M. Nicholas Burke, MD, discusses Acute Coronary Syndrome.
Welcome to cardiovascular conversations with Minneapolis Heart Institute. Your podcast for the best in cardiovascular content, cardiovascular conversations is a new, creative and engaging content source for the latest and greatest in cardiology topics and innovation. We are your hosts, Fred. Um, use. And I'm Jason Hicks. Enjoy the podcast. Welcome back, everyone. Today we have a special guest, Dr Nick Bourke, who is an interventional cardiologists with Minneapolis Heart Institute. We're discussing a CS or acute coronary syndrome. Under the umbrella of a CS is stem E or S T elevation M I and semi or non s T elevation M I and unstable angina. Dr. Burke will be dissecting these topics as well as the classifications system MH area first to as their level one through level five heart protocols. So, Dr Burke, A C s syndrome is often used as a constellation of symptoms related to myocardial ischemia. Can you walk us through or break down the categories of a CS and the importance of each? Yeah, acute coronary syndromes There. There are three kind of major diagnoses within acute coronary syndromes. The one that everybody is worried about. And when people talk about having a myocardial infarction or a R a heart attack. What we're referring to is what's called an s T elevation myocardial infarction or a stem e, and that is diagnosed based on the patient showing up generally with chest pain or shortness of breath. Something along those lines in an electrocardiogram. Reese E g very clearly showing what's called s T segment elevation myocardial s t segment elevation on the E C G. Um, there's in that generally represents a complete occlusion of a major vessel feeding the heart. Um, in a little less severe than that, at least in the acute situation is what's called non s T segment elevation myocardial infarction. And that's where the patient comes in with chest pain. They may or may not have obvious electrocardiograph IQ changes, but they don't have s t segment elevation on their e c g. And they generally have evidence of, uh, myocardial damage predominantly based by an elevated troponin in the bloodstream. And that often represents a sub, totally occluded vessel or a vessel that's mostly closed. But that hasn't completely closed, and it can also represent a closure of a smaller side branch that's not picked up by the E C G. The third diagnosis in that is unstable angina, which is sort of the prelude or the warm up up to those other those other syndromes where you have a diminution of blood flow to the heart muscle. But it's not severe enough to cause any cell death or damage, so you don't see an elevation and proponent. And of course, you don't see the S T segment elevation with both unstable angina and non S T elevation myocardial infarction. You may see other electrocardiograph IQ changes that give you a tip off that that's what's going on. S t segment Depression, T wave inversions, etcetera. Can I ask you a little bit more about some of the terminology? So I like a CS because it allows us to, as you just said, create sort of this umbrella under which all of the coronary artery disease pathology exist. I think, though it's it can be confusing still in medicine. Sometimes we still see, even in the current literature reference, key wave non Q wave, um, throwing around some of these terms that maybe I think in medicine sometimes don't do a good enough job of reading ourselves up on and moving on. To what? What are we actually all talking about? So that we're all speaking the same language. But it's safe to say that what you just referenced are the terms is the terminology that we ought to be using right now. If I'm gonna call you Dr Burke and say, Hey, I've got this guy here with chest pain. I think he has had a an end stem me, not a non Q Wave Em I anymore. Okay, regarding unstable angina this term for me. And I think for a lot of emergency practitioners, primary care providers is a little bit nebulous because I think we were all taught. Wow. Okay, you've had again with terminology, Crescendo, angina it. Now you are having angina. That's not like your usual chest pain anymore. But I think it goes beyond that, doesn't it? It's not just the patients who, while they've had a change in their usual stable angina, can you talk to us a little bit more about what is unstable angina to you? How we should be viewing it, Aziz, the referring providers, unstable angina. Think of it for me as the patient is trying to have a heart attack, not hasn't had the heart attack yet, and generally that is a new onset or a precipitous change in their in their engine, a pattern if they happen to have angina beforehand. But if it's new onset, and particularly when it comes on with rest at rest or very minimal exertion, it can also be described as a change in an journal pattern if it's with significant activity if it hadn't been present before. Because it's a new onset and what the idea is, is that something precipitously has changed in the coronary anatomy, and that's changed fairly abruptly