

When we talk about PAD, the major symptom we look for is claudication. It's often talked about as being the classic symptom. The problem is it's only present in less than 15% of these patients. So if we wait for these claudication symptoms to occur, these ischemic symptoms that occur from decreased blood flow into the muscles with exertion, we're going to miss almost 90% of the cases. So waiting for us to develop claudication symptoms or even other signs of ischemia, such as wounds that won't heal or gangrenous changes, mean we're going to miss an awful lot of these patients. Another problem we have is that peripheral arterial disease begins in our teenage years and progresses until we die. It really never gets better. We have ways of slowing down the progression. We have ways of going in and cleaning out diseased arteries. But even then, they're never actually fixed. So the process continues. So ideally, it would be nice to know PAD is developing before it reaches a symptom of ischemia. We don't treat heart attacks only when people have them. We like to reduce the risk factors by controlling their blood pressure or their lipids years in advance. But unfortunately, with PAD, we don't tend to treat things until they become symptomatic. So, we miss a lot of stuff. 

And this disease is dangerous. The more severe stage, the CLTI, we have an amputation rate of one-third to two-thirds of patients by 4 years. And by the end of the first year, patients with CLTI, 25% of them will have passed away. By year 5, over 60% will have died. The mortality rate for this disease is worse than the majority of cancers, except for possibly pancreatic and lung. So we really should be taking it more seriously than we are. 

And we're not doing a great job with it. A study was done year before last that looked at 2017 Medicare data of patients who had CLTI and a foot ulcer. This resulted in over 33,000 amputations. Now, of those 33,000 amputations, two-thirds of them did not receive a revascularization procedure in the year before they had the amputation. Over 90% of them did not even have an angiogram before they took the leg off. And of the patients who had an amputation, almost half of them were above the knee. So this illustrates that we're not catching the disease early enough in its process, and even when we do, we're not necessarily treating it as actively as we could. 

We know the basic diagnostic techniques of this are checking pulses of the foot and the leg, doing pressure measurements such as the ankle brachial index, to get an idea of the perfusion of the leg, especially what gets to the ankle. So basically, it's the ankle pressure divided by the brachial pressure, giving us an index that we say the average is 1.0. If it is less than 0.9, we say they have PAD. If it is above 0.4, we say the vessels are non-compressible. And we see this a lot in patients that have hardening of the arteries, especially those with diabetes or renal insufficiency, where they have a lot of atherosclerosis of the arteries themselves. So the ABI isn't as useful in those. In those cases, especially with the high ABI, we use the toe-brachial index, similar type measurement, but we use the toe and the ankle as the numerator and denominator to determine the index. And if the TBI is less than 0.7, we consider these patients that have PAD. Now, the toe-brachial index is very useful in patients that have atherosclerosis, especially of the foot. One of the other problems we have is over 70% of the patients that have CLTI have below-ankle disease, meaning the arteries are calcified very hard, so the ABI doesn't do a good measurement. Toe-brachial index does a better job of giving us in those cases. 

And also personally, I recommend that all of us that are seeing these patients have just a handheld vascular Doppler and learn how to use it, because we can do a lot of work just with that at bedside with checking out the different pulses of the foot and leg and giving an idea of the general health of these larger arteries using that method. 

So how does this work? You probably are all familiar with intermittent pneumatic compression therapy and have used it to help treat these venous and lymphatic diseases. How they gradually compress to different levels in a sequential matter, basically milking fluid out of the foot into the leg and up into the thigh. And most of these devices tend to be full leg from the foot all the way up to the thigh, are rather large, but are very, very useful for healing a lot of these disorders. The therapy we're talking about today is a modification of this. The modifications are the pneumatic compression cycle is quite different than what you normally would have for the venous or lymphatic devices. And the device only goes from the foot below the knee. So it's much lower profile and lighter to use than these other type of devices. 

But the compression and pneumatic cycles are different. What happens with this is there is a very rapid compression, less than half a second, as compared to a gradual type that we would see in other devices. Also, the compression is at a higher pressure. It gives 120 millimeters of pressure, the average systolic blood pressure. So 120 millimeters of mercury in less than half a second. But it only remains compressed for 3 seconds. And then it relaxes for 17 seconds. And then the cycle repeats. So there is 3 cycles per minute, and the treatment length is usually 45 to 60 minutes. And we recommend this being done at least once a day, but two or three if it's possible. The more treatments, the more effect we have. And different types of compression pressures have been measured in research. And they have found that the 120 millimeters of mercury compression gives the greatest arterial effect. 

