Kendal Williams, MD (Host): Welcome everyone to the Penn Primary Care Podcast. I'm your host, Dr. Kendal Williams. So, the number one cause of death in the world is a condition known as atherosclerotic cardiovascular disease. It is the cause of heart attacks and strokes, the number one reason people die. Forty percent of people in the world will die of this. And much of our efforts, therefore, in the primary care clinic, are spent towards identifying people who are at risk and managing those risk factors. And we've talked about those issues in prior podcasts. What we haven't talked about is the management of folks who already have significant atherosclerotic cardiovascular disease, who have coronary artery disease, so disease specifically in their coronary arteries.

And in order to do that, I brought on two experts at Penn who've really devoted their careers to this phenomenon. Dr. Dan Kolansky is a Professor of Cardiology, Professor of Medicine here at Penn. He is the Associate Chief of Clinical Affairs in Cardiovascular Medicine. He is the Director of the Cardiac Intensive Care Unit at HUP. Dr. Kolansky, honored to have you on.

Daniel Kolansky, MD: Kendal, thanks. It's a pleasure to be here to talk about one of my favorite topics, which is coronary heart disease prevention and treatment, what we can do to identify it. So glad to be part of it.

Host: With us also is Maureen Julien. Maureen is a nurse practitioner at Penn. She's an NP in Cardiology. She's worked very closely with Dr. Kolansky, has a vast knowledge of this area and works with patients every day. Maureen, thank you for being here.

Maureen Julien, NP: Thank you for having me. I'm excited to join Dan and represent the voice of advanced practice.

Host: And many of our listeners are advanced practitioners. And let's start with a very basic question, and that is what's happening in the human body when people are developing cholesterol plaque that may then lead to the blockage of their arteries? Dan, what's happening in that process?

Daniel Kolansky, MD: Yes, Kendal. So, we call this, as you said, atherosclerotic heart disease or coronary heart disease. And as you said, it is the leading cause of death worldwide. We had a nice phenomenon where that trend was decreasing a little bit. But then, in the last few years, we've actually seen it increasing again, there's some concern about that. There may be some relationship to COVID, whether it's inflammation or changes in people going to physicians and practices. But nonetheless, it is a concerning uptick. So, coronary heart disease or atherosclerotic heart disease is a buildup of plaque, generally chronically, but sometimes acutely in the coronary arteries, leading to insufficient blood supply, lack of blood supply to certain areas of the heart, leading to symptoms of such coronary insufficiency, which are angina, shortness of breath, sometimes exertional fatigue, and also being a risk factor for the development of heart disease. And so, that's it in a nutshell.

We often look at this in two sort of large buckets, one being the acute presentation, so patients who present to the hospital or to the clinic with unstable angina, or acute myocardial infarction, and we can get into that a little bit later. But the second big bucket is those with chronic coronary artery disease, and they may present either symptomatically or even asymptomatically. And I think that's a large group of patients and people that the primary care group is seeing and needs to evaluate, and we need to look for those folks and identify them because of risk factors, and then to work on strategies for both prevention, treatment, and even detection of coronary disease.

Host: One of the analogies I give to patients is this is like rust in cars. You know, a lot of cars are going to develop rust over time. It's kind of a natural process in a sense. But, you know, you want to keep it from killing the car, right? And so, you have to control it. Dan, I actually want to go down because I have some questions to just about cholesterol plaque itself.

Let's go from a clean, pure artery, completely unblemished, and somebody starts to build up cholesterol plaque. And then, take us through what can happen to that plaque. And then, eventually, of course, it begins to calcify and harden and so forth. But I want to spend a few minutes just on that plaque itself and how that develops and how it evolves.

Daniel Kolansky, MD: Sure. So, it's a really interesting and good question. So, it's the basis for atherosclerotic heart disease. So, plaque develops, and we've known for decades now that it happens early in life. There were autopsy studies decades ago, even from the Korean War, showing that 18, 20-year-olds began to have fatty streaks in the coronary arteries. And while those are not obstructive in any way, they're the precursors for what develops ultimately as a coronary obstruction. And so, those fatty streaks over many years can develop into a minor or modest obstruction. We talk about either on an angiogram, something that we call sort of luminal irregularities or mild plaque. And I think what we're really talking about is, you know, 10%, 20%, 30% narrowings in the arteries, clearly not enough to obstruct blood flow to the point of giving symptoms.