and in those situations, the patient's air at the greatest risk for that to transition further to a non stem e or an S t elevation or stem E which, of course, carries a very you know, much higher mortality and morbidity with that. So Dr Burke, with that, then you're just talking about how the corner vessels change. Can you talk us through the path of physiology of what happens with those vessels? Um, you know, heart attacks don't occur because our blockages, you know, become 49% blocked in 50% 51 52. That's not how that happens. They can grow very, very slowly like that, but that's a very stable situation. What happens in acute coronary syndromes is plaque rupture, so you have a blockage or or erosion. You have a blockage anathema sclerotic plaque in the artery that becomes inflamed. So there's inflammatory cells present than in lesion. And what happens then is that in significant cases the plaque will rupture. It will break open or erode on the top, and when that happens, that exposes a very irregular surface to the blood. So the plaque may rupture and break and somewhat narrow the vessel itself, just by virtue of the fact that the plaque is now protruding mawr into the Lumen of the vessel. But then you have this very irregular surface that's exposed to the blood and blood does what it's supposed to do when it sees an irregular surface. It forms a clot so that you don't bleed to death when you get a paper cut, so you get a combination of plaque rupture and erosion and or erosion, and then traumas formation. And it's generally the thrombosis formation that actually closes the vessel that causes theater event. Now, if people are lucky, they that may heal up. And that's how you find people who come in with 90% blockages. But they're nice and smooth, and they've been that way for a while. If they're unlucky, they completely closed. The artery has the incidents of a. C s. As we as we just discussed it in your practice or with literature support that it's actually remaining stable or are we really seeing a pretty significant incline in this? We're not seeing an incline on, and I think the reasons behind that are a few. But I actually think that we're we're practicing much better Preventative care. Ah, lot of people, a lot more people around statins, the cholesterol lowering agents. Blood pressure is, you know, mawr controlled than it had been in the past. Hopefully, you know, it's interesting, though, because, you know, this go runs counter to the obesity epidemic that we're seeing, and I suspect that that will rear its head as well, and we will start to see mawr complications from that over time. I'm wondering if it would make sense, and I think that will be able to derive some questions out of each one of these is for you to break down for us. A level one. Ah, level to a level three and level four. And I think that they're inherently are gonna be some obvious questions. It'll pop up that we can just throw out and we'll be able to have some good discussion about each of these. So I'm wondering if we might be able to start with the big one. The one that we all worry about that we don't wanna miss ever. The level one myocardial infarction or stem E. I'm using those terms interchangeably correctly. Right? Correct. Okay, So can you just give us an example? Yeah, maybe you know any pearls that you have in there, and then what we ought to be considering doing with these patients? Well, the nomenclature, the levels. Level one, Level two, etcetera is a Minneapolis Heart Institute specific thing. Perfect. And we labeled the and this started with our treatment of S T elevation myocardial infarction. You know that the classic situation is a 65 year old smoking diabetic, hypertensive, overweight guy shows up with an hour of crushing stub, sternal chest discomfort radiating to his left arm, making him feel short of breath, a little bit sweaty and perhaps a little nauseated. And his electrocardiogram will demonstrate s t segment elevation in two or more continuous leads on the electrocardiogram and that persons having an S t elevation myocardial infarction. Historically, the treatment for that has evolved since I've been in practice fairly dramatically and initially, autopsy results showed us that thrombosis was really kind of a key player in that. So the initial treatments for stemming or myocardial infarction were bed rest. Then it was found that aspirin decreases mortality. So the aspirin is helpful. Beta blockers, which lower heart rate and blood pressure were found to decrease mortality. But the big change came when the clot dissolving medications came out the thrum politic therapy, and this was medication that was delivered intravenously that would make the blood super thin and dissolve clots. And they it worked. It lowered mortality substantially and improved outcomes. The problem with that was that there was about a 1% incidence of interest cerebral hemorrhage with that therapy. So and an interest cerebral hemorrhage, when your blood is very thin, is almost always lethal, extremely, extremely debilitating. So you were