good morning folks uh this is Dr Rob cvis I'm aab addiction Doc and today I have the honor and privilege of um just talking with a colleague of mine Dr Phil AIA who is a cardiovascular surgeon good morning Phil thanks for taking the time early this morning um what's interesting unlike a lot of folks in our space is that um you and I have a lot of parallel Synergy uh what separates us is the diaphragm uh I'm a surgeon who started out bariatric surgery and realized that I could fix weight but I couldn't really fix why people gained the weight in the first place and that led me down a pathway of understanding metabolic Health you in a very similar way are a surgeon who is a cardiac surgeon or a cardiovascular surgeon operating on the heart and blood vessels a large part of your work I assume is fixing pla in blood vessels the we'll talk about plaque in a second because most people have an imagination of what it is you and I have held it in our hands um and you have walked that backwards uh in a brilliant way to say okay why is this plaque here what are the more effective strategies to uh prevent it and then to stabilize it and to reduce the ongoing uh uh production of that plaque and in a very similar Trend we've kind of met together at a metabolic interface where we are looking at insulin resistance as a problem um can you walk me down that pathway of how your life is evolved in that regard as a surgeon going backwards if I can put it that way yeah sure thing and it it is uh quite interesting that we kind of AR arrived at this same place you know essentially trying to keep people off of our operating tables exactly and you know I think um uh similar to you you know it's been both a personal and professional Journey uh you know for me I uh going back a decade was you know a morbidly obese pre-diabetic heart surgeon and I kind of started asking you know how can this be uh you know we had gone through all the education that we went through and um you know I was unable to uh manage my own health essentially and I was following the advice that I had learned to give and it wasn't working and I started to also at the same time wake up to the fact that you know we we give patients this these this advice about how to be healthy that eat less move more uh you know eat a lowfat diet manage your cholesterol in our in in the case of my specialty and it obviously wasn't working for them it was working for it was great for our business well exactly I guess it depends on what your goals are ultimately and we can talk about maybe uh the system doesn't have have the same goals that the individuals might have exactly I know smoking and and carbohydrates are your best friends in terms of what you do surgically certainly uh and so you know I started to uh through a series of events you know uh really the seminal event for me was I was at a Society of Thoracic Surgeons meeting so the biggest meeting of Heart and Lung surgeons in the country and Gary TOS happened to be the guest speaker uh Gary had at that time just rid uh the case again sugar and um of course before that had written good calories bad calories and why we get fat and you know Gary talked about those Concepts how it wasn't necessarily the amount of food that we were eating but the type of food we were eating and how those specific Foods were driving us to eat more food and cause obesity and um you know and that resonated with me personally and I I went on a low carb diet after uh reading Gary's books and uh I had great success losing weight reversing my pre-diabetes and then I started asking you know why did I hear about this from a journalist and that's not a knock on Gary in any way uh but here we are had gone through all this education and I never heard these Concepts from my medical school uh professors from my colleagues uh you know and so that got me asking some different questions but ultimately what I came to realize is the surgery that I do the surgery that you do um it's great to be able to offer that to patients but you're never as good after the surgery as you would have been if you didn't need the surgery in the first place oh that's I love that line by the way I say that again yeah you're never as good after the surgery as you would been if you didn't need the surgery in the first place love that and and you know that's really what it comes down to and when I you know started really thinking about what you know why did I become a physician what is our role as a physician um it it's to help the patient the best way we can and um and that's what led me to you know conclude that the best way that I can help patients is to keep them off the operating table and you know because of that changed around my practice similar to the way you have uh still operate as a heart surgeon but also have a tele medicine practice wrote a book all of that stuff now to try and keep as many people off the table as possible and I just want to uh um if folks are interested Phil like myself is a clinically practicing surgeon or or actually let me remove that word metabolic health specialist primarily focused on cardiovascular disease and if you look in the show notes uh Phil's contact if you're interested in Consulting with him in the show notes are his access details it's important to know that up front so he is available for consultation uh Phil I love that uh can I ask you a personal question um and we can edit this out if you're not willing to say this what do you know what your CAC score is your car arric calcium score yeah uh my CAC score is zero it's been zero twice now three years apart I'm am just about to turn 5050 years old as we record this and and mind is zero as well and I think it's an important concept that at least by the thinking of that cardiothoracic Society it is not possible to be fat and have a high LDL and a high cholesterol it's in congruent with a zero CAC score and the only thing that I would change is you use the word pre-diabetic you and I were never pre-diabetic we had insulin resistance but genetically our body is so good at turning sugar into fat it never harmed our blood vessels our diseases are going to come from insulin not from sugar but you see other folks and I think this is a very important narrative and um Matt Bud was talking about this a little bit ago I'll go into Matt in a second is that uh cardiologists and cardiovascular surgeons see more diabetics than endocrinologists and um so the disease that you treat at least in a metabolic space is more for the diabetic side the diabetic genetics rather than folks like yourself and myself who have zero CAC scores so it's it's an important concept uh that I just want to reinforce to the