This Cardiovascular Medicine webinar is designed to develop a framework to recognize, diagnose and manage mechanical complications of myocardial infarction. Mayo Clinic cardiology experts
Jeffrey B. Geske, M.D., and Mandeep Singh, M.D., moderate the webinar.
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Mayo Clinic Medical Professionals — Cardiovascular Diseases. Hi everyone, good afternoon. My name is Man Deep Singh and I'm a professor in the department of cardiovascular disease and I come to you live from Rochester Minnesota and today in the quarterly webinar series of acute coronary syndrome would talk about mechanical complications in patients with acute coronary syndrome. In patients with acute myocardial function. Um It it is my distinct pleasure and honor actually to introduce to you with Jeff Boesky, whose been recently promoted to a position of full professor. Congratulations. And he needs no introduction. He has co anchored R. C. V. Board of your course for as long as I remember and actually helped me pass those with flying colors and he teaches medical students very very passionately. He is leading the research in Holcomb patients. Does echoes. I don't know what else he does but he does a lot of things And he's a above all I think he's a great educator, I think that's his his uh suffix. I would say if I have to say Dr Yassky the educator. So with those words, let me pass it on to Dr Gorski who will talk about the mechanical complications in patients ridiculed myocardial function. Dr kinsky, Good afternoon. Well thank you so much, Man Deep for the kind introduction. I I appreciate that. I'm looking forward to speaking with our web audience. Look forward to your questions at the conclusion of the presentation and speaking about mechanical complications and patients with acute m I I have no disclosures other than that I have a little bit of a quirky sense of humor. So that may come into play as we go through this topic. Our learning objectives for this talk are really threefold. We plan to diagnose mechanical complications of me. We plan to develop a framework to recognize both rupture and non rupture mechanical complications. And then once we've identified and diagnosed those we want to select appropriate management strategies for these patients who oftentimes are some of the sickest patients that we will take care of in order to do that. I think it's important to have a framework to kind of organize and categorize mechanical complications. And I would broadly initially divide those into both rupture and unruptured complications. And within the unruptured group I would further subdivide into profound LV failure. RV infarct, LV, aneurysm, ischemic M. R. And dynamic outflow tract obstruction. Whereas within the ruptured group that can really happen at one of three locations. It can either be in the papery muscle, in the septum or in the free wall and we'll go on to further divide the free wall into frank or complete rupture versus a contained rupture. Also known as a pseudo aneurysm. But let's first dive into the unruptured complications and talk about profound LV failure. When we say profound lb failure, we're really referring to cardiogenic shock in the setting of acute. M. I. This is a decreased cardiac output in the setting of adequate intravascular volume with signs of reduced perfusion. I think it's good to have agreed upon definition that we can think of the human dynamic parameters that we'd be referring to here would be a systolic blood pressure, less than 90 or a map less than 60. That is sustained classically. 30 minutes would be the time frame. But I don't know any of my CCU colleagues who start a timer and at 28 minutes say no, it's not cardiogenic shock yet. Really, I think these are just parameters to help us think about this condition as a whole as the cardiac output drops things back up so we increase our primary kepler wedge pressure, left atrial pressures as the heart begins to back up in the setting of acute M I really were thinking about extensive myocardial infarction as the number one cause of cardiogenic shock. Many times. This will be in an anterior distribution but not always just knowing that the LED supplies so much of the my cardi. Um You need about 40% of the Maya Cardio loss to hit cardiogenic shock. Again, this is a round number. But as far as what we're talking about to drive cardiac pump function down into this state, about 40% of my cardio loss is enough to do that. There are some non infarct causes pulmonary embolism aortic dissection with acute Jr, a pickle ballooning. We're not really going to dive into those cardiogenic shock itself is an enormous topic and so I recognize that this is not specific to the mechanical complications, but it is something that I think is very german during this talk to mention that there are not in for causes. When we when we see these patients they tend to be older patients. Those with less reserve, they tend to be diabetics with anterior infarct as we mentioned. And if they've had a prior myocardial infarction, they've already lost some myocardial, it takes less incremental loss to get to that 40% threshold that causes profound LV failure. This happens most commonly in those with multi vessel disease or left main disease. Again thinking about the