Ep. 54: “The Stents I Didn’t Get”: One Man’s Journey From Scary Scan to Smarter Questions — with Steve Kaplan, Author and Tech Entrepreneur

A high coronary calcium score can feel like a verdict. Steve Kaplan got a 641 at age 67 while he was still outpacing younger riders on the mountain bike trails around Lake Tahoe. Within months, several cardiologists told him he needed stents or a triple bypass. In this episode, Dr. Regina Druz talks with Steve about the year he spent questioning that plan. Steve built and sold two IT consulting companies and wrote nine technology books before he wrote a book about his own coronary artery disease, and he turned AI into a research partner that helped him interpret lab results and cardiac imaging reports and bring sharper questions to short appointments. Listen for the scan result that landed on his phone during a flight home from Cedars-Sinai, why a stent pioneer told him to skip the angiogram altogether, and the freeway analogy that made two seemingly conflicting test results make sense. Dr. Druz explains what a coronary calcium score can and cannot show, how she uses small doses of statins to help stabilize plaque, and what the ISCHEMIA trial found about stents in stable coronary artery disease.

Watch on YouTube: A video version of this episode is available on the Own Your Heart Health YouTube channel. Subscribe to be notified of new episodes.

Episode Chapters

[00:00] Meet Steve Kaplan, From Sickly Kid to Athlete
[04:43] A Calcium Score of 641 Changes Everything
[07:48] Triple Bypass Advice and a Stent Pioneer’s Verdict
[13:12] Using AI to Find the Right Heart Scan
[18:52] What a Coronary Calcium Score Can’t Show
[24:21] How Statins Stabilize Plaque in Small Doses
[28:59] Steve’s Medication Plan and Photon Counting Scan
[33:20] How Scanner Technology and AI Affect Cardiac Imaging Results
[43:08] How AI Helped Steve Ask Better Questions
[50:43] Heart Attacks vs Stable Disease and the ISCHEMIA Trial

Transcript

[00:00] Meet Steve Kaplan, From Sickly Kid to Athlete

Dr. Regina Druz (00:02): Welcome to Own Your Heart Health. I’m Dr. Regina Druz, your holistic cardiologist. This week, we will dive into common heart health concerns, uncovering root causes and unpacking scientific discoveries and controversies. The information provided does not constitute medical advice. Please contact your healthcare practitioner before making any changes that may impact your health.

Welcome, everyone. Well, you know me. This is another Friday Fun Day. Yay! So today I’m with a very special guest. Usually on my shows, I have medical professionals or wellness professionals, entrepreneurs, scientists. But today, actually, I have someone who is a book author who also has lived through some of the most difficult times that patients experience when they are found to have cardiovascular disease.

And who is willing to share his story so that you can learn from it and maybe ask your doctors the right questions, look at the right resources, and as always, we’ll provide those to you. Just a little word of advice. Whatever you hear on my show when I discuss it with colleagues, whether medical colleagues, wellness colleagues, or even patients, remember that this is not medical advice. This is just something that comes to us from our life experiences.

And while we weigh in with our expertise, the particular situation that you might be in health-wise, it is important for you to discuss it with the physicians and medical professionals who are taking care of you so that you get the right health outcome and are not sort of just running around guessing what should be happening with your heart health. So today I’m welcoming Steve Kaplan to the show. Steve, welcome. And please introduce yourself and tell us who you are, where you’re from, and what is going on.

Steve Kaplan (01:58): Thanks, Dr. Druz, and thanks for having me on the show. Steve Kaplan. I live up in Lake Tahoe, just across the California border on the Nevada side, and have been up here about fifteen years. And before that, I spent most of my adult life in the Bay Area in California.

Dr. Regina Druz (02:21): Okay. And what brings you to our show today?

Steve Kaplan (02:27): You know, I love your format and the guests you’ve had on the show, and I thought it’d be a great opportunity for me to be a guest and hopefully help get the word out to a lot of your listeners about the things that I’ve learned in my heart journey.

Dr. Regina Druz (02:44): All right. So let’s go right into it. Tell us about your heart journey. What happened? How things started, how things panned out. First of all, you’re here to tell your story, which is always great. You know, for anyone with a heart journey, we always want to make sure that a person is here in front of us able to tell their story. Right. You know. And I think these days we’ve gotten pretty good at making sure that patients, whatever the heart story is, make it back to the other side. But you know, tell us the heart story.

Steve Kaplan (03:13): Well, I’ll kind of start before that, growing up as a kid, which was in Pittsburgh, Pennsylvania. I was very sickly as a kid and small for my age, and like I said, I was about as coordinated as a shopping cart with three wheels. And then I got encephalitis at eight years old and almost died, you know, barely made it out of the hospital. So that was kind of my background. And you know, my grandparents immigrated from Pinsk. I understand you’re also from Ukraine. I don’t know if that was the work ethic that got instilled in me or not, but anyway, I learned to work hard and eventually got into wrestling in high school. In the beginning, there were five ninety-eight pounders, and I was number five on the team. By the time I graduated, I was MVP, and then wrestled in college. Not very well, but made the team. And started running and ran a marathon and coached wrestling and then got into mountain biking and snowboarding and so on.

Dr. Regina Druz (04:26): So you were a pretty athletic individual, right? Probably more so than the majority of people, right? There are a lot of people who play sports in their youth, but it sounds like you were athletic even beyond just the college athletics, for example.

[04:43] A Calcium Score of 641 Changes Everything

Steve Kaplan (04:43): Yeah, nothing natural at all. And I’m still uncoordinated to this day, but I work hard at it. And that kind of shaped my life in my sports and in business. I started and ran and sold a couple of IT consulting companies, sold them both eventually to publicly traded companies, and wrote nine different IT-related books, including different editions. And yeah, I felt very healthy, strong. Mountain biking up in Tahoe, especially with people visiting me from the Bay Area at lower altitude, I could usually outride even guys 15 years younger.

But then my wife, Wendy, was seeing a functional doctor, and I decided to go in on a session with her. Based on my family background (my dad had a quadruple bypass at sixty-one, and both of his brothers had heart disease) and on some slightly elevated lipid scores, based on those factors, she said I should get a coronary calcium scan, which I’d never heard of. But I went in, you know, confident that I would get a score of zero, and it came back at 641. And so that kind of blew my world apart.

And I did what a lot of people do when they get really bad news like that and don’t know what to do, which was nothing. So I kind of just ignored it for about seven or eight months, until that same functional practitioner had me get more comprehensive lab work done, and

Dr. Regina Druz (06:28): Mm-hmm.

Steve Kaplan (06:29): one of the numbers, especially MPO, myeloperoxidase, if I’m not saying that right.

