STEMI part 2- Questions and case scenarios- Elias Hanna

I will continue talking about STEMI management. I will mainly use the questions and clinical vignette format for explanation purposes. So, true or false: Q waves and acute STEMI imply a poor prognosis with limited value of reperfusion.

True or false: Q waves often take 12 hours after STEMI onset to develop.

So I will answer both: those are false. Here is the explanation: Q waves often develop at 1 to 14 hours after STEMI onset, while the ST segment is still elevated. You can see here the progression. So, actually, 30 percent or so of STEMIs have already Q waves by one to three hours, and it increases with time. Q waves are associated, yes, with a more delayed presentation, larger infarct, a bit less myocardial salvage, and worse short-term prognosis. However, Q waves are not synonymous with irreversible myocardial damage and may very well reflect stunned myocardium that is electrically silent but not dead. And Q waves do not preclude reperfusion therapy. In fact, significant myocardial salvage is achieved in over three-quarters of patients with Q waves, with a salvage index of over 50 percent of the area at risk. Also, 40 percent of acute Q waves regress by six months. Q waves may be seen after non-STEMI and the transient ischemia of a few hours without extensive necrosis. In those cases, Q waves are usually not very deep, but nonetheless, they are significant. So you can see, go from non-STEMI ST depression to Q waves: pathologic Q waves, albeit not very deep. Persistent Q waves at more than six months are more concerning than acute Q waves that are seen in the first few days.

For STEMIs alike, the really bad Q waves acutely are those that look like this: very deep Q waves with minimal residual R, so very small R to Q ratio, and only mild residual ST elevation, mild ST to Q ratio in multiple leads. Those Q waves suggest old MI, over 12-24 hours, even if ST elevation persists. Keep in mind, persistent ST elevation does not mean the infarct is acute. With such pattern, persistent ST elevation usually means an infarct of several days old. And in fact, this fits with the old trial where 68 percent of late-presenting patients still had ST elevation on the EKG. This was 1 to 28 days later after the infarction. You can have, you frequently have persistent ST elevation for several days, if not more, after an acute infarct. So, ST elevation does not necessarily mean the infarct is still acute; it could be subacute or even chronic. In cases of dyskinetic or aneurysmal infarct, but account for the patient description and for ongoing pain.

So, really, in order to call STEMI or Q wave infarct late, it's best to have all those three features combined: so that EKG pattern, also a patient description of pain onset more than 24 hours, and the third is no ongoing significant pain with distress. If you have all three features, then the MI is late and no PCI is indicated if the artery is occluded, even if ST elevation persists, as per the old trial. Now, coronary angiography is still warranted, as I explained, you do it, and if the artery is not occluded, then PCI is still warranted beyond 24 and 48 hours, only included arteries that are totally occluded. Now, if you have two out of the three of the N factors, possibly late, you have to individualize. Ongoing significant pain with distress is the feature that will push for PCI, regardless of the other two. Now, if you have no ongoing significant pain, like you have number three, and the MI patient description is over 24 hours, yet the EKG does not show deep Q waves or does not show Q waves at all, even in that case, it is likely that the MI is old, even if you don't have this EKG pattern. Not ongoing pain, patient description more than 24 hours: two out of those three, it is likely that the infarct is more than 24 hours. Keep in mind that actually in the old trial, 33 percent of patients did not have Q waves. So you really don't need absolutely to have this pattern or even Q waves to call the infarct old. You have to take into account those three, and sometimes two of the three are enough to call it old without the EKG pattern, but it's best to have all three. This is when you're most certain. Keep in mind that I'm also talking about STEMI, meaning I'm not talking about non-STEMI, where evidently the perfusion several days later is totally appropriate. Talking about STEMI, so you need it to have had at some point evidence of persistent prolonged ST elevation at some point, or persistent ST elevation at this point. So I'm not applying those features to non-STEMI. Keep that in mind. Okay, so this is another illustration. This is the late bad Q wave: the deep one with mild residual R and ST elevation in multiple leads. This is what is concerning for late infarct. Compare it to those early Q waves that you may see in the first few hours of an MI. This is how they look: you still have a big R, a significant ST elevation compared to the Q wave, ST to Q ratio.

So this is a patient who had chest pain starting three hours ago. He has significant pathologic Q waves, meaning they are wider than one box and deeper than one box in leads II and aVF, but nonetheless, they are not very deep. They are in that pattern, so they fit with a rather early presenter. Now, it's true the Q wave in lead III may look like this one: it is deep with mild residual R wave, but in order to call it late bad Q, you need to have it in multiple leads, at least two leads, and inferior STEMI in my experience, and probably in three to four leads for anterior STEMI, the ones through at least V4. Even that pattern that may look bad still benefits from PCI if pain started less than 24 hours ago, and especially if the pain is ongoing. Again, you account for all those three features. If you have that EKG pattern, but you don't have those other two, you only have one basically, then you should consider the infarct infarct onset as less than 24 hours and that the patient will benefit from PCI. Also, even if it is late, the patient still benefits from coronary angiography and from PCI if the artery is not totally occluded. That's why there is a value of late coronary angiography. This pattern: do not give thrombolytics, certainly not if over 12 hours. So we may do cath and PCI, but I would certainly avoid thrombolytics for that pattern that is highly suspicious for some significant delay in presentation.

