Chapters Transcript Video Acute Coronary Syndrome Pharmacology Dr. Krishnan describes the most commonly used pharmacological agents in Acute Coronary Syndrome. Uh, good morning, everyone. Um, and, uh, thanks for giving the, giving your time. I think, uh, this is a great opportunity to kind of go over some basic topics, um, and, uh, it's a, it's a good way for me to kind of refresh the basics as well. So. Um, over the next, uh, you know, 20 or 30 minutes, I thought this, we could start off with something that we see very commonly, uh, pharmacology of ACS, um, and please feel free to stop me at any time, um, and if you have any thoughts, experience, or questions, uh, please feel free to ask. Um, and, uh, you know, uh, if there's any other topics that you guys have in mind, uh, you know, Larina and Matt Brubacker know who are kind of spearheading this, uh, and hopefully we can learn together, um. So this was a, this was an interesting quote that I came across and uh you know, this is by one of the Stanford professors, and he says that a little bit of slope makes up for a lot of Y intercept. So essentially what that means is um in non-mathhematical and philosophical terms is. That little increments of improvement make a much bigger difference than someone who is better off starting off but doesn't change or improve themselves, right? So uh just we're, you know, we'll we'll we'll kind of build on a little bit of knowledge every single time we do this. Um, so let's go over some of the learning objectives that I thought would be a good place to start here. We'll go over some basic understanding of commonly used agents in acute coronary syndromes or ACS. Uh, we'll talk a little bit about the types of antiplatelets and their properties. Uh, we'll talk a little bit about, you know, uh, what, how do we choose one over the other, the duration of DAPT, and how to risk assess patients and de-escalation strategies, especially in patients who are high bleeding risk. So I know this is, uh, you know, there's a lot of information on this slide, but let's break this down, and this is one of the, one of the slides from the most recent European Society of Cardiology ACE guidelines, which came out, I think, a year and a half ago, and essentially we're this is the physiology of what happens when someone were to have plaque rupture, which you can see in the top left of your screen right there. When there is plaque rupture, there is exposure of collagen and a disruption in the endothelium to platelets, right? And what that happens is it kind of triggers the intrinsic and extrinsic coagulation pathways, and they kind of meet at this final common point at factor 10. Um, uh, which is right here, um, and then, um, that in turn leads to the production of thrombin, uh, which in turn leads to the conversion of fibrinogen to fibrin, so fibrin is the mesh. Where the platelets kind of stick against and that's what clot essentially is, right? And at various points of these activation pathways, both in the coagulation as well as in the platelet factors is what our different drugs work and kind of understanding a little bit about why we use, you know, different medications is kind of based on this. So for example, When we put patients on a heparin drip, which is UFH on fractionated heparin, it works on factor 10 and thrombin. Um, we don't use enoxaparin as commonly, but enoxaparin has a lot more affinity for factor 10A rather than thrombin, it inhibits that. Um, and at the same time, on the, on the other hand, when patients have heparin-induced thrombocytopenia and we use medications like algatroban or bivalirudin, those are direct thrombin inhibitors, so those take care of a little bit of the coagulation pathway. Now, on the other end, when we give patients antiplatelet agents such as aspirin, it prevents platelet activation using the thromboxane A2 receptor. Uh, a separate receptor, the P2Y12 receptor, has a couple of different binding sites, and we have a few medications that act on that, and we'll talk a little bit about important properties about these and why these work the way they do. And um the final common pathway which is uh GP2B3A inhibitors uh which are used in patients who are unable to take P2Y12 receptors um. Or, or, uh, are in cardiogenic shock and they don't have oral access, uh, so that we can use, uh, eptifibotide and thyrofiban. We use, uh, thyrofiban here at Centera, uh, so that's really when you look at it, the final common pathway, right? So that prevents the platelets from kind of linking together with fibrinogen, so even if they don't have anything on board and they have a stent put in, uh, Tyrofiban alone should be enough because it's the final common pathway there. Uh, but that this is like a basic understanding as to, um, you know, the, the, the overall physiology and where the different pharmacology targets are. Um, now, uh, so when we talk about the different platelet agents, um, and this is important, uh, because it all antiplatelet agents, even in the P2Y12 receptor antagonist family are not created equally, so what does that mean? So let's start off with Plavix or