audience yeah I think it is important uh to note that and uh you know the work of uh Joseph craft and Gerald Ren uh in the cardiovascular space uh it shows us exactly this you know um in one of uh Jerry revens you know uh talks um you know he basically makes the comment that the um coronary artery disease the aosc orotic heart disease patient without diabetes has simply not been diagnosed uh in other words people aren't looking for it in the right way and and as you mentioned it's not even really about diabetes per se it's insulin resistance and now that I know to look for this um I see this every day you know in my surgical population um when you look for it properly almost every patient that ends up on my operating table is insulin resistant um and we can't say the same thing about cholesterol uh elevated LDL cholesterol is really a 5050 uh shot you know when you end up on my operating table but insulin resistance is nearly Universal and we have all the data we need on this it's not debatable uh you know it's interesting when I talk to my Cardiology colleagues these days and um I don't necessarily try and convince them you know I know within the low carb community of course cholesterol is a very controversial topic and you know and I it's not about convincing cardiologists that cholesterol isn't the issue it's really just opening their eyes up to the fact that insulin resistance is a much bigger issue so you can look at the cholesterol we can address the cholesterol all okay maybe and I'm sure we'll get into all of that uh but we do have to acknowledge that insulin resistance is a much bigger problem always has been and everyone understands this and the literature strongly supports that um yet you know it it's not the way that our practices are geared because you know it's not the main messaging from the Health Care system and there are many reasons why that is uh but that's what I really try and wake people up to um we can figure out what the role of cholesterol may or may not be in this whole process but we have to acknowledge that insulin resistance is the primary driver and a much bigger risk factor so let's let's try and fix that let's try and diagnose it uh to start with and I I appreciate that and we're going to get into those weeds in a second I'm want to put your surgical hat back on CU we have this unique opportunity you and I of talking about something that we've seen um which other people imagine but they've never seen um I've done a fair amount of peripheral vascular surgery especially when I was younger because of the in the smoking era so we did aaa's before they had end endovascular surgeries and that kind of thing you've done the same um can you describe uh in as Vivid a way as you can and I I call it kind of the snot-like substance that is plaque that is this collection of stuff because everybody has an imagination but nobody's held it and touched it and felt it can you describe as a surgeon what you feel what you see not in the conies and are the conies the same as the of the larger vessels but what does all of that look like when you get in there yeah so typically you know when we're actually taking the plaque out which you know uh to set the stage in the cardiovascular surgical world uh what I do on a usual basis we don't actually take the plaque out we basically are working around it we're re-rooting the plumbing around it hence the coronary artery bypass being the most common operation we do but you're right in other vascular beds like the cored arteries in the neck or the the peripheral arteries uh in the uh in the extremities and um you know at abdominal aortic aneurysms are probably the most dramatic example of this uh and of course remember that well although it's not something I commonly do today um you know that plaque is often this kind of um mushy cheesy type uh substance um and you know seeing that and holding that and touching that you can certainly understand how we got to where we are today because you look at that and you're like this is fat this is you know butter this is cholesterol uh this is what it looks like so of course it must be the fat that we're eating and the cholesterol that we're eating and the butter that we're eating that's causing this plaque um now just because something makes good sense doesn't mean it's true and of course we know that those two things what you eat and what ends up in your blood vessels are not directly connected and it's not as simple as if you eat the cholesterol you eat the saturated fat that that's what ends up in your bloodstream it's not a drain that's getting clogged by bacon grease but but here's an interest again from a surgical's perspective from a visualization of the vessel because this is debated and discussed in our scientific groups a lot by people who've never seen touched and felt and scraped out or bypassed what you and I have done and you're right cored inct me want to come back to this we remove the plaque and then we try to revize same thing with the AAA we we put a Graft in there to squash it but um where is the blood vessel when you've got this plaque where is the blood vessel in this where's the blood vessel wall is this stuff in the wall has it exploded is on the out is it on the inside where is the The Vessel wall in the plaque yeah so the vessel wall is going to be on the other side of the plaque from where the blood is um and you know this plaque ends up being a interface between the vessel wall and the blood uh and that should tell us some things uh and the other thing that's real striking that again I didn't fully appreciate but now I think back to is the inflammation that is always uh there when you do scrape this plaque off the vessel wall underneath is clearly not normal and um you know the kateed is a great example because typically you know we're clearing the plaque out and we get to a normal area you know at the lower you know what we call the proximal end of the plaque closer to the heart and you can see that interface between where the blood vessel wall has not been damaged and there's no plaque no cholesterol build up and you know then you scrape out this area of plaque and you see the damage underneath and if it was just a matter of you know the cholesterol basically just sticking to the wall as people picture you know why would it occur at that spot and then a millimeter next to it you have a normal blood vessel that doesn't have any plaque attached to it because the LDL cholesterol is evenly distributed in oura bloodstream it's one of the you know kind of laws of of fluid physics that things are going to evenly distribute throughout a compartment of fluid and so it doesn't make