017 - Why Hospitals Still Push $20,000 Stress Tests (And What Actually Saves Lives)

Hey, welcome back everybody. Uh, I am here today with, uh, the good Dr. John Osborne and JD Enright, uh, here at Dallas, Texas. They've allowed me to kind of come hang out with them for the day. So, um, and I should start with, they, they, they run Clear Cardio here, and CLEARLY is something that we use in our practice, the CT angiogram with the AI evaluation, which is just very— it's the future of cardiovascular screening, really. So whenever I reached out to Cleerly and I wanted to get a cardiologist that was not on their payroll, that I could really get the straight story, they gave me his name right off the bat and reached out to him, and he was very gracious with his time. And Dr. John Osborne is trained at— you did your You did your residency down at Brigham and Women's?

Yeah, Brigham and Women's Hospital. Now, so Mass General and the Brigham are all now one part of the same organization. So now the latest name is called Mass General Brigham or MGB, not MGA. This is an MGB, which is the smaller of the two, as I recall. But if you're into English sports cars. But yeah, so it's Mass General Brigham is where I did my training.

Yeah, yeah.

In internal medicine and cardiology. Got my— also, I was in the MD-PhD program prior to that, so I picked up a PhD, which, you know what BS is, right? Yeah.

Yeah, right?

Bachelor's degree. MD is more dung.

Oh.

And PhD is piled higher and deeper.

Piled higher and deeper, yes.

So I've got all that squared away.

All this doctor humor is killing me.

Yes, yes.

A lot of slapstick.

So anyway, but yeah, so I did all my training in Northeast, And then rationality overcame me and moved to Texas. Been here 28 years and—

Oh, really?

Yeah.

Straight out of residency, came right here.

But fellowship.

Yeah. Or fellowship.

Sorry.

Yeah. So I did my 7 years at the Brigham and did my training there and then came down to Texas and never looked back. You know, one thing I got to say, and you appreciate this too, I love telling people, particularly the Northeasterners, whom I love, I'm from Boston, so yeah.

Yeah, exactly.

So I love saying the one great thing about Texas is never once have I had to shovel heat off my driveway.

So there you go. Just hail.

There's that.

Just hail.

I've seen that. Off your roof, maybe.

Yeah, exactly.

Anyway, but yeah, so I've been here.

You're also a cardiologist as well.

Yeah, I was going to say. So my journey was, I trained in general cardiology. One of the other little notable things about my training is, again, this is just pure luck, that in the Department of Genetics at Harvard is an amazing lab. And back in the '90s, we were doing what's called positional cloning, which is now a legacy technology after we cloned the human genome. But we were doing position— positional cloning, which is unbelievably tedious to do. and I won't bore the details, but this lab was the lab that came up with, identified all of the genes that caused hypertrophic cardiomyopathy, which is a fairly common genetic form of inherited heart disease. And then also we did a lot of dilated cardiomyopathies as well, doing all the genetics behind that. So I spent 2 years in my time at Boston in the Department of Genetics at HMS doing that positional cloning, which was really great. So I went from a physiologist— that was my PhD— into a molecular geneticist. And so that was kind of my evolution. And then as a cardiologist, I was always interested in the noninvasive stuff, right? Echos, and nuclear cardiology, and stress tests, and vascular, and ultrasound, and all those kind of tools. And really wasn't terribly interested on the interventional side, like doing stents. A lot of my colleagues were, but I wasn't.

Mm-hmm.

I remember at the Brigham back then is we'd get people from all over the place, right, coming to get their caths at the Brigham. And we'd cath them, and we'd see some— we'd call it lumpy, bumpy stuff, right? No blockages, but it wasn't completely normal.

Right.

And we'd say, eh, lumpy, bumpy. Not necessarily to them. We'd say, oh, you're good. There's no blockages. Oh, that's good. And then fare thee well. And I'm going, but wait a minute. Isn't that kind of like saying you got a polyp, and we're trying to diagnose— early, you know, colon cancer or things that lead to colon cancer. And I thought, that's kind of a little bit wrong. We just say you're fine, right? Go off, marinate for a while, and maybe if you're lucky, you come back and we balloon you or stent you or bypass you. And I thought, that's weird. So that was kind of my genesis of preventative cardiology, going, wait a minute, we're seeing stuff that's important and actionable.

Mm-hmm.

Although, as it turns out, even on a heart cath, we're really seeing late disease, right? Because disease always starts in the, in the donut, right? If you got a donut, right, it starts in the donut, not the hole.

Right.

And, and the plaque will grow outwards literally for— could be decades, right? And you could have a, a normal heart cath or even maybe a little lumpy bumpy, and you could still have a considerable amount of plaque that could rupture and kill you. And so there was no such thing as preventive cardiologists back then. This is the mid-'90s. And so I basically, and almost without thinking, I'm going, you know, I really need to understand all of these things on the imaging side. How can we detect it early? And then on the therapeutic side, once we do detect it, what to do about it. So along the way, in no particular— in retrospect, yes, perhaps I had a plan, but no particular Uh, way, uh, you know, got my internal medicine cardiology, and then I got boarded in nuclear cardiology, boarded in echocardiography, boarded in, um, later cardiac CT when the first of those machines came out in the early 2000s, uh, got boarded in hypertension, got boarded in lipids. Um, so I kind of put together all the, the, the big parts of preventive cardiology because there was no training program. So I just kind of put together my own training program and got 7 boards out of the whole thing. So very expensive wallpaper, I like to say. Yeah, I've seen it. Yeah.

I actually put it all in new frames and everything so it's—

Exactly.

To match the decor in the clinic.

Right.

That was cheap.

So that was my journey. And then, you know, in the last maybe 10 or 15 years, we've now come up with this concept of preventative cardiology, which is really twofold. One, early detection, not late detection, which is historically what we waited for, as you know, working all those years in the emergency room.

Yeah.

And that's really done with cardiac CT. I mean, that is the tool, right? I don't do stress tests anymore. They're not accurate, they're insensitive. Any blockage less than 70%, they'll be normal. 25 to 40% false negative rate, where there is a severe blockage and it misses it. 25 to 40% false positive rate, which then, Gets everybody riled and excited and patients and docs. And we'd cart them off to the emergency— to the cath lab, spend another $20,000 cathing them, putting catheters, you know, via the groin.