clopidogrel. It only inhibits 35 to 40% of platelets, right? So which is, you would, you would assume that if you're giving someone 600 mg that more than 40% of platelets would get inhibited, but that's really not the case even in patients who are, who do not have the, uh, you know, the, the, the gene polymorphism that makes them, uh, Plavix non-responders, only about 40% of the platelets are inhibited. Um, which, and it's a prodrug which becomes an active metabolite, um, now, on the other hand, when you compare it to medications like Effient or Prasagrel or Brilinta or Tyagrelor, they have approximately 80%, uh, platelet inhibition of platelet activation, so these are more potent drugs, um, interestingly, Prasagrel is a drug that does become a metabolite. Uh, but we, you know, this is, this is not, this is not something that you can have a resistance or tolerance to, um, and, uh, ykagorlo is actually a completely active drug, and the metabolite that is formed by the body is also active, uh, but it is a reversible inhibitor of the P2Y2 receptors and again it, it has approximately 70-80% platelet inhibition. Which is why, uh, and, and the other important point is the onset of action of each of these medications is different, and this is important when you're seeing a patient in the ED with a STEMI who needs immediate platelet inhibition where giving them Plavix 600 mg, unless they're, you know, above the age of. 80 elderly um doesn't, would, would give you platelet activation in 2 to, you know, inhibition in 2 to 6 hours, um, so that's probably by the time you're already put the stent in and which in in the, on the other hand, medications like Effient and Brilinta give you a lot more factor activation, um, which, which, which is clinically important. Um, the, the peak effect, uh, is another, uh, interesting concept, um, even with 600 mg of Plavix, you're getting the peak effect, so the platelets start getting inhibited, but the peak effect is approximately 7 to 8 hours. So even if you were to give them 600 mg at, you know, midnight, their peak effect is around 6 to 8 a.m. On the other hand, Effient and Brilinta have a lot more faster effect, which is why we prefer these medications when you want kind of immediate platelet, uh, inhibition. Um, the, the, uh, you know, there's a lot of data out there that's comparing Brilint Effient to Plavix and vice versa, uh, but really the two big trials that kind of put Effient, um, and Brilinta respectively on the map were the Triton, TIME 38 and the Plato. Uh, and these showed that compared to Plavix, there was a significant reduction in MI stroke, uh, a composite of death MI and stroke, uh, with, uh, both of these medications, uh, and there was a significant, you know, 1%, but still significant reduction in mortality, uh, with compared, uh, Brilinta comparing to Plavix, so they didn't look at a mortality benefit in the case of Effient, um. And there, but this comes at a cost, right? So this comes at, you know, a slightly increased risk of bleeding which is more prevalent in the older population. So again, you know, the higher risk subgroups where you want to avoid Brilintata Effient, really when you look at the data is those above the age of around 80, uh, Effient, uh, specifically, it's a black box warning for prior stroke or TIA, uh, which is an absolute contraindication. So if you're not sure if the patient had a prior stroke or TIA, I would, you know, probably don't use it. Um, relative contraindications are weight below 60 kg and age above 75. Some people do use half dose Effient. Uh, my recommendation would be if it's below 60 kg, I think we can do half dose, but if they're above the age of 75 to 80, then maybe using an alternative, um, antiplatelet agent, right? Um, the, the other question that we see commonly, especially in terms when we, uh, come into, uh, the hospital and we have a large NSTEMI population, so the question always is, do we preload them or not? Um, there's multiple trials, um, and these are some of them, including a Swedish registry which have kind of conclusively proven that there's no benefit of preloading these patients with a non-ST elevation MI. Uh, there's actually a higher bleeding risk, especially if you cap them within 24 hours, which which almost never happens at the heart hospital, but at, uh, some of our other hospitals we're, we're pretty good about capping them the next day. Uh, um, I know Beach General, uh, does, does, does an excellent job of that, um, so I wouldn't preload these patients, right? Uh, it's safe to not preload. Um, and I'm also gonna give you a little bit of data, so this, this is a trial that kind of compared Effient and, uh, Brilinta or Prasagrel and uh Tyagrolo. So this was a big randomized open label trial. Uh, these were patients who presented with acute coronary syndromes, and then they randomized them to getting either Brilinta or Prasagirl, and the primary endpoint was a composite of death, MI or stroke at one year. But the even more important endpoint was uh a secondary endpoint which was a safety endpoint of bleeding, uh, so they looked at over 4000 patients