Transcription
I want to continue talking about important STEMI ideas, but also, am I in general? I will start with this: the interpretation of the spectrum of troponin level. I see a lot of fellows not knowing how to interpret troponin values, so I tried to put together a guidance that you cannot find in any guidelines or books. So here are a couple of questions: Does troponin level help distinguish the four major categories of myocardial injury? And when does troponin peak after MI onset? A lot of fellows somehow don't know the answer to that question. So first, before I detail the troponin, I want to quickly remind you of the four major categories of myocardial injuries.
So, one: in order to call myocardial infarction, you need to have a troponin elevation, but also that's not enough; you need to have evidence, clinical evidence of acute ischemia, such as symptoms or EKG abnormalities, mainly dynamic ST elevation or depression or evolving Q waves or deep T inversion over five millimeters. Or the third possibility here is wall motion abnormalities on Echo, plus on top of that, you need to have troponin rise and fall of over 20 percent, uh, when it's rechecked at two to three hours. So if you have those, then you can call it myocardial infarction. Then you distinguish the three types: if it is a setting of demand-supply mismatch, then it would be type 2 MI. And there are two types of type 2 MI: with underlying CAD or with no underlying CAD. Then, if the context suggests the primary coronary process, then it is a type 1 MI, non-STEMI or STEMI. It is important, type 2 MI, to distinguish the type 2 MI with underlying CAD or with no underlying CAD because the long-term prognosis is different. The type 2 MI with underlying CAD is a closer long-term prognosis to type 1 MI.
Now, if you have a troponin elevation but no clinical evidence of ischemia, then this is what we call a non-MI troponin elevation or non-MI myocardial injury. That's an extremely important entity, and in the era of high sensitivity troponin, this is actually the most common cause of troponin elevation in the hospital. It's not type 2 MI; it's non-MI myocardial injury. And there are two types of that: if there is a troponin rise and fall, it will be an acute non-MI myocardial injury; if there is no troponin rise and fall beyond 20, it's a chronic myocardial injury. Those are the patients who have a chronic advanced CKD or chronic cardiomyopathy, chronic advanced heart failure, or elderly with chronic hypoxemia, chronic anemia. Those species may live with a slightly elevated troponin above injury cutoff.
Okay, now how do you distinguish those beside the context? The more you have a pronounced ST abnormality or angina or troponin or Echo, the more you progress from injury to type 1 MI. Specifically regarding troponin, beside the EKG and the context, you may use high-sensitivity troponin to distinguish between those four major types of myocardial injury. Here is a high-sensitivity troponin classification that I made; you will not find this in any book. I try to correlate levels with a diagnosis of what type of MI or injury you have. Now, there can be a lot of overlap, but this is a general guide. There is usually an injury cutoff, which is a 99th percentile for the assay, and keep in mind that there are multiple high-sensitivity troponin assays available. And there are two types of troponin: you have the troponin T and the troponin I, and there are grossly two different types of values and cutoff, one for the high-sensitivity troponin T, which is an assay by Roche, and another one for all of the high-sensitivity troponin I assays, and there are many manufacturers for that. So, for example, at University, we have HS troponin T; at the VA, we have HS troponin I. Cutoffs are different, and importantly, the troponin I is usually four to ten times higher than troponin T for the same degree of myocardial injury. So know that when you get a transfer from another institution using high-sensitivity troponin I and there is a higher discrepancy with higher value, so when your troponin is a thousand, it's the other one could be ten thousand. At lower value, it's three, four times higher; the higher you go up, the larger the discrepancy.
And here is how I classify them again; there is there is potentially a lot of overlap, but above 22 for our assay, through quantity, this is what you start getting injury. Between 22 to 100, it's oftentimes myocardial injury. Between 100 and 2 to 300, it's frequently either non-MI injury or type 2 MI with no CAD. Between 2,300 and a thousand, you're starting to think there is CAD, whether it's type 2 MI with CAD or type 1 MI, non-STEMI type. And above a thousand, this is where you're thinking it's an acute occlusion MI, even if the patient doesn't have a clear STEMI on the EKG. This is an occlusion MI, whether STEMI or STEMI equivalent. Again, there is a lot of overlap, and definitely the type 1 MI, non-STEMI, could be diagnosed with a troponin of a just 22, just above cutoff. The idea though is that those higher, more serious diagnoses can be seen with lower troponin value; however, the less serious, more benign diagnoses here in this area are usually not seen at higher troponin value. Please don't rule out upon MI based on a troponin that is only 40. Yes, you can have type 1 MI in the right context, and here is where you use your EKG and your other features. Another specific cutoff is this: the one thousand. Really, when you have over 1,000 with our assay or 10,000 with a troponin I, it is usually an occluded artery. And like I said, this is kind of my own classification, but there is some data that can support those levels and cutoffs that are used now.