If we use this type of therapy, the research has shown that we can increase the arterial blood flow in the calf by about 274% in patients that have relatively normal circulation. But in patients that have claudication, the mean flow could be increased by 174%. 

For patients that have claudication, walking distance is a measurement that's often used to determine how significant their disease is. Initial claudication distance is when the first claudication symptoms develop, and absolute claudication distance is when the claudication gets so bad they have to stop walking. So these are two measurements terms that are used for this, and studies that have been done show that we can increase the initial claudication distance and the absolute claudication distance by between 100% and 200% by using this type of treatment. But again, these type of benefits are seen over a prolonged period of time. We're usually talking about 3 months for a treatment of this before we really get an idea of how much good it's going to do. So it doesn't really give as acute a benefit as it does. And this has to do a lot on how it affects the macro and the microvascular system. We'll talk about this a little bit as we go on. 

In the diabetic foot, we can increase the skin blood flow immediately after cuff deflation of a compression. But we see a second increase in perfusion that happens a few seconds later that's basically a vasoactive response where we get a dilation of arteries that are proximal to where the compression was. We'll again talk about this a little bit more, but there's a different phase where we don't just get the initial, but we also get a delayed response. And patients that have diabetes and CLTI, we've found an improvement in limb salvage rates and wound healing and an overall increase in blood flow, which can help their situations. 

In fact, this is useful even in patients that have no option for revascularization. There is a category of patients who are not candidates for any sort of vascular treatment such as bypass or endovascular treatment. These are called “no option.” Now we tend to look at them as “few option” because we do have some different types of procedures out that can help these patients. But there are certain patients that really didn't fall into any category of treatment in the past. In that, the most severe of the severe patients, we have found that we could increase the blood flow to the leg. With long-term use, we can increase capillary blood flow. We can improve claudication distance. If someone has had an intervention, we can reduce postoperative swelling and help normalize skin microcirculation after the procedure. And overall, we can improve limb salvage rates and wound healing for these most severe patients. 

In fact, the American Heart Association/American College of Cardiology has made this a recommendation for patients who are not an option for patients. Now, why this is important is we often think of compression therapy as being contraindicated in patients that have PAD. And it makes sense. If you're going to squeeze the arteries closed, it's not good if they already have a compromised arterial system. But because this is a recommendation for it, it means it must help in a different way than standard compression would. And we'll talk about why that occurs. 

There's basically five major techniques or thoughts as to why this helps. The first group we'll talk about are those that affect the larger vessels, the macrovascular system, and those that affect the microvascular system. And we'll talk about these a little bit each separately. 

First, the macro system. We can increase arterial inflow, we can increase shear stress in the arteries, and something that's called transitory hypoxic stimuli that causes upstream vasodilation. The first of these mechanisms is how it affects the arterial-venous pressure gradient. Now, the AV pressure gradient is how blood circulates in the body. Blood goes from high pressure in the arterial system to lower pressure in the capillary and finally lowest in the venous system. But how the blood gets back to the heart is by contraction of the muscles in the calf and the leg, which squeeze the blood back. But this is basically how circulation works. 

We can change how the blood flows also by changing the AV pressure gradient. If we force the blood out of the foot and the leg by squeezing the veins in this area, it forces blood into the thigh. In doing so, you're reducing the venous pressure, improving venous outflow, and increasing the AV pressure gradient, which tends to drive arterial blood into the system of the legs. So, this is how we really thought this technology worked before. It was basically, we squeezed it, it pressed it, we reduced the blood in the veins, they went into the arteries. And this is a major component of how this works, but it's not the only one, because it also increases shear stress in the arteries. 

Shear stress is the force exerted by these red blood cells against the endothelial walls, this friction of the blood that develops. Because we have found that this friction in high-stress situations tends to be protective to the arteries; but in low stress, it tends to cause more problems with the endothelial system, and atherosclerosis tends to develop. 

Now, one of the reasons this is, is because nitric oxide is produced when shear stress increases. Nitric oxide is one of the most potent vasodilators in the body, so it causes these arteries to dilate. It's also very important for the health of the arteries. And it's also a little bit of a blood thinner itself. We hear about nitric oxide a lot in healthcare today because as we age, we lose the ability of our tissue to make it. So by age 60, we've lost about 85% of the nitric oxide that our body could make when we were younger. So we'll see a lot of different types of treatments tend to increase nitric oxide production, and certainly for arterial supply, it's extremely important. 

