Vascular surgeon Shant Vartanian, MD, presents an update on understanding and managing abdominal aortic aneurysms and peripheral artery disease – prevalent age-linked disorders with significant morbidity and mortality. He provides clear criteria on risk factors, explains the value of the ankle-brachial index, offers keys to slowing disease progression, compares open and endovascular repair of AAAs, and gives priceless tips on diagnosing and relieving claudication.
My name is Sean Pertania and I actually grew up on the peninsula. I was born in Belmont um in the late 70s and then uh moved to Burlingame. I went to Burlingame High School, and then Stanford, and then I did all my um residency uh research and fellowship at UCSF and I've been on faculty here since um uh 2010, uh, I'm sorry, 2012. And uh it's, um, it's great to have such deep connections to the community. Um, and to practice in our San Mateo clinic, which used to be Bay Meadows, which I remember, remember fondly is where I learned to play golf at the little run, uh, nine-hole course inside the racetrack. So, um, for sure, things have changed a lot, um, uh, in the area and for sure in my specialty, vascular surgery. Um, I'm gonna talk, I think today about, um, two things that I get referred to most that seems to have lots of questions and anxiety, um, peripheral arterial disease, and I, um, spontaneously added. Aortic aneurysm very briefly just to um um make it maybe a little more comprehensive and interesting um for uh the audience. So, what is our scope of practice? Who do we, um, who do we treat um and see at our CTO clinic? Um, well, certainly more than just aortic aneurysms and peripheral arterial disease. Um, but carotid artery disease is I think a common one as well, asymptomatic carotid artery disease. Um, we'll get follow-ups for incidentally found aortic dissections. Um, sports medicine is a growing one, particularly, um, young adults and athletes with, uh, thoracic outlet syndromes. Diagnostic testing, we can do um the full gamut at San Mateo as well. And I will say, um, we have had great um reviews from our patients because it's so accessible. They could pull off the freeway, park, and be in our clinic within minutes. Um, and it's nice to be able to do point of care testing at the time of our initial evaluation for vascular surgery. So, um, aortic aneurysms, just, um, real quickly, I don't know, um, how many people knew, but actually, um, Einstein died of an aortic aneurysm. Um, and like many things in his life, he was just a little bit ahead of his time. Uh, he actually had it reinforced by a really famous general surgeon back in the day, um, Doctor Nissen. It's, um, there were limits on what they could do. They would try to take a mesh and wrap it around the aneurysm so that the aneurysm wouldn't grow. We now know that that's a failed concept and despite having it fixed in 1948, Einstein actually died of a ruptured aneurysm in 1955. Just as doctors Cooley and Debeke, pioneers in cardiovascular surgery, um, came up with a way to replace the aorta with initially homograph, so basically fresh cadaver aorta, they would just swap it out. Uh, but Debey very famously on his wife's sewing machine and a sheet of, um, polyester from the fabric store, um, sewed the first, um, the cron graft, and that has essentially been Um, largely unchanged and what we use to replace the aorta over the last 70 years. Um, and I'll show you a little bit about how times have changed in terms of how we can do that. Um, so what is an aneurysm? You know, an aneurysm is basically a dilation 50% over its nominal diameter. There are nomograms you can look up what's normal for different parts of the artery. I would say that circulatory system is like a tree. As you go up the tree, every branch should be a little smaller than the one, below it. Um, so if, if it's too large on the, on the other side, then, um, that meets the definition of an aneurysm. Um, not all aneurysms are the same. Um, what we're going to focus on today are the degenerative aneurysms that are a result of smoking, and that's by far the most common. Um, and it's important to understand the ideology of the aneurysm because it changes the natural history and how we choose to surveil or um do an intervention for each one of them. Um, why are aneurysms dangerous? Uh, well, it gets back to your, um, uh, physics, high school physics, Laplace's law, uh, where, uh, tension in the sphere is proportional to the radius of that sphere, um, wall tension. And so, the larger, um, the wall radius, the more wall tension there is on the surface. And of course, like any other structure, uh, if you exceed the, the rupture threshold, it can be catastrophic. So, the analogy I often tell patients, um, when you have a balloon and you start blowing up the balloon, it's very difficult. But once the balloon gets large, it's very easy for it to get larger. And so it is with aortic aneurysms. Um, Uh, we learned very early for abdominal aortic aneurysms that the risk of rupture was proportional to the size, and there's lots of great natural history data on that. And, um, early in the, um, establishment of the treatment paradigm, we've, as a society said, you know, we will only fix these when the risk of death is higher than the risk of doing nothing. Um, and so, it turns out the early operative mortality for aortic aneurysms was somewhere on the order of um 5 to 10%. Uh, and they established that threshold that we use today, um, 5.5 centimeter aortic aneurysm because the risk of natural, the natural risk of rupture was the same as the mortality of surgery. Um, so, what's new in vascular surgery? The minimally invasive repair is new and as a result, the risk of death from repair is plummeted. Um, and so, one of the controversial topics now is, wait, should we still be using the same thresholds for repair or should we revise this to an even lower threshold for intervention? Um, and I'll get into a little bit about why that necessarily hasn't changed. Um, but that was the magic number, 5.5 centimeters. Um, we've