Heart Disease Through the Lens of Metabolic Cardiology

Welcome back once again as we continue to take a deep dive into vascular disease, metabolic cardiology, which is basically the concept that this is the new anti aging, literally controlling the skin that surrounds all your arteries. This is where your age is, this is where it lives. And we can measure it, we can treat it, and actually give you a better outcome than typical standard stuff. It's being overlooked by our colleagues in the biohacking and regenerative world when this is literally where our age exists, which is in our arteries and capillaries.

Yeah. You are as old as your blood vessels.

You are as old as your blood vessels.

And you can do all the fancy stuff you want to do, but you gotta. This is where the rubber meets the road.

It is. And so I want to talk about heart disease, coronary artery disease, but a couple preliminary things. The first is we will talk about heart disease and primary strokes or brain disease. But what people need to realize is we're ultimately talking about old arteries in the heart. Old arteries, arterioles, capillaries in the brain. But you can have this in any organ. You can get kidney disease, which is more common in diabetics and people with high blood pressure. You can get erectile dysfunction, which the urologists now consider to be one of the early signs of heart disease.

Harbinger of badness to come.

Yes. You can get this in your eyes and get retinal in issues. Blindness, obviously, dementia, mild cognitive impairment. You get peripheral vascular disease in your hands and your feet. So literally you can get this in any organ in your body. It's just as far as killers in our country. Heart disease is, you know, number one. And then neurological issues is like number number three.

It goes where blood goes. Right. Blood vessels go everywhere. Yes. So anywhere that blood is flowing can be affected or damaged. It's the target end organ issue that you have to be concerned about. And the big ones are the ones that get the most press because they're going to kill you and they're going to increase your morbidity and that's your brain and your heart. But I mean, God, kidney disease and all the patients that are on dialysis or liver failure, if there's a vascular pathology behind it, or lung disease, you've got pulmonary artery hypertension. Like there's just so many layers to this that just kind of fly under the radar, which is a little bit concerning. But the reality is, is that we're talking about vascular disease. Right. We're gonna talk about some specific target end organs. But this is vascular disease and the metabolic flexibility or inflexibility that goes along with your vascular disease and it is treatable. Treatable?

Yeah. Irreversible. If caught early enough, a hundred percent. I, I would, I've had patients caught later with calcium scores of 2000. I've got the calcium scores down to 1,500. 1200.

Yeah.

So. So I don't ever lose hope in people because I've seen people come in with early onset Alzheimer's. And actually I had one gentleman early in my career with this, actually. Him and his wife fired me after his early Alzheimer's became mild, cognitive impairment became normal. And it was funny to see his personality come back. And he was a painter and he started painting again. And after about a year, his wife and him were like, we're so happy. Thank you, Dr. Hartman, but bye. And I was like, I'm happy for you.

So that's interesting you say that because I say this to patients all the time. I say, first of all, I don't believe that anything is irreversible until I'm proven that it's irre. Until it's proven to be irreversible. So I'm not going to give up hope until we feel like we should give up hope together. Two, If I do my job right, and this is not good business, but, but it's good medicine if I do my job right, someday you probably shouldn't need me anymore. But that's really the funny part of what we do is if someone gets better, like sometimes they walk like you said, but sometimes, and this is a patient that said this to me last week, she's like, I feel amazing. You're not going to fire me now, are you? I'm like, why would I fire you? She's like, because I'm all better. I'm like, you can stay as long as you want. She's like, I'm afraid to leave. I don't want to go anywhere. I feel great. I'm like, of course, of course you can say, like, that's the goal. Like continuity of care and having that person that got you there, helped you there, helped you on your journey, keep an eye on you. Like that's, that's really what it's all about.

But you know, the older you get, you don't heal quite as well as you did when you're younger.

Yeah, for sure.

But even they've done, even the 110 year old individuals that you still have stem cells in your 110, it might be one stem cell line.

Yeah.

But you still have them yeah, you can still self heal and self repair a little bit.

Yeah, you know, so definitely.

So heart disease. So heart disease basically is vascular disease of the heart. So why don't you, you know, maybe talk about fat around your heart? Maybe talk about visceral fat. Yeah, talk about this idea of disease in general.