sense if it's only the cholesterol that these plaques occur in one place and a millimeter next to it in the same blood vessel you have absolutely no plaque with a pristine uh blood vessel wall yeah so I I just want to reinforce a few things because most folks have not been there and touched that and felt that the first thing is the plaque is on the inside the vessel wall is on the outside the plaque isn't at least when we operate on it not inside the vessel wall may have started there a little bit but it's outside of the vessel wall it's in the Lumen secondly it's very Frable it's very snotty it is not like this smooth thing it's not this uh linear thing or even you can see the calcified stuff that it's the snot likee stuff that can break off very easily um and then the blood tries to worm its way through that and these occur as you said as Islands in various areas sometimes you'll see a stretch of it but there is native almost normal looking vessel now I haven't looked under the microscope at the normal sides but at least macroscopically you don't see that but this is an important consideration for me the reason why I as a general surgeon saw a lot of plaque is because we I grew up in the smoking era where the majority as you said the cids the aaa's the lower large vessels are were primary targets of nicotine or of smoking whereas with the hypoglycemic um disease we primarily see it on your Turf in the cardiac vessels there's a lot of patients who have uh significant coronary artery vascular disease but very little plaque elsewhere if they are diabetic do you have any insights or understanding and I think it's important for people to know because there's a lot of argument about whether CT is a correlate for uh uh plaque in the heart do you have any idea why these two very similar inflammatory processes have different places they exhibit their disease one more broad spectrum one more direct and also um what is the best testing for you conserve not obviously operating but what is the best way algorithm for people to know what their plaque level is from a diabetic perspective yeah and and we can talk about the second part of that first um because there is this difference that you mentioned and you know uh the honest truth is we don't understand all of the reasons why there is this difference um you know first and foremost it may just be a size issue understand that we're talking about coronary arteries that are you know usually one and a half maybe up to about three or four millimeters in diameter um versus you know very tiny you know uh I need to use magnifying glasses to operate on these things it gives you an idea of how small they are uh and then we're comparing it to the kateed artery which is usually going to be you know somewhere in the uh let's say 10 to 20 millimeter so almost a 10x size difference and then you get to the abdominal aort um which at its normal size is about four to six cmers and you know of course when it get becomes aneurysmal that we're operating on it it's oftentimes larger it is larger than that um so one is a size issue and then there's probably something to do with the flow Dynamics related to that and uh there are some other factors that come into play um but because of that difference in plaque doesn't occur the same that in the heart as it does in the katas as it does in the femoral arteries um I believe that the best strategy if we want to know if there's plaque in the coronary arteries is you need to look at the coronary arteries and the good news is we have a great way of doing that today we have the coronary artery calcium scan the C AC scan and it's going to show you if there's any calcified plaque in your coronary arteries let me stop one second pH if I can because we've actually talked at loggerheads a little bit that snot like substance that we see has very little calcium in it the calcium occurs kind of underneath that and you can see the calcium on x-ray so what we were talking about earlier on was the soft pla component uh can you make a distinction between the hard PLA and the soft PL is the CAC SC measures the hard PLU the calcified bone likee PLU as a so if you think about the way I look at it if you look at a bone with a piece of cartilage on it uh the soft block is like the cartilage and the hard the calcified part is a bit like the bone can you make a distinction between that and help people to understand calcified versus non-calcified plot and the role of the CAC score in that yeah so you know the they definitely are two different points in the process uh and you know again there's a general concept out there that it's an evolution right you go from you start with what's called a fatty streak which is basically just a little bit of this substance that starts to build up on the blood vessel wall and then it's a gradual buildup process and at some point either due to just simply time or other factors this calcium starts to come in and you now get a calcified plaque uh and the reality is is that they go together um it's not clear that by the way it is actually a a a straight progression um there seems to be sometimes you get more calcified plaque for different reasons uh you may not have as much soft plaque uh but regardless they almost always exist together when the disease is significant um it is certainly possible that you have some soft plaque you don't have calcium in it and we don't see that on the CAC scan but the reality is is that's not clinically relevant um the chance have you SE have you seen a patient with a zeroc CAC score with a large burden of soft plock um not what I would call a large bur burden you know we we are so good at Imaging now and we can talk about the other Imaging study the CT angiogram which shows us in fine detail the soft plaque uh that yes we do see some soft plaque with a CAC score of zero uh but it is incredibly rare to see um a large burden of soft plaque you know to the point that someone might need a stent or bypass surgery with a CAC score of zero or you compromise flow toward a heart attack or a stroke or a heart attack correct with the caveat being that you know sometimes people do have heart attacks with CAC scores of zero and that should really open our eyes as well because we should say well how can this be they don't have plaque or they don't have calcified plaque at least and then they have a heart attack and again that should alert us to the fact that maybe plaque isn't even the whole story maybe there are some other things going on that might be causing heart attacks like blood clotting um and I you know blood clotting is a significant part of all of this we GNA talk because that that is something that