The last way it affects the major arteries is this transitory hypoxic stimuli for upstream vasodilation. Now, this is a big term, but basically what it means is when the body senses compression to an extremity, when it gets squeezed, the arteries proximal to that area dilate. It's a reflex. It's a protective mechanism because the increased blood flow that gets into the area that’s compressed. How this works, though, is that the intermittent pneumatic compression for arterial disease has a very rapid and fast and strong compression, which triggers the proximal reflex. So the arteries proximal to it dilate, but the compression only lasts for 3 seconds, and it relaxes. So by the time the proximal arteries dilate, the compression ends. And so you're actually increasing blood flow into the area using a reflex. So this is how this differs also a lot from how the venous and lymphatic work and why this can be useful in patients that have some arterial insufficiency where you wouldn't want to use the other ones that have constant type compression over longer periods of time. 

So the last group of theoretical reasons why this work have to do with the microvascular system. Now, these take a few weeks to actually become measurable, but we see that we get an upregulation of angiogenic growth factors, VEGF and MCP1, along with a whole bunch of other ones, that we see are very important for growth of new arteries and development of collateralization within the arteries that we have. We also see these factors are very important for wound healing. But we see an increase in these growth factors after a few weeks of using this therapy. 

And we also see a change in the veno-arteriolar response in the capillaries. Now, this is actually in the capillary bed where the oxygen transfer can occur. You all know blood gets in through the arteries, then into arterioles, which go into the capillaries, and it's perfused in the capillaries. Blood comes out the other side into the venules, which goes back into the venous system. It goes like that. At the base of these tiny arteries that go into the capillary bed is a structure called the precapillary sphincter. This tiny structure controls whether blood gets into the capillary bed or not. When the sphincter is closed, blood goes directly from the artery into the vein, this arterial shunting that we see. When it is open, blood's able to get into the capillary bed and perfuse and exchange its oxygen. So the body has this mechanism because if we're laying down, the sphincters close. If there's too much oxygen in the tissue already, the sphincters close, and the blood just goes over back into the arterial system and goes somewhere else to work. But in certain diseases, such as diabetes, where we see this autonomic neuropathy, we will see these precapillary sphincters remaining closed longer, which is one of the problems we have with healing in diabetic wounds. This therapy seems to cause these capillary sphincters to stay open longer, to perfuse the capillaries and their tissue to a greater extent than they would without the therapy. 

So those are the 5 mechanisms that seem to help most as to why this works. Now, there are certain patients that we don't want to use this for. And usually these are the same patients you wouldn't use any sort of pneumatic compression of extremities. Patients that have an active DVT or a pulmonary embolism, we don't want to use these for. If they have significant congestive heart failure, we don't want to overload the heart. So we know with all these types of pneumatic devices, we really stay clear of them in the more severe stages of CHF. If a patient has quick or rapid advancing disease of the arterial system where we see wounds getting worse faster or gangrenous changes increasing. We don't want to use this because there's always a risk of forming these microvascular blood clots that can occur. So if a patient's really getting worse, this is not something to be used. This type of therapy is mostly for patients that are either advancing in PAD or are relatively stable where you're trying to help their arterial system. Really our gain is seen more in the longer term as compared to an acute impulse to increase the blood flow. And my personal recommendation, if somebody has an ABI of less than 0.5, I would recommend they be also under the care of a vascular specialist. Because in those patients, the likelihood of them needing an intervention is potentially imminent. So you want the vascular team working with you when you're treating these patients. And vascular specialists are also using this therapy along with it. But I like this therapy because it is something that can be utilized by a non-interventionist who still may have a reduction in their arterial blood flow. 

So Darren, I'll turn it over to you. 

Darren Behuniak: Great. Thank you, Dr Evans. Really appreciate all of your insight there. And as Dr Evans mentioned, we met at a focus group where we were, it was a podiatry-focused collection, and we really wanted to understand. We had known that there was previous technology out there that was very popular in the late 90s and early 2000s. Over 60 studies performed on IPC for PAD. And we just kept seeing so many of our patients with lymphatic and venous disorders that also had arterial disorders. So we set out to try to make something that was based on previous technology and all of the studies, but at a more affordable price point. And that's what we've done with the Artaira device. I'll get into a little bit about the device, but more so about the reimbursement. Some of these topics Dr Evans covered. 

