Can You Reverse Heart Disease? What My Plaque Scans Showed | Dr Campbell Rogers

For decades, cardiology has been really good at treating the numbers that predict heart disease, cholesterol, blood pressure, a risk score on a chart, but those are just estimates of risk across the population. They don't necessarily tell you where the disease is actually forming in your arteries right now. Two people with identical numbers can have wildly different amounts of plaque. A growing movement argues that we should stop treating the statistics and start looking directly at the arteries themselves, finding plaque early while it's still soft and small and treating it long before it ever becomes a heart attack or a stroke. That shift in mindset could change how any of us monitor our own risk. Can we now accurately see disease and measure its progress years before it would ever cause symptoms? Can that picture actually guide better decisions? What to treat? How aggressively and when? And how much can we trust the technology that produces it? My guest today has lived on both sides of this. Dr. Campbell Rogers is an interventional cardiologist who ran the cardiac catheterization lab at Briegum and Women's, taught at Harvard, and led cardiovascular R&D in the device world before becoming the chief medical officer at Halflow, a company using AI to measure plaque from an ordinary CT scan. To put this technology to the test, I did something personal. I had Halflow analyze my own arteries scan twice 16 months apart. In this episode, you'll hear how Campbell reads my results, but more importantly, what this technology means for anyone trying to understand their own heart health. And where the evidence is genuinely strong versus where we may be getting ahead of it. With that, please enjoy my conversation with Dr. Campbell Rogers. You trained as an interventional cardiologist. I believe you ran the the cath lab at Briegum and Women's and you taught at Harvard and at Harvard MIT Sciences program. How did you first get pulled toward the cardiovascular system and then towards coronary artery disease? Oh, that's a good question. Going way back in my going way back in time. You know, I think in medicine people are drawn to things they have personal experience with and a family member, etc. often. And they're drawn to things in which they see mentors and where I trained at Briegum and Women's there was just an incredible tradition of cardiological care, cardiology care, academic work, you really in a world-leading way. And those were the people I saw and learned from. So I was drawn to it. You see great people doing amazing things and you kind of want to emulate them. And then what particular point would you say in your career you became specifically interested in coronary artery disease and atherosclerosis? Yeah, very early on. I think there were two things in my experience that led me to it. One was in my early training, even as an intern, fresh out of medical school in the late 1980s. I trained at the Briegum where there was early adoption of really advanced coronary disease care, including giving drugs to dissolve blood clots that were causing heart attacks when that was really new. And then opening up arteries that were blocked with balloons and then with stents. And seeing that happen and honestly seeing the change that came to patients when one fixed their acutely blocked coronaries was incredible. I mean, I would analogize it to I expect what is the the gratification that for example, surgeons see or orthopedic surgeons, somebody comes in with a broken bone and they fix it and immediately someone is really treated for what was ailing them. That kind of rapid fixing and gratification really appealed to me. And you know, everyone's different in what they go into medicine to me that ability to see a problem that's causing a problem for a patient perhaps threatening their life and then fix it had a lot of appeal. What does running the cath lab actually mean if someone's unfamiliar with cath lab? Does that involve some of the things that you just mentioned, balloons and stents? Or what does that look like on a on a day to day? It does. And it's really I think central to hopefully the discussion we're going to have today. So what's called to avoid the shorthand a cardiac catheterization laboratory is a place it's think of it to a lay person. It's it's akin to an operating room. So it's a place in which procedures are done, invasive procedures and there really are two sorts. One is to diagnose what may be wrong. So somebody goes in not knowing and they have a diagnostic test. Think of it like an x-ray and then that it reveals what may be wrong. The second of the two is treatment. So often what's wrong can be fixed using similar invasive tools and that also takes place in a cardiac catheterization laboratory. I mean the word catheterization means using small tubes a catheter to go from some artery or vein and somebody's risk during their leg and then snake them up using x-ray guidance so that they're in and around the heart and then around the coronary arteries. So that's that's quite invasive compared to what we're going to spend a lot of time discussing today which is cardiac imaging. So presumably a lot of those patients you were seeing had fairly extensive or kind of late-stage disease would that be right? Yeah so that really you've gone right to the number of the issue and so here I described those two worlds of a catheterization laboratory the diagnostic piece and the treatment piece and they're both the you know the involved invasive procedures involving the heart and these things have risk etc. And the truth of the matter is that until quite recently the only way to really diagnose whether someone to your question had extensive disease or only a little bit of coronary artery disease or actually maybe no coronary artery disease. The only way to know was one of these invasive procedures and so the observation that I made just in my practice in running the cathlete but also it's been published in as well documented as follows that if somebody goes in for historically if somebody goes in for an invasive procedure to see do you have coronary disease? The answer to that that needs fixing that needs something invasive done so you're in an invasive procedure only about a third of patients who enter a catheterization laboratory with that question end up having the answer be yes you had an invasive procedure and we found something wrong and we're gonna fix it in basically said differently two thirds of patients who go in for an invasive procedure end up with good news great news you know mr. Smith great news we did an invasive test and we found out you don't have coronary disease it's really good news the problem of course is that to get that answer was an invasive test and it was expensive and it's a risk etc. So that's it's not always people with advanced disease historically it's often people who have no disease yet to document that they've had to go through this invasive procedure for those who want familiar with hot flow how would you how would you describe hot flow? So hot flow really it's a technology which you know a couple of decades ago arose from scientists at Stanford University and initially the focus of hot flow was to say this exact problem I just described that people go on doing invasive procedure and then often are told we don't need to do anything and basically to fix it to try to improve that ratio so rather than a third to increase it to a much more frequently if you're gonna have an invasive test it's because you need to have an invasive treatment so what hot flow initially our initial product and analysis was we take images gathered non-invasively non-advasively from a CT scan done of the coronary arteries so a non-invasive test we take that information and then we apply artificial intelligence to the images and advanced computation to the images and derive information about blood flow into the arteries so if someone is told hey you know what you may need an invasive procedure we're worried you have coronary disease that may need an invasive fix we can say ahead of time you can have a CT scan you then have the heart flow the product that that's associated with is called fractional flow reserve or FFR abbreviated we can provide this FFR information and you know what if it's not terribly bad you don't need to have an invasive procedure you need medical