trading a couple percentage mortality points of the benefit with the thrown politic medication, but you had the trade off of an uptick in the increase of stroke. Nonetheless, the overall wash was that it was of benefit to use these therapies fast forward a few years, and it was determined that a mawr effective way of dealing with this is with an invasive procedure where you go in and do an angiogram, find the blockage and open it up and with initially with balloons. But Aziz, the therapies developed in step balloons and stents. This improved our outcomes substantially in terms of lowering mortality, and it also didn't carry with it that 1% risk of an interest interest cerebral hemorrhage because people weren't on the's super potent clot dissolving medications. We do use some blood thinning medications while we're doing the procedure, but nowhere nearly as potent as were given previous to this with with the throng politic therapy that was all great if you presented having a heart attack to a place that did angioplasty and stents. Now most of the population doesn't live that close to PC. What we call ah PC I center of perky Tania's coronary intervention of a center that does angioplasty and stenting. So those people were still treated with from politics. If you presented to ah hospital that had that capability, well, lucky for you, you've got the better therapy, one of the E D docks that you guys will work with, Dave Larson, who was working with us, said, Why can't my patients here in Laconia get the same therapy that those presenting at the Minneapolis Heart Institute, too? And that was the genesis of the Level one program? There was some studies done in Europe in very small geographic areas like the Netherlands that showed that if you transported people for angioplasty and stent emergent Lee, they did better. Even if you had to transport them and get the angioplasty and stent, then if you gave them the throne politics. It was said that this couldn't be replicated in the United States because of competing healthcare systems and insurances, etcetera, etcetera. But we started that program here, and that was the Level one protocol that subsequently was spread out throughout the state and had is now the model for how heart attacks were treated pretty much worldwide. Assuming they have the ability to transport people for for that type of thing, a t least in the developed world. So and it certainly is in in the United States that actually came out of partnership between Richie Medical Center and the Minneapolis Heart Institute. And it was it was really nice because we started doing it. Ah, couple other systems in the state started doing it at the, you know, shortly after we did. And my take on that was, if what we do causes you to raise your bar good on us and good on you for doing the right thing for the patients. So that's in a nutshell. That's treatment, you know, for S t elevation. Myocardial infarction. So can we branch off onto that from that? A little Not into any of these other levels of chest pain yet, but I would like to hear from you about that study. What did we find with that study? And by doing so, what are we talking about? In terms of morbidity, mortality decreased for our patients with primary PC I, as you say. Well, if you look at heart attacks in general, somebody showing up with an s t elevation myocardial infarction untreated? Let's let's assuming that the patient makes it to the hospital. So there there's We're not talking about people who diet at home in their sleep. Um, if they make it to the hospital. The mortality from a myocardial infarction a stem e is about 13% aspirin lowered that down to on this is all comers. Aspirin, meaning all patients not just selected patients, is part of a study. Aspirin lowered that down another 2 to 3% so 11 10 11%. So it made a significant improvement. Beta blockers lowered that further one or 2% and throw politics got us down into the 6% range 6.5% range In terms of mortality from myocardial infarction, that's pretty good PC. I now 5% mortality with very limited complications from the procedure itself, made a dramatic improvement in in terms of what we can dio in terms of survivability. But what we showed actually and that this is really exciting is and and we had a particular protocol where we for people who the problem is is that you've time is muscle, so you need to open the artery. However you get the artery open, be it clot dissolving medications or be it angioplasty and stenting as soon as possible. You need to be what we call door to balloon under 90 minutes. And if you're under 90 minutes, you've substantially decreased mortality. There's a law of diminishing return. So at some point, you know, further detriments in time are not going to result in an improvement in mortality. But the main cut off in the goal for every PC I center was a door to balloon of less than 90 minutes. Well, we counted that 90 minutes from your door, tow our balloon, right, and there were also. But there are people who presented even further away that we couldn't get them here