Chapters Transcript Video Ischemic Heart Disease Click here to view presentation deck Back to Symposium Hi, good afternoon, everybody. Thank you for joining us this afternoon. And after lunch hour, I know it can be a little tiring, but thanks for uh hanging out with us today. So when we were given this talk, um the three of us got together and we're like, how do we come up with a plan so that we, it's all cohesive and uh there's some take home points. So the crux of the matter is when a patient walks into our office and they have chest pain, the onus is on us to do the right thing. And the question is the moment we type into epic. Uh What kind of a test we want? A million tests pop up. There's um um there's uh exercise stress test, there's exercise stress echo, there's pharmacological stress, nuclear, there's a pet scan, there's a stress MRI there's a coronary CT A. So the bottom line of the evaluation is, what are we trying to achieve? What we're trying to achieve is to risk stratify patients into lower intermediate high risk categories. We're trying to reduce mortality, we're trying to reduce clinical events and we're trying to assess all these things while we take the patient's um characteristics into account, whenever we talk to a patient, we're automatically inherently applying Bay theorem to our um patient's life. We are taking the pre-test probability of disease. And we are considering what the outcome of our testing is going to be and finally deciding how we're going to manage the patient. And all of that goes into uh choosing the right test. Main considerations for uh evaluation include the clinical evaluation, the clinical perspective, the functional capacity of the patient, the left ventricular function and the coronary anatomy. And the whole idea behind stress testing is identifying and defining these things so that we can tell the patient this is the risk of your disease. This is the risk of me sending you for an invasive angiogram and the risks of the angiogram are less or the risks of the benefits of the angiogram outweigh the risks and hence it's beneficial to you. So how do we get to that point? The factors associated with higher risk of mace on the left side, we have a whole host of factors that are patient dependent. These occur when we review the chart, these occur when we talk to the patient on the right side. Yes, that's the data we get after we've spoken to the patient, after we've talked to them about their primary risk factors, but we cannot take testing in isolation without putting it together with the patient. Both of those things need to be taken into account. And why is that? Where do we have proof for such a concept? And we do. So, the history is basically a paramount part of any form of evaluation. If you look at the graph, um there's seven factors that they list out. None of those factors are based on the results of testing. All of those factors are risk factors that the patient comes to you with. Have you ever had heart failure? Do you have a history of hypertension? Are you older than 75 years of age? Do you have diabetes? Do you have, have you had strokes? Do you have evidence of peripheral arterial disease? Are you a smoker? Most of these things can be derived from the history of the patient themselves. And if you look at the graph, the population at risk decreases as the number of those risk factors increase. And even though the numbers for higher number of risk factors are lower, the incidence of cardiovascular disease death and M I or strokes is much higher. The moment we have multiple risk factors in the same patient. So even before we order a test, we already know who is a high risk patient who is gonna have disease and who are we going to have a lot of things to do for? So what are the tools at our disposal whenever I pull this graph up the med students who've just done their patho or their step one or step two, they know exactly what we're talking about. And as you get to the fellowship that level, they're like, I don't know, I just know what test to order don't bother me with these things. And the thing is the physiological aspect of cardiac disease is just as important to understand, to realize what, what test that we want to order. The sensitivity and specificity of each test is determined by where they are on this curve. The first thing that changes when we have obstructive epicardial disease is that we have perfusion anomalies. After perfusion anomalies, we get diastolic dysfunction, then we proceed to systolic dysfunction, then we get ischemic changes and then we get genal symptoms. So when patients come to us and tell us I'm having shortness of breath, the shortness of breath, most of the time is going to be because of diastolic dysfunction as opposed to having se severe systolic dysfunction or other ischemic changes because the first step is that A TP is necessary for calcium cycling in the left ventricle. And if your calcium cycling is not appropriate, your heart gets stiffened every time we exercise and that leads to pulmonary edema and leads to shortness of breath. So when a patient comes to us and says I'm short of breath, we have to start thinking of ischemic heart disease and as the symptoms progress, the sensitivity and the specificity of a finding disease become even more. Uh even higher. And in the past when these things came