Thursday, September 19, 2024 | New York Academy of Medicine (NYAM)
1216 5th Ave, New York, NY 10029
Dr. Amir Ahmadi highlighted the need to transition from focusing on risk factors to directly addressing coronary artery disease. He pointed out the shortcomings of current risk assessment methods and stressed the importance of early detection and treatment of atherosclerosis. By using a real-life example of a low-risk patient who unexpectedly suffered a myocardial infarction (MI), he illustrated the gap between current prevention strategies and actual outcomes. Dr. Amadi pointed out that many MI patients do not fit high-risk profiles and often show no prior symptoms, making traditional methods inadequate. He proposed a new approach that focuses on detecting and treating atherosclerosis and plaque progression using advanced imaging and AI to identify high-risk plaques and tailor treatment, aiming to reduce the incidence of myocardial infarctions (MIs). Lastly, Dr. Amadi highlighted future advancements in imaging and AI that could further improve early detection and treatment of coronary artery disease.
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Transcript of Dr. Amir Ahmadi's Presentation:
[David Maron] [0.32s] We're gonna start with session 1.
[David Maron] [3.12s] My name's David Marron, and my co moderator, Mike McConnell, we are the Stanford gang, and we're up here with the Mount Sinai gang.
[David Maron] [11.92s] And, our our first, speaker this morning is, doctor Amir Amadi.
[David Maron] [19.77s] And, doctor Amadi is at Mount Sinai.
[David Maron] [24.81s] He's director of cardiovascular CT and MRI research and director of the valve clinic and director of the lipid clinic at, Mount Sinai St.
[David Maron] [35.29s] Luke's Hospital.
[David Maron] [36.89s] And his presentation this morning is shifting from treating the risk of disease to treating the disease.
[David Maron] [44.13s] Doctor Amadi.
[Amir Ahmadi] [47.57s] Doctor Marin, it's an absolute honor and, pleasure to be here among this amazing, amazing faculty.
[Amir Ahmadi] [54.99s] I'm covering actually for, doctor Narula who couldn't be here today.
[Amir Ahmadi] [59.63s] So I'm sorry for the inferior replacement, but I'll try my best.
[Amir Ahmadi] [66.01s] As you can see the title, what I'm going to talk about is the vision of prevention future that I think in, cardiovascular disease.
[Amir Ahmadi] [75.84s] What I think we we need to do, and I think this is shared by the audience here, is to start seeing the disease itself, which is a disease of the coronary arteries.
[Amir Ahmadi] [84.67s] And I'm only talking about the disease of coronary arteries, and treating it as opposed to guesstimating.
[Amir Ahmadi] [90.91s] So I'm gonna start with a real life case.
[Amir Ahmadi] [93.56s] His name is not Sam, and this is not his picture, but the case is real.
[Amir Ahmadi] [98.67s] This is this is about, 3 or 4 weeks ago in our CCU.
[Amir Ahmadi] [103.16s] So he's a 50 year old gentleman.
[Amir Ahmadi] [105.00s] He's a physician.
[Amir Ahmadi] [105.72s] He doesn't have any past medical history.
[Amir Ahmadi] [108.12s] It comes with these, risk factors.
[Amir Ahmadi] [110.73s] His LDL was 110, A1C of 5.4, no hypertension, ASCD risk score was calculated based on the calculator at 2.6%.
[Amir Ahmadi] [119.37s] He plays indoor soccer every Thursday or night and he doesn't have a chest pain and he claims to be good.
[Amir Ahmadi] [125.72s] How do you categorize his risk?
[Amir Ahmadi] [127.97s] So according to guideline, this is a low risk guy.
[Amir Ahmadi] [130.76s] And does he have any need for anything else with regards to prevention of cardiovascular disease?
[Amir Ahmadi] [136.04s] So if I saw him and anybody else that practices guidelines in the clinic, we would probably reassure him.
[Amir Ahmadi] [142.40s] We'll say, yeah, keep on the good work, diet, exercise, Mediterranean diet, and whatnot.
[Amir Ahmadi] [147.92s] So what happens is that on a Saturday morning that I'm rounding, we get a coach STEMI.
[Amir Ahmadi] [152.31s] He comes with a chest pain while having brunch.
[Amir Ahmadi] [154.94s] He rushed to the hospital.
[Amir Ahmadi] [156.31s] This is his ECG.
[Amir Ahmadi] [157.66s] You don't have to be a cardiologist to say that this is abnormal.
[Amir Ahmadi] [161.10s] And he goes to cath lab and he has a proximal to middle AD, 99% occlusion, the haze area that you see in there.