reliably in 90 minutes. So we actually broke that down in what we call zone one end zone, too. Zone one of the patients that we can get to our cath lab in an artery open reliably in under 90 minutes. Further out, what we developed was a protocol where we used what we call a farm ako invasive strategy. And this was really the brainchild. Dr. Tim Henry, who was along with Dr Dave Larson were the primary movers in the level one protocol. So a big shout out to him is well in this. And what was done then is, rather than giving the full dose of Trumbull Isis, we gave a half dose thrombin from politics. We saw dramatically reduced stroke rate with that and about 60% of the patients with that by the time they got to our lab already already had an open artery. Now the artery was severely blocked still, and it had a lot of clot in there, so we still needed to do some work on it. And what we showed through that is that the mortality for those patients was the same. So what that means is, if you have a heart attack in, uh, China or South Minneapolis or right across the street from Abbott Northwestern Hospital, your chance of dying from that heart attack is the same for the patient who presents in blue Earth. Okay, Yeah, that makes sense. Which is amazing. It really is. It makes me feel better about wherever I decided to have my heart attack. Anything else in terms of treatment, things that we need to be considering or something that might be new or, um are evolved in terms of treating Stem me. No, you know the treatment. They We have newer anti platelet agents that have been demonstrated to be of benefit we chose to use to Kangra lore. There. There's Takagi allure. And then there's price of grill, which is the other newer anti platelet agents. A supposed to clopidogrel or Plavix? They're more potent anti platelet inhibitors. They work more quickly, so that's become the standard we chose to Kangol or because with Presser Grill, there's a black box warning for people who are older or who have had a prior TIA or stroke Not to use that. But different places have different protocols on that, so that's changed a little bit. But our basic treatment in terms of getting the patient as fast as possible to the cath lab opening the artery placing a stent hasn't changed in many years. E. I mean, they're drug eluting stents, which we've been using since the early 2, 2000. They've looked at a lot of different things, like whether catheters that suck the clot out make make an improvement. They really don't seem to We get a beautiful result in they're going in there initially with a balloon. Just open up and restore flow and then putting in a stent to make sure we've got a nice final loom until we get a good result on the artery. Very good. Very good. So moving along, then toe the level two that would put us in? Yeah, level two. So it became clear that we protocal ized the therapy for stem E. Everybody knew exactly what to dio. When a stem e roles in you get the e k g. It says stem e you basically just pulling the trigger and put the patient on rails and away they go We didn't have that for other forms of acute coronary syndromes, unstable angina, non s t segment elevation, myocardial infarction. And we put those together because the treatment strategies for those are the same. There s oh, they're treated identically. You could just think it's non non stem me as a little bit more severe than unstable angina. And it's important to note that if you don't a non stem e which basically is trying to become a stem me if you don't treat the non stem e aggressively. The mortality is non of non stem ease is the same as stem e, so you need to treat these things aggressively. And a zai described before the unstable angina and non stem e we protocal eyes that as well and said, Okay, what does the data shows the best treatment for these people? Well, the best treatment for them is aspirin, heparin and an angiogram. Fortunately for May, the angiogram doesn't have to be done immediately, which is a bonus, because that means I have to get up a little bit less frequently in the middle of clothes is long as the patients not having any more discomfort If they're having active, ongoing chest discomfort. We treat that as a stem e, so we call that a Level two emergent, and we bring those people directly to the cath lab. If they're symptom free with nitroglycerin, heparin, aspirin, that sort of stuff and feel fine will sit on them until the next basically the next working day, and do the do the angiogram. Unfortunately, the data has shown that that's a safe and effective way to do that, that we don't have to take people do all people directly to the cardiac cath lab in an emergency. And we define those people is people who present, you know, a nuance said unstable type of angina associated with either elevated proponent, which would be a non s T elevation myocardial infarction. Significant electrocardiograph IQ changes, particularly S T segment depression, which is indicative of mild cardio s Kenya or anterior T wave inversion. And this is would be a