This is another case here to illustrate again those late presenters and EKG pattern. So this is a 71-year-old man, dialysis patient, diabetic, presents with 30 hours of chest pain, worse than two hours ago during dialysis, but now is minimal. He has ST elevation in leads V2 through V4, was really profound Q waves and no R wave, and actually the Q is much deeper than the residual ST elevation. Take that EKG pattern along with over 24 hours of pain and no ongoing current chest pain: you really have no indication for emergent PCI in this patient, despite the persistent ST elevation, which I said is very commonly persistent several days after an infarct. So you really have no indication for emergent PCI. You may need to do elective PCI if he keeps having recurrent pain, but no indication for emergent PCI. We did do PCI on this patient; he had a totally occluded LAD. We did follow the ESC guidelines using 48 hours as cutoff instead of 24 hours. However, six months later, you can see the Q waves never vanished, and he had no improvement of his apex. So I'm not sure the reperfusion helped him here, keeping in mind that he had all three features consistent with late presenters.

This is another case. So this is a 68-year-old man. He had indigestion for 18 hours. He still has mild ongoing pain, and he looked in distress. Should he undergo late PCI of an occlusion? He has Q waves in the inferior leads, and he has mild subtle ST elevation in those leads, less than a millimeter, with some reciprocal ST depression. Yes, this is a late STEMI by the EKG features I explained, but he likely still derives some benefit from primary PCI because his pain is less than 24 hours and he still has ongoing distress. We took him to the lab; we treated an occluded proximal RCA. EKG remains unchanged after PCI. Now I will give you that same EKG, but I will change the scenario and see if you would manage this patient differently. So this is a 68-year-old man. He presents with off and on episodes of chest pain. He does not have any significant distress currently. He reports a prior history of a large MI two years previously. We don't have an old EKG, but that's all we have, and we have this history. This patient, I would not take him to the lab emergently, as ST elevation in this scenario is not acute STEMI, and Q waves are not acute STEMI in this case. Rather, they are old STEMI with dyskinetic myocardium. You have a chronic persistent ST elevation with Q waves and either inverted or upright T waves. In those patients with a chronically dyskinetic or aneurysmal myocardium, those ST elevation may last months and years. So definitely do not take this patient urgently. This patient had all three bad features, so definitely do not take him emergently. The worst: you take him emergent, you find an occluded RCA; there is no indication to fix it, and you may engage into fixing a CTO of the RCA here.

Another question that often comes up: does viability testing help in late presenters with occluded culprit artery? So let's say here this patient: he's presenting late, we decided not to take him emergency and not to open an occluded LAD later than 24 hours. Okay, should we do viability testing? Maybe if it is viable, we can open it late. Well, the answer is no. In fact, in a substudy of the old trial, patients who received a viability testing, in those patients, viability did not predict a benefit from late PCI. So viability testing was not useful to decide about later reperfusion. It was, even if you're viable, there was no benefit of late reperfusion. In fact, you must prove ischemia to benefit from late PCI more than 24 hours, especially on exercise testing, meaning you need to have chest pain or extensive ST depression on exercise testing, plus or minus large reversibility on nuclear testing. So you must prove ischemia, not viability. Ischemia was an exclusion criterion from the old trial, not viability. So what is, what's the difference? A lot of people don't understand the difference. So this is what viability means: viability means that fixed defect. It means at rest you have the infarctic territory uptake significant more than 50 percent nuclear agent at rest with no dramatic change with stress. So we have significant nuclear uptake that doesn't vary significantly with the stress. Ischemia means that you have a defect at rest that gets dramatically more extensive and more severe with stress, and the key word is dramatically, not mild reversibility, dramatic reversibility. And we're talking in a patient who's had an infarct here specifically. So after MI, you prove that there is dramatic worsening of the defect in severity and extent around and inside the infarcted area, and more importantly, to be more specific, it has to be exercised in my opinion and document severe ST depression and angina with low-threshold exercise. Those are the patients who would benefit from late PCI, not those viability based on the old trial and old trial substudy. Okay, the lack of ischemia means that the myocardial territory is already receiving enough blood supply for whatever tissue that is viable. That's why there is no value of revascularization. So it has to be ischemia. And this is the old trial. It took STEMI or Q wave infarct older than 24 hours, mostly older than 48 hours, 1 to 28 days old specifically, and it showed that they did not benefit from PCI and had a trend toward harm, more frequent reinfarction. They included those patients: totally occluded artery, akinetic or dyskinetic infarct wall, not three-vessel or left main disease. And that's why late coronary angiography is still useful if your artery is not totally occluded. You're not in OLD if you have a three-vessel or left main disease; you're not in OLD. You may still qualify for revascularization and CABG and no recurrent rest or low-threshold angina, no severe ST depression on stress testing, no cardiogenic shock. And as I explained, uh, 67 percent had Q waves. Not all patients had Q waves. So you don't absolutely need to have Q waves to be called late MI. Conversely, having Q waves does not mean you're late either. You have to look at the pattern of the EKG and the full three features that I explained.