therapy and etc. and symptomatic control but you don't need invasive procedure so it can help some of those people in that the two-thirds of people that would otherwise go and have an invasive procedure done and and not require some type of surgery correct and it turned out we reduced that the what's called a negative invasive angiogram rate meaning negative meaning you don't need to have fixed we reduced it by about two-thirds though we showed you know multiple big clinical studies this made a real difference for patients and just to be clear I would presume both of these people if not all of these people that we're going in and having an invasive kind of procedure to look at the the block the blockages in their arteries these were people that had symptoms that is correct by and large the overwhelming lions sure yes and that's actually kind of dogmatic in coronary disease I'm sure we'll talk more about this but historically that in the absence of symptoms, it really didn't make sense to think about aggressive treatment. So the blood flow analysis, which is where hot flow kind of started, that analysis is more important for the person who already has moderate to severe plaque and you're looking to see whether that plaque is kind of affecting them in a functional capacity. It is more important for deciding is it functionally impacting them today? Yes, but I want to caution, it's not more important for the long-term health of the patient, where there are other metrics looking at the actual disease, at the plaque, which can dominate. But for deciding, does somebody need an invasive procedure to put a stent in? And let's be clear, stents are incredibly effective, as is bypass surgery, at limiting symptoms for people who have them, improving outcomes, preventing future heart attacks, probably preventing death from heart attacks, in a subset of patients, they're incredibly effective. But there are also therapies for people who don't need stents. Is it the plaque level camel, like the absolute amount of plaque that is responsible for blood flow restriction? Is that something that's being quantified where you know, okay, once the average person has tends to have this amount of plaque in this artery, we tend to see, you know, a kind of blood flow restriction, which is causing symptoms? The short answer is no, that there is not a direct link. And one person may have a large amount of plaque, which is not actually limiting blood flow. Another person may have a relatively modest amount of plaque, but you know, bad luck, it's all in one place and it's narrowing and limiting blood flow quite a lot. Today in practice, and I'm not sure if this is in the guidelines or not, when would someone be referred for that blood flow analysis that you guys do? So today, coronary CT angiography is indicated for people with symptom suggestive of coronary disease, meaning chest pain or being out of breath with exercise, feeling palpitations, there are a whole bunch of very sometimes vague symptoms which can reflect coronary disease. So a coronary CT angiogram is indicated. In fact, in the guidelines, it is the preferred test above things like stress testing and nuclear testing and all those other somewhat the column old fashion tests. CT angiogram is done. And then heart flow, the FFR component, is indicated in the guidelines if someone has a narrowing between 40% or 40% or 90% meaning the artery used to be 0% narrowed and now it's narrowed down to 40 or even 90% narrowed. That's the range that guidelines indicate should have an FFR done. And back to your earlier point, you're saying that that's it's been validated or shown that this can be beneficial in changing the kind of treatment or further investigations that a cardiologist may refer to their patient to. Yes, and most specifically whether or not they may benefit from an invasive procedure. Yes. Talk to me about when heart flow decided to add on this additional assessment of plaque. So you've begun looking at that blood flow as you mentioned and then you've shifted and a lot of our conversation today is going to be on plaque analysis. Was that always the kind of destination? Was it starting with blood flow and then moving into this kind of detailed quantitative analysis of plaque? I think you know for for the company from the very beginning our mission has been to improve diagnosis and care of patients with coronary disease. And that includes where we started, which is okay, let's make sure the right people are triaged into or out of invasive procedures. But all along I think the recognition has been that coronary plaque is present and I'll give you a couple of factoids. One is that we've talked a lot today about symptoms. Do someone have chest pain bubble? The proportion of people who present with a heart attack, who have had symptoms before that heart attack is very small. It's under 50%. So if as a field and for us as a company if we're going to improve care of patients with coronary disease, if we're going to wait for symptoms to develop to then say okay great news we're here we're going to help that's good but it's not enough. And the identification of coronary disease earlier using coronary CT and geography, the same basic tool we use for FFR. You can see the plaque that's how coronary CTA was developed. And so I think from the very beginning there was a realization look we need to start off with a you know as a startup company we were a startup company start off with this single product make sure that it's validated and make sure it's effective and in the guidelines and getting out there. But all along there was this notion coronary CT and geography provides incredibly rich information that we should be able to mine apply different sort of analytic techniques to and provide back to clinicians and to patients. Let's start with the difference between a coronary CT and geography standard type. Perhaps some of the listeners have even done this themselves and you typically you get a report back and that report says you know maybe it says that you have no disease, atherosclerosis or it says mild or moderate or severe and often there's a coronary calcium score done at the same time so perhaps you get a number for that. How is that scan, that investigation and that report different to the half-low analysis of these scans? Let's separate it into three different buckets rather than two because you mentioned calcium score which is a very important and useful tool just to be clear. So calcium scoring has been done historically and is done today using a CT scanning machine same machine same type of machine but I would say simplified compared to what we're going to talk about next which is a coronary CT and geography. It's simplified because it doesn't require intravenous injection of x-ray die, iodine contrast, doesn't require that and it can be done very quickly and it's relatively ubiquitous one can get it quite easily. So that's calcium scoring and that provides information is there calcium, let's like mix up your bones, is there calcium in the coronary arteries where of course it shouldn't be and if there's calcium in the coronary arteries you know that's not not how God made us that indicates there's some coronary disease. So that's a calcium score. The next of the three is then okay a coronary CT angiogram and that's a step up in terms of detail and information available. So a CT angiogram requires an intravenous an IV to be placed in your arm and then x-ray die, iodinated die to be given, not radioactive die let's be clear, but iodinated die to be given and as the die passes through the heart vessels the CT machine operates very quickly and takes pictures of the coronary artery. So they're outlined the inner the channel is outlined with die and that provides incredibly rich information. Are there narrowings as we talked about is their plaque does one have a congenital anomaly so you're born with coronary arteries of a certain unusual shape sometimes that poses risk etc. So that's the coronary CT angiogram. The third of the three to your question is okay what does heart flow provide. So heart flow provides information derived from that coronary CT angiogram from the second of our three along this journey. This coronary CT angiogram images they're sort of the they are x-ray images they come to heart flow. We do an analysis involves a lot of artificial intelligence and a lot of computation. It involves an