marker, potentially for a high risk lesions such as approximate left, anterior descending or if the person's had a recent positive stress test. So if they've had a recent positive stress test, they've already shown us that they probably have cardiac disease. And now they're presenting with an unstable situation. And those people are treated in the same way they're treated with heparin. Aspirin. Nitrates is needed and transferred to a piece. Tow us because these are all I'll come or admitted to the hospital. If they're presenting to the idiot Abbott, they're all transferred or kept in at Ridgeview because of the cath lab there overnight and then receive an angiogram, basically the following hospital a hospital day. Dr. Burke, you just said so we have these level to emergent patients. So just toe sort of summarize, I think. What I what it was I heard you say out of this is we have the non stemming the end stem e patients who have essentially positive biomarkers. They have elevated troponin, and they have a concerning enough history in that they're continuing to have chest discomfort or their annual equivalent. Those patients do need to mawr emergent Lee, go to the cath lab in my correct. Okay, Now, we also have this. Yeah, if you're if you're having, but I was on a roll. Well, I know, and I will let you get back on the road. But if you're having s Temi equivalence on your your E c g But you're having crescendo chest pain. Is that an automatic indicator? So you're doing nitrates. You're doing paying control with whatever allergies, if you wanna go with this person continues to have this crescendo. Isn't that an indication to go to the Catholic? Yes. Okay, that that's what I wanna dio e Think what you're driving at is that there's the again. There's a spectrum and there are people who you know, had two hours of chest discomfort and then feel better. Maybe some thrombosis formed in that artery. And then the body's natural, uh, system Liszt. That promise. And it's no longer so inclusive, but they're still it extremely high risk because they've got this ruptured or ulcerated plaque in their coronary arteries. There is a subset of these people who have ongoing chest discomfort, even though they haven't there. E k g does not say stemming does not say s t segment elevation myocardial infarction. The fact that they're having ongoing symptoms tells us that they have ongoing a scheme, er ongoing, my cardio at risk. And those people we treat the same as we do. Ah stem e bring them emergent Lee to the cardiac cath lab. And that's also regardless of the of their biomarkers, if they're if they have a concerning history and findings on BCG, whether they're trope is elevated or not, they're going to go to the Catholic because you can't get their pain under control, right? And they may have presented early enough so that their proponents or not, elevator Yeah, so your first opponent, even though it's negative, doesn't mean that they don't have a new acute coronary syndrome. So in terms of the non stemming, we have the Obviously. We've seen a lot of these patients in our career, and it's not uncommon to have them will come in with chest pain and their chest pains now gone. But lo and behold, there troponin is elevated above baseline. Those kinds of patients at our facility or other similar facilities. Let's just say we don't have an interventional Cardiologists who's gonna be available in the next 24 hours ought to come to a tertiary center e. Abbott, because they'll need that cath Correct. No reason we treat them that way is because people that have had s T segment changes on their e k G or positive biomarkers, particularly or recent positive stress test have an improved outcome with an early invasive strategy, meaning and by early invasive, I mean angioplasty and stenting when appropriate. So those are the people who benefit from going directly or fairly quickly to the cath lab. There's a segment of the population that doesn't necessarily have toe have that, and that's where we get into a level three. What, what we're talking about thes air people who've got fairly classic symptoms, but they don't have any of the other high risk features. So the level threes are the people that otherwise have high risk for coronary artery disease. Diabetics, prior history of corner vascular disease, etcetera, who we feel should probably be kept locally in the hospital and then received the stress test. If the stress test is markedly abnormal, or if they have recurrence of symptoms that they can't make go away really easily. If the stress test is abnormal now you're in the level two category or if they have recurrence of symptoms, they can't make go away. You're now in the Level two category, so they hold on to these people. If the stress test looks okay, those people can probably be safely discharged. Essentially, what you're saying, then, just to briefly review level three, I think we'd all agree that these air these air not are low risk. No patients, but they happen to not have those findings on the K G or biomarkers that we would hope would just be