microbial territory that supplied but this last one at first caught me off guard early use of beta blockers in large influx because I generally think of beta blockade as being a good idea. You know this ends up being supportive. It's so much a part of the chronic care of patients with C. I. D. So what is the data that goes into early use of beta blockers and large influx causing profound LV failure. It really comes from the first key trial that we will discuss today that being the commit trial and commit was an enormous trial. This looked at greater than 45,000 patients who were having an acute M. I. And it randomized them into patients receiving protocal. Ized high dose, met Oprah law versus placebo. And I think you know if you just see meta prolonged versus placebo then that's fine. But the devil is in the details here because the meta prologue group received five mg I. V. Every 2 to 3 minutes. So long as their systolic blood pressure was not below the nineties or they weren't profoundly braddock arctic. And then immediately thereafter began loading with 50 mg of oral metaphorical every six hours. Such that within the 1st 24 hours in a patient who may have been beta blocker naive they perceived 200 mg of the total. Well what happens when you bury someone in a mountain full of meta protocol? Well you do decrease re infarction and ventricular fibrillation. But we also saw that in the first 1 to 2 days you have a lot more cardiogenic shock. The person already has an insult going on. And then if you load them up with high dose protocol eyes, beta blocker you end up with travel. So my take home point from that is to avoid high dose particularly I. V. Beta blockers and acute. M. I. When you're when you're doing it in a protocols fashion. That doesn't mean you couldn't give beta blockers in acute. M. I. But it does mean do so judiciously cardiogenic shock is a villain. This is something that has high mortality. And even though it occurs in a minority of patients undergoing microphone function it accounts for a disproportionate amount of the mortality. And so should we be treating those patients more aggressively. Should we be emergent lee revascularization, patients who present an LV failure either with P. C. I. Or or emergent cabbage. That was the subject of the shock trial. And the shock trial was a much smaller trial than the commit trial that we just talked about cocktail looked at 300 patients who had Stamey and presented with cardiogenic shock and it split them half and half between medical stabilization, which actually could include fiber analysis, tells you a little bit about the age of the trial versus those undergoing emergent revascularization which was split again about half and half between Pc. I. And cabbage. And what did we learn from the shock trial? We learned that there was initially no mortality benefit seen. Kind of surprising actually. Right. But that was looking at 30 days. And if you looked at subgroup analysis, those younger patients, those less than 75 years old did benefit from early revascularization at 30 days and at one year. And if you did further analysis though and looked at the overall cohort at six months, one year and six years. So beyond that initial 30 day endpoint, we saw that revolves cries patients did do better. So summarizing that, what is my take home point? Well the guidelines tell us do early revascularization. If you're young, Less than 75 years of age presenting with profound LV failure in the setting of M. I. You should pursue revascularization within the 1st 36 hours. And they actually extend that to all patients. Even those older than 75 based upon that additional follow up data. So my summary is early pcr cabbage should be considered for patients presenting with cardiogenic shock in the setting of acute M. I. Particularly if they're less than 75 years of age. Should we be using balloon pumps knowing that this has high mortality. Should we protocal eyes use of balloon pumps in patients with profound LV failure. Is there evidence for that? That was the shock to trial and shocked too. Looked at 600 patients with non ruptured cardiogenic shock and protocol eyes them to receive balloon pump or not and found that protocol eyes use of balloon pumps had no mortality benefit at 30 days for one year. Very interesting to see how the guidelines interpreted this trial. My thought is don't use balloon pump as a first line agent and that is kind of what they said but then they said if you don't use a first slide agent and the patient is not responding then it's class two A to still use it as an older guideline. And if you go across the pond to europe they actually say don't do it. So a little bit of conflicting thoughts there and I think that perhaps the stems from evolution of mechanical support. That balloon pump is perhaps not our best option in many patients. Things like an impeller can provide very high level support and this can actually be placed even subclavian. This provides up to five leaders of continuous support can be kept in place for some time up to up to 60 days and can really serve to stabilize patients as a bridge to Salvador transplant. So I wonder if some of the recommendation guideline differences, they're actually relate to alternative mechanical support. This can be a very challenging