Yeah.

Now we go through the wrist into their heart only to find out you're fine. But again, you could still have plaque that I can't see in a heart cath. So cardiac CT is really the dominant strategy to be able to assess the status of your coronary arteries if you have plaque or blockages. And then the big, big excitement in the last few years, as you know, is now adding AI on top of that data. which allows me to see literally stuff that I could not see before.

Yeah.

And, you know, how AI works, we take that, that incredible massive gigabyte, gigabytes worth of dataset, the raw data, the 3D high-resolution data coming out of the CT machine. We then send it up to the cloud, process it using Clearly, which will do a couple of things. One, it will look at every single one of the millions of pixels that make up that high-resolution 3-dimensional dataset. It will then on top of that, When we look at what we call grayscale, so imagine a chest X-ray or an X-ray or CAT scan or MRI, those are all grayscales, right? It's black to white, gray in the middle.

Right.

Our eyes can see or delineate about 50 shades of gray.

Like the movie.

Like the movie, exactly, right? I know where your head is.

Yeah, well, you know, why did they call it that? Well, there's gotta be a reason. Now we know.

Exactly.

Now I can see 50 shades of gray.

Now you see, you're learning new stuff.

Who'd have thought?

Exactly.

Right?

It's worth the trip already. Tune in, tune in. It is, right? 50 shades of gray. Trivia central. So our eyes can see 50 shades of gray, right? However, every one of the millions of pixels coming out of the CT machine is electrically encoded, electronically encoded, with over 2,000 shades of gray. So imagine our eyes could see not just red, green, and blue, but infrared, ultraviolet, X-rays, microwaves, gamma rays, right? The entire electromagnetic spectrum We can now see with the AI.

I would see that movie.

Yeah.

2,000 Shades of Gray.

2,000 Shades of Gray.

Yeah, yeah, yeah. The next generation. I can't wait to imagine. Yeah, yeah, yeah.

Whoa.

Life after 50 Shades.

I'll keep that in mind.

That would be great.

And then lastly, it will then give us— so seeing what cannot be seen with our eyes and then quantify that.

Yeah.

Down to a 10th of a cubic millimeter, which is an infinitesimal Volume.

Yeah.

So it really is just remarkable. And it's the cool thing is it really, it's so accessible, right? You know, you can order clearly.

Yeah.

You can order clearly.

The nice thing. Yeah. With the AI piece, it almost brings guys like me who isn't, you know, I prior to that, I wouldn't feel comfortable really reading one.

Right.

And I can get that information and it quantifies it.

You only have to do about 10,000, then you get good.

Yeah.

But yeah, it's phenomenal for me.

It's really the democratization of imaging, right? Yeah, that's a good way to put it. Lots of complicated things happen from the data and the AI and all that, but it really now becomes accessible to a lot more people. And also, I think, understandable to our patients too.

Yeah, yeah. And it does, you've talked about this on your podcast like crazy, but that soft plaque versus hard plaque, And calcified plaque, which doesn't matter so much, and then the soft plaque, which is what— and then it delineates that even further into low-density soft plaque, which has been— I mean, we found some stuff on our patients that were really moving in a different direction that would, I feel, drastically changing their outcomes 5 to 10 years based on this stuff.

You're saving their lives.

Yeah, you're getting cheesy, but yeah, pretty much.

No, you are. I mean, seriously.

Yeah, it is life-saving.

It's okay to be cheesy. Absolutely.

So, so a little kernel truth here, but JD and I have kidded about having, you know, on those construction sites, no accidents for 370 days or something. You know, we need to have the lives saved.

Yeah.

You know, I mean, it's a little cheesy, but.

Right, right. But it is. I mean, that's what we're doing. But I was looking at— you wonder why it's not part of the vernacular, part of what we're doing, like colonoscopies and all that sort of stuff. And then I was looking at— I mean, this might be sketchy, and I may want to edit this out, I imagine.

Ooh, do it now.

But I mean, hospitals make— I was looking at what specialties make the hospitals the most money.

Oh yeah.

And you know what it is?

Oh yeah.

I mean, it's cardiovascular. There's no incentive. Why, I mean, why would you, I mean, if you're not an MD—

By the way, I love this controversial stuff. Let's keep this going.

But if you're not an MD or DO, but you're a CFO, you're going, hey everybody, don't change a thing.

Doing good.

We're doing phenomenal.

We're gonna buy a new cardiology wing.

Oh yeah.

You're giving free coupons for a month's worth of fast food to all of your patients. Here's all the fat food you can eat. Just come on in, 'cause we'll see you in about 3 months.

Oh yeah, it's terrible. Even now, I mean, they try, but it's still a bunch of carby stuff. Even in the doctor's lounge, there's still a soda machine where I have privileges.

So 20 years ago, well no, 25 years ago, You have to do this 200 hours of training in radiation to get your license here in Texas. So I did all that. It was down at St. Luke's in Houston. So as it turns out, St. Luke's, which is a notable place for cardiology and for bypass surgery, the home of DeBakey and Cooley and those guys, right?

I have no idea who those people are, by the way.

In the basement of St. Luke's was actually the most profitable medical device company McDonald's.

Oh my gosh.

Per square foot. That was it. The most profitable McDonald's. And I remember going down there and, you know, there weren't many places to eat. So food desert, right? So I go down there and try to find something to eat. But I remember seeing on the menu, and this is incredible, you know, they had French fries. They had small, medium, large. Then they had maybe extra large. Then they had something beyond that, only in Texas. They had the bucket. It literally was—

A bucket of what?

A bucket of fries.

Of french fries and potatoes.

A bucket of fries.

Really?

I mean, like this big, which is— well, anyway, it was a bucket.

Wow.

Right? Sitting at St. Luke's in the basement, in the most profitable, busiest McDonald's, you could buy a bucket of fries, which again is perfect. Create the problem. Fix the problem.

Yeah, right. Fair enough.

I mean, isn't that insane?

Yeah. So that's like being a diabetes doctor and owning Willy Wonka's chocolate factory. Exactly. Like, why not?

You guys will make—

in one door, out the other. Make money on both ends. Yes, exactly.

Yeah. Yeah. So the first— whenever I reached out to you the first time, uh, I remember we were talking and I was listening to everything you're doing and I thought, you're a rare bird.