Dr. Regina Druz (06:34): Yeah. Thank you.

Steve Kaplan (06:38): I write all these words in the book, and I know how to spell them, but speaking them is not necessarily my forte. But anyway, that was quite elevated, and both her and my MD said, you know, you need to see a cardiologist. And

Dr. Regina Druz (06:53): Okay.

Steve Kaplan (06:54): I just never saw myself as a cardiology patient, so it was hard. But I went in and saw him, and he told me that I needed to get an angiogram. And I wasn’t so thrilled about them sticking a wire up into my heart. What else you got? And I ended up getting a CCTA scan at a local hospital. With what I’ve learned now, I would never have done that back then, because it was a fairly low-resolution scan and didn’t have AI and some other things. But

Dr. Regina Druz (07:31): What year was that, roughly?

Steve Kaplan (07:33): That was 2024. September 2024.

Dr. Regina Druz (07:37): Okay. So it was a couple of years ago. Technology was already on the market for the AI quantitation for CCTAs, for sure. Okay.

[07:48] Triple Bypass Advice and a Stent Pioneer’s Verdict

Steve Kaplan (07:48): It was. And then that scan came out really bad. I mean, for me, it said, you know, seventy to ninety-nine percent blocked in two or three of my arteries. So I went back to the doc, and he said, you’re probably gonna need a triple bypass. And that really blew my world apart. And all of a sudden, the stent was looking pretty good. And we were on a trip in Costa Rica, so I saw a doctor down there, and he reviewed it. He also said, yeah, you probably need a triple bypass.

And so I was feeling really down and dejected, because I saw my dad, you know, it was hard on him, and I didn’t want them cracking open my sternum. And on top of all that, when I first got that first CAC number, 641, that night lying in bed, my chest was hurting, or pressure.

Dr. Regina Druz (08:44): Mm-hmm.

Steve Kaplan (08:44): It had never happened to me before. And it was fine when I was exercising or whatever, but at night, or when I thought about my heart, I’d feel it again. And so then with these bypass recommendations, I said, I gotta do something. I’m gonna go crazy. And so I started listening to heart books, listening to and reading everything I could find. I started researching like crazy. You know, in Tahoe, I kind of toned down my mountain biking and so on, and started doing more long hikes with one AirPod in my ear and the other one listening for bears. I would go out and, you know, listen to these books, and so I started learning more and more.

And, you know, long story short, I ended up seeing about eight cardiologists originally. They all said I needed an angiogram or stents or bypass. One of them, who I got through a friend, told me, well, I don’t think you need stents. And he went over the trials with me, COURAGE and ISCHEMIA and ORBITA and FAME 2, and that for asymptomatic, stable individuals, a stent doesn’t reduce the risk of heart attack or associated mortality.

And so I was feeling pretty good until I got another, more advanced CCTA scan, because I knew better now. A 640-slice resolution, and I got a more involved AI test that gave me FFRCT, as you know, an estimated measurement of the blood flow in my LAD, my widowmaker. And it said it was only 0.69 (it’s supposed to be at least 0.8) and said I was 72% blocked. And so that report went to my cardiologist, and at eight a.m. the next morning, he called me. Never a good sign. And he said, Steve, I’m changing my recommendation. You need to get an angiogram and probably stents.

So, you know, I kept pushing and pushing. But he also had given me a stress echo, an echocardiogram, where I hit 17.2 METs, which is, you know, very, very good for my

Dr. Regina Druz (11:02): Very impressive. Yeah.

Steve Kaplan (11:05): And I still felt strong, and my heart rate recovered quickly as well. And then Dr. Zeger, he’s in the book, showed me these studies. And so I kept telling people, well, you know, I’m willing to get the angiogram and the likely stents, but tell me how the stents are gonna help me. And nobody ever could. Then

Dr. Regina Druz (11:30): Okay.

Steve Kaplan (11:32): finally, through a friend, I met Dr. Tim Fischell. He wrote the foreword to the book. Just a quick background on him: professor of medicine at Michigan State, Cornell, Harvard, Stanford trained, top of his class at Cornell, co-invented the drug-eluting stent, the most common stent in the world. Millions of patients bear his fingerprints. He has started around 10 cardiovascular companies and has over 100 vascular patents. So I thought, if anybody on the planet is going to tell me to get a stent, it’s Dr. Fischell. But he actually did not. He reviewed all my scans and lab work and everything else. He said, Steve, don’t get a stent. It won’t do you any good. He said, don’t even get an angiogram, because if you get an angiogram, there’s something known as the oculostenotic reflex. Yeah, that tends to

Dr. Regina Druz (12:32): No, yeah. So let me sort of stop you for a second. You’re mentioning a lot of terms, and I know that some of our listeners may be familiar with the terms and some may not. So rest assured, we will define all the terms and speak a little bit about the trials so that we’ll put it all in context so that you understand exactly what’s going on. But you know, Steve, clearly you’ve done your homework, and you had access to some of the docs that are sort of, you know, in places that write the guidelines, right, and author the studies. So you are fortunate in that regard. So Dr. Fischell said you’re good, you know, but what did he say you should do instead of the stents?

[13:12] Using AI to Find the Right Heart Scan

Steve Kaplan (13:12): Well, he said, don’t even get an angiogram, because if you get an angiogram, they’re gonna give you a stent. He advised keeping my blood pressure perfect and reducing my exercise intensity by about ten to fifteen percent. If I did have any chest pain or shortness of breath, don’t bother getting any more imaging, you know, go straight to the cath lab and get a catheter angiogram.

But by that point, I already had an appointment set with an interventional cardiologist. And so I met with him, and he knew Dr. Fischell. They’d been on a panel together, but it didn’t change his recommendation. He said, no, you need to get an angiogram. And I didn’t want to do it.

A real big part of the story I should have mentioned is that in the beginning of all this, I was using AI as kind of a search tool. Being in tech, I was kind of working with AI. But by this point, I was using it as a total, I’m gonna call it a medical partner, you know. My research staff, my chief of staff for preparing all my notes, my synthesizer to look at my labs and my physician visits and my functional data and my watch output, you know, everything, and synthesize it all for me.

And so it was a really interesting thing, because when that cardiologist realized that I wasn’t going to get an angiogram, he suggested a nuclear PET, which I’d heard of, but I didn’t really know a lot about. And he even booked it for me at the hospital. And by this time, I’d learned not to walk into a scan without doing my research.

Dr. Regina Druz (14:57): Prepared.