I will move on to the next topic. Also, I will use a clinical vignette. You have a 51-year-old man, staggering chest pain for the last week, followed by constant chest pain and indigestion for the last 20 hours. This is his EKG. He has extensive severe ST elevation in the leads V2 through V5. He's already having Q waves, and his presentation is a little late. Nonetheless, ongoing pain, 20 hours, definitely benefits from PCI, not thrombolytics beyond the 12 hours. So we took him for a PCI, and we did a PCI, primary PCI, and stenting of an occluded, 100 percent occluded proximal LAD. We had a great angiographic result and TIMI 3 flow. He has mild residual chest pain with no distress. Like I said, it's very common to have residual chest pain; we don't worry much about it. It has to be severe, severe pain with some distress to make us worry. To add mild lingering pain, nothing concerning. This is his EKG post-PCI. What is the problem with this EKG post-PCI? So the problem with this EKG is persistent ST elevation. Remember what do we call persistent ST elevation after thrombolytics or after PCI? We aim for a reduction of ST elevation of at least 50 percent, preferably 70 percent. Most commonly, we use the lead with the worst ST elevation, and we see if it declined 50 percent at least. Okay, and we can see here it was about seven millimeters in lead V3; it went down to about four millimeters, so less than 50 percent. Same in lead V2, it declined but less than 50 percent. So no significant resolution of ST elevation; that's concerning. Now we don't call that aneurysm yet or this kinetic myocardium yet. It has to persist for significantly longer than one hour after PCI to call it so. It has to persist for several weeks after PCI to be concerning for dyskinetic aneurysm. However, even its persistence at one hour after PCI is already concerning for impaired long-term outcome and long-term mortality and long-term recovery of that anterior wall and apex. So the questions are though: are those, is this EKG phenomena common after PCI? We described how common it is after lytics; it happens in 30 percent after lytics, and in that case, we do rescue PCI. Now, how about if it happens after PCI? How common is it, and what do you do about it if it happens after PCI? So actually, this is quite common, based on many studies, persistent ST elevation after primary PCI, meaning resolution less than 50 to 70 percent, is common and is seen in about 30 percent of patients. Even 20 percent do not have 30 percent serial resolution. So 20 percent have barely any change of their ST elevation. Now why does this happen? Three mechanisms I want really to know those three mechanisms very well: distal microembolism, embolization of the thrombus. So we achieve good epicardial results, but the coronary microcirculation is plugged. Microvascular spasm, and this is a target of therapy, or very importantly, number three: myocyte injury and edema from ischemia or even reperfusion. So you can get sometimes irreversible reperfusion injury. Late presenters have this phenomena far more commonly. Imagine late presenters for limb ischemia; we worry about reperfusion injury and compartment syndrome. It's the same thing with late presenters and PCI. You can get irreversible perfusion injury, and that's one reason why you can get further or persistent at least cellular injury, edema, and even cellular death, and that can explain that persistent ST elevation. So it's most commonly in late presenters; it is associated with the worst long-term prognosis in terms of myocardial recovery and in terms of clinical outcomes. What do you see on the angiogram in patients with persistent ST elevation? What do you expect to see? So you may see in those patients what we call angiographic no-reflow. You open that artery; it looks great. The epicardial vessel looks great, widely patent, but the microcirculation is plugged. So you may, we have angiographic no-reflow. So impaired, sluggish flow despite wide macrovascular patency. That's the definition of no-reflow. You have to have a resolution, near full resolution of the epicardial stenosis to talk about no-reflow. However, no-reflow is not very sensitive, meaning most patients with that microvascular plugging they will have TIMI 3 flow, but they will continue to have persistent ST elevation. It means TIMI 1 to 2 flow is seen in 5 percent plus PCI whereas persistent ST elevation is seen in up to 30 percent of PCI. Okay, so if you have very impaired microvascular flow, you will see no-reflow and persistent ST elevation on EKG. If you have somewhat impaired microvascular flow, you will have TIMI 3 flow; you will not have no-reflow, but you will have persistent ST elevation on the EKG. Now, if you have excellent microvascular flow, and this is what we shoot for, you'll have TIMI 3 flow and resolution of ST elevation, and the prognosis is progressively better in those three, going from this to that. Okay, the reasons for angiographic no-reflow are the same three reasons as persistent ST elevation, except they need to be more severe to see it and on the angiogram than to see it on the EKG. So what do we do about it? Unlike persistent ST elevation after thrombolysis, persistent ST elevation after successful PCI does not dictate any further procedure unless, unless what? So basically, persistent ST elevation tells you, you know, the prognosis is impaired. Unfortunately, there isn't much we can do. Partly it's impaired because of the late presentation, but you should do something if the patient has severe pain or angiographic no-reflow. When you have that extreme form that manifests as angiographic no-reflow or or persistent severe pain, you should do something about it. And what can you do about it? This is what you can do about it: the sequential treatment any interventionist needs to know those three. So one, the easiest one is intracoronary vasodilators. Now keep in mind, intracoronary vasodilator, try not to give them via the guiding catheter, try to give them via distal lumen catheter. Why? Because there is impaired distal flow. If you inject them via the guiding catheter, they are not going to make it distally. So to make it easily, you advance like a dual-lumen twin-pass catheter distally, and you inject through it any of those four: adenosine, verapamil, nicardipine, nipride, usually in that range, 50 to 200 micrograms. Keep in mind nitroglycerin, you may try it, but it typically does not dilate the microcirculation; it dilates the epicardial vessels. So those are the ones you need to use. If those don't work, the second line of treatment is glycoprotein inhibitor, eptifibatide. Also, you can give it, give it systemically, but consider using it distally via that dual-lumen catheter because this will attenuate and try to dissolve those distal microemboli. Okay, the third line of treatment is balloon pump. Balloon pump does not improve coronary flow in patients with severe stenosis; it is not going to be able to push flow in diastole through an obstructive lesion. However, once you relieve that obstructive lesion, the diastolic augmentation will improve coronary flow and will improve coronary microvascular flow. So actually, balloon pump is an excellent treatment for microvascular flow after opening the epicardial stenosis. So if I give you that same patient scenario, same EKG, but instead of telling you his chest pain is almost resolved, I tell you, well, he has significant residual chest pain and distress on the cath lab table and it has a slow TIMI 2 flow, what do you do? Well, in that case, we have to do that three sequential treatment.

