Transcription
Good morning folks. Uh, this is Dr. Rob Cvis. I'm an addiction doc, and today I have the honor and privilege of, um, just talking with a colleague of mine, Dr. Phil AIA, who is a cardiovascular surgeon. Good morning, Phil. Thanks for taking the time early this morning.
Um, what's interesting, unlike a lot of folks in our space, is that, um, you and I have a lot of parallel synergy. Uh, what separates us is the diaphragm. Uh, I'm a surgeon who started out in bariatric surgery and realized that I could fix weight, but I couldn't really fix why people gained the weight in the first place. And that led me down a pathway of understanding metabolic health. You, in a very similar way, are a surgeon who is a cardiac surgeon or a cardiovascular surgeon, operating on the heart and blood vessels. A large part of your work, I assume, is fixing plaque in blood vessels.
We'll talk about plaque in a second because most people have an imagination of what it is. You and I have held it in our hands, um, and you have walked that backwards, uh, in a brilliant way to say, "Okay, why is this plaque here? What are the more effective strategies to, uh, prevent it, and then to stabilize it, and to reduce the ongoing, uh, uh, production of that plaque?" And in a very similar trend, we've kind of met together at a metabolic interface where we are looking at insulin resistance as a problem. Um, can you walk me down that pathway of how your life has evolved in that regard as a surgeon going backwards, if I can put it that way?
Yeah, sure thing. And it, it is, uh, quite interesting that we've kind of arrived at this same place, you know, essentially trying to keep people off of our operating tables.
Exactly. And, you know, I think, um, uh, similar to you, you know, it's been both a personal and professional journey. Uh, you know, for me, I, uh, going back a decade was, you know, a morbidly obese, pre-diabetic heart surgeon. And I kind of started asking, you know, "How can this be?" You know, we had gone through all the education that we went through, and, um, you know, I was unable to, uh, manage my own health, essentially. And I was following the advice that I had learned to give, and it wasn't working. And I started to also, at the same time, wake up to the fact that, you know, we, we give patients these, these, this advice about how to be healthy: "Eat less, move more," uh, "You know, eat a low-fat diet, manage your cholesterol." In our, in, in the case of my specialty. And it obviously wasn't working for them.
It was working for, it was great for our business.
Well, exactly. I guess it depends on what your goals are ultimately. And we can talk about maybe, uh, the system doesn't have the same goals that the individuals might have.
Exactly. I know smoking and and carbohydrates are your best friends in terms of what you do surgically, certainly. Uh, and so, you know, I started to, through a series of events, you know, uh, really the seminal event for me was, I was at a Society of Thoracic Surgeons meeting, so the biggest meeting of heart and lung surgeons in the country. And Gary Taubes happened to be the guest speaker. Gary had, at that time, just, uh, written "The Case Against Sugar," and, of course, before that, had written "Good Calories, Bad Calories" and "Why We Get Fat." And, you know, Gary talked about those concepts, how it wasn't necessarily the amount of food that we were eating, but the type of food we were eating, and how those specific foods were driving us to eat more food and cause obesity. And, um, you know, and that resonated with me personally. And I, I went on a low-carb diet after, uh, reading Gary's books. And, uh, I had great success losing weight, reversing my pre-diabetes. And then I started asking, you know, "Why did I hear about this from a journalist?" And that's not a knock on Gary in any way, uh, but here we are, had gone through all this education, and I never heard these concepts from my medical school, uh, professors, from my colleagues, uh, you know. And so that got me asking some different questions.
But ultimately, what I came to realize is the surgery that I do, the surgery that you do, um, it's great to be able to offer that to patients, but you're never as good after the surgery as you would have been if you didn't need the surgery in the first place.
Oh, that's, I love that line, by the way.
Yeah. You're never as good after the surgery as you would have been if you didn't need the surgery in the first place. Love that.
And, and, you know, that's really what it comes down to. And when I, you know, started really thinking about what, you know, why did I become a physician? What is our role as a physician? Um, it, it's to help the patient the best way we can. And, um, and that's what led me to, you know, conclude that the best way that I can help patients is to keep them off the operating table. And, you know, because of that, I changed around my practice, similar to the way you have. Still operate as a heart surgeon, but also have a telemedicine practice, wrote a book, all of that stuff now to try and keep as many people off the table as possible.
And I just want to, uh, um, if folks are interested, Phil, like myself, is a clinically practicing surgeon, or, or actually, let me remove that word, metabolic health specialist, primarily focused on cardiovascular disease. And if you look in the show notes, Phil's contact, if you're interested in consulting with him, in the show notes are his access details. It's important to know that upfront, so he is available for consultation.
Phil, I love that. Can I ask you a personal question? Um, and we can edit this out if you're not willing to say this. What do you know what your CAC score is? Your cardiac calcium score?
Yeah. Uh, my CAC score is zero. It's been zero twice now, three years apart. I'm, I'm just about to turn 50, 50 years old as we record this.
And and mine is zero as well. And I think it's an important concept that, at least by the thinking of that cardiothoracic society, it is not possible to be fat and have a high LDL and a high cholesterol. It's incongruent with a zero CAC score. And the only thing that I would change is, you use the word pre-diabetic. You and I were never pre-diabetic. We had insulin resistance, but genetically, our body is so good at turning sugar into fat, it never harmed our blood vessels. Our diseases are going to come from insulin, not from sugar. But you see other folks, and I think this is a very important narrative, and, um, Matt Budoff was talking about this a little bit ago. I'll go into Matt in a second, is that, uh, cardiologists and cardiovascular surgeons see more diabetics than endocrinologists. And, um, so the disease that you treat, at least in a metabolic space, is more for the diabetic side, the diabetic genetics, rather than folks like yourself and myself who have zero CAC scores. So it's, it's an important concept, uh, that I just want to reinforce to the audience.