I've separated out my head a lot so I want to discuss that in a second because you I I I mean this is just ridiculous how much information you are sharing that just blows my mind and helps people to understand this as a process because there's so much misconception because we haven't seen it I mean this is just blowing my mind sorry um so right it's claing versus plaque and cling is acute it occurs rapidly whereas the plaque has been there for a long time and that's to understand and the two can go together or separately yeah so you know to Circle back to you know what can you do you know what our best test to determine are you at risk for you know a heart attack for atherosc orotic disease um the answer comes back to the coronary artery calcium scan is the screening test you know I always liken it to the mamogram let me stop you for a second so the the CAC score is there for Progressive chronic disease yeah okay and it's the it's probably the most commonest indicator of a potential heart attack it it seems to be the best predictor that we have better than you know for instance blood cholesterol levels uh it's clear that the CAC scan is a better predictor of cardiovascular risk than blood cholesterol levels are and um the the good news about the test is it's easy to do um it's basically you know it's fairly inexpensive uh and um it's universally available especially here in the US may not be so in some other countries but um because of that it makes a great screening test and and I think it should be done to why do family practice doctors not do this we we do colonoscopies we do mammograms yes they should be done but the majority of Americans are going to die of a heart attack why are we not doing this as a routine screen perhaps at the age of 40 or 45 like the indicators for those other screens prostate rest colon it it it is ludicrous yeah it's a great question and it's one I ask all the time and quite frankly I've never been able to get a good answer to and the only thing you have to Circle back to is it would fundamentally change the Paradigm around how we manage cardiovascular disease and that's going to disrupt a lot of well-entrenched things uh in our medical system what is your total cholesterol uh when I check it it runs anywhere between two 250 and 350 typically you're going to die have a heart attack in about 10 seconds if you don't take a stattin so but you got a zero CAC score so a conflict of knowledge right there but I want to get back to the the CAC score and I think uh I'm going to throw something out just because there's a lot of talk about the absolute number the CAC score is not sensitive enough to give us an absolute number it gives us kind of a space that this disease you don't have it you got a zero or you've got a low likelihood of it or it is intermediate or significant but a lot of people say oh my score was 120 now and now it's down to 100 and I'm reversing my CAC score uh or it's cly if it goes up significantly but they it's not that sensitive because the read everything else where there's a range within which uh it can occur it's it's less sensitive and I want to talk about ctas but what do you think of the reversal two questions here the the reversal of a carard Arctic calcium score and also all the products the nac's and all the products that are being pushed out there to potentially reverse or stabilize the plot there's some Merit to it but I can you give me your thoughts on those two things can it be and can it be dissolved and is there validity to take those medications to do so yeah great question so first of all you're right you know the variance in the CAC score we have to acknowledge and I tell people you know that variance may be about 10% or so um outside of that um you can lower your score I have seen people scores go down in my practice um but I don't think it's really all that important to be honest it's more important that you stop the progression that your score doesn't continue to go up and again we know that that's the natural pattern um CAC scores in multiple Studies have been shown to progress on average somewhere between 15 and 25% per year if you don't change the course if you don't change the course if you're just sort of following it uh and we know that that progression or lack of progression is as strong maybe even a stronger predictor of risk than your absolute number is so you know to put this in very real terms I see patients that have CAC scores of a, 1500 even up to 2,000 and it turns out that they don't have any disease you know at that point that needs an intervention they don't need a stent they don't need bypass how do you know that what do you what do you do to figure that out usually it's going to be either a CT angiogram or uh an invasive anagram what we call a cardiac catheterization to get that detailed look at the blood vessels and there are some other factors that come into play um but you know if you take those patients and they're high score and um you do what we do and we'll get into that and you stabilize their score so their score is 1500 today a year from now their score remains 1500 and five years from now their score remains 1500 those people are at very low risk for having a heart attack you can have someone on the opposite end their score is 100 or 200 let me stop you for a second there they're at low risk for a heart attack from Progressive disease but they're not at low risk for a heart attack from a sudden blood clot or a clock rupture there's a difference uh uh I just want to make that distinction because I don't want to lull people into a sense of security in that regard well yeah you know and again none of this is saying you ignore the disease that's there there are there are things that we're doing to manage it um but overall they're at low risk of having a heart attack even taking into account you know I'm not saying there zero risk but they're at low risk so you're right very important to differentiate our sort of medical ease you know low risk doesn't mean no risk um but on the other end of SCA of the scale you have people who they come you know with their CA they get their first CAC score and let's say it's a 100 or 200 and again low risk of disease today but they come back the following year and they haven't made changes and now their score you know is 250 and then it's 300 and and then it's 500 you know that person even though their absolute score may be lower five years later than the first scenario they are at higher risk of a clinical event because they have this progression and this is another important point that you made earlier about the CAC score it's a way to follow disease progression and this is