[Amir Ahmadi] [168.45s] And, unfortunately, he has a great outcome.
[Amir Ahmadi] [171.57s] But it cases like this makes me always think that how could have this been prevented?
[Amir Ahmadi] [177.90s] And is this a rare event?
[Amir Ahmadi] [181.74s] So aside from working in CCU, I also work in a prevention clinic for the past, 7 or 8 years.
[Amir Ahmadi] [190.26s] And when I think about coronary disease in general, I put it in a timeline as it's seen by a cardiologist.
[Amir Ahmadi] [197.70s] So it starts with birth and it goes to the first prevention visit.
[Amir Ahmadi] [202.94s] The point of the first prevention visit for us is to basically prevent the first MI.
[Amir Ahmadi] [208.94s] So from a perspective of me myself as a prevention doctor, I try to prevent the MI.
[Amir Ahmadi] [216.68s] But when I run on a CCU and I look at the person with an MI, I ask myself, why did this happen?
[Amir Ahmadi] [224.44s] The problem is that between these two perspective, there's a huge disconnect that I'm going to talk about now.
[Amir Ahmadi] [231.25s] As people that actually end up with MI are not always the people that we have predicted them to have the problem and the disease.
[Amir Ahmadi] [238.94s] And I think the solution to this disconnect that we have is to rethink about pathophysiology of MI and rethink of strategy of how we can actually see, our patients and what we do for them.
[Amir Ahmadi] [252.18s] So let's start that.
[Amir Ahmadi] [254.26s] From the prevention perspective, who who is at risk and how we can prevent the MI?
[Amir Ahmadi] [259.56s] So our framework, even though we like to be very you know, we sound very sophisticated, is that we basically do 5 things in our clinics as it re relate to prevention of a lot.
[Amir Ahmadi] [270.13s] We either reassure people or we ask them to lifestyle modify or we do medical treatment, or we send them for more testing, or we send them to invasive testing for revascularization.
[Amir Ahmadi] [280.27s] How do we do that?
[Amir Ahmadi] [281.87s] The 2 gateways that we use is either risk factors for the first three or symptoms for the next 2.
[Amir Ahmadi] [289.07s] And what we are trying to do is to prevent either MI or we prevent the symptoms or relieve the symptoms or improve the quality of life.
[Amir Ahmadi] [298.03s] How did we get here?
[Amir Ahmadi] [299.75s] It's basically as doctor Harrington were, was mentioning, over the last 50, 60 years of, science, we had amazing data that shows on a population level, for example, risk factors are important.
[Amir Ahmadi] [315.19s] So that lead us to focus on risk factor and risk estimate scores.
[Amir Ahmadi] [320.20s] We also learned that symptomatic patients are more likely to have events, and therefore, we started to focusing on symptoms.
[Amir Ahmadi] [326.85s] For example, we have chest pain guidelines as opposed to coronary disease guidelines.
[Amir Ahmadi] [330.69s] There is a quite a bit of focus on on symptoms there.
[Amir Ahmadi] [334.13s] And our noninvasive testing prior to the evolution of CT scans, we're very much focused on detecting ischemia and obstructive lesion because they were more likely to cause events.
[Amir Ahmadi] [345.85s] So that was the focus on ischemia or obstructive lesion.
[Amir Ahmadi] [350.25s] But when you look at it from MI and go backward, you have a patient.
[Amir Ahmadi] [354.56s] You're like, how did this happen?
[Amir Ahmadi] [356.00s] Could I have predicted this?
[Amir Ahmadi] [357.52s] We need to start thinking about, the usefulness of these criteria, the symptoms, the ischemia, or or the risk factor in in predicting.
[Amir Ahmadi] [366.89s] And and, you know, the question of why did this happen and could have been prevented or not.
[Amir Ahmadi] [372.13s] So when you think about symptoms going backward, we know that symptoms are unreliable because only 1 third of people actually present with stable ischemic heart disease.
[Amir Ahmadi] [383.57s] 2 third of people, the first presentation of their coronary disease is either death or MI.
[Amir Ahmadi] [387.99s] So we cannot rely a symptom as a gatekeeper.
[Amir Ahmadi] [391.99s] We we look at risk estimates score.
[Amir Ahmadi] [394.15s] This is a beautiful paper done in 2018 by a young MI registry group in Boston.
[Amir Ahmadi] [399.88s] And what they looked at is people at age of 50 or lower that presented with their first event.
[Amir Ahmadi] [406.61s] And there they asked the question, if I saw this person 2 days ago in my clinic with this risk profile that they presented, before their MI, could I have predicted this in mind?