also, um, understood that not everyone's rupture risk is the same, and we now try to individualize, um, the decision to intervene. Things that have clearly been shown to make an impact. Number one, female gender, and lots of people argue you should have a, you know, 5 millimeter lower threshold for women. Ongoing smokers, COPD, aneurysm shape turns out makes a difference, and there's now emerging biomedical imaging techniques such as this uh finite-dimensional analysis where you can um really try to calculate the wall stress being applied on the aneurysm and try to establish a threshold for repair that is appropriate for that individual patient. Uh, in the future, uh, which one of my partners is studying are biomarkers and genetic profiling with circulatory, um, tests. So you can do a blood draw and try to risk, um, adjudicate the, um, uh, chance of rupture, uh, for individualized patients. Um, so, who, um, is at highest risk for aneurysm growth, progression and death? Um, aneurysms, abdominal aortic aneurysms are by and large a disease of smoking. Uh, and it's pretty unusual to see an abdominal aortic aneurysm in somebody that isn't a former smoker or an active smoker. Um, and it's both an issue of the duration of smoking, uh, and the volume of smoking. So, it's like a classic dose, um, Uh, um, relationship, uh, response. Um, and, um, multiple studies have shown aneurysms or patients that continue to smoke are at risk of aneurysm growth. Um, so, uh, we get asked a lot, is there anything I can do to change my risk of this aneurysm growing? Number 1 by a mile is stop smoking. That will slow the rate of aneurysm progression. If you continue to smoke, smoke, your aneurysm will continue to grow. Um, if they quit smoking, um, it doesn't necessarily get them out of the woods, um, but it does slow the rate of progression. Um, and, uh, also been shown, though not as, um, dramatic of an impact is diet to a degree. So, fruits and vegetables, nuts and fish are all protective meats seem to increase your risk of aneurysm progression. But again, these are really minor gains, minor influence. It's um smoking, um, by, you know, an order of magnitude that is the predominant pathophysiology and aneurysm progression, um, uh, over time. Uh, one other really interesting observation, which I think is really um important because we're a progressively diabetic society, diabetes is actually protective against aortic aneurysms. Um, and, uh, it's not really well studied. It's, um, possibly due to glycosylation of some of the connective tissues, um, that, that line the aortic wall. Um, there is some speculation that perhaps metformin, the drug itself is what's protective and not the condition of diabetes. Um, this is all that's being sorted out. Um, but interestingly, in a progressively diabetic society, diabetes is protective against abdominal gainers. Um, so what is the normal rate of growth? And this is super important because we'll see patients with small aneurysms far more commonly than we see patients with large aneurysms. Uh, and we know, um, due to the law of Laplace, the rate of growth or this wall tension increases with size. So smaller aneurysms, um, grow slower than larger aneurysms, and the normal rate of growth for most aneurysms that we see in the 4 centimeter range is about 3 millimeters per year. Um, so this is great when we do our initial, um, uh, intake with somebody with a new diagnosis of an aortic aneurysm. Let's say that one that's at 4 millimeters, and we say if you stop smoking, And we keep an eye on this aneurysm. Um, it's only gonna grow, you know, 2 to 3 millimeters per year for most patients, and the threshold for repair is typically 5.5 centimeters. So you can do a back to the napping calculation and say, you know, don't worry, we're gonna keep an eye on this, but it's unlikely you're gonna need to repair for, let's say, you know, 3 to 5 years. Um, and in some ways, this is a, uh, wake-up call. Um, again, it's commonly smoking-related and so it's an opportunity to deliver a message linked to a behavior modification that can, um, hopefully, um, be impactful and, um, help prevent, um, growth. Um, because of this data, the rate of growth data, Um, and, um, other data that's been out there, um, there are now, um, pretty clear recommendations that have been endorsed by the US Preventative Services Task Force. We do all our surveillance with abdominal ultrasound, so it's very low risk. Um, it is very cost-effective, uh, and there is a strong recommendation, uh, for, uh, any, particularly men over the age of 65 with any history of smoking to get a screening abdominal aortic ultrasound. Um, uh, it, there was some backlash when this recommendation was made because it specified the male gender. Um, uh, CMS adopted this and expanded it to women as well. So now, as a part of a Welcome to Medicare, uh, onboarding, and abdominal aortic aneurysm screening is reimbursed for, uh, any patient over the age of 65 with any history of smoking. Um, for aneurysms that are identified, um, our surveillance interval varies by aneurysm size because of the rate of growth. So, aneurysms under 4 centimeters, we don't look again for 3 years. Aneurysms, uh, between 4 and 5 centimeters, we'll look again at, um, 12 months, and once you're at 5 centimeters, you're approaching the threshold for repair and that's when we'll do, um, imaging every 6 months, um, to capture them early. Um, there have been studies that have looked at the safety of doing a, a, a surveillance program like this, and it turns out it's very safe. There's very low risk of harm to the patient by doing surveillance all the way up to 5.5 centimeters, particularly in men. OK. So let's say it reaches size threshold. Um, how do you repair it? This is, again, um, the old fashioned way. There's two ways to, um, work on the plumbing, as I like to tell patients. You can either replace the pipe or you can reign it. Um, the old fashioned way is to replace the pipe and, um, for the aorta, you would clamp the aorta above and below, open the aneurysm