Steve Kaplan (14:59): Yeah. And so I asked AI, okay, you know, it’s at this hospital, this is the type of scan it is. Is it gonna give me the information I need to know what to do regarding a stent or not? And it said, well, I’m not sure. It looks like they have one of the best scanners in the country, but ask them these questions. So I emailed the radiology department, and they emailed back saying, no, we don’t do that, that, and that. So, like most nuclear PET scans, they looked at blood flow, but only at a global level. And even that was a calculated number, not measured directly.

Dr. Regina Druz (15:37): Mm.

Steve Kaplan (15:39): So for me, where I had this widowmaker that appeared to be seventy-two percent blocked, 0.69 FFR, it would have been pretty much useless to me, whatever it showed. And so I used AI. I said, well, where can I find one that will help me? And there weren’t very many answers at that time, but Cedars-Sinai in LA came up.

Dr. Regina Druz (16:00): So

Steve Kaplan (16:02): I flew down to Cedars, got the scan. I was on the plane flying back home from California, and my portal dinged, and my results were already in. And I knew this was the moment. I was either gonna go to the cath lab or not. And I opened it up, and it said, yeah, your blood flow is not only normal, it’s almost twice normal.

And at that point, I realized that, you know, I need to write a book about this, because I’m on a lot of Facebook heart groups, and people asked me a lot of questions about my journey as I went along. And I just realized that so many… When I got that first score, I was scared and frustrated and confused. And for a while, I even got into the, you know, the anti-statin Facebook groups, which are huge, over a hundred thousand members.

Dr. Regina Druz (16:59): I think I’m going to be permanently banned from that one, but okay, go on.

Steve Kaplan (17:07): Oh gosh. A reporter even interviewed me because of my participation, for an article, the anti-statin article. And you know, just as an example, this would happen all the time. A member would join, and she’d say, my cardiologist prescribed, you know, forty milligrams of rosuvastatin, and I don’t know what to do. And inevitably, the replies would start coming in. Just throw away your pills, and don’t tell your cardiologist. And I knew, even though I was still, you know, confused and scared and reaching out, I still knew that was really bad advice. And then I realized I did it myself. I had cut my statin dosage, you know, by three-fourths. I didn’t even let my doctor know.

But eventually, you know, using AI and finding other people to listen to, I kind of got pulled out of that. And my dad was a smart guy. He had two PhDs, and he was a big early Bayesian methodology practitioner. Bayesian reasoning is a kind of probabilistic reasoning. And so I rediscovered that, and I started using that as my North Star for what I should do next in this heart journey. You know, because for every person you can find saying, you know, lower your ApoB and your LDL, et cetera, there’s somebody else saying, no, it doesn’t even matter. You know, it’s good for you.

[18:52] What a Coronary Calcium Score Can’t Show

Dr. Regina Druz (18:52): So it’s funny, because in your story, I really see how impactful it is, because so many patients that come to us have lived either a similar story or a portion of what had become your story, right? Because this is kind of that crux, that tension in cardiology, is that we have great tools, and we’re constantly expanding in terms of our technological capabilities. But the answers that we get are from large clinical trials that are population-focused. They’re group-focused. And it’s really challenging to apply a lot of these answers to a person in front of you, because there are so many unknowns. But one interesting thing I want our listeners to understand, to reflect on, is that the coronary calcium score (and we talked about it on the show, and I talked about it in some of my videos) is actually a great test.

It’s easily accessible. It tends to be inexpensive. There isn’t very good insurance coverage. Sometimes they cover, sometimes they don’t, but at most, it could cost, you know, maybe two, three hundred dollars, often even less than that. There are some medical groups or facilities that honestly give it for free, because that’s an opportunity for them to get some patients in who are looking for preventive cardiology evaluation or potentially need more than just a prevention action, may need treatment and intervention, which is kind of where your story goes.

But the coronary artery calcium score, as good as it is, actually shows us only calcified plaque, right? So the best-case scenario, the coronary artery calcium score is zero, which means there is no calcification in the coronary arteries. This patient typically has a very low risk of events in the next 10 years. This is what we consider short term. They have the best prognosis. The problem is that young people, especially women, almost always have a calcium score of zero. Why? Because the plaques are there, but they’re very small. They’re so-called soft plaques, right? So they haven’t had a chance to calcify yet, because this is a lifelong process.

And believe it or not, and that’s going to bring us to the story and the statins, this process of arterial plaquing is not an adult phenomenon. We pick it up in adulthood, but this process actually starts in childhood. We do know, and you know, I’m going to bring my little model here. So if you’re listening to us, thank you for listening. But if you can watch us, this would be very helpful to you. Because when we start, we start with a nice, sort of pristine, beautiful endothelium, just one cell thick, lining every single vascular surface in our body. And we have, you know, a little membrane that separates it from the muscular portion of the artery, right? Because the artery has to contract, it has to expand. And of course, there’s an outer covering that just protects the arteries, you know, sort of sheathes them, right?

So the process that starts in childhood is when ApoB-containing particles literally go right through this one single cell lining, the endothelium, and they get stuck right below it, right? And this process is called transcytosis. Now, it’s an important process, because this is how our blood brings cholesterol to our tissues, right? Cholesterol is really not a villain. We need it. We need it for our cell fluidity. We need it to repair ourselves. But how will it get to every single cell that we need to maintain? You know, they can make their own cholesterol. Pretty much every single cell in our body makes its own cholesterol. So the supply is there. But when the blood brings it through, it actually doesn’t need any receptors. It literally sort of goes in as if it were filter paper, right? And this process is called transcytosis.

So what happens is that we know from studies in very young individuals, you know, children who perished from traumatic experiences, soldiers on the battlefield, right, who had autopsies, we know that they have these little deposits in their arteries, and they’re called fatty streaks, right? So when people say, oh, LDL cholesterol or ApoB is not important for heart disease, they’re basically arguing with a biologically proven fact that this process of transcytosis is taking place.

Now, obviously, as one goes down this, you know, vascular tunnel, the endothelium, what’s lining our arteries, is subject to multiple influences: inflammation, oxidative stress, various disruptions, flow disruptions, right? You may not be super inflamed. Maybe your inflammation is normal, but there are local flow phenomena, because blood flows through the blood vessels at a certain speed, at a certain angle. There are shear forces. And depending on how these flow phenomena and other factors in your environment affect you, we start building plaques.

So we know that people in their 30s, about 10% of those individuals, plus or minus, will have some sort of plaque in some sort of vascular bed. You know, there have been multiple studies in that regard. There was a recent study called REACT, where they actually did 3D imaging, 3D ultrasound, something that we’re looking at at Holistic Heart Centers. And we know that young individuals have soft plaques. And very often, just like, you know… Steve, how old were you when this calcium score was obtained, if you don’t mind sharing?

Steve Kaplan (24:18): No, yeah. I was sixty-seven when I got the first score.