You're not the average—

I mean, I was thinking the way you guys make money is doing interventions. And I say all that to— I mean, I love my cardiologist.

Oh, absolutely.

They're doing a great job, and I appreciate everything they do. If I'm having a heart attack—

But when people didn't detect the disease early.

Yeah, yeah. It's just something that needs to be layered onto the whole picture. Right, right.

And I kid about putting my interventional colleagues and surgeons out of business, but in reality, I mean, it is a team. It's just, unfortunately, we have not spent enough time effort, thought on, well, wait a minute, that person that had that heart attack, what's been going on with them the prior 20 to 30 years? Because we know the disease is there and it's detectable.

Yeah.

So I think we're just adding on to the pie now. I think down the road there may be some shifts, and I think there may be some of my interventional colleagues that see the light of prevention and go, wait a minute, I'm a recovering interventional cardiologist, and now I'm interested in how do we detect it early and prevent it so we don't need to put people Through mechanical procedures.

So you guys are the 2 doctors here. I'm curious, is there data going back to like the 1700s or 1800s? You know, I know there wasn't great medicine back then, but that shows people having heart attacks and strokes, or did they even know what those were back then? Or you just— they died? I don't know.

So just died. So, so that's a great question, right? The first medical case history, the first medical description of angina. Angina, right? Angina.

What is angina, by the way?

So angina basically is when your pipes are too small to supply enough blood flow to the heart muscle.

When you say your pipes, your actual—

Your arteries.

Your arteries, right. Your arteries are too small, there's not enough blood flow.

So it's kind of like an engine, right? So you apply a load, exercise, running, mowing the lawn, doing physical activity. You apply the load, The engine needs more fuel, blood, and when there's a discrepancy, when the load is too high and the pipes aren't big enough—

You're starving the engine.

Yeah, and you start getting typically, now again, the problem is, and as an ER doc, you know, there's all these different manifestations of what we call ischemia, that is an imbalance between the load and—

The demand.

And the demand, right? But classically, typically, Heaviness, tightness, pressure, ache, burning, that kind of thing. May or may not radiate to the neck, jaws, back, shoulders. Could have nausea, shortness of breath, sweating. I've said this a few times, but unfortunately, it can also just manifest as nothing. It can manifest as fatigue. It can manifest as just shortness of breath.

Got it.

Flu-like symptoms, throwing up, nausea.

Sounds like everything can be a symptom of a PEA. That's the problem, right? That's the problem. Like, my God, I probably had 6 heart attacks on the way here today.

Exactly.

I had sweating.

And survived every one of them.

terrible food. I felt nauseous. I was like, oh my God, I must have angina.

That's really the medical crux of the problem is it can show up in any number of different ways. Anyway, but that's angina.

So you got to— okay, got it.

Angina and angina. Appreciate it. Yeah. So, and that diagnosis of angina, which is a late, late stage of disease, was really what is how the entire cardiology—

Back in the old days.

Medical industrial complex is built on. It's finding the blockage, and then if you find the blockage, you fix the blockage.

But in the 1700s, 1800s—

The first description of angina is 1812. Wow.

Really.

So relatively recently.

War of 1812, I got it.

Yeah, right? So part of that was, People never lived long enough to get— most people, the majority of people never lived long enough to get—

Oh, because disease, quality of life, just on average.

So 100 years ago, average lifespan was 47.

Wow.

Okay, which means that pretty much everybody in this room except Yvette is dead.

Wow.

Well done.

Right?

Wow. Yeah.

Yeah.

You can't see her on camera, but she's right over there.

She never got old enough.

The prettiest one in the room.

Largely.

Yeah.

Because it is an acquired disease, right? No one starts off black.

Yeah.

It is 100% acquired disease, right?

It's like that because your arteries are like slip and slides. Yeah. Remember the slip and slide?

Yeah.

Before they outlawed it because all these old guys were breaking their backs.

And lawn darts.

And lawn darts, yeah. But it's like the slip and slide, right? Remember the slip and slide?

Yes.

Exactly.

Yeah, so it's interesting that only until relatively recently Was angina identified, named, and described in medical literature?

1812.

1812.

Wow. Yeah. Okay, 'cause the reason why I was asking is I wasn't thinking, what an epiphany. I wasn't thinking about mortality rates being because they, we just didn't live as long because life was sucky back then. It was really hard, right?

Yeah, it was.

We went to work when we were 11.

Tuberculosis, cholera.

Yeah.

Trauma.

Yeah.

Inflammation.

Flu. Like just the flu.

Yeah, right.

How many people did the Spanish flu kill?

A million.

A million, right? So crazy.

50, 60 million.

Yeah, the world was just out to get you. It's like living in Jurassic Park again, right? Everything was out to kill you. Got it.

Or Australia.

Yeah, fair enough. So aside from that, right, aside from that, what I was thinking, where I was going with this was, is it also diet-related? Like lifestyle and diet-related? So are more people having heart attacks and strokes nowadays at earlier years or earlier ages because of the foods we eat.

Oh, yeah, absolutely.

And we see a disparity. You know, I'm curious what you both think. A disparity between like the US versus, say, other countries that aren't so fat foodie. Is that even a word? Like, I don't know.

So a great example of that is Finland. Okay.

Yeah.

So Finland, up until about 30 years ago or so, had some of the highest rates of heart disease in the world.

Really?

Yeah.

The Finns?

Finland. Yeah, the Finnish.

Okay.

And a lot of it was they ate an incredible amount of saturated fats and just nasty stuff.

Right.

Really?

So the Finnish people, to their credit, realized this is not good. We're leading the world in something we do not want to lead the world in, which is heart disease.

Yeah.

So they started at a cultural, governmental, societal level and said, we need to change these things that we can change. Now, there's a lot of factors that are certainly genetic related to heart disease, but, you know, those are genes. But let's attack the environment.

The things we can control. Yeah.

Yeah. And so they, via, you know, getting people to— with a lot of governmental nudges and societal changes and food changes and all that, dramatically lowered the risk of cardiovascular events in Finland.

Where are they now?

Do you know where they are now? Oh, they're really on the low end of things.

This happened, what, in the '60s, '70s?