Another idea: how long does it take for high-sensitivity troponin to rise, and how long does it take for it to peak? It takes high-sensitivity troponin one to three hours to rise after MI. It may take up to three hours. If it is less than MI cutoff by three hours, you already ruled out myocardial injury. However, it takes 24 to 36 hours for that troponin to peak in non-reperfused MI, and if you've done PCI early, like in STEMI, it peaks usually about 16 to 18 hours. It peaks earlier and sometimes higher peak but narrower peak and smaller area under the curve of myocardial mass injured. So 24 to 36 hours for peak in non-reperfused MI, 16 to 18 hours in reperfused MI. Notes regarding that idea: one, a high plateaued troponin supports a presentation of over 24 hours; you're bouncing around that plateau here. A very high plateau troponin, thousands for the high-sensitivity troponin T with the minimal delta or with decline retrospectively supports late presentation of STEMI equivalent, more than 24 hours. There is an important idea I want you to know is that in non-STEMI, you have your event here, you have your severe ischemia, then that ischemia resolves, let's say with medical therapy, and the patient is waiting for cath. Now, the troponin will continue to rise until 24 plus hours after the event, even if ischemia is alleviated. Residents and sometimes fellows worry, you know, the troponin is still rising, now the patient is feeling fine, but the troponin is still rising a day later; it's still rising. They think that the ischemia is still ongoing; that's incorrect. The troponin peak reflects the past; you're seeing the past 24, 36 hours ago when you're looking at the troponin peak. So if the troponin keeps rising and the patient is not having chest pain in a non-STEMI setting, this is not ongoing ischemia; this is a troponin seeing the past. Okay, on the other hand, in the case of STEMI, by the time you peak and reach those very high values near plateau, you're already late; you already missed your best reperfusion window. You need to recognize subtle STEMI by EKG early before you reach those very high values. Another thing is after it has peaked and it's declining or you're at the plateau level, you can use you can use the troponin to diagnose recurrent infarction; usually it over 20 percent rise of troponin is the agnostic of recurrent myocardial infarction.
A few other notes related to troponin: here I mentioned that the significant delta of troponin at two to three hours is 20 percent; however, for the low troponin values below that 50 to 100 range, it's 50 percent delta that is significant based on several data. Another important note here with the low troponin below the MI or injury cutoff within that zone, you have a very low troponin zone, either undetectable, less than six usually, or detectable but low, less than 14, with low delta, less than 50 percent. So you have that very low-risk zone that allows you to discharge the patient at two to three hours after presentation to the ED. Now, higher values than that lows on, you know, whether from here all the way 200 or even 2 to 300, frequently, like I explained, do not mean type 1 MI or coronary angiogram; they generally require at least observation and workup, and they look at the underlying context: is it type 1 MI or is it a secondary process causing injury? So you don't always need coronary angio for those patients, but above that very low zone, you need some workup and at least some observation; it depends on the context and other ancillary findings, such as the EKG.
All right, so I'll move to another topic. This is a 64-year-old man with no significant past medical history. He's presenting with 10 hours of intermittent left arm and left jaw pain, started at rest. He's hemodynamically stable, and he has no heart failure. This is his presentation EKG, so look at it and tell me what do you find on it. By the way, the doctors who are involved in the care of that patient initially, they were not very impressed; they saw that this patient has mild ST depression. The question here: this EKG has mild ST depression; is this a non-STEMI, or are there findings suggestive of subtle STEMI? And the answer is: this patient, it's true, he has ST depression diffusely, but it is most pronounced in leads V2 through V4. So whenever you have diffuse ST depression, but it is most pronounced in any of the leads V1 through V4, particularly in a case where you also have a pronounced R wave that is tall and wide in either V1 or V2, as in this case, it is tall and it is wide, more than a box in V2, so it is, beside that ST depression, tall and wide R wave in V1 or V2 and an upright T wave; this is strongly suggestive of a posterior infarct, and this should be treated as a posterior STEMI. And keep in mind, to call it posterior STEMI, that ST depression in the leads V1-V4 only needs to be 0.5 millimeters, simply because normally we have mild ST elevation in those leads, so a little bit of ST depression is already significant in those leads. And this is how that ST elevation would look if you perform posterior lead EKG; that big R will be Q, and you'll have ST elevation with T inversion; that's what that upright T is important, because it suggests posteriority inversion. Now, keep in mind that practically, posterior EKG may not show you this because the posterior leads are very far from the heart, so the whole QRS and ST, everything is shrunk down; that's why the cutoff for ST elevation, the posterior leads, is a half millimeter, but you may not even see it, and I've had posterior infarcts with no ST elevation in V7-V9; you may only have that mild subtle ST depression and most pronounced in V1 through V3. So in this particular patient, the pattern was not recognized at the outside institution; they kept checking troponin, and it eventually went up to over a thousand, 36 hours later, and as I explained earlier, with that troponin T over a thousand, that is strongly suggestive of occlusive MI, and so in retrospect, that supported the diagnosis of posterior MI. By now, unfortunately, he is 48 hours