Dr Thomas Nero speaks with Dr Aaron Baggish about coronary artery disease in the endurance athlete (and non-athlete as well!) They discuss cardiovascular testing in Masters athletes including ETT, coronary calcium scoring and CT angiography as well as risk factor identification, inflammation, physical & emotional stress and ongoing research. Dr Baggish is a Professor of Sports Cardiology at Université de Lausanne and founder of the Cardiovascular Performance Program, Massachusetts General Hospital, Harvard Medical School. He has been team cardiologist for USA rowing, US Soccer, and the New England Patriots. He was the medical director for the Boston Marathon and is a consultant to the IADA, IOC and FIFA.
Dr Thomas Nero speaks with Dr Aaron Baggish about coronary artery disease in the endurance athlete (and non-athlete as well!) They discuss cardiovascular testing in Masters athletes including ETT, coronary calcium scoring and CT angiography as well as risk factor identification, inflammation, physical & emotional stress and ongoing research. Dr Baggish is a Professor of Sports Cardiology at Université de Lausanne and founder of the Cardiovascular Performance Program, Massachusetts General Hospital, Harvard Medical School. He has been team cardiologist for USA rowing, US Soccer, and the New England Patriots. He was the medical director for the Boston Marathon and is a consultant to the IADA, IOC and FIFA.
G ood morning and welcome to future pulse. I'm Dr. Thomas Nero. And with me today is Dr. Aaron Baggish. It is, , very early in the morning here in, uh, New York and Connecticut and, , a bunch better midday in, , Luzon where Dr. Baggish is welcome.
Thank you very much. Great to be with you, Tom.
, so I've been looking forward to this for an extremely long time.
I'm a, , reformed triathlete. , and, , I initially met Dr. Baggish, I want to say I was about 15 plus years ago at one of the sports cardiology conferences, and I decided that he was the person I most wanted to become when I grew up. Um, unfortunately there was already Dr. Baggish in that position. And, , so I'd really never got the opportunity to do that.
, but, I am, a little bit jealous. . You used to be the director, or I guess you are still the emeritus director of the, , cardiovascular performance program at the mass general. And now you're at, , in Luzon, , Switzerland. .
, and, , tell us a little bit about why you made that move. I'm, uh, I'm intrigued.
Well, first off, perhaps the thing I'm most proud of is actually starting the cardiovascular performance program at MGH. It was really the the country's first dedicated sports cardiology resource for athletes and active people, and the program is thriving. There are an amazing team of people that continue to see athletes from all over the country, and it was a great place to work, and I'm still very much engaged.
But for me, The time had come for a new set of challenges, and it turns out that Switzerland is really the home of sports policy. Most of the major sports organizations that oversee international competition are based here, and I was increasingly doing work with many of them, and my wife and three children and I thought a European chapter sounded like a fun challenge, and so here we are.
Well, I am a little bit jealous. , the skiing over there is absolutely spectacular. And the food is much better.
I would agree on all fronts.
All right. Well, today we're going to be talking about ischemic coronary artery disease in athletes. , we're not going to be talking about a number of the other topics that have been covered a lot in the press recently with sudden death in athletes, , and issues with hypertrophic cardiomyopathy and other arrhythmias.
. So I wanted to talk more about some things that have been creeping up in our program. And, , it is an issue that , a lot of our endurance athletes , are questioning. And I guess it comes back to the big question of, , is there a maladaptive, , issue With endurance exercise, we all know that looking back at the physician's heart study in the nurse's heart study from the 60s and 70s that we saw this J curve with exercise, and it's been replicated in a number of different studies.
And that's always been intriguing and we've. Blown it off in the past is saying that there are other issues here, or maybe we were looking at the data incorrectly, but there's been a number of registries that have shown the same thing. So how do you approach this? And , what are your initial thoughts?
, at the risk of starting, , by sounding like a skeptic, I want to be clear that most of the epidemiologic literature that focuses on health outcomes in truly high level endurance athletes or competitive athletes that are aging, um, are simply underpowered to make any real conclusions. , the fact is 100 percent crystal clear that if you go from doing , No physical activity to some form of exercise, you improve health outcomes, and the more you do, the better it tends to look.
What I think we all need to be aware of is that , the curve does flatten out, meaning above a certain point, you're not going to get any more bang for your buck, whether it's preventing heart disease or trying to simply live longer or outrun cancer, by doing more than, say, two or three times physical activity recommendations.
So, the curve flattens, but I think it's a mistake when people start talking about there being a true uptick in, in, Adverse outcomes among those that push themselves hard as they age. Yep.
