Chapters Transcript Video Treatment of STEMI Click here to view the presentation deck Back to Symposium Good afternoon guys. Hi, I'm AnAnd Krishnan, one of the neuro interventional cardiologists with Brian. So we just decided between the two of us that we might be the most inexperienced panel, but we're certainly the better looking one. So, uh and also, uh you know, I have no disclosures. Uh The only thing is I am looking for a PC P in the Virginia Beach. So if you like uh the presentation, please take me on as a patient. Um I know we, yeah, Brian needs one too. Um So, uh you know, I have 20 minutes to do this talk. We're gonna go over some basics. Nothing fancy. These are all cases that I have done. Um And uh, you know, door to lunch time is 20 minutes. So I'd rather be doing a semi, I think that would be easier. All right. So these are the learning objectives and um you know, uh the, the most of the guidelines and I'm happy to share my slides is from across the pond. Uh because these are the more newer guidelines from the European Society of Cardiology and this is the, you know, the citation for it. So, feel free to take a look at it and starting slide, right? So in God, we trust but all others must have data. So this was a oncologist and you know, cardiology is really built on data. So as much as possible, we're going to hit up on some of the major trials and just to give you a flavor for why we of the things that we do right in acute coronary syndromes and really, you know, kind of piggybacking on Brian Stock. Acute Coronary Syndrome is a spectrum and you can have patients who are having minimal disease with no EKG changes to patients who have cardiac arrest and ST elevations with the PH of 6.8 and who are not breathing, right? So, uh really the the key thing is you want to rest stratify these patients and any sty talk is going to be incomplete without actually talking on the high risk and sty. So, uh hopefully I'll have time to touch base on that. Uh I'm not gonna touch base too much on the EKG uh assessment because Dan Thibodeaux made my life easier. So that makes me fly through some of these slides. But these are some of the pearls, right? So uh in V two and V three, the guidelines actually say that the ST emi criteria is is not one millimeter, it's actually different. And that's because those leads are closer to the heart and hence you have a slightly higher threshold to call a semi. So it kind of makes sense intuitively um everywhere else. Anterior one millimeter really is the way to go here. Uh Other key pearls and inferior stem, you always get rights sided precordial leads because you're always worried about an RV infarct. Uh posterior leads are also a good idea, especially in V seven to V nine. So you just kind of uh go just below the scapula. Uh again, uh these are especially if you have uh t elevations or inferior uh ST elevations. And uh again, Dan touched on this topic. So if you have ST depressions and multiple leads and you have elevations in a VR, that's actually a mirror and you're worried about multivessel ischemia. So this patient in your office, if they're having chest pain, most likely has left main or multivessel disease. So uh call me or Brian. Um going forward first case, this was my first week uh as an attending in Sana, still getting oriented by Doctor Alamar. He was in the back room. He's one of my senior partners, but essentially 71 year old female suffered a motor vehicle accident. Luckily no trauma came in uh after cardiac arrest, three vicar fibrillation shocks and this was her EKG. So you get because of lack of time. Uh 10 seconds, look at this, you get an A, if you call inferior ST elevations, you get an A plus. If you also recognize that she also has a posterior infarct because you have uh you know ST depressions in V two V three with upright T waves. Uh So when you flip that EKG or you, you know, you look at the mirror image, you actually have ST elevations there. So this is a quick way to see that this patient actually is potentially having an infero posterior M I right. So again, you know, the the point of the slide is how quickly what is your total ischemic time of that patient? Because the minute the artery occ includes the patient, the ischemic time has started, you're on the clock, it doesn't matter when you diagnose the semi, the ischemic time is almost always longer than when the diagnosis of ST elevation M I or an A CS has been made, which means that you have to really, you know, try to be quick about opening up the blood vessel. So, uh she presented to a primary PC facility and hence you go down the first pathway. Um So you, you know, you have um about an hour to uh you know, door to balloon time here, a couple of key trials. So, you know, anytime the patient is coming to a Cath lab or even if they're having an A CS picture, one of the medications we always use is aspirin, right? So this was one of the trials that put aspirin on the map. Um you know, potentially they could have come up with a better name. But this was back in the nineties. Uh and it showed that aspirin actually reduced ischemic events without a significant increase in bleeding when compared to fibrotic therapy, which was kind of the first clot busting medication that came up. Then we had the cure trial, which kind of talked about Plavix. And then this was another medication which showed that with every addition of Plavix to aspirin, you actually reduce ischemic events by 20%. Uh which again, uh with, with some increase in bleeding, but the benefit far outweighed the risk. And then one of the newer trials which had uh Tagar come up further showed that when you add Tagar compared to Plavix, in addition to aspirin, further, you get a 20% reduction in ischemic end points. So really the guidelines are shifting towards it and someone who's having a CS especially a stemi you really wanna do tag or um ideally