after pain onset; he has no residual chest pain; he was transferred to us; we did a coronary angiogram, so here is what he had: he had a dual LED system, and the LED diagonal has severe stenosis, as we expected. He has an occlusion of the for the second obtuse marginal branch; you see it here with a stump, okay, and he also had severe RCA disease, a proximal and this. So you know, he has occlusion of the OM; it's 48 hours late; he's not having any ongoing chest pain anymore; PCI of that OM is not definitely indicated per the old trial that I discussed in prior talks, so you may just refer the patient for CABG of the LED and the RCA or perform PCI of the LED and RCA, and that's the reason why, like I explained, it's still useful to perform coronary angiography late in those patients. Let's say though, here I decided to give this patient the benefit of the doubt, and they tried to recanalize that OM, and let's say that I also want to refer this patient for CABG for his multivessel disease. So how can I time things? How can I recanalize the OM in a timely fashion, yet also refer the patient for CABG in a timely fashion? We do just angioplasty of that OM; again, it's a questionable indication, but I wanted to give the patient the benefit of the dog, so we wire it and open it with balloon to obtain a decent angioplasty result with TIMI flow, no stenting, no Clopidogrel, and then we refer the patient for CABG that can be performed one to seven days later, and the LED and RCA disease; this is not what I would call a stable CAD disease; this is the multivessel disease that you see in a patient with a STEMI, as multiple trials have shown, including what we call the COMPLETE trial and the recently presented and published BioVasC trial. Non-culprit disease in STEMI is an unstable disease that has a significant risk of progressing to MI in the next six weeks and especially within the next year. So while this disease might have been pre-existent to his event, by definition, the multivessel disease you see in a STEMI is unstable disease, even the non-culprit disease is unstable, and that's why we recanalize non-culprit, even asymptomatic disease in the setting of STEMI or non-STEMI.
This is another case: a patient presents with chest pain that has lasted two to three hours earlier today and has now resolved, and we're three hours away from his chest pain. His EKG is shown; should he undergo emergency perfusion? If you look at this EKG at first glance, it looks unremarkable, but if you look carefully, there are a lot of subtle findings: one, you do have ST depression in V1 through V3, isolated ST depression in V1 through V3, which again, in this patient coming with chest pain, it would worry me; not just ST depression, it's mild, half a millimeter, which is already significant in the right context, but you also have big and wide R wave, big R wave in V2 and wide and wide R wave in V1 with an upright T. So this is already consistent with the posterior injury and the right compact context, but not just this: you have pronounced QRS in all the inferior leads, 2, 3, and aVF, which in the right context in this patient may suggest evolving Q waves. And not just this, there is a third major finding here: the morphology of the ST, especially in V5 and V6; if that was all you had, that ST morphology in V5 and V6, you may call this, this is just early repolarization; however, in the context of the other findings, this ST morphology in V5 and V6 is concerning for STEMI; it's subtle ST elevation with somewhat is shrinking QRS; early repolarization, you usually have big QRS here; you have an ST elevation that is subtle, especially in V6 with a shrinking QRS. So that is actually, in conjunction with the other findings, concerning for a lateral STEMI. So now you have multiple indicators of posterior, inferior, and lateral STEMI. So although it is subtle, this is, in my opinion, is subtle STEMI, and he should qualify for emergency perfusion. Unfortunately, most doctors will overlook such EKG, and they will only be alerted when 24 hours later the troponin is over a thousand or over 10,000 for the troponin I, but by then, troponin is looking at the past; by then, you're already over 24 hours late. So you really want to see the present through the EKG; the troponin will help you make a diagnosis when it's already quite late; the troponin level. And this is another even more subtle EKG, and look at the EKG; he has again subtle ST depression in V1-V3 here; R wave is not big yet; it will become big as in posterior Q waves eventually, and you have another finding; look at that ST. Beside the ST depression in V1-V3, the ST-T morphology in V5-V6 on an aberrant beat is quite concerning; you have what we call the domed ST-T morphology; look, if this patient was asymptomatic or if I was seeing him in clinic with some vague symptoms as an outpatient, I would not worry about this EKG morphology V5-V6, but in this context with those ST depressions here and that ST-T morphology, I would worry about the subtle STEMI in this patient, and those are the features you can use in those subtle cases. So this is the domed morphology here that I described; okay, this is that domed fused ST-T in one dome, one convex dome; you can have it like this; it could be like that. The other morphology I described here is that you're starting to have a Q wave and is shrinking QRS along with ST elevation that supersedes and size the whole QRS or comes close in size to the whole QRS, or if you have also ST elevation with terminal T inversion; that's also concerning for an injury. I wouldn't call this Wellens; I would call it Wellens if you don't have a Q and pronounced acceleration, but if you have Q and/or significant acceleration, this pattern wouldn't be called Wellens; it would be called STEMI. So those morphologies, along with the posterior injury idea, suggest what we call posterior STEMI in both those patients, and both those patients eventually had very high troponin value that fit with occlusive MI, and both of them had occlusions of obtuse marginal branches, large obtuse marginal branches.