[Amir Ahmadi] [417.34s] Could I have actually started them on statin?
[Amir Ahmadi] [420.06s] And what you can see is pretty surprising that people that are in the high risk, people that have familial hypercholesterolemia, people that have diabetes only constitute a very small portion of the whole population of MI.
[Amir Ahmadi] [432.30s] And at the bottom, what you see here is that people actually that, that have low risk or borderline risk constitute about 70% of people who came with MI.
[Amir Ahmadi] [443.76s] So I took that idea.
[Amir Ahmadi] [445.44s] And over the last 4 years, we did this in Mount Sinai and Mount Sinai in Morningside.
[Amir Ahmadi] [450.24s] We just presented this few weeks ago in London in the ESC conference.
[Amir Ahmadi] [454.16s] So we looked at people with a type one MI, 65 years or younger.
[Amir Ahmadi] [458.63s] And we said, what if we saw these people 2 days prior to their MI?
[Amir Ahmadi] [463.03s] Could we have predicted this based on the two main gateways that we have to prevention, symptoms or risk factors?
[Amir Ahmadi] [470.15s] So from the statin indication, ACC 2018 guidelines, what we found out is that 47% did not meet their requirement for being on statin or doing further testing.
[Amir Ahmadi] [483.47s] And from the symptom standpoint, we looked at we we took the historical, basically perspective, and we asked the patient, when was the very, very first time that you had any pain?
[Amir Ahmadi] [495.13s] And in 62%, that wasn't more than 2 days ago, more than 48 hours.
[Amir Ahmadi] [502.02s] And in about 54% of the patient, it was the same day as the presentation.
[Amir Ahmadi] [507.46s] So you put it together, intermediate or high risk is about 53% of the patients.
[Amir Ahmadi] [515.01s] Lower borderline risk is about 47%.
[Amir Ahmadi] [518.38s] Symptoms for more than 2 days is about only 38%, asymptomatic up until presentation 62%.
[Amir Ahmadi] [525.10s] This is our gateway.
[Amir Ahmadi] [527.01s] We put it all together.
[Amir Ahmadi] [529.23s] The Venn diagram shows that 32% of your entire MI remember, every 34 seconds we have an MI.
[Amir Ahmadi] [536.99s] Entire first MI, 32%, 1 in 3 are people that are low risk that we don't even give them statin and people that are asymptomatic.
[Amir Ahmadi] [547.42s] So why is this happening?
[Amir Ahmadi] [549.59s] Are we wrong in our risk estimation?
[Amir Ahmadi] [552.14s] Not really.
[Amir Ahmadi] [553.02s] The risk estimations were fantastic at a population level.
[Amir Ahmadi] [556.38s] So high risk people are more likely to have event than low risk.
[Amir Ahmadi] [559.87s] Schemic people are more likely to have event than nonschemic, and symptomatic more likely than nonsymptomatic.
[Amir Ahmadi] [565.87s] The issue is that when you scale it to a population, the population of low risk, the denominator is much bigger than the high risk.
[Amir Ahmadi] [574.43s] Same with skimming, same with, symptomatic and non symptomatic.
[Amir Ahmadi] [578.91s] So when you scale it and when you look at the MI going backward, even though they have the low risk or nonschemic or nonsymptomatic, they have a smaller portion of the pie.
[Amir Ahmadi] [589.60s] Because the pie is such bigger pie, the absolute number actually becomes a substantial number.
[Amir Ahmadi] [596.56s] And more MI comes from the low to intermediate risk group than high risk.
[Amir Ahmadi] [600.16s] More MI comes from the nonschemic group and asymptomatic group.
[Amir Ahmadi] [604.05s] So that's what I call MI paradox.
[Amir Ahmadi] [606.85s] So what's the solution?
[Amir Ahmadi] [607.97s] We look at pathophysiology.
[Amir Ahmadi] [610.21s] Pathophysiology is that you start with a plaque, you go through progression, you go through progression to get to a stage of vulnerability, which I'm gonna allude to in a second, and then you have a plaque rupture.
[Amir Ahmadi] [620.37s] So the pathophysiology is not telling anything that is lie.
[Amir Ahmadi] [624.45s] It starts with a plaque.
[Amir Ahmadi] [625.97s] It ends with a plaque rupture.
[Amir Ahmadi] [627.49s] It's all about plaque.
[Amir Ahmadi] [628.93s] So what we can actually do is to realize this disconnect and move forward.
[Amir Ahmadi] [634.18s] So what we believe in in terms of pathophysiology is what I just showed.