But the key to this device is rapid high pressure. And those sequences, that's what all of the studies were done on. And at one point, Medicare was covering these devices. And they came back and said that there weren't enough studies. We all know that they can be finicky. Our feeling is that at that time, there were a lot of manufacturers that got into the game and were making these types of devices, but they didn't operate the same way as what all the studies were based on. There were multiple seconds in between. The garments didn't fit the same way. And I've outlined some of the way ours look now. They just weren't the same, but they got flooded. So we feel like it was more of a fiscal decision. They've since kind of realized that this device can help in the long run save costs. The critical component, though, again, is this high pressure, rapid inflation, and garments that are easy to get on and fit snugly. We show this to a lot of our patients. We have a video even for the clinicians as well, or the caregiver at home, to really show them how to get the garment on and make sure that this device works properly. 

You saw a picture of the device, and we'll get back to it. But everything that we've done at AIROS, even on the lymphatic and venous side, has been with user-friendliness, ease of use in mind. If you know these patients, they will get prescribed devices, and compliance is key. And if it's difficult to get on, if it's confusing, they will not use it. So that was the biggest thing with our design of this device. Having a big color screen on there, especially for the elderly patients. Previous technology that's been out there weighed about 27 pounds. Ours is less than 7. It has a handle on it, so patients can move around their house and use it as needed. We also have a usage tracker built into the software, so we could tell if the device is being used or not. And we're exploring some Bluetooth capability that will be able to transmit that data, especially for payers, potentially down the road. That's something that's on our development roadmap. 

As far as the market and how this is getting paid for and the types of patients. So Dr Evans covered a lot of this. These are the before pictures of some of the patients that we have, and we're having extremely tremendous success closing some of these wounds. We’re actively trying to do some studies that match what's been done before. But at this point, we're focused on some of these patient case studies, which we can get out to everyone and we'll be getting out there to the podiatric community, the wound care community, and the vascular community in posters and at trade shows and online. So that's really what we're focused now because we know that this technology works and now it's a matter of getting it to these patients, especially those that are non-surgical. They don't want to have an invasive procedure or there's other reasons where they can't. We say the “last resort,” so when amputation is all that's left, this is a device that can be tried and used. And as Dr Evans said, it's adjunctive therapy. A lot of these patients will still have to maybe have a procedure, but it can help, and it can even help afterwards, help those procedures become more efficacious. 

As far as who we're working with, and again, so our goal is to work with the durable medical equipment community and these folks that are already talking to many of the same, we say call points. So podiatrists, including podiatrists that own their own DMEs, we're actively discussing with, the podiatrists can write for this, like they can for some of the other items. So when we were coming to market, that was a big factor for us, the fact that podiatrists who own their own DME could purchase directly from AIROS, and we help them with billing and the like. So obviously vascular, cardiovascular, wound care, and family docs and general practitioners. We’re just trying to make people aware that this is out there. Obviously, they're not performing a lot of those surgeries, but if they know that it's out there, maybe they could get them to a specialist and have them ask about it. And as mentioned, we're very interested in developing some sites where we're going to be doing our own studies. 

Getting down to the reimbursement, this is very important because the utilization, as Dr Evans mentioned, of intermittent pneumatic depression for PAD and treatment of symptoms of PAD, it really fell after Medicare decided in about 2015 to not pay for them. Originally, they were. They cited that there weren't enough studies. We don't think that that's really where it was coming from, maybe more of a fiscal decision. But the fact is that they are now paying for this device again. And they have it set up. And this is Medicare. Commercial insurance is starting to follow suit a little bit, but Medicare is paying a device rental. We're seeing it's now beyond 10 months when the original setup was a 13-month rental, and that's what we're seeing now. In the first month, Medicare will pay the EO699 code. That is for the half-legged garments. So they pay for the two garments or the one garment in some cases, and then the rental goes from there for 13 months. And it's about $537 per month. That's the allowable. There are a number of ICD-10 codes that are out there. They really fall under peripheral vascular disease is really the main code. And then there's a number of different ones. I gave one example here of arthrosclerosis, native arteries with intimate included claudication. There's ones that are with wounds. So there are a number of them that are out there and we'll get into what's needed for a billable claim in a second. The other place that we really wanted to focus was the VAs. And so that was really, again, our plan was to help a lot of those VA patients and also have a device that would be affordable for even a cash pay through a DME. And we've done that. As we've gotten out there, and really, once we got through FDA, Medicare started paying for these again. And so now it's better for everyone when that's the case. 

