Transcription
Okay, so I will continue talking about the differential diagnosis of Wellens’ syndrome and STEMI equivalents. Okay, so this is a patient, a 56-year-old female, HIV active, cocaine user. She comes in with chest pain off and on for the last five days, including a long severe pain last night. She is chest pain-free now. What is the diagnosis and how urgent is the angiogram? This is Wellens’ syndrome. Now, is it a STEMI though? So I would take this patient to the lab urgently or not urgently? How would you take this patient? Now this, this is at 7:00 PM in the evening. Would you take him right now, or can he wait till the morning?
So, one, I’m going to explain to you how Wellens’ looks exactly. This is truly a Wellens’ syndrome, the way it looks. One, Wellens’ is not a STEMI. So, by definition, you do not have ST elevation over one millimeter. You do tend to have a little bit of ST elevation, as you may see in V2 V3. It tends to be subtle, less than one millimeter. More importantly, it’s a specific morphology. It’s not just biphasic T or inverted T; it’s a specific T morphology where you have a straight, especially you see it here, is straight or convex ST segment that suddenly takes a sharp turn down into a T wave. The sharp turn should be almost 90 degrees into a T wave. So it’s not a shallow curve into a mildly inverted T; it’s a deep turn into an inverted T wave. It might be biphasic, as it looks here in V2, or it might be just deeply inverted T. And in most cases, you have something like that, the deeply inverted T, not biphasic. 75 percent of the cases are deeply inverted; 25 percent are biphasic. You should not have Q waves as well. If you have ST elevation more than one millimeter or Q wave, then this is a STEMI. And actually, you can have the exact same morphology in a STEMI. Keep that in mind. We do not call it Wellens’. So you can have a full-blown ST elevation that eventually progresses to this shape. This is not called Wellens’; this is called STEMI. At one point in STEMI, you do evolve actually into similar morphology of biphasic T and deep T inversion. It’s not Wellens’; it is a STEMI.
Okay, so in this particular case, it’s Wellens’. Another feature of Wellens’ is that those T abnormalities are predominant in leads V2 V3. They usually extend between V1 to V5, but they are very predominant in V2 V3. They are not diffused. So the question now, should we take him to the lab urgently since it is not a STEMI and since the patient is chest pain-free, as is the case in typical Wellens’, you can wait till next day on this patient. If it is in the middle of the day and you want to take him urgently, it is fine, but you do not have to take this patient urgently. You, you can wait till next day, as we did in this patient.
Okay, now what does Wellens’ tell you? Wellens’ tell you, in the original paper in the 1980s by the Wellens’ group, showed you that patients with this pattern, 100 percent of them had severe LAD stenosis proximal to the second septal, and 75 percent of those patients went on to develop a full-blown large infarct if they were left unrevascularized. So it’s a high-risk feature that often progresses to a large infarct. Now what happens if you record that EKG few minutes later? What will happen to that T wave ST elevation? You need to know the pattern of Wellens’, and this is what happens if you record it a few hours later. Typically, the T wave will become deeper and deeper as time goes by. Then eventually, the T wave will start regressing progressively until it becomes normal. This is how, what you need to know. This is a very important slide of how you get Wellens’ and the EKG natural history. In this case, when this patient had chest pain the night before or a few hours before, she had, even though we didn’t document it, she had ST depression or ST elevation transient. Now after the pain resolved and you’re recording EKG afterward, then she developed the Wellens’ biphasic T waves. Then she progressively develops the Wellens’ deep T waves, and the more severe the ischemia, the deeper that T wave. Then she progressively reverses back to biphasic T before normalizing. So Wellens’ means that at some point before you get that EKG, she had a profound ST depression or ST elevation, but now you’re seeing post-ischemia. Wellens’ is a post-ischemic EKG; it’s not an actively ischemic EKG. Hence another reason they tend to be chest pain-free during the EKG recording, during the finding. Hence the reason you can wait until next day to catheterize the patient. Okay, and that will deepen with time, as you can see in V2; it’s getting deeper with time. It’s not that ischemia is getting deeper; it’s a reflection of the initial ischemia that now has resolved or is temporized. This is the cath on this patient. Now you will see this is as bad of a Wellens’ as you can see that mid LAD is subtotally occluded. You have to me too flow; it still has a flow. And if you go to the original publication by Wellens’, 18 of those patients had total LAD occlusion. Yet again, I don’t believe a cath is urgent, and it’s not recommended for it to be urgent as long as she is chest pain-free and no ongoing ST depression or ST elevation. She underwent stent, and she did fine. Actually, her apex has recovered at one-month echocardiography. I’m going to give you other examples of Wellens’ T wave. Those are from my book, so those are two other cases. Again, look at the morphology; know it well. It’s a straight or convex ST segment, very important, then you dive deep into a T wave very sharply, almost 90 degrees, 60 to 90-degree angle. Again, V2 V3 predominantly, a little bit in before V5, but it’s not diffused. This is another case of what we call deep T inversion Wellens’, but again, straight or convex ST and sharp dive into the T in at least one lead in those leads V3 before it’s smoother, but it is steep in V2. Both those patients had severe proximal LAD 90% stenosis, two different patients on the case I showed. Note that this is not a proximal LAD; this is after the first septal; this is mid LAD, and Wellens’ doesn’t have to be proximal LAD. In the original paper, they defined it as a lesion before the second septal, so it could be mid LAD. Those are, this is a summary of all those Wellens’ features: symmetric and deeply inverted T wave or positive-negative biphasic T wave, predominantly in V2 V3, you know, ST elevation, no Q wave. You frequently have a prolonged QT interval, as in any post-ischemic EKG. Post-STEMI, your QT interval will prolong as well. It happens similarly in Wellens’ syndrome. Chest pain-free during the recording.