Yeah, looking at the, um, the mass registry, we saw in there that as people Increased up their activity that they had increased risk factors, especially interesting. Alcohol was one of them. I, I fully expect that dietary changes were also part of it. , there's no way that you can exercise for 5, 000 kilojoules per week and not be eating more carbohydrates.
, , and there may also be other issues with family histories that were underrepresented. , when we look at family histories, we're really only getting half of the story because half the people are going to have the gene and half the people are not going to have the gene approximately.
Yeah, that's right. , you're getting at this broad issue of unmeasured confounders or poorly measured confounders. And when we talk about the master's athlete exercise literature, , the major weakness, and this is not a fault of the investigators that do these studies. It's just incredibly difficult to appropriately adjust for some of the things that we know in clinic translated to outcomes.
And perhaps the most important one you mentioned is dietary intake. I , there's this pervasive view among people that are fit and highly active that the furnace is hot, so it will burn whatever you put into it. And that's potentially true from a maintenance of weight and body composition perspective, but we know that poor macronutrient choices affect arterial health, and it is almost certainly one of the unrecognized reasons why people get into trouble.
, 2023 was a great year for research. , I have been intrigued by more papers this year than probably any year in my career. Two that came out, , that were really interesting to me were , the Masters @ Heart Study, , and MARC 2.
, Masters at Heart showed something very interesting is that as you increased up to the highest level of endurance athletes, they had more soft plaque in their coronary arteries. And just to remind people, Masters at Heart, , studies a number of things, but in addition, they have a. , CTA or coronary CT angiography, , arm in it, , where they looked at plaque and they saw that there was, , plaque stabilization up to a certain point and then an increase in soft plaque at the peak, uh, versus Mark 2, which was also an excellent study by an excellent team, , that showed, , increased, , hard plaque and also, but I marked increase in overall plaque, which was again, somewhat interesting and maybe speaking more to these co founders.
Yeah, it might be worth for the audience just very quickly, , reviewing the literature base upon which these two studies came out, , because there's some important, um, Precursor work that people should be aware of. And this goes back now, you know, close to 20 years where initial studies looking at male marathon runners showed that higher levels of coronary calcification, very, very complex studies involving cohorts, which this was not a huge surprise.
Lots of smokers, lots of alcohol consumption.
, and probably the most famous was a 2008 European Heart Journal publication looking at a group of 50 male marathoners and comparing them to sedentary controls who were adjusted for framing and risk score, basically. And it turned out that the marathoners had more coronary artery calcification, and that was for many people kind of the first shot across the bow that maybe there was something maladaptive.
. There was then a series of two studies published in 2017 in circulation, um, one from the UK and one from the Netherlands, in which, for the first time, exercise dose was looked at. And the major findings from those two studies was that the more exercise people did across the lifespan, the higher their CAC scores were.
And so that really started asking the question is this a maladaptive phenotype that we should care about in clinic or is it a marker that has really no relevance at all? And I will tell you the two studies you just talked about really emphasize the complexity of this conversation. And what I would encourage the listeners to remember is that coronary calcification, and we'll talk about soft plaque in a minute, but coronary calcification is a nonspecific marker of injury and repair.
So we develop calcium in our coronaries whenever there's been some sort of perturbation, whether it's traditional atherosclerosis with lipid rich plaques or in the case of master's athletes, simply mechanical twisting and kinking over many years, which leaves calcification in the absence of true athero.
So probably want to unpack this spectrum of calcification a little bit more. But again, I just want to remind the listeners that this, this has been a question that's been alive for two decades and it's one that we're actually not anywhere closer to fully understanding, but I, but I have some good thoughts for people.
, so we'll get back to that. What are your thoughts on the two trials that did come out this year , with masters and, , MARC two? , what are their limitations and what did you find out that you found that was helpful on them?
Well, the first is that both of those studies were done by incredibly accomplished groups, friends of mine, people that I consider real experts in the field. And what's, what's remarkable, and this is a reflection of where the field of sports cardiology has gone, is that instead of just relying on observational convenience samples, these investigators really develop protocols.
assess people prospectively over time. And so the quality of the data is really quite high. I think as we briefly alluded to earlier in the podcast, the major challenge here is what was measured, but more importantly, what was not. So let's go back to sports cardiology one on one, and that is that no amount of exercise uh, confers immunity to true coronary disease that hurts people.
So lipid rich plaques, proximal , L. A. D. disease, things that get people into the cath lab and by revascularization. , another way of putting this is that you simply can't outrun risk factors. So in the aging athlete with hypertension, dyslipidemia, family history, a couple of cigarettes a week, whatever it may be, you can't outdo that by pushing your body harder and harder.