But as you wisely get at, what happens to that plaque? So, there's a couple of courses it can take. It can hopefully be arrested or interrupted if we get to the right preventive therapies, and we'll spend some time on that tonight having to do with lipid management and blood pressure management. The plaque can slowly progress and become now 50%, 70%, 90% narrowings and it becomes more fibrotic, harder, perhaps more calcified, and patients begin to experience typical anginal type symptoms. Or finally, it can result in a plaque rupture. And that plaque rupture is really what is accounting for the acute myocardial symptoms. And when we say plaque rupture, it doesn't have to be the 90% blockage at all. In fact, it's more likely to be the non-critical blockage, 50%, 40% narrowing, where suddenly because of blood pressure or other stresses, that plaque becomes exposed to all the sticky things in the blood. So, the platelets begin to adhere and aggregate and form a thrombus. And then, that thrombotic occlusion can be subacute, maybe 95% causing angina and unstable angina, or 100%, causing an acute ST elevation MI, the sort of feared complication, which is a total occlusion of the blood vessel, which needs prompt intervention. So, that's what can happen to the plaque from a big picture, either slow progression or an acute obstruction.

One more thing to throw out there is that some of that slow progression, if it continues over a long term, can result in a silent occlusion of a vessel, something that we call often a chronic total occlusion or a CTO. And that may be identified later in its course with angiography or CT scans and represent a silent occlusion or a silent myocardial infarction. So, big spectrum of what can happen and that's why we need to get on this early and treat with preventive therapies and ultimately with other therapies.

Host: I think it was a revelation to me to recognize that it wasn't simply the slow buildup of plaque, progressively blocking the vessel, but that you could go from 40% and get this plaque rupture that was dramatic. Now, I have this idea in my head that fresher plaque is a little bit more unstable and more dangerous as opposed to more fibrotic calcified plaque, and we're going to talk about calcium scores in a minute. So, I'm constantly having this conversation with patients about the significance of their calcium score. And one of the things I tell them is, you know, the calcification process is actually kind of a good thing. So, is that correct, Dan?

Daniel Kolansky, MD: Yes, that is correct. So, just to restate, you're exactly right. And Maureen and I, in our practice, deal with this frequently, that the idea is that some of the softer plaque that is not being modified, perhaps with appropriate medical therapies, is at more risk of plaque rupture. So, in some cases, we worry a little bit more about the patient with a lot of risk factors, diabetic, hyperlipidemia, soft plaque, 30-40% plaque, and they're at risk for plaque rupture and acute coronary syndromes, whereas calcified plaque, fibrotic plaque, may become something that results in long-term anginal symptoms or insufficiency because of a high-grade obstruction, but maybe less prone to the acute myocardial infarction.

So, I think that idea is correct, and it's an important one. It's hard to get your hands around because patients and people see their CT scans and their scores and say, "Gee, I've got a 70% calcified plaque. I'm at risk for everything falling apart." And while they're certainly at risk, it may not be the same way that they're thinking about the risk.

Maureen Julien, NP: You know, plaque rupture is one of the ways that I talk to my patients about statin therapy. Soft plaque is a risk for plaque rupture. And statins lower cholesterol numbers, which is great. And we know the lower the LDL, the better. However, it also helps to harden and calcify the plaque that you have there. And it kind of smooths it out. And I explained to patients, now you are at less risk of plaque rupture and what we're trying to prevent is a big heart attack. I do get a lot of buy in when I'm able to explain it to patients like that.

Host: I read an article a couple of years ago that said that that process of plaque stabilization when you're on a statin happens in about a month or two. That within that period of time, you've stabilized your plaque to the point where at least it's a little bit less risky than it was before. Does that sound right?

Maureen Julien, NP: Sounds about right. And the other thing that unstabilizes plaque can be tobacco. Smoking, you know, makes the plaque more porous and can be more set up for plaque rupture. So, I also try to sell that when asking people to, you know, quit smoking.

Daniel Kolansky, MD: That's all absolutely right. And, you know, interestingly, there have been some studies with the early initiation of high-dose statin therapy after an acute coronary syndrome, and it does tend to help prognostically. And so, I think that idea of early plaque stabilization by high dose statins is a real concept. And so, yes, we encourage that, both in the acute coronary syndromes, but also in the office with soft plaque.

Host: I think we've seen the same thing in stroke as well, that 80 milligrams of Lipitor started in the hospital. It was a SPARCL trial. I may have that wrong. But, you know, it showed that, within the month, the next month, that stroke risk was reduced. And that's obviously dealing with the same process, it's just a different organ. I don't want to spend too much time on plaque, but this is the root of the whole thing. And I think understanding this plaque itself is very important to this.

But I actually wanted to ask about hypertension because, Maureen, you had mentioned smoking. We know that diabetes is a risk factor for plaque development. You know, high cholesterol is also a risk factor for plaque development. But hypertension, from my understanding, it's an independent predictor, if you will, or independent cause of plaque formation. Is it that it causes stress on the vessel? Do we know why?

Daniel Kolansky, MD: Yeah. I think that we do believe that it causes sheer stress on the blood vessels and leads to increased plaque formation. And so, it's critically important to treat hypertension for the plaque aspects. There's also the cardiovascular demand aspects of hypertension and the development of left ventricular hypertrophy from hypertension that also plays a role.