and, uh, the primary endpoint which was a composite of death stroke or uh of uh death stroke, uh, or MI. Um, was, uh, favorable. Prasagril did better, which meant that, you know, in layman's terms, Prasagril gives you better ischemic risk reduction profile right at the end of the day, um, and interestingly, the safety endpoint, there was no difference, so this was kind of like finding a little bit of the holy grail, right? You get better ischemic risk protection, but you don't get, uh, a bleeding, you know, increased bleeding. Um, which is why, uh, the, the European guidelines and, you know, uh. Are, are, are giving a two-way recommendation for Effient over Brilinta in ACS patients who proceed to PCI, um, interestingly enough, when they look, when, when all the trials for Prasagril were done, they were randomized to uh gettingrasagrel downstream, so after we already knew their coronary anatomy and they were going to get a stent, um, so which, which also gives some additional information that you don't always have to preload, right? So, you know. In, in a medication, let's say you have a patient who's having an NSTEMI, aspirin, heparin drip, uh, for platelet inhibition and prevention of further in coagulation cascade, and you take them to the lab, they have a, they, they have a culprit lesion, you stent them, you can load them with Effient, um, you know, after, towards the ending of the case, or before you put the stent in, um, and that is. You know, in fact, superior in terms of ischemic risk. Now it could be the drug, but it gives additional kind of information that, uh, waiting to to load them with a potent, uh, P2Y2 receptor antagonist is OK. Uh, the, the ACC or the American guidelines don't specifically state, uh, you know, uh, this, this, uh, Effient over Brilinta because there's only one randomized trial, but it's, it's, it's, it's an important trial to know about. Um, but then, you know, the second question is, do we use it for everyone, right? So if they're so much better, do we use it for everyone? Now that's where a little bit of the caveats come in. Um, the trials, the, the landmark trials were all done with 1st generation drug eluting stents, and now we're in the era of 2nd generation drug-eluting stents, which are better, thinner struts for using IIS to optimize stents. Uh, which means that, uh, you know, uh, these, these ischemic risks might be lower just with the better mechanical nature of the stents. Um, I would, like I said, you know, avoid it in patients above the age of 75 or 80, um, and there's some data to support that. So there's the popular ADE trial which looked at non-ST elevation MI and patients with age above. 70 and compared Plavix versus Brilinta and what they noted was there was lower bleeding with the same mace and mortality favoring Plavix, right, so which, which was a little different from what the Plato trial showed, but again, it's the devil is in the details. There's there's more than one thing that goes into it. Uh, again, the sweetheart registry, which wasn't a randomized trial, but it was registry data which looked at Brilinta versus Plavix. Again there was higher bleeding and mortality in those above the age of 80 years, um, you know, favoring Plavix. So again, when you're when. We're looking at these patients who are increasing order, you know, in the in the 75, 80, um, it's, it's not wrong to not use a more potent P2Y4 receptor antagonist because the benefits of those potent agents is kind of negated by uh the higher bleeding risk. So, uh, and, and, you know, the final point is, when should we use Plavix, uh, or when should we use the more potent agents like Brilint and Effient, uh, with in those with higher ischemic risk, more complex procedures, multiple lesions, bifurcations, complex interventions, diabetes, CKD, or those who have ACS. If they're, you know, below the age of, uh, uh, you know, they're not in the, in, in the advanced age subgroup, these are patients that we should preferentially be looking to use the more potent P2Y 2 receptor agents. Uh, and on the flip side, what is the role for Plavix? Uh, it, it's in stable coronary artery disease undergoing a PCI. Uh, patients are on concomitant DA use. The data for using Eliquis and anything other than Plavix is really non-existent based on trial data, and the bleeding risk is, is significantly higher, so. Any patient who's requiring Eliquis uh or have post-op Afib or an LV thrombus, we should preferentially be using Plavix, uh, patients who've gotten uh thrombolytics, uh, these are patients, the trials only looked at patients, uh, they were subsequently loaded with Plavix, again, we don't, uh, there is some signal towards increased bleeding risk with the. More potent P2Y2 receptor uh agents, so that is somewhere where we should be using Plavix, um, for example, patients who got a transfer from Sasi and or who got analytics and came in with, uh, a STEMI, these are patients who I would give Plavix to and not, uh, uh, Brilliant or Effient to, and those who are unable to top potent P2Y2 receptor antagonists. Um, so this is kind of a flow chart that kind of