And at some point, if those risk factors aren't adjusted for or treated, more importantly, you're going to end up with coronary disease, particularly if there's a family susceptibility. So what the two 2023 studies remind all of us, about is that in the clinic when we see Masters athletes, we simply cannot assume that because they're putting in 15 hours a week on the bike or they're racing Ironman twice a year that we don't have to worry about them.
Indeed, we have to step back and think about them just like every other patient and risk stratify them and aggressively manage those risk factors.
And I do think it's important to look at them versus them, not them versus other patients. , when one of our patients come in and say, Hey, , I was doing great. And then all of a sudden. I'm not doing great anymore. , , I'm still running five miles a day, but it's a little slower.
, or, , , I'm having reflux disease and I just, I don't know where it's coming from. Um, you know, we've certainly found a number of patients who have exercise induced atrial fibrillation, uh, as well as ischemic coronary artery disease, uh, because we looked for it and other people , had not looked for that in those patients because they just assumed that they were too good. , and also, using CT angiography to assess rather than putting them on a treadmill because on a treadmill, they'll, , go to Bruce five and you'll be reassured that they're doing well.
But at the same time, there's maybe something that's still undergoing there because otherwise they'd be able to go to Bruce six or beyond.
Yeah, I think it's really easy in the context of a busy cardiology practice where you've got 20 30 follow ups in a row and some really sick people walking through the door to take the master's athlete that tells you that they've gone from running, you know, a seven minute mile pace to a 745 minute mile pace seriously.
You're saying to yourself, God, this guy's still 10 times healthier than anyone else I'm going to see today. Why should I bother? But the truth is, is that most master's athletes know their bodies well and most of the diseases we care about, they can really get them into trouble. often presents subtly with mild performance decrement as the primary sign, if you will.
So when the athlete comes in and tells you about something going on, take the time to do a little more history digging. It could just be they're tired, stressed, going through a marital problem, whatever it is, but it could be the primary presentation of obstructive coronary disease. So just take that real seriously.
, there are risk factors that were under assessing their phenotypes, um, how does one assess this? , looking at the research that's coming out now, , you can't necessarily just look at their lipids, their lipid profiles look adequate.
, we haven't necessarily looked at their , lipid sub fractionations. , we do see that they have, , some elevation in, , high sensitivity CRP, , but not all of them do. , there have been, uh, mixed results on interleukin one. , there's been some results , in research strategies on interleukin six, but these are not things that we can look at, , routinely.
, so when you have someone who's coming in and says, well, you know, I have these risk factors, but I'm really, I'm exercising a lot and I love it. , but I'm afraid , of dropping dead , on the, on the course. How do you work with them? , what are you thinking about in the back of your mind, as far as where the research is and , how that may impact them?
Well, I'll tell you, and this is just a very basic, simple approach. When someone comes in and shares with me that they're concerned about a bad outcome, the very first question I have for them is, Why? Why are you concerned? And the person that endorses having something changing in their body, they're developing discomfort, they're developing performance decrement, that's very different than the person that says, Oh, well, you know, one of my training partners had something bad happen and Woken up to that.
So first differentiation is people that may be manifesting early symptoms of disease versus those that just have a general risk because of an anecdotal experience or something they've read in the newspaper. The second thing is that, you know, you ran through a number of interesting ideas around the use of biomarkers to restratify people.
And I don't think we're really there yet in this population. So I fall back on some simple things that again, I can't show you good science to prove, but I just know anecdotally having done this for so long that it translates into risk, and I'll give you my list of things. So the first is a family history, and this is where, as we talk more about the 2023 studies, um, we really have the probably one, if not the most single and important unmeasured confounder.
When we talk about the genetics of coronary atherosclerosis. We don't fully understand it. We obviously have now polymarker risk scores and things that have some ability to differentiate between high and low risk. But in the clinic, that stuff is still pretty hard to use. But simply ascertaining whether mom, dad, or any first degree relative, had premature atheros, so before 60 for a man, before 55 or 50 for a woman, your metric, um, that speaks volumes to me.
And I risk stratify those people aggressively. I mean, we should talk a little bit more about exercise testing because I don't want to throw that out. It's still a very important tool in the clinic, but that one I pay close attention to. Second thing, and this is again always underappreciated, is psychosocial stress.
, the physiology around stress and how it affects vascular health is becoming clearer and clearer. And there is no question in my mind that people that are living through intense periods of stress, whether it's in the workplace or at home or with relationships, that that is contributing to an atherogenic risk profile.