a decision to make, when to proceed with mechanical support. I'm always glad to have my colleagues in the Cath lab like like DR Singh to help guide that decision making and to help select the correct support. Let's move from the LV now to the RV. So we've done profound LV failure. What about right ventricular infarct and right ventricular failure complicating acute M. R. Thankfully RV. Infarct occurs in the minority of infarct about 10% and is much more common in inferior stem is likely because this is stemming from R. C. A coronary distribution. Oftentimes occurs in a proximal R. C. A. Lesion. Think about the RV branches coming off high on the R. C. A. To supply right ventricular myocardial. How we diagnose this? We look for one millimeter S. T. Elevation in leads V. One and then placement of right sided leads. So leed V. Four R is another place to recall right sided leads. Aren't done unless you ask for them. So if you're suspicious of right sided infarct. An RV in part to make sure that you pursue right sided leads because this is really the most sensitive BCG marker for RV injury. What does that look like here we have an example of an R. V. In park. You can see here circled S. T. Elevations in V. One and then I just had to relabel V four V five V six as the our leads because this is being done in that distribution. So this had to be asked for to place the right sided leads on echocardiography. We can see here an RV that's not doing so hot, there's global severe hipaa kinesis, there's RV dilation. It's actually quite a bit bigger in this view than the left ventricle. We can see septal flattening and this is a patient that is running into trouble from a significant RV. In farm. As the RV becomes acutely ischemic, it develops systolic dysfunction. Therefore the RV stroke volume goes down and the peak RV. Systolic pressure goes down. We can't generate that forward flow. And because we have that decrease in RV forward stroke volume, the LV actually becomes under filled, the LV pre load goes down and as the LV pre load goes down we slide down our starling curve, our L. V stroke volume goes down and therefore we have a total decrease in cardiac output, both RV and LV output. Now as the R. V becomes sick, it dilates. So it tries to slide up its starling curve but it actually ends up taking up more space within that fixed pericardial con fine and can squish that under felt LV. Further decreasing LV filling. There's a classic triad of symptoms and presentation of RV and farts and I think it's important to recognize this. A classic triad of hypertension, clear lung fields and elevated J. V. P. Now if you look at this triad you could say other things can look like this honestly tamponade can sometimes look like this and you may have to look at other things to help distinguish them. But I think that those clear lung fields really help to distinguish a predominantly RV issue from an LV issue. And I would recognize this triad. Sometimes patients undergoing RV infarct will develop unexplained hypoxia. And if you have a patient with diagnosed RV infarct either from that E. C. G. Criteria that echo that we looked at or you're just suspecting it based on the clinical trial that we said and they have unexplained hypoxia. Think about the fact that in the setting of an RV infarct you develop high right atrial pressure and you can actually pop open a patent foramen oval because of that and develop a right to left shunt you can shunt blood at atrial level because of high right atrial pressures and develop a shunt related hypoxia that won't respond to supplemental oxygen because that blood is not going through the lungs. How do we treat RV infarct well prompt re perfusion that's a theme that we saw in LV and parked and profound LVMH Park. Same thing here. Prompt re perfusion is key. In addition we want to maintain RV preload. Now this can actually seem counterintuitive in the setting of an RV. In part you can develop jugular venous distention because blood is backing up are a pressure is increasing. But despite an elevated GDP we actually want to give these patients fluids because they're LV is so under felt. Their LV pre load is low that giving additional fluids actually supports the RV and LV function you may require into tropes in these patients and they can really escalate quickly from being very sick. You may need to restore a V synchrony if they go into atrial fibrillation and avoid hypoxia. Now we learned with one mechanism of hypoxia if you can you want to provide additional support to avoid this because this further increases pulmonary vascular resistance can increase RV after load and worsen the entire problem. These patients can be very sick. So don't forget that mechanical support may be needed as you're pursuing prompt re perfusion. Think about whether this patient deserves mechanical support as there are options out there. I've shown to hear when being the protect duo the other being the RV in Pella. These are things that may be needed to support these patients as you're pursuing ivy, food resuscitation, coronary revascularization treatment of hypoxia. All of these different things in concert. What's next move on to LV Aneurysm. Oh the aneurysm occurs in less than half less than 5% of the time. It's very infrequent, tends to be in patients