Yeah, exactly. So the good news is that a lot of this, there's lots of tools to treat heart disease, right? Diet, exercise, lifestyle, medications, et cetera. But just a good lifestyle, Knocking out the smoking, right? Because there was a lot of smoking. Cleaning up the diet.

Processed foods.

Processed foods.

Because they didn't have processed foods back in the 1700s, 1800s, right?

No.

Everything was grown locally.

Yeah.

And it rotted if it was out too long.

If it wasn't eaten.

Exactly. You know what I mean? I had just the other day, I went into the refrigerator. I'm like, wait, this has been in the refrigerator for like 7 weeks. And I opened it up. I'm like, I could probably still eat this. I'm throwing this away. Like, there's no way I'm eating this now because it's probably— Full of something that's keeping it alive for so long, right? So, like, so we're living longer is what I'm hearing, docs, right?

Right.

We're living longer.

Which is a good thing.

Which is a good thing, but we're eating really crappy foods for the most part. Most of us are, because we live fast lifestyles. We're picking up foods, everything's processed. The stuff comes from all over the world. It's shipping in. Like, how often do you live next to a farm where you're buying strawberries and meat, right?

Right.

So, it's preservatives, whatever. So we're living longer and we're eating worse. So the disease has a chance to really proliferate, progress. And that's what you guys think, that why we're dying of heart attacks and strokes? Why it's the number one cause of death?

Peak in the US, peak cardiovascular death was in the '60s.

Oh, okay.

From the '60s till the early 2000s, we really reduced it a lot, right?

Really?

So less smoking. Statins came into the scene. We, we better understood things like high blood pressure and better treatments for high blood pressure, etc. So there was a dramatic decline from peak heart disease in the '60s till the early 2000s. Okay. Now, at the same time, overlying that was processed food and the food industry, mass food industry, and all of those things.

Mm-hmm.

So, and the other thing is, as we quit smoking, right, we all gained weight.

Visceral fat.

Visceral fat.

Yeah, and snacking at the middle of the night.

So it went down and down and down every year consistently, which is remarkable. I mean, imagine if I'd said cancer death rates in roughly about 40 years fell by 60%. Well, yeah, we didn't do that, but they did fall for cardiovascular disease.

Got it.

However, 2011, they started going back up. Now, less smoking, but now we have an obesity epidemic, which then causes diabetes. That visceral fat causes high blood pressure, cholesterol disorders, hypertension, all of those other nasty things, sleep apnea, DJD, et cetera. And so we've been losing the battle since 2011 here in the US.

That's so interesting. And I know this is your podcast, but I like— just reel us in anytime you want, because we could talk forever. But just to that point, this is a personal reference point that I have, and some of you who are watching your podcast, your listeners, your followers, may resonate with this. My wife is Mexican, and we've been married for 27 years. I met her 28 and a half years ago while I was in Mexico City.

Mm-hmm.

And I remember what it was like in the 1990s in Mexico, and it was very far and few between where I saw what I consider to be overweight men and women, mainly women because that's what I focused on back then before I met my wife. So I didn't see a lot of overweight women, okay?

Yeah.

And it was like, wow, this is unique, right? This was unique. What I, over the 27 years that I've been married, I have noticed, however, that Mexico has changed a lot. And now it's hard to find a woman that isn't overweight.

Yeah.

Or a man that isn't overweight. I've seen it in my own in-laws. I've seen it in friends and family members that I've created over the years. It has been dynamic, and I've thought about that. I'm one of those guys, like I'm sure you guys and a lot of your listeners are, you latch onto something, you wanna know why. You go down that rabbit hole. And so I did my own little backdoor research kind of thing, and it turns out that I identified there was a point in time right around 2011, 2010 timeframe when Mexico opened up Broadly to fast food restaurants, to Americanization. It's the number one country in the world for consumption of Coca-Cola products.

Exactly.

They drink— if you've ever been to a quinceañera or a party, they have 10 2-liter bottles everywhere, and it's sugar, sugar, sugar, sugar, sugar. Tons of sugar, saturated fats. Adopted because it was the cool thing to do, the American lifestyle, because— and the American companies just flooded in. NAFTA, all of that stuff that opened it up to free trade, whatever. It was, it was our lifestyle that was affecting their lifestyle. Yeah, that's my own conclusion. I don't have any facts behind that other than what I've read and what— in my own deductions.

But yeah, so I'll go be— okay, number 1 per capita intake of Coca-Cola, Mexico.

Mexico.

Number one cause of death in Mexico is diabetes.

Diabetes, yeah.

Wow.

Oh yeah, that's which is related to everything that you guys and then of course those patients diabetes die of cardiovascular disease. But yeah, heart health. Yeah. So number one cause of death in Mexico is diabetes.

No kidding.

And that occurred in a generation.

Yeah. My brother-in-law has diabetes. He's in his 50s and he has diabetes pretty severe. You know the feet things and whatever and we're trying to deal with that. But Yeah, I mean, you know, and guess what he does? He throws big '80s parties full of 2-liter bottles of Coca-Cola. Yeah, right. I know, I know it's a stretch, but anyway, sorry, back to you.

No, no, I— so, you know, on that note, what I'd like to talk about, a few things, is, you know, obviously a lot of my, my listeners don't know about Clearly and all that sort of stuff, but The thing is, with it being actionable, and you just had a guy in here earlier where you'd done some things, and then part of the protocols that we work with are based on some of the papers you were an investigator on. But you just had the guy in here that had, within a year's time—

Mark Cozart.

Yeah, really a decrease in his plaque load, which you're looking at things and actually staging them based on plaque load. which you can see.

Right.

Of course, it diversifies it further, which is very helpful. But for— and based on that plaque load, you're rechecking it in 1, 2, or 3 years. But for him, he had significant load, and then you rechecked it. So talk about that case, because I thought that was pretty cool. I was just eavesdropping.

Yeah, so using AI to detect heart disease and quantify it, which is really incredibly important, because if you'd had— You had someone who had known heart disease, stents, balloons, bypass surgery, heart attacks, strokes, whatever, right? Has known heart disease. And then, you know, treat them with all the appropriate pillars of prevention, which is diet, exercise, non-pharmacologic things, medications, et cetera. What we could not answer until just a few years ago with the ability to identify and quantify very accurately plaque is you couldn't ask your doctor, After all my diet, exercise, weight loss, medications, etc., is my plaque better? You couldn't answer that. Now, if you had cancer, you'd get worked up. Hopefully we detected early. We would stage you, we would treat you, and then we'd restage you to know, is the cancer gone? Is it better? Is it worse? Right? That's just the typical modus operandi of cancer oncology care.