So, I think, Kendal, to your point, when Maureen and I see a patient in the office, and we do a lot of what people might call just preventive cardiology, but it's all in the same realm of atherosclerotic coronary vascular disease, we go through that checklist of four or five things with every single patient. So, we ask about family history and therefore the genetics that underlie this. And there are certainly people who are more prone to this than others. And we don't entirely understand the genetics, but there's a lot of interesting work being done on that. And we check on hypertension. Obviously, we talk about lipids. We talk about diabetes. smoking, and the last one being exercise. So, we go through that checklist in nearly every patient that we're seeing who's at risk for or who has coronary disease. And I think for the primary care physicians and practitioners out there, you know, that's the things to run through in every office visit to make sure that those are being adequately thought about and treated.

Host: So, we're going to go through a stepwise approach to evaluating the types of patients that we see. We're going to actually start with the asymptomatic, and then we'll talk about the stable and then the unstable. And then, give you all a peek of what happens in the cath lab. So, I think that, as a primary care physician, the most common scenario that I see is I have a patient, I've identified them potentially at risk for atherosclerotic disease, I'm trying to decide on, whether I should start a statin off, and then I get a coronary calcium score. And that comes back and, you know, if it's elevated, over a hundred, then I know there's significant, potential coronary artery disease there, and then I may be dealing with a patient who's asymptomatic but at risk. Maureen, how do you look at these coronary calcium scores in your practice?

Maureen Julien, NP: Sure. We use them a lot. We use it for risk stratification, you know, in patients who are coming looking for opinions about their risk. And a lot of times, we have patients coming with that result in hand. The majority of those patients, like you said, are asymptomatic. Any score outside of zero is actually abnormal. And we tend, you know, to have a discussion about that and tend to be aggressive in our lipid-lowering and statin use, even for lower calcium scores. But certainly, you know, greater than a hundred and then over 300, certainly at higher risk in the short term, three to five years of a myocardial infarction or stroke.

That's good, hard data that helps patients to understand risk. That score can be used with the Astro-CHARM score app calculator and can help give you a risk score over 10 years. That can also be helpful in conversations with patients. You know, I would say almost everybody who comes with an elevated calcium score, whether it's one or a thousand, we're talking about statin therapy in our practice.

What to do when it is very elevated, certainly when you're over a hundred, and certainly as you approach, you know, the thousands, we do think even in asymptomatic patients, we really should rule out left main and proximal triple vessel disease. So, a stress test in some form is usually where we will go. I don't know if we want to go down the vein of stress testing.

Host: Yeah. No, that's a good thing. So, here's how I do this. If it's under a hundred, I start people on a statin. But if they're not having any symptoms, I don't do anything. If it's over 300, I refer them to you or one of your colleagues with the intention and the expectation that they're probably going to get a stress test to determine. And then, the 100 to 300 folks, it's kind of a mix, I suppose. Is that how you do it? Do you stress everybody who's over 300, is my question.

Daniel Kolansky, MD: So, I think that's a really good approach, as we just discussed. Any elevation is abnormal and warrants treatment. Above some moderate number like 300, we do stress people. Now, if they're very active and physically fit and don't have any symptoms, you might not do a stress test and follow them and consider them just a higher risk individual, or we might, for reassurance, proceed with a stress test. And sometimes with an alternative that we can talk about at some point, which would be a coronary CTA, to give us some information about anatomy. But I think a stress test is the starting point for most of these patients who have moderately elevated risk.

Host: We want to get into stress tests, but I have a question here. If you put somebody on a high-dose statin, say you do 20 of Crestor or 40 of Lipitor or 80 of Lipitor, what is your expectation to happen to that patient? Because we talked about that within that one to two months, they're going to get some plaque stabilization. We know that statins alone lower the risk of MI. You can correct me on this, about 30-40%, something like that. In my folks that I get on statins, of course, I have a limited sample size, they almost never go in for an MI, they never get any problems, they always do well. Of course, you're seeing a different population, you're seeing folks who get on high-dose statins and maybe still have an MI, but what is your expectation about the power of those statins, practically?

Maureen Julien, NP: I mean, my expectation is lowering that LDL, you know, by 50% with that first dose. And then, I'm going to escalate it to, you know, in most of my patients try to get down to an LDL in the 50s if, you know, I'm worried about them and they do have some risk, like an elevated calcium score.

I think you're right. I think we're talking about two different populations. We don't get as many patients coming into Cardiology, you know, with no risk factors and no known coronary disease. Anecdotally, I can say in our practice, we've had patients with bad family history. So, you know, it can still happen, but we do the best we can for the greater good by using the best data that we know. And that's lowering that LDL as low as possible.