So in order to get a patient a device, a diagnosis of peripheral arterial disease or PD or PVD, any kind of clinical documentation, which you're all used to, pointing to symptoms, rest pain, night pain, ischemia, intermittent claudication, and any kind of ABI test or TBI tests or any other vascular testing that's been done, that allows in the prescription. And that allows the DME that we work with to get a device, get it to the patient's home, set it up for them, just like they do for the lymphatic and venous ones. And they handle all the paperwork. And we're actively doing inpatient surveys to be able to follow up and get pictures when possible, 30, 60, 90 days out. And that's really the phase that we're in right now. 

At this point, we'll allow some time for questions. And I just really like to reiterate what we're going for here and what we know is possible is helping a lot of these patients that have no option. This device is not for everyone. And Dr Evans, when we're speaking at the conferences and talking to clinicians and the doctors and to wound care nurses, it's not for everyone, but we believe it can help many, many people. And we're committed to doing that, working with the DMEs, even with financial hardships, being able to get this device on patients and helping potentially save a toe. That is our main goal. And we'll leave it up for questions. Thanks very much, everyone, for joining us. 

Dr John Evans: Yeah, and I'd like to add something just at the end as to why I feel that really all of us in our profession should be aware of this treatment. Because when it comes to peripheral arterial disease, the treatment options of the patient are, 1) guidelines-directed medication, to take medications for their cholesterol, for their blood pressure, for their diabetes. These type of situations to make themselves as healthy as possible, to eat well, to sleep, to exercise, which is one of the most important treatments that we don't tend to recommend as much, to stop smoking. And these are basically the treatments that we have for PAD at this point. We have certain medications that we can take that can improve circulation, your different antiplatelet and anticoagulant agents. And some of the other medications that have been shown to increase walking distance. So we have some drugs that can be taken. And after that, we tend to refer to vascular specialists. And often they will perform these procedures where either a surgical bypass is done or they'll do an endovascular procedure. Now, these procedures are amazing what they're able to do now. So right now, that's basically the treatments we have for this disease. 

What I think is important is I look for things that other than vascular specialists can do, something that those of us that aren't vascular surgeons or interventionists can help our patients with. If they have wounds or if they have claudication or these other types of aspects of PAD that may not require an intervention at this point. And that's where this falls. This can improve the arterial circulation in the leg. It, again, is not as powerful as an intervention or probably even as the drug therapy is, but it's something that can fit into that category that the patient does for themselves. So the patient has agency over their treatment, something they can actually do to help themselves. It's non-pharmacologic and it's non-surgical or interventional. So it fits into the category of something we can do to add these patients that may have wounds that won't heal, that have arterial insufficiency, or have symptoms that may lead to tissue loss such as gangrene or other issues like that. So I think it's important for us to be aware of it. In the right patient, it can be very, very useful. So I think we should at least be aware of the treatment and how it works. Thank you.

Darren Behuniak: Thanks, Dr Evans. One last thing I'll add, we are very open to consignment setups, and we've done it for many podiatrists and some of the wound care centers and vascular offices already. So if it's something you'd like to try in your office, touch and feel and try it on a patient, we're absolutely open to that and do that all the time. So we'll reach out, or please reach out to us if that's something that you would like, and we'll make it happen. And with that, I think we'll open it up to some questions. 

Hi, everyone. On behalf of Dr John Evans, love to thank you for attending the session. We hope it was informative. We have time for a few questions here that have come in during the session. I'll run through them now. Looks like some I can answer on the billing and reimbursement side, and some Dr Evans can answer from the clinical side. 

So the first one is: “What exact findings have to be present for Medicare to cover? Is prior authorization required, and does AIROS do that for the doctor?” So as far as getting the prescription for this EO675 arterial device, our Artaira, the main things that are needed are to support the prescription for the device are a diagnosis of peripheral vascular disease or peripheral arterial disease. Any kind of supporting notes or studies, such as an ABI or TBI, anything from a clinical note standpoint, presence of a wound, intermittent claudication, any kind of ulcers—diabetic foot ulcers or arterial ulcers—anything that can be in there, Medicare has deemed it as a quote-unquote case-by-case basis but from what we're seeing, as long as all of those elements are in there, that would be good to support the prescription for this device. We'll send some follow-up materials that speak to that, kind of a checklist to ensure everybody's clear on what exactly is needed to get that done. 