Which is rationalized.

Yeah, I mean, it makes sense, right? You'd want to know, okay, did the treatment that I did—

Work.

Work. In the world of cardiology, couldn't even answer that. I could say, well, your cholesterol's better, and blood pressure's better, and your weight's better, and blah, blah, blah. But in no way could I answer, is my plaque better? What AI now allows us to do is detect plaque across an incredible spectrum, right? From— we can also say, There is no plaque. End of stop, full stop. End of story, full stop. Boom.

With certainty.

With certainty, right? Which only occurs in 1% of kind of the middle-aged population. Or we can say, yeah, you have some plaque, you have no symptoms, there's no blockages, your stress test would be normal. There'd be no way to detect this. Again, if you've heard this earlier, except if we did an autopsy. But let's do the virtual autopsy as well. We call that cardiac CT with AI. Or we'll find, you know, yeah, and then, you know, depending upon how much plaque you have, we can put you in these different stages that do 2 things. One, we have stage 1, 2, and 3 for atherosclerosis stages. If you're 1 or 2 or 3, that dictates both what we might recommend to do to treat it, which obviously, you know, stage 3, you kind of get the whole kitchen sink thrown at you, as you can imagine.

Mm-hmm.

And then it also dictates When we relook, when we look under the hood again to make sure not only are the numbers better and I'm weighing less and I'm not smoking and my cholesterol is better and blood pressure and all those checkboxes. Right. But we really want to know, are all of those surrogates translating into is the plaque better?

Yeah.

And it's interesting. Most time, yes. But I've also run into people who have phenomenal numbers.

Yeah.

And they got more plaque.

I was going to ask you that. So, you know, have you had people that have like a really low ApoB and have significant disease and vice versa?

I mean, right. Right. No, I've had— I can give you examples. One is a doc that I've known for 25 years, had a high calcium score, got him— we did Cleerly and all that. And he was pretty well treated. But, you know, we really ratcheted down. He had a lot of disease. Right. Really ratcheted things down, got him on all the right drugs, lost a lot of weight. Everything looked perfect. So I said, okay, let's take another look. Yeah, his plaque got worse.

Huh.

No, here's— I mean, there's always tweaks we can do, but in his case, for a year— so we added colchicine.

Yeah.

Right?

Yeah.

Right? So I mean, lipids look good, blood pressure looks good, he lost weight, but his CRP was still high.

Okay.

So we added colchicine. So there's always something we can do. But had we not done that, I would've gone, I don't know, everything looks good. And his plaque was progressing. Another guy—

'Cause he had this low-level inflammation going on.

Exactly, right?

And colchicine really added—

Yeah, yeah, yeah, so we used an anti-inflammatory drug.

A cheap drug.

Yeah, cheap, right? Well tolerated, we've used it for decades. So cardiac CT and AI was really helpful in that case. And without the AI, I mean, I couldn't have looked at his images and go, They would look the same by my eye, right? Having done 20,000 of these over the last 25 years. But AI told me that he was progressing and his lipid actually, his lipid-rich soft plaque actually was going up.

Yeah.

I said, okay, what are the things we throw at this? So we added on a drug that's been available for decades and safe and well-tolerated and cheap. So I'll let you know with his next scan what things look like, okay? But it provided very useful actionable data to say—

Precision, yeah.

The numbers are the numbers, the surrogates are the surrogates, but is the plaque better? And I could not have done that without cardiac CT and MRI. No more guesswork, right?

Short, those days are over.

Exactly. And then the opposite, right? A guy who works out 6 days a week, looks incredibly healthy, bad family history. Lipids were really pretty unremarkable. No blood pressure issues, no diabetes, glycemic issues, no smoking. Anyway, We put him in the scanner, and this is really eye-opening to me. Again, a lesson that I learned, because I learn lessons every day.

Humbling.

It is very humbling, right? AI, CT and AI is very humbling. So we put him in the CT machine, and his coronaries looked perfect. I've read 20,000 studies. I think I'm reasonably good. Coronaries looked fine. We get the AI back.

Yeah.

His score was 400.

You're talking about— 400 millimeters, cubic millimeters.

Stage 2.

Oh my God.

No blockages.

Yeah.

Okay.

The AI lit up his vessels. Yeah.

Right.

I couldn't see it.

Sure.

Right. Very humbling. But that's okay. I'll use the technology I got to use.

You're still good.

400 and not a speck of calcium.

Oh, wow.

Because he'd had a calcium score before and I said, I'm not going to trust it. So we did cardiac CT again. It looked fine, but the AI, it was amazing. It was a light show with his AI when we did the AI. I mean, it just lit up. So with that in mind, we tweaked things, put him back in the scanner because he's stage 2. So he has 2 years to rectify his wayward ways.

Mm-hmm.

We did all the right, you know, fixed all that again. His lipids were normal, really didn't have any other factors, but Fixed all that. Rescanned him 2 years later, 200. 50% reduction.

Excellent.

Yeah, which also to me, now this is my hypothesis, it also suggests to me, if you catch somebody really early on in that process, the plaque is probably more malleable versus I got a lot, a lot of plaque, I got lipid-rich plaque, calcified plaque, et cetera. This is just hypothesis for everybody, but it is very interesting that that N-of-1 experience, and to see such rapid change, that maybe the earlier we catch it, the more we can really have a big, big impact.

It responds faster in the earlier stages.

Yeah, isn't that interesting?

Yeah, very interesting.

It's hypothesis, but it is intriguing. I mean, this is where science comes from.

It'd be an interesting study.

You make hypothesis, and then you study it.

I might fund something like that. I'd be open to funding a study like that.

As you talk about regression of plaque, I had a patient, Big car guy. You always know when he's coming because you can hear whatever cool car he's driving. It just will shake your soul.

I think I passed him one night.

V12 Hemi or something.

But they're cool. They're cool. I mean, always very— but anyway—

No replacement for displacement.

Yeah.