the slam dunk. But they're concerning enough when we run them through, and we'll get to this in a little bit because I think you know where I'm going with this, um, various accelerated diagnostic pathways or protocols. But these air patients that we shouldn't have to think too hard about if their story is reasonable, they have the risk factors they need. Mawr work up provocative testing and the like because then they'll declare themselves okay. This does not appear to be cardiac. Or you know what? You just bumped yourself up to a level two and you're going to do better if we actually do that. That's correct. With an invasive strategy. Once you're in the Level two zone. Okay, fair enough. So I think that what we're bleeding into now is is what differs level three from level four. So maybe you could talk about that a little bit. And how we as primary clear primary care clinicians, emergency clinicians should be approaching these ultimately lower risk patients? Well, you know, level threes or people who have what you feel to be a prior probability of having coronary artery disease that's high. What we have is really a modified Timmy risk score, taking kind of the most important features from the Timmy score and say, if you have any of these. Your prior probability of having the disease is high enough that we think that it's best to do. Initially, the recommendation was that you actually even admit the patient to the hospital and do the stress test before they're discharged. Now that has not been validated. Perspectively to say. Can we spend some of these people home? Can't do all these people have to be admitted. I can't tell you affirmatively that that's absolutely the best way to do this. You can protocal eyes, medicine toe a point, you know, to do that type of study would require thousands and thousands and thousands of patients and multi centers and whatnot. So this was our best guesstimate the safest way to treat these people. If you're 35 year old smoker and has classic symptoms, they probably need some kind of a stress test, you know, or some type of provocative or imaging you know, being a CT corner angiogram or be it a stress test of some capacity if they don't have those other high risk features and they're symptom free. And they've ruled out for a myocardial infarction, meaning you've had cereal, cardiac enzymes and proponents that air negative. Whether or not you can send those people home are based on those type of criteria. And then for kicks, we threw in level five for those people who are obviously non cardiac eyes. There any plug that you'd like to make for Minneapolis Heart Institute? You guys have been fantastic. I think, in terms of producing fairly well founded algorithmic approaches for a lot of us out there. Is there anything that you'd like to talk about with regard to mh I in that? Yeah, there's an app for that. Fantastic. Um, waiting for the Minneapolis Heart Institute app. And we have all of our protocols on a nap that you can download on the APP store. It's works both for Android in in Apple. Uh, products. Um, it's got all of our protocols. It's got our acute coronary syndrome protocols. Got all of our cardiovascular emergencies protocols. Cool it for out of hospital cardiac arrest. Uh, ECMO, e cpr, all of the other cardiovascular emergencies. Including, you know, abdominal aortic aneurysm, critical limb ischemia. Uh, sending aortic aneurysm, etcetera, all of theirs around there. Also, there's a huge amount of information on which test when to use in terms of what? What's the best stress test or what's the best test to get for people to try toe? Determine whether or not they've got obstructive coronary artery disease? The new anticoagulants is all on their how to switching anticoagulants. What are the indications? So there's just a huge amount of information right there at your fingertips. Awesome. Well, we've been talking today with Dr Nicholas Burke, Minneapolis Heart Institute. Interventional cardiologists. Thanks so much for your time. We learned to town was fantastic. Yeah, thanks for listening to cardiovascular conversations with Minneapolis Heart Institute. If you haven't already done so, be sure to subscribe to the podcast. And for lots of excellent clinical tools, be sure to check out the APP for Minneapolis Heart. For more information, please also visit Minneapolis Heart Institute at Minneapolis heart dot com. That's mpls heart dot com And don't forget to review us a swell. This is Jason Hicks and I'm Fred Meuse signing off until next time. See you soon. Another member use a reproduction of cardiovascular conversations, is forbidden without the express written consent of Minneapolis Heart Institute or align a Health. Cardiovascular conversations should not be used for legal purposes, and it does not take advertising money. The content is informational only and is not to be used as a substitute for medical decision making or as medical advice. Some of the opinions of the hosts and guests are their own and not those of Minneapolis Heart Institute or align a Health, another one.