individual trained analyst for every single case going through and quality checking and quality assurance etc. And then information goes back to the clinician who originally ordered the CT angiogram who's taking care of the patient and that information includes and it goes back in about an hour between an hour and an hour and a half. So this is a very fast process. The coronary CT angiogram is done. Information comes to heart flow. We send back information to the clinician and it says are they're blood full limitations etc. Is there plaque present and again and really importantly let's measure how much plaque there is and this is really the number of the issue for this discussion. How much plaque is there quantitatively not on some sort of scale but and what's it made of is their calcium are there signs of plaque that's higher risk all of that we provide back for clinical use. Okay so let me throw this back to you just so that we're we're on the same page here. The AI coronary plaque analysis or AI CPA which is what heart flow is doing a more detailed understanding of someone's plaque burden. So the standard CT angiogram kind of gives you an indication of do you have mild disease or moderate or severe but this deeper analysis tells you more clearly the absolute amount of plaque you have but also the type of plaque the composition of that plaque. And so my next question to you Campbell is with that information what's the benefit of having that information over just the information in a traditional CT. I was trying to think of analogies in medicine that sort of would be relevant. And these tools to quantify coronary disease in a way that cannot be done without them. You know, they can't be done by somebody just reading the CT scan as a clinician. An analogy would be something like with the invention of X-rays over 100 years ago. Prior to the invention of X-rays, if someone fell down and hurt their leg, clinician wouldn't know is the bone broken. Physician could say, "Look, I'm going to do a physical exam. I'm going to assess it. I can't be totally sure often if the bone is broken. All of a sudden, X-ray is done, and now there's no question. It's there, it either is or it isn't. And the clinician has immediate new information. That's how I think about these tools for assessing coronary disease using AI from CTA, for so-for-the-cornary plaque analysis. One can now look at a patient's coronaries. And this was never possible before and measure the extent of disease. Not guess about it, not rely on the patient's risk factors or the fact that they had a family member who had coronary disease, but it's patient-specific. You either do or don't have it. And if you do, here's how much of it you have today. It's hard to overstate the revolutionary nature of this for coronary disease. It's very exciting as a time in the field. And does understanding the type of plaque that someone has, if it's low attenuation plaque or non-calcified plaque versus calcified plaque, does that help you determine that patient's risk? Does it help with risk assessment? It does, and I'm going to give a couple of, say, editorial comments as well. It does. So there is very good data that the -- and this is not -- won't surprise anybody. But the more coronary plaque one has, the worse the prognosis, the higher the likelihood of eventually developing heart attack or developing chest pain or needing a stent, or dying from heart disease. So the more -- and specifically, the more plaque without calcium, the more non-calcified plaque. But here's my editorial comment. This is an area now that these tools exist, and they're quite new, that we, as providers, need to have a lot of humility, because we're now able to look at coronary disease in a way that was never possible before. So we are going to learn -- so for anyone to be dogmatic and say, "Okay, great. I know exactly what -- you know, this type of plaque is associated with this type of outcome, and this change over time. The science is in development, and the clinical studies are ongoing using these tools." And again, I think humility for us in the field, humility is a good thing to have, because we're going to learn a lot about coronary disease that we have not been able to know before. There's some established or accepted numbers when it comes to plaque volume. I think listeners of this show will have heard previous guests talk about, young adults in the early 20s in the Korean War, who post-Altopsies showed that they had atherosclerosis at a very young age, and that this is a disease that occurs across the lifetime. It's about lifetime kind of exposure and burden, and if atherosclerosis isn't your cause of death, most people are going to die with some degree of atherosclerosis. At least that's what I've had previous guests share with us, and you can comment as to whether that's something you agree about. But is there an established amount of plaque that you would say is where things become problematic? The short answer is no. I agree with everything you said about the prevalence of atherosclerosis. Those early Korean War victim data studies are solid, and they looked at the aorta and saw plaques, fatty streaks, and the aorta of those soldiers. It's very common, and it's gotten more common for a whole variety of reasons over the last few decades. I think the way that we look at it is there's an age component to your question. One way to think about it is, and we have for our plaque analysis, we now have this information as part of what the clinician gets back, and it says, "Follows, "Okay, I have a 40-year-old male with this much plaque." We have looked at a population of nearly 300,000 people, and I can tell you from that population amongst 40-year-old males, this example patient has more plaque than 90% of them. That tells you something. So let's say I'll make up the numbers. Let's say they have 100 to big millimeters of plaque. They're 40 years old, and that again, let's put it in the 80th percentile for 40-year-old men. If you then switch and say, "It's no longer a 40-year-old man," excuse me now, it's a 70-year-old man. They're no longer in the 80th percentile. They may now be in the 20th percentile. So you need to know the age, the sex of the patient, and couch it at least in terms of that framework. That makes sense. So it's not just how much plaque do you have, but how much plaque do you have at a certain age, and then comparing that and contrasting that to your peers at the same age? What can you tell us, Campbell, about how accurate, reliable these plaque measurements are against the gold standard? So, intravascular ultrasound, that invasive kind of assessment where you're getting in and really being able to understand exactly how much plaque someone has. How does this AI analysis of CT and geography compare? So that's a critical question, because look, one could bring forward a tool and say, look, great news. We're able to extract information about plaque from CT. The immediate question, any clinician and any patient should ask, is, okay, good. You say you can do this. Prove it. Tell me, if you say, I have 100 cubic millimeters of non-calcified plaque. How do you know that's true? How do I know I can trust that number? So you put your finger on assignment. The answer is, in clinical studies, as in anything in medicine, the proof of the pudding is in clinical studies, comparing to a recognized gold standard. And the gold standard, as you reference, is intravascular ultrasound, which involves putting a catheter down the coronaries with an ultrasound transducer on it, imaging plaque that way. That has been done for decades. It's a standard, very invasive, but a standard tool. So, for example, for heart flows, plaque analysis, we've done a clinical study, totally prospective, totally blinded, where we, or patients agreed, consented to have an ultrasound done and to have a CT done. And then in a totally blinded way, we compared the two. So we had a choral apthic, the ultrasound, say, okay, here's how much plaque Mr. Smith has. We took the CTA. We said, okay, here's how much plaque we think Mr. Smith has, and we compared the two. And they actually compare extremely well. And this is all published in peer-reviewed literature, et cetera, et cetera. And it has to be prospective, because if you go about it and say, well, look, you know, we happen to have a few patients who had intravascular ultrasound, and they may have had a CT as well. So we're going to look retrospectively and see how they compare. There are all sorts of biases, either intentional or unintentional, which can seep into such an analysis. 