sac and replace that with the dcron graft, the polyester tube that we've been using forever. Um, how does that work in the modern era? Super durable. Works great if you can select the right patients who are at, you know, low or moderate, um, anesthetic risk. Um, despite that, it is a major operation. Um, there's a roughly 15% chance of cardiac um, uh, morbidity, typically, um, atrial fibrillation, 2 to 5% risk of MI depending on their pre-op risk stratification. Um, there's a number of other lower risk, um, and low magnitude. Or low frequency uh complications that can occur with open repair. Um, but I think the hardest thing for the patients is the recovery. So they spend about 3 or 4 days, um, in the ICU and they'll be in the hospital about 1 week. Um, and just because they get discharged home doesn't mean they're back to where they were preoperatively. The recovery is really 2 months, um, in turn, until their energy level, um, until their appetite, um, until their strength really returns to where it was preoperatively. Um, so it's, it is a big operation. It's major vascular surgery, um, and offering it to patients should be done, um, cautiously. Um, in, uh, you know, I don't like using the word disruptive innovation very much because it's so hackneyed, but for sure, um, it applies to the minimally invasive, uh, repair of the, um, abdominal aorta. Um, this was the initial description done in Buenos Aires, um, in the late, uh, or I'm sorry, in the mid 1990s, and all they did is they took a, a, um, Palmas stent, which is basically a balloon, a hand-mounted balloon stent, and they sewed a dcron graft to it. They put it on a catheter, advanced it into the aorta and somebody who wasn't a candidate for surgery. And inflated the balloon. So, it's like a wind sock here and it, um, fortunately for them, kind of sealed this into place and now your circulation goes through the graft instead of into the aneurysm sac and, in theory, depressurizes this. Um, they, you know, realized that most of these problems involve the aortic bifurcation and so there were some modifications, but this really, um, opened people's eyes on what is possible in a minimally invasive way. And now, uh, there are at least, you know, 8 commercially available devices, um, with, you know, more similar than dissimilar that largely do the same thing. Um, and what they are, these are, um, metallic, um, um, frameworks with, um, uh, fabric, either, uh, Gore-Tex or Dacron, and that line it and help exclude the aneurysm sac. Um, uh, I often show patients, um, this animation just to kind of get them comfortable with, um, what the repair looks like. You'll see lots of patients have EVAR in their chart. What is an EVAR? Well, um, an EVAR, an endovascular Aneurysm repair, um, is like building a ship in a bottle, um, and I'll show you why. But one of the key things here is the patient experience. The patient doesn't have to be under general anesthesia. They can be awake. Um, you just need some local anesthesia where you access the groins. This is the aneurysm right here. Um, as always, first order of business is to put in a wire into the circulation. Um, this is a particularly complex aneurysm because this aneurysm extends down into the, um, common iliac and the pelvis. So we'll have to exclude anything that's abnormal. Um, and what the way these devices work, um, these devices are made out of, um, this spring that's, um, nickel titanium alloy. It's, um, uh, super elastic with shape memory. So, they're designed to be in a very specific shape, but they're compressible. And as soon as you release, um, the constraining mechanism, it springs back up to that shape. And so, they're designed is basically a pair of pants, um, and you, you know, there's different sizes and you pick the sizes that you want. And then from inside each one, you can then extend the pair of pants into a sealed zone of normal artery above and below the aneurysm. Uh, and, um, the reason why we can do this under local anesthesia is because the arteries don't have somatic nerve endings. They're totally insensate. So, patients might feel pressure with like a balloon angioplasty, but in something like this where you're just realigning it, they cannot appreciate, um, uh, any kind of discomfort. Um, and, uh, so here you go. And then this is the aneurysm usually starts at the renals. Here's the other pair of pants. Um, and then like I said, just like building a ship in a bottle, we'll advance another, um, device to bridge the gap here. And then the circulation will be able to work its way from the aorta above into each one of these branches into the limbs and the pelvis without actually communicating with the aneurysm sac. Patients get discharged home the following day. Um, it doesn't take a lot out of them physiologically, so the recovery is very brisk. Most patients just need some Tylenol on discharge. Um, they're up and they're walking around normally on the following day. Um, there's a big push, at least for the less complicated ones, to make this a reimbursed procedure in ambulatory care surgery centers. Right now, it's hospital-based, so there's that overnight admission. Um, but just to give you an idea on the safety profile for the majority of these patients. Um, it was very controversial when it came out. Um, industry has done a great job of progressing the technology. Um, there have been a series of random randomized trials now comparing the two unequivocally, and the vascular aneurysm repair has a much lower, um, 30-day mortality, much lower morbidity, um, and I'll show you now, 80% of all patients that get repairs are done minimally invasive and the 20% are because they have really complex anatomy. Um, you'll see this a lot in CT scan reports, an endoleak. What is an endoleak? Um, well, um, uh, an endoleak is basically any circulation in the sac outside of your stent. Um, you know, the illustrator here shows you that there's one, artery in and two arteries out, but in truth, there's dozens of arteries, little branches all along the aortic aneurysm. Every