And so I spend lots of time talking to people about stress management, and that may be as simple as doing things like meditation or yoga. It might be. Ending relationships. It might be getting therapy. There's lots of things that can be done there, but I think that's important. And then the
the two remaining are dietary intake and training approaches. So with dietary intake, I mentioned this earlier, even if you can maintain a lean body mass, By eating lots of calories and exercising a lot, the choices of where those calories come from are really important. And it turns out that it's not the high cholesterol foods that people worry about, like the eggs and the shellfish that really bother me.
It's the simple starches. So anything that's white or beige, that's been refined, cracked, put in a box, that stuff is poison for the, for the coronary arteries. And so And it turns out that there it's a very common part of the Masters athlete diet. So just simple changes moving toward unrefined grains, brown rice, I'm really reducing the use of energy gels and power bars, like not a big believer in that stuff.
And then finally, and we'll talk about this more when we get back to calcification, it's the approach to training. And when I say approach, I mean it's what the annual calendar looks like. The single biggest, I think, pitfall of most aging athletes is they don't spend enough time resting and recovering.
And we need rest and recovery. We needed to perform well, but we also needed to stay healthy. And so I have over the years kind of arbitrarily come up with this three month rule. And that is that all Masters athletes should spend at least three month of the year in a phase of what I term active recovery.
Doesn't mean they can't exercise. It just means they should be reducing volume by at least 50 percent and really staying away from intensity. And that heals everything. It heals vascular lesions. It heals musculoskeletal problems. It brings relationships with spouses who don't like you being out all weekend back together.
So it's good on a number of fronts.
Periodicity, whether you're talking about short term periodicity, Moderate term periodicity, long term periodicity, uh, there's a lot of really interesting, , research that's gone into that, .
And even , four or five year where you go three years and then that fourth year you have to, you should take it down again, um, reassess where you are before you start going back up if you're trying to be competitive .
Yeah, Tom, I'm really glad you brought up the term periodicity. It's one that many cardiologists are not necessarily familiar with because it's much more of a sports science term. And a lot of the literature has looked at periodicity as it relates to long term achievement of goals, whether it's winning competitions or placing, whatever it is.
But it turns out, and I think this is actually an area of future research that we need to pay better attention to, is that Periodicity probably is an important determinant of health outcomes. And I, I, I honestly, one of the things I always ask my master's athletes patients is, does exercise rule your life or do you let life rule your exercise?
And the answer to that question tells me which bucket they're in. People that place exercise first and foremost above everything else are periodize. And those that allow some of the normal ebbs and flows of life, whether it's a particularly difficult year at work or a Kid leaving home and going to college that allow those things to actually pull away from their exercise a little bit.
I'm less concerned about those people because there's some natural periodization there.
So let's go back to the testing questions or testing issues that you wanted to cover, especially about exercise testing, , coronary calcium scoring, CT and geography , and CPET.
So, um, let's start with the tried and true exercise treadmill test. Um, not a perfect test. should obviously be considered a screen for obstructive coronary disease. But what I think we often forget is that the most important metric we get for maximal effort limited exercise testing is either a directly measured peak VO2 or a surrogate in the form of estimated METs.
And this has been true for longer than probably you and I have been practicing medicine, is that the peak performance on a treadmill test is the single best prognostic. prognosticator of how long we live and how well we live.
, and just to jump in here for just a second, that it is not just someone getting up to 80 percent of their maximum predicted heart rate, , because that is very misleading in the master's athlete. They need to do it up to, to up to symptoms or up to their maximum, , because below that really is not going to necessarily help us.
yeah, I would say nine out of ten Masters athletes that I see for a second or third opinion relay the same story when they tell me about their stress test and that is that they told me I had done enough and they stopped me. That is simply, unfortunately, although it may be inconvenient from a scheduling perspective, it's bad medicine.
Most of what we learn about diseases that affect people manifest in the last 10 percent of their exercise spectrum. So when we exercise these people, we need to be sure that they stop us. Either they can, simply can do no more, or whatever symptoms they're presenting with are manifest. And that gives us a high quality exercise test.
Pharmacologic stress testing, 85 percent max predicted, should just simply never be used in this population.
You had alluded to the question of getting up to an estimated VO2 max or, or a calculated VO2 max versus a true VO2 max. , are there times when you are deferring and getting the full CPET? , I'm usually only using it, for patients who I'm unclear about why they're falling off their curve rather than , looking for ischemic coronary artery disease.
Yeah, I mean, I'm a little biased because I have had the luxury, both in Boston and here again in Switzerland, of working in a place where I have an exercise lab at my fingertips as part of my daily practice. So I very infrequently do exercise testing without metabolic gas exchange. I just find that from the perspective of, um, really being sure what peak capacity is, that a measured VO2 is far better than an estimated VO2.