Daniel Kolansky, MD: Yeah, I totally agree with that. And well said, and I think it also brings up the question of how low to go. And so, that coronary calcium scan that you just talked about tells us that going back to first principles, that these people have plaque, and it's been accumulating since whatever age. And so, the lower the better for the LDL cholesterol. We have traditionally followed guidelines that talk about the definition of coronary disease. And once you have plaques, we sort of call that a coronary disease equivalent. You have the disease. And so, we really want to treat to the coronary disease guidelines. And those have traditionally been less than 70 or, the European guidelines, less than 55. And I think with all of our modalities, we really want to try to get patients into that lower zone, acknowledging that you get the most bang for the buck with that initial treatment with a statin and dropping it perhaps 40%, 50%. But there may be continued benefit by lowering that cholesterol even further.

Host: We talked about stress testing a little bit. And Dan and I, you and I were talking about in sort of our prep meeting for this podcast that we may want to come back and do a whole podcast on stress testing and cardiac imaging, but there has been a sea change in the last few years that we should at least bring up, and that is really the development of coronary CTA. Let me just tell you what I understand of this, and I'll start off of our conversation and then you could correct me.

Stress testing, you're going to pick up blockages that are 70% or greater. But as you noted, the plaques that are 40-70% percent are potentially just as risky, but you won't necessarily pick those up on the stress test. So if you're trying to determine the risk of this patient in front of you, we often think about doing stress tests when we're working up chest pain, but that's not really the question we're at, especially in this circumstance. You're trying to figure out what's their risk in the next year, especially maybe somebody you're just doing it because their coronary calcium score is 350. My understanding is that's where coronary CTA has really helped, is that it's helped us identify folks that are in this 40-70% range. We can still see the 70% plus folks on that scan, but that we're also identifying this whole group of folks that have submaximal, if you will, plaque blockage, but enough that they could be a bit damaging.

Daniel Kolansky, MD: Sure. I think that's a really good way to have set that up. To add a little bit of color to that, you know, the stress test is one of the tools, and we'll get back to this when we get to the cath lab, that helps identify physiology, right? So, the physiology of coronary heart disease is something that we're always excited about. And it tells us with exertion or with activity is the degree of stenosis present likely to be causing ischemia, likely to be causing lack of sufficient blood supply to the active cardiac muscle. And so, stress tests help in the physiology, and they help also in the exercise portion of physiology. In other words, does somebody have symptoms with exercise? So, we use that as part of the tool.

But you're right, CTA, in its pure state of just looking at the vessels, tells us a lot about the presence of plaque and does the patient, the person have mild, moderate, or severe plaque. And that's going to color how you approach their treatment. When you find somebody who has two or three vessels with 40-50% narrowing and is asymptomatic, you'll likely say, "Well, they don't need a cardiac catheterization and a stent, but they sure should be considered for the maximally aggressive secondary prevention that we can do." And that's going to include not only the statins and cholesterol lowering, but aspirin, antiplatelet agents, all of the things that we think are very helpful in secondary prevention. So, we put the patient into the bucket now of having asymptomatic, moderate coronary disease. And we should do everything we can for secondary prevention and prevention of plaque rupture and plaque progression.

Host: Maureen, if I send my patient to you with a calcium score of 367, they're not symptomatic, they're not a high exerciser though. They walk their dog. Are you going to send that patient for a stress test or a CTA? And how do you make that decision?

Maureen Julien, NP: Yeah. I mean, I think I would have a discussion with the patient. I really do like stress testing. I think it really gives you a lot of good information, like Dan was saying about patient's activity level and when they're pushed beyond just walking the dog, what really is going on there. You know, a lot of times we have patients who come with shortness of breath, which is a harder symptom sometimes to tease out. And you may find that patients are just deconditioned and they really just aren't able to exercise to a good level. And it's really deconditioning and not really coronary artery disease that's driving their symptoms.

So with 367, with walking a dog, mildly active, I would stress them because I want to know what they're doing on the treadmill and get that information. If the stress test turned out positive, then, you know, we're at the crossroads of a CTA versus a cardiac cath.

Host: Is there a situation where that asymptomatic patient, you might go directly for CTA? So, let me give you an example. I have a patient, she's 62. She exercises all the time. The calcium score was really high. We don't really know why because everything else about it is good. Stress testing her is actually going to be a little bit of a problem. It might get hard to get her heart rate up because she's actually pretty fit. So, that might be a situation where I might think I would just go right to CTA, just so I want to get to know how much disease she has. But is there any other scenarios where you might go right to CTA?

Daniel Kolansky, MD: I think that's a really good one. Whenever there's ambiguity as well, patients have had some symptoms that we can't really get our arms around. That might be another helpful scenario. We, in our practice within the last year, have had two patients that one of whom had a negative stress test, but had some funny symptoms and a high calcium score.