with anterior infarct and a decreased incidence. Uh now that we have more timely re perfusion LV aneurysm while it most typically shows up in the apex, I've shown here an example of a basal inferior finding and this involves all layers of the myocardial and will have a broad based neck, a broad based neck. Now the reason I think that's important is because these true aneurysms don't rupture and they look different than false aneurysms which we'll talk about later on. Here's a nice cardiac M. R. E. Example of a true aneurysm shown here in the same distribution of that illustration that we looked at a basil inferior distribution. While these don't rupture, they can be associated with significant arrhythmias. You can get thrombosis formation in these there can be other complications but they do not rupture. Talk about ischemic mitral regurgitation. Ischemic mitral regurgitation is the consequence of LV. Remodeling acutely. This can occur because of ischemia to the papery muscles whereby you can have a retraction of that mitral valvular apparatus and tenting of the mitral leaflets more chronically as the LV dilates. You can end up having remodeling of the LV that stretches the mitral annulus and further tense. That mitral leaflet by pulling on that sub valvular apparatus. Here is an example of what this can look like. This person is suffering an inferior lateral myocardial infarction. You can see in that inferior lateral wall that there is a kinesis. Their poster mitral leaflet has become tethered and anterior mitral leaflet override has occurred, which results in an e centric post early directed might regurgitation jet. It's important to recognize because this really affects forward flow in addition to resulting in potential pulmonary edema. Treatment of this again involves timely re perfusion. You may need to use diuretics in these patients with pulmonary edema and after load reduction allows for additional forward flow. It kind of makes the path of least resistance for blood to go forward as opposed to ejecting retrograde into the left atrium and into the lungs. The more my trigger irritation that you have post. Am I the worst you do. Let's move on to our last unruptured complication that of dynamic outflow tract obstruction and while not common. I think that this one is really important to recognize. This happens in a pickle infarct where we lose our a pickle contract. I'll function and we developed a compensatory hyper dynamic basil contract. I'll function which can result in dynamic outflow tract obstruction akin to the path of physiology of hypertrophic obstructive cardiomyopathy. Now this results in hypertension because you lose forward flow out the output track. But interestingly the treatment differs from all of the other forms of hypertension that we've discussed so far you want to confirm the diagnosis. You might suspect it initially by hearing a dynamic murmur. But confirmation is really gonna be through transfer asic echocardiogram and in this hypotensive patient undergoing acute M. I. We're actually gonna give them a beta blocker. Remember when we said that that could be problematic and actually can promote profound LV failure. But in this case we have a different mechanism. Even though hypertension is still presenting, beta blocker actually actually helps to prevent that hyper dynamic basil function. We want to avoid positive ana tropes which again are the treatment of choice in someone with profound LV failure and you want to avoid an intra aortic balloon pump. So the mechanism really differs despite an end or pathway result of low blood pressure. So think about the mechanism of what's going on with hypertension and the setting like um I don't use a default treatment for everyone because the mechanical complications differ from one of but shift gears a little bit into the rupture complications. We've talked about unruptured complications now rupture tends to occur in the first week, classically days 2 to 5. My my pathology colleagues tell me this is when the myocardial kind of looks like mushed peas as all the granular sites are kind of distributing within the myocardial we'll lose structural integrity of that. My cardio wall and it's right from my cardio complications of rupture, we said we can divide these into different groups. Let's start by talking about papillary muscle rupture, papery muscle rupture is uh it's important to know because the pectoral muscles are a sub and a cardio structure. And unlike many of the rupture complications that will talk about that only occur really in the setting of trans mural infarct papery muscle rupture can occur with trans mural infarct stemming or actually in the setting of n stem the sub and a cardio ischemia. We tend to lose flow to the southerner cardamom first. So this is an area frequently affected by myocardial infarction and it tends to be for paper muscle rupture that it's not symmetric which peppering muscle is involved. This is much more commonly involving the poster medial pepper muscle and that really relates to the blood supply because the poster medium pepper muscle has a single blood supply from the P. D. A. Whereas the anterior lateral pepper muscle splits its blood supply from the led and the circum flex. So in those patients that may it may actually be