[24:21] How Statins Stabilize Plaque in Small Doses

Dr. Regina Druz (24:21): Okay, so 67. So you definitely were beyond the age when your dad had a heart attack, right? And you had no symptoms, and you were super active, right? So by the time people are in their 60s, we kind of do expect some plaque formation, right? We expect, you know, some alteration in what’s happening in the blood vessels. We expect some calcium buildup. We could get some narrowing of the artery, but very often people who are active, who are exercising, form so-called natural bypasses. So they may not even know about their arteries, and their exercise tolerance continues to be excellent.

And these areas which are calcified are usually much more stable. They’re not going to give us this scenario here, which is what we call thin-cap rupture of the plaque. It’s called a fibrous plaque or fibroatheromatous plaque. The cap of it is too thin, there’s no calcification, it ruptures, and of course, you could see all this, you know, sort of blood and thrombus. That’s basically the heart attack situation, right?

So what statins do is that statins actually fortify the cap, right? So they take people from this thin, sort of fragile scenario to a scenario where their plaques become calcified. And that’s, of course, stability. And you know, statins also, as drugs, augment nitric oxide, which is what the endothelium uses for its protection, right? So for anyone who says, I am absolutely not going to take a statin, even though I have coronary artery disease, I would say do reconsider, because a statin does not always mean that you’re supposed to be on a very high dose.

Actually, what we often do with our patients is that our doses are minuscule. And the reason why our doses are so small, you know, like one of my colleagues calls it microdosing. You know, microdosing is in vogue right now because of GLP-1s, but we’ve been microdosing statins for the past five years. So microdosing statins allows you to tap into what’s called the pleiotropic benefit, where there’s nitric oxide augmentation, and actually even a change that is happening here.

And this may be a little bit too small to see, but these sort of blue dots are supposed to represent immune system cells called macrophages. They get inside that area below the endothelium where cholesterol is accumulating, and they try to digest it, so they sort of become very bloated and can’t get out, and they’re called foam cells. And so then the rest of the immune system cells come in, and the whole process starts. And Steve, you mentioned MPO, and that’s what we see, right? We see high MPO, because we know there is some vascular remodeling happening from those immune system cells.

But statins are capable of turning them off, right? So these cells are below the endothelium. They’re stuck, and they are sort of transmitting, like, SOS, SOS, SOS, come and clean it up. You know, what statins are doing is changing the secretory phenotype to make sure that these cells are capable of kind of turning themselves off and protecting the, you know, turning off the plaque, right? Changing the plaque into something less inflamed, you know, a little bit more stable. So that’s how statins work.

And you don’t necessarily need, you know, it’s not a dose-dependent effect. It’s just a class effect. And so if you’re using a smaller dose with supplementation, with lifestyle, and sometimes non-statin alternatives, you can actually get stabilization without experiencing side effects. So you know, this is what I think is missing in this discussion, because, you know, cardiologists are sort of in this camp saying you must reduce LDL at all costs. And they’re not wrong, because LDL reduction, ApoB reduction, is very powerful. It may even result in plaque regression. But in this other camp is, as Steve, as you’re saying, the Facebook group that says, throw out your scripts, throw out your tablets, don’t take them.

You know, both of these groups still agree on the vascular biology. So the question is, how does one get to plaque stabilization using the least aggressive treatment? And that aggressive treatment is predicated on the person’s risk. So when we do have a high-risk situation, of course we need to treat more aggressively. So Steve, you had a change of heart, and you told me in your notes that you didn’t get a stent, but you embraced aggressive medical therapy. Tell us about it.

[28:59] Steve’s Medication Plan and Photon Counting Scan

Steve Kaplan (28:59): Well, yeah, I went on a statin and then decreased the statin. And once I started using, you know, I say Bayesian reasoning, looking at the evidence and understanding the evidence hierarchy, with randomized controlled trials at the top of the hierarchy, then I went back with my new cardiologist, and we arrived at a statin level that made more sense. And, you know, I toned back the most severe part of my exercise. I already ate a fairly good diet, but I ate better. I went to the Mediterranean diet and cut out most red meat. I tried to do pretty much everything I could do to make things better.

It’s kind of funny, though, because my dad, again, was very anti-medicine. And I have four siblings, and all five of us grew up resisting medicine. But I have a little five-pound chihuahua named Piper. And a couple years ago, my wife Wendy and I… Piper was having trouble breathing at night, and the vet was closed. We stayed up with her all night and took her to the vet in the morning, and the vet said, you know, she’s got congestive heart issues. She’s not likely leaving. And we went back the next morning to say goodbye, and she saw us and perked up. And they put her on twice-daily heart medicine.

And this was in the winter, and the next summer, I was up hiking trails with her. And I remember when it hit me on one trail. I wouldn’t let her get too far ahead of me, because she’s the perfect size for a bobcat or coyote snack. But she was a little bit ahead on the trail and looking back at me, and I’m just thinking, you know, this medicine really works. She would be long dead if she wasn’t on that medicine.

So I went back to my cardiologist and said, what do you think about ezetimibe? He said, yeah, let’s add that. And then, you know, I got my LDL down into the forties, but my ApoB was still stubbornly in the mid to high sixties. Which is great if you don’t have severe heart disease. But for me, at high risk, you know, I thought it needed to be lower, and he agreed. So I went on Repatha, and, you know, I drove it way down after that.

So that’s the… And of course, you know, I take baby aspirin, although I’ve had to stop that due to stomach ulcers. So I’m kind of looking for an alternative right now. But those are certainly the cholesterol-lowering medicines I take. And I take supplements that I try to ground in science. It’s not always possible, but, you know, I use my best guess. And that changes as well. Like, I was really into nattokinase for some time, but then I stopped that as new evidence came in. So yeah, I’m just trying to stay on top of the medicine.

Just a couple of weeks ago, I got a photon counting scan by Dr. Filippo Cademartiri in Milan, Italy. He’s one of the pioneers of the scan, which, being newer, is still highly dependent upon the practitioner. Yeah. And so I had him do my heart and my neck, my carotids. Carotids, how do you say…

Dr. Regina Druz (32:46): Think of carrots.

Steve Kaplan (32:48): And the good news was that the CCTAs I got had dramatically overestimated the stenosis. Instead of 72% in my LAD, for example, the photon counting scan showed it was only 48%. The bad news is that in my carotid, my right one, I still have a significant amount of low-density, non-calcified plaque. The worst kind, the soft plaque. And

[33:20] How Scanner Technology and AI Affect Cardiac Imaging Results

Dr. Regina Druz (33:20): But you will follow it. So you see, this is an important point, I think, for our listeners. You know, we’re going to look back at the coronary artery calcium score. So the coronary calcium score, as I said, a score of zero is the best scenario, but it does not rule out soft plaque. So young people tend to have soft plaques. Older people may also have soft plaques, so they may have plaques which are inflamed.