And from a physiology perspective, what you learn when you look at gas exchange curves from submaximal exercise, So measuring ventilatory threshold, looking at oxygen pulse, things that come out of a traditional CPET test, if you will, I find incredibly useful. So I, I do it with every patient. I appreciate that may be difficult for some labs, but that's been my practice.
And it also does help with assessment of, , anaerobic threshold, , and specifically for, exercise prescription around anaerobic threshold although , , one of the concerns or one of the, , limitations is that it is specific for the exercise that you're doing, your heart rate is going to be different.
, and your anaerobic threshold different on the bike than it will be on the run versus in the swim , and rowing. It's all going to be different. You have to do it , in the environment that you are looking at.
Yeah, that's, that's an incredibly great, good point. I mean, most high level sports cardiology programs will be able to exercise people on a bicycle, a treadmill, and in many cases, a rowing ergometer. We deal with lots of masters rowers in our practice. And what I would say is that exercise is definitely modality specific.
And if you're using exercise to prescribe doses, meaning if you're using the test to give people thresholds, and it really should be done on the modality that you're using. Sending them out into the world to do, but that's a luxury for many people.
, what are you going to be looking at other than their peak, , exercise capacity, ,
I'm looking at some basic things I'm very interested simply in their heart rate Delta So their heart rates are where they start and where they finish Very interested in their heart rate recovery kinetics that tells us a lot about fitness and also indirectly Can tell us something about the presence of coronary disease I'm still a believer and some may criticize me on this on the simple exercise ECG It turns out that all the false positives exist and I have this discussion with patients the negative predictive value of a pristinely normal ST segment across all 12 leads.
A peak exercise is usually a very reassuring sign. So I'd pay attention to the basics because they really matter. And as you were alluding to with gas exchange, you have the ability to measure ventilatory thresholds. We tried to move a little bit away from the turn in aerobic threshold because that that comes from an old literature when it's which people thought you quote turned on your anaerobic metabolism.
That's not what happens, right? It's just simply that you outstrip your lactate buffering capacity and lactate starts to accumulate at a certain threshold. But that can be a great tool to use people to help them understand how to gear workouts toward a recovery or base building approach versus one that really is required for competition level intensity.
And maybe at some point we could get into MAF training and all the rest of that.
, I can talk about MAF training all day. I'm a believer with some caveats.
So, so am I, I was talked into it by a friend who's a master's, , outrigger canoe racer, and he had me dive into it, to help him. And, , it really has, changed the way that I talk about prescription for exercise. . Although, , we had talked a lot about in the past about, , limitations of high intensity interval training.
Again, maybe something that we will be able to get into. If not, we may have to do a separate podcast on those things. , so, uh, back to, , coronary calcium scoring. , so do, what do you see as the, , utility of this , in the master's athlete?
In isolation, zero. I simply do not order coronary calcium scores on my Masters athletes without angiography. And this gives me a chance to go back and talk a little bit about the calcium physiology story. So, if you look in Masters athletes, you will find coronary calcium. Maybe not the majority of the time, but a significant minority of the time.
The problem is that you won't be able to figure out easily why it's there. So on one end of the spectrum you have the pristine risk factor master's athlete who's been at this for 40 years, who's been at the top levels of sport, who has a CAC score of 400 or 500 or even sometimes into the thousands. You look at their coronary arteries by any form of more invasive imaging, whether it's CTA or conventional angiography with OCT or whatever your pleasure is, and you see that they have wide open huge macrovascular vessels with what we refer to as a salt and pepper calcification pattern, where there's just pixelations of calcification, usually on the greater curvature of the proximal LAD, sometime the RCA, but that's simply a mechanical stress phenomenon.
It comes with the arteries seeing lots of shear flow, lots of shear stress over so many years during exercise, And the arteries develop microinjury and what happens is calcification is a marker of that repair. There is zero risk in that end of the spectrum and there the calcium score ends up getting people into trouble because we don't know what to do with it.
On the other end of the spectrum you have the true atherogenic masters athlete with uncontrolled risk factors, bad family history, terrible diet, smokes on the weekends. They may have the same CAC score. But you look at their arteries and they're the type of arteries we see in textbooks when people define atherosclerosis.
Lipid rich cores, calcified plaques, sometimes soft, sometimes stable, sometimes unstable. So the CAC score in isolation doesn't help you, right? If you want to really take a look at coronary biology and differentiate the person you should be concerned about versus the one you should be less concerned about, it really requires CT angiography.