And sure enough, the CTA led us to very high-grade proximal disease. And we've had a couple of patients like that. So, I think if you're trying to identify, again, it's interesting. This is really, Kendal, an evolving area. So, you're in the cusp here and you're out in front. There have been a couple of big European studies now that have suggested that the early identification using CTA as a first modality in such patients leads to better outcomes.

So, you might ask, well, why? It doesn't cure anything. And I think part of it is that when you identify 30%, 40%, 50% narrowing, you're much more likely to get on to aspirin and to anti-lipid agents. And that's in fact what was shown in the European studies, so that you're ultimately getting to a much faster treatment effect when you start with a CTA.

So, I think you're right on the cutting edge of what's being done. We used to use it primarily to rule in or out coronary disease in low-risk patients, primarily in the emergency department settings. And you're familiar with that. You've seen patients go to the ER. They have some atypical chest pain. They can get a CTA in 30 or 60 minutes, there's no obstructive disease, home they go, and that's great. But now, it's become more sophisticated, and so we do use it in settings like that.

Host: So, that's the asymptomatic population. And the symptomatic population are going to present with chest pain, chest discomfort, chest discomfort with exertion, shortness of breath, and so forth. And, you know, traditionally, we've divided those into stable versus unstable angina versus NSTEMI versus STEMI. I think one of those categories may be sort of fading away.

The stable folks are the folks that have predictable chest pain with a certain level of exertion, and you're comfortable that it's stable. The NSTEMI folks are people who present with non-ST elevations MI, maybe it's better to talk about the STEMI people first because the others are just the NSTEMI, who have troponin rises and symptoms. And so, those are if they have ST elevation MI or ST elevations, they're in ST elevation MI. If they're not, they're NSTEMI. Now, the other category I learned was unstable angina, but with increasing sensitivity of troponins, does that category even exist anymore, Dan?

Daniel Kolansky, MD: It does, Kendal. So, what we're talking about is just to put a little information around this is the high-sensitivity troponins, which over the last five, six years have replaced the traditional troponins. And they will pick up any degree of mild myocardial cell stress and damage. So, there are many scenarios where you can have what's referred to as myocardial injury without really being an MI. And that can come from a variety of cardiac stresses. So, hypertensive crisis, congestive heart failure with an exacerbation, certainly in people who have some degree of renal insufficiency and they don't clear the troponins as easily, all those will yield a mild or modest elevation in troponin. And we have to be careful not to lump all of those into an acute MI category. We don't see this so much in the office, in the primary care group, but we do in the emergency department and in the hospital. But nonetheless, we know and your folks will see this that if a patient comes in with chest pain, there are now rapid rule-out protocols. So, one-hour negative high-sensitivity troponin or over three hours that are negative, that can rule a patient out from the acute syndrome and then, get out of the hospital, out of the ER, and can work them up appropriately.

The ones with the moderate elevation, it comes back to first principles. What are the symptoms really doing? Is it the patient that you're suspicious, right? They do have some risk factors. They're a diabetic. They have some atypical but ongoing symptoms with exertion. They're recent, they're progressive, they have a little bit of a high-sensitivity troponin rise. That's the unstable angina, we can call it a non-ST elevation MI. Probably the best term for that is the acute coronary syndrome. Somebody where there is probably some degree of plaque rupture or thrombosis going on and having chest discomfort, maybe a high-grade stenosis, and those people need attention.

Host: Let's talk about the NSTEMI folks. These are the folks that come with symptoms. They have a troponin rise. They're not an ST elevation MI. Actually, just back up and frame this, Dan, of, you know, who's going to end up in your cath lab? Well, the STEMI folks are going to your cath lab, so we don't really need to talk about them anymore. It's the NSTEMI folks and the stable folks that we have some confusion about. So when do you cath the NSTEMI folks? What is driving that decision?

Daniel Kolansky, MD: Right. So, we've switched gears a little bit now from maybe the office population to somebody where they've called the office and said, I've been having symptoms for a couple of days and you say you better get to the emergency department because we don't want to miss an acute coronary syndrome. So, they show up now and they are in acute coronary syndrome. They have a little troponin rise or certainly progressive symptoms. The truth is that the majority of those patients in the U.S. in our current care do make their way to the cath lab.

Now, you have to frame it. You have to ask the question, is it, are they appropriate for cath and intervention, or should we start with a little bit of medical therapy? So, all those patients get an antiplatelet agent, perhaps a beta blocker or two, decrease their cardiovascular demand, maybe they get an anticoagulant for the first 24 hours. And if they completely cool off and they don't have high risk features like ongoing symptoms or ST depressions on ECG, and they have normal LV function on an echo, well, they might go into the lower risk category, but still acute coronary syndromes. So, there may be some who you will defer a cath. You know, in the old days, we would sort of maybe give them a couple days and then do a stress test. And only if that was positive, go to the cath lab. I think these days we much more frequently go earlier to the cath lab, try to identify high-risk plaque knowing that we can potentially treat it with coronary stenting revascularization or exclude it and then just get them onto the appropriate medical therapy.