Okay, so mild ST elevation below guideline cut point that is having a morphology consistent with the STEMI, or if you have evolving Q waves with it, as in this particular case, this is usually subtle STEMI and would qualify for primary emergent PCI if chest pain is ongoing or if chest pain is less than 24 hours, even if it is even if it is no longer ongoing, as in this particular patient here. If the pain is over 24 hours and the patient is no longer having chest pain, you should still do coronary angiogram, as I did in that first case here; you should still do coronary angiogram; however, if the artery is occluded and troponin is in the very high occluded range, confirming a significant large STEMI equivalent myocardial injury, then this patient would fall under OASIS trial, and he has a questionable PCI benefit. So definitely do not give fibrinolytics below those cut points; you need to have different STEMI to do fibrinolytics, not subtle STEMI, but do primary PCI. Now, in those patients, even when late, as I showed in the case earlier, I may more readily do PCI even late in those patients with subtle STEMI, as I would in non-STEMI, where there is no timeline cut off for benefit of PCI. This is particularly the case in those late subtle STEMI if the troponin is below the STEMI levels that I defined earlier, which indicate that the patient did not have a large area of myocardial loss. You know, sometimes those subtle cases may be managed in between STEMI and non-STEMI, but to give you the definite answer, they are best managed emergently as a STEMI, and you may ask yourself: why is ST elevation so so mild in those cases that I've shown? There are several reasons; one of them that could justify late PCI and that could justify managing them as non-STEMI to a degree is the fact that ST elevation is so mild because you have some collateral flow that limits the injury; you have maybe this lesion was chronically 90%, and now it occluded, and so you already have a grade 3 collateral that limits the injury and limits the elevation, or you may have an artery that spontaneously canalizes and it's subtotal at this point rather than total occlusion, which also limits the injury, or you have ischemic preconditioning, as I explained in a prior talk; all those who will limit the ST elevation and will limit the myocardial injury and may justify later benefit from PCI, and they may explain why sometimes the troponin may not rise to STEMI levels, although it may, in all the cases I've shown today, it it throws to a STEMI occlusive levels the troponin. Another explanation is that MRI area may be large but not well seen by EKG 12-lead; that's why it's often occurring in posterior and lateral STEMI more than it occurs in anterior STEMI, and/or it could be the third option is that it's a small MI territory, you know, a relatively small diagonal or small OM that is not well seen by the EKG 12-lead. So this subtle STEMI and STEMI equivalent EKGs have been put together by a group in Minnesota, and they have called them OMI, subtle occlusion MI. I prefer to use the term subtle STEMI and STEMI equivalent, which is the term I've used way before the Minnesota group described that OMI, but be familiar with that term and be familiar with that entity, subtle STEMI.
So those are examples of subtle STEMI, including the ones I just showed: basically subtle ST elevation but morphology consistent with STEMI, sometimes with a subtle or glaring reciprocal ST depression or T inversion, sometimes with evolving Q waves, and sometimes with a shrinking QRS; sometimes you have subtle ST elevation, but the ST depression is more obvious, and that will be a hint to the fact that ST elevation is real and it's a subtle STEMI. Again, sometimes the evolving Q waves or the shrinking QRS. Then the second the second big entity is the ST depression maximal in any of the leads we went through before, indicating posterior OMI. Then you have the winter hyperacute wave, which I described in my ST talk; those are basically tall hyperacute T waves with an upsloping ST depression, mainly in the anterior leads, and they indicate an anterior MI with an occluded LAD; there are those that subgroup of patients that may never progress to ST elevation; they are just stuck at the phase of hyperacute T wave with an upsloping ST depression; those should be managed as a STEMI. Then you have the category of left bundle branch block or ventricular pacing with discordant ST elevation, more than 25 percent of the QRS height.