Those are some cases that people call Wellens’ that are not Wellens’, and I do want you to know those so uh you don’t make misdiagnosis and rush a patient to the cath lab unnecessarily. Case one A, here you see this morphology. Anybody can tell me what this is, and you can put it in the chat box. So this is a patient with ST elevation and fairly deep and fairly abrupt biphasic T wave, but look at the ST; it is more elevated than in Wellens’, and this is something I showed last week. This is a young black man who’s asymptomatic. This is another EKG I showed that week, but it’s a similar morphology, that very common morphology in young black men, the early repolarization variant. So this is not Wellens’; this is a young asymptomatic patient, incidental EKG, and importantly, they tend to have pronounced ST elevation. Early repolarization ST elevation before the T inversion. Also, they tend to have a pronounced, very pronounced QRS, as in early repolarization. Early repolarization is often in young people associated with very prominent QRS. So this is not Wellens’. B, Case B is a very important one that is very common, and I want you to know it well. What is the diagnosis here? Look at this; you’re having a biphasic T wave with a straight convex ST in lead V4 and a little bit in lead V5. What is the diagnosis here? And look at the QRS. This is a 45-year-old severely hypertensive man. I’ll tell you the diagnosis. Yes, it’s LVH with a strain pattern. So what happened? This is what you call the transition lead T wave. So you have LVH, and you’re going to have ST depression and particularly DPT inversion in leads V5 V6. On your way between upright T to negative T, you get a biphasic T wave in one lead typically. Again, this is a T inversion of the transition lead. This is a not Wellens’. C, I want you to look at this. This is a patient, a 52-year-old man who is presenting with chest pain. He has this in leads V4 V5 only, and you can see this is not Wellens’; it’s concave; it’s not straight, the ST segment, and it’s a very smooth; it’s a smooth downslope; it’s not a very sharp downslope, and it’s only in V4 V5; it’s not V2 V3. This patient has been cathed three times because of that EKG at various institutions. Whenever they see this, they call it Wellens’; they cath him; he does not have CAD. Troponin was undetectable. This is just a normal variant T wave in the lateral precordial leads. This is the case here. Again, the morphology is not suggestive of Wellens’. This patient is coming with chest pain, but the ST segment is clearly concave, and it’s a very shallow downslope of T. It is not Wellens’, yet I will tell you this patient with chest pain had 90 percent proximal LAD stenosis. Still, I would not call him Wellens’. In this particular case, those T wave abnormality did reflect an LAD stenosis, but I still, I would not call them Wellens’. You, you do need to have a specific morphology to call it Wellens’. Everybody understands those features I described. Now this is another case here. Is this Wellens’ syndrome? This is actually diffused inversion everywhere, and the answer is no. Yes, I agree with you; the answer is no. This is not Wellens’, and here is why. This is what we call a global T inversion. Unlike Wellens’, one, it’s very diffuse; it’s almost in all leads; it’s in over six to eight leads. So it’s diffused, not localized to the precordial leads, particularly V2 V3. That’s one. Two, the morphology is different, and you have a smooth downsloping ST, not a straight or upsloping convex ST. You don’t have that steep downslope, slower upslope. So this is not Wellens’. Look how Wellens’ looked like. Those two cases, compare it to this. So this is what we call; it’s an established entity, very important entity called the global T wave inversion, and it tends to have that very deep T inversion in more than six to eight leads. The inversion frequently over 10 millimeters. Now what is the differential diagnosis of global T inversion? The reason I want you to distinguish it from Wellens’ because Wellens’ is very specific for ischemia, but those other patterns, while they can be seen with ischemia, are not specific for ischemia. So global T inversion can be seen is in ischemia, but it’s not specific for ischemia. So anybody can tell me what is what other diagnosis can be suggested with this pattern? So one differential diagnosis is any intracranial process, bleeding, stroke, or any other process. A second big differential diagnosis and probably the most common differential diagnosis is actually ischemia, except it’s not called Wellens’, but it is diffuse ischemia, severe ischemia. A third differential diagnosis is hypertrophic cardiomyopathy, especially the apical variant, but actually any hypertrophic, even the non-apical variant, can lead to that pattern. A fourth diagnosis is any high catecholamine tone, such as cocaine use, Takotsubo cardiomyopathy. It’s actually a very common pattern in Takotsubo cardiomyopathy. At some point in the course, early in Takotsubo, you get ST elevation, RST depression. Takotsubo will mimic STEMI acutely; it’s hard to distinguish it from STEMI. It tends to be less pronounced of an ST elevation, but it will mimicking STEMI. Then a few minutes or hours later, you get the deep T inversion pattern, and frequently you see the Takotsubo patient at this stage, this stage of a deep T inversion. This particular patient had Takotsubo. So this is when you see the patient frequently, over 80 percent of the time, at the DT inversion pattern. So again, Takotsubo is another differential. Those are the top four differentials. Other differentials: pericarditis can give it, PE, advanced AV block or post-AV block can give you that pattern. Um, good. Another thing I want to point out is in any process that leads to diffuse finding in all the leads will lead to an opposite finding in lead aVR. So you have diffuse T inversion all leads, need how, look how you have upright T wave in lead aVR. Normally, T wave is inverted in aVR. aVR is an interesting lead; it shows you the opposite of what is found in all the other leads. Anybody has questions regarding this, you can ask or in the chat box. Yes, type B versus type A Wellens’; it’s really not important. The difference is really this. This is what we call the type B Wellens’, this one, what you see here, meaning the