So he asked me a question, and you can elaborate on this further, and I went back and being the epidemiologist, as you talk about regression of the plaque, it's like, where does it go? And I knew there's receptors on the liver, it's excreted, et cetera, but if it's in an artery, it has to go through the capillary system, back to the venous system, back to the, and all that. As it reabsorbs, what's the general, I mean, high-level explanation of—

So, and again, if you quote me, date me. So this is what we believe right now, that the bad plaques, the lipid-rich plaques, the actual lava plaques, are embedded in the vessel wall, when we really turn off the fertilizer, right? So your cholesterol is X.

Yeah.

We lower it by 50, 60% lower than X, right? There is no further infiltration of lipid from the vessel, from the, from the, you know, from the, from the blood.

Right.

Into the plaque anymore. We have macrophages. They will start eating it up. But usually that whole system is so overwhelmed by how much lipid is coming in, which by the way, your lipid levels aren't very helpful to understand if you have plaque or not, because it's very complex how much lipid is coming in, how much is being metabolized, eaten up by your macrophages, the garbage truck cells of the body. But if we really turn off the lipids, and there's usually blood pressure and glycemic issues and all that that I won't get into.

Sure, yeah.

We'll keep it pure in the lipid space. If we really turn off that faucet, we now give the body the opportunity to basically metabolize that lipid.

Mm-hmm.

And so we do see, in fact, it's really fascinating, and this is really great news for everybody. On one level, it's sort of easy to understand that because it is a very slow glacial process, right? That when that occurs, yes, we can see reversal, Yeah. Uh, in an anatomic level, right? So, you know, the, the, the, the hole is bigger, right? Uh, but that's a very, very slow process that occurs months to years. AI will, will see that change long before we can even say it anatomically as far as the degree of narrowing. Okay, so AI is a, is an early leading indicator, right? Uh, so yeah, we can reverse plaque in an anatomical structural way. However, the best news is— but that takes months to years. The best news is, and we already have— we had a lot of data even before we had the era of cardiac CT, and that if you look at events, right, which are ruptured plaques, when you begin to lower cholesterol, the reduction in events begins to occur within days to weeks. Well, that's long before we see any anatomical difference, right? This is also before AI.

Mm-hmm.

But that's long before you see enough plaque resolve, the vessel is bigger in an anatomical structural way. So what's occurring at the functional physiologic basis, right, is that we're very, very quickly rendering those plaques, which are rupture-prone or vulnerable plaques, when we target that plaque, diet, exercise, cholesterol, smoking, whatever might be appropriate, Then we rapidly convert those plaques from active, growing, rupture-prone, vulnerable plaques into stable plaques. And that occurs in days to weeks. So which is exciting. Yeah, we don't have to wait or get through months to years because we're changing the physiology of plaque, not necessarily the anatomy, but the physiology of the plaque within days to weeks when we began to do all this.

Which is remarkable.

Which is fantastic. Right. Which makes me feel great because I can say, hey, and now the interesting thing is The, the contrafactual to this is, conversely, if you have plaque and you stop the drugs, most of the data was with cholesterol drugs, but if you stop the drugs, the plaques rapidly wake up. So if you stop your cholesterol-lowering drugs—

Yeah.

Yeah, they're gonna rapidly convert from stable, quiescent plaques to vulnerable plaques. And that, again, occurs in weeks.

So the big take-home there is just because you have a lot of plaque and say we do your CT and it's like, oh, you're riddled with stuff. And they're like, oh, crap, what can I do? Well, you can make a difference within a week by just tweaking some things.

And it's really important that you do.

Yeah.

Yeah. Right.

Like Mark, who was sitting here earlier, who you happen to be out there waiting to get in to speak with us.

Yeah.

He was late stage 3. He had over 1,000 total plaque burden.

Yeah.

1,000 millimeters of plaque.

That's—

yeah, that's a lot. And, you know, with the AI too, it gives you very accurate measurements of stenosis. Not that I really worry about that because it's all about plaque. But it's interesting, in 90 days, right, over that 90 days before he came to see me, he'd had at least one stress test, a nuclear stress test, right? You know, lots of radiation cost, whatever. And it was perfectly fine. Right? Well, if you look at his cardiac CT, I didn't make this point out, but if you look at his cardiac CT and the narrowings, he had 3 vessels that were greater than 70%, and his stress test was completely normal.

And he had no symptoms.

And no symptoms.

88, I believe he had 88%, a 90%, and a 79%. Yeah, exactly.

How did he come to you guys in the first place?

He got lucky.

Yeah, I mean, he went through 3 other cardiologists before another one of my patients, they're also in aviation, Talked to him and said, hey, I know this crazy doc, Dr. Osborne.

He had 2 heart catheterizations. So his story, real quick, was he went for a general checkup. He's very active. He's a contractor, building contractor. He's in his 60s, but the guy's— he's changing, running up ladders. Guy's in great shape. He just went for a general checkup. They did a stress test, EKG, whatever. They went, mm, I don't know, something maybe, whatever, calcium, whatever. He ended up going 2 heart catheterizations, 3 cardiologists, to the point where within 90 days of him having a general checkup, they wanted to do major open-heart bypass surgery, and the testing of his arteries showed that his arteries were too narrow, and they were thinking about taking—

Cadaver veins.

Cadaver veins. So immediately he started freaking out. He's thinking he's gonna drop dead. They're telling him he's gonna die.

Sure.

to meeting with us, and now we're sitting on the couch with him a year later, and we've reduced his total plaque burden, soft plaque.

Right, over 30%.

36.4%.

In one year.

In one year.

And what's remarkable is we got it, he also had a cardiac, he had 2 cardiac cath, cardiac CT, so they used the right tools, at least one of them, not an angiogram, and so we got the cardiac CT that he had done before at the other hospital, We finally got that in our talons. And so then we could do the comparison from prior CT that was not done by me, but elsewhere. So we got that data, did AI on that, did AI on the one that we did, and we could see in just 1 year with just all the diet, exercise, weight loss, working with our nutritionists and stuff, over 30% reduction. You have the number?

36.4%.

36.4%. Percent reduction in plaque.

Converting that—

And that's in the soft—

Calcium.

Yeah. And in 1 year.

That's remarkable.