Yeah, I think it is important, uh, to note that. And, you know, the work of, uh, Joseph Kraft and Gerald Reaven, uh, in the cardiovascular space, it shows us exactly this. You know, um, in one of, uh, Jerry Reaven's, you know, uh, talks, um, you know, he basically makes the comment that the, um, coronary artery disease, the atherosclerotic heart disease patient without diabetes has simply not been diagnosed. In other words, people aren't looking for it in the right way. And, and as you mentioned, it's not even really about diabetes per se, it's insulin resistance. And now that I know to look for this, um, I see this every day, you know, in my surgical population. Um, when you look for it properly, almost every patient that ends up on my operating table is insulin resistant. Um, and we can't say the same thing about cholesterol. Elevated LDL cholesterol is really a 50/50, uh, shot, you know, when you end up on my operating table. But insulin resistance is nearly universal. And we have all the data we need on this. It's not debatable. You know, it's interesting when I talk to my cardiology colleagues these days, and, um, I don't necessarily try and convince them. You know, I know within the low-carb community, of course, cholesterol is a very controversial topic. And, you know, and I, it's not about convincing cardiologists that cholesterol isn't the issue. It's really just opening their eyes up to the fact that insulin resistance is a much bigger issue. So you can look at the cholesterol, we can address the cholesterol, all okay, maybe, and I'm sure we'll get into all of that, uh, but we do have to acknowledge that insulin resistance is a much bigger problem. Always has been. And everyone understands this, and the literature strongly supports that. Um, yet, you know, it, it's not the way that our practices are geared, because, you know, it's not the main messaging from the healthcare system. And there are many reasons why that is. But that's what I really try and wake people up to. Um, we can figure out what the role of cholesterol may or may not be in this whole process, but we have to acknowledge that insulin resistance is the primary driver and a much bigger risk factor. So let's, let's try and fix that. Let's try and diagnose it, uh, to start with.
And I, I appreciate that. And we're going to get into those weeds in a second. I'm want to put your surgical hat back on, 'cause we have this unique opportunity, you and I, of talking about something that we've seen, um, which other people imagine, but they've never seen. Um, I've done a fair amount of peripheral vascular surgery, especially when I was younger, because of the, in the smoking era. So we did AAA's before they had endovascular surgeries and that kind of thing. You've done the same. Can you describe, uh, in as vivid a way as you can, and I, I call it kind of the snot-like substance that is plaque, that is this collection of stuff, because everybody has an imagination, but nobody's held it and touched it and felt it. Can you describe, as a surgeon, what you feel, what you see, not in the coronaries, and are the coronaries the same as the of the larger vessels, but what does all of that look like when you get in there?
Yeah, so typically, you know, when we're actually taking the plaque out, which, you know, uh, to set the stage, in the cardiovascular surgical world, uh, what I do on a usual basis, we don't actually take the plaque out. We basically are working around it. We're re-rooting the plumbing around it, hence the coronary artery bypass being the most common operation we do. But you're right, in other vascular beds, like the carotid arteries in the neck, or the, the peripheral arteries, uh, in the, uh, in the extremities, and, um, you know, abdominal aortic aneurysms are probably the most dramatic example of this. And of course, remember that, well, although it's not something I commonly do today, um, you know, that plaque is often this kind of, um, mushy, cheesy type, uh, substance. And, you know, seeing that and holding that and touching that, you can certainly understand how we got to where we are today, because you look at that and you're like, "This is fat. This is, you know, butter. This is cholesterol." Uh, this is what it looks like. So of course, it must be the fat that we're eating, and the cholesterol that we're eating, and the butter that we're eating that's causing this plaque. Um, now, just because something makes good sense doesn't mean it's true. And of course, we know that those two things, what you eat and what ends up in your blood vessels, are not directly connected. And it's not as simple as if you eat the cholesterol, you eat the saturated fat, that that's what ends up in your bloodstream. It's not a drain that's getting clogged by bacon grease.
But, but here's an interest, again, from a surgeon's perspective, from a visualization of the vessel, because this is debated and discussed in our scientific groups a lot by people who've never seen, touched, and felt and scraped out or bypassed what you and I have done. And you're right, carotid and, uh, I want to come back to this. We remove the plaque and then we try to revise. Same thing with the AAA. We, we put a graft in there to squash it. But, um, where is the blood vessel when you've got this plaque? Where is the blood vessel in this? Has this stuff in the wall? Has it exploded? Is it on the outside? Is it on the inside? Where is the, the vessel wall in the plaque?
Yeah, so the vessel wall is going to be on the other side of the plaque from where the blood is. Um, and, you know, this plaque ends up being an interface between the vessel wall and the blood. Uh, and that should tell us some things. And the other thing that's real striking, that again, I didn't fully appreciate, but now I think back to, is the inflammation that is always, uh, there. When you do scrape this plaque off the vessel wall, underneath is clearly not normal. And, you know, the carotid is a great example, because typically, you know, we're clearing the plaque out, and we get to a normal area, you know, at the lower, you know, what we call the proximal end of the plaque, closer to the heart. And you can see that interface between where the blood vessel wall has not been damaged, and there's no plaque, no cholesterol buildup. And, you know, then you scrape out this area of plaque, and you see the damage underneath. And if it was just a matter of, you know, the cholesterol basically just sticking to the wall, as people picture, you know, why would it occur at that spot? And then a millimeter next to it, you have a normal blood vessel that doesn't have any plaque attached to it? Because the LDL cholesterol is evenly distributed in our bloodstream. It's one of the, you know, kind of laws of of fluid physics that things are going to evenly distribute throughout a compartment of fluid. And so it doesn't make sense if it's only the cholesterol that these plaques occur in one place, and a millimeter next to it in the same blood vessel, you have absolutely no plaque with a pristine, uh, blood vessel wall.