biphasic T wave. This is what we call type A Wellens’, which is a deep T inversion. Okay, so I don’t care about this classification; it’s not important, and you often progress from this to that anyway, as I showed you, go from biphasic to DPT inversion. So it’s not important. What’s more important is a morphology, straight or upsloping ST segment that dives into a sharp T wave, whether it looks biphasic or it looks deep T invert deeply inverted; it’s the same to me. So type B versus type A is not important in my opinion; it’s the same thing, no difference, and they evolve into one another. You go from biphasic to DPT inverted, and eventually you progress back from deep T inverted to biphasic to normal. Any other questions regarding this? No questions. I’m going to move to the next case. So this is an 86-year-old man who has a history of CKD and severe heart failure with preserved EF. He’s presenting with severe back pain for the last three days. His troponin is elevated at one. So what do you think the diagnosis is here? I mentioned last week, look at it. I mentioned last week, posterior infarct. Is this a posterior infarct? So look at this case. You have diffuse ST depression everywhere, in every single lead. It’s not localized to leads V2 V3 V4. If it was localized or very predominant in leads V2 V3 before, I would call it possible, even if you have mild ST depression in the other lead, but in this case, I see depression is profound in all of the leads. So this is not posterior MI, and you have ST elevation in lead aVR. So what you answered in the chat box is correct. This is suggestive of left main disease. Diffuse ST depression with ST elevation in leads aVR and or V1. This would be suggestive, in general, the pattern of left main and or severe proximal LAD and or severe three-vessel disease. Now why does this happen? Diffuse subendocardial ischemia will give you ST depression, and this is the axis of the ST looking away from the heart. Okay, now anything that looks away from the heart will look upright in lead aVR. So we have diffuse ST depression; you will have ST elevation in aVR, and you will have ST elevation in lead V1 commonly because lead V1 looks away from the heart. It’s the same thing that happens in pericarditis. In pericarditis, the axis of ST is going the opposite way; it’s going toward the heart, and therefore you get ST elevation everywhere, and you get ST depression in aVR and V1. Okay, so that diffuse ST depression implies diffuse subendocardial ischemia with ST elevation aVR and V1. We call it diffuse, and it’s over eight leads in the original publication, but now six leads has been embraced by the ESC guidelines. Okay, it doesn’t have to be left main; again, it could be proximal LAD or a three-vessel disease ischemia. This patient specifically had tight left main, and we took him to the lab, and we stented it. We took him emergently to the lab. So those are two questions I will need to highlight here: does it have to be left main, and should he take him to the, should he be taken to the cath lab emergency? So when it is left main, your ST elevation is much more in aVR than in V1, and it actually, you may only have ST elevation in aVR and no ST elevation; we want always in conjunction with diffuse ST depression. So we never talk about ST elevation in aVR as suggestive of left main without diffuse ST depression. Okay, so you always have to have diffuse ST depression in on top of that you have ST elevation in aVR and V1 that could signify left main when ST elevation aVR is much more pronounced than it is in V1. Conversely, if ST elevation in aVR is equal to the ST elevation in V1, this would suggest proximal LAD disease or three-vessel ischemia. The idea is the following: so when you have three-vessel ischemia, you will get diffuse ST depression, and you will get ST elevation in both V1 and aVR equally. Now when you have left main or proximal LAD stenosis, beside the diffuse myocardial ischemia, you get proximal basal septal injury, transmural injury, which gives you this axis of repolarization across that septum. This is the axis of the septal injury. Okay, you get it in left main and proximal LAD, which gives you an even more pronounced ST elevation in aVR and V1. This vector will look towards V1 as well. There is a catch though, with left main ischemia, you’re also getting posterior left circumflex ischemia that counterbalances that basal septal injury, and that’s why with left main that posterior ischemia will cause ST depression V1 as eventually it counterbalances that ST elevation from the basal septum and eventually end up with no ST changes in V1 or mild ST changes in V1. Conversely, you get a lot more pronounced ST changes in aVR. That’s why left main is that specific special subset of those etiologies here that gives you more pronounced ST elevation aVR compared compared to V1. Proximal LAD or three-vessel disease lead to equal ST elevation in both aVR and V1. You kind of got the point here. So it’s all about the basal septum injury and about the fact that in left main you have left circumflex ischemia that counterbalances that basal septal injury and annihilates the ST elevation in V1 but not in aVR, which is a different axis. Always in EKG, you have to look at axis of the polarization and axis of repolarization to understand how QRS and how ST respectively project in that lead. Should we cath this patient emergently? So it is not a STEMI as the elevation aVR and V1 is not a STEMI. Diffuse subendocardial ischemia in the non-STEMI ESC guideline, it’s considered one of the indications for urgent, immediate invasive in less than two hours. This is not the case where we follow door-to-balloon 90 minutes, but this is a case where we managed on STEMI urgently as an other indications in less than two hours. That’s according to the ESC guidelines, and I agree with it, but there is a catch though, like in any of those recommendations, you have to take into account, as I did in this case, how profound the ST depression is and how profound the ST elevation in aVR is. Over one and a half millimeter is very concerning for left main; that’s one, and aVR more than V1 is concerning for left main; that’s one idea. So profound, how profound the changes are. Number two, how persistent they are. If they are transient for a few minutes and they uh evolve