I will move on to the next idea here. So a 55-year-old man presents with shock and severe pulmonary edema. His wife notes that he complained of chest pressure for several hours, four days previously. EKG shows inferior Q waves and one-millimeter ST elevation. No murmur is heard on exam. Echo shows inferior akinesis with a mild MR. What is the next step? Coronary angiography and PCI? Coronary angiography, PCI, and balloon pump? Right heart catheterization and Impella CP? This question is in my book, by the way. A lot of those information and images are from my book. So this patient has cardiogenic shock. He's presenting four days late. One may justify, of course, it's cardiogenic shock; it doesn't matter when he presented; he needs to undergo reperfusion and potentially support device. That's the idea to justify B. However, the answer is actually C, TEE, sorry here for the typo. The answer is C. The idea you need to know is the following: inferior MI by itself rarely causes cardiogenic shock. So the classic teaching is always that whenever you have an inferior MI, you have to think that this patient has either RV shock or mechanical complication or bradyarrhythmia causing the shock. You have to rule those out before calling the shock as purely due to the inferior MI. So you suspect in this patient mechanical complications, specifically MR, papillary muscle rupture. And the problem is that papillary muscle rupture can be deceiving on physical exam and can be deceiving by Echo. Why? Because when you have papillary muscle rupture, you get that acute massive MR, and you get that huge V wave with near equalization of LV pressure in late systole. This attenuates your murmur for one; it also attenuates your color Doppler velocity, particularly in late systole. Also, your MR jet is eccentric, so it's eccentric, and it's a brief cutoff V wave cutoff MR Doppler. Those are frequently missed by TTE. In fact, you may see it on Echo itself; you may see a mass, a piece of papillary muscle had a flopping in the LV and to the LA, but color may be deceiving. So on this patient, papillary muscle rupture is highly suspicious. You should do TEE and rule that out before you proceed with treating just the coronary and using support devices for straight irregular cardiogenic shock. Your duty, then you do coronary angiogram, then emergent surgical mitral valve replacement. So again, the classic teaching is inferior MI with shock, think this: RV shock, mechanical complication, relative bradycardia or AV block, or he has a prior MI or LV dysfunction. The least likely is just the inferior MI. In that case, it will be a super dominant tract with apical, posterior, and lateral involvement. Now, shock with inferior MI: always doing emergent Echo. If the emergent TTE is suspicious but not definitive, as in this particular case, for mechanical complication, a TEE. If the patient is around the PCI or around cath time, do an LV gram. LV gram has a very high yield for diagnostic diagnosing mechanical complication if well done; it probably even has a higher yield than Echo. If this patient was presenting within 12 hours with cardiogenic shock and inferior MI, I would take him for cath, but before I do the PCI, I would do an LV gram in a patient like this, make sure no mechanical complication, then I will do the PCI. Good question. It doesn't have to be a TEE in this particular patient here. You could take him for coronary angiogram and LV gram and balloon pump, then send him for surgery if you indeed confirm that he has MR by LV gram. So that's another option.

I want to give another case scenario. This case scenario is very dear to me, and I'll tell you in my clinical experience I have yet to see a doctor clinically make the right diagnosis on those patients. So a 68-year-old man presents with inferior and lateral STEMI. He undergoes primary PCI of a large thrombotic codominant proximal left circumflex. He has been doing well, but then he suddenly develops near syncope on day 2, blood pressure 70 over 40, pulse 35. No murmur is heard. EKG shows sinus bradycardia with re-elevation of the ST segments in the inferior leads by several millimeters. What is the most important next step? Immediate coronary angiography? PCI? Immediate echocardiography? Immediate placement of a transvenous pacemaker? He is very slow and in shock, and he has re-elevation of the ST segments. What's the answer here? I'm going to go back to that case. I'll give another case. This is a patient I had a week ago. This is an 80-year-old female, late presenter, 48 hours late. She had pain 48 hours ago, no residual chest pain. This is her EKG. She has ST elevation in leads V2, V3, V4, and V5, no Q wave. Now keep in mind, the lack of Q wave doesn't mean she's not late. I think this patient is late; she's over 24 hours, and she has no ongoing pain. She has two of those three features, including that very important number three. 33 percent of all patients did not have Q waves, still did not benefit from PCI. Not all late presenters…

Have Q waves, and that depends on how transmural your M4 and the location of the impact. Sometimes the impact is not fully transmural, so you don't form Q waves. Sometimes you have two competing—in fact, you have an infarct in the anterior wall, but you have an old infarct in the posterior wall, and that precludes you from having Q waves. And sometimes conduction abnormalities can preclude you from having Q waves. So not all late presenters have Q waves; so we don't—we're not absolutely obliged to take this patient late. We may put her in the old trial nonetheless, because I like to have a QRS; I like to have all three features—a deep QRS, to avoid doing late PCI.