Yeah, so I, I just want to reinforce a few things because most folks have not been there and touched that and felt that. The first thing is, the plaque is on the inside. The vessel wall is on the outside. The plaque isn't, at least when we operate on it, not inside the vessel wall. May have started there a little bit, but it's outside of the vessel wall. It's in the lumen. Secondly, it's very friable. It's very snotty. It is not like this smooth thing. It's not this, uh, linear thing. Or even, you can see the calcified stuff. It's the snot-like stuff that can break off very easily. Um, and then the blood tries to worm its way through that. And these occur, as you said, as islands in various areas. Sometimes you'll see a stretch of it, but there is native, almost normal-looking vessel. Now, I haven't looked under the microscope at the normal sides, but at least macroscopically, you don't see that. But this is an important consideration for me. The reason why I, as a general surgeon, saw a lot of plaque is because we, I grew up in the smoking era, where the majority, as you said, the carotids, the AAA's, the lower large vessels, were primary targets of nicotine or of smoking. Whereas with the hypoglycemic, um, disease, we primarily see it on your turf in the cardiac vessels. There's a lot of patients who have significant coronary artery vascular disease, but very little plaque elsewhere if they are diabetic. Do you have any insights or understanding? And I think it's important for people to know because there's a lot of argument about whether CT is a correlate for, uh, uh, plaque in the heart. Do you have any idea why these two very similar inflammatory processes have different places they exhibit their disease, one more broad spectrum, one more direct? And also, um, what is the best testing for you, concerning, not obviously operating, but what is the best way, algorithm, for people to know what their plaque level is from a diabetic perspective?
And, and we can talk about the second part of that first, um, because there is this difference that you mentioned, and, you know, uh, the honest truth is, we don't understand all of the reasons why there is this difference. Um, you know, first and foremost, it may just be a size issue. Understand that we're talking about coronary arteries that are, you know, usually one and a half, maybe up to about three or four millimeters in diameter, um, versus, you know, very tiny, you know, uh, I need to use magnifying glasses to operate on these things. It gives you an idea of how small they are. Um, and then we're comparing it to the carotid artery, which is usually going to be, you know, somewhere in the, let's say, 10 to 20 millimeters, so almost a 10x size difference. And then you get to the abdominal aorta, um, which at its normal size is about four to six centimeters. And, you know, of course, when it becomes aneurysmal, that we're operating on it, it's oftentimes larger. It is larger than that. Um, so one is a size issue, and then there's probably something to do with the flow dynamics related to that. And, uh, there are some other factors that come into play. Um, but because of that difference, plaque doesn't occur the same that in the heart as it does in the carotids, as it does in the femoral arteries. Um, I believe that the best strategy, if we want to know if there's plaque in the coronary arteries, is you need to look at the coronary arteries. And the good news is, we have a great way of doing that today. We have the coronary artery calcium scan, the CAC scan. And it's going to show you if there's any calcified plaque in your coronary arteries.
Let me stop one second, Phil, if I can. Because we've actually talked at loggerheads a little bit. That snot-like substance that we see has very little calcium in it. The calcium occurs kind of underneath that, and you can see the calcium on X-ray. So what we were talking about earlier on was the soft plaque component. Uh, can you make a distinction between the hard plaque and the soft plaque? Is the CAC scan measures the hard plaque, the calcified, bone-like plaque? As a, so if you think about the way I look at it, if you look at a bone with a piece of cartilage on it, the soft plaque is like the cartilage, and the hard, the calcified part is a bit like the bone. Can you make a distinction between that and help people to understand calcified versus non-calcified plaque, and the role of the CAC score in that?
Yeah, so, you know, they definitely are two different points in the process. Uh, and, you know, again, there's a general concept out there that it's an evolution, right? You go from, you start with what's called a fatty streak, which is basically just a little bit of this substance that starts to build up on the blood vessel wall. And then it's a gradual buildup process. And at some point, either due to just simply time or other factors, this calcium starts to come in, and you now get a calcified plaque. Uh, and the reality is, is that they go together. Um, it's not clear that, by the way, it is actually a, a, a straight progression. Um, there seems to be sometimes you get more calcified plaque for different reasons. Um, you may not have as much soft plaque. Uh, but regardless, they almost always exist together when the disease is significant. Um, it is certainly possible that you have some soft plaque, you don't have calcium in it, and we don't see that on the CAC scan. But the reality is, is that's not clinically relevant.
The chance, have you seen, have you seen a patient with a zero CAC score with a large burden of soft plaque?
Not what I would call a large burden. You know, we, we are so good at imaging now, and we can talk about the other imaging study, the CT angiogram, which shows us in fine detail the soft plaque. That yes, we do see some soft plaque with a CAC score of zero. But it is incredibly rare to see, um, a large burden of soft plaque, you know, to the point that someone might need a stent or bypass surgery with a CAC score of zero.
Or a compromised flow toward a heart attack or a stroke or a heart attack. Correct.
With the caveat being that, you know, sometimes people do have heart attacks with CAC scores of zero. And that should really open our eyes as well, because we should say, "Well, how can this be? They don't have plaque, or they don't have calcified plaque, at least, and then they have a heart attack." And again, that should alert us to the fact that maybe plaque isn't even the whole story. Maybe there are some other things going on that might be causing heart attacks, like blood clotting.