and improve, you might be able to wait till next day. Three, how persistent the patient’s symptoms are. So in the absence of severity of those features, you may be able to wait; it may not be urgent. What are other cases beside that EKG of urgent cath and non-STEMI? The three big ideas: one is, as you all know, refractory or recurrent chest pain that we all know it, but there are other ideas such as hemodynamic instability, electrical instability, meaning sustained VT, and acute heart failure. So hemodynamic instability, you have to be careful; not every shock qualifies for urgent cath. Okay, cath, you have to make sure it’s cardiogenic shock, and typically it will be a shock associated with profound ST segment abnormality, whether it’s elevation RST depression. So shock with profound ST depression; that’s another indication for urgent cath. Heart failure; they put it in all guidelines as an indication for urgent cath, but I don’t agree with that, and actually JACK 2021 review doesn’t agree with that. Most acute heart failure, you need to stabilize them before taking them to the cath and decompensate them during the procedure. The only acute heart failure you have to take emergently is acute heart failure with hemodynamic collapse or the acute heart failure that is massive, that’s already intubated with concomitant profound ST depression. So that’s the only acute heart failure with profound ST depression, profound persistent ST depression and requirement for ventilation or profound shock. The only acute heart failure that you need to take urgently, not all heart ischemic heart failure. Most ischemic heart failure can wait until you’re stabilized so you can do your procedure with less risk and less risk of decompensation and pre-procedural ischemia and hypotension. Okay, there is another idea related to this topic. This topic is so important because that EKG we see it so often. I’ll tell you that most often when I see a similar EKG, maybe not as pronounced but similar diffuse ST depression, most often in my experience is not even severe ongoing myocardial primary myocardial ischemia. Most often in my experience, this is actually secondary myocardial ischemia, frequently like profound anemia, a profound shock from another reason. You have a patient who’s coming with fever, pneumonia, septic shock; you get diffuse ST depression with ST elevation in V1 and aVR. You have a patient with COPD and profound hypoxia as he’s getting intubated, his SpO2 is 60; you get that EKG. So beware of that EKG; you will get it whenever you see it; you have to take the contexts into account. Don’t trash those patients with profound anemia and hypoxemia of another source or shock of another course source. Don’t rush them to the lab. Keep those ideas in mind, very important. Okay, there’s another differential diagnosis even for that. So I mentioned diffuse ischemia, including left main ischemia. I mentioned secondary ischemia, very important, depending on the context. There’s another differential. This patient, what’s the diagnosis on this EKG? So he has diffused ST depression with ST elevation in aVR. He has a quite a prolonged QT, and he has a double hump T. You see that double hump T. This is what, this is another cause of diffuse ST depression: hypokalemia. It will give you, anything that gives you diffuse ST depression can give you ST elevation in aVR and V1 that look away from the heart. Anything that gives you diffuse ST depression can give you ST elevation in V1 and aVR, regardless of having that septal injury; you don’t need to have it; that is a special to the left main and proximal LAD, but anything gives you this will give you ST elevation aVR and V1. This weekend I was called by another institution for transfer for STEMI or acute MI based on that EKG. Well, again, this is a patient with afib; he has diffuse ST depression with ST elevation aVR and V1 suggestive of diffuse ischemia, but there is a catch. This patient is coming with nausea and fatigue and vomiting, no chest pain, and the potassium is 2.6. So this is another hypokalemia EKG. This one, the potassium was 2.6 as well. So keep in mind that EKG is not a slam dunk. Don’t immediately rush those patients to the to the lab. Keep in mind that this pattern could be secondary myocardial ischemia from another process, and it could be hypokalemia. And even when it is a primary ischemia, if it is not profound or persistent or the pain is not persistent, if none of this is present, then you could do it on cath. This patient potentially a few hours. This is another case, moving to another topic. This is a 51-year-old man who presents with chest pain, dyspnea, and pulmonary edema on chest X-ray. His blood pressure is 220 over 110. He has no prior EKG. What’s the diagnosis here? Is this a STEMI? So here I’m moving to the topic of left bundle branch block. Okay, and you left bundle branch block with chest pain. Should we take this patient to the cath lab? Does he have a STEMI, and why if he does or if he doesn’t. One, the first idea to know regarding left bundle and STEMI. Left bundle branch block is often not STEMI. STEMI very rarely, rarely causes left bundle branch block occlusion because the left bundle is supplied by both the LAD and RCA, is only affected in extensive
Infraction, as an illustration of that, in gas to one trial only one percent of Sami had left. Bang the branch block on presentation, so LeBron the double block is rarely a STEMI. In fact, most studies show that a new left bundle branch block is just a chronic cardiomyopathy. It could be chronic ischemic cardiomyopathy or frequently chronic non-ischemic hypertensive cardiomyopathy. So left bundle branch block in new left bundle branch block is not acute ischemia overwhelmingly. Only up to 10% of patients with an ischemic cardiac presentation and a new left bundle branch block have a STEMI equivalent with acute coronary occlusion on angiography. STEMI is even far less likely. If you take all comers, those in your bundle branch block, including patients with atypical pain and atypical presentations and heart failure, if you include all those, STEMI is even far less likely in your left bundle branch block, probably less than five percent. This shows you how unlikely STEMI is with left bundle branch block. Yet you can have, of course, STEMI with left bundle branch block.