And so when we do coronary CT angiography, which, Steve, is what you had, right? The abbreviation is CCTA. That’s where things get really interesting, because recent advances in coronary CT made it possible for us to quantify, with artificial intelligence, two really important areas, right? One area is what actually is the blood flow, relatively speaking, down a vessel which may have plaques. And so we measure something called fractional flow reserve, and, you know, these numbers do correlate to the ones that doctors get in a laboratory when they insert a catheter into the coronary artery and insert the wire for measurement, right? So the invasive, non-invasive correlation is pretty strong.

And so we know that we are able to tell whether or not there is some lack of oxygen coming to the area of the heart that a specific coronary artery is feeding. And this is what ischemia is. So a person may have no symptoms, they may have a lot of symptoms, they may have sort of symptoms. You know, they could have vasospasm, which I think, Steve, maybe that’s what you had after your diagnosis. You got, you know, anxious and upset, and at night you would get some chest pain just thinking about it, right? Even though you didn’t have classic angina when you were exercising.

So we are able to tell, using this FFR measurement, should we worry about the blood supply for this individual, right? We have three main arteries and sort of a big chunk out of which two of the main arteries come out, called the left main. And so we need to know, is this a situation where their heart somehow is not getting enough blood supply? And remember, these are measurements at rest. This person is not exercising, not doing anything.

Now, the problem with AI quantitation right now is that it appears to be highly dependent on the protocol that is being used, and on the AI itself. And you mentioned that you used AI extensively as sort of your medical, you know, adjudicator, if you will. And I use AI quite a bit as well. But when it comes to cardiac imaging, we know that the technical properties of the scanner itself, some of them are pretty specific properties that you wouldn’t know about as a patient at all. And even your referring doctor may not know about these. You have to be a cardiac imager to know this.

And so not only the scanner parameters, the acquisition parameters, but also the AI algorithm itself is not apples to apples. So, you know, you may bring the exact same CT angiography, the exact same test. You may feed it into this AI algorithm or that AI algorithm and get very different results. So this new modality called photon counting CT, which is a new emerging modality, overcomes a lot of these limitations.

But you know, I feel like we actually do much better with our patients, because we scan their carotids pretty much all the time. Carotids, and, you know, their heart, their ultrasound, their echo, their abdominal aorta. And we’re just expanding pretty much into whole-body ultrasound, because there are so many vascular structures. So we can tell, as time goes on, if there are changes in the blood vessels.

Now, this is hard, because there’s also a lot of variability, right? So this is where I think the friction comes for a lot of patients, is that they’ve committed to do things well. They’re taking medications or not taking them, you know, they’re doing some of their lifestyle modification. And you know, there’s so much effort, there’s so much intensity, and they then come, for example, for a carotid scan, or they come for a CT, and they’re not seeing much change, or they’re seeing some worsening, or they’re seeing plaques go through different changes, right? Some become better, some become worse.

And I want to tell you guys that this is 100% normal, because there is about a three-year time span for any change that’s going to happen in a blood vessel, which is a stable change or chronic change, not an acute change. Obviously, if it’s an acute MI and, you know, there is rupture of some of those atherosclerotic plaques, that doesn’t take three years. That’s sort of immediately apparent. But for the blood vessels to shift, for the vascular biology to shift, it’s a multi-year phenomenon.

So you can drop your LDL and your ApoB in about 12 to 16 weeks, and you’re going to be great. But you need to keep it like that for three-plus years for your blood vessels to even begin to show changes. And when those changes do happen, they change by maybe, like, one percent, two percent, right? And this is called percent atheroma volume. So I want you to be realistic and not necessarily run to your doctors and demand that they put AI onto your scan and show before and after and tell you exactly, you know, what those changes are.

But the point is that we also have some other really exciting tools. And I’m personally very excited. And I don’t know, Steve, if you had access to it, but there is a technology right now, also based on CT angiography, that can actually measure the degree of inflammation in the fat that surrounds the coronary arteries. The company is called Caristo. They just got FDA approval here in the United States. It’s been used in Europe quite extensively. And this scan is called CaRi-Heart, hopefully I’m pronouncing that correctly.

And so CaRi-Heart is actually able to tell us how much inflammation there is, right? You saw those little blue cells in my little model, right? You know, that’s what makes the fat that surrounds the coronary arteries inflamed. And that usually transmits into artery inflammation, because these structures are very close to each other, right? They’re basically all jammed in a tiny little space. Your coronary arteries are anywhere from two to four millimeters in diameter. You know, you need a special magnifying glass to see it.

So the point is that we are getting better, I think, at being able to figure out whether the effort the patient is making, whether it’s a statin, Repatha, ezetimibe… And we’ll talk about these drugs a little bit in November, because I’m waiting for the American Heart Association trials to drop and, you know, disappoint us on the whole Lp(a) story. But the point is that we want to measure things where they count, because we know how hard it is for patients to keep up with this effort, you know, and wait for years to figure out if things are happening positively or negatively in their blood vessels. So, does that parallel your research? Is that what you discovered in your journey and in your book research?

Steve Kaplan (40:43): I didn’t know about the…

Dr. Regina Druz (40:45): CaRi-Heart? Caristo?

Steve Kaplan (40:47): What you just mentioned sounds really interesting. But

Dr. Regina Druz (40:49): It’s very interesting. And I think, you know, it’s even more interesting because these fat deposits, some of course are around the arteries, and they’re meant to be there because they serve a protective function. At least when we were younger, they serve a protective function. Once it becomes inflamed, that’s certainly not protective anymore. That’s detrimental. But there are also these fat deposits sort of on top of the heart, and this is called epicardial adipose tissue, or EAT. Right. And the one around the coronary arteries is called perivascular adipose tissue. I’m not sure if it’s abbreviated as PAT or PVAT, but they just have names based on location.

And so this epicardial adipose tissue is actually also very active. And we know from studies that it does play a role in the pathophysiology of heart failure, especially heart failure with preserved ejection fraction. We’re in the midst of a huge epidemic of heart failure with preserved ejection fraction, and that tends to tilt more toward women and people with hypertension and diabetes. It’s much more difficult to treat than heart failure with reduced ejection fraction, which is what it sounds like your dog had. And medications right now for heart failure with reduced ejection fraction are absolutely extraordinary. You know, the impact that they have, both for functional class and actually for mortality reduction, is extraordinary. So, you know, this is not one of those things where you can only go lifestyle and skip medications if you have it, right? So that’s kind of, you know, the mindset here.