And, uh, I, you know, blood clotting is a significant part of all of this. We're going to talk, because that, that is something that I've separated out in my head a lot. So I want to discuss that in a second, because you, I, I mean, this is just ridiculous how much information you are sharing that just blows my mind and helps people to understand this as a process, because there's so much misconception because we haven't seen it. I mean, this is just blowing my mind. Sorry.
So, right, it's clotting versus plaque. And clotting is acute. It occurs rapidly, whereas the plaque has been there for a long time. And that's to understand. And the two can go together or separately.
Yeah, so, you know, to circle back to, you know, what can you do? You know, what's our best test to determine, are you at risk for, you know, a heart attack, for atherosclerotic disease? The answer comes back to the coronary artery calcium scan is the screening test. You know, I always liken it to the mammogram.
Let me stop you for a second. So the, the CAC score is there for progressive chronic disease. Yeah. Okay. And it's the, it's probably the most common indicator of a potential heart attack. It, it seems to be the best predictor that we have, better than, you know, for instance, blood cholesterol levels. It's clear that the CAC scan is a better predictor of cardiovascular risk than blood cholesterol levels are. And, um, the, the good news about the test is it's easy to do. Um, it's basically, you know, it's fairly inexpensive. Um, and, um, it's universally available, especially here in the US. May not be so in some other countries. But, um, because of that, it makes a great screening test. And, and I think it should be done. To why do family practice doctors not do this? We, we do colonoscopies, we do mammograms. Yes, they should be done. But the majority of Americans are going to die of a heart attack. Why are we not doing this as a routine screen, perhaps at the age of 40 or 45, like the indicators for those other screens, prostate, breast, colon? It, it, it is ludicrous.
Yeah, it's a great question, and it's one I ask all the time. And quite frankly, I've never been able to get a good answer to. And the only thing you have to circle back to is it would fundamentally change the paradigm around how we manage cardiovascular disease. And that's going to disrupt a lot of well-entrenched things, uh, in our medical system.
What is your total cholesterol? When I check it, it runs anywhere between 250 and 350. Typically, you're going to die, have a heart attack in about 10 seconds if you don't take a statin. So, but you got a zero CAC score. So a conflict of knowledge right there. But I want to get back to the, the CAC score. And I think, uh, I'm going to throw something out just because there's a lot of talk about the absolute number. The CAC score is not sensitive enough to give us an absolute number. It gives us kind of a space. This disease, you don't have it, you got a zero, or you've got a low likelihood of it, or it is intermediate or significant. But a lot of people say, "Oh, my score was 120 now, and now it's down to 100, and I'm reversing my CAC score." Or it's, uh, if it goes up significantly. But they, it's not that sensitive because the read, everything else, where there's a range within which, uh, it can occur. It's, it's less sensitive. And I want to talk about CTAs. But what do you think of the reversal? Two questions here. The, the reversal of a cardiac calcium score, and also all the products, the NACs, and all the products that are being pushed out there to potentially reverse or stabilize the plaque. There's some merit to it, but can you give me your thoughts on those two things? Can it be, and can it be dissolved? And is there validity to take those medications to do so?
Yeah, great question. So first of all, you're right. You know, the variance in the CAC score, we have to acknowledge. And I tell people, you know, that variance may be about 10% or so. Um, outside of that, um, you can lower your score. I have seen people's scores go down in my practice. Um, but I don't think it's really all that important, to be honest. It's more important that you stop the progression, that your score doesn't continue to go up. And again, we know that that's the natural pattern. Um, CAC scores in multiple studies have been shown to progress on average somewhere between 15 and 25% per year if you don't change the course. If you don't change the course. If you're just sort of following it. Uh, and we know that that progression, or lack of progression, is as strong, maybe even a stronger predictor of risk, than your absolute number is. So, you know, to put this in very real terms, I see patients that have CAC scores of 1, 1500, even up to 2000. And it turns out that they don't have any disease, you know, at that point that needs an intervention. They don't need a stent, they don't need bypass.
How do you know that? What do you, what do you do to figure that out?
Usually, it's going to be either a CT angiogram or, uh, an invasive angiogram, what we call a cardiac catheterization, to get that detailed look at the blood vessels. And there are some other factors that come into play. Um, but, you know, if you take those patients, and they're high score, and, um, you do what we do, and we'll get into that, and you stabilize their score, so their score is 1500 today, a year from now, their score remains 1500, and five years from now, their score remains 1500. Those people are at very low risk for having a heart attack.
You can have someone on the opposite end. Their score is 100 or 200.
Let me stop you for a second there. They're at low risk for a heart attack from progressive disease, but they're not at low risk for a heart attack from a sudden blood clot or a clot rupture. There's a difference. Uh, uh, I just want to make that distinction because I don't want to lull people into a sense of security in that regard.