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There are four flavors, like cherry salt, lemonade salt, orange salt and pineapple salt. Receive a free element sample pack with any order at drinkelement.com/simon. The Keto CTA paper, which I know you're familiar with, and they ran some of their scans or all their scans through through half flow in their most recent preprint. It was interesting to me that their primary outcome used Q&A, which I hadn't heard of. I believe it's a research tool. It's not something that's available to patients or individuals. Do you know much about Q&A and how does that compare to half flow in terms of the way that it analyzes Plak? I tell you what I do know. And again, there are others I'm sure with much more experience with it. To reiterate what you said, Q&A is largely a research tool used by Core Labs has been used for decades. For Core Labs for measuring Plak, it's quite labor intensive, so it doesn't lend itself to routine clinical use based on that. It also involves quite a bit, I believe, of operator interpretation. So some subjectivity or risk for inter-observer variance. So I think some of that may see them, but I don't know. Certainly used widely. There are lots of very good publications, which are relied on Q&A as a research tool. Back to your earlier comment around a coronary artery calcium score. You mentioned this three different buckets of things like we can measure a coronary artery calcium score, traditional CT and geography, and then the AI-driven analysis of the CT and Geogram. What would you say to the person who's had a coronary artery calcium skull done? And it was zero. And so they have been led to believe that means that they're at very low risk of cardiovascular disease and don't have atherosclerosis. Is that the case and is there value in someone with a coronary artery calcium score of zero doing this AI-driven analysis of a CT and Geogram? I would separate the two conclusions you just deposited. One is they have very low risk, and the second is they don't have coronary disease. Because I'll answer those two differently as conclusions from a calcium score of zero. Calcium score of zero does impart very low risk, and that's been proven across large studies etc. It does not say the patient does not have coronary disease. Like those are two different things. Somebody certainly can have plaque in their coronaries that is non-calcified. So calcium score, you know, it is invisible to a calcium score. That does exist. And I think I would say to a patient like that, look, your calcium score of zero is great. That's awesome. Your prognosis, your risk of having a heart attack and dying or having a stent, blah, blah, blah, blah. Over the next several years is very low. Full stop. It does not tell you you don't have coronary disease. So you should see if you know this is a concern. You should understand your risk factors. You should understand your lipid levels. They should talk to a physician. And depending if you were someone who has very high risk, despite a calcium score of zero, there may be a role for imaging with CTA. Again, I would emphasize though that today, CTA is not indicated in the guidelines, it's not paid for by insurance companies, blah, blah, blah, blah. Unless a patient has symptoms. Does it mean it's not used in those patients or that symptoms, but just for everyone's aware, for patients or that symptoms is currently not indicated, which is a whole different discussion that we can have. Tell me about that. Who do you think is the ideal personal persons that can benefit, whether it's risk assessment or treatment or both from having a CT and geogram done and then going that next step and having the AI analysis done? Certainly it's patient only to start with the sort of the easy ones. It's patients who have symptoms of coronary disease who are not a cute leel, but have symptoms. The guidelines is Class 1A, it's the top ranked test. That's not the core of your question. For patients who don't have symptoms, I think there are certainly patients who are very high risk, people who are in high risk occupations, they think of pilots and first responders and so forth. For whom it may be warranted to understand do they have coronary disease. Next would be people who have coronary calcium. Let's talk about this. We've said calcium scores are great, if they're zero, your prognosis is good. But if they're not zero, they indicate that you have, the patient has coronary disease. Then it doesn't have to be more than a calcium score of over five or ten. Any coronary calcium period means you have coronary disease. In that setting, I think there is a relatively, an increasingly strong case to be made, that understanding not just the calcified plaque, but also the non-calcified plaque can be super helpful. And if the calcium score, especially if you look at the guidelines, anywhere from say 1 to 300, there's a lot of subjectivity in there of how much therapy should someone be on medical therapy. Once you get over 300 or 400 of calcium score, the guidelines are pretty aggressive. Most people would say you should be treated aggressively. But in that kind of, call it the middle range, there's a lot of ambiguity. The final point I would make is, and this is really for clinicians, it's that in treating coronary disease with medicines, talking with the patient, there's a conversation about look, whatever your LDL is high, and you need to take a medicine to lower it. You have risk, you need to take a medicine. And for many patients, it's super abstract. It's kind of like high blood pressure, you can't feel it, you can't see it. And so the adherence of patients with medicines is notoriously poor. So we see value in potentially using the CT angiogram and the plaque measurements to go to a patient as a physical care clinician. Go to a patient and say, look, it's not just your LDL measure. Use your coronary disease. Here it is, I can show it to you. Now here's why you need to do the following to take medicines and modify lifestyle and so forth. Is this where cardiology is moving? Do you think, and is there evidence to support this idea that you treat the plaque and not necessarily just the number? So if we say, for example, we take a 30 year old who goes in and sees his doctor and his APOB is super elevated, tries to make some lifestyle changes. It's still elevated. His doctor speaks to him about lowering that with a drug and he's left wondering, well, do I have disease? And we know that some people, for whatever reason, they have elevated APOB and are not getting the same disease as the next person who has the same APOB. So is that where we're moving? Where it's treating the actual plaque, seen on imaging versus just the biomaco? 100%. And it's back to the analogy earlier. Again, this is where we need humility. It's like X-rays over 100 years ago. It's no longer guesswork. One person's sore leg after they twisted their ankle may have a broken bone. Another may just be a strain. One person's APOB is X may have diffuse severe coronary plaque. Another person may have whistle-clean coronaries. And now we can know the answer to that. So why wouldn't we use that information? Now, hastened to say, we need to continue to gather the clinical evidence that these are the right choices so we can, you know, compel patient physicians, guideline writers, etc. to move in this direction. It's not just take my word for it. We have to prove it. But to your question, is this the direction that's going? Absolutely. And what are the downsides, barriers, or risks of scanning more people, other than, you know, there's a cost and accessibility component? Are there any safety issues with performing more CT, angiograms like radiation or other things that, like the intravenous iodane contrast? There are radiation as the main one. I'll talk about it in a second. The contrast, you know, for people who are not allergic to contrast medium, which some people are, is really quite benign. The volumes of contrast used are really small. So that really is important, but it's relatively minor. The radiation is not minor and although these CT angiograms are quite parsimonious when it comes to how much radiation they use, any radiation is greater than zero. So it is