segmental vessel has paired arteries for the back and the spinal cord. Your IMA kind of comes in there too at the bottom of the sack. Um, is an endoleak bad? Well, they're super common. They're present in roughly 25% of all cases that we do, um, but they're rarely pathological. Um, you need a surgeon to look at it, understand the etiology of the endoleak, and almost all, um, just get observed and we only stage an intervention if it's a very particular endoleak or there's still aneurysm growth despite having an intact repair. OK, so, um, just to give you an idea of how transformative this was, the technology was, I think the initial device was introduced, um, uh, and FDA approved in the late 1990s, uh, and now, um, this is the solid black line at the top. 80% of all repairs are being done, um, endovascularly. Uh, in the early days, there is a cutdown to put devices in. The devices have been miniaturized and now it's totally percutaneous, um, so the recovery is even better. And what happened to our population over time? Um, well, if you look at, um, uh, mortality, mortality plummeted like a rock, there was that 5.4% that was stable and still is stable for open repair. Um, but since we're doing so many more of these percutaneously, uh, I'm sorry, endovascularly, the overall mortality is at 2%, um, and, you know, in elective repairs, it's probably much lower than that. Um, and here you go. So, um, in terms of death from AAA, death has plummeted because we're doing, um, so many more elective repairs and patients that probably were not candidates for open repair, um, because of age or cardiopulmonary disease now can be safely repaired, um, without, um, putting too much stress on them. Um, so, uh, I love this slide. It's one of my favorite slides. I show it everywhere. Um, I just showed you that we're doing a great job of reducing death in AAA, and what I've really just shown you is the very back end of this curve here where these two lines cross. The, uh, data. The line is um cigarette, um, smoking usage, number of cigarettes, and then, uh, this solid black line is AAA mortality. This is more than causation, uh, or correlation. There's definite causation that's been shown between smoking and mortality and as our population stops smoking, so too has death um from AAA dramatically. Um, so we've made an impact on, you know, the people in front of us, but the far more important thing is smoking cessation, particularly. Um, uh, for aneurysm progression. OK, so for Triple A's, in summary, highest-risk populations, anyone over the age of 65 with a history of smoking should get screened. Um, smoking cessation slows rate of expansion. Um, we have some better risk stratification and we're trying to apply a little more of an individualized approach to a threshold for repair. Um, but the reality is the overwhelming majority of patients now can have a very safe, um, uh, minimally invasive repair, uh, with low risk of morbidity, mortality, and a very brisk recovery. So, Um, that's, uh, triple A's in a nutshell. Um, peripheral arterial disease, um, what is peripheral arterial disease? People think that it's just atherosclerosis of the legs and technically, it's, uh, in any non-cardiac vessel. Uh, and, um, uh, you know, interestingly, there are, uh, afro-prone areas. It turns out one of the big stimulus for atherosclerosis is a hemodynamic stimulus. Um, so, turbulent flow, um, gives you low shear in that location. Low shear activates endothelium, activated endothelium in the setting of all these other inflammatory, um, signals results in the development of atherosclerosis. Uh, and so, uh, these ather-prone areas very classically involve, um, parts of the aortic arch, the carotid bulbs, um, the visceral branches, uh, and branch points in, um, the pelvis and the lower extremities. Um, so, uh, these are atherprone areas and we know, you know, um, Uh, where to look to find the burden of the disease. Um, there's a technical definition as well for the lower extremities. An ABI of less than 0.9, um, is, you know, basically, um, diagnostic. It's what's used in all, um, um, clinical studies. Um, an ABI is super easy to do. You don't have to send them to us to do it. If you have a, typically, uh, we use a manual sphigmomanometer. Um, check the pressure in both arms and use a Doppler pencil to, to get the occluding pressure in the radials and then apply it into the limbs as well. Um, you, you know, if you're experienced and you have the stuff there, you can do it in under 10 minutes. I understand you probably all have busy clinics, um, and it's easier to send them for the test. Um, uh, so oftentimes what we'll do is if someone has a high diagnostic suspicion on onboarding, we'll get an ABI before we see them just to confirm, um, the diagnosis. Um, OK, super high prevalence, um, unlike aneurysms which are regressing, um, the prevalence of PAD is increasing, roughly 30% increase, um, particularly impacting, um, uh, low and middle-income countries and, um, low socioeconomic, um, regions throughout the United States. There's a rapid progression. Uh, of, um, PAD, um, regionally and worldwide. Um, the prevalence now stands, um, on the order of 12% of the general population. Who is at highest risk? Um, I'll show you some data. Age is a big deal. Um, it's, there's almost a hockey stick type curve with an inflection point once you get to the 7th decade of life, uh, even the absence of other traditional Framingham risk factors. Um, the three highest risk groups, patients over the age of 70. Patients over the age of 50 with a history of smoking or diabetes or patients over the age of 40, which is pretty young, uh, with diabetes and at least one additional, um, uh, risk factor, um, for PAD. Uh, all your classic Framingham risk factors apply, um, but some really stand out, smoking, diabetes, and age. Those are, um, top three by a mile in terms of risk of developing peripheral disease. And here it is, skip this one. Uh, OK. Prevalence by age, this time stratified by male and female gender. Um, and you can see under the age of 