I'll move on to another idea here. This is a patient who presents a severe back pain for the last couple of days. What is this EKG? What does it suggest? So you have ST depression in over six leads, pronounce ST depression in more than six leads with ST elevation in V1 or aVR; this is not a STEMI, but it is what we call a high-risk non-STEMI with extensive subendocardial ischemia, suggestive of either three-vessel disease and/or left main disease. So again, diffuse severe ST depression in more than six leads with ST elevation in V1 and/or aVR; it's usually left main or three-vessel CAD, high-risk non-STEMI, not a STEMI. The idea is when you have diffuse subendocardial ischemia, will diffuse ST depression; you will get ST elevation opposite to the heart; this is the ST depression vector, vector, those black arrows, and so we'll get opposite, mirror image ST elevation in the opposite leads, which happen to be V1 and aVR, which look away from the heart; so you get ST elevation in those leads. Another explanation is that when you have severe left main and proximal LAD ischemia, you can get injury at the very base of the heart; this big white arrow here, which can cause ST elevation in V1 and aVR. So that's the explanation of why we get ST elevation V1 and aVR opposite to diffuse ST depression, but also basal septal injury. Okay, an important idea is, like I said, you get ST elevation in V1 and/or aVR, but if ST elevation is more pronounced in aVR than in V1, that's more concerning for left main, especially when ST elevation is over 1.5 millimeter and more pronounced in aVR than V1. If ST elevation is equal in aVR and V1 or more pronounced in V1, it's usually not left main; I mean, it's very serious with this EKG; it would be more vessel ischemia or proximal LAD than a left main. So that's why that aVR is often worrisome. Keep in mind though, to worry about those elevations in aVR and V1, they must be accompanied by ST depression in other leads, diffuse depression in more leads, not just ST elevation in aVR. And like I said, this is not STEMI, but those are the European non-STEMI guidelines, and they suggest you…
Treat it almost like a STEMI in a sense that you need an immediate invasive strategy, less than two hours, in those non-STEMI patients. Uh, I don't always take all those diffuse, diffuse ST depression urgently to the cath lab. I take into account the depth of the ST depression, the height of the ST elevation in AVR, and especially the persistence of that. Frequently, you get this pattern and during chest pain, then you know with medical therapy early on, within the first 15 minutes, that EKG improves and the patient is chest pain-free. I think it's no longer emergent; you should still do it soon, within the next few hours, but I don't think it's any longer emergent. Okay, so take into account persistence of ischemia and the depth of those ST abnormalities.
Another important idea here is that when you have this pattern, it's not always a primary coronary process with left main ischemia, even when you have that pronounced ST elevation AVR. Keep in mind that it could be a secondary coronary ischemia, and I've seen that pattern frequently. Patients who are coming with septic shock, profound hypoxemia, profound anemia, profoundly bleed, you can get secondary myocardial ischemia with diffuse ST-segment abnormalities and ST elevation in AVR and V1. So take the context into account; it may be profound demand-supply mismatch, not a primary coronary process.
This is another case. So this is a recent case we had a week ago. It's a 71-year-old man; he has metastatic melanoma. He presents with acute chest pain, no shock. So this is his EKG, and this is EKG 15 minutes later. Can somebody tell me what's the diagnosis here? So this patient has diffused ST depression with ST elevation in AVR and V1, more pronounced in AVR than V1 and over one and a half millimeters. So it's strongly concerning for left main disease. This is, by the way, not a posterior STEMI, evidently because ST depression is not most pronounced in V1 through V3; it's diffuse and more pronounced actually in the lateral leads. Now, the difference between this patient and the prior patient I showed is that this patient also has some ST elevation in the inferior leads. Okay, so while the totality of the EKG suggests definitely left main ischemia, plus or minus three-vessel ischemia, he also has ST elevation inferior leads, particularly on that EKG you see 12, in these three; it's also II, III, aVF. So one may think, is this an inferior MI? And we are taught that when you have simultaneous ST elevations and ST depressions, the ST elevation is the primary process, while the ST depression is reciprocal to the ST elevation. This type of EKG is an exception, and actually this EKG is fairly common. It suggests that the patient has left main and/or three-vessel ischemia. In this case, it is left main ischemia with an RCA CTO, so that the ischemia is much more pronounced in the inferior wall. When the left main gets ischemic, the RCA, which is being supplied by collaterals from the left, and the left main gets more ischemic than any other territory and gets so ischemic that you develop an inferior, not just ST depression, you develop ST elevation injury. It's very important to understand that because this is not a primary RCA STEMI. You do need to take this patient emergently to the lab; you will find an RCA occlusion, but please don't make the mistake of trying to wire the RCA; that's not the culprit. The RCA, that EKG strongly suggests the RCA is actually a CTO, and the main culprit here is the left main with collaterals to the RCA. Now that is indeed what this patient had. So he had a very tight, critical stenosis of the left main, and he had an occluded RCA, and you can see the collaterals to the RCA. Those are what we call Grade Three collaterals, meaning you can see reconstitution of the epicardial vessel, in this case the epicardial PDA and the epicardial distal RCA, and this is the RCA; it is occluded, but somebody may get tempted with this EKG to try to wire it; that will be a wrong next step. What is acute here is the left main; the RCA, the CTO, both by EKG feature and by the fact that you have Grade Three collaterals. Grade Three collaterals take at least, usually two weeks, to form, as I explained in a prior talk, so they do suggest some chronicity. Now, evidently, you could have 90 percent for several months and form more collaterals and now have 100 percent right now. So Grade Three collaterals don't absolutely prove that you, in fact, or that your occlusion in the right is not acute, but putting everything together, this is a CTO, and what you should fix is the left main. My colleague did this case, and they did the right thing here; they did not bother going after the right; they stented the ostium of the left main.