about, the only thing we really had was EKG S. So EKG S, they are very, very good tests. If they're positive, their spec specificity is very high when we have a positive treadmill stress test. But because of such a high specificity, we are going to miss changes that haven't occurred by the time those ischemic EKG changes take place, we're gonna miss diastolic dysfunction, We're gonna miss perfusion anomalies, which is where our rest of our stress testing comes into play. Perfusion anomalies with a spec study are one of the first changes that take place. We can test that with a spec study. We can do a pet study, we can do an MRI study. After that, we have diastolic changes which can be evaluated with an echocardiogram. Then we have sec uh systolic changes that can be uh detected with echo and MRI. And as we progress up the curve, we see more and more testing. Um um um tests that open up to figuring out what's going on with the patient and lastly to make it even more complicated. Now, we've added coronary CT A to the mix. So now we've taken a physiological change in the heart and said, hey, what do we do with the anatomy of the coronary? How does that come into play? So, choosing the right test for the right patient is very, very important. And I think um Angie uh kind of alluded to this. We need to have a pre-test probability while deciding what test do we want to use? Do we want a test that has a very high negative predictive value? Do you want to rule out a severe obstructive epicardial coronary artery disease or do you want a test that has a very high sensitivity or where does your patient live and where do we want to decide? So, from a framework of evaluation of patients, I put these tests into two or three categories. One is functional assessment, which is how much can they work out or what are the changes that take place in the body? When a patient is exercising, this can be what their heart rate does. Heart rate recovery is a very good prognostic indicator of things to come. Blood pressure changes when people are exercising are very, very important. So that's the functional aspect of it then becomes the anatomy or the anatomical aspect of it, which is defined by the coronary uh CTAs. And the third one is the physiological changes taking place in the myocardium that occurred due to the epicardial disease that take place. Those can be evaluated by any of the functional tests, which can be a stress echo, a stress spect or a stress MRI. So these are the three buckets, overarching buckets that we deal with things that favor use of CT A are going to be things like a patient who's younger does not have severe calcification. You're suspecting they have plaque, but your pre-test probability of severe plaque is low or is a 2530 year old who says that they have chest pain and you suspect some, something like an anomalous coronary artery um to be causing their symptoms. So in those patients go for the CT A, go for AC T A first. If we have a patient who is older, who has smoked their whole life, who has ESRD has diabetes that was uncontrolled for a prolonged period of time. The probability of epicardial coronary artery disease is going to be very high. The probability of having significant calcifications is going to be very high in those te uh patient type of patients choose a test that is going to be able to determine the physiological assessment of the myocardium, choose a test such as a stress echo, A stress MP I or a stress MRI between the stress echo and the stress MP I. The main difference is the patient's uh body habit is if we think we can get, get great pictures from the echocardiogram, echocardio, echocardiogram is great. If we think uh that uh we're not gonna be able to get good pictures from the echo. Do a stress nuclear study, both are level two in the guidelines. The evidence is good when we get a good test. If we don't get a good test, if we get artifacts in either one of the tests both of them are going to be riddled with questions. So where is coronary CT A in all of this? Where do we stand? So the promise and the Scott Hart trials that you talked about were great. So they compared CT versus functional assessment and neither strategy was superior at two years and there we have it both are just as good at two years. However, at five years, the CT scan was much better at preventing uh issues. And why is that? The answer is straightforward. If we think about it, the CT scan will pick up non obstructive plaque, we will be able to tell you your patient has established disease. You're going to have a conversation with your patient saying look, you have non obstructive plaque, you need to be on a statin. Whereas in the older times these patients, they were not getting a prevention therapy because hey, your stress test is normal, you don't need therapy. So the outcomes, the longitude and the long term outcomes are much better with a AC T scan as opposed to a spec not because we're identifying more obstructive disease, but because we're able to identify more non obstructive disease, which we are acting on much sooner. So where does the anatomy part of this lie? Where, how do we decide is anatomy better or is functional stratification better? So there were multiple trials that tried to answer these questions. It all started with the courage trial and the presenters of the ischemia trial. One