another fault in how it gets used in the medical system because you're right most PC s don't order the CAC but if they do they think of it as a one-time test and it's clearly shouldn't you know it needs to be used as a way to follow disease progression and it's very good at doing that uh so again it's something that I ask all the time why aren't we doing this if the patient has a nonzero CAC score that score should be repeated in a short period of time in my mind in my practice it's typically one year uh you know and maybe you could say that's a little bit too aggressive but I really don't think it is because I want to know is your plaque getting worse are you accumulating new plaque that is really the key question than having a heart attack yep that's that you know okay don't do anything but then I'll see you in the ER when you're clutching your chest that that's we have to put it into the risk so I love that narrative that's that's a really good narrative what about nuclear medicine stress tests or or stress tests in terms of flow and and cardiovascular risk yeah they play a role in figuring out where you are on this kind of risk uh progression but they're not a good screening test and unfortunately they have become sort of the most common uh screening test um really you know nuclear stress test or stress tests in general um are really only are best used in patients that are having symptoms that we're trying to figure out the likelihood that these are cardiac symptoms um and they're also an adjunctive test that if you've established someone has some disease and you know they're if they're not having symptoms and you're trying to elicit symptoms because you're basically provoking their activity so for patients that aren't really active um it's not really all that useful if they tell you well not having any symptoms and chest pain of course being the main symptom shortness of breath related uh in cardiovascular world but if a patient is just sitting on the couch the fact that they're not having chest pain doesn't really mean anything so a stress test can be a good way either you make them walk on the treadmill you physically provoke them or you give them medication that speeds up the heart rate and chemically provoke them and now you figure out does that uncover symptoms yeah I like the new the stress test primarily as a sign of immediacy is there an immediate need to intervene and couple of couple of comments because as you said one of the one of the steps is to do a a Cath and the cardiologists to my mind are somewhat Cavalier about caths or they used to be um and and they're two concerns number one the majority of cardiologists have never seen uh like we talk about earlier plaque disease they don't they don't conceptually understand what it absolutely looks like so when they do a balloon when they put a stent in the risk of knocking something off the risk of having a shower the risk and often they get away with it but we so often see um the troponin the cardiac numbers going up which is basically a measure of a heart attack when we have a calf so I try to keep a calf back when I recommend a calf to a more likely like a greater likelihood of inter vention rather than a screening tool I don't know if you share that sentiment can you comment a little bit on Rising um measures of muscle damage or muscle injury which are the tronin and also uh cath risks especially cath risks yeah definitely so and and you're right you know the the catheterization which is an invasive test you know we actually you describe what a c is yeah definitely so you know we actually have to get a a catheter that's where the name catheterization comes from into the blood vessels uh that we're interested in in this case the coronary arteries on the heart how do you get there how how do what's the pathway to get there yeah exactly so typically you're going to enter the blood vessel the artery either in your wrist or in your groin those are the two arteries we use for Access and then you actually have to put a catheter and and we're talking about pretty small you know you remember how small I said those blood vessels are so now we have very small catheters uh that we then get up either through the arm through the big blood vessel the aorta into the coronary arteries which come off the aorta uh uh or we're coming from the groin all the way through the aorta to those coronary arteries and now we put this catheter into the artery itself and we inject d uh that we can then see on an X-ray machine uh it's a video you know so it's not a static x-ray picture that people might be used to it's a uh moving picture and we can actually watch that die go through the blood vessel and we can see where the blood vessel might be narrowed where this plaque is um now the interesting thing that people don't understand is the catheterization doesn't actually allow us to see the plaque um it shows us the narrowing in the Lumen of the blood vessel the channel That the blood is going through how wide or how narrow that vessel is exactly but you're not actually really seeing the plaque sometimes you can see those little bits of calcium uh but it doesn't give us a good image of the plaque like the CT angiogram does um and uh it's a little bit of a different perspective so um the in the um the uh you know that can actually lead you to some false conclusions about things um because you're only seeing how narrow the blood vessel is you're not actually seeing how much plaque is there uh and those are two different things uh again getting into the minutia but that the other risk also fil just when you and I operate on vessels um we clamp above and below and one of the reasons we clamp is not just blood flow but it is because debris dur during manipulation of the vessel can travel Downstream and we always clamp disly and then we clamp well we clamp proximately then we clamp disty but um and then we have to I remember and it's been a while since I did vascular Cy we have to fastidiously wash out that debris that gets knocked off to in the handling I don't think in talking to them most cardiologists understand how fragile some of that plaque is and I'm assuming the Keds are not that much different than the other vessels and we do see increase in muscle uh damage measurable muscle damage when you do cats what do you think about that is that an important consideration when you're deciding to have a uh an intervention done um what is that risk because you do get little Showers of tiny fragments of that of that plaque of that gelatinous plaque what are your thoughts on that yeah you know so I think um catheterization is definitely not a risk- free free procedure no