because you do have an improvement in um ische you know, in, in ischemic outcomes and tag actually showed a mortality benefit as well. So this is like the one of the most basic slides. Uh and uh 11 of the key points here is that duration of action and uh half life are two different things. So, pharmacokinetics and duration of action are two different things. And this is really a key point as to why these medications act the way they do and why we pick the doses that we pick. So, aspirin only has a half life of 30 minutes. But because it irreversibly affects the thromboxane A two receptor. It, the platelets are made every week in the body. So you're poisoning platelets with aspirin and the, the, the duration of effect is 5 to 7 days, but the, the medicine is gone in 30 minutes. So, you know, it's the same reason if you were to take ibuprofen and then take aspirin later uh or Ibuprofen right after you take aspirin, sometimes the aspirin may not work. Uh Plavix. On the other hand, uh depending on the dose, uh usually starts working with the, the first few hours. But again, uh it is an irreversible inhibitor but only inhibits about 30% of the platelets. So the 600 mg inhibits about 30% of the platelets within, you know, 2 to 4 hours. So that's one of the reasons why a cardiologist, uh especially an interventional cardiologist will always be like, please give them 600 do not give them 300 cause it takes forever to start acting, especially if you're gonna put a stent in them. Um And tag is one of the uh reversible binders. Um It has a longer half life. Uh and, but it, you know, has a similar uh duration uh of uh effect essentially, but it inhibits 80% of the platelets. So that's why it's more potent than uh Plavix. Uh So this is uh you know, a fun picture that kind of talks about everything your body goes through when there's a clot. Um you know, when, when, when there's clot rupture, the coagulation pathway is activated. But at the same time, the platelets are activated. And essentially what happens is is that, um you know, to put it in a nutshell is that there is fibrin Stans, fibrin strands that form a mesh and then the platelets kind of stick on to that mesh and that's how a clot is formed. So all of the medications that we use affect different parts of this pathway to kind of get the best anti uh you know, clot effect, as you would say. So, fibro analytics acts um you know, on uh the fibrinogen uh um uh pathway there. Aspirin works on the thromboxane A two receptor. Uh your P two Y 12 inhibitors like Plavix and tag are gonna act on the AD P receptor. And then, you know, um uh you know, some of you might have heard about medications like a grast. These are two B three inhibitors. This is like the final common part pathway that prevents platelet, uh you know, aetion and aggregation together. So, you know, that's our bailout drug in the Cath lab. Uh where if everything fails, if you're not sure if they have taken Tagar or Plavix or Aspirin. Um in, you know, in this patient, for example, when she had a CPR uh and a cardiac arrest Agris sta is your go to drug. And then Heparin and uh Bivalirudin are again acting on uh factor uh two and factor 10 A to prevent uh clot formation, more clot from propagating. So, uh this was my case. So, you know, this was that lady who went in, I had to go groin, uh some pictures, uh essentially, uh we're seeing the left coronary system on the, on the top left here and you can see that she has a completely occluded, the arteries that coming down, they have to go all the way down and around the heart towards your, I wanna say, uh left hand side. Yeah, my left and your left as well, um towards your left hand side. And then that is where the semi was. So it's feeding the infra posterior of the heart. So it kind of fits with the EKG, but she also has some disease in the right, which looks chronic. So we're not gonna touch that. Um And then, uh the next few is we take other pictures of the left uh coronary system to make sure she's not having. She does have some osili again, this is chronic. We're not touching it today. Um And then on the bottom view, uh I have two wires down. It was a bifurcation lesion. Uh Lucky me on my first semi. Um And then we uh put in a balloon and then our door to balloon time was like 25 minutes as soon as she hit the cat lap. So that was great. And then finally she ended up getting four stents, a bifurcation stent into that uh other blood vessel that's going towards the, towards your uh right. Um And uh she did great. Uh Actually she left the hospital a week later. Um So the second case, this was a case out of fellowship. I don't know if you guys have been to Vermont, but Rutland um is one of the, is, is in Southern Vermont and this was a uh gentleman who came in with chest discomfort on and off. He had no known uh C ad and uh EMS was called and they drove him to the Rutland Ed. Um This was his EKG and here the ST elevations are kind of subtle and, you know, always, uh I was taught to look at the, the R wave more, you know how big the R wave is and to a certain extent and compare the ST changes through the R wave. You often cannot expect two millimeter ST elevations when the R wave is only one millimeter tall. Um but he was having symptoms, again, symptoms trump everything else uh in a patient who was having chest pain. So this was how far he was from University of Vermont where our Cath lab is, it's more than 100 and 20 minutes away. And hence, he did not present to a primary PC I facility. And now the decision pathway is that he needs to get clot busting medications and the reason and, and, you know, he, uh, he got TNK, he continued to have chest discomfort on and off without unresolved changes. So we activated a semi and he came up to the Cath Lab and that really is, is that, you know, the data suggests that within the 1st 2 to 3 hours, uh, clot busting medication