60, um, it's a pretty low incidence in the general population. This is from Nhanes, um, 2000 participants that had ABI data available. Um, but once they get over the age of 70, um, it, it's, uh, increases substantially. In patients over the age of 80, it's well over 25% have, um, uh, um, diagnosable peripheral arterial disease. OK. Um, when I see a patient with PAD, um, a really easy framework is, is this asymptomatic? Is this claudication, or is this limb-threatening problem? Um, because it has totally different ramifications for, um, the workup, interventions, and the conversation we're gonna have and potential treatment. Um, asymptomatic is, um, by far the most common, 3 times more common than patients with claudication. Um, these are patients that will typically have an abnormal pulse exam picked up on, um, on physical examination or commonly in our area, patients that are getting lifeline health screening, um, and just get a screening ABI and there is some abnormality. Um, um, asymptomatic disease, why does it matter? Well, uh, you know, PAD is a manifestation of systemic atherosclerosis. Um, and, uh, just because they have an abnormal ABI doesn't mean that they have, um, uh, uh, um, afro and other parts of the body. If you have a diagnosis of PAD, you roughly have a 20% chance of having some elements of coronary disease and some elements of coronary artery disease. Um, so, uh, I, you know, I don't have a lot of jokes for the medical students in clinic, but my favorite is a knock knock joke. Uh, it goes something like this, knock knock, who's there? Abnormal ABI abnormal ABI who? It's not a joke, it's a wake-up call. So, if you get, if you, if you have an abnormal ABI, even if they're asymptomatic, what you should really be doing is trying to identify risk factors that um have led to this, that probably would lead to coronary disease, cerebrovascular disease, and stage your efforts and your interventions for the fate of the patient, not for the fate of the limb. Um, other important point about ABIs, um, the worse your ABI, um, the worse your prognosis from cardiovascular mortality. Um, and just to kind of, I mean, logically it makes sense if you have a really high burden of atherosclerosis, your ABI is going to be lower, and if you have a really high burden of atherosclerosis in your limbs, you probably have a higher burden of atherosclerosis, uh, in your heart or in the brain. Um, so, um, there is emerging evidence that if you were, um, in the vascular medicine world, um, to superimpose ABI into your risk models, your risk calculations, etc. you might be able to refine that, particularly in subpopulations. Um, we don't typically do that, but that is kind of where the, where the ball is moving to. Um, and I think it just drives home the point that there is some, um, information in an ABI in an asymptomatic patient, even if we're not gonna stage, um, a particular invention. Um, what about screening then? Should we be screening all these patients? Um, should we just get ABIs in patients over the age of 70? Um, this has been studied exhaustively. This is a meta-analysis with something like 100,000 patients, um, uh, that got published as part of the US, um, Preventive Services Task Force. Ultimately, they decided to give it an indeterminate recommendation. An ABI is easy to do, it's cheap, it's low risk, um, but they weren't showing, um, enough of a benefit for the general population to endorse screening. Uh, what you should really use it is more selectively in patients, high-risk patients, subpopulations that uh might be, um, uh, that might do better with more aggressive or targeted medical therapy. Um, and that's typically how we use it in our practice. Um, so patient's asymptomatic PAD, it's really non-invasive testing to make the diagnosis and then work on risk factor modification. OK. What about claudication? This is another super um common referral um to our clinic. Um, I have pain in my legs, um, and, uh, you know, a pulse exam was difficult and it gets sent to us. Um, so, the, a couple of things about claudication. 9 times out of 10, um, you can make the diagnosis very accurately with a thorough history, uh, in a physical examination. Claudication has some very unique features, very reproducible onset. The problem is the muscles at rest are well profused and they have to experience a certain amount of physiologic stress in order to develop lactic acidosis and that's the pain signal. Uh, it turns out that the level of physiologic stress is always the same. So they'll say reproducibly, I know I can get to this bus stop before I have pain. Um, if I'm not walking, um, as far, I don't get pain. If I walk slower, I don't get the pain. If I walk up a hill or on stairs where there's more physiologic stress, then you get the pain. That's a key part of it. It's very reproducible. You need the stress component and you need the reproducibility component. Um, it usually is quickly relieved with rest. So if they rest and for most people, 5 minutes can be as long as 15, but if it persists for longer than that, it's almost certainly not, um, uh, true claudication. Uh, and this is the other key one, it's not affected by position. So if they tell you they have the symptoms lying in bed or when they're seated, um, then that's not, um, a manifestation of peripheral arterial disease. Um, the classic claudication is calf claudication. It's certainly the most common. It tells you the problem is, um, well, the problem is more proximal. You, you get, um, symptoms one level below where the problems are, um, but you can have what's called Laric syndrome, thigh or buttock claudication that's a little different than the classic symptoms. It can give you hip pain that gets, um, mistaken for arthritis, and oftentimes there's impotence due to occlusion of the internal legs as well. Um, and less commonly foot claudication. That's, um, that's pretty unusual. Um, I would say, uh, somewhere between 10 and 20% of the patients we get referred to for claudication do not in fact have claudication. And that's