undergoing an RV infarct they could further on end up having peppering muscle rupture because that R. C. A. Tends to provide the P. D. A. And about 70% of people. So in someone with an R. C. A. M. Farc think about this as a potential complication. These patients present with acute severe mitral regurgitation and flash pulmonary edema as we begin to eject blood rapidly into the left atrium. Now we're objecting less blood out the aorta. So you have this sudden profound dropping forward stroke volume that can result in cardiogenic shock. Now our barrel receptor reflex sees this profound decrease in forward flow and can actually increase our system of vascular resistance in an effort to maintain an organ perfusion. But that actually increases LV. After load and further causes much regurgitation of vicious cycle can develop unless we quickly turn this around and seek guidance or seek repair of this mechanical complication. These patients present with acute dismay and pulmonary edema. They are sitting bolt upright in bed and respiratory distress and will they have a murmur? Well they might or it might be very soft or it might actually be absent if you break that mitral apparatus. And it's almost like there's no mitral valve there. You can lose the gradient between LV. And L. A. And you may have a rapid equalization of LV. And L. A pressures during systolic ejection. Therefore you may have no murmur at all. Here's an example of this. We see here this this case, we see that the poster media popular muscle is taking a vacation into the left atrium. It's not sticking down in the ventricle. And and as one would expect you can see there is torrential, profound wide open mitral regurgitation. How much mitral regurgitation. I mean literally you could drive a truck through this mitral regurgitation. That's how much there is this person is in profound respiratory distress there in pulmonary edema, they are rapidly decompensating. So once you've identified this, you've confirmed it with echocardiogram. The treatment is urgent surgery. You may need to stabilize the patient within the trucks with the balloon pump but rapidly get them to the O. R. I would not take this person back to the cath lab to redefine the coronaries before taking them to the O. R. Time is of the essence. You need to get them there and all those surgical mortality is high. Non surgical mortality is even higher. Let's talk about septal rupture as the next of our rupture complications. Septal rupture is shown here. This is showing a transfer resting echocardiogram at the basal level. And you can see there's lots of continuity of the myocardial at that basil in furious septum. If we put some color over that area, you can see that there is lots of tissue integrity and a shunt that has developed at that basil in furious septum. Now this can really take one of two flavors of VSD in the post infarct setting. One is anterior, which is not the one that we just showed anterior influx tend to be associated with a wraparound LED and tend to cause an atypical VSD. The other flavor is the one that we just saw and an inferior infarct. You can develop a basil inferior VSD. And unfortunately that's the nastier version. These ones think about it. There's a lot of important structures right there. There's the conduction system. There's the a V valves and these can many times have a very sore Sir pigeon this course. So these patients with VSD will present with hypotension, shocked dysosmia pain and a harsh systolic murmur. A harsh systolic murmur frequently accompanied by a thrill. And this harsh, loud, vigorous thrill associated member is a good way to to tell us apart of VSD. And a paper muscle rupture. Remember, pepper and muscle ruptures can actually be completely Oscar literally absent whereas this tends to be quite loud. Another thing is that pulmonary congestion is unusual in these patients, although they will develop a left to right shunt acute pulmonary edema is less common, which brings us to the age old adage that a new murmur with the patient laying flat. Not in pulmonary edema, pulmonary distress. That's A VSD. Whereas if the patient sitting bolt upright in respiratory distress and may even have an absent or very soft murmur or think about acute. M. R. These patients shunt from left to right, they developed an acute increase in their pulmonary blood flow therefore, and they have an oxygen step up in the RV. If we if we do a cath interestingly because of the increased flow through the primary vascular bed, you can end up getting a little bit of increase in those pulmonary pressures and you can see if you have a swan Ganz catheter of the waves. A V. Wave is not a great way to tell apart acute. M. R. From VSD from pepper muscle rupture from A VSD. They actually both can get a V. Wave in Papua muscle rupture. The V. Is from the torrential Metro regurgitation, its volume from the ventricle. Whereas in A VSD you can get a V. Wave from that increased blood flow, shunting left to right into the right ventricle and then across the pulmonary bed you can get volume from the vein. So in a popular muscle rupture you get A VSD from the ventricle or V. From the ventricle. Whereas in A VSD you get a V. Wave from the pulmonary veins from increased flow through the pulmonary bed. So don't rely on a V. Wave to