procedure is in medicine where we always have this risk benefit equation and um you know and so that really should enter both the patient's mind and the operator's mind the the cardiologist doing that Cath um you know need to think about that and is this the right test uh for this situation and you know it used to sort of be the only option we had uh now we have non-invasive ways of looking at these blood vessels the CT angiogram and I think that has changed the game and honestly medicine um the Health Care system is still catching up with that it's still understanding that I I I do think catheterization is still overused it's not as overused as it used to be but it's still overused and it's not something to be taken lightly you know it is a procedure it does have very real risks associated with it and so we need to take that into consideration and more so um also what we're starting to understand is there used to be sort of a knee-jerk reaction that you did a cast cation you saw a blockage the blockage looked bad and the inclination was we need to treat that blockage we need to put a stent in or we need to do bypass surgery we're now understanding that you know um the the look the percent narrowed that the blood vessel is on that catheterization is not the whole story as to whether or not intervening on that blockage putting a stent or doing bypass is actually going to benefit the patient uh so this is where we get into the concept again that you mentioned earlier of is there aeia is there reduced blood flow associated with this that's really the key question and we again have better ways today of assessing that um and you know we can get very technical but there are some things that can be done during a catheterization to actually measure the blood flow and now determine does this warrant treatment or n perfect so you've mentioned it a few times and I want to go there between a CAC score and a calf lies the CT angram and the biggest issue is cost and uh cost die has to be used and radiation is a little higher but can you explain to me the value of a uh um a CT angram over between a Cath and a CAC Sport and I really look at it from two perspectives it shows me Anatomy kind of a little bit of static Anatomy because it's still a CT scan but it also shows flow can you explain that the uh so we're looking at function as well as function and provision of oxygen and and correlates with oxygen and nutrition to the heart muscle as well as the plaque burden how do you use CAC scores how do you view them how does your brain work when you're thinking about a CAC uh sorry a uh CTA yeah so you know all of the things that you said the CTA is more detailed and because we're now giving d uh but we can give that d now into a just a simple intravenous line we don't have to get the catheter up to the heart um we can now see the actual flow through that blood vessel we can see how narrow that blood vessel is similar to what we were talking on the catheterization and with the most advanced version of the CT andram available today we can actually do what is the most advanced what is the most advanced one so it would be one with what's called ctfr fractional flow Reserve that's the measurement of is this narrowing actually reducing blood flow uh through the blood vessel so that can all be done today um you know that's not as commonplace you know the standard ctog may not include that uh you know when you go get your CT angiogram but it's still a much more detailed look and now it can give us a sense of okay there's plaque there um is this plaque we need to worry about in the sense of you know the patients at sort of imminent risk uh and is you know uh is reducing blood flow uh so I use it again as the second level test if I am particularly concerned because either the CAC score looks bad or the patients having symptoms that I'm concerned about I think the CT angiogram um is now a great option before you go and take that risk of the invasive catheterization um it gives us a good road map we have an idea going into the catheterization now of what we're dealing with and you know we can have the discussions about you know stance bypass that type of stuff uh so it's an intermediate step for me now some people say well if it gives you such a great view why not use that as your screening test and of course you know um uh Dave Feldman and Matt budoff are currently doing this study you know lean mass hyperr study and they chose to use the CT anagram because it's more detailed uh and in an ideal world yeah we would get that great picture every time the downsides like you mentioned are more radiation exposure more more cost and you have to give this die which occasionally can cause some issues pretty rare but occasionally can cause issues uh so you take all of that into consideration and as of today the CT angiogram in my mind um is not ready to be used as the widespread screening test but it's a great secondary test and I have a pretty low threshold for ordering it these days I think the key you've mentioned these words but a CAC score is a global screening test if you want more detail a diagnostic test is the CT anagram because it gives you both Anatomy it gives you soft plock and it gives you flow uh and that's a computerized calculation then the therapeutic intervention is a calf or your hands so uh you know that's the way that I look at the escalation of these I want to flip a little bit I know time is an issue for both of us but the way my brain works when it comes to Therapeutics so okay I've got a burden of disease I look at the evolution of plaque and the treatment of plaque from three using three different words the the first one is plaque stabilization plaque rupture which is the most questionable one the second one is um if you've got a burden of plaque and you've changed your diet and you reduced your uh um uh you're managing your diabetes or whatever it may be uh it really is about the risk of developing a clot on top of that plaque or even a clot where you don't have that clots in the but clotting disease as you said is a significant factor in both stroke and cardiovascular disease probably definitely more so in stroke but also in cardiovascular disease so the second word I use is anti-coagulation and then the third word that I use and I'm working backwards to cause is ultimately the the the word that is associated with all cause plaque disease and you're never absolute but that is inflammation so the the the other word that I use and so I use anti-inflammation and that's both a dietary strategy you're going to quit smoking plus certain medications anti-coagulation and then anti-pla disease which for me is the