a factor to consider. There's quite a literature on the tiny effect of these doses of radiation on long-term risks, for example, of cancer. But there was a literature on it and people need to be aware of that. But there's very, very modest doses of radiation. We're going to walk through my own scan results and the half-flow analysis of these. And I, for background, for listeners who haven't caught my previous episodes, I've had a scan back in 2024 and then I had a follow-up scan in 2026, which was about 16 months later. Before we get there, they're kind of just a little bit more information that I'm interested in on exactly what happens when the lab sends you the scan. you just walk us through in a little bit more detail. How does hot flow perform that analysis? And how, how and pull is the machine that's used for the scan, the types of images that come through the overall kind of protocol at the center where you have your CT and Geogram? So the logistics of what happened, our CT and your grant is done, the images come to us. And the first thing we do is we do an assessment of quote, image quality. And that means are the images, sharp, I call them loosely speaking, are they sharp enough for us to then do our detailed AI analysis? And the answer to that is not always yes. It's yes, the images are good enough about 97, a little more than 97% of the time, but it's not 100%. And the reason that other two or three percent we don't provide an analysis is the images are just too fuzzy. There may have been inadequate medications given at the time or other factors that may factor into that. Once it passes that bar though, it then goes into our automated process with the people periodically doing QC checks, et cetera, as I described. Now, to your question about the technique at the site, it does make a difference. Each site has its own unique scanner. And there are a whole variety of different types of CT scanners. They have their own unique procedure, if you will, for exactly how that camera, how the scanner is used, what medications are given, et cetera. So we at HeartFlow spend a lot of time working with CT imaging sites with our customers to get them to really understand here's what you need to do to make sure the images are optimized. So that's point number one. It does make a difference. The second is, if one is comparing, and we're going to talk about this in your case, I mean, if one is comparing two scans over time in the same patient, has the disease gotten worse, better stayed the same. Back to my fracture analogy is the bone healing, or is it not healing? The more one can have the same scanner, the same technique, then, and now makes a difference, for sure. Yeah, and I'll point out to the listener, because of that, I had both my scans at the LUNQIS Institute in LA, so the same center. And I actually requested to make sure it was the exact same machine and protocol to try and reduce some of that variability there. So let's get into my results, Campbell, perhaps we start with the baseline. And then we can walk through the changes that were observed on my follow up scan, which again was about 16 months later. So maybe walk us through the top line takeaways from the 2024 baseline scan. And for those who are watching on YouTube, you'll be able to see this on screen as well. Sure. So Simon, what you're looking at here is your heart, your coronary arteries. And this is the heart flows, so-called user interface. So your clinician would have access to this and be able to go in and look at it just as we're going to do now. So what you see here, it's a heart flow analysis. Here is your date of birth. And here is your age, as of when the scan was done, December 3rd, 2024. So to start with, what you see on the left are the coronary arteries, these kind of sneaky looking things. This big tube in the middle is the aorta, which brings blood out of the heart to the rest of the body. And the coronary arteries branch off of it, as you see. And what I'm going to do is I move it. You can see there are multiple arteries that bring blood to the heart. Your right coronary artery is shaped like a C over here. Your left anterior descending is here. And your left circumflex is this one that comes down around the backside of the heart. Now, what you're looking at, you see these areas of yellow. And that's where you have coronary plaque just as we've been talking about. So we can actually zoom in on that and look at that and say, OK, here's where some plaque has developed over time over your 38 years. And then if we said, OK, amongst your earlier discussion, amongst 38-year-old men, where does this put you? And we have a wealth of data and 38-year-old men. And so this is actually, if you look down here at the bottom, the total plaque that you have is 116 millimeters cubed. That puts you in the 89th percentile, meaning you have more plaque than 89% of 38-year-old men whose scans have come to us. Point number two is we've talked about flow and fractional flow reserve. That's this. I'm going to click this little lever up here. And this shows, hey, great news. There is no limitation of blood flow. If there were, it would appear yellow or red. But there's nothing. It's all blue and blue green, which is all normal. So your blood flow is normal to your heart, despite having plaque. We're going to switch that back off. And then the last thing we can do is we can say, well, what is this plaque made of? So now what I'm going to do is I'm going to go to this middle panel. And I'm going to grab this with my mouse, this little slider. These three stripes in the middle are your left main and left anterior descending arteries, strung out from the beginning at the top to the more terminal ends at the bottom. And we're going to sort of scroll down like this. I'm moving it down. And I'm going to draw your attention. I'm going to pause here. Draw your attention to this little bow tie over here. This shows exactly where as I scroll, where in your artery we're looking. And finally, over here to the right shows this is where the plaque is. Here's the artery. There's got a gray shape here, which is bringing blood to the heart. And here's the plaque. It looks sort of like a cap on top of the artery. It's not narrowing the lumen. It's great. Not limiting blood flow. But there's plaque there. And just to then quantify this, if we're going to go back to the very beginning, you, 2024, had plaque in your left main artery. That's right here. You can see a little bit of calcium, mostly non-calcified, which is yellow. Calcimus blue. And then the plaque goes away. And then down here in your left anterior descending, you have another area of plaque. Switching gears for a second here, folks, to talk about Shopify. Shopify is the e-commerce platform that we use at 38 Terra to sell our science-backed gut health products into the US, the UK, Australia, New Zealand, and soon to be Canada. 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Sign up today at Shopify.com/proof. The more I've learned about the supplement industry, the more selective I've become about the supplements that I put into my body. This category has a real trust problem. Like regulation, easy manufacturing, labels that don't have to disclose everything that's inside the formula and so on. So when I find a brand that is doing the work properly, I tend to stick with them. That's why I partnered with Momentus. They built what they call the Momentus standard, which is a commitment to testing, to transparency and label accuracy. That frankly, very few other companies in this category bother with. Every product is independently certified by NSF for sport or in form sport, which means it's tested for contaminants for heavy metals and band substances and verified to actually contain what the label claims. Two of the supplements I take every single day are made by Momentus, their plant-based protein and the career pure, creatine monohydrate. The protein blends P and rice for a very strong amino acid profile, supporting muscle adaptations from resistance training, and tendon ligament and muscle recovery from playing pedale. And on creatine, the evidence has been quietly stacking up over the years, not just for muscle strength and power output, but for healthy aging, particularly cognitive performance and when combined with resistance training, bone health. Right now, Momentus is offering listeners up to 35% off your first order with the