I took the patient for the lab, and we did PCI of an occluded LAD, but it was probably not warranted. Now, after doing PCI of the occluded LAD, this is her EKG. As expected, as the elevation did not get better—in fact, it may have even gotten worse—she still feels fine clinically; no issues. Twelve hours later, she got up to go to the restroom, and she had a pre-syncope, a blood pressure systolic 75, pulse of 40 beats per minute. She has significantly worsening ST elevation on telemetry. She lied down; she felt a little better, but 10 minutes later she has a progressive bradycardia, then a systole, and she dies. What's the diagnosis? The diagnosis is free wall rupture, and you need to think about it in any patient with such a scenario. Free wall rupture is the most common and the most underdiagnosed mechanical complication. If I ask what's the most common mechanical complication, a good proportion of physicians will say papillary muscle rupture or ventricular septal rupture. That's not true; free wall rupture is far more common than the other two, and it's the most underdiagnosed mechanical complication. It's seen in at least one and a half percent of patients treated with PCI, compared to less than 0.5 percent of the other two; three percent of patients treated with thrombolytics; and at least six percent of patients not reperfused.

What are the risk factors? It's late or no reperfusion, as in this patient; severe hypertension; female sex; older than 65-70; as anticipation first MI; and as anticipation and absence of collaterals. And that was interesting in this case: when I took her to the lab, I fixed the LAD, but even 48 hours later she had absolutely no visible collaterals to her LAD. She had all of those features. And when does that free wall rupture develop? Most doctors think that the peak frequency is at three to five days. That was correct in the pre-reperfusion era. In the reperfusion era, most mechanical complications—all three of them—occur in the first 24 hours. The second peak is at three to five days. Why is that? Myocardial rupture of any sort—any tear, whether ventricular septal rupture, free wall rupture, or papillary muscle rupture—it occurs at the border zone between the infarct and the normal myocardium. It's a high shear stress area; you have hypercontracting myocardium here and akinetic dyskinetic myocardium here, so you get the rupture at this point normally. Now, in the pre-reperfusion era, as I explained in the past, you get progressive LV remodeling and dilatation, so much so that your wall stress and shear stress increases progressively over the course of the days, and the shear stress at that junction, border zone, gets worse at three to five days, so that was the peak; rupture was at three to five days. Nowadays, with reperfusion, we don't get that as much; therefore, the peak is no longer at three to five days, and it is at least as likely to happen the first day. It may even hypothetically be favored by the perfusion injury in those late presenters on whom we do reperfusion. When you do a PCI on this patient, you're one—you're creating reperfusion injury potentially; we don't withhold PCI because of this concern, but that is a concern. And two, you may create a rush of blood to that necrotic area, so we can create myocardial hemorrhage, which is a frequent component of free wall rupture. So that's why it's seen more often in the first day in the current era.

In the shock registry now, through our rupture often leads to tamponade and a bradycardic PEA, and it's often nonsalvageable. It commonly has one of the following prodromes before you go into PEA: recurrent chest pain; re-elevation of ST segments—very important. When you see the elevation of ST segments, a lot of doctors rightfully think about thrombosis, and yes, that should be a top consideration, but don't forget free wall rupture. You get local pericardial irritation with free wall rupture, and therefore you get re-elevation of the ST segment. You also get bradycardia, and you get vagal effect and syncope. So remember those; anytime you have those, think free wall rupture, even if it is transient. Now, most often, if this progresses to PEA, the patient is not salvageable, so even if you miss it, it probably unfortunately doesn't make a difference. However, it will make a difference in those cases—in 30 percent of the cases—you develop those prodromes, but you don't go into full-blown PEA and tamponade, why? Because the rupture temporarily seals itself with the clot and pericardium, so you develop either a localized pericardial effusion or what we call pseudoaneurysm—it's a rupture that is sealed by pericardium and clot. This is where it's important to recognize those problems, and it's again up to 30 percent of the cases you can save—30 percent of those patients. This is where it's important to recognize those prodromes and to do immediate echocardiography, contrast, look for any effusion. Again, a lot of times it's not dramatic effusion; it's a localized effusion or a pseudoaneurysm, so look carefully at all the walls; look at flow across any LV defect, whether by color or by contrast; and any doubt here, and eventually to confirm, you have to do CT or MRI.