So we're, we'll talk about the plumbing aspect of it and then we can kind of talk about the. We're not going to get into arrhythmias and electrical. All right. So we're going to talk about the plumbing aspect of it and we can talk about maybe even some of the architectural and anatomical remodeling that occurs. Things like cardiomyopathies, congestive heart failure, that kind of thing. So this is specifically about the blood vessels that supply the heart, the coronary arteries. And the coronary arteries are basically broken up. There's branches, there's the left main, the left anterior descending the right coronary, and then there's other sub branches, circumflex, osteol, etc, and they're there to basically supply blood flow to the heart. That's this huge muscle that's pumping out the rest of your blood or portion of your blood to the rest of your body after it's been oxygenated from your lungs. So pump, pump goes out, feeds all the other tissue, comes back, gets oxygen, goes back to the heart, pumps on, back out. So the heart itself, obviously, in order to do this work all day, every day, requires a blood supply. And those are called the coronary arteries. When those coronary arteries are getting damaged over time and you start to accumulate plaque in that coronary artery space that starts in the wall first and then starts to push into the lumen, you start to get a little bit of tightening of that vessel. And even then that soft plaque is still reversible. It could break off. It's called a thrombus. So it can break off and embolize, go to a smaller blood vessel. So what wasn't a problem because it was in a larger caliber blood vessel is now a problem because it went to a smaller caliber blood vessel. So now you have that twinge of angina and someone tells you you had a minor heart attack. So those plaques can break off and cause problems by embolizing. It's also the mechanism by which they can get into the blood vessels and go up to the brain and cause a stroke. An embolic phenomenon that typically happens when you have a dysrhythmia like atrial fibrillation. The other issue that Happens over time is that as that, that plaque starts to kind of get calcified, it's getting stabilized, it's not gonna break off anymore, but it's getting bigger and bigger and pushing into the lumen. And now we have what's called stenosis. But the artery itself is hardening, so you're losing flexibility, you're losing compliance. Blood pressure's going up, it's exacerbating the problem. Increase in heart rate, increase in shearing forces. There's just stress and strain being put on these blood vessels. So now we have this self perpetuating mechanism of those three finite mechanisms that we previously talked about. Inflammation, oxidative stress, vascular, immune dysfunction, plaque is getting worse and worse and worse. Stenosis is getting tighter and tighter. And so you go from no disease to some disease, to worsening disease, to I'm symptomatic with exertion, I got that chest pain when I was shoveling snow, to now I'm symptomatic at rest, to now maybe I'm having my event, which we call a myocardial infarction or heart attack. Myocardial ischemia is another way of saying that it's more diminished blood flow, but typically reversible. The infarction is when there's a big enough hit to the wall of that heart that you now have damage. And that damage is usually permanent, but can sometimes be salvaged. We used to believe it was absolutely irreversible. We now know you can salvage it. So as those blood vessels get tighter, as the disease gets worse, it becomes multivesal disease, maybe, or just one, one vessel disease that's getting worse and worse and tighter and tighter. Eventually you're taking time bomb of a myocardial infarction at that point in time. Now you have a degree of comorbidity that goes along with that heart attack or heart disease. You're gonna have hypertension, you're gonna need to be on other medications, all hands on deck for all your risk factors at that point. As far as conventional medicine is concerned. Statin, aspirin, probably beta blocker to decrease the workload of the heart, decrease the myocardial oxygen consumption. Basically how hard the heart has to work to pump out blood. Maybe you're straining the vessels, maybe you're straining the valves, maybe the heart itself is remodeling because it's a muscle that's working harder. If you work your bicep at the gym, it gets bigger. So now you have hypertrophic cardiomyopathy, or maybe the heart Gets a little bit thinned, and now you have dilated cardiomyopathy or you catch some disease and now you have restrictive cardiomyopathy. There's all these things that can kind of go along with it, with the goal being that now at this point in time, it's not a goal, but the result being now at this point in time, your heart is damaged or the vessels are damaged and now you're kind of stuck in that situation. So the key is to prevent it before it gets to that point.

Yeah. And I think with what you ended with. That is where in our current system that cardiology excels when you have cardiomyopathy, when you've got these structural abnormalities.

Yeah.

This is where our system is really good. Yeah. You have that acute event, I mean, in our country hospital right across the street, you can get stinted, open back.