tell these two apart. Instead look at the position of the patient and as well think about their murmur. A thrill. You're thinking VSD soft, maybe an audible murmur, pulmonary edema, rapidly progressive. Think about Katherine muscle rupture VSD. You're again going to think about emergent surgical repair. These can abruptly expand in someone who is more human advocacy stable. They may become less human chemically stable. But know that in those inferior ones like the one that we showed sometimes this can be really technically challenging and a surgeon may say, no, let's let's stick with medical management with kind of stabilization and that maybe the treatment of choice also know that when you have an interventional colleague available, it may be the right thing to think about non operative closure of A VSD with something like a perky tania's closure device. Hi operative mortality in these patients. Our last of the rupture complications is that a free wall rupture will talk about frank rupture to start. This is a dramatic, often fatal complication. Many times. This presents as an elderly woman with her first my cardio infarction, that's in the entire distribution. An elderly woman with her first entry, am I you think about a complication that can progress to this? A little bit of a graphic video here here we see a free wall rupture in an elderly woman presenting with her first interior. My this person was rushed down to the operating room. You can see the heart still beating. We've survived long enough to get them to surgery, but you can see how this could rapidly result in pericardial tamponade and patient death. Unfortunately, many times this presents his death. This is a frequently fatal event. But if you get a pulseless electrical restaurant unheralded bagel event, you should be thinking about free will rupture. Especially in an elderly woman presenting with her first interior macaron function. The last part of this free wall rupture that's contained. This is sometimes called a pseudo aneurysm. I don't love that term, a pseudo aneurysm because to me that doesn't sound as much like a rupture complication. And it actually sounds a lot like a true aneurysm, which we talked about before, that broad based neck. Those don't rupture, but these terms are synonymous uh incomplete rupture. Sub acute rupture, pseudo aneurysm. And this is where just a single layer of organized rhombus or pericardium is sealing that, that perforation. This may be a clinically silent event. Or maybe someone who has a stuttering chest pain that occurs in that correct 2-5 day window. And if you see a new pericardial effusion in someone who's posting my that should raise your suspicion for this. When you see a pseudo aneurysm, a pseudo aneurysm unlike a true aneurysm will have a narrow neck. So narrow neck. Think about rupture complication. Broad based neck. Think about a non rupture complication and I think that's important because clinical management of these will differ. Here's an example of a pseudo aneurysm. If you look here out at the LV apex in this 14 review you can see that there is flow from the LV apex out into this space, this eco lucent space out of the apex and this is someone who has developed an atypical pseudo aneurysm. He's gonna have unpredictable pretty progression to true. To complete rupture. This is something that deserves urgent surgical management. We've gone through a lot of different complications in this brief 30 minute talk, spending profound LV failure RV infarct LV aneurysm Ischemic, M. R dynamic outflow tract obstruction papillary muscle rupture septal rupture. True frank, free wall rupture and contained rupture. I would like to leave you with one slide of pearls. If you've drifted off, it's been a busy webinar, you're joining us in the afternoon in the evening, come back for one slide. These are the things I think are really high yield avoid high dose protocol. Ized I. V. Beta blockers in large ACUTE. M. I. You got to think about what you're doing because we know that these can result in profound LV failure. This can result in cardiogenic shock. So as you're thinking about use of beta blockers be judicious If you have a patient presenting with acute. M. I. particularly if they're less than 75 years old and they've developed cardiogenic shock. Think about early re perfusion. And truthfully the guidelines would support early re perfusion in all patients. Not just those less than 75 RV. Infarct has that classic triad that we talked about Of hypertension, clear lungs and elevated J. V. P. Reap refuse them in timely fashion. Give them I. V. Fluids and know that these patients can progress progress quickly quickly. You may need to give them in the tropics support or even mechanical support to get them through that acute event. True and false aneurysms. Even though aneurysm sounds the same. True aneurysms have a broad based neck. They involve all layers and they are not rupture complications. They can still have a rhythm, a genic complications and all of complications. But they don't rupture. Whereas a narrow neck is something you should be thinking about. Rupture complications and this is someone that deserves urgent surgical evaluation. Think about rupture in an elderly woman presenting with her first interior microphone infarction. Especially