summarizes. The duration of DPT, the type of DAPT in the 25 guidelines, uh, for both STEMIs and non-STEMIs, and then we'll kind of go through specifically, uh, what, why each of these classes were given. We went through some of it, but we'll, we'll talk a little bit more about the bleeding risk and the de-escalation strategies. Uh, it's color-coded, so anything in green is a class one recommendation, uh, and anything in yellow is a class two recommendation. Um, so we'll go through the non-ST elevation, um, uh, MI, uh, or ACS first, so in patients who had a PCI, uh, PCI performed, um. And if, if they're not on any chronic anticoagulation, right, uh, then you ask them, uh, you know, do they have a prior history of TIA or stroke? And if the answer to that is no, uh, and they're not an advanced age person, you can do aspirin and a potent P2Y12 receptor antagonist based on the data that we just showed. Um, now, if these are patients who are at a high bleeding risk, that's where you're kind of taught thinking about de-escalation strategies, and there's been a wealth of trials that have come out since the, the, you know, the older guidelines, and more and more data is building to suggest that the default strategy may not be one year of DAPT it can be shorter, um. And the simple reason for that is most of your stent thrombosis risk, which is close to 10 to 15% uh in the first year, is really in the 1st 30 days of PCI and hence, as long as you cover that 1st 30 days with DAPT, ideally with a more potent agent, you can kind of largely reduce the ischemic risk, and thereafter, the minute you were to stop the uh the aspirin. Uh, then you have a significant reduction in bleeding risk. Right now, the guidelines haven't adopted that uniformly. Even the latest, uh, ACS guidelines, uh, on the editorial, there was a lot of discussion amongst, uh, you know, many, uh, experienced operators on do they truly believe that as a class one indication that everything needs to be for 12 months, but, you know, as. It stands as of now, it's a class one indication to give DAPT for 12 months in those who do not have a high bleeding risk and ideally with a potent agent. Now, if you want to reduce the bleeding risk, uh, there's a couple of ways you can do it. Now, if the patient were to be on Brilinta, you can do 3 months of DAPT and then stop the aspirin and just continue the Brilinta for 12 months and then stop the Brilinta and switch them over to aspirin. There's a lot of data that was looking at Brilinta and de-escalation strategies. On the other hand, if the patient were to be on Pasagrel, when you look at the trial data, the similar trials for just stopping the aspirin at 3 months and just using Pasolol alone do not exist. Now, common sense wise, I think it's reasonable to kind of do the same way, because when you look at the pharmacology of both Effient and Brilinta, it's very similar in terms of platelet. Inhibition, but that being said, one optional strategy is to de-escalate to aspirin and Plavix, right? So, uh, in patients, you know, at least 1 month of DAPT, ideally you wanna push it to 3, but 1 month, uh, like, you know, most of the stent thrombosis risk is gone, not to say it's, it's, it's completely gone, but it's gone at 1 month and then you de-escalate, um, and then for most patients, you do DAPT for 12 months, and this is kind of similar in, in STEMI situations as well. Now in patients who need chronic anticoagulation here, you wanna do aspirin and Plavix, there's no data to suggest you use anything else, and you know, the data at Plavix and OAE is for, you know, you do triple therapy with aspirin for 1 to 4 weeks. Most of us stop it at 1 week or even before they leave the hospital, um. And then you continue Plavix and OAC for at least 4 weeks, but ideally 12 months, um, again, if, uh, you know, they have a high bleeding risk or they have a bleed, then I think it's reasonable to maybe stop the Plavix and switch them over to aspirin, but, um, again that's, that's a little bit of a data-free zone. Um, and, um, in patients who are medically managed, uh, really the data exists for aspirin and Plavix, but, uh, there is some data for aspirin and Brilinta, but I, I don't think this portion is super important, you know, 9 out of 10 times, uh, we, we are taking up patients with non-STEMIs for invasive strategies, so the patients who we don't do it are really the elderly patients, and then you ask yourself, really, even without. A stent, do I put them on Brilinta? and I wouldn't, I wouldn't, I usually never do DAPT on uh medical, medically treated older patients with NSTEMI, um, we'll just do a short duration of DAPT for about a month or just aspirin and Plavix, uh, would be the way to go, um, and, uh, the class 2. Uh, the, the, the class 2B recommendation again, if you're doing angiography in 24 hours, then you do not have to routinely pre-treat them. If you're gonna wait more than 24 hours, it's a 2B recommendation to load them again, this, uh, we don't do routinely and I don't think we we we should do it because a lot of these patients have multi-vessel disease and now they're awaiting