The next question is for Dr Evans here. The question is, “If the Artaira device is pushing the blood down, doesn't that make lymphedema and swelling worse?” So I'll let Dr Evans speak to that. 

Dr John Evans: Yeah. And again, thank you, Darren. And thanks, everybody, for joining us today. This potential therapeutic option can be very important to our patients because it gives us something that we can use in addition to all those that are provided by our vascular colleagues. It's something that we as podiatrists or wound care specialists can initiate to help our patients to heal and to give them a little bit more of a likelihood of saving their limb. 

And how this works is similar in a couple of ways as to the lymphatic or venous devices, in which it does push the blood out of the foot and leg. But by doing so, and affecting the arterial-venous pressure gradient, by doing so, it's driving blood from the venous system primarily into the arterial system. The majority of reservoir of blood in the leg are within the veins, because the veins can distend and they tend to hold more of a volume of blood in them than do the arteries. So when you do compress the veins, you press the blood into the arterial system, not just through the heart, but also through any collateralization or such that goes up along the limb. And plus, since these compressions begin distally, and one of the other differences between this type of device and the venous or lymphatic devices is this device is simply below knee. It just affects the foot and the leg. So when it contracts, it's not going to push blood all the way up. So it really isn't driving blood out of the area as much as pushing it up, which is primarily the venous system, and then allowing it to spread into the rest of the arterial system that way. So in effect, it's not milking everything out of the leg. 

The other difference has to do with the duration of the compression, whereas with the venous or lymphatic devices, there's a longer compression cycle in which you're basically milking the blood out of the leg. This isn't. This is a very rapid and short duration, only 3 seconds, of a compression. So after the relaxation, the blood's going to go back where it was unless you're able to drive it somewhere else. And if it's going to drive it out, it's going to drive it proximally, but also to extend to its lateral or medial area from it. So it's a little bit different than you might think with these other type of devices. 

Darren Behuniak: Very good. Thank you. This next one is clinical related, and I believe we have a slide on it, but I'll just kick it to Dr Evans: “What studies have shown what percent increase in arterial flow is achieved using the device?” I think there was a study that was mentioned, but I'll let you handle that one. 

Dr John Evans: Yeah, there's a few that have looked at that specifically, but generally we've just seen increases. One of the drawbacks of having such a heterogenicity of studies is they all follow what may be different protocols. And so it's difficult to look at apples-to-apples in some of these studies as compared to just looking at the overall benefit of the intermittent pneumatic compression therapy itself. But one that we had studied looked at patients who had relatively normal circulation. After a compression, you would increase the blood flow to the foot and leg by about 274%. And of those who had claudication, it was about 174%. Now, again, this is generalization. But the idea being, we see a significant increase in the arterial flow after a compression of this type of a device. 

Darren Behuniak: Very good. We got another one that just came in. I'm just jotting a note down, and this just came in. “Has Medicare come out with a paper or LCD—local carrier determination or local coverage determination—describing what's needed for coverage?” This arterial device, this type of arterial device, EO675, has been a part of the national coverage determination for years. The LCD, that was disbanded around November of 2024, did not cover the devices, and so once that LCD went away and went back to the national coverage determination, that's when EO675 started to get paid for again. And that's where we're at. 

And then there's another one about just some... So as far as the paper and what is needed for coverage, again, we'll send out a checklist follow-up of what exactly they're looking for. We just got through 13 months to 13-month rental, as we mentioned. There was a number of them that got through and went all the way through to 13 months of coverage that started last year. So we know that they are covering and expect some of the commercials, more commercials to come on as well. But again, we'll share that information so that everyone knows and it's clear what is needed for the script. 

Dr Evans, another one related to CLTI: “So to help guide expectations for CLTI patients that are very challenging, what is the percentage of limb preservation versus limb amputation with IPC?” I know that's a study we're looking into, but Dr Evans, I'll let you address that. 