Why is left bundle branch block confusing? Left bundle branch block normally intrinsically will cause opposite ST changes. So if you have, you have a prolonged QRS in lead one, you will have opposite ST changes in lead one and aVL, in and two and all the leads with an upright QRS. You have negative QRS and the precordials V1 through V3; you will have opposite upright ST elevation in those leads. Okay, so inherently it could be confusing when you have STEMI and left bundle branch block. Is this ST elevation secondary to bundle branch block or is it ischemia? So if you have somebody with concordant ST changes, so we have ST elevation in lead one or you have ST depression in leads V1 through V3, this is what we call concordant ST changes, same direction as QRS. This is a STEMI. This is a very specific finding, the concordance finding, and implies a STEMI concomitant to the left bundle branch block. However, you may have a STEMI without concordant ST changes. Take, for example, the patient with anterior STEMI due to proximal LAD occlusion. Inherently, he will have ST elevation injury in the leads V1 through V3. It may be localized to the lead V1 through V3 in which leads left bundle branch block is also causing, causing ST elevation. So in that case, with a proximal LAD occlusion and ST elevation limited to V1 through V3, discordant to QRS, how can you tell whether that ST elevation is partly due to STEMI, not left bundle branch block?
The way of telling is to look how discordant it is. So it is discordant, but how excessively discordant that ST elevation is. In the past, Sgarbossa, in the 90s, used the scheme where five millimeters was considered possible STEMI. This should be abandoned in today's criteria. So several papers, including one study I did at Louisiana State University, show that the Sgarbossa criteria is actually very non-specific and non-sensitive. 10 to 15 percent of left bundle branch block have five-millimeter ST scorings without any STEMI based on multiple studies, not just that. Having less than five millimeters of discordant could be STEMI, so you could miss it also by using that feature. It's very non-specific, very non-sensitive. So this is the more specific and sensitive feature is to look at the relative discordance, the ratio. So don't look at the absolute value, look at the ratio. So look at this patient, for example. This was a patient with left bundle branch block and inferior STEMI. Okay, so he had ST elevation in lead AVF that's about two millimeters only, but his QRS is only five millimeters. Two divided by five is 40 percent; it's over 25 percent. It is a STEMI. Also, in lead three, he had an ST segment, and we measure it at the J point, okay, it's about here. He had, and I like to take it one box, like I explained, like many other authors, one box beyond the J point. So he had ST elevation of three boxes and QRS of nine boxes, so that was a 30 percent or so ST/QRS ratio, over 25. So the over 25 is much more sensitive, with almost 100 percent sensitive and 88% specific for STEMI in both my paper and the Smith paper. So 100% sensitive, 88% specific for STEMI. Some have fine-tuned; Smith has fine-tuned this ratio to 20. I did 25 in my paper. I still think it's best to use the 25, and this is how we measure it. You measure the QRS and mainly the S wave, and you measure the ST segment and you calculate the ratio. That's another case. This case, it's also, this is anterior STEMI with left bundle branch block, as you can see now.