But importantly, what Dr. Osborne was saying earlier is we didn't have to wait for that whole year to reduce his risk of heart attack or stroke. That happened with the days and weeks.

Yeah.

Right?

And I think that's really important.

It is. It is.

People get, you know, like some people, they come in and they don't know where to start kind of thing. They get overwhelmed. And, you know, like if your office is completely trashed, where do I start to clean it up? Well, if you do something Right then, it makes a difference right then.

Exactly.

Right? It's very immediate, which is great. And it's something I like to share with my patients too, because it's kind of like saying, okay, well, you got cancer. We'll give you treatment. It'll be a couple years long. We'll give you treatment. Now, if you do not die, within 2 years, the cancer will be better. But I don't know, in the next 2 years, God knows, right? I mean, uh, but imagine you say, okay, once you start the chemo, The cancer will be on the run. And that's really what we're doing with cardiovascular chemo, right? Your diet, exercise, whatever medication you use.

Yeah. Well, I think what you guys are doing is great. One more point I want to make is that, and it just happened fairly recently, you really can't tell by looking at somebody. Have you been shocked? Like, I've had— I have one guy that—

Oh, this is what Jay-Z said, and I use this all the time, right? Cardiac CT and AI, unbelievably humbling, right? You'd think, I've been doing this 30 years, I got good spidey sense. No, no, no. I want to hear your story.

No, I mean, yeah, this guy's in his 40s. He's a trainer.

Not—

I mean, just kind of fit and— but lean. I mean, handsome man. Just looking at him, you'd never know. I got his—

He was a month— a week older than you.

No, no, no, he wasn't that guy. But he was— It was just— and he had to— I mean, his lipids were high. He didn't want to do any intervention. This is right before he started doing Clearly.

Of course, because I feel fine.

And so, yeah, he wanted to do some other things.

The mirror makes him look like a million dollars.

Yeah, he was looking at all the noise from a cardiologist saying statins are bad and medicate and all that kind of stuff. So he's getting some bad information. And some people, you just listen to them. You can't really—

Sure.

Anyway, he's had a bypass. He's doing great, but in his 40s.

So he had an event.

Yeah.

So he had a heart attack.

Great, great guy. I mean, I really love the guy, but just kind of a rough, rough deal. But he's doing great and all that stuff.

Everybody think it's not me.

But my point is that it's so shocking that— and somebody can look terrible and they have great—

So my joke, Kevin, is I'll see The big Texan, barely fits through the wall, through the door rather, through the wall, through the door, right?

Well, they could go through the wall.

And I just see them, right? And I like to say, belt at 45-degree angle, belly enters before the nose, you know what I mean? And I'm going, yeah, 5-vessel bypass surgery. And I've had these guys, I'll say guys, 'cause I'll be sexist about that, but I've had those guys walk in, I'm going, yeah, 5-vessel bypass surgery, right, spidey sense. Yeah, nothing, right?

Clean as a whistle.

And then I've had the 33-year-old guy who had Lp, familial hypercholesterolemia. It was all his mom's fault, as it turns out. Actually, got Lp from dad and familial hypercholesterolemia from mom. Oh my God. So the guy flew for the Air Force, pilot, all that stuff, and actually went to the Air Force Academy. And so he was told by the flight surgeon when he was in his 20s, said, man, your cholesterol's high. Better eat right and exercise. Okay, the guy's a triathlete, Ironman, nothing bad ever crossed his lips, no other risk factors for heart disease, perfect blood pressure, never smoked, did everything you'd like, and was ripped, probably 7% body fat. He went to bypass surgery at age 33.

Oh my God.

Now, here's the good news. That was 20-plus years ago. He's never had another intervention since then, By that point, his disease was so extensive he needed mechanical fixes, but we got his cholesterol under control in a few weeks, and that was it.

So the new vessels aren't going to end up like the old vessels.

Exactly.

'Cause they can, they can turn into them.

And then the next generation is his— he had me see his daughter, right?

That's right.

Look who his dad was.

One of our patients.

Guess what? I mean, and she was, 18, because I'm an adult cardiologist. She was 18, but she was still in high school and obviously perfectly healthy kid. But no one had looked at her lipids or put all this together. We checked her lipids. Yeah, looked just like dad's. So by the time she was 18, she got started on drugs. Looks like. And then nothing will happen to her.

Yeah, right.

Which is great.

You know, that's a good point. Even if, you know, somebody is— if they've already had intervention, Stents, bypass, whatever, this tech is still very useful.

Oh, absolutely, right? So, you know, we can, we can look at your graphs, we can look at your stents. You know, everybody wants to know, are they okay? Which is fine, and we will, and that's fine. I mean, you get all that data for free, but really it gets back to, I want to know where your plaque is, what your plaque volume is, you know, what your lipid-rich plaque is, your soft plaque, and, and you're going to get that. So Now, I will say for the audience, if you've had stents, you can get your CLEARLY, you can get to the AI. According to the FDA, it has not been FDA approved for bypasses. We call it CABGs, coronary artery bypass grafting, or bypasses. So if you've had bypass, they will reject the study, FYI. So that's—

It doesn't mean the study isn't accurate.

It is.

Right, I mean, I think there's still value. I could look at it qualitatively. I could see lipid-rich plaques, and in the old days before AI, I'd have studies, I'd look at the old one and the new one, and I'd say, okay, look, there's more calcium here, there's less lipids. You could do it in a qualitative sense, but I'm so spoiled with AI that that's the old days.

Sure, yeah.

But if you've had bypass right now because of FDA clearance, the AI company will kick that out, unfortunately. But cardiac CT is still very, very useful. You can look at all the graphs, and you can look at the natives, and you can see lipids and stuff. But you can't apply, unfortunately, and this is just an FDA clearance hickey for the time being, that'll be fixed in the future. You can't apply the AI to that, just because it's not cleared.

But for stents and things?

But for stents, yeah, all day, every day. So, no matter where you are, either prevention, you've never had issues, or you're already on the other side of the heart attack, or stents, or again, bypass surgery, cardiac CT is phenomenal. If you've had cardiac CT, for the moment, Can't do it. But even— but with stents, we absolutely can do AI and then measure exactly how much plaque you have, lipid, and then, you know, use that to follow that.

In fact, in fact, I would say anybody who has stents, I would highly recommend it because—

There's probably even more.