So, for example, imagine that same patient I gave you here, this one, but with a slightly different scenario. So 12 hours later, she develops pre-syncope while getting up to the restroom; blood pressure 75, pulse 40. Blood pressure and pulse improve as she lies down, and with—they gave her saline fluid bolus—she remains uncomfortable and hypotensive. A lot of doctors here, they see an elevation on telemetry; they will be thinking about putting a temporary pacemaker and take her back to the cath lab for pacemaker and for repeat coronary angiogram for those ST elevation. Wrong. You should think: first, rule out rupture before doing all this. Uh, they may even give you a scenario: she had all this, but now she's feeling okay; blood pressure improves; she goes back to sleep. Well, everybody may feel happy, but no, don't feel happy. Even having those temporary symptoms should alert you to a sealed rupture and should trigger the workout. Okay, I go back to that initial scenario I gave you; the answer to that was B: immediate echocardiography, because of the concern of free wall rupture, not taking him back to the cath and doing PCI and pacemaker. Importantly, in your board, they may give you even a different case scenario; they may give you a patient who never developed any symptoms; she's feeling okay all along, but you do an echo on her; she's totally asymptomatic, and you see moderate pericardial effusion. Any moderate pericardial effusion, including—including asymptomatic, incidental pericardial effusion on echo post-MI, should be highly suspicious for a sealed free wall rupture and should trigger MRI or CT. So, in a board, you can have a question like this where they give you a long scenario; they talk about non-sustaintability; they talk about EF; and they throw in a small statement about pericardial effusion—one centimeter or more pericardial effusion—and they tell you what to do next. Well, the answer here will be C: don't get distracted by ACE inhibitor or whatever; monitor the patient in the hospital for a longer period of time; repeat echo and obtain cardiac MRI or CT. That should be the answer in that case. So remember that hint in your board: moderate pericardial effusion, and in your real life, suspicious for free wall rupture. Now, free wall rupture is most common—just so you know—in the anterior and lateral wall, so it's most common in LAD, left circumflex, and sometimes it's just a small diagonal. In fact, I've seen it with a small diagonal branch.