Interestingly, this case is easier because she had concordant ST elevation in leads 1 and aVL, but she also had this concordant and the discordant in these V1 through V3 is striking for STEMI. Look in lead V2; you have ST elevation that is almost the size of S waves or QRS. So we have ST to QRS ratio of almost 100 percent. So that alone, even not looking at the concordance, would have told me there is a STEMI. Same here, it's about three millimeters, and the whole QRS is about eight millimeters, so that is excessive discordance. So excessive discordance in relative terms, not absolute terms. This is the first patient I showed; he has this concordant ST elevation over five millimeters, yet the ratio is barely 10 percent. This patient does not have STEMI; he has malignant hypertension with hypertensive cardiomyopathy. This illustrates the importance of relative discordance as opposed to absolute discordance. This patient has a huge S wave, and the discordance ratio is barely 10 percent. Conversely, this is the last patient I showed; she has this concordant ST elevation less than five millimeters, yet a ratio that exceeds 25 percent, and she has anterior STEMI. Those criteria also apply that this, that excessive discordance and any concordance apply for LVH and for V paced rhythm. One important tip about LVH: LVH gives less discordance than left bundle branch block, and therefore in LVH you can use absolute discordance over 2.5 millimeters in the precordial leads or over one millimeter in the inferior lead is suggestive of STEMI based on that paper. So generally overall, use the relative discordance in all cases. In LVH, you could use some degree of absolute discordance, but I want you to remember the relative discordance. In the 2013 STEMI guidelines, new or presumably new left bundle should not be considered diagnostic by acute MI isolation. So this is eliminated from an MI consideration. 2020 ESC guideline: hemodynamically stable patient presenting with chest pain and left bundle branch block only have a slightly higher risk of having MI compared to patients without left bundle branch block. Roy is asking about right bundle branch block. So yes, prognostically speaking, in STEMI, right bundle branch block is as bad prognostically as left bundle branch block. So if you have a true STEMI with right bundle branch block, your prognosis is as poor as a true STEMI with left bundle branch block. Acute right bundle branch block with a STEMI implies acute proximal LAD occlusion. So it's a before the first septal; it's the first septal infarction that causes right bundle branch block. It's a big LAD infarct that causes a right bundle branch block. That said, right bundle branch block doesn't cause, because it does not cause ST changes. Right bundle branch block normally should not cause any ST abnormality, definitely no ST elevation. It can cause a slight ST depression in V1 through V3, but no ST elevation. So that's why right bundle branch block is extremely important prognostically if it is a true STEMI, but it does not cause any diagnostic challenge. You're not going to miss a STEMI in a patient with right bundle branch block. That's the idea. So right bundle branch block is very bad when it's associated with STEMI, but does not cause diagnostic confusion.
I want to describe a quick case here. A patient presents with chest pain that started four hours previously and inferior ST elevation. His pain has just resolved with aspirin and nitroglycerin, but ST elevation is persistent. Should we undergo emergency perfusion? Pain resolved, but ST elevation is persistent. Very common scenario. My answer to this is he should be undergoing emergency perfusion. Correct, and here's the reason why. I mentioned the prior talk: transient STEMI. If chest pain resolves and ST elevation resolves, then you can wait till next day, and this is what we call transient STEMI, a subgroup of which is self-aborted STEMI, but this is not the case. You still have ST elevation; therefore, you still have ongoing ischemia and severe ischemia and injury. He should be cased urgently. Those are the indications for emergent cath in STEMI: persistent ST elevation less than 24 hours for symptom onset, even if symptoms have resolved, or persistent symptoms even if you're over 24 hours from presentation. Okay, I will move to another case here. This is a 39-year-old man who's presenting with palpitation. What is the diagnosis here? Look at this EKG carefully. He has ST elevation leads V1, V2, V3 and has some ST depression diffusely with a shape suggestive of pseudo-right bundle branch block in V1. It's not really a right bundle branch block because QRS is not wide in the other leads. This is what you call pseudo-right bundle branch block. So yes, this is a Brugada pattern. Now, can this be, I mean, is it when you see it, it has to be Brugada? It's not STEMI, and why is this patient tachycardic? He has sinus tachycardia. What can come to your mind when you see somebody with a Brugada pattern, yet he's tachycardic? What's the immediate thing that should come to your mind? And it came to my mind as I was communicating with Wasawat immediately as I saw, as I saw this EKG: fever. So here's the differential for this EKG. So in an asymptomatic patient with a screening EKG on whom you find this, it's a slam dunk; it is a Brugada. It's a downsloping; we call it coved ST elevation with a pseudo-right bundle branch block in lead V1, V2, and V3. So this is the type 1 Brugada pattern, which is the real Brugada syndrome. Now, in a patient with symptoms, be careful, such as this patient, be careful. This pattern may be Brugada pattern, and because the patient is tachycardic, you have to think Brugada pattern induced by cocaine and fear or fever. Cocaine is a sodium channel blocker, and therefore it can elicit Brugada pattern. Brugada pattern is due to a loss of function mutation of the sodium channel, so in the phase one of depolarization. So therefore, if you have anything that inactivates those sodium channels, such as cocaine, some anesthesia, fever, you will get Brugada patterns. So think of that fever. In this case, this patient had a fever of 39.5 that elicited this pattern. Keep also in mind, he's taking, are you sure he doesn't have PE? PE can give you the exact same EKG. I've seen it in the past; I showed it in my prior talk, very similar ST segment in PE. So think in the proper case context. Think, could this be PE with RV injury that looks like Brugada? In fact, importantly, any case of RV injury can give you this pattern. Example: RV contusion. I had that on my board exam. A soccer player tripped and fell on his chest; he did not pass out; he had the chest injury and rib fracture, and he had