because there are a number of um syndromes that mimic claudication. Most commonly, um, uh, spinal stenosis, uh, or radiculopathy sometimes. Um, rarely, a compartment syndrome or, uh, there's, uh, venous claudication symptoms that can develop as well. Um, but a lot of these can be teased out with just really careful history. Um, and if you need to, that's where the ABI is useful, adding some objectivity to very subjective, um, history and physical examination. And again, ABI is really easy to get, really easy to do, and then if you do an ABI that shows an uh less than 0.9, then, then you've made the diagnosis. Um, there are patients rarely that kind of are, um, in this gray area where it seems like it's claudication. They do have palpable pulses and their ABI is close to normal. Um, uh, in those situations, we do something called an exercise ABI, um, and, um, during exercise, your, um, peripheral systemic resistance falls dramatically. And what that does is it, it drops your pulse pressure. So if you see, um, Uh, if you do an exercise ABI in somebody who is essentially close to normal, you'll see their ABI drop dramatically during exercise. Um, there's a couple of ways to do this. We can, you know, we use, uh, you can either put them on a treadmill, um, and, and I, I don't recall if you have a treadmill at, um, Cemetery or not, but there are bedside exercises that you can do very commonly, we just do heel raises. So you just have a patient grab the edge of the gurney and just do um 20 calf raises over a period of 2 minutes and then recheck the ABI and that usually is enough um physiologic stress to, to give you a change um in your pressures. Do we get diagnostic imaging for, um, uh, claudication? Almost never unless we're planning revascularization. So we don't need a CT scan, we don't need an MR, we don't need an angiogram. Um, and the workup, it's really just, um, um, history, risk factor modification. We'll get into all this here, um, um, uh, and an ABI just for, um, confirmation. OK. This is one of my favorite natural history studies. Um, I doubt you can do it. I doubt it would get through an ethics board today, um, but it was, um, uh, a study of patients with claudication, um, from the Manchester Royal Infirmary in the 1940s. Uh, and what they did is they had 1500 patients, um, and they diagnosed, diagnosed them all with angiography. Angiography back then was crazy. It was a direct aortic puncture. They'd take a needle and just right in the back and puncture the aorta blindly. And then fill it with dye and shoot an X-ray. Um, so we know these patients for sure had, um, true claudication, and then they put them on a treadmill every 3 months and they said what would happen. I just want to remind you, and this was in the 1940s, so no aspirin, no statins, no medical therapy available. Um, and the other key difference is, um, how much our populations have changed. Diabetes was only present in 4% of their patients. Um, today, um, it's, you know, in our practice, it's probably closer to, you know, 50%. Um, what happens to a patient with claudication if you just watch them? Well, um, 55% improved. They improved probably because they're putting these patients on treadmills. 35% never changed. Um, 10% had worsening symptoms, but that doesn't mean they lost their limb. Less than 5% of patients progressed to amputation. In the 1940s, no medical therapy. Patients that probably continued to smoke. Um, so, claudication, um, uh, uh, um, is a quality of life problem. Uh, it's not a limb threatening problem. And I think that's one of the key messages we try to drive home to patients. Now, quality of life is important and you know, we do a lot to help people, you know, um, uh, feel better about themselves, um, uh, but we have to understand what the natural history is in order to stage an intervention that is, um, of the appropriate risk-benefit profile. So, um, goals of therapy. Um, two things. Uh, a, um, I didn't put in there, but the risk of cardiac death, um, in that natural history study was something like 20% over six years. Um, so, the goal of therapy is still feed the patient over the limb. It's about risk reduction and preventing coronary events down the road, and then the next stage is functional improvement. Um, you guys are primary care doctors, so I'm not gonna hammer home this point. You know what to do for, um, medical therapy, um, patients with alpha sclerosis, right? Smoking cessation, dyslipidemia, diabetes, hypertension. Um, uh, we now recommend, um, a single agent antiplatelet therapy. These patients are different than the general population, um, because they have some manifestation of atherosclerosis. This is not the same as just the, the general population. This is secondary prevention. Um, and then, what, what else can we do to improve the limb function? So there's 22 things we can do, pharmacotherapy and exercise, 3 things in surgery. We'll go, go through them in that order. Um, so, in the United States, FDA has two medications that have an approval for use in PAD. One is elastazol, the other one is pentafityline rental. Um, Europe also has, uh, naphtidofural. We, we don't have that, but I mean, maybe you've got a patient that gets treatment in Europe and comes to your clinic. They might be on that medication for that. Um, Trental is an old medication. It got it approved by the FDA in 1984. I question whether it would get approved. It had, if it had to go through the, um, uh, investigational new drug process today for lack of efficacy. Um, the idea was it reduced blood viscosity and maybe slowed platelet, platelet aggregation. Um, commonly, patients will have nausea, headaches, drowsiness, and anorexia. More problematically, it can exacerbate hypertension. Um, I still see patients on Trental that come to our clinic every once in a while, and our first order of business is largely to discontinue it. Um, some of the early studies showed that there was a clinical benefit, but multiple studies have showed, have failed to show an improved ABI either both resting or exercise