I have some other ideas that are important as well. I will move to a totally different topic that is very important because there are no good guidelines regarding the management of left ventricular thrombus, and most of the data guiding us are very old. So I tried to put together how to manage LV thrombus, giving you a straightforward algorithm and management strategy that applies to acute MI with thrombus; it can apply also to non-ischemic cardiomyopathy LV thrombus or chronic cardiomyopathy LV thrombus. So this is a case: 65-year-old man, he had anterior STEMI four months ago; he received primary PCI; his EF was 25 with apical akinesis and LV thrombus. He was placed on warfarin plus clopidogrel. Now, four months later on echo, his EF has improved; his apex has improved; it's still abnormal, but it has improved; LV thrombus has resolved. Should we stop anticoagulation, and can you use NOAC instead of warfarin? Keep that question in mind; I'm going to give you some explanation, and I'll try to answer it again. So LV thrombus is seen in five to ten percent in the PCI area, particularly with anteroapical infarct. You need to know the timeline; it usually forms within the first week, three to six days after MI, most thrombi form in that time frame, and actually it can commonly form in the first 24 hours; at least 25 percent of thrombi form fairly quickly in the first 24 hours. If your thrombus forms beyond the first week, particularly up to two weeks, in the absence of anticoagulation, what's the risk of stroke or embolization with LV thrombus? The risk is about 10 to 15 percent versus one percent in patients who don't have LV thrombus or atrial fibrillation who have a STEMI but no LV thrombus or atrial fibrillation. In two old landmark analyses, nearly all embolic events occurred within three months of MI, and these are some of the references; most of them are, as you can see, from the 80s and 90s. This is where we got the understanding of the natural history of LV thrombus. So nearly all embolic events occur within three months of MI, and mostly in the first two weeks. After this period, LV thrombus becomes organized, scarred, and unlikely to embolize. In fact, after three months, the organized thrombus has a beneficial effect as it adheres to the dyskinetic apex; it kind of grabs the edges of the impacted territory and may prevent further MI, bad remodeling, and zone expansion, and it can reduce the paradoxical dyskinetic myocardial motion by a plugging effect. So it may be good to have a chronic, organized thrombus; it reduces dyskinesia. With anticoagulation, 60 to 80 percent of thrombi resolve; the rest become organized, fibrotic, and laminated. Now, which features are concerning for late embolization beyond three months? Some studies suggest that a mobile or a pedunculated thrombus bulging in the LV has the highest common embolization than a laminated mural thrombus; that is likely true. However, up to 40 percent of emboli occur in patients without pedunculated or mobile morphology. Patients with a basically laminated, non-mobile thrombus. So having a laminated, non-mobile morphology can be reassuring, but that's not absolutely reassuring since a substantial proportion of emboli still arise from those thrombi. So more importantly than the pedunculating morphology, the single most important predictor of embolization from LV thrombus is persistent severe heart failure or persistent severe akinesis or severe LV dysfunction, as has been shown in a couple of papers, including one recent in JACC 2020. So that's the most important determinant of whether you should anticoagulate beyond the three months. And uh, these are some of the guidelines. The STEMI guidelines from 2013 recommend warfarin therapy for LV thrombus in the STEMI setting, and they suggest limiting it to three months. This strong guideline from 2014 suggests also three months of warfarin in patients with ischemic stroke or TIA in the setting of acute MI complicated by LV thrombus. Interestingly, even in patients who had a stroke from an LV thrombus, they only recommended three months of anticoagulation, not a lifelong. A lot of us treat those patients with warfarin forever; maybe we're overtreating those patients. And this is a text of the AHA stroke guidelines: After three months, the risk of embolization diminishes as thrombus becomes organized, fibrotic, and adherent. However, patients with persistent mobile or protruding thrombus may remain at increased risk of stroke and other embolic events beyond three months. So they are not definitive about what to do beyond three months, but they give a definite indication for three months only; beyond that, it's questionable.