kind of black box of everything what do you think about that and how do you think about that in your management of your patients outside as a as a non-surgeon if I can put it that way yeah I mean I think that's a a good construct to think about and that does guide you know some of the things that I typically are recommending to PTI to manage this disease um and you know uh but I even kind of step back uh you know and say at a higher level you know is the intervention that we're using whether we're talking about a pharmaceutical a dietary change or a a true intervention a stent or bypass surgery is that intervention addressing the underlying root cause of the disease process uh and that's a question that we really don't ask enough in medicine uh and this broadens Beyond cardiovascular disease but to keep it to cardiovascular disease you know we we had the discussion earlier we talked about inflammation we talked about insulin resistance these are root cause issues that ultimately lead to cardiovascular disease and is what we're doing addressing that and the simple you know on many you know the simple answer I guess I'll just stick with it is the surgery that I do the stents that get placed do absolutely nothing for the root cause of the disease we have to acknowledge that not saying they shouldn't be used but they don't address the root cause the Pharmaceuticals um you know did a very poor job now that might be changing we have these newer Pharmaceuticals uh that are not cholesterol lowering medications um but they do they do on some levels start to address the insulin resistance and we're even more looking at the information tell me what you're talking about in that class which drugs reduce in uh insulin resistance we're talking about the glp1 uh Inhibitors atjar and that indication that's new entry there's another uh a patient and a buddy of mine David na uh uh nebor who is a uh he's actually an electrophysiology cardiologist and done amazing well he works in our space but he brought something to my attention in December of 2023 the FDA approved culturein as a therapeutic drug for uh uh in a in a similar vein to gp1s with a much greater reduction in cardiovascular risk than statins it was head-to-head compared by statins and I've got a video on that coming up have you heard about that what are your thoughts on culture scene which I'm just starting to explore um what do you yeah so this is looking at the inflammation part of this and uh culture scine has now been demonstrated in two trials uh they were called the low Doo trials lowd dose culture scine uh to reduce the risk of cardiovascular disease uh of clinical events I should say heart attack um as well as Statin uh did and um you know there there's some caution around using them there's some other effects we have to think about uh but you're right they now have gotten that indication and I'm starting to see that used more in practice and um you know there's always been this talk around statins um that you know maybe the effects that we see from statins are not due to their cholesterol lowering but due to their anti-inflammatory effects which they do have uh one very interesting cl to my mind is that when you say look statens you know I've got a Zer C score I don't want to be on a stat well it's got that anti-inflammatory protection but I'm not willing to to take a Statin drug that has a massive side effect profile if there are other medications that give me the same or better anti-inflammatory value at a specific point that I know how they work culine works on lucaites aspirin works on platelets um that has a clot reduction anticoagulation because that's what we're talking about we've now shifted Away From Plaque which is it doesn't really work there now we're talking about anti anti-coagulation and anti inflammation um and there are far more direct better drugs with a lower side effect profile as you mentioned the GP 1's now we've got the culture scene I uh uh like aspin quite a bit that was my PhD but um I I know that time is time is getting short what I want to ask you is a let's role play a little bit I come into your office I'm on a ketogenic diet let's say I'm even carnivore um but I've got a uh some idiot called Dr cus did a CAC score I'm 60 years old and he found that my plaque is500 and I'm petrified yeah but I'm asymptomatic I exercise I eat a Kil I hate the word I eat right or healthy because that's more whole grains and fruit but I I'm a carnival yep by the way my CSC is called zero so what is okay I've walked into your office what testing do you do I've got a CAC for 1500 multivessel disease but Main and L and lad what take me from there yeah so you know the the the first discussion point is going to be you know do we get a CT angiogram or not and you know if you're truly asymptomatic and you're op you know you're exercising at a high level um you know that's a pretty good indicator that you're not at risk but I know you know many people they just get worried about the picture on the CAC score they want to know you know how much at risk am I and think that's a great situation for using the CT angiogram uh so that's probably going to be my go-to in this situation and then the second part of that discussion becomes okay if we determine that you don't need an intervention today you don't have that bad of blockage anywhere that we're thinking about a stent or bypass um now it becomes we need to follow this over time we need to make sure it doesn't get worse and to do that we need to address all of the factors uh because just because you've been carnivore for a while or low carb keto whatever we want to say um doesn't mean that you've totally fixed your insulin resistance doesn't mean that you've reversed your inflammation all the way we need to check this stuff and this is where the blood work comes into play uh and that's where we really get into the nuance and the detail of all this blood work and of course the cholesterol issue then comes up on second that is the place where I see the most in congruity with with non-metabolic Physicians like yourself they have no clue of how to interpret the blood work they're obsessed with lipids and they don't look at the diabetic or the insulin resistant side of things at all yeah and and you know they're not even obsessed with lipids they're obsessed with one number on the lipid panel that really doesn't tell us a whole lot about the lipids the LDL C the LDL cholesterol level um and that really doesn't tell us you know it doesn't tell us anything about the quality of the lipids which I think is really the issue that we should be narrowed on and of course that's related to insulin resistance um