while on this medication. And I'm gonna show you one example I'm here coming up. Um, this is a far more effective, and this is a first-line agent for me, um, for, um, a patient who comes in with a new diagnosis of claudication. It's elastazol or Pletal. Um, it's a phosphodiesterase inhibitor and a direct vasodilator. Um, the big issue, um, is, um, patients have symptoms of flushing and you cannot use it in heart failure. Um, so you cannot use this in all the patients that come to you, but in the patients that, um, fall outside of those two scenarios, um, we always will try elastazole as a first-line therapy. Um, and it's been shown to improve maximal pain-free walking distance in as short as 4 weeks of therapy. OK. This is a great um comparative effectiveness trial. This was, um, published in um JAMA I wanna say roughly 2010 or so. Um, randomized placebo-controlled with three arms. Um, uh, there's the elastazol, rental, and placebo. Um, rental and placebo were identical. These are the bottom two lines, so you get no benefit of rental over placebo. Mind you, all patients improved, and this is study effect. Patients being on treadmills, patients being motivated, patients quitting smoking probably, um, but elastazol for sure had documented improvements in, um, treadmill testing up to 6 months, um, on, on that regimen. So, um, if the patient can tolerate it and there's no contraindication to its use, um, it's a good way, um, to get a little bump in functional, um, improvement, um, with the pharmacotherapy. Um, other things that have been shown to work, this one's interesting, ramipril. Um, uh, this is, um, a randomized placebo-controlled trial, um, 200 patients getting ramipril with significant improvements in pre-free, uh, maximal treadmill walking times. Um, so, uh, what we typically tell, um, our colleagues in, you know, internal medicine and primary care is to consider an ACE inhibitor as a first light agent in treatment of hypertension in patients with PAD cause you might be able to kill two birds with one stone with this medication. Um, and then of course, uh, nephtudofuryl oxidate, not available in the United States, um, but also been shown to increase, um, walking times on treadmill. OK, what about exercise? So, uh, we say exercise, but what, what do we mean by exercise? We really mean just light exercise, light aerobic exercise, walking, basically. Uh, and there's lots of evidence of the biomechanical and biochemical changes that happen when you apply light exercise to the vasculature. Um, uh, and it's not purely, um, a, a mechanical issue. For sure, you can remodel the collateral vessels around an occlusion, but it is also an issue of, um, tissues being much more efficient in extracting oxygen due metabolic exchange. You see this in the performance athletes all the time, you know, they might have, you know, they might develop, uh, um, with very high intensity training, they might develop lactic acidosis at a certain threshold, but with just vigorous training, they can extend that over time. So, same applies to Um, you know, a patient in their 60s with claudication. Um, what is, um, the right exercise? It's been studied extensively. Walking is the best, superior to cycling, um, although we use cycling sometimes, um, stair climbing, um, uh, uh, uh, weight training, um, upper arm exercise, etc. So we're not asking for a lot, we're just asking for a walking program. A low-intensity looks like it works just as much as high-intensity. And the key threshold that's been established is your walking session must be 30 minutes, 3 times a week. If you exceed that, you're gonna start really seeing the benefits of a walking program. Um, if you're below that, you're not gonna get as much out of it as you could. Um, when we say walking for 30 minutes, a lot of these patients, claudicants, can't walk for 30 minutes without pain. Um, we reinforce, um, uh, it's, um, OK to stop when you have pain. Uh, A, you're not doing any damage by experiencing pain. Uh, let the pain go away and resume walking and just try to make the total time walked 30 minutes. And over time, they'll see an improvement. Um, Turns out it's um difficult to get people to adhere to a walking program. There are a number of apps that are available that can be downloaded. Um, uh, there are services, um, phone-based services for coaching, basically. Um, a supervised exercise program has been shown to be far more effective. That's when a patient comes to a center and literally has, you know, in this case, a physician coach who is making sure that there's adherence to the program. If they do that, then you really garner all the benefit out of that. Supervised exercise programs are now reimbursed by Medicare. Unfortunately for us, there's not a lot of options in the Bay Area and we've been trying to work with um Mills Peninsula um down in Burlingame to be able to um structure a program for that. Um, SET, excuse me, um, for supervised exercise. Um, who do we offer procedures to? Remember, it's a quality of life issue. Um, uh, the fate of the limb is relatively benign. You really want to target people with a pretty profound functional impairment that is impacting their daily living. I will say, um, more often than not, when we see somebody, we say let's try, uh, pharmacotherapy, risk factor modification, exercise program for 3 months, and let's, and then we'll discuss a procedure if you're still not happy. 