Dr John Evans: Yeah, again, it's generalized results on that. Although the overall results have shown that there is a moderate-to-significant improvement in the limb preservation rate on using this procedure. And that's one of the driving forces why the American Heart Association and American College of Cardiology, when they were developing their 2024 PAD treatment guidelines, listed this as one of the recommendations of treatment for patients that have no option. So ideally, if you have a patient who reaches the CLTI level, we are recommending that you have them working with a vascular specialist. Because when anyone reaches a level of this chronic limb-threatening ischemia, the mere definition of that means they are in the range that they are probably going to need an intervention. So we want people working with vascular people at that point. And one of the other important points about this type of treatment is, this is not a primary treatment for arterial insufficiency for patients who have CLTI. This is an adjunct to everything else that they should be doing, which could mean an intervention. It's going to mean guidelines-directed medication, ideally some degree of exercise therapy that would be initiated, which is something we really haven’t talked about much, but we should because it's been found to be useful in all stages of PAD. But this is an adjunctive treatment. The real benefit here is if you've got a diabetic foot wound and you know there's some degree of arterial insufficiency, this is something that can help them. But if they're on that CLTI stage, we want them working with a vascular specialist, because this may be something that would be benefit to them that doesn't involve drugs or an intervention itself, that the patient has some control over, it gives them some agency over their own care. So I would never think about this as either/or. If you think a patient is reaching the level that they may need an intervention, get them to somebody who can make that decision for you so you're not the only one who's making that. Because just for medical-legal persons, we know patients that have PAD, these are high risk, and we're trying to keep them from losing their limb, but they are on that pathway. If we can delay it as long as possible, that's what we're looking for. But anyone who is in that situation, I would definitely defer to vascular and then discuss with them, is this something that could be adjunctive to whatever they're doing? 

Darren Behuniak: And to piggyback on that, just another question, and a really good one, and one message that we're absolutely trying to communicate: “Beyond the no-option patients, shouldn't we offer it earlier upstream? Which group of PAD patients beyond no option have seen the most success with IPC?” So Dr Evans, if you could address where—and this is something we're trying to educate the vascular, podiatry, and wound care community—where does this fit into the patient treatment? And clearly it's adjunctive, but does it make sense? And we think it does, but how does it make sense to use this type of device earlier once PAD symptoms arise? 

Dr John Evans: That's an excellent point. Peripheral arterial disease develops throughout your life. I mean, it begins in your teenage years, and it gradually worsens until you die. It doesn't really get better. But we don't tend to diagnose it until they reach some degree of critical ischemic stage. Either they've got a wound that won't heal, they've got gangrenous changes, something like that, or claudication. So we're missing the boat. We're not even identifying the disease until it's well down the road. So this type of therapy, in looking at the research that's out there, has been useful in all stages of PAD. Not just in the worst, even thought it’s shown benefit when patients have no options at all. But the benefits occur all during its stage. So really, this is useful in any stage of PAD. It's also useful after an intervention. If they've had a bypass or an endovascular procedure, this has been used and studied and found to reduce post-op swelling and increase the skin perfusion to augment the procedure that's being done. 

The thing is, the research that's been done has not been as deep as we would like. And AIROS has been looking at that. There are some other companies also looking at this because we're finding this is something we could be using more, but it hasn't really been looked at. But it's relatively safe and they are low risk. So its utilization is just beginning. And right now, we're trying to get the word out that it's an option for these patients that we should at least be aware of and decide whether it's something we would like to do. 

Darren Behuniak: And then the last one, I think we're up against time, just related to, piggyback on what we're saying. I think we've kind of addressed it, but: “How do we know when a patient could benefit from endovascular procedure versus the use of the Artaira device?” And really, they're used in conjunction and adjunctive therapy. Dr Evans, just to make a finer point on that, that's really what we're talking about here is the adjunctive nature of this device. 

Dr John Evans: Exactly. We want that patient to be seeing a vascular specialist. Because if you feel that they may be at that point, well, that's good enough for us. We want to get them checked out. And then the vascular specialist can decide, do they want to watch it for a while? Maybe utilize this to help it along the way? Or is it really time for them to get an intervention and then decide whether it might be used after that? So if you come across that situation, get them to vascular as soon as possible. 

Darren Behuniak: Very good. And with that, I think, again, we're up against time. So we appreciate all the questions. There'll be some follow-up materials coming out, again, including that checklist as far as what's required for coverage. We really appreciate everyone taking the time. We look forward to more of these discussions with Dr Evans and other members of the wound care and vascular community going forward. And we wish everyone a great day. Thank you.