Well, yeah, you know, and again, none of this is saying you ignore the disease that's there. There are, there are things that we're doing to manage it. Um, but overall, they're at low risk of having a heart attack. Even taking into account, you know, I'm not saying there's zero risk, but they're at low risk. So you're right, very important to differentiate our sort of medical ease. You know, low risk doesn't mean no risk. Um, but on the other end of the scale, you have people who, they come, you know, with their CA, they get their first CAC score, and let's say it's a 100 or 200. And again, low risk of disease today. But they come back the following year, and they haven't made changes, and now their score, you know, is 250, and then it's 300, and then it's 500. You know, that person, even though their absolute score may be lower five years later than the first scenario, they are at higher risk of a clinical event because they have this progression. And this is another important point that you made earlier about the CAC score. It's a way to follow disease progression. And this is another fault in how it gets used in the medical system, because you're right, most PCPs don't order the CAC. But if they do, they think of it as a one-time test. And it clearly shouldn't, you know, it needs to be used as a way to follow disease progression. And it's very good at doing that. Uh, so again, it's something that I ask all the time, why aren't we doing this? If the patient has a non-zero CAC score, that score should be repeated in a short period of time. In my mind, in my practice, it's typically one year. You know, and maybe you could say that's a little bit too aggressive, but I really don't think it is, because I want to know, is your plaque getting worse? Are you accumulating new plaque? That is really the key question.
Than having a heart attack. Yep. That's that, you know, okay, don't do anything. But then I'll see you in the ER when you're clutching your chest. That, that's, we have to put it into the risk. So I love that narrative. That's that's a really good narrative. What about nuclear medicine stress tests or or stress tests in terms of flow and cardiovascular risk?
Yeah, they play a role in figuring out where you are on this kind of risk progression. But they're not a good screening test. And unfortunately, they have become sort of the most common, uh, screening test, uh, really, you know, nuclear stress test or stress tests in general. Um, are really only are best used in patients that are having symptoms that we're trying to figure out the likelihood that these are cardiac symptoms. Um, and they're also an adjunctive test that if you've established someone has some disease and you know they're, if they're not having symptoms, and you're trying to elicit symptoms because you're basically provoking their activity. So for patients that aren't really active, um, it's not really all that useful. If they tell you, "Well, I'm not having any symptoms," and chest pain, of course, being the main symptom, shortness of breath related, uh, in the cardiovascular world. But if a patient is just sitting on the couch, the fact that they're not having chest pain doesn't really mean anything. So a stress test can be a good way, either you make them walk on the treadmill, you physically provoke them, or you give them medication that speeds up the heart rate and chemically provoke them, and now you figure out, does that uncover symptoms?
Yeah, I like the new, the stress test primarily as a sign of immediacy. Is there an immediate need to intervene? And couple of couple of comments, because as you said, one of the, one of the steps is to do a, a cath. And the cardiologists, to my mind, are somewhat cavalier about caths, or they used to be. Um, and, and they're two concerns. Number one, the majority of cardiologists have never seen, uh, like we talk about earlier, plaque disease. They don't, they don't conceptually understand what it absolutely looks like. So when they do a balloon, when they put a stent in, the risk of knocking something off, the risk of having a shower, the risk, and often they get away with it. But we so often see, um, the troponin, the cardiac numbers going up, which is basically a measure of a heart attack when we have a cath. So I try to keep a cath back when I recommend a cath to a more likely, like a greater likelihood of intervention, rather than a screening tool. I don't know if you share that sentiment. Can you comment a little bit on rising, um, measures of muscle damage or muscle injury, which are the troponins, and also cath risks, especially cath risks?
Yeah, definitely. So, and, and you're right, you know, the, the catheterization, which is an invasive test, you know, we actually, describe what a cath is.
Yeah, definitely. So, you know, we actually have to get a, a catheter, that's where the name catheterization comes from, into the blood vessels, uh, that we're interested in, in this case, the coronary arteries on the heart.
How do you get there? How, how do, what's the pathway to get there?
Yeah, exactly. So typically, you're going to enter the blood vessel, the artery, either in your wrist or in your groin. Those are the two arteries we use for access. And then you actually have to put a catheter, and we're talking about pretty small. You remember how small I said those blood vessels are? So now we have very small catheters, uh, that we then get up either through the arm, through the big blood vessel, the aorta, into the coronary arteries, which come off the aorta, uh, uh, or we're coming from the groin, all the way through the aorta to those coronary arteries. And now we put this catheter into the artery itself, and we inject dye that we can then see on an X-ray machine. Uh, it's a video, you know, so it's not a static X-ray picture that people might be used to. It's a, uh, moving picture, and we can actually watch that dye go through the blood vessel and we can see where the blood vessel might be narrowed, where this plaque is. Um, now, the interesting thing that people don't understand is the catheterization doesn't actually allow us to see the plaque. Um, it shows us the narrowing in the lumen of the blood vessel, the channel that the blood is going through, how wide or how narrow that vessel is.
Exactly. But you're not actually really seeing the plaque. Sometimes you can see those little bits of calcium, but it doesn't give us a good image of the plaque like the CT angiogram does. Um, and, uh, it's a little bit of a different perspective. So, um, the, in the, um, the, uh, you know, that can actually lead you to some false conclusions about things, um, because you're only seeing how narrow the blood vessel is. You're not actually seeing how much plaque is there. Um, and those are two different things. Um, again, getting into the minutia. But the other risk also, Phil, just when you and I operate on vessels, um, we clamp above and below. And one of the reasons we clamp is not just blood flow, but it is because debris during manipulation of the vessel can travel downstream. And we always clamp distally and then we clamp, well, we clamp proximally, then we clamp distally. But, um, and then we have to, I remember, and it's been a while since I did vascular surgery, we have to fastidiously wash out that debris that gets knocked off to in the handling. I don't think in talking to them, most cardiologists understand how fragile some of that plaque is. And I'm assuming the carotids are not that much different than the other vessels. And we do see increased muscle, uh, damage, measurable muscle damage when you do caths. What do you think about that? Is that an important consideration when you're deciding to have a, uh, an intervention done? Um, what is that risk? Because you do get little showers of tiny fragments of that, of that plaque, of that gelatinous plaque. What are your thoughts on that?