3 out of 4 patients are happy and they're not interested in having a procedure. Um, uh, as a profession. Uh, we also realized that, you know, in these minimally invasive interventions, there's a really limited durability. And so you want to choose patients with the right anatomy so that the risk-benefit profile really match. Um, so basically, procedures where you'll know you'll get a sustained benefit, um, over at least 2 years. Uh, otherwise, you're probably not doing anybody any favors by doing multiple interventions to keep a stent open without any real significant functional improvement. OK. Let's skip this. OK, so, another excellent, um, comparative effectiveness trial, randomized trial looking at optimal medical therapy, supervised exercise program, and, um, stenting. And it, um, this study got um a lot of praise because it addressed all the other studies that showed the same thing but had some criticisms. Basically, they cherry-picked the patients that were gonna do the best with a percutaneous intervention with a stent. So they, so that was, you know, just to help um um silence the criticism of the studies before them. And then um they looked at the um optimal medical therapy in this, in this case with the um um statin, uh 81 mg of aspirin and then a supervised exercise program. Both arms got optimal medical therapy. One arm was exercise, one arm was revascularization. And then they did two things, um, uh, tread, treadmill testing because you have really objective evidence of what happened, um, and then secondary endpoints like quality of life and uh the more subjective stuff. Uh, and these are the key results. Um, the panel here on the left is peak walking time. The green line is supervised exercise, red line is a stent, uh, blue line is just the medical therapy. So, everyone did a little bit better at 6 months, but the walking program outperformed the stenting and even though, um, the trial, uh, the supervised exercise program was only for 24 weeks, the results persisted over a year beyond when the study concluded. Um, more so than you what you got with the percutaneous revascularization with the stent. Um, and then, um, this is claudication onset time. Um, so the claudication onset time, you know, both groups did well. It tells you that the stent group, you know, had effective revascularization. They were able to, um, uh, you know, walk without onset of symptoms, but it's the behavior modification and the walking, and when you had patients with pedometers, even the patients that got stents, very few actually went out and were actively walking more. Um, so there's that component as well, uh, the behavior modification that goes with, um, uh, um, supervised exercise. Um, so, you know, that's why the first-line therapy now for patients with claudication is, um, risk factor modification, optimum medical therapy, and supervised exercise. We'll try that for 3 months and then we'll reassess. Um, And here it is in, in text, textual format. OK. And then the last thing I wanna say here is um limb-threatening ischemia, which is the majority of our practice and something probably very um few primary care doctors have to see frequently, but it is a time when an urgent referral is actually, actually um necessary, um, because Uh, this is where time is tissue and patients really face, um, amputation. It used to be called critical limb ischemia. We've moved away from using that terminology. Now we call it chronic limb-threatening ischemia. Uh, and what it looks like is an ulceration, which oftentimes is mistaken for a little trauma from their shoe. Um, rest pain, which is dependent rhubar that oftentimes gets mistaken for cellulitis, and more obviously, a gangrenous toe. Um, and just to give you an idea what this looks like by pictures, um, I can't tell you how many times this picture on the left, um, will, will go to the ED with a painful foot, um, and we'll get placed on a course of antibiotics. It won't get better, a new course of antibiotics, and it won't be until their 3rd effort where they say, well, you know, the pulse here is normal, let's refer them to a vascular surgeon. Um, so this is, um, uh, um, dependent rhubar. Uh, unlike cellulitis, when you elevate this leg, it will blanch immediately. So what this is, is, you know, the tissues are so starved, there's, um, uh, basically vasodilation, maximal vasodilation in order to increase the profusion even just a little bit. Um, it's trying to compensate for, um, ischemia, uh, in the foot and, um, obviously once you elevate it and the pressure gradient, um, changes it, it totally goes away. And then this image here on the left is an ischemic ulcer, and again, this is um, uh, pretty mild physical exam finding. Um, they're typically very painful. Um, oftentimes diabetics still have neuropathy and are insensate. So you, so you, you just have to, unfortunately, take the sock off and look at the foot and make a, make a, um, uh, uh diagnosis by exam. Um, this is a real big problem. Um, this is a curve of mortality, and the annual mortality is, um, roughly 15%. This is a big randomized trial from about 15 years ago looking at bypass versus balloon angioplasty. Um, again, this kind of speaks to the burden of atherosclerosis that these patients have, that it's a systemic problem, uh, and these patients are often near end of life due to cardiovascular morbidity and mortality. Um, uh, these patients will have classically severe pain if they're not diabetic, that's unrelenting and very difficult to treat with medical therapy. Um, you really need effective revascularization to address the pain issue. Um, you know, your skin protects you from the outside environment. Um, when you have these chronic open wounds, um, bacteria can come in and give you an infection, particularly in diabetics, and that's the pathophysiology of limb loss and diabetes. It's the ulceration that lets, um, the medics for infection. Developed. Um, and these patients often have loss of ambulatory function, deterioration in their functional status, um, that, uh, kind of compound the cardiopulmonary, uh, manifestations of their underlying disease. Um, the risk of amputation is roughly 20%, um, in the 1st 6 months unless you do one of three things, effective revascularization, um, hopefully not amputation, although some patients that's the right answer. Uh, and patients that are really at end of life, um, we seek, uh, more of a palliative wound care kind of option. Um, That's largely what I have. I think we kind of came in right on the, just, just under the time limit. Um, uh, again, um, we treat lots of things, but certainly happy to, um, uh, take all your PAD referrals that you feel are critical.