So Steve, how did AI help you? Sort of tell us that, because, you know, I just came back from an AI in healthcare meeting yesterday in New York City, and I spoke to a couple of companies and some really serious, you know, investors. And one of the issues that they brought up is trust, right? Because AI models are probabilistic. They’re not deterministic. And, you know, today they say two plus two is four, and tomorrow they say two plus two is four point two. It’s sort of like that, right? Because it’s a probabilistic estimate, not a deterministic calculation. But how did you use AI in your patient journey?

[43:08] How AI Helped Steve Ask Better Questions

Steve Kaplan (43:08): Well, like I mentioned, it really evolved. I used it originally as just kind of a search tool, but then I learned I could upload my labs into it and upload my visit reports into it. And so I started using it much more as a reasoning partner and, you know, ultimately kind of ran everything by it. I know with my first cardiologist, AI helped me write questions to him that I put on the portal, and he never even responded to those. I would never have been able to even come up with them. But I fired him after that.

Dr. Regina Druz (43:49): You fired him because he didn’t respond to questions, or you fired him because he didn’t agree with AI? Like, which one?

Steve Kaplan (43:55): No, because he didn’t respond at all. Okay. I actually ended up going through 10 cardiologists by the end of the journey.

Dr. Regina Druz (44:08): Cardiologists, please listen. There is a lesson here. You must respond to your patient inquiries, acknowledging that AI is not you, but it could at least give them some focus on what to ask you. So please, please take a listen here, okay?

Steve Kaplan (44:23): Well, and AI helped me understand the whole thing about what stents do and don’t do, you know. It helped me with the studies after Dr. Zeger told me about them. And I had already made an appointment with a cardiologist at a local community hospital, ranked third in the country, though, for cardiovascular care. And I met with him, with my wife Wendy. And he looked at my reports, and he said, you know, with his fingers, this is a normal artery. Yours is seventy percent blocked, like around here it goes. So we have to put a stent in and open it back up, or you risk a heart attack. And by that point, I already knew that was not correct, not for me.

Dr. Regina Druz (45:02): The main

Steve Kaplan (45:04): danger was plaque rupture, not, you know, stenosis. That’s as best as I could tell, anyway. So, you know, using AI like that to become more and more sophisticated, to find that the nuclear PET that I was scheduled for wouldn’t have addressed my…

Dr. Regina Druz (45:24): Specific question that you had to ask. Yeah.

Steve Kaplan (45:26): Finding the one in Los Angeles. So I’d say probably the biggest thing it helped me with is synthesizing everything, including research, and helping me ask better questions than I could have ever begun to do on my own.

Dr. Regina Druz (45:42): Yeah, and I think that’s quite a legitimate use. And, you know, at Holistic Heart Centers right now, we will actually be providing a patient agent. It’s completely internal to us, so it’s only for existing patients at this point. But this is really to help them interact with their medical information and understand, based on the curated literature and verified sources, how their medical information, the studies, the tests that accrue with us, what does it actually mean, right? And this is very important, because when you are in these general frontier AI models, they tell you sometimes what you want to hear.

You know, I had patients come to me who invented some sort of cardiovascular risk stratification scores and asked AI if they were doing better or not so bad for their age group. And of course, it agreed. It said, your score is not so bad, and you’re doing great. But then when you look at it, it was completely not the real situation. But the point is that being able to bridge some of those gaps, you know, in patient education and access to information, is really important. Like even, you know, figuring out, let’s say, medications and medication side effects, right? This is another very important category. But that element of trust and that element of continuity, this is a difficult one, you know, for AI to develop. But obviously, we are working on it.

Something that you mentioned in your story also is very important, which is that you are a person of means, right? And you had an opportunity to reach out to some of the physicians that are fairly well recognized in their field and, you know, to travel to different locations to get what you needed to get. Do you feel that AI, in many ways, for people who are not able to do that or not willing to do that, democratizes access, right? In other words, does it really open up the opportunity to someone who can’t buy a ticket and go to LA, or buy a ticket and go to Milan and have a photon counting CT if they want to? So, yes or no? Does it level the playing field?

Steve Kaplan (48:02): I would say absolutely, to a large degree. And like I say, even though I had the resources to do things, I did a lot of things that I wouldn’t have done if I had known how to consult AI better back in those days, including getting a CCTA on a 256-slice scanner without AI. And that was just a waste of money, time, and radiation.

Dr. Regina Druz (48:26): Well, but by the way, you can take those images and feed them through AI. Nowadays, they do have this capability. We can do it retro, a retrofitted determination, if you will. Among your 10 cardiologists, well, we know one didn’t answer your questions, so we know one outcome. But among your 10 cardiologists, how responsive were they to your AI information sharing? Let’s put it that way.

Steve Kaplan (48:56): I would say pretty responsive. I mean, I also learned, you know, how to choose cardiologists better who would fit with me. It was part of the whole process. But I found the people, on the whole, to be very responsive and, you know, very smart and sincere. The first one I fired, but all the rest were just more of a natural transition.

And, like, the interventional cardiologist who really wanted me to get the angiogram, you know, he wasn’t wrong. It’s just a different opinion. And in my particular case, it probably wouldn’t have helped me. But two experts can still look at something and interpret it in very different ways.

And in fact, when I went to Cedars-Sinai and I got my results back, sitting on the plane, I said, well, you know, I got the CCTA that showed I was seventy-two percent blocked and an FFRCT of 0.69, and you’re saying my blood flow is nearly twice normal. One of these must be wrong. And AI said, no, it’s not. Think of a freeway, like you have to go somewhere on the freeway. And the FFRCT is saying we have seventy percent lane closures on that freeway, so you’re likely to have some severe traffic.

Dr. Regina Druz (50:31): Yeah, some congestion.

Steve Kaplan (50:32): Yeah. But the nuclear PET scan is saying, oh yeah, the highway has seventy percent lane closure, but we measured traffic at rush hour, and everything’s going smoothly.

[50:43] Heart Attacks vs Stable Disease and the ISCHEMIA Trial

Dr. Regina Druz (50:43): Yeah, exactly. So that’s a great analogy. And I also want to circle back and give our listeners a little bit of a framework here. So stents, and actually what preceded stents, balloon angioplasty, revolutionized cardiology. They were probably the single most impactful cardiovascular intervention, outside of bypass surgery, which of course was tremendous. But if you don’t need surgery, stents were very impactful.