Oh, yeah, absolutely. More reason to come in because you know for sure—

Because not only did you have plaque, but you had plaque that ruptured and tried to kill you.

That's right, exactly. So Come on in and let us, because again, stents only resolve the symptom. It's not addressing the root underlying cause of the disease, which is the liquid plaque, lipid plaque.

So I would say the only people I wouldn't recommend cardiac CT and AI on, you don't have a pulse and you're not breathing. Now you can get beautiful CT images if you don't have a pulse. Yeah, oh yeah. There's no motion, don't have to pre-medicate them. But yeah, that's gonna be a problem. But other than that, yeah, I think anyone—

Do you see that the future of cardiovascular screening, that this will eventually be something that you do every 5 years or 10 years or whatever?

Yeah, I mean, everything's here. The hardware, the software, the understanding, the biology, the literature. But as you know, medicine changes very, Very slowly. Very slowly, right? I still remember, as a resident in internal medicine, we were talking about doing stool guaiacs combined with a left-sided sigmoidoscopy, right? And is that, how does that compare to colonoscopy? I mean, just crazy stuff. No, we don't do any of that stuff. You just put a scope up there and down there.

Yeah, in fact, this is interesting for your viewers. In 2009, Texas was the first state in the United States, in the entire union, to pass a law. A bill was passed in the House and the Senate here in Texas that was the very first heart attack prevention law.

Mm-hmm.

That required private health insurance, not Medicare, Medicaid, Medicare Plus, but private health insurance companies, healthcare insurance companies in the state of Texas, to cover all Texans for a minimum testing. So in order to prevent heart attacks and strokes at the time, it was calcium score because that was state of the art. It was like, if you have a calcium score, then you probably blah, blah, blah. You know, we all know that now is not— it doesn't matter so much anymore. But it was all they had at the time. And they covered like, I think it was $200 or something like that was the average.

Yeah, they pay $100 for your calcium score.

Yeah, $100.

15 years ago.

And they were required to do it. That was a long time ago. Right now, Clear Cardio, along with Clearly, and Jim Min, who's their CEO and chairman of the company, one of the co-founders, is— and I are working with Senator Angela Paxton. So Senator— and she's the wife of Attorney General Ken Paxton.

Right.

She's a Texas senator, and she's driving the bill that we worked together with her on. to amend that law, because it's been, you know, how many years? 16 years-ish. So to include CT and AI analysis as part of that, and increase that coverage amount to cover a portion of that, or if not all of it. And because that is the standard now, and because we know definitively it works.

And as much as we tend to evolve very, very slowly in medicine, very, very conservative, I have to tell you, and we just found this out last week, I am incredibly excited to note that of those that are supporting this, we have the Texas chapter of the American College of Cardiology, which is huge, because we have lots of my interventional colleagues in there, but those that understand this go, hey, this is very important. We're all working together. And we'll find stuff that people didn't know about, and they'll be taken care of. But the other thing is, just as big, if not even bigger, is the Texas Medical Association, which is huge. It's 56,000 physicians in Texas, and they're behind this as well, which is really— I think it's, you know, we're crossing our fingers.

We're very optimistic that this is going to happen. And so we've got a number of our existing patients.

Texas is leading the way, which is phenomenal.

When you think about the dollars it's going to save.

Oh, gosh.

Billions.

$20,000 heart cath, several thousand dollar nuclear stress tests, all that kind of stuff. Yeah, I mean, and you get the answer, right? It's not, oh, we did an EKG, and now you do a stress test a few weeks later, and that looks funky, and then a few weeks after that, a heart cath, and all the— during the time you think you're gonna die. And I mean, just the delay, the time, the cost. I mean, one tool, done. That's it. It's binary. If you got a problem, we'll see it. If you don't, you don't.

And I'm from Boston, you know, but I'm very pleased to say that I'm I have a Texas implant now, and I love Texas, and so many— for so many reasons.

You've been grafted.

Yes, I've been grafted. That's a cardiovascular joke, by the way. But so to see that Texas led the way way back then, and now we're upgrading that to be today's version of that, and leading the way again. I think you're gonna see the dominoes fall in the rest of the country when they see the value of that proposition.

2009, calcium scoring, no one had heard of this, right? I mean, I'd been doing it for over 10 years by that point, but no one had heard of this. And so it was a big, big deal to advocate and talk about calcium scoring and doing it and paying for it, right?

Mm-hmm.

Now, in 2025, guess what? Yeah, I mean, a lot of people, I mean, we still, it's still underutilized, but And again, it's not perfect. You can miss stuff and all that, but it's better than no cardiovascular imaging. But now a lot of people are beginning to start doing calcium scoring, right?

Yeah, sure.

That's much more notable. So we're kind of where we were with cardiac CT and AI, where we were 15 years ago with calcium scoring. But we're hoping to turn that around and really advance this so that we don't have more useless deaths for a disease that is detectable, decades before you get in trouble, and we have incredible arrays, as you well know, of tools to treat and stop and reverse plaque. The problem is the early detection.

We need the cardiac MRI. And RFK just the other day, right? RFK just the other day, 2 days ago, you sent me the article, was very audible about how important this type of imaging is.

Yeah, so I think it's changing, and we're gonna go after Texas first, and then next the nation.

Well, that's a big state, so. No small feat.

9th largest economy in the world.

Yeah.

Well, man, thanks for letting me hang out with you guys.

Yeah.

Oh, gosh.

Thanks for having us on your podcast.

Thanks for letting me use your wonderful place. And yeah, do you guys have anything else you want to say? JD?

No, just, you know, we did an earlier podcast with you on our, you know, Prevention is Power podcast. And so thank you for participating.

Sure.

We are very grateful for fellow Preventionists, I guess we call ourselves, who are out there trying to save people's lives every day. So thank you for what you're doing. And, you know, we're going to send everybody who's in the Oklahoma City area to your place to get all the things that you— the benefits that you provide. Yeah.

And it's great to meet fellow travelers, right? And one of my favorite quotes from Ben Franklin, he says, we all must hang together Otherwise, we'll all hang separately. So here's to hanging together.

Yeah, fair enough. Yeah, absolutely. Well, thank you guys, and thanks everyone for listening. And until next time, see ya.