uh CABBG uh and that further delays their uh kind of care, um. So, uh, and, and then this is just one of the, one of the slide, uh, from both the ESC guidelines as well as the most recent, uh, American guidelines, um, uh, the, the key point here is that they, they've made a change to the statement in patients with ACS, and the key statement here is who are not at high bleeding risk, right? So, uh, they should do that for 1 year to reduce major adverse cardiac events. So at not at high bleeding risk is the key point here. And uh again, the same thing is said in the EAC guidelines, a year of DAPT even in ACS unless there is high bleeding risk, but this automatically means that we have to assess bleeding risk in all of our patients, and there's a couple of ways that you can do it. Uh, the, the, the, the, the ACC guidelines talk about, uh, an, uh, academic Research Consortium high bleeding risk score, which is an RCHPR score, and the presence of at least one major or two minor criteria is kind of, these are patients who have been identified at high bleeding risk on both internal and external validation, right? And when you look at some of the major criteria, um, there's uh. It's, it's, it's, some of, some of this is pretty intuitive, um, patients with CKD, that's a lot of our, uh, complex intervention patients, um, hemoglobin level is 1, less than 11, um, if you want to use, uh, patients who have liver cirrhosis, uh, platelet count less than 100,000, um, so the these are all some of the major risk factors, and the, the minor criteria again age more than 75, moderate CKD. Um, and you know, a, a hemoglobin level that's in the intermediate range but not the, not the low range, and any ischemic stroke, uh, that is not meeting, um, uh, high risk criteria, which is moderate to severe ischemic stroke in the past 6 months or intracranial hemorrhage, so this is, this is present in a lot of our patients, so in these patients, you, you, there is data to suggest you don't have to do. Uh, DAPT for 12 months, you can get away with doing it for 3 months and then stopping the aspirin, in fact, there's a wealth of data that says it's, it's better, um, the precise DA score was a score that was derived from 8 data sets and. The Masterdap trial and other trials looking at short-term dual antiplatelet therapy use the score. It's easy to calculate, and a score above 25 identifies high bleeding risk. So these are the five things you kind of enter it in MDCalc, and it tells you what your precise DAP score is. There's there's, there was a paper recently that spoke about how the RKHBR is a better tool to assess and it picks up higher bleeding risk patients better than the precise TAP score. Nevertheless, I think as a first step, it would be better to use some bleeding risk assessment strategy and then kind of. You know, going into the nitty gritty of it because I think the precise t score is easier to use and easier to incorporate in your note, and it kind of tells it, um, you know, gives the picture with a point scoring system. Uh, so then if you do have patients, uh, you know, how do we switch between them, and this is a chart we always look at and always pull it up, and when you think about this, uh, it is something that is intuitive, uh, once we understand how these medications work, so, um, what do I mean by that? We spoke a little bit about the duration of action of some of these agents before, and also the half-lives of these agents are very different than the duration of their action, um, for example, uh, Plavix has a very short half-life compared to Brilinta, Brilinta hangs around in the system for approximately 12 hours, which is why every time you switch a patient from Brilinta to Plavix. Uh, you have to be careful and give a washout period of 24 hours. So even if someone got a stent yesterday and you're switching them over from Brilinta to Plavix, you have to give them a 24 hour washout period with the last Tyagar dose, so you don't give them the p.m. dose and you have to reload, because if you were to give the patient Brilinta and Plavix. By the time the Plavix gets a gets a chance to act on the platelet, the Brilinta is still hanging around. By the time the Brilinta is gone, the Plavix is also gone because the half-life of Plavix is very short, um, and now that doesn't mean that the platelets are not inhibited for 5 to 7 days. Once the platelets are inhibited by Plavix, it's inhibited, but the, but for the drug to act on the new platelets that are forming, um, it needs to have a 24 hour washout period. And similarly, when you're when you're going from Uh, Prasugrel to to Plavix, same concept, because Prasagril has a long half-life, you have to wait, uh, at least 24 hours, um, and vice versa for Prasagrel and Effient, um, and you know that that's, that's kind of the main key concept of why we wait, uh, the times that we do. Um, now, This was an interesting paper that came out last year, almost 2 years ago now, and it kind of talks about. You know, gives a little bit of information on in the patients with some of the highest bleeding risks, specifically in diabetes, right, because