Here is how I put it together myself; this is my algorithm. So one, perform echo with contrast within 72 hours of an event. If the echo is negative but the patient has a high-risk feature, large apical akinesis or dyskinesis, repeat the echo with contrast at two weeks and consider MRI, CT. There is an issue of sensitivity; echo without contrast has less than 50 percent sensitivity for LV thrombus; echo with contrast has 64 percent sensitivity, and MRI and CT have close to 100 percent sensitivity. That's why in some of the old studies there are, there is a substantial proportion of patients of patients who had post-MI stroke who had no LV thrombus or atrial fibrillation, and it's assumed that those patients have an LV thrombus that was missed by echo. Okay, so if you have high-risk features, you know, one, repeat the echo two weeks with contrast for sure; you need contrast and may consider MRI, CT. Now, if LV thrombus is found, what do you do? You give either warfarin or NOAC; you don't absolutely need to give warfarin; NOAC is acceptable, and I will show that in a little bit. You give that for three months, then you repeat the echo at three months. At three months, you decide to continue anticoagulation if all those criteria are met: one, the bleeding risk is not high; two, you have one of those two ideas here: the LV thrombus persists and it is mobile and pedunculated, or much more importantly, even if the LV thrombus has gone, if you have severe apical dysfunction or heart failure, if those persist regardless of persistence of LV thrombus, you should strongly consider giving anticoagulation beyond three months. So basically, you continue it beyond three months if the bleeding risk is acceptable and either one of those two is present: the LV thrombus persists and is mobile and pedunculated, or it doesn't persist, but you have severe dyskinesia or akinesis, large area of akinesis still, or you have severe heart failure. On the other hand, if you have somebody who's LV thrombus has resolved or persists but it's small and laminated now, and the apex area has mostly recovered, there is still a small area of hypo- or akinesis, but the apex has mostly recovered, and the patient has no heart failure, then I would not continue anticoagulation beyond three months; then you would stop anticoagulation in those patients. Now, if you stop it, repeat echo within the next three months to detect LV thrombus recurrence. LV thrombus recurs in 15 percent of patients; this is based on a JACC review from 2022. I will show you the NOAC. So NOAC compared to warfarin; keep in mind that there is no, there has never been a randomized trial of warfarin versus no warfarin in patients with LV thrombus. Warfarin use is based on old retrospective data; they have been used and found to be comparable to warfarin in several retrospective studies and in one meta-analysis, this one. There are two small randomized trials, one from Egypt and one from Israel; this is the more recent one from Israel. They found that NOAC is non-inferior to warfarin in patients with LV thrombus, like me. What is even more important is thrombus resolution, because like I said, even late persistent thrombus doesn't worry me much if it is organized and laminated; it can have helpful effects, like I said; it can improve and reduce myocardial LV remodeling. What would worry me more is, does he still have a severely reduced EF, in general severe dysfunction of the apex, or does he have severe heart failure? You know, it's a patient who keeps coming with congestion; that's what I worry more about, even if it is not there. If you have severe apical dysfunction, that persistent akinesis and heart failure, it's going to come back once you stop anticoagulation, or it has a high likelihood of coming back, and when it comes back, that freshly reformed thrombus will have a significant risk of embolization. It's even worse for it to disappear and reappear than to stay there; when it reappears, it will take time for it again to get organized again, so there will be a time frame, as it is reappearing, where you have an increased risk of embolization, higher than if it never resolves.
Excellent question. So the question is to give prophylactically in a patient with a large akinetic area and especially with heart failure, clinically even with no evidence of LV thrombus, to give them anticoagulation. I think this is an outdated strategy by today's standards; I prefer not to give anticoagulation to such patients. Rather, if you really have serious concern about apical thrombus that is that is formed and missed on your echo or that will form, is to do what I highlight here under number one: is to repeat your echo again at two weeks and probably, if you're that concerned, rather than put them on prophylactic anticoagulation without being certain, just do MRI, CT on him. So to answer the case I showed, the patient's apex has improved, the LV thrombus has resolved; should he stop anticoagulation? Probably yes, stop anticoagulation; the risk of emboli is very low at three months, even with persistent LV thrombus, as long as thrombus is laminated, and NOAC versus warfarin, I answer that yes, either one is okay, but this patient doesn't need any anymore.
I have some material that is highly relevant for board exams; they always ask those questions on board exams. I had those on my initial board certification, on my recertification. So I want to give some board questions related to conduction disease and STEMI. So one, does right bundle branch block occur with inferior or anterior STEMI? Can anybody answer that question? Right bundle branch block occurs typically with anterior STEMI because the right bundle is supplied by the first septal perforator; that's why when we do alcohol septal ablation for HOCM, have the patient get right bundle branch block. So the right bundle is from the septal of the LAD, so it's an LAD, not an RCA. Number two, in STEMI, which one implies the worst prognosis, left bundle or right bundle branch block, and along this question, does left bundle branch block occur with inferior or anterior STEMI? Okay, here is the answer. So right bundle and left anterior fascicle are supplied by the LAD first septal, so they imply proximal LAD MI. Conversely, the HIS, the main left bundle, and the left posterior fascicle have a dual supply from the LAD septal branches, using multiple septal branches, not just one, and the AV nodal artery. So in order to impact those, left bundle and left posterior fascicle, it is difficult to affect them, and in order to affect them, you typically need to have multivessel disease; you, for example, you have an occluded LAD, but you also have a CTO of the right or a critical right, or vice versa. And actually, if you look at a