[Amir Ahmadi] [638.50s] What we are actually practicing this is a reverse engineer of what we're practicing.
[Amir Ahmadi] [643.30s] We are kinda like practicing under the assumption that risk factors should be there to pre to basically cause the disease.
[Amir Ahmadi] [651.03s] Disease should cause symptoms, and symptoms should cause MI.
[Amir Ahmadi] [654.47s] That's wrong.
[Amir Ahmadi] [655.67s] The reality is that there is atherosclerosis that cause MI.
[Amir Ahmadi] [660.28s] There is not a one to one relationship between risk factors and an atherosclerosis.
[Amir Ahmadi] [664.21s] Meaning in 2 twin brothers with exactly same profile, one might have atherosclerosis, the other one might not.
[Amir Ahmadi] [669.96s] And there is so much more to it than than just presence of 1 to 1 risk factor to atherosclerosis.
[Amir Ahmadi] [675.89s] And some people have symptoms and some people don't.
[Amir Ahmadi] [678.29s] So we can't rely on those things.
[Amir Ahmadi] [680.53s] So we can reverse engineer DMI.
[Amir Ahmadi] [683.17s] Why MI happen?
[Amir Ahmadi] [684.13s] Because of a plaque rupture.
[Amir Ahmadi] [685.41s] Why plaque rupture?
[Amir Ahmadi] [686.37s] Because it progressed.
[Amir Ahmadi] [687.33s] Why it progressed?
[Amir Ahmadi] [687.97s] Because it existed.
[Amir Ahmadi] [690.04s] So very simple.
[Amir Ahmadi] [691.88s] And there is a reason for its existence, but it's much more complicated to try to figure it out and guesstimate its existence or not.
[Amir Ahmadi] [701.32s] So we have these identifiable risk factor, genetic factor, environmental factor, inflammation x, which is probably 50,000 other factors.
[Amir Ahmadi] [708.61s] And in 50 years from now, they're gonna figure out and they're gonna laugh at us.
[Amir Ahmadi] [711.65s] But you guys didn't know that.
[Amir Ahmadi] [713.17s] But what we can do with this framework is that we can actually start thinking about a personalized treatment based on detection of atherosclerosis, maybe intensifying the treatment based on presence of progression, and and thinking about revascularization if we see plaque that is at the risk of rupture.
[Amir Ahmadi] [733.53s] And when we talk about progression, it's not just a lumenal progression.
[Amir Ahmadi] [737.61s] It's a progression of features that gets the, lesion more and more close to a mice.
[Amir Ahmadi] [743.45s] So that's an increasing necrotic size, thin fibrous cap formation, and exposure of that to a shear stress that can cause a plaque rupture.
[Amir Ahmadi] [751.33s] So when we think about this, we need to redefine this whole concept of high risk plaque as doctor Naghavi did that in 2003 with his from vulnerable plaque to vulnerable patient.
[Amir Ahmadi] [763.26s] What I'm trying to do here is to remind us that this is not a binary concept based on presence or absence, but it's actually quant quantification of some plaque features.
[Amir Ahmadi] [774.12s] It's a dynamic concept because our medical therapy changes it.
[Amir Ahmadi] [777.63s] The natural progression changes it, and it's a lesion level concept.
[Amir Ahmadi] [781.32s] And and it's a marriage between the physiology and pathology at a lesion level.
[Amir Ahmadi] [784.53s] And and what we can do in in the near future is to the lesion level.
[Amir Ahmadi] [786.34s] And and what we can do in in the near future is to marry these two concept in order to have a better understanding of who benefits from aggressive medical therapy and who benefits from revascularization, which I'm I'm just gonna fly through these slides that, that kinda like the presence of, plaque allows us to individualize our medical treatment, which I'm going to call it a personalized optimal medical therapy as opposed to Optima medical therapy based on overall plaque and individual plaque features, and it can guide us to revascularize both for symptoms and for MI prevention.
[Amir Ahmadi] [821.74s] And we have tools that is combination of CT scans and AI.
[Amir Ahmadi] [825.68s] And this is an example of it, from a Lucid company that can guide us towards the risk for symptoms and the risk for MI prevention.
[Amir Ahmadi] [834.17s] And I think to wrap it all together and bring it back to the population level, I think there are very interesting efforts that you can actually reduce the need for contrast in these images and by AI or to try to detect non calcified plaque, plaque features, even physiology based on a non con imaging in the next few years.
[Amir Ahmadi] [856.43s] So with that, I thank you.
The presentations were hosted by I-ELCAP – The International Early Lung Cancer Action Program.
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