code, [email protected]. That's livemomentus.com and use the code, theproof. So that's as of 2024, that was what was seen. Campbell, just a quick question. On the left anterior descending, where you were showing that cap of plaque and you mentioned that blood flow is not affected, is that typical in early stage disease where the plaque is kind of growing outwards out of the vessel rather than inwards in causing obstruction? Yes, it's not universal, but it's quite common. The term of art, if you will, the clinical term is remodeling. So the artery remodels and gets bigger so that it kind of knows plaque is growing. It wants to keep it from narrowing the lumen. So the whole artery gets bigger in a way that can accommodate the plaque yet not common. compromised blood flow to the heart. And just to be clear, when we think about the risk of that plaque, one aspect of that is it affecting blood flow. And in this case, you're saying it's not. But is there also some risk in whether that plaque kind of ruptures and ends up traveling down through the artery and causes a blockage elsewhere? Yes, exactly. And it's a great, it's a great illustration of what coronary disease risk is. So let's talk about that. The primary mechanism of heart attacks is that a plaque, such as this, and use the term rupture, would rupture. All of a sudden, in the blink of an eye, for reasons that remain not fully understood, the plaque will suddenly kind of pop as if it were a blister. And it will cause a blood clot because all of a sudden, all of this cholesterol and all this abnormal disease tissue is exposed to the blood, which is flowing right here in a blood clot forms. And then there's a problem with blood flow because now the arteries totally blocked or nearly totally blocked. And the left anterior descending brings blood down. It's the biggest of the three coronary arteries in you and in most people. And it brings blood to a big chunk of the pumping chamber, the left ventricle of the heart. And that, I think, will be something that we might come back to that when I discuss a little bit later, my decision around how I'm going to treat this. And it'll be something I unpack further in an episode with Dr. Dansofer, who's helping me with the treatment side of things. But let's move through to 2026 because this so far sounds a little bit morbid and I'm sure people want some good news. All right. So Simon, now we've switched and now we're looking at your second scan, which was done about 16 months after the first one. So now we're up here in April, 2026. You've now had a birthday. So you're 39 years old. And a couple of things changed, which is really interesting. And as a reminder, here is the coronary arteries. They look the same as they did in terms of their basic shape and structure. We still see here is this plaque in the left anterior descending, this yellow area. But a couple of things have changed. Number one, if we look down here at the total volume of plaque, it now has fallen to 60. Your percentile, both you had a birthday, so your older and the amount of plaque has gone down. So now you're down in the 80th percentile. You were in the 89th percentile as a reminder, year and a quarter ago. And then what we're going to do again is look down by scrolling down this. The first thing I want to highlight and I'll show you side by side images in a second is that in your left main artery, there had been a plaque before and we don't see it anymore. No, it's gone. It was small, but it's gone. In your left anterior descending will come down and this area where there had been sort of that big thick plaque, we talked about it rupturing and so forth, appears less. It's, you know, the yellow area is less and this quantification of plaque in the left anterior descending is less than it was before, especially this non-calcified yellow plaque. So again, we'll look at them side by side in a second and an exact comparison, but it's really interesting to see this difference. And I want to heart them back. One of the things I said earlier, which is these sort of learnings, you know, some may say, oh, we don't see that or that doesn't sound like coronary disease. Let's have the humility I've been asking for. We've never had tools to look at this. So how do we know that this hasn't happened before? We don't know. And here we have really good imaging done at a wonderful place in Los Angeles. It does world class imaging. If all of this AI overlay and okay, here's exactly what happened. So let's use that to understand both for you as a patient, what's important. And then for the field, how can these tools perhaps be used more broadly? Just a quick question on the percentile. So you mentioned there that on the 2026 scan with the reduction in plaque, which was about a 40% reduction, or maybe a little bit more during over that 16 month period. So annualized would be a little less than that. You said it put me at about the 80th percentile. Do you know Miami heart that cohort? I looked at that and at least in their youngest age kind of bracket, they had 40 to 44 year olds. They didn't have a bracket under that level of total plaque volume put me at about the 50th percentile. Is that just differences in kind of the population characteristics in those in the two different groups, the all of the people that you've scanned versus their population? It's possible. I think again, I'm not as familiar with the I'm familiar with the publication from Miami heart that used I think a different tool that didn't use the heart flow plaque analysis, which as I mentioned has been validated as the only one that's been validated prospectively. So I really can't speak to the, are there differences in population? Is it the tool that's being used that is a little, is over calling disease in that case, etc. So your percentile drops I don't know. And then just in terms of validation, we were speaking before about validating against intravascular ultrasound. And so presumably, and I haven't dug into these studies, but presumably that's validating in subjects that have quite a lot of plaque. And I've had several people kind of comment on my level of plaque and saying, look in the scheme of things, it's very small amount. It's a mild amount of plaque. And one of the questions I had for you was when you're using AI to analyze plaque in someone who has a small amount of plaque, how accurate is that measurement of plaque and is there, is there likely any kind of noise as you get down to small amounts of absolute plaque levels? To speak specifically to our data against intravascular ultrasound, which you asked about, the way that we did that only prospective study was as follows, we looked at individual plaques. So the patients tended to be patients who were undergoing invasive procedures. You're absolutely right. So overall, they perhaps had more disease or a population of higher disease than would include you. But the way we looked at it was by lesion. So Ivis is a very specific tool. I'm going to image from here to here and quantify the plaque. And we did the same. So the comparisons we made and were published were at the lesion level, meaning that even though the patient may have had more lesions, the per lesion agreement is what we're talking about here. We cite specific disease and that's what we've quantified in Valdez. So in that paper, there are lesions ranging from very small plaque volume such as you have to bigger lesions with more plaques such as people with higher disease burden might have. And what do we understand about measuring change in plaque over time with hot flow? So using me as an example again here, I measured 16 months apart from baseline to follow up. Then I was reading that ACC scientific statement and they had some wording in there that suggested optimal time interval was perhaps five to seven years. And then I started thinking with someone that has a small amount of plaque like myself, did I wait long enough to get an accurate, reliable kind of pulse check on what the difference in plaque is truly. I think this again, I keep coming back to the same theme, I apologize. This is about having humility. We don't know. And in that scientific statement, you're right, there's a range, I think it goes from two years on up as a recommendation. It shouldn't be done sooner than that because it makes sense sort of in a in a broad way, of course. But there isn't any real, you know, large volume data on this