registry like GUSTO I, the culprit is kind of half and half, LAD or RCA culprit, to have a left bundle branch block in MI. But more importantly, it's very rare to have left bundle branch block in MI; only one percent of STEMI had left bundle branch block. Most left bundle branch blocks are cardiomyopathy, hypertensive, or chronic ischemic cardiomyopathy, valvular cardiomyopathy; they are not acute ischemia. Okay, and if it happens from acute ischemia, it's usually multivessel disease. Both right bundle branch block and left bundle branch block are associated with the same increase in mortality; left bundle branch block because it implies a large infarct with multivessel disease; right bundle branch block because it implies a proximal LAD. In fact, before that, I always tell fellows in the cath lab that first septal is a holy vessel; if you M4 the LAD after the first septal, you may not get cardiogenic shock; you infarct before the first septal, you get cardiogenic shock. So, and that's why right bundle branch block is associated with high mortality because it implies an infarct before the first septal. So new bundle branch block is associated with right or left, with two- to six-fold increase in in-hospital mortality, heart failure, and renal failure because it correlates with a more extensive infarction, higher risk of cardiogenic shock. Another thing is that those acute bundle branch blocks, even without having a AV block, they do correlate with a high risk of progression to complete AV block, 20 to 40 percent. Now, usually not a permanent complete AV block; it usually resolves, but it's an AV block that persists usually for days and requires temporary pacing. So higher risk of progression to complete AV block; the bad prognosis, though, is not due to that progression to complete AV block; it's due to the association with a much larger infarct and cardiogenic shock. So this is a board question that I had: One, is a standby temporary pacemaker, transvenous pacemaker, indicated in acute bundle branch block, even without AV block? And this is the answer; this is based on the old guidelines before 2013, all the STEMI guidelines. It's one, it has to be in the setting of anterior MI, which is where you get those bundle branch blocks; you typically need to have some LAD involvement to have a right or left bundle branch block. So in the setting of anterior MI, you're having a new bundle branch block plus long PR; those are patients where, based on the old guidelines and for board answers, it's still advised to put a temporary transvenous pacemaker prophylactically. This is just a bundle branch block; a new bundle branch block; it, transcutaneous pacing pads, which are the same as the defibrillator pads, are enough, but keep a high alert; 20 to 40 percent risk of progression to complete AV block. But this is the board answer that I had: new bundle branch block plus long PR; they want you to put a temporary transvenous pacemaker.
Now I describe bundle branch blocks; now I want to describe what to do for AV blocks. A patient with inferior STEMI just underwent primary PCI of the proximal RCA; in the CCU, his monitor shows complete AV block with a junctional escape rhythm of 40 beats per minute for 5 minutes, which subsequently resolved; he felt dizzy but did not experience chest pain; reconnaissance; what is the next step? Continue to monitor; place a transvenous pacemaker; give atropine or aminophylline. The answer is A, continue to monitor, and here is the explanation. So complete AV block in the setting of inferior STEMI is usually well tolerated, as in this patient; he was dizzy, but he didn't have significant severe hemodynamic compromise. So it's usually well tolerated and does not require temporary pacing. So even if he wasn't in persistent AV block, here I made it easy; I said it stopped spontaneously in five minutes, but let's say he was in persistent AV block; even then he would not need temporary pacing unless, so it's persistent plus refractory to medication, atropine or aminophylline, plus associated with severe symptoms or hemodynamic compromise, which is usually more seen in those inferior infarcts with RV shock. The reason it's benign is that the AV block is at another level, and sometimes, especially in the first day, it's a purely high AV block. So if symptomatic, if persistent and symptomatic, you may treat it with atropine up to two milligrams, mainly effective in the first 24 hours, or aminophylline, which is effective the first 24 hours or beyond the first 24 hours. Okay, so it's persistent and symptomatic and refractory to meds; this is when you consider pacing. If it is persistent and he's minimally symptomatic and no hemodynamic compromise, you may not give it anything. This is the last question: A patient with anterior STEMI just underwent primary PCI was a proximal LAD; so this one is anterior STEMI; in the cardiac care unit, his monitor shows AV block, complete AV block with a slow escape for only 15 seconds, which subsequently resolved; he feels well; his EKG shows right bundle branch block, again proximal LAD, right bundle branch block, and residual anterior ST elevation with Q waves; what is the next step? Monitor; transvenous pacemaker; atropine; aminophylline. The answer here is B, place a transvenous pacemaker. Another question I want to ask you: How effective is atropine and aminophylline in those patients? And let's say this patient had a persistent AV block; should you try atropine and aminophylline? So the answer is that atropine and aminophylline are not effective, and here's the explanation. Complete AV block in the setting of anterior STEMI requires transvenous pacemaker placement, even if transient; it is a high-risk rhythm and associated with a four-fold increase of mortality, mainly related to the large size of the infarct and pump failure rather than AV block. Atropine and aminophylline are ineffective in infranodal block, and there is a theoretical concern about aggravating, actually, the infranodal conduction, simply because you increase the sinus rate when you give atropine and aminophylline; when you increase the sinus rate and the atrial bombardment of the infranodal area, you get what we call concealed conduction that further reduces how many of those sinus beats get through the infranodal area. So in theory, you may aggravate the infranodal conduction because of that concealed conduction process. So the ACC 2018 bradycardia guideline suggests giving atropine for acute MI AV block at the nodal level; they suggest against trying atropine in infranodal AV block. So they don't say directly, don't use atropine in anterior MI; they say don't use it in infranodal block, but indirectly, by all we know, they are kind of suggesting to avoid it in anterior MI.