, I'm fond of saying the only thing CAC scoring does in athletes is ensure sports cardiology referrals because you don't really know what to do with the information.
Well, our jobs are going to be safe for a number of things that are probably not necessarily just the Masters athletes, but, for the people who are not getting into athletics, we'll be able to, , have our careers without them necessarily having limitations.
Um, so in Europe, you have a lot more ability to obtain CTAs. Um, they're relatively, they're inexpensive over there. Uh, they moved over to the many years ago and for. Partially historic partially for economic reasons. We're not doing that quite as much that United States. Although I think we are catching up.
, I agree with you. , anything that hint at something that's wrong. I'm trying to move to CT and geography to try to differentiate. , I'm still surprised at the amount of true atheroma that I'm seeing in those athletes. , but also maybe our population is, is different , but I'm seeing more than I would expect.
Yeah, and I think, again, this gets back to the issue of, um, of exercise not conferring immunity to true athero. And there are risk factors that we, we know of and that we oftentimes ignore in these healthy people. And there are risk factors that we simply don't understand. So I think the more we look, the more we find.
And the big question that I don't think anyone can fully, fully reconcile yet is the degree to which exercise and isolation stimulates or at least accelerates that process. And that is, that's the question that was, I would say raised again by the two 2023 studies you mentioned, but simply not put to rest.
. I think these studies, , are, , a stepping stone we can't point to a definite mechanism. And if you can't do that, then you haven't solved the question. We need to look at this more in trying to differentiate, true disease from epiphenomenon and disease that we can then, , intervene upon because that's really what everyone's asking about, right? What can I do to make things better for me, , in the long run? , so where do you see , , research going?
, I share your enthusiasm for some of the things coming down the pipeline around better arterial plaque characterization, particularly when it gets at the pathophysiology, which I think inflammation is probably going to end up being the one that we really all gravitate to and ideally maybe in some space down the line have ways to treat, although I think that's probably not going to be a tomorrow solution.
I do want to just make one point about serial calcification. or serial cactus scoring. Just you know this. But just for the rest of the listeners who may do this less often, when a masters athlete comes to you with a coronary calcium score above zero and you do things to them to ostensibly make them healthier.
The most important of which is started on a stat. And then we can talk more about my my views on that. Do not repeat the calcium tests to show that you have done something good, right? Because most of the things we do, will cause the calcium score to go up and so your patient will feel as if you have failed them and your recommendations were faulty when in reality, in that situation, increasing calcium is actually a good thing.
Yeah, , I'm definitely in the one and done camp. , I did recently, , speak with Matt Budoff, , who is the godfather of coronary calcium scoring, uh, and, and brown CTA in the United States, and, , he does recommend a Q5 year, but knowing where the curves are going to go, , greater than expected, less than expected.
, because there are some data coming out saying that in non athletes. Specifically non athletes, , that that curve, , may be helpful to determine whether or not you are aggressive enough. But yeah, I agree once.
There's your risk. Let's move on.
Yeah, and I have a great deal of respect for Matt and if I had a CT question, he'd be the person I'd go to to ask it, but I will also point out that the reason CAC scoring has become such an important part of general cardiology is we have such robust outcomes data associated with it. No one can argue that in a typical , cardiology patient that CAC scoring can be used to move the risk needle in one direction or another, but we do not have that data in Masters athletes, right?
There is no data set available at this point, which shows us beyond a shred of doubt that a CAC score means anything in this population. And again, I go back to this, this challenging triangular argument, right? We know that peak levels of fitness are the single best predictor of how long we live and how well we live.
Right. We know that the fitter you are, the more likely you are to have CAC and the higher your CAC seems to be. So which of those two is right? Is it the CAC or is it the fitness level? And I would say it's probably some combination. I just want people to be clear that it's premature to think about CAC scores as having the same prognostic value in very fit athletic people as it is in a sedentary population.
So, , looking about more again at the, upcoming research, what research are you interested in as far as, , masters athletes in coronary disease? , whether it's with inflammation or in, , gene expression or something or anything on those along those lines.
Okay.
Yeah, I wish I had more enthusiasm for gene expression work. Again, I'm fascinated with the human genome. I'm also humbled by just how many Millions, if not billions of dollars have been put into trying to understand how to leverage that to improve outcomes. And it's been, I would say, not a great return on investment for me.
The things that I'm really, really most interested in seeing happen in the future is for us to better understand the impact of chronic inflammation and how that affects the exerciser. Right? We know that. chronic inflammation and the non exerciser is a bad thing. But we also know that part of the benefit of exercise is that you have a short term pro inflammatory response followed by a longer term anti inflammatory response.