Up, thrombolytics, bypass surgery, less than three hours, cardiac rehab, all the different medications.

But you can extend less than three hours. Yeah. I mean super fast. So this is where we excel and in our country, and we're really, really good, is that you've got the cardiomyopathy, you, you actually need to use a beta blocker to decrease the oxygen consumption. Okay.

Or a diuretic because you have congestive heart, you're pulling lung, you're pulling fluid on your lungs or on your legs.

Or some of the newer, the newer medications like Aleskranon that actually are work through the renin system. Like that's where we're amazing. Everything you said before, that is the metabolic cardiology world to build up. And that's where our system doesn't do. And that's kind of what we talk about. You know, you mentioned plaque, the plaque stabilization. You can actually measure an unstable plaque with an LP PLA 2. If that's elevated. You know, you have plaques that are unstable and something as basic as omega 3s can help stabilize those plaques.

Myeloperoxidase is another one that's unstable plaque and dysfunctional hdl.

Yeah. And so on. Plaque size, you know, if the plaques are getting bigger, you actually have a way now to clearly testing. You can actually look and see how, how big the plaques are. You can do a CIMT and look in your carotid and see how big they are in your, in your neck.

And it clearly shows not only how big they are, but the morphology of the plaque. So is it soft? Is it calcified? Where is it? And then is it lipid rich? Does it have a necrotic core all these things matter. Is this a plaque that's dying on the inside or is this, it's going to have even more of an immunologic inflammatory response. Or is it just a lipid rich plaque? Or is it an unstable red hot pimple that's about to pop? Or is it a calcified plaque that's stable but problematic because it's stiffening your artery? That information is incredibly important. In the CIMT study that you were mentioning, estimating vascular age. Right. It's measuring things.

And again, if you have an elevated cimt, we can use things like garlic, we can use things like high doses of vitamin C, we can use things based on the biomarkers to actually and then recheck on it. Calcium score. If you have a calcium score which measures that. You know, one of the things I find fascinating, and this is Environmental Protection Agency data, this is not fancy functional, this is just regular government data in Haynes data actually that 30% are inhanes that 30% of all heart disease in our country can directly be related to lead exposure. So all of a sudden in our world, if someone comes in, we need to be lead experts. Yeah, it's if you have a solid plaque elevated calcium score, most likely you've got some lead. What's your lead levels? And so all of a sudden now addressing that, if you have stenosis and hardening, measuring that like through the calcium score and our CLIO score, but if someone's blood level is up, all of a sudden addressing that becomes a leverage point. And then the small vessel disease you kind of alluded to, you know, these are all big things. When you do stents, when you bypasses. So many people have small vessel disease, that's kind of like erectile dysfunction of your heart where it's a little small things we use, we use sildenafil, we.

Use Viagra, which, phosphodiesterase inhibitors, which increase.

Nitric oxide, which is exactly what nitroglycerin does, is what our nitrates do. So literally we're doing the same thing for the penis as we do for the heart. That's a small vessel disease. And we don't have a good therapy per se drug for that. But on the functional medicine side, if you measure all these little small biomarkers, you now actually hit that and improve the small vessel disease. So, you know, it's really interesting, I think, to realize where traditional cardiology has its place and is super amazing and this is the best country in the world for that stuff.

Yeah.

And for this other metabolic Cardiology stuff that we just talked about. Not so much. Yeah, that we, you have to see someone like us to even talk about it.