diabetes is a hypercoagulable state, and even if you can argue that patients are at high bleeding risk, these are potentially patients at the highest ischemic risk as well, um, and what they looked at was uh abbreviated antiplatelet therapy versus uh standard antiplatelet therapy, um. They, uh, essentially, and this was a pre-specified analysis from one of the key trials called the Master DPT trial, and in this trial, they had approximately 1500 patients with diabetes, um, and. And of a total of 4500 and odd patients, and they, uh, overall, they looked at two co-primary outcomes, which was net adverse clinical events, which was a composite of both ischemic and bleeding events, and then they looked at major adverse cardiac or cerebral events, so just basically looking at ischemic risk. And then they looked clinical at just bleeding risk, so one was a composite, which is net adverse clinical events, so this is important for the patient. This is essentially balancing out ischemic and bleeding risk, and then they looked individually at ischemic risk as well as bleeding risk, and uh what they found was that in high bleeding risk patients with diabetes, they did have higher risk of uh major adverse cardiac events um. Compared to non-diabetic patients, so this is patients without diabetes, this is patients with diabetes, so when you, when you look at uh the, the net adverse uh clinical events, it was. insignificant, uh, but their bleeding risk per se in these patients with diabetes was slightly elevated, um. And abbreviated therapy compared with standard therapy was associated with similar net adverse cardiac events and major adverse cardiac events, um, and also had, so when you look at the ischemic risk in these patients, even if they have diabetes, uh, shortened antiplatelet therapy was better in patients who had a hiding risk. Uh, and this did not come at a, and that does not, did not come at a risk of increased ischemic risk, but it did have lower bleeding risk, so this essentially validated the concept that shortened antiplatelet therapy can be used in patients. Who have diabetes, um, which is one of the most common, uh, chronic issues that we have in our patients that increases ischemic risk, uh, but lowers bleeding risk if you were to shorten it without any change in ischemic risk, so this. Is important concept kind of basing strategy on what we should be doing in patients, even if they have diabetes, as long as they have high bleeding risk, we really have to think about, uh, you know, shortening their DAPT duration after ACS um. And uh so what are the ways that we can do it? And there's there's a couple of ways uh that you can uh kind of de-escalate here, uh, one way is to consider abbreviated Pythagorlor therapy, which means uh we just do Pythagorlor monotherapy or Brilinta monotherapy after 3 months of aspirin plus Brilinta. There's a, there's the the landmark trial that looked at that was the twilight trial which showed there was a 44% reduction in bleeding risk without change in ischemic risk. Um, so then the corollary question is, can we use this in patients, uh, with, uh, who, who we just put on Plavix or Prasagrl? Intuitively, the answer for Plavix is no, because remember we're not genetic testing a lot of these. Patients and Plavix non-responder status would mean in about 30% of our patients that they're not getting any antiplatelet therapy, right? So if, if you stop the aspirin in 1 to 3 months, but they're just on Plavix and they're a non-responder, uh that is uh that is a significant, uh, ischemic and stent thrombosis, so I would not recommend doing just Plavix monotherapy, um. Effient again or Prasagril alone, there is no trial data, but intuitively you potentially can, right? Uh, because the way how Brilinta and Effient act in terms of platelet inhibition is very similar. Now, what about de-escalation strategies, and this is something that we commonly see in our patients who uh at Centura, who we get, who we load them with Brilinta, but then they cannot afford Brilinta, uh, but they also have a history of stroke, um, or, um. Uh, you know, TIA, uh, in these patients, I think there is, like we said, there's, it's a class 2B recommendation to go from, uh, a more potent P2Y2 receptor to a less potent one. personally, I would avoid this, uh, but you know, in those who cannot use Prasagrel and cannot afford Tyagor, I think, uh, you know, 30 day coupon and then switching to aspirin plus Plavix, I wouldn't stop the aspirin, it's gonna be aspirin plus Plavix, uh, is a reasonable strategy, but. Again, the guidelines give it a slightly lower recommendation as very validly compared to the first, uh, one which is uh monotherapy with a more potent uh P2Y12 receptor agent. Yeah, um, so I think those are, that's, that's kind of a short summary on ACS pharmacology, and if, if any of you have any questions or any comments, uh, I think we can use the next like 5-10 minutes to go over that, um, but, um. Yeah, um, that would be, I think that's the end of my presentation. Published April 30, 2026 Created by
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