So it gets more complicated. I think we have to be really careful how we measure it. I would say that probably measuring a single CRP at an office visit is not a particularly useful thing. And we're going to need to move to a point where we can actually start looking at area under the curve in these people, which is something that's coming.
But, um, still a couple years out. And the other thing that I'm fascinated with and I think has a real potential to move the needle is better understanding the biology that relates, as I mentioned earlier, psychosocial stress to vascular biology. It is becoming really clear that what happens in the brain has important cross talk with our coronary tree.
And I think there are going to be opportunities there to really improve long term outcomes and reduce the risk of the stuff we really care about, which is revascularization, MI, and sudden death.
So how are you measuring that? How are you looking at things like vascular resistance? , there was a, a number of studies in meditation and vasodilatory effect, , nitric oxide effect.
, so there are two types of measurements that are relevant. One is how you're measuring the psychosocial stress itself, and there is typically some combination of, , more traditional neuropsychologic batteries around stress, but also increasingly using brain imaging. So PET and CT, functional CT, functional PET, to look at brain activity and to understand how that tracks with what's happening in the vasculature.
And then, Looking at vascular function can be done lots of different ways. It can be done noninvasively through radial tonometry. I think we're probably moving more toward doing CT based things with provocation like exercise and NO, but it's a field I'd say it's in its infancy. It's really exciting.
, there's so much that we can, learn, , in the next, . Five, 10 years. And, , the amount of data that we're getting, is growing exponentially, , especially with things like wearables, which is a completely other again, hour long conversation.
Uh, and that at some point I may, tap you again to talk about that
yeah. Well, if you're, if you're interested in doing that, just let me know. , my group in Boston was asked by, by JACC last year to put together a state of the art review on wearables and cardiovascular medicine. And we thought it would be an easy thing because we talk about it every day and we do it, but it's such a complicated topic with a lot of noise and questionable amount of signal.
So, um, anytime you want to take a dive, let me know. Cause I love it.
I will promise you we will be back and we'll talk about that because, , you know, we're talking about amazing amounts of data .
, so, , before we, , leave today, , the two questions that I have is, uh, first off, what do you think is the correct minimum amount of training for people to get the maximum benefit? Not necessarily for athletes, but for all patients.
So, the most recent 2018 HHS Physical Activity Guidelines, um, which suggest 150 minutes of moderate or 75 minutes of vigorous activity a week, are predicated on some really strong epidemiologic data, which shows that that's where the curve starts to flatten out. I would say that in the six years since that guideline has been published, There have been a number of studies.
One is recent is this past week in circulation for interested readers. There was a great us based study looking at physical activity and long term outcomes. And what I think we're realizing is that the physical activity guidelines are probably an under representation of how much activity we should get.
So I think probably doubling those is really the goal. And that boils down to an hour a day. And it's a lot. And I understand for many people. That doesn't sound like a lot of fun. But if the if the question is, what is the. best amount of exercise, the best dose to maximize outcomes. My current synthesis of literature is it's probably about twice physical activity recommendations and that can be some combination of both moderate and vigorous to get you there.
And so on the flip side of that, what do you think is the maximum level that people that regular people, people who are not in, specific competitions, should be doing and training per week, just on a, on a base level.
So there is a much more complicated answer and that's where I think it all boils down to the individual patient or athlete and they're oftentimes the same in front of you. Um, there are some people who can handle and can thrive with exceptionally high doses of exercise without any complications, and there are some that can't.
So, to me, this kind of gets at the question about, in a similar way that we talk to our patients about alcohol consumption. And, and that is, how much alcohol can you drink before bed? Before it has any meaningful negative effect on your life. So if that's one half of a beer before it qualifies, before it impacts your sleep, your relationships, your ability to work, then that's too much.
If it's two beers, then that's too much. Exercise is the same, right, in that There are some people that are really fragile, and this is less often a conversation about heart disease, but more a conversation about musculoskeletal health. If you're routinely hurting yourself, your knees, your ankles, your hip, your back, it's probably too much exercise, or at least you're not doing it right.
But there are plenty of people that can handle quite healthfully huge doses of exercise over long periods of time. And you know, the truth is, is that many of them are using that exercise to self medicate something, whether it's underlying anxiety, depression, disordered sleep. And so to take that exercise away from them for no good scientific reason, has as much chance of doing harm as it does good.
And the last question before we leave, is, about statins. And, , you had alluded to statin use, , and, I know that I get a lot of resistance when I talk to athletes about statin use, um, but I do use it routinely and I try to push it in the right, in the right patients.