of the first statements they said is we need to be courageous enough to follow the recommendations of the Courage Trial. The Courage trial basically said that if you have myocardium, that is less than 10% of the myocardium at risk, you can manage them medically without requiring intervention if they remain asymptomatic with maximum medical therapy. And maximum medical therapy is antianginal therapy which includes beta blockers, nitrates controlling blood pressure, preventing worsening of atherosclerotic disease, things like that, the things that are all in the guidelines. So as long as our patient does not have a very high amount of myocardium at risk, we can still manage them noninvasively with just medications. Ischemia trial, took this further because now we have anatomy definition. They excluded patients who had left main disease, proximal led disease. And once again, they tried to evaluate patients on the basis of invasive therapy versus conservative therapy. And on longitudinal outcome, the results were great. Uh conservative therapy works very, very well. Not every, not every lesion needs a stent. So the goal and the overview of ischemia evaluation in our offices is basically we need to decide how we're gonna do noninvasive testing. Is there a high clinical uh pret pre likelihood of disease? Is there a low to moderate um risk of um disease? And then we choose the right test once we choose the right test in chronic stable uh coronary artery disease then we try medical therapy. If we don't have high risk features, if we have high risk features, and if we think that the revascularization is more beneficial than the risk of the disease, then we go ahead and we refer for invasive angiography. Now that being said none of the tests is gold standard. The gold standard still remains as my interventionalist. Tell me the table of truth. So the invasive angiogram will still be the gold standard because we are riddled with artifacts either from calcium, either from um significant subcutaneous tissue, either from contrast, percolation on the coronary CTS from attenuation artifacts in nuclear imaging from other artifacts and echo. So as much as we can risk stratify patients if your patient remains symptomatic and clinically, your evaluation does not match the evaluation that was presented to you by the noninvasive test. The tiebreaker is going to be an invasive uh evaluation and that may be necessary for a lot of patients and it's OK. We none of the tests is wrong. It's just that we don't have 100% answer in a noninvasive fashion. So, noninvasive risk stratification, there's criteria for a high risk patient. But using just the um just what we know about patients, anybody who has left main disease, who has proximal led disease or who has a low ef because they have multiple areas in the heart that are blocked. We know by default, they're gonna have high risk disease. These are things that we don't need to read about. We just look at the patient and we talk to them if they're having persistent symptoms, despite their heart rate being control, blood pressure, being controlled. Uh despite being on two antianginal therapy, then we know they're a high risk patient and we need to send for an invasive angiogram. So although we have all these risk stratification tools, but we also over experience and clinical evaluation, the tools exist inside us if we talk to the patients well, and we know whom to refer for invasive uh strategy and appropriate revascularization. So what do the guidelines say? The first line test is always functional assessment if we can get it done. However, the caveat is that although the specificity is high, the sensitivity is lower. So once again, if the clinical situation does not match the results of your testing, do more testing or refer for an invasive strategy in most patients with established ad using additional imaging modalities is warranted. It's OK to order a second test, it's OK to order another test, we need to give our patients answers so that the bottom line is when they go home, they're at peace and they are on the right therapy. And that's what we're here for. In 2021 the guidelines were updated and cardiac CT was upgraded in recommendations to become one of the first line tests. It's a great test when used in the right patient in the right setting. Repeat imaging of an asymptomatic patient. This commonly comes up into question. My patient had PC I uh several years ago. Currently, they're on isosorbide, they're on beta blockers, they're on aspirin. They're doing fine. Do I need to reimage them? So the, the answer will be if on that initial test, they had residual obstructive disease that was not revascularized or there has been a change in symptom subset. It might be reasonable to offer them a noninvasive evaluation. It's rarely appropriate to repeat a stress test within two years of a prior stress test. Symptomatic patients with C AD or CCT A defined um severe disease. FFR like Angie talked about less than 0.8. They should theoretically be referred for an invasive angiogram and that concludes uh just a basic framework of when to order what test, what each tests mean and how to choose the right patient. Do we have any questions? Published Created by Related Presenters Manik Veer, MD Cardiology View full profile
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