this EKG, and they asked me what to do with it. This EKG in that board question to me was not Brugada; it was RV contusion. Okay, regardless of whether it was RV contusion or Brugada, the treatment is conservative and observation. So anyway, you can see it with RV contusion; you can see it with anterior MI. So don't ignore anterior MI. Consider doing a quick bedside echo and look at the full context to assess whether this could be anterior MI and consider, you know, following the troponin to see that. Hyperkalemia can give you such a pattern, but I'll show you more hyperkalemia; it's not perfectly the same. So we got the differential diagnosis of Brugada pattern. It's not always just the genetic; it could be RV injury from PE, contusion, could be MI, it could be hyperkalemia. And the note on Brugada: what they call type 2 and 3 are very non-specific and mean nothing. We should really only be talking about type 1 Brugada, and we should just say Brugada syndrome for type 1 Brugada pattern only. Type 2 and 3 are only meaningful if you can make them evolve into type 1 by giving procainamide, but I would only do that in a patient with syncope. So really, there is only one type of Brugada, which is this pattern. The other ones that have no prognostic value by their own. This is a hyperkalemia EKG. Again, you have what looks like Brugada in lead V1, V2, but the difference is the T wave morphology. It's a very narrow, peaked T wave that pulls on the ST. Okay. This is another hyperkalemia EKG that again can look like Brugada. Indeed, we want, that's how I always imagine it, that T is being pulled here, so it becomes narrow and it pulls on the ST segment, and it can create diffuse ST depression. Okay, it can create here diffuse ST depression and that narrow T with ST elevation at times. So you can have ST elevation as well as diffuse ST depression hyperkalemia. Keep in mind the T wave of hyperkalemia is very different from the T wave of STEMI. Typically, the hyperacute area of STEMI tends to be wide, not like this; it tends to be wide, more than high, although on occasion it can look like this, but the, it tends to be wide more than high. So this is a patient I had when I was a fellow, but it was a dazzling case to me, so I saved that EKG. He's a 63-year-old man in the surgical ICU. He had extensive bowel resection for carcinoid four days previously. He's having acute onset of chest tightness and dyspnea. His blood pressure is 180; he's tachycardic. Should you perform cath on this patient? A cold STEMI has been called by the surgeon. This is a specific morphology. Back then, in 2009, it was not described. I wish I published that case because two years later somebody else published a series of those cases. This is a special morphology. Look at it in a critically ill surgical or medical ICU with chest pain and this particular morphology. This is not a STEMI; it can be STEMI, but is often not, and this is the name of this pattern. It was described two years after me, and it's called the spiked helmet sign. This particular ST morphology where you don't have an isoelectric TP segment. So you have the TP goes down-sloping, then all of a sudden it shoots up; it gives a spike, then it domes; it's a spike, then a dome. It's hard to tell what's QRS, what's ST; it's all fused together and giving that morphology of spike and dome. Okay, so this is a spiked helmet sign. It looks like basically like a Prussian hat; it's almost the whole thing is like a dome, up, down, dome, and on top of it you put a spike, typically, and most often described in the inferior lead. Again, in critically ill surgical or medical patients, it tends to be transient, and in a case series of eight patients described in 2011, none of those patients had a STEMI. None of these patients had an MI by markers, and 75% of them died. So they tend to be non-cardiac critically ill patients with a transient finding. So what I suggest to you to do: one, recognize the pattern; to repeat EKG; it will normalize half an hour to an hour later. Now, why does this happen? There are various explanations. One explanation was, and the one I thought of when I saw that EKG in 2009, because we cased that patient and he had no CAD and his troponin remained negative, I thought of lead artifact because he was breathing heavily. It could be a mechanical stretch on the electrode in those patients with abdominal illness, breathing heavily. That was one theory; that's why you don't have an isoelectric baseline in those inferior leads. Another theory that is more standing today is that this is due to high catecholamine tone, okay, high adrenergic tone. That's why, for example, this pattern has been described; the spiked helmet pattern has been described in Takotsubo and seen in critical illness where you have high catecholamine tone. This is another pattern that I had at the beginning of this year here in Iowa. Again, I was called at 2 AM; a medically ill patient; she has multiple spinal surgeries; is coming with MRSA bacteremia and epidural access; she started to complain of acute chest pain and dyspnea, and she has this EKG. It's a very characteristic EKG. So it's an interesting morphology in lead one and aVL. It's hard to tell; kind of like the other EKG I showed you, cannot tell what is QRS, what is ST; they are all fused together in one dome. It's also the same in the prior one; they are all fused together in one dome, and they are fused together in one dome, except there is a spike on that dome. In this pattern, there is no spike; they are all fused together in one dome, and they don't look like a dome; they look like this. So this is a spike and dome morphology. This is how ours look; it's called the shark fin pattern. So they are fused together in one triangle that looks like a shark fin in those patients. You still have an isoelectric TP, and that pattern can be seen in any lead; more, it's not more commonly in the inferior lead, unlike the spiked helmet, which is typically described in the inferior leads. So anyway, this is the shark fin pattern. You have a shark fin in lead one and aVL and the reciprocal sharp triangle in three and AVF. Again, whatever causes a change in a subset of leads can cause opposite, opposite change in another subset of leads; that doesn't necessarily mean STEMI. So anyway, I recognized that pattern, and I still took her to the lab, and she had normal coronary artery. Troponin did not go up much; it went up to a mild degree, like 0.1. If you, if you Google shark fin pattern, you will find tons of online blogs suggesting that shark fin pattern is an ominous type of STEMI, yet there is only one case report of shark fin that turned out to be an acute LAD STEMI, only one case report in 