It's. It's crazy. It's night and day and again, like I walked in both worlds. I currently walk in the prevention one, but I, I've been on that other side. I mean, every ER that I've ever worked in has a code stemi, which basically means that someone's coming in with an ST elevation mi, meaning an active acute heart attack. You hit the code button and it's all hands on deck and it's get them to the cath lab as quickly as possible and it's all timed and everybody's involved and you're, you're quite literally saving lives because time equals viable tissue. This is the same thing for strokes. Every hospital has a stroke alert. If you've ever gone to visit someone in the hospital and you hear code stroke bed six, er, that means someone's having a stroke and they're about to take them immediately to the CAT scanner to see if it's ischemic or hemorrhagic. And if it's non hemorrhagic, they're giving that person clot busters or they're putting them on a hyperinret. You got to perfuse that tissue because as soon as you're getting blood flow to that tissue that was previously not getting blood and, and oxygen and nutrients, you're preserving that tissue, you're preventing irreversible damage. And that was great for a little while. It's stressful as hell, but it was great for a little while. This is so much better because now you're meeting people years before that happens and you're preventing that from happening. You're changing the trajectory of a life by saying, this is where I see your risk to be. This is where your anatomy currently resides and this is what we are going to do about it. And then you retest it. Now this is where your anatomy resides, which is better than it was. Your cimt, this is a real patient. CIMT study just decreased by two and a half years. She reverse aged her blood vessels by almost three years. And when the tech was had her on the table and was ultrasounding her carotids, it's called a carotid intimal medial thickness. So it's measuring the two of the three layers in that carotid artery and it's calculating a score that gives you an estimation of vascular age. And she came to me with one already done by a Previous provider. And it had her vascular age estimated to be five years older than she was. And she was like, screw this. And so we got to work and she just got one updated and now it's equal to her current age. And over the course of time, it's been about a three year adjustment. And so the tech was just like, wait a minute, Wait, wait, what? And she's like, what's wrong? She's like, why are your blood vessels so patent? She's like, why are you so upset about that?

It doesn't happen. It's not supposed to happen.

Literally, that's what he said. He's like, this isn't supposed to happen. And she just smiled and like, that's so profound. And that's pretty amazing. And. And the goal is to get to that point. Like, the goal is to prevent having an old vascular age, older than you or having a lot of calcification. But if you have it, it doesn't mean you're out of luck. It just means we gotta work harder. That's it.

I remember having a conversation with Dr. Dave Spring, who's a very well known lipidologist, probably one of the top lipidologists in the world, at least our country. And it was interesting because his perspective was huge. He was doing this back in the 70s where he was like, I would have like five heart attacks a night. People are coming in dying in the ERs, because we had nothing for them. We had like bypass. Yeah, that's kind of it.

Bypass and aspirin.

Yeah. And it's kind of. And so when all of a sudden statins came around, it's like, oh my gosh, like it went from crazy busy ers to like, not that many. And they realized, hey, statins will stabilize these, you know, impending doom patients. And so, you know, because we're medical doctors and we cut our teeth in the regular world, you know, you and the er, me in the hospital and outpatient, you know, you have to have a respect for where standard of care is amazing. But with. But back then we didn't understand like any of this vascular biology stuff. We didn't know any of this stuff. And so I think being able to 100% individualize the care for people, if you are a vascular path, maybe you need a statin. If you've had a recent event, maybe you need a statin. But if we can catch these people 5, 10, 15, 20 years before when they've got a less than 50% blockage on their, you know, their calf and maybe a 50 or 60% blockage in their carotid and elevation. The cholesterol, HSCRP, but no actual disease. It's like, cool, because we can now.

Do all the other things, fine tune it, get it better. And if you need a statin, it's not the end of the world. I mean, just get to the minimal effective dose that hits your marks and make sure you get that person on CoQ10. Make sure you're monitoring their A1C and their insulin. Make sure that they're not having muscle aches. Make sure that it's not doing more harm than good. Just. I call it thoughtful medication. You know, like I. I tell patients, I'm not anti pharmacology. I'm pro. Thoughtful drug. Like, if you're gonna give somebody a drug, do it thoughtfully. Know the side effects, know the nutrient deficiencies that occur, and give them the minimal effective dose for the shortest period of time. That's gonna change their trajectory.

Well, there, you know, two interesting data points to that as well, that half of all people who go to the ER with the first heart attack have a normal cholesterol. Yeah. So cholesterol by itself is not determinative. The second thing is that when they did, when. When Crestor first came out, it was like one of the most studied stats at that point in time. They had all these, like, as you know, all the. All the studies were named after planets like Pluto and Saturn. They had kind of all these weird, kind of bizarre names, but they could not correlate the cholesterol coming down with the outcomes. So some people take the stat and the cholesterol would come down, some people take it, it'd go up, but everybody had better outcomes. And it was like, what is it that we can track with that correlates with the improved outcomes? And it was information. Hscrp.

Yeah.