Host: Is there a role for CTA in this situation where you're trying to decide that they need a diagnostic cath?

Daniel Kolansky, MD: So, I think in the acute setting, unless you're really trying to rule in or out, like you're just not sure, is this coronary disease or is this hiatal hernia or musculoskeletal or something else? That's where it's helpful. If you've convinced yourself that there's a high probability that this is coronary disease and that there's troponins and/or EKG changes involved, then I don't think a CTA adds very much because you're going to get that information from a coronary angiogram in the cath lab. In the outpatient setting, as we've talked about, there are lots of reasons where you could do a CTA. And in the low-risk patient with chest pain, I think is another good area to do that in.

Host: Yeah, Dan, the last one I want to talk about is these stable folks, and I actually share at least one patient with you, an older gentleman who appears to have stable angina. I think he's in his 90s. And I'm always, "When should we cath them? Should we cath them? And I know that's the decision you go back and forth with, but your tolerance of risk is greater than mine, you know, I think. Because I always want to say, "Well, let's just open that vessel and get rid of this problem." But what about that stable patient?

Daniel Kolansky, MD: I think, Kendal, it goes back to the first things that you brought up on this podcast, which is what's the nature of this coronary disease? So, you've decided it's not a plaque rupture, it's not an acute problem, but it's perhaps a chronic or progressive problem. And then, we get to how much can medications relieve the symptoms, and also is this causing other problems? Is there a deterioration in left ventricular function? Is there shortness of breath and congestive heart failure? Those are higher risk features that would make us go for an intervention.

Somebody who has mild chronic symptoms that are reliably controlled with medications, you're right, we have a little bit of tolerance. But we certainly want to help patients feel better. Now, the kind of scenario you brought up, we also have to balance risks, right? Now, there's not a lot of risk with our interventions in the hospital or in the outpatient cath lab. But there's nothing we do in medicine that doesn't carry some risk when it comes to invasive therapies. So, we look at renal function, we look at age, we look at vascular disease, we look at stroke risk, and we try to balance that. And we'll see if he does need another cath in his mid to late '90s or not. That would certainly be something we wouldn't have considered decades ago. But I think the field has expanded and we're all about, you know, helping people live a fulfilling life with less pain and less risk. So if that's appropriate and there's good conversation with the patient and his or her loved ones about it and about the risks, then we're willing to consider that as well.

Maureen Julien, NP: I think that's the important point with this, with chronic stable angina, is that it really is about their symptoms and quality of life. It's not a life-saving procedure. So, really having that shared decision-making discussion. And if the patient is risk-averse and content with their quality of life and, you know, using nitroglycerin PRN, sometimes that's an okay place to stop.

Host: Do you sometimes think in your head, listen, I've had this person on a high-dose statin for 10 years, I can see there's this very heavily calcified plaque, it's a stable situation. Is that kind of something that goes into it? It's all calcified basically, so less risky situation.

Maureen Julien, NP: Yeah. I guess we can never really know, you know, what plaque will turn into a plaque rupture. But as we've talked about the softer plaques that haven't been treated are the higher risk. But, you know, there's entire conferences called the Vulnerable Plaque, people talking about how can you anticipate which plaque, you know, will become unstable.

Host: So most of us, we'll never get into the cath lab. I had an opportunity when I was a medical student actually rotating with Dr. Kolansky, I think. But I will probably never get there again. So, what happens behind that door, behind those curtains is really a mystery to me, Dan. And so, I actually want to spend a little time, because I think we're all very interested in what goes on, and how you get these vessels open, the various tools you use, and the challenges you face. Can you just take us into the cath lab for a typical case, and what happens?

Daniel Kolansky, MD: Sure. I'd love to. Maureen can add a little bit of the flavor of how the patients are handled in the pre and post procedure areas as well, which is important, to your audience. So in the cath lab, we have the great privilege of doing both diagnostic and at times therapeutic work to really help patients, and diagnostic catheterization. And we're here pretty much focused on coronary disease, so we'll skip the valvular stuff for now. We can always come back to that. But the coronary disease diagnosis, we do get a pretty definitive diagnosis from an angiogram. So, how do we accomplish that? You know, as you went through this and perhaps some of the older members of the group, you remember femoral access and lots of bleeding and that kind of concern. Things have gotten better over the last 20 years. Probably the great majority of our access is through the radial artery. It's smaller, it's less prone to bleeding, and consistently patients prefer that. And patients typically come in and say, "Can you use my wrist for the catheterization? And the answer is generally yes. There are obviously a number of occasions when we can't, the vessel size is incorrect for us, or there's tortuosity, or there are other reasons that patients can't use a radial approach, in which case we use a femoral approach, and I think that's improved as well, and there's less bleeding and pain and complication.