so in some ways you can just say well let's just figure out if the patient is insulin resistant uh and I that like I said earlier you know when I'm talking to my Cardiology colleagues today this is the main point I try and get to them is you can talk about the lipid but we need to acknowledge that insulin resistance inflammation are bigger risk factors so let's assess for that as well that this patient is not diabetic because their LDL is high and you're treating diabetics with high LDL exactly so no okay so what what medication strategy let's say I I'm insulin sensitive yeah but I've got a 1500 um a nuke Med is negative a um my echo is fine which they love to do I didn't we didn't get a chance to even talk about the value of Echoes because everybody gets an echo when they walk into a doctor's office but um CTA shows the 1500 pla burden low level of soft pla good flow what is your preventive medication strategy I'm on nothing yeah uh so my preventive strategy is is centered around you know the making sure that you're not insulin you remain not insulin resistant and low inflammation and from a dietary standpoint the best approach to that clearly is a low carbohydrate diet um you want to eliminate processed food you want to eliminate things like vegetable and Seed oils uh these highly processed fats and um you know I lean towards the animal-based side although I admit you can do this you know as a you know with a plant-based approach there are some other nutritional considerations that come into play but you want to eliminate processed food first and foremost you want to be managing your insulin resistance and your inflammation beyond that I don't really don't think there's any Pharmaceuticals that are useful in this situation um I think you can look at some of the supplements like we talked about that are targeting those things that we talked about blood clotting uh inflammation uh and the plaque uh you know calcification problem process and this is where we get into things like vitamin K2 uh and its role in uh calcium deposition uh we can talk about things like nyas as a you know anti-thrombotic agent preventing those blood clots um and maybe a couple of other things like nitric oxide like vitamin E uh that can help to lower that blood vessel uh inflammation and help to repair that blood vessel wall uh so those are the things I think about uh but you know it basically comes down to we want to make sure that you're not insulin resistant we want to make sure that your inflammation is controlled and then we want to follow this plaque over time with the CAC score or even in some situations a repeat CT angiogram at an interval to make sure that it's not getting worse and if they were still instant resistant um with some weight on them you'd recommend a glp1 as not to get them to lose weight or anything but to help to accelerate the Improvement in their uh insulin resistance would yeah I think that's where the glp 1es start to come into the algorithm and again we're still figuring it out I I think the drugs are widely overused in general uh but I do think they have a role because of that mechanistic they're actually attacking that root that root cause the insulin resistance uh and so I can see a role that they may play and that they're starting to come into the algorithm but they're certainly not my go-to you know uh as I know you have said many times you know it it it's not a pharmaceutical only approach the glp 1's may be an adjunct to the diet and lifestyle and again it's clear that the best diet for reversing insulin resistance is a low carbohydrate diet I I agree completely that it is a multiactor thing and we there's so much Synergy uh here Phil I I know time is out I'd love to there's so much more that I want to discuss I we both had uh we we both work uh we both CL clinicians I really really value this how can people because that last question is pretty much what you do in the non-surgical realm you got a surgeon's hat on and that is that is that correct and how can people access you to get that testing done to get that work up to get that interpretation which is really what they buying they're not buying the blood work they're buying the interpretation of the blood work which is more accurate which is more of a story of where they currently are that you and I have an expertise in that other folks don't they look at numbers and throw pills at numbers as you said uh LDL or whatever it is we understand the story we understand the narrative how can people access you um how do they get hold of you and the show notes will have these details in yeah definitely so and we're definitely going to have to do part two and get into some of this even deeper uh but you can find me everywhere at iFix Hearts uh is just the simplest thing you can go to iFix hearts.com you can set up a call with my team to talk about joining the practice having that evaluation done uh social media everywhere is iFix Hearts as well and uh you know like you uh am on this mission to spread this word um to not only get this information to more patients uh but also to get this information to more doctors so that the patients can then access doctors that think this way and recognize these things and we can get people more effectively taken care of and you know ultimately we can keep more people off of our operating table you know the point that I want to leave people with is um just how common heart surgery has become how big a problem heart disease is and just because we are better at keeping people alive with heart disease uh similar to The Diabetes story uh we really should be looking at this as a treatable reversible disease rather than just this chronic disease management that we take people through and um you know the answer is the more proactive you are the more you take charge of your health uh the better you're going to end up being so find a good clinician like Rob uh who understands this and can really help you uh manage this problem and uh instead of the passive approach that our health care System tends to take the vast majority of people find out they have heart disease when they have the heart attack uh and that is just simply unacceptable in my mind too late exactly oh I love that to end on Phil this has been absolutely wonderful you've blown me away with some of the statements that I'm going to steal from you the the the lines it really is that thinking and we really have to grow ourselves as a specialty in metabolic Health where you come from Cardiology cancer Family Practice uh uh Gynecology wherever it may be the central point is the narrative that we just had the metabolic Health side thank you so much thank you Rob