Now, when you have that sealed rupture with persistent hemodynamic compromise but no PEA arrest, those are patients you want to undergo emergent surgery, but before emergent surgery you may take them to the lab and stabilize them by putting ECMO. You know, that's one thing that could be considered in those patients with persistent hemodynamic collapse while awaiting surgery. Another idea I want to mention: free wall rupture is the third most common cause of death in acute MI after out-of-hospital arrest and cardiogenic shock. It's actually the second most common cause of sudden death in acute MI. It is seen in 12 to 30 percent of early sudden death after MI. I want to give another case scenario: this is a 65-year-old female, hypertensive, no prior CAD history. She had chest pain four days ago. She presents with dyspnea, severe hypoxemia or pulmonary edema, and low blood pressure of 85 millimeters of mercury. EKG shows inferior Q waves with about one to one and a half millimeter ST elevation. We did right heart cath on her, and this is the wedge pressure. What diagnosis is suggested by this wedge pressure? She has a massive V wave; look at that V wave; it almost reaches 60 millimeters of mercury. The mean wedge pressure is about 30 with a V wave of almost 60 millimeters of mercury. What gives you such a huge V wave? So, MR is possible, yes. Now, this is the full right heart cath; you can see the RA pressure, PA pressure, and don't forget another diagnosis in acute MI that gives you a big V wave: LV cardiogenic shock; severe LV failure can give you a massive V wave. There's another diagnosis that can give you a big V wave; we always check for or to step up in those patients: VSD, or ventricular septal rupture, VSR, can cause massive V wave. Okay, and this is what this patient had; her SaO2 was 38 percent; her PA SaO2 was 80; she had massive O2 step up, so she had ventricular septal rupture, and that massive flow that recirculates back to the left ventricle and the left atrium creates that massive V wave in the left atrium. So, after echo confirms the diagnosis, what's the immediate next step? So, again, to summarize: 65-year-old female, inferior MI, she's presenting several days late with cardiogenic shock and pulmonary edema, and she has massive V wave, and we diagnose on the right heart cath that it's likely ventricular septal rupture, not papillary muscle rupture, although you can have both as well, so keep that in mind, but the—the findings are totally consistent with ventricular septal rupture. So, after echo confirms a diagnosis, what's the immediate best step? Coronary angio and PCI; emergent surgical correction after coronary angio and balloon pump; Impella CP, then Impella 5 if needed, and balloon pump. The best answer is C. So, his explanation: it's not A; it would have been appropriate if the patient had cardiogenic shock, even if she's presenting late, but she doesn't have a mechanical complication, but again, this is inferior MI with cardiogenic shock; indeed, she did have a mechanical complication, so that's not the right answer. The B, C, and D are appropriate, but the most appropriate is likely C. Why isn't it emergent surgical correction? A lot of people think emergent surgical correction is the answer for VSD; it is the answer for mitral valve papillary muscle rupture; it's not the best answer for ventricular septal rupture. Why? And here's the answer: it is very difficult to sew ventricular septal rupture early on, as the margin of that rupture—of the tear—are necrotic, friable, and mushy. The same limitation applies to percutaneous plug, and in fact, even if you correct it early on, you may create secondary tears and rupture post-op. That's why surgical or percutaneous mortality improves if you can wait more than seven days, so you have a harder tissue to sew on, and if possible, if you can wait more than three weeks. And in fact, data shows that the operative mortality is over 60—60 to 88 percent—if you operate the first day versus 30 percent if you wait more than seven days and 10 percent if you wait more than three weeks. Now, of course, this is partly what you call survival bias, meaning patients who survive more than seven days are less ill and more likely to survive; it's not just the surgery. Nonetheless, because of that technical issue and that survival data, try to wait before doing surgical repair or percutaneous repair. We do know that you do need to repair it eventually, because 95—94 percent of unoperated ruptures die at 30 days. Unclear how many unoperated ones die in the first one or seven days, but this is kind of the approach: you try to wait at least seven days if you can, so try to stabilize hemodynamics with the balloon pump or better with Impella CP, and try to wait more than seven days before surgical or percutaneous repair. In patients who are stable with a small ventricular septal rupture, you can even try to wait three weeks. Patients with severe shock may not be able to wait that long; those may require emergent surgery versus practically more aggressive stabilization with better support devices, and the best support is ECMO plus Impella. In one study in Circulation, in one mathematical model, has shown that Impella 5 appears to be the device with the most reduction of left-to-right shunting and most improvement of forward left ventricular flow into the aorta and the best improvement of wedge pressure. But if you want to stabilize the full hemodynamics and the potentially concomitant LV and RV failure, then you combine ECMO and Impella 5. So, in those cases, you get the most improved left-to-right shunt and wedge pressure and the best improvement of systemic flow and systemic pressure. You don't have to jump directly to ECMO plus Impella. So, in this particular patient, she is not in severe shock; you may start with something milder in philosophy; you may even start with volume pump; it's not incorrect, but probably the best answer is Impella CP, but be ready to quickly upgrade, depending on the patient's progression—upgrade from CP to Impella 5 or balloon pump to CP to Impella 5 plus ECMO as needed. Okay, and try to make them wait before surgical correction if you can. In this particular patient, a balloon pump was placed, and this was her SvO2—the mixed venous O2 in the SVC; it was 39 after we placed the balloon pump. What happens? You reduce left-to-right shunt because you improve forward flow, and therefore, because you improve forward flow, one—your SvO2 will improve; you have better left-sided flow, so it becomes 56 percent, and two—you get less step up because you're having less left-to-right shunt, so the step up improves; the SVC O2 improves; also the V wave dramatically declines after putting a balloon pump, and it will decline more if you put Impella. In this patient, this patient is stabilized on a balloon pump, then Impella, and she was operated nine days after this, which is 13 days after her MI, using double patching of the VSD hole. Unfortunately, she still died of postoperative complications, and this is, you know, the recommendation from the American Heart Association: we suggest delaying surgery when feasible in hemodynamically stable patients without respiratory failure to allow for better patient selection. And this is from the European guidelines; same idea: they suggest delayed elective surgical repair may be considered in patients who respond well to aggressive heart failure therapy and support devices, and they indicate that early surgery is indeed associated with high postoperative mortality. So, try to wait if you can. And I mentioned here the very high mortality of ventricular septal rupture. The mitral valve surgery, on the other hand, has a lower mortality; it has a mortality of 20 to 25 percent. Part of the reason is that in mitral valve surgery you don't have to sew the necrotic muscle; you can just put mitral valve replacement, and commonly that's the treatment: mitral valve replacement, not repair. That's why the mortality—the surgical mortality—of mitral valve replacement in acute MI is lower than correcting ventricular septal rupture. Another idea I want to describe here is that the ventricular septal rupture occurs probably with similar frequency in anterior and inferior or inferolateral infarctions, whereas we know papillary muscle rupture is more common in inferior infarct—of the posterior medial papillary muscle, which has a single perfusion from the RCA or the circumflex, whichever is dominant, whereas ventricular septal rupture occurs with similar frequency in anterior and inferior infarction. Anterior infarction are more likely to cause apical defect, whereas inferior lateral infarction are more likely to cause basal defect at the posterior basal septum. Posterior ventricular septal rupture poses additional technical challenges; they are more difficult to fix, and they have higher mortality, as in the patient I showed, because the heart must be elevated in order to sew, so it's an additional difficulty. Also, you have a nearby posteromedial papillary muscle and valve leaflet and PDA in close proximity that you need to avoid injuring. Another idea: LV gram, like I mentioned, is an excellent tool to diagnose all three mechanical complications, and this is LV gram for ventricular septal rupture. Use an LAO view; LAO view that looks in this direction will lay out the septum very well, especially eleocranial, and will show you very nicely the ventricular septal rupture and the filling of the right ventricle.