So, patients come in, and we generally look at it as an outpatient procedure. They come in in the morning or the afternoon. And increasingly, there's less focus even on being NPO for 12 hours like there used to be. There's several studies now that have shown that really you can eat up until about two hours before a procedure and the anesthesiologists have bought into that. That prolonged NPO is no longer necessary. Patients come in, we meet and greet them in their patients rooms. We make sure that their labs, their typical labs are okay. We think about things like renal function.

And assuming all that's a go, we typically bring them into the cath lab, give them a little bit of sedation, using agents like Versed and Fentanyl. So, patients are awake, but it's conscious sedation monitored by an experienced nurse, generally safe. Patients are very comfortable. They often say it really wasn't nearly as bad as they expected. Using some local lidocaine, we place a sheath in the radial artery, put our catheters up and take some pictures. That whole thing takes about 20 minutes typically in a good setting. And then, we have diagnostic information. At that point, we make decisions. The easiest, well, probably the easiest is that the arteries are wide open and that there's no obstructive disease. And, patients are happy to hear that they don't need any intervention. We take out the catheter, we put a little pressure dressing over the wrist, give them some fluids and get them home in about two hours. So, that would be one scenario.

Another is that we identify one or another obstructive blockages, and we say this is consistent with that stress test that Dr. Williams ordered a while ago and it shows lateral or anterior or inferior ischemia, and there's an obstructive lesion. And it looks like it's something that we can treat with a balloon and a stent, and we go forward and we can talk more about that and we place a stent.

Sometimes, this is a discussion for They can get a little bit more detail, but sometimes we can do physiology in the cath lab, which is really exciting. So, we do what we call the equivalent of a stress test. We have a couple of modalities for doing that now. The most common is to put a little pressure wire sensor across a narrowing and ask the question in one of these intermediate narrowings that maybe is only 50% or 60%.Is this the cause of this patient's symptoms? And if the indications are positive, like a positive stress test that are consistent with ischemia, we may well go ahead and treat. If, on the other hand, the obstruction does not appear to be severe, and the physiology is negative, we'll stop and say, let's look for some other causes for your symptoms. So, the studies have shown again and again that physiology-guided intervention, whether it's a stress test before, or an FFR measurement in the cath lab yields better results, better long-term outcomes. That's the quick look behind the cath lab curtain. And we can talk about some more things as you're interested.

Host: Well, I want to hover on this physiology aspect because, you know, traditionally, always, the downside of diagnostic catheters, "Oh, you just get anatomical information. That's why you needed the stress to do that." But now, in the cath lab, you're really able to sense whether or not this particular obstruction is causing an actual ischemic situation, right? I guess there could be other things. There are collaterals that can develop. you know, there's, I don't know, the individual muscle tolerance. I don't know exactly what all the factors that may be in this. But, you know, there are things that determine whether that actually is ischemic. And you mentioned FFR, which is fractional flow reserve. What is that, Dan?

Daniel Kolansky, MD: So, the big picture is you're exactly right. The big picture is we're trying to if a particular lesion is resulting in ischemia in a particular territory of the cardiac muscle. And so, fractional flow reserve or FFR was one of the first of the physiologic measurements, and everything else has been a little bit of an offshoot. We now commonly use something called IFR, but it's another version of the same thing to determine whether it meets this narrowing, this intermediate or moderate narrowing, it meets the cutoff to be qualifying as an ischemia-producing lesion.

Interestingly, we even have FFR that can be done now without actually putting a wire down the coronary. So in the cath lab, we have a new system that's appropriate for some, but not all lesions where just using some advanced imaging and physiology, we can take the angiogram through some computer software simulations and give FFR based on angiography alone. And so, that's been a real, really nice advance. It's just one more opportunity we have to get that. And also, we'll talk about CT scans on another podcast hopefully, but FFR has now been applied in the same way to CT scans. So, you can specifically order a CT FFR. And if they find a narrowing, they'll apply the FFR technology.

But back to your question, the big question is how does that help us? Well, it tells us if that narrowing is likely to be causing ischemia or not. If it is, that may well be responsible for the patient's symptoms. And if we can relieve that obstruction, they're going to feel better if it says that it's not producing ischemia, then putting a stent in there may not make them feel better and subject them to whatever the small risk of stenting and its after-effects are.

Host: I had an experience that I think a lot of faculty at Penn have, and that's that they learn from their residents. I don't rotate on Cardiology anymore or Oncology or some of these other things, and the residents come back and talk about these technologies and IFR and, of course, you try to look like you know what they're talking about, then you go read about it. But IVUS, you know, intravascular ultrasound is another tool. I remember a conversation with a resident talking about IVUS and thinking to myself, "What the heck is IVUS?" How are you using intravascular ultrasound?