in that 2 to 5 day window where the mic Rd um looks like smushed peas. The patient's lying flat and they've got a thrill VSD. If they're sitting upright in pulmonary edema, think about palm might regurgitation even if the murmur is not present and know that a V. Wave is not the best way to distinguish between acute M. R. And A. VSD. With that. I would like to thank you for your attention during this webinar. I'd like to thank you dr Singh for inviting me to give this. It's really an honor to be here. I look forward to any questions that may come from the audience and I would like to acknowledge even going into those questions that these patients can be critically ill and that a team based approach is so important. You'll notice a lot of these patients. We brought in our surgeons, we brought in the Cath lab for timely re perfusion. We're utilizing our ICU resources and while I am an imager and someone who has a passion for structural disease and for many of these complications, I will admit that the team based approach. Getting that surgical consult, getting the Cath lab to advise you. Getting the ICU team is really an important step in managing these acutely ill patients. So I look forward to your questions. Thank you so much. Okay thanks Jeff. What a wonderful talk. What what what a delight. Um Let me start off from your last half of the presentation from a ruptured perspective having worked in Cath lab for three decades. Um I think there is complementary information to be had by doing an LV angiogram. If we suspect for example A VSD. Or a popularly muscle rupture. Especially if we can't hear RMR murmur and then the step up from RV. Or audit to R. V. Or R. V. Two P. I think is a critical information to be had if Echo is not readily available in in in a patient who has a P. A. Uh and and cardiac arrest and then economic show just medical refuge in. Um My my question to you um is that if you think that this is the kind of approach if a patient has a cardiac arrest um in the field or in the do you do echo before you send these patients to Cath lab? That's one question I want. And the second one, what have you seen in terms of temporal trends over time with very aggressive and timely primary pc. A analytics being given very aggressively because all these data that's coming up is not contemporary. It's kind of quite old. Yeah. And maybe maybe I'll answer your second question first because I think you've hit the nail on the head every single one of these mechanical complications that we talked about today. We've seen a decline in incidence of these as we pursue timely re perfusion and you'll notice the number one treatment for many of these is timely re perfusion. So I I think that that kind of really serves to emphasize that point. And and I'm I'm very grateful for this because many of these mechanical complications have such high mortality even when the management is done correctly. So I think it's a great point that although these are not as common as they once were, that they still occur and they may occur in patients who have had reduced access to care or prolonged time to re perfusion. That should raise your radar to suggest that these patients may be at higher risk for such mechanical complications as as far as your question regarding uh kind of triage of patients presenting with uh you know out of hospital arrest and things. I do think that um that there is some uh individual care that needs to be occurring there if you're having a patient that has having S. T. Elevation on their resuscitated rhythm. And I think that timely re perfusion is really of the essence. Um We didn't get into this talk into going through you know, targeted temperature management and some of the ways that that has improved outcomes and out of hospital arrest. But I do think that especially if the clinical suspicion is high for for a CS and for that is the cause of an out of hospital arrest then getting them to the cath lab without delay is is very important. Um I do think as well that that echo serves a very key role in diagnosing confirming and following these patients. And um this will depend on on the availability and access to to to uh to echo. But I will say I'm very proud of our ICU group and and much of our cardiology group who's adopted things like handheld echo things that can be done on the fly as you're making some of these decisions. Many of the of the physicians in our ICU are are very facile obtaining a quick echo images that can help to confirm LV function that can look for that new infusion. But I think too as you pointed out, if you are in the Cath lab and you have someone who is critically ill and they've just had a P. E. A arrest or their human dynamics are unstable and you're concerned for a mechanical complication then getting information expeditiously whether it's an LV graham, whether it's a right heart cath to look for a step up. I think that knowing those additional things in timely fashion to guide surgical management is really important because you don't want to call the surgeon and say, hey I think we might be having a mechanical complication. They say great I'll come and help what's the complication. And then you say I don't know yet. I think that having that confirmation step. Whether it's trans thoracic echocardiogram