I will give one more idea here: I have a 67-year-old man; he has a prior CABG and non-bypassed right coronary artery. He presents with a generalized chest discomfort for 12 hours. He has inferior ST elevation, particularly in lead III. So we performed PCI of an occluded right coronary artery. This is the EKG one hour post-PCI; you can notice his ST elevation did not change much; it went from four to three millimeters in lead III; not a good response, even though he did not develop Q waves in leads II and AVF. The recovery of his inferior wall is unlikely in light of the persistent ST elevation. Persistent ST elevation after PCI is at least as bad and likely worse than Q waves; usually Q waves are present with persistent elevation, but not always. This is the second case that I show of that sort; this patient had persistent ST elevation post-PCI and bad prognosis; she eventually died, yet she did not develop Q waves. Now, 36 hours after PCI, which is 48 hours after his STEMI onset, he develops this on telemetry, so he gets a couple of PVCs, then he goes into sustained VT, and that sustained VT—monomorphic VT—degenerates into V-fib, so he got defibrillated. No significant angina; EKG after the VT is similar to the post-PCI EKG. On echo: inferolateral akinesis, EF 36 to 40 percent. What's the cause of his sustained monomorphic VT? Is it ischemia? Is it stent thrombosis? And the current ischemia of that inferior wall? Should he get ICD, life vest, or should he get emergent cath, or the combination of all this? Why does he have VT? It is not ischemia; it is a scar; that's the answer I want, and here is why: the first 48 hours after a large acute AMI, whether STEMI or profound extensive ST depressions, non-STEMI, and very large troponin rise, V-fib or polymorphic VT is an ischemic rhythm due to potassium fluxes and abnormal automaticity. VT—in this case, that early VT, V-fib—affects short-term but not long-term prognosis. So, if you don't die from that early V-fib out of hospital, you're likely to have a very good prognosis; it doesn't affect your long-term prognosis, that early V-fib, and no indication for ICD for the first 48 hours, V-fib or polymorphic VT. Now, more than 48 hours after an acute large infarct, any VT—monomorphic, polymorphic, or V-fib—is indicative of scar and is not a primary electrical ischemic process. In those cases, data shows that VT correlates with pump failure, extensive myocardial damage, and increased long-term mortality from both heart failure and VT, and therefore you absolutely qualify for ICD, class 1 in the ACC guidelines. Unfortunately, ICD may not eliminate the whole risk of this patient because VT correlates not just with future risk of VT, it correlates with pump failure and extensive myocardial damage and risk of death from myocardial failure. Now, the third idea that is dear to me is that monomorphic VT, even if it is early—early or late—monomorphic VT indicates a scar, increased long-term events, and warrants an ICD. Even if it is early, monomorphic VT typically results from scar and is not due to acute ischemia. As per the guidelines for VT, it may rarely be seen in acute MI, even early on in the first 48 hours, almost like our patient, but even in this case it is likely a marker of a permanent substrate from a prior scar. So the patient who has it early on likely has a scar from an old prior inferior infarct, and he's having a second inferior infarct now, or his presentation is later than we think; we think it's 12 hours; maybe it has been going on for much longer than the patient realized it. So, in those cases, when you have monomorphic VT, you do have an underlying permanent substrate and scar, and you have a high risk of recurrence. Ischemia may facilitate the induction of monomorphic VT but is not the underlying cause of it. Okay. Now, on the other hand, direct V-fib or polymorphic VT can be due to acute ischemia, but they don't always mean acute ischemia. Keep in mind the scar also can give you direct V-fib and polymorphivity; they do worry us about acute ischemia, and they do want us to make sure we eliminate acute ischemia, and we do cath, but they don't necessarily imply ischemia; they can be seen in scar. Acute ischemia is implied when you have ischemia on EKG—ST depression profound or ST elevation—or the timing is less than 48 hours after a significant infarct. Rely on the EKG to decide whether there is recurrent ischemia, not so much the troponin, because the arrhythmia itself and the cardiac arrests can cause a rising troponin. Okay, VT that is monomorph—monomorphic or even polymorphic—outside the setting of acute MI on EKG usually signals an underlying scar, and its inducibility is not affected by revascularization, even if a lesion is found. There was an old but very good study by the Brugada, published in 2001; they took patients with monomorphic VT—inducible monomorphic VT and CAD—that is not acute MI; they fixed the CAD, then they repeated the EP study, and they showed that fixing the CAD has absolutely no effect on the inducibility of monomorphic VT. Therefore, according to the ACC guidelines that I'm quoting here, in patients with ischemic heart disease and sustained monomorphic VT, coronary revascularization alone is an ineffective therapy to prevent recurrence. Beware of coronary angiographic findings in the setting of monomorphic VT. This is from my book: a coronary stenosis in a patient with monomorphic VT is a frequently incidental stenosis, the treatment of which does not affect VT recurrence. So it's fine to treat the coronary stenosis in a patient with monomorphic VT for another reason: he may have angina, so you may treat it for that reason; you may treat it for heart failure reasons, but just don't think that I'm treating the CAD and I'm protecting the patient from VT; I'm not; he still needs to have an ICD. So this is how we manage this patient. So we had sustained monomorphic VT about 48 hours after his STEMI, kind of right at the cutoff zone; he had later MI presentation, and his monomorphic VT is related to his scar; it's not acute ischemic VT, and the hint in his case is the persistent ST elevation post-PCI, which is another reflection of late reperfusion with persistent cellular injury. He did not have signs of acute ischemia; there was no reason to do emergent cath. We did cath anyway next day, and it shows that the RCA is widely patent. He had actually multiple recurrences of sustained monomorphic VT that we stabilize with antiarrhythmic therapy. Eventually he underwent ICD; I will not put life vests in this patient; he does need long-term treatment of the VT related to his scar.