Daniel Kolansky, MD: That's a great question. So, intravascular ultrasound or IVUS or, more globally, intravascular imaging, because there are a couple of other intravascular imaging techniques. So, the traditional coronary angiogram, it's been around for a long time, uses contrast, outlines the vessel. We can see obstruction, intravascular ultrasound and other intravascular imaging techniques. Look from the inside out and we see not only stenosis, but composition of plaque. And we use it in two ways. We use it to help diagnostically, what's the composition of the plaque, how tight is the narrowing? But we also use it in our therapeutic endeavors. When we place a stent, we very often then follow it with intravascular ultrasound, both before and after, actually, to make sure that we're doing as good a job in expanding the stent and opening the vessel as we can.

So, one practical example is we know that one of the tricky things for a long time in stenting has been if there's a lot of coronary calcification present. We've talked about calcium right from the beginning of this podcast. If the calcium is really heavy, in the plaque that we're treating, it can make it difficult to expand the stent. If you can't fully open the stent, then you're left with a partial narrowing, that's not a good situation. So, how do we get by that? Well, we've always had a lot of tricks to do it, but intravascular ultrasound at least helps to tell us if there's significant calcification there. And then, we may choose a different tool to help open the artery before we finish with a stent.

One of those tools might be currently one of the newer generations is lithotripsy or shockwave, which is Intravascular lithotripsy, just like it has been used for other kinds of calcified areas in the body, to crack the plaque and allow expansion, hopefully safely, and allow us to place a stent. So, those are just examples of tools that we now have, and it makes the procedure more accessible, we think safer, and yields better results long term.

There was an interesting cath lab experience, but what was that all about? So, we think of these as a variety of tools to correct the problem and open the vessel. I would turn to Maureen for a second and just ask her to talk a little bit about the patient experience with the cath and the post-cath management because she's the one that often gets those phone calls. Hey, I was in the cath lab yesterday. What are some of the things that we're thinking about now? And you'll get them in your office practice as well.

Maureen Julien, NP: Yeah. I think a lot of the patients, you know, go through without any sort of complications or complaints I think we get a handful of people who will call with some soreness, tenderness, swelling, at the cath site. And, you know, we talk through that. Sometimes, we'll see them in the office. Most times, we're able to just kind of, you know, follow it and, you know, don't need to do any sort of imaging. If we are concerned, certainly, we bring them in for ultrasound. We want to rule out a pseudoaneurysm or an AV fistula and correct that, if we do find that. I will say, you know, in my 20 plus years dealing with interventional Cardiology, the risk of pseudoaneurysm and AV fistula has dramatically gone down since we've been using radial artery primarily. We certainly don't get as many of the vascular complications as we used to in our earlier days.

If patients are stented, guidelines suggest that patients should go to cardiac rehab. So, that's certainly part of our post-procedure management. Patients who go to cardiac rehab, I tell them, "Do better, live longer." So, that usually is motivation enough for them to do that. You know, they're qualified for 36 sessions, 12 weeks, three times a week. Penn has a facility down at Pennsylvania Hospital. But we certainly use local facilities as well, whatever's convenient so that the patient can get there.

Majority of the patients do really great without a lot of complaints. We see them in the office and hope for a symptom resolution. Sometimes, you know, we have to tease out some kind of post-procedure symptom. Rarely are they related really to a real issue that needs to be addressed, kind of going back to the cath lab. So, yeah, patients generally do really, really well and are back to themselves within two days back to regular work and, you know, whatever exercise they want to be doing.

Host: Then, we're into this whole area of secondary prevention. How can we keep those vessels from clogging back up again, keeping those stents open and so forth. So for that discussion, we're going to have to bring you back, because I was too long-winded in my questions. This is actually too fascinating an area to cover in just one podcast. This is such an important area. It's so much a part of what we do as physicians. As we said, it's the most common cause of death in the world. So, spending a couple of podcasts really going over it is, I think, well worth the time.

Daniel Kolansky, MD: We're game. We'd be delighted. I will say, I think there's a few, there will be some takeaways for the primary care group that we really would like to impart having to do with duration of antiplatelet therapies and which therapies and how aggressive to be with cholesterol-lowering. And there are just so many new-- you know, you've had, Dr. Soffer and others on the podcast, there are so many new approaches to lipid lowering that we incorporate into our practice that we think is just so important. But I think as a primary care physician and primary practitioner, we want to get the word out that lipid-lowering attention to risk factors are important, and antiplatelet therapy is important, and delighted to talk about that, and types of stents, and all the ramifications during part two.

Host: Yeah, that's great. So, this patient we've been following through in this podcast will now come back into our practices, and we'll be sharing them with Cardiology and trying to figure out the best approach moving forward. That's going to be part two.

Thank you everyone for joining the Penn Primary Care Podcast. We'll see you again for part two.

disclaimer: Please note that this podcast is for educational purposes only. For specific questions, please contact your physician, and if an emergency, please call 911 or go to the nearest emergency department.