Yeah, you know, so I think, um, catheterization is definitely not a risk-free procedure. No procedure is in medicine where we always have this risk-benefit equation. And, um, you know, and so that really should enter both the patient's mind and the operator's mind. The, the cardiologist doing that cath, um, you know, need to think about that, and is this the right test, uh, for this situation? And, you know, it used to sort of be the only option we had. Uh, now we have non-invasive ways of looking at these blood vessels, the CT angiogram. And I think that has changed the game. And honestly, medicine, the healthcare system is still catching up with that. It's still understanding that. I, I, I do think catheterization is still overused. It's not as overused as it used to be, but it's still overused. And it's not something to be taken lightly. You know, it is a procedure. It does have very real risks associated with it. And so we need to take that into consideration. And more so, um, also what we're starting to understand is there used to be sort of a knee-jerk reaction that you did a catheterization, you saw a blockage, the blockage looked bad, and the inclination was, "We need to treat that blockage. We need to put a stent in, or we need to do bypass surgery." We're now understanding that, you know, um, the, the look, the percent narrowed that the blood vessel is on that catheterization is not the whole story as to whether or not intervening on that blockage, putting a stent or doing bypass, is actually going to benefit the patient. Uh, so this is where we get into the concept again that you mentioned earlier of, is there ischemia? Is there reduced blood flow associated with this? That's really the key question. And we again have better ways today of assessing that. Um, and, you know, we can get very technical, but there are some things that can be done during a catheterization to actually measure the blood flow and now determine, does this warrant treatment or not?
Perfect. So you've mentioned it a few times, and I want to go there. Between a CAC score and a cath lies the CT angiogram. And the biggest issue is cost. And cost, dye has to be used, and radiation is a little higher. But can you explain to me the value of a, um, a CT angiogram over, between a cath and a CAC score? And I really look at it from two perspectives. It shows me anatomy, kind of a little bit of static anatomy, because it's still a CT scan, but it also shows flow. Can you explain that? The, uh, so we're looking at function as well as function and provision of oxygen and and correlates with oxygen and nutrition to the heart muscle, as well as the plaque burden. How do you use CAC scores? How do you view them? How does your brain work when you're thinking about a CAC, sorry, a CTA?
Yeah, so, you know, all of the things that you said, the CTA is more detailed. And because we're now giving dye, but we can give that dye now into just a simple intravenous line. We don't have to get the catheter up to the heart. Um, we can now see the actual flow through that blood vessel. We can see how narrow that blood vessel is, similar to what we were talking on the catheterization. And with the most advanced version of the CT angiogram available today, we can actually do what is the most advanced. What is the most advanced one? So it would be one with what's called CT-FFR. Fractional flow reserve. That's the measurement of, is this narrowing actually reducing blood flow, uh, through the blood vessel? So that can all be done today. Um, you know, that's not as commonplace. You know, the standard CT angiogram may not include that, uh, you know, when you go get your CT angiogram. But it's still a much more detailed look. And now it can give us a sense of, okay, there's plaque there. Um, is this plaque we need to worry about in the sense of, you know, the patient's at sort of imminent risk? Uh, and is, you know, uh, is reducing blood flow? Uh, so I use it again as the second level test. If I am particularly concerned, because either the CAC score looks bad, or the patient is having symptoms that I'm concerned about. I think the CT angiogram, um, is now a great option before you go and take that risk of the invasive catheterization. Um, it gives us a good roadmap. We have an idea going into the catheterization now of what we're dealing with. And, you know, we can have the discussions about, you know, stents, bypass, that type of stuff. Uh, so it's an intermediate step for me now. Some people say, "Well, if it gives you such a great view, why not use that as your screening test?" And of course, you know, um, uh, Dave Feldman and Matt Budoff are currently doing this study, you know, lean mass hyper responder study. And they chose to use the CT angiogram because it's more detailed. And in an ideal world, yeah, we would get that great picture every time. The downsides, like you mentioned, are more radiation exposure, more, more cost, and you have to give this dye, which occasionally can cause some issues, pretty rare, but occasionally can cause issues. Uh, so you take all of that into consideration. And as of today, the CT angiogram, in my mind, um, is not ready to be used as the widespread screening test, but it's a great secondary test. And I have a pretty low threshold for ordering it these days.
I think the key, you've mentioned these words, but a CAC score is a global screening test. If you want more detail, a diagnostic test is the CT angiogram because it gives you both anatomy, it gives you soft plaque, and it gives you flow. And that's a computerized calculation. Then the therapeutic intervention is a cath or your hands. So, you know, that's the way that I look at the escalation of these. I want to flip a little bit. I know time is an issue for both of us. But the way my brain works when it comes to therapeutics. So, okay, I've got a burden of disease. I look at the evolution of plaque and the treatment of plaque from three using three different words. The, the first one is plaque stabilization. Plaque rupture, which is the most questionable one. The second one is, um, if you've got a burden of plaque and you've changed your diet and you've reduced your, uh, um, you're managing your diabetes, or whatever it may be, it really is about the risk of developing a clot on top of that plaque. Or even a clot where you don't have that. Clotting disease, as you said, is a significant factor in both stroke and cardiovascular disease, probably definitely more so in stroke, but also in cardiovascular disease. So the second word I use is anticoagulation. And then the third word that I use, and I'm working backwards to cause, is ultimately the, the, the word that is associated with all-cause plaque disease, and you're never absolute, but that is inflammation. So the, the, the other word that I use, and so I use anti-inflammation, and that's both a dietary strategy, you're going to quit smoking, plus certain medications, anticoagulation, and then anti-plaque disease, which for me is the kind of black box of everything. What do you think about that? And how do you think about that in your management of your patients outside, as a, as a non-surgeon, if I can put it that way?