Why? Because we learned fairly quickly that for patients who are having a heart attack (nowadays it’s called acute coronary syndrome, and there are different types of heart attacks, about five different types), let’s just talk about a scenario that everybody knows, because it’s in the movies and the internet and whatnot, right? A classic heart attack. Somebody grabs their chest and says that they’re having chest pain. They’re rushed to a hospital. And we have this door-to-stent time of 120 minutes. That’s actually a national guideline. So if you choose to have a heart attack, please choose to have it in a large populated city where you’d be within that 120-minute period. Of course, I’m being sarcastic here, but it is what it is.

And so we know that in that situation, in that acute situation, stents save lives. Balloons save lives too. They were just not as great, because about 30% of individuals would end up restenosing the area where balloon angioplasty was performed. But stents were absolutely a game changer. They save lives, they save hearts. And we have a saying in cardiology that time is muscle, right? If you allow the ischemia that you already learned about to go unchecked, the heart muscle essentially destroys itself. So this is why every second, every minute counts. And that 120 minutes is not some sort of, you know, number out of the sky. That’s really based on serious clinical trials. So there is no argument with this.

If you’re having a heart attack, if you woke up today and you have chest pain, crushing chest pain, and it’s not going away, please call 911. Please go to the emergency room. Please get that stent. You cannot argue with that. If you are an older individual and you’re scared because you came to a parking lot to go to a grocery store and you realized you cannot walk more than 100 feet without chest pain, please go to the ER. Please do the same, because this is a life-saving procedure.

Stable coronary artery disease, Steve, which is what you had, right? That’s a different story. And so COURAGE was the first trial. Look for the article on my website. I’m going to put all of those trials together for you so that you understand what they are. There were other trials as well, and probably the largest trial was called ISCHEMIA, right? So it was, you know, sort of very clear-cut. They took patients who didn’t have terrible disease.

I already mentioned that there are certain blockages that we always have to treat interventionally, whether it’s surgically or with stenting. We can’t not do it, because basically, you know, I recently saw a patient whose arteries were literally 99% blocked in every major artery. And there is nothing else you can do. There is only one choice here. You have to revascularize them, right? So that’s high-risk anatomy.

But the ISCHEMIA trial took a lot of individuals, over 5,000 individuals, who were not in that very high-risk group. But they did have ischemia, they did have blockages. And they said, okay, we’re going to give one group whatever is appropriate state-of-the-art medical therapy now, and then another group, in addition to that medical therapy, will get revascularization. So they will get a stent and maybe a bypass surgery.

And so they did all of that, and they found out that in that particular situation, which is a lot of people (and I think, Steve, you are sort of representative of that), in that particular situation, there was no benefit to revascularization. Yes, people who got stented or had bypass surgery, if they had symptoms, got nearly immediate symptom relief. But it wasn’t that they died less of cardiac events, and they certainly didn’t die less overall, right? So it’s cardiovascular mortality versus total mortality.

So this is very important, then, because when you are in front of your doctor and the doctor says you need a stent or you need bypass surgery, you need to understand why. And maybe some of the AI opportunity is just to go there and say, what are the clinical studies? How can I, as a patient, understand the merit of this proposed treatment for me personally?

Now, there are other factors, because as we’re getting better with this technology, as we understand more about the impact of genetics and oxidative stress and just all these other features that maybe we didn’t have just a few years ago, we’re able to get these answers precise and personalized, right? And so that’s what we’re coming into. But you do need to know what the evidence base suggests.

And for a lot of patients who are at, you know, this stage, going to my diagram, whose plaques are sort of right here, they’re obstructing blood flow. This is about 70% stenosis. So this is about what you had in your arteries, right? You can see that the artery lining is kind of pushed inward, right? We call it negative remodeling. All this stuff below the surface has been piling up, you know, there’s calcification, of course, and whatnot. But for a lot of these patients, lifestyle modification and medications are a very good strategy.

And giving them a stent in this area is not necessarily something that is going to be of benefit, unless they have symptoms that we can’t control with anything else. Or, as I said, they have coronary anatomy, blockages that are so dangerous or so severe that just giving them medication is really not appropriate, you know, and that could lead to a worse outcome.

So the purpose of this is not to… You know, I don’t want to fall into the trap of saying no stents for you, right? That’s not it. The purpose is to really give you the tools and to give you the story. And Steve, thank you so much for sharing your story, so that you understand that you have options, right? And these options are very important, because at the end of the day, it’s your heart, it’s your health, and you want to do the things which are right for you. And what may seem like the right thing a couple of years ago may not be the thing that is right today, right? Because the information is changing constantly. And I do think that that’s where AI will, in many ways, give us that opportunity for better patient education and really give patients some tools that could enable them to have informed discussions.

Steve Kaplan (58:04): Yeah, I agree completely.

Dr. Regina Druz (58:06): Good. So tell us about your book and where people can get your book, because it all started… You said you put your journey into your book. So tell us about that.

Steve Kaplan (58:16): It’s on Amazon.com: paperback, hardback, Kindle, and an audiobook version is coming in two or three weeks. That’ll be on Amazon Audible. I do have a funny story I just wanted to tell you real quick about it, though. Sure. About four weeks ago, I don’t know why, but my blood pressure started climbing. You know, I take it every day. And one morning it hit 187.

Ooh.

The systolic, the top number. And I was thinking, you know, this is ER territory. And I was thinking, well, if I have a heart attack, it’s really gonna be bad for book sales.

Dr. Regina Druz (58:57): It wasn’t gonna be terrible.

Steve Kaplan (59:01): Then my brother chimed in later, saying, well, maybe you should write another one called The Stents I Should Have Gotten, so we can publish it posthumously if we need to.

Dr. Regina Druz (59:13): Very funny.

Steve Kaplan (59:15): But, you know, I wrote it because of all the people on Facebook asking me questions, and, you know, wanting to help people avoid all the wrong turns I made. And, you know, I’m a patient. I don’t pretend at all to be a cardiologist, but I do talk a lot from the patient side. A lot of other people shared their stories with me that I put in the book, especially a lot of asymptomatic individuals. And I think that reading it will help people get more context, learn more, and most importantly, become, like you say, the CEO of their own heart healthcare. The average cardiologist has 15 minutes per patient. That’s just not a lot of time to learn everything and synthesize everything, so they can use AI to do all that, to connect the dots. Because at the end of the day, it’s our hearts, it’s our health. We have to be responsible.

Dr. Regina Druz (1:00:13): That’s right. And that’s why this podcast is called Own Your Heart Health, because the whole idea is to make you the owner of your heart health, so that you take responsibility and you take the actionable steps. And, you know, on the subject of AI, there was a very interesting thing shared yesterday at one of the panels in the meeting that I attended. One of the participants said, well, we often talk about human in the loop, but it’s actually the reverse. It’s AI in the loop, as part of the human interactions. And I think that’s what your story shows us, you know, AI in the loop that has given you some guidance and some opportunity, at least to ask the right questions, to find the right physicians, to get the right level of care that works for you, and it continues to be a partner.