on what what changes, how quickly it changes. So to say, oh, we know it's too soon. We don't believe this. We don't have an experience upon which to make such judgments. I'll tell you for our product, for our analysis, we have a lower limit. If it's anything below one millimeter of calcified plaque or two millimeters of total plaque, we don't call that as plaque. So we say, okay, there may be small changes that, you know, we can't be totally sure of in the one or two millimeter range. That's not what we're talking about here in your case. These are changes, you know, of tens of millimeters of plaque and we have a lot of confidence that given everything you said, same imaging site, same scanner, same technique, great imaging, I think no reason to disbelieve this. And I'll tell you a bad reason to disbelieve this is, oh, we just don't expect this because we haven't been able to look at it. I think I know the answer to this, but something that that I was thinking about when reflecting on the Keto CTA study, the first study they published, it was retracted and then the preprint along with my own results. And let me just give you, and you know this, but the listen is some more background here. I also had my scans analyzed by clearly and by QAGIO to Matt put off very kindly ran my scans through QAGIO and that's usually, or it's not something that's available to the public. As we mentioned before, it's a research tool, but it allowed me to kind of compare and contrast between these different tools, which I thought was interesting given a lot of the conversation around Keto CTA. And first thing I'll say is that all of these analyses actually did agree with each other at a high level. in that they all showed I have quite a small amount of of clock. But there was some disagreement in the absolute amount of clock, albeit all of them saying it was low, and then also the direction of change over that 16 month period. And it would be easy for me to just use heart flow and kind of hope that that is the most accurate one because that showed the best result. And that would be my as a patient, that would be my bias. I'd look to that one and say, look, that showed 40% regression. Great. So my question to you is the way that I was thinking about this and also the key to CTA results was that both in my case and in the case of the subjects in that study, we're looking at people who have low amounts of clock, scans done over essentially a year. So I was thinking based on that scientific position statement that maybe there is some noise here and maybe there needs to be some more validation between serial scanning between baseline and follow up in subjects with low amount of clock from these different analyses. Do you have a different view on that and why there is some disagreement in the results that I have and how I should think about which one is likely to be most accurate or reliable? Yeah. So I think, look, as you've I've gotten a sense in this conversation, we at heart, quote, take tremendous pride and put a huge amount of faith in our clinical data, published, great journals, prospective, we validated, blah, blah, blah, we've talked about that. The other vendors in this space have not published purely prospective, Ivis comparisons. So that's kind of just point number one. So we have, so we stand on the evidence that when we measure plaque and we say it's this much, that's how much it is. In terms of the key to study, we just, you know, I know what's best of it was originally published in a very good journal of the Jack family of journals and it was then retracted and I don't know the details. Retracting peer reviewed literature is quite unusual and usually belies something in the methodology or the analysis, which wasn't totally done according to the sort of optimal scientific principles, but I don't know the details of that. It was retracted. We did do an analysis ourselves of the key to data. It's been presented as you alluded to in public settings. It has not been published in your peer review journal yet, but it's been presented. We have no line of sight to what the other vendors did or any we have never seen any of their data except what was published. I want to come back to you though and you ask the question is more data needed to know, so what do you make of their regression that we showed? Of course more data is needed on a population data and basis and we at Hartflow are doing prospective studies of bunch of them looking using serial imaging. You will also see the same coming from pharmaceutical companies using this in lieu of hard clinical endpoints looking at regression. There is a large NIH, this will be interesting for you, a large NIH funded study, the title is preempt, PRE-EMPT funded by the NIH in young people with small amounts of plaque looking at what does it take to regress plaque? I think it's a couple of years between scans there. We are the tool that the investigators and the NIH chose to use in that study. So you take all of that, the other is more information needed. Of course, to me that more information is what do we learn about a population of patients like you Simon? What happens to most people? What are the outlier cases? That doesn't mean we need more studies to know whether or not to believe what you saw. You're the patient, you're an M of 1, you had a validated tool showed these changes. I believe them. That doesn't mean everyone like you would have the same response. That's not how biology works. You did. That's great. We need to know what does a population do or what for people like you, what drove that change and that kind of thing. I also think this is a good example of how this type of analysis can guide clinical decision-making because in 2024 when I was speaking with Dansofer and others about whether I should commence lipid-loan therapy, my ApoB just through lifestyles at about 70 to 80. Most people would say that's a very good ApoB level for someone who is otherwise fit and healthy and doesn't have other risk factors like L.P. with L.A. or high blood pressure, etc. But I do have a strong family history of early cardiovascular disease and we know that probably up to 50% of cardiovascular disease has a genetic component. Back to what we were saying earlier, you can have two people with the same ApoB and different disease burden. Running the CT angiogram and even just getting the baseline analysis and seeing that there is some soft block that's in there in particular. That was enough for Dan to say look based on the wider body of literature looking at regression and significant regression. Getting ApoB down below 40 milligrams per desi liter makes a lot of sense. I just want to communicate that to the audience because that really is the basis for me and I'll have a dedicated episode on this starting some monotherapy so that my ApoB is down to that level where we see more regression. Even though I've seen some regression on the half-flow analysis, the idea being that there's no blood flow restriction but back to your other point. I want that soft block that's there to be smaller and also more stable. Everything you said makes perfect sense and Dr. Soffra is a guru in this area and his guidance will be wonderful. So on that note, I'm interested in what literature is out there that speaks to tracking treatment response with hot flow if there's any data out there at all actually watching how block changes or stabilizes when you lower someone's ApoB with medications. Does that data exist? It does. There is some and as I mentioned, we are gathering more and there will be much more forthcoming but I'll give you an example of what does exist and it's quite compelling so it's a relatively sort of an important but a niche of patients I'll describe. As a study, the publication was in the Journal of the American Medical Association, JAMA-cardiology in February of this year. It was a study from Emory University in Atlanta and it looked at men with prostate cancer who were randomly assigned to either of two medications, what are called Androgen Deprivation Therapy to help treat the prostate cancer. So there are two of these different drugs, randomly assigned and the end point of the study was looking at coronary plaque and did a change. Why would they do that? Because one of these two Androgen Deprivation Therapy drugs is known to be associated with higher rates of coronary disease. So they were trying to see does this other newer