I mean, I think that's a, a good construct to think about. And that does guide, you know, some of the things that I typically are recommending to patients to manage this disease. Um, and, you know, uh, but I even kind of step back, you know, and say at a higher level, you know, is the intervention that we're using, whether we're talking about a pharmaceutical, a dietary change, or a, a true intervention, a stent or bypass surgery, is that intervention addressing the underlying root cause of the disease process? Uh, and that's a question that we really don't ask enough in medicine. Uh, and this broadens beyond cardiovascular disease. But to keep it to cardiovascular disease, you know, we, we had the discussion earlier, we talked about inflammation, we talked about insulin resistance. These are root cause issues that ultimately lead to cardiovascular disease. And is what we're doing addressing that? And the simple, you know, on many, you know, the simple answer, I guess I'll just stick with it, is the surgery that I do, the stents that get placed, do absolutely nothing for the root cause of the disease. We have to acknowledge that. Not saying they shouldn't be used, but they don't address the root cause. The pharmaceuticals, um, you know, did a very poor job. Now that might be changing. We have these newer pharmaceuticals that are not cholesterol-lowering medications, um, but they do, they do on some levels start to address the insulin resistance. And we're even more looking at the information.
Tell me what you're talking about in that.
class which drugs reduce in uh insulin resistance? We're talking about the GLP-1 uh inhibitors, Atjar, and that indication. That's a new entry. There's another uh a patient and a buddy of mine, David Na, uh uh Nebor, who is a uh he's actually an electrophysiology cardiologist and done amazing well. He works in our space, but he brought something to my attention. In December of 2023, the FDA approved colchine as a therapeutic drug for uh uh in a in a similar vein to GLP-1s with a much greater reduction in cardiovascular risk than statins. It was head-to-head compared by statins, and I've got a video on that coming up. Have you heard about that? What are your thoughts on colchine, which I'm just starting to explore?
Um, what do you? Yeah, so this is looking at the inflammation part of this, and uh colchine has now been demonstrated in two trials, uh they were called the low-dose trials, low-dose colchine, uh to reduce the risk of cardiovascular disease, uh of clinical events, I should say, heart attack, um, as well as statins did. And, um, you know, there there's some caution around using them. There's some other effects we have to think about, uh, but you're right, they now have gotten that indication, and I'm starting to see that used more in practice. And, um, you know, there's always been this talk around statins, um, that, you know, maybe the effects that we see from statins are not due to their cholesterol-lowering, but due to their anti-inflammatory effects, which they do have. Uh, one very interesting clue to my mind is that when you say, "Look, statins, you know, I've got a zero C score, I don't want to be on a stat," well, it's got that anti-inflammatory protection, but I'm not willing to to take a statin drug that has a massive side effect profile if there are other medications that give me the same or better anti-inflammatory value at a specific point that I know how they work. Colchine works on leukocytes, aspirin works on platelets, um, that has a clot reduction, anticoagulation, because that's what we're talking about. We've now shifted away from plaque, which is it doesn't really work there. Now we're talking about anti-anti-coagulation and anti-inflammation. Um, and there are far more direct, better drugs with a lower side effect profile, as you mentioned, the GLP-1s. Now we've got the colchine. I, uh uh, like aspirin quite a bit. That was my PhD, but, um, I, I know that time is time is getting short.
What I want to ask you is, let's role-play a little bit. I come into your office. I'm on a ketogenic diet. Let's say I'm even carnivore, um, but I've got a, uh, some idiot called Dr. Cus did a CAC score. I'm 60 years old, and he found that my plaque is 500, and I'm petrified. Yeah, but I'm asymptomatic. I exercise. I eat a kilo. I hate the word I eat right or healthy because that's more whole grains and fruit, but I, I'm a carnivore. Yep. By the way, my CAC score is called zero. So, what is? Okay, I've walked into your office. What testing do you do? I've got a CAC for 1500, multivessel disease, but main and L and LAD. What? Take me from there.
Yeah, so, you know, the the first discussion point is going to be, you know, do we get a CT angiogram or not? And, you know, if you're truly asymptomatic and you're op, you know, you're exercising at a high level, um, you know, that's a pretty good indicator that you're not at risk. But I know, you know, many people, they just get worried about the picture on the CAC score. They want to know, you know, how much at risk am I? And think that's a great situation for using the CT angiogram. Uh, so that's probably going to be my go-to in this situation. And then the second part of that discussion becomes, okay, if we determine that you don't need an intervention today, you don't have that bad of blockage anywhere that we're thinking about a stent or bypass, um, now it becomes, we need to follow this over time. We need to make sure it doesn't get worse, and to do that, we need to address all of the factors. Uh, because just because you've been carnivore for a while or low carb keto, whatever we want to say, um, doesn't mean that you've totally fixed your insulin resistance. Doesn't mean that you've reversed your inflammation all the way. We need to check this stuff, and this is where the blood work comes into play. Uh, and that's where we really get into the nuance and the detail of all this blood work. And of course, the cholesterol issue then comes up.