Steve, thank you so much. I learned a lot, you know. I’m super grateful that you shared your story. And if we help even one individual to ask better questions and maybe change their mind and get better care for their heart and their overall health, that would be tremendous. And I’m looking forward to reading your book. I got the PDF, you know, and I have a lot of PDFs, but for sure, I’m going to give this one a read.

Steve Kaplan (1:01:31): Thank you so much. And I also learned a great deal. So thank you for sharing all your experience.

Dr. Regina Druz (1:01:36): You got it. You got it.

Thank you for tuning in to Own Your Heart Health with Dr. Regina Druz. This podcast is powered by Holistic Heart Centers. If you enjoyed the show, please rate and review us on your favorite podcast platform. To learn more about our services, visit HolisticHeartCenters.com and subscribe to our YouTube channel. The link is in the show notes. See you next week.

If you want to know where your own cardiovascular risk sits before that conversation, the HeartWell Quiz is a starting point.

Frequently Asked Questions

What does a coronary artery calcium score show, and what can it miss?

Dr. Druz calls the coronary calcium score a great test: easily accessible and inexpensive, at most a couple of hundred dollars and sometimes free, though insurance coverage is inconsistent. But it shows only calcified plaque. A score of zero means no calcification in the coronary arteries and, typically, a very low risk of events over the next 10 years. It does not rule out soft plaque, which has not yet had time to calcify. Young people, especially women, almost always score zero even when small soft plaques are present.

Does a high calcium score mean you need a stent?

Not necessarily, and that is the heart of Steve’s story. After a score of 641 and imaging that suggested severe narrowing, he was told by several cardiologists that he needed an angiogram, stents or a triple bypass. Dr. Druz separates two situations. In a heart attack, stents save lives and time is muscle. In stable coronary artery disease, which is what Steve had, the ISCHEMIA trial found that adding stents or bypass surgery to medical therapy relieved symptoms but did not reduce cardiovascular or overall deaths. Some blockages are so severe that they must be treated with a stent or surgery, so her advice is not “no stents” but to understand why a procedure is being proposed for you.

When is a stent urgent?

During a heart attack. Dr. Druz is unequivocal: if you have crushing chest pain that is not going away, call 911, go to the emergency room and get the stent. The same applies if you suddenly find you cannot walk more than 100 feet without chest pain. In those situations it is a life-saving procedure.

What did the ISCHEMIA trial test?

As Dr. Druz describes it, ISCHEMIA enrolled over 5,000 people who had ischemia and blockages but were not in the very-high-risk group. One group received state-of-the-art medical therapy; the other received the same therapy plus revascularization with a stent or bypass surgery. Revascularization gave people with symptoms nearly immediate relief, but it did not reduce cardiovascular deaths or deaths overall.

How do statins stabilize plaque?

Dr. Druz explains that statins fortify the thin cap over a plaque, moving it from a fragile state toward a calcified, more stable one. They also augment nitric oxide, which the artery lining uses for protection, and they help turn off the inflamed immune cells trapped beneath the lining. She describes using very small statin doses in her practice, alongside lifestyle, supplements and sometimes non-statin alternatives, to reach plaque stabilization without side effects, and says treatment should match the person’s risk. Talk with your own clinician before changing any medication.

Why can a CT angiogram and a PET scan seem to disagree?

Steve’s CT angiogram with an AI blood-flow estimate (FFRCT) suggested a 72% narrowing and a value of 0.69, while a PET scan at Cedars-Sinai showed blood flow he describes as nearly twice normal. The analogy AI gave him: one test counts lane closures on a freeway, the other measures traffic at rush hour. Dr. Druz adds that AI results on CT angiography depend heavily on the scanner, the acquisition protocol and the algorithm, and that photon counting CT overcomes many of those limitations. Steve’s later photon counting scan put the same narrowing at 48%.

How long does it take for plaque changes to show on a scan?

Dr. Druz says LDL and ApoB can drop in about 12 to 16 weeks, but the blood vessels need those levels maintained for three years or more before they even begin to show change, and then the change in percent atheroma volume may be only one or two percent. A follow-up scan that looks the same, or slightly worse, is normal and does not necessarily tell the whole story.

How did Steve use AI in his heart journey?

He started using it as a search tool, then uploaded his labs and visit reports and used it as a reasoning partner: to write questions for his cardiologists, to check whether a scan would answer his question before he booked it, and to find a center that could. Dr. Druz calls that a legitimate use, with a caution: general AI models sometimes tell you what you want to hear, and trust and continuity still come from the clinicians you work with.

Should you stop a statin your cardiologist prescribed?

Steve describes how, frightened by his first score, he joined anti-statin groups online and cut his own statin dose by three-fourths without telling his doctor, something he later recognized as bad advice. He returned to his cardiologist and they agreed a plan together. Do not start, stop or change any medication based on this episode; talk with your own clinician first.

Show Notes & Resources

Guest: Steve Kaplan, Author and Tech Entrepreneur

Steve Kaplan is the author of “The Stents I Didn’t Get,” a patient’s account of his own coronary artery disease, available on Amazon in paperback, hardback and Kindle, with an audiobook to follow on Audible.

Before his heart journey, he built and sold two IT consulting companies, both to publicly traded companies, and wrote nine IT-related books.

He lives in Lake Tahoe, on the Nevada side of the California border, where he mountain bikes, snowboards and hikes.

After a coronary calcium score of 641 at age 67, he spent a year working through ten cardiologists, advanced cardiac imaging and the clinical trials, using AI as a research partner, and chose aggressive medical therapy instead of stents.

Topics & Resources Mentioned in This Episode

Coronary artery calcium score — what it shows, and why a zero does not rule out soft plaque
COURAGE, ISCHEMIA, ORBITA and FAME 2 — the stent trials Steve reviewed
Stents in a heart attack versus stable coronary artery disease
Statins — how they stabilize plaque, and small-dose statin use
Ezetimibe and Repatha — part of Steve’s cholesterol-lowering plan
CCTA, FFRCT, cardiac PET and photon counting CT
CaRi-Heart (Caristo) — measuring inflammation around the coronary arteries
Epicardial fat and heart failure with preserved ejection fraction
AI as a patient’s research partner — and its limits
Dr. Tim Fischell — co-inventor of the drug-eluting stent, who wrote the foreword to Steve’s book
Dr. Filippo Cademartiri — photon counting CT, Milan
Cedars-Sinai — where Steve had his cardiac PET scan
“The Stents I Didn’t Get” — Steve Kaplan’s book, on Amazon

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