drug perhaps have that kind of side effect if you will less often. So they did serial imaging, CT scan at baseline, randomly assigned patients, re-emmaged them a year later just as in your case, Simon's same scanner is all at Emory's same protocol very well done and they used the heart flow plaque analysis as the tool to measure plaque and low in behold, they found that the more the drug associated with coronary disease risk showed much more progression over a year of coronary plaque than did the alternative drug. So again, it's a prospect of randomized trial. This is the end point. They showed a really big difference. This tool is so precise. It took them, I think, all round number. It was about 65 patients who were randomized. I think about that. Usually we think about randomized trials. There are thousands of patients, 65 patients, ish total and they were able to show this really important observation about coronary disease and a high risk group of people using this tool. So that's coming. And again, this was, this is published in a great, very high impact journal. So yeah, it's cool to see this beginning, but we're at the beginning of this journey and we need to understand how does it change and who does it change, how fast does it change, and what do those changes mean clinically? What do you think about this idea that that soft plaque, non-calcified plaque, sort of turning into calcified plaque on on treatment? And someone might see when they commence lipid lowering therapy, particularly statins, their coronary artery calcium score goes up. But what do you think about the idea that that is usually good sign and is pointing towards stabilization rather than worsening of diseases? That's something that you tend to agree with. And is that something you see on hot flow scans with people that are on stunts? Yes, and yes, I believe in it. It's been increasingly shown in the medical literature for quite a while, just using calcium scores, not just not even coronary CTA or the AI plaque analysis. And we do see it absolutely. And I think most people, I agree, think it's a sign of vascular healing. And earlier, I mentioned low attenuation plaque. Just to be clear, is that, is that a type of plaque that the hot flow analysis looks at specifically? And what is it about low attenuation plaque that makes it riskier or more vulnerable than other soft plaque? So yes, it is. So we report volumes of low attenuation plaque. You didn't have any. So we didn't see it in your analysis. When it exists, we do measure it. It's a subset of the non-calcified plaque. So you have non-calcified plaque of X and a piece of that May and some patients be so called a low attenuation plaque. There is some literature that suggests low attenuation plaque is associated with higher rates of heart attack and death and that kind of thing. I think the jury's probably a little still out on that. You mentioned earlier Simon, the recent American College of Cardiology Scientific Statement in that statement. I think conventional wisdom for now is non-calcified plaque as a whole. Again, up with a small portion, maybe low attenuation. But non-calcified plaque as a whole is probably the best indicator of risk overall. So a low attenuation plaque, yes, some literature. And then jury's perhaps still out a little bit of how different that risk is than that which is associated with overall non-calcified plaque. Most people listening, myself included, are really most concerned with the outcome, not having a heart attack or a stroke. The blood test isn't important and the measurement of plaque isn't important. But that's what we really care about in real life, right? Beyond reclassifying risk and kind of changing what gets prescribed, do we have evidence yet that using the AI coronary plaque analysis leads to fewer heart attacks and strokes or is that the missing piece of data that would kind of get more of the preventive cardiology community on board using this as a screening tool? So yes and yes. We have some data on that. There is more coming. I'll give you a couple of examples of what's coming, what to look out for in a second. But to your first question, what patients care about, of course it is. I mean, the old saw of somebody, you know, you do something, a patient does something because they want to dance at their daughter's wedding, right? That's the, which is, you know, compelling. And as someone who's danced at both of his daughter's weddings, I know exactly what that means. And that's, of course, what matters is the end of the day. The connection of these tools for coronary disease management and good clinicians guiding patients in their preventive course is essential. And there's a way marker on the way to showing reduced death and heart attack rates. And that way marker is lowering LDL. We have already shown it published in a study called the side that use of this plaque tool led to meaningful reductions in LDL, you know, think of APOB, et cetera, lower lipid levels associated in contravertibly in dozens of trials for decades with lower rates of heart attack and cardiovascular death. So that's the way marker. And I think that's been proven in their more studies. In terms of real heart end points, I mentioned this, this study showing LDL changes, we are following those patients over time. It's a study called Decide, DEC IDE. We expect one year data and longer to be coming out over the balance of this year and beyond, so in relatively short order. And it'll be very interesting as those data come through to be able to to your point to say to patients and clinicians, if this is used, you can expect fewer heart attacks and deaths. And that will be a very powerful statement. I think we're well on the way there with these surrogate markers, but we need to take that last step, of course. - Look forward to those results. And we'll make sure that we share those with everyone here. Just to leave people with something a really practical takeaway. Remind us in your view, based on the literature. Who of our listeners right now, if they haven't had a CT angiogram, who would it be most important to go and have a conversation with their physician or referring doctor about going and getting this scan done and having the AI, coronary, prochanalysis done with it. - So number one, patients who have symptoms, the symptoms chest pain, et cetera, done deal. Patients who don't have symptoms, who have positive calcium scores, especially in their ranges, we talked about one to maybe 300 or so, where there's real ambiguity about how aggressively treated those patients should be. I think there's a real role, and there's some indication in the most recent guidelines from the American College of Cardiology earlier this year that there's a role for CTA imaging in such patients where there's ambiguity about lipid lowering therapy. So that's warranted, I think. And then finally, there's this whole group of people who just want to know. And I know it sounds silly and kind of vague, but we have this tool now that people just one can know if they have coronary disease. It was never possible before. And to be clear, patients who fall into back category are gonna be paying for it out of pocket. Insurance companies aren't covering this. Yet, but that's another use case that I think we see growing Simon. And again, people have discretionary money they spend on their health. And this is one potential use of that for sure. - Well, thank you very much for being with us today, Dr. Rogers is an incredibly important topic we're talking about, the disease that's still responsible for the most deaths globally, and I've certainly learned a lot today. So I'm really grateful for your time. Are there any final words that you want to leave myself or our listeners with? Is there anything that we didn't cover that you really wanted to? - No, I just wanted to again, express gratitude for being here, including me in this, for sharing your own health journey and letting us at Heartflow be a part of that and wish you all the best. - Thanks, appreciate it. We'll chat soon. - There you have it friends. I hope you enjoyed this episode. If you did and want to stay up to date with future episodes, be sure to hit that subscribe button on YouTube and follow on Apple or Spotify. - Finally, thank you for showing up and the effort that you're making to take control of your health. I look forward to hanging out with you again in the next episode.