So what is, what is your approach to statins and what do you think that, where it has the benefit and where it has the harm?
So, big believer, both in the primary and secondary preventative settings, athletes with elevated LDL cholesterol should be on a statin if they can't get it into a very clear goal range with dietary modifications, which is the majority of people. So, primary prevention, big believer. Secondary prevention, even bigger believer, when someone has had an event, they need to be on a statin and that's a lifelong thing.
I think where my practice pattern may differ from some others is the use of a statin simply because of a coronary calcification score in someone that has otherwise normal lipids. I discuss it with patients. I explain what we know, what we don't know, but I also remind them that statins are not necessarily risk free.
And that about 30 percent of true high level exercisers that take them are going to have subjective complaints that come from the statin. So I'm okay if someone has an LDL of 90 and a CAC score of 100, leaving them off the statin. Now, there will be those that disagree with that, but I'm just sharing with you my practice patterns.
I'll also say that statin prescribing presents inordinate opportunity for creativity, right? So the concept of just giving someone a single high dose statin every day for the rest of their life doesn't work for that many people. I love varying up timing. Sometimes people can get by with one or two statin doses a week.
Sometimes they take holidays during their training period. So there's always an opportunity and it's all, it's got to be an iterative process with athletes.
And , the most important part of a statin is starting the statin. It's sort of like the most important part of exercise is putting on your shoes. You get a bigger bang for your buck at five milligrams of rosuvastatin, , than you do at 20. Although , for my coronary disease patients, I'm always starting out on high doses, statin, you know, I'm on a high doses statin.
, but for those patients, , they shouldn't look at it as saying that we're not giving them the benefit if we start them on five milligrams of Rosuvastatin and get their, lipids down 30 to 40% rather than 50%.
And I will, just going back to the secondary prevention thing, I'm obviously a doctor that helps people prioritize exercise and get them doing back what they want to do. But in the post MI setting, if the question is, should I be pushing my body hard again immediately or should I be on a high dose statin?
If you have to choose one, it's the high dose statin and put exercise on the back burner for at least 6 to 12 months. We know that statins do most of their benefit from a repair mechanism perspective within the first year, if not two after an MI. So that's got to be at the top of the list, not getting back to your marathon training if you can't do it on a statin.
So the next question, , I'm going to ask, which again, I, I said there were only gonna be two questions there. I guess there were three. , was, and this one we can, , eliminate the answer to is. What are your lipids? When I talk to other lipidologists and other cardiologists, , , I've been interested in the past two years that the answer has been lower and lower.
Yeah, I've been dealt some good genetics and maybe the fact that I do pay attention to what I eat helps, but I've been squarely in the 70 70 club for many years, so an LDL below HDL above 70, and as long as that stays like that, I'll consider it a victory.
I have a , family history of ischemic coronary artery disease. Um, and although my CTA is normal, I do have significant inflammation on my, , FAI. And, , that seems to increase cardiovascular risk.
, but based on that, , and a persistent LDL around 100. I actually started myself on the statin,
yeah, I agree with you. And to make myself be as imperfect as I really am, I should let the listeners know that when we do research studies where we use CT or MR, I always try to volunteer and be the first person to go through. And I've got measurable coronary calcium in the place you'd expect it in a lifelong athlete on that greater curvature of the LAD with the lipids I just mentioned.
And I've got some hinge point fibrosis in my left ventricle where the RV insertion comes in, which again is a very common finding in masters athletes. So. None of us are immune to finding things on imaging, it's just a matter of the choices we make around them.
. I will also say that, , I said mostly vegan diet. , I do cheat. And when I go skiing, I definitely cheat. Uh, and I, and I enjoy it.
well I hadn't eaten a morsel of mammal meat in ten years, but moving over to Switzerland where the quality of the meat is so much better, I've started eating some small quantities of beef again. And if I take six months off of my life because of that, it's actually a price I'm willing to pay.
Well, especially if you're eating in Switzerland. I think that it may be a little bit different there than, than it is in other places. Uh. Well, Dr. Baggish, I can't thank you enough again, uh, for being here with us today. I think this has been really enlightening and, I look forward to other conversations that you and I may have, um, and also all your work that you're doing, , you have, , changed the landscape of the way that we look at, , sports cardiology over the past, 20 plus years.
And, um, I, personally thank you for all the work that you do because, , without you, , I don't think we would be in the place where we are today.
Well that's kind of you to say, and it really has been a pleasure speaking with you, and let's get back and do wearables, that would be fun.
Very good. I'll make a plan on it. . Thank you.