On second, that is the place where I see the most incongruity with with non-metabolic physicians, like yourself. They have no clue how to interpret the blood work. They're obsessed with lipids and they don't look at the diabetic or the insulin resistant side of things at all. Yeah, and and, you know, they're not even obsessed with lipids. They're obsessed with one number on the lipid panel that really doesn't tell us a whole lot about the lipids, the LDL-C, the LDL cholesterol level. Um, and that really doesn't tell us, you know, it doesn't tell us anything about the quality of the lipids, which I think is really the issue that we should be narrowed on. And of course, that's related to insulin resistance. Um, so in some ways, you can just say, well, let's just figure out if the patient is insulin resistant. Uh, and I, that, like I said earlier, you know, when I'm talking to my cardiology colleagues today, this is the main point I try and get to them is, you can talk about the lipid, but we need to acknowledge that insulin resistance, inflammation are bigger risk factors. So let's assess for that as well. That this patient is not diabetic because their LDL is high, and you're treating diabetics with high LDL. Exactly. So no, okay.
So, what, what medication strategy? Let's say I, I'm insulin sensitive, yeah, but I've got a 1500. A nuke med is negative. A, um, my echo is fine, which they love to do. I didn't, we didn't get a chance to even talk about the value of echoes because everybody gets an echo when they walk into a doctor's office. But, uh, CTA shows the 1500 plaque burden, low level of soft plaque, good flow. What is your preventive medication strategy? I'm on nothing.
Uh, so my preventive strategy is is centered around, you know, the making sure that you're not insulin, you remain not insulin resistant and low inflammation. And from a dietary standpoint, the best approach to that clearly is a low carbohydrate diet. Um, you want to eliminate processed food. You want to eliminate things like vegetable and seed oils, uh, these highly processed fats. And, um, you know, I lean towards the animal-based side, although I admit you can do this, you know, as a, you know, with a plant-based approach. There are some other nutritional considerations that come into play, but you want to eliminate processed food first and foremost. You want to be managing your insulin resistance and your inflammation. Beyond that, I don't really don't think there's any pharmaceuticals that are useful in this situation. Um, I think you can look at some of the supplements like we talked about that are targeting those things that we talked about, blood clotting, inflammation, uh, and the plaque, uh, you know, calcification problem process. And this is where we get into things like vitamin K2, um, and its role in, uh, calcium deposition. We can talk about things like nias, as a, you know, anti-thrombotic agent, preventing those blood clots. Um, and maybe a couple of other things like nitric oxide, like vitamin E, that can help to lower that blood vessel, uh, inflammation and help to repair that blood vessel wall. Uh, so those are the things I think about. But, you know, it basically comes down to, we want to make sure that you're not insulin resistant. We want to make sure that your inflammation is controlled, and then we want to follow this plaque over time with the CAC score or even in some situations, a repeat CT angiogram at an interval to make sure that it's not getting worse.
And if they were still insulin resistant, um, with some weight on them, you'd recommend a GLP-1 as not to get them to lose weight or anything, but to help to accelerate the improvement in their, uh, insulin resistance? Would? Yeah, I think that's where the GLP-1s start to come into the algorithm. And again, we're still figuring it out. I, I think the drugs are widely overused in general, uh, but I do think they have a role because of that mechanistic, they're actually attacking that root, that root cause, the insulin resistance. Uh, and so I can see a role that they may play and that they're starting to come into the algorithm, but they're certainly not my go-to. You know, uh, as I know you have said many times, you know, it, it, it's not a pharmaceutical only approach. The GLP-1s may be an adjunct to the diet and lifestyle. And again, it's clear that the best diet for reversing insulin resistance is a low carbohydrate diet. I, I agree completely that it is a multi-factor thing, and we, there's so much synergy, uh, here. Phil, I know time is out. I'd love to, there's so much more that I want to discuss. We both had, uh, we both work, we both clinicians. I really, really value this. How can people? Because that last question is pretty much what you do in the non-surgical realm. You got a surgeon's hat on, and that is that is that correct? And how can people access you to get that testing done, to get that workup, to get that interpretation, which is really what they're buying? They're not buying the blood work, they're buying the interpretation of the blood work, which is more accurate, which is more of a story of where they currently are that you and I have an expertise in that other folks don't. They look at numbers and throw pills at numbers, as you said, LDL or whatever it is. We understand the story, we understand the narrative. How can people access you? Um, how do they get hold of you? And the show notes will have these details in.
Yeah, definitely. So, and we're definitely going to have to do part two and get into some of this even deeper. Uh, but you can find me everywhere at iFixHearts. Uh, is just the simplest thing. You can go to iFixHearts.com. You can set up a call with my team to talk about joining the practice, having that evaluation done. Uh, social media everywhere is iFixHearts as well. And, uh, you know, like you, I am on this mission to spread this word, um, to not only get this information to more patients, but also to get this information to more doctors so that the patients can then access doctors that think this way and recognize these things, and we can get people more effectively taken care of. And, you know, ultimately, we can keep more people off of our operating table. You know, the point that I want to leave people with is, um, just how common heart surgery has become, how big a problem heart disease is. And just because we are better at keeping people alive with heart disease, uh, similar to the diabetes story, uh, we really should be looking at this as a treatable, reversible disease rather than just this chronic disease management that we take people through. And, um, you know, the answer is, the more proactive you are, the more you take charge of your health, uh, the better you're going to end up being. So find a good clinician like Rob, uh, who understands this and can really help you, uh, manage this problem. And, uh, instead of the passive approach that our healthcare system tends to take, the vast majority of people find out they have heart disease when they have the heart attack, and that is just simply unacceptable in my mind. Too late. Exactly. Oh, I love that to end on. Phil, this has been absolutely wonderful. You've blown me away with some of the statements that I'm going to steal from you, the the the lines. It really is that thinking, and we really have to grow ourselves as a specialty in metabolic health, where you come from, cardiology, cancer, family practice, uh, uh, gynecology, wherever it may be. The central point is the narrative that we just had, the metabolic health side. Thank you so much. Thank you, Rob.