And so it's one of those things where if you're checking these markers, if your HSCRP is already normal, okay. And your PARCO number is already okay, and your cholesterol is normal, then probably a statin might not do a whole lot for you. Why do you have disease? Let's look elsewhere. And you might find out that you have an infection, you have a dental, you have root canalis infected, and we have untreated sleep apnea. You know, and so you live in a moldy house or you work, you have chemical exposure, you work at. You know, we have a lot of big chemical companies around here. And yeah, it's amazing how many of our patients get heart disease from, from the Workspace. And so buying that for the individual, using the armamentarium that we have, but also individualizing absolutely everything.

Yeah, yeah, agreed. And the heavy metals, for sure. I mean, that's a huge point. It's not just lead. It's all of them. And correct. And looking at maybe serum, which I know you do, but I also like looking at urine. Provoked metals. Seeing a body burden and then having them play detective in their life to make sure it's past pretense and not ongoing, and then gently get them out of their system and teach them how to detox their life. It's. Anything that you can do will move things in the right direction. There was a study that was done with blind IV chelation. It was a subset of patients that had known coronary artery disease. So they all had documented catheter catheterization, documented coronary artery disease. And they put everybody on a statin and aspirin standard of care. Half the group stayed on statin and aspirin. Half the group stayed on statin and aspirin and got IV chelation. They didn't even measure metals. And then they recapped them six months later, and there was 30% regression of stenosis in the chelation group.

Was this TAC1 trial?

Yes.

Okay. So the interesting thing about that trial is the expectation when that trial was done was it's not gonna work. So it wasn't powered to prove that the chelation worked. It was basically set up. We're gonna see failure. We're gonna do no difference. And so we saw the difference. They were like, crap. We didn't measure metals, and it's not powered. So that led to TAC 2 trial. We actually. For our research company, we were actually approached to do the Tac2 trial. We talked about doing it, but there's some things about it I wasn't super excited about. So. But it's interesting, even in research like that. Like, I think the tack. True. Still ongoing right now. We're waiting for it to come out. But they. They did a trial they didn't look at.

Yeah, they had metal. They didn't even look. They just like, here's some. Here's some IV EDTA or DNSA or.

Whatever it was just so. And that's. That's where.

But even then, it's like, edta. Was it pulling out metals or was it breaking up biofilms from infections? Like, who the hell knows?

Oh, it's also antioxidant.

It's a preservative.

Yeah. EDT's a preservative in our vials. On. On blood, right? Yeah, it's in the vials.

It's like, what was it doing? Well, we don't know. Cause they didn't measure anything. Cause they just assumed it was going to fail.

It reminds me of that study that came out. I don't know if you're. This was before. This was before I think you came and joined me. Where the study came out that showed fish oil caused prostate cancer. Do you remember that?

No.

That was maybe 10 years ago. And it was study. And they did blood levels of omega 3s and they saw that in prostate cancer patients, their blood omega 3 levels were elevated. Oh, my gosh. News flashed. Sounds almost like the Women's Health Initiative news flash. Fish oil causes prostate cancer. Okay. It didn't run off like the Women's Health Initiative did and mess us up for 20 some years. But this is about six months where all my patients were scared of taking fish oil. Right. So I got the article and looked at it. They didn't ask the patients if they were taking Omega 3s. They didn't ask them. They're taking a supplement. The brand? Nothing. They purely just did a blood level and they assumed if the blood level was elevated, they were taking a supplement. Therefore, fish oil causes prostate cancer. And my thinking is maybe your body's trying to fight it off and maybe it's by its natural response. My theory is just as good as your theory. But the headline was Fish oil calls us prostate. Yeah. So I just have to remind people, when you hear things that don't sound quite right, don't assume it's correct. Actually read the literature, read the data, which is what we do. So.

Yeah.

But anyway, so stroke. That was hard.

That was hard. Yeah.

We'll talk about stroke next.

Yeah.

But hopefully this information's helpful. The reason we're talking about this is for people to realize that, you know, vascular disease, this is the overlooked thing in a modern error and of fascia flame, fancy things in the functional medicine world of gadgets, of optimization, anti aging. And we're forgetting the thing that's been staring us in the face for decades, that we have things we can do for and we can measure. And so that's what we're going to talk about. And next in that lineup of vascular disease, which includes every organ in your body, we're going to talk about strokes next.

Yeah. Cool.

All right, take care. We'll talk to you soon.

See it.