2021. Actually, there are more case reports or a larger case series of shark fin in Takotsubo. So here is my take on this: shark fin pattern is a non-specific pattern that could be STEMI, but can be seen in a critically ill patient and can be triggered by high catecholamine tone, very similarly to spiked helmet sign. That's the reason why we see it in Takotsubo. Again, when you see shark fin pattern, it could be STEMI, but I have no data suggesting, no large series telling me it's most often STEMI. Repeat EKGs, do echo; those are the things that will help you in those patients. Your LV will be hyperdynamic rather than akinetic in those, in those contexts. Okay, this patient; we repeated the EKG; it normalized spontaneously. So this is a 63-year-old woman; she's a smoker; she has severe hypertension and no prior cardiac history. She's presenting with severe hypertension of systolic blood pressure of 200 and chest pain for three hours prior to presentation, and this is her EKG. Is this STEMI? When I look at that EKG, if that was a 23-year-old man, I would have been less concerned; I would have thought maybe this is early repolarization, but early repolarization is very uncommon in a 63-year-old woman. She has ST elevation in leads V2, V3 through V6, subtle, not bad; it's about two millimeters in lead V2, one and a half in V3, you know, one and a half in V4, V5, but importantly the morphology of ST elevation in lead V4 and V5, it's a domed morphology. You see the STT are fused together; the ST is straight into the T wave; there is no concavity in any of those leads; it's a straight STT fused in one dome. Another idea is the STT size in two leads approximates the QRS size. So whenever I see that STT dome almost equal to the QRS size or exceeding half of it, I kind of worry: is this a shrinking QRS and rising STT as in STEMI? That's what you have in STEMI: shrinking QRS before it becomes equal and rising ST. So that was very worrisome to me. The other thing that was worrisome is no other explanation. If this patient had a big QRS of LVH, I wouldn't be worried about that ST elevation; I would have called it opposite discordant ST elevation less than 25 if she had big QRS, but she doesn't have big QRS and no early repolarization. I mentioned in the past, early repolarization is very common in young men; it is fairly common in middle-aged men, actually, in V2, V3; it's seen in, you know, 30 to 40 percent of men, up to 30 to 40 percent of men, even in the lateral and inferior leads is seen in five to ten percent of men. So you can see it in middle-aged men, middle-aged to older men, but in women it's two to four times less common. So it's, you know, very uncommon in an elderly white woman. This is early repolarization in a 52-year-old woman where early repolarization is not common, but you could still say this EKG has classic features of early repolarization. You have very notched J-wave with very concave ST segment and very prominent QRS; STT is much smaller than QRS. That's characteristic of early repolarization. You tend to get in early repolarization, pronounced QRS, and STT is much smaller than the height of the QRS. So this was a classic early repolarization in an older woman. This is not the case here. So for those reasons, no other explanation, and the worrisome morphology, I decided to take her urgently to the cath lab. You could do a bedside echo to help you as well. So I took her urgently, and she was, she had a proximal LAD 100% occlusion. I recanalized it; I put a stent; we had TIMI free flow; everything looked good. Then all of a sudden her pressure was, throughout the case her pressure had been 180 millimeters of mercury, then within 15 seconds her pressure went from 180 millimeters of mercury to zero millimeters of mercury. Her rhythm did not change; she remained in sinus rhythm with a full collapse over pressure and practically a PEA cardiac arrest. What's the diagnosis here? We resuscitated her; I did more angiogram while we're doing CPR; I could not see any perforation; I did bedside echo during resuscitation; we couldn't see any effusion; we could not get her back, and she eventually unfortunately passed away. So what is the diagnosis here? I want you to know the diagnosis because I recognized it and I wrote it in my report even before the autopsy, way before the autopsy. Somebody mentioned PE. No, she did have acute LAD occlusion. It's hard to have two diagnoses. Is what I wrote in my report, based on our reviews of the angiogram and the sequence of events, we do not suspect a coronary or aortic complication directly related to our procedure; no perforation, no coronary dissection, no ventricular arrhythmia. We suspect that the abrupt PA collapse is due to coincidental ventricular free wall rupture in the setting of anterior STEMI in a hypertensive elderly female patient. That was my diagnosis that same night, and two weeks later the autopsy confirmed she had free wall rupture. She had, in retrospect, all the risk factors for that. She is, this is the common scenario: first MI, elderly female, severe hypertension; those are the risk factors for mechanical complication; that also applies to papillary muscle rupture and ventricular septal rupture. So she had those risk factors, and that's why she had free wall rupture. Another common misconception is: when does free wall rupture or all the mechanical complications occur? What, what time do they peak at? How many days after infarct? There's a common old teaching of three to five days. Three to five days was in the 1980s; people still use that, but it's incorrect by today's standard. The peak, according to the SHOCK registry, which is not even that novel; SHOCK registry is from the year 2000s, late 90s, 2000s; the peak mechanical comp, the peak rate of mechanical complications occur the first 24 hours of AMI. That's the first peak. The second peak is three to five days. The idea is in the reperfusion area you're not getting any more, the rupture that you used to get at three to five days. Three to five days, what happens then? That infarct zone, soft zone, starts extending and extending, and it pulls the tension on the normal myocardium, so that the junction between the normal zone and the infarcted zone ruptures. This is where you get the rupture at the junction between the infarct and the, and the normal myocardium, and it happens three to five days later. It used to happen three to five days later as that infarcted zone thins out and stretches out, but that doesn't happen in our days. In the reperfusion area, the infarct zone continues to have good turgor and it does not extend. That's why statistically most of your ruptures will happen in the first 24 hours, and that
Fits in this lady.