is, is, is, is as good as primary PC I. So if any of you are vacationing in Hawaii, apart from Honolulu, a lot of places don't have primary PC I cause you're in the island. If someone, you know, has a heart attack, they're getting clot busting medication and then they're gonna get shipped over to Queen's Hospital most likely. Um And uh but, but the key point to remember is that even though they get fibri lytic, almost always data has shown that primary PC I even after that uh is, is better for ischemic and mortality events. And um as the longer the ischemic time goes, the clot busting medication doesn't work as well. So if someone is having chest for the past 8 to 9 hours, and it's fairly consistent that, you know, the artery probably occluded 8 to 12 hours ago, the clot busting medication is not going to work because remember that coagulation pathway and that clot forming pathway is kind of pretty much that train has left the station So your best bet is to open it up, uh, with, uh, with a balloon and a stent. Um, and, uh, from the guidelines you have within 10 minutes of someone hitting the Ed, if you're at a non primary PC I center to get an EKG and to actually give the clot busting medication. Um, and Ed doctors would run through the checklist because that's what they did in the stream trial from which the guidelines take the recommendations. So, um I think if I have a couple of more minutes, I'm gonna do one more case. This was the case I did last Friday. Um When I was uh my first day of orientation at uh the Virginia Beach Hospital, 54 year old gentleman uh has all the risk factors under the sun for cardiac disease came in with one week of progressive chest discomfort which was worse on minimal activity. Saw him as a N ste E as a consult on the floor. And his EKG uh you know, you could argue is there something in V two V three? But then uh it wasn't two millimeters. So it wasn't enough to call a sty uh but his symptoms were concerning. So I got a stat echo on him and here, you know, he, he has a high sensory and an EKG doesn't meet sty criteria, but he's having chest discomfort and you're pretty sure this is an N sty, right? So, you know, one of the well validated scoring systems we have is called the gray score. And it, you know, less than 140 means they are low risk Andy, more than 140 is high risk endy. And again, this, this is not something set in stone if your lowest patient is having chest pain. Now, all of a sudden, you know that low risk kind of goes out the window, they're having ST elevations, it's different. Uh but he was not having but uh chest discomfort actively. Uh but when you kind of do the score, when you go through it and MD Calc and Dyna Metics have that, he, he scored way above the 140. So this is someone again for triaging purposes, is someone who needs a cat ideally within the next 24 hours, right? Even if he's electrically hemodynamically stable and if he were to score less than 140 on the grade score, then you can kind of put it out up to 72 hours. Um And that is really, you know, when, when you have patients which are, you know, vying for beds in a ordinary center, uh this is important, this is an important piece of information that you want to keep in mind. Um that kind of helps you risk stratify the patients with a validated scoring system and kind of tells everyone the same story. So if I'm seeing a patient at the heart hospital who was transferred in from another center. And the note says, gray score of 190 that pretty much tells me almost everything I need to know about that patient in my head, about what this patient needs going forward, right? Um So this was this echo um ideally, you want everything to thicken nicely and that is the an an Antero seal wall that is not thickening uh right from the mid all the way to the apex. And then here we have contrast uh the outer end of the screen where the picture is, is again the anterior wall, the anterior wall is not moving. So this is something that I'm, you know, in my head, I'm like this is a middle lady or a big diag that's, that's, that's on the verge of causing a sty. Um So this was his right. It was, it was, it was, it was, he had small vessels uh which was interesting because he was a 52 year old man and he wasn't small. But this was this diabetes, does this to your vessels? For reference, the catheter is a two millimeter catheter. Ideally, you want your RC A and your left, you know, your RC A and a man to be at least uh three millimeters. Uh but in his, it was barely and this uh this is what we had so that long vessel that goes down uh the front of your heart, that's the led and he had an occlusion uh like a 95% thrombotic lesion in the proximal to mid led. Um And then we, in the last image, we have a wire down there, we ballooned it. Um And then um we put in one long stent 275 by uh 38 I believe. And he had a good result. He left the hospital a couple of days later on aspirin, high intensity statin and ticagrelor because that showed mortality benefit than Plavix, especially given his young age. Um But apart from that, you know, summary slides, always think history always do a physical exam. EKG is key, but you know, you can always get an echocardiogram. That's, that's a great test as well. Uh to kind of see if there's wall motion abnormalities, helps you to stratify these patients. Um And then, uh you know, triages triad strate because not all end sties need to go right away, but all stem is obviously uh you're on the clock for them. Um And then this is the final slide last year of fellowship for me. Uh These are my mentors. They taught me everything I know about cardiology over the past four years. Uh So any Google reviews and yelp reviews go to them. Thank you. Published November 5, 2024 Created by Related Presenters Anand Muthu Krishnan, MD Cardiology View full profile
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