whether it's the LV graham, whether it's human dynamics to support this are important but know that that some of these can look alike. And I emphasize that a little bit when we talked about comparing dynamic outflow tract obstruction and cardiogenic shock to conditions that could mimic one another but have very different treatments. Similarly if you have someone with a swan and you see a V wave that's not enough, you need to really put on your thinking hat you need to make sure that you have differentiated between these conditions because the management can really differ and expeditiously figuring that out as important as human dynamics. Clinical stability can rapidly change in these patients. Yeah. Thank you. Thank you very much. I have a few questions before that. I also want to make a comment about the beta blocker issue. I think this is the same team um that don't start beat up lockers just before sending the patient or non cardiac surgery. They don't have the same favorable outcomes in comparison to a patient who has been chronically on beta blockers. And maybe we have to change our team here as well that don't super load them with high dose of beta blockers and beta blockers is something that we want to shy away from in a sick individual. That is not our priority? Um The question we have from the audience one is what do you think? Is there a difference between the outflow obstruction that you see in doc Kosovo cardiomyopathy representing versus the scenario that you described in terms of L bot obstruction and hypertension. Yeah. So I think that Takasu bow associated dynamic outflow tract obstruction and a pickle and my associated dynamic outflow tract obstruction. The the human dynamics and physiology are the same and the two scenarios can look honestly very similar and echo as well. You need that you need that kath to know. Do we have an L. E. D. Occlusion here that's caused an atypical infarct. Do we have a you know a 99% stuttering lesion in the L. A. D. Or is this a Takatsu bow? But from the standpoint of dynamic outflow tract obstruction mediated hypertension. I think that we're really talking about the same path of physiology there. Yes. So regardless if you have hypertension and you're suspecting Takasu boer ethical. In fact a true plaque rupture and you have hypertension treat, treat them the same way. Do not get bothered about whether it's Takasu bow or it's a true plaque rupture. The management is pretty similar. Absolutely. And I think if you're wondering between those two conditions not because of the presence of the dynamic alpha tract obstruction but the clinical scenario is unclear if this is a Takatsu bow or if this is an apple infarct you need to air on the side of defining the coronaries and and and and determining the direct invasive coronary angiography, what's going on and I think that's really important because absent that there's echo findings are really not going to tell you if this is an atypical infarct or Takatsu bow and the management is going to differ. I think that's the key point which is if we suspect Takasu Bow it is not by our clinical suspicion or demographics or by echocardiogram coronary angiogram needs to be performed for us to be sure whether this patient has struck a super or not because almost 90% of a CSR plaque ruptures and North Takasu goes yeah and you might have a clinical you might have a clinical scenario that doesn't involve coronary angiogram. But it's it's more the exception than the rule. If you have someone who has well defined coronaries, maybe they just had a C. T. A. Of their chests because the clinical scenarios unclear and you have the coronaries well defined and they just had the death of a loved one and they wouldn't want an invasive procedure but there are scenarios where you may not go forward with coronary into them. But I think the default needs to be to define the coroner. So um uh the second question I have from the audience is how would you treat true aneurysm. Now given the stitch trial results which have been very equivocal um If you find a true aneurysm, what are your guidelines in terms of conservative management versus sending them for a repair of true aneurysm. Yeah that's a good question. Um I think that uh that it's there's probably not a straightforward answer. So first off, I'll just say that I don't think there's a single answer that applies to all patients in that question. Um I would really want to know a lot more about about the scenario because you have a large pseudo aneurysm that's profoundly affecting LV function. I think that there's some benefit to focusing on LV function. Uh you know, therapies, beta blockers, ace inhibitors but the presence of true aneurysm, some somewhat the the the horses left the barn and you've got some uh irreversible damage there. Um I think the time that we've seen the most aggressive management and I think appropriately so is when there's been um arrhythmia associated with this. True aneurysm can be an itis for ventricular arrhythmias and I've seen cases where we've gone in and done ventricular applications, but also where we've gone and done aneurysm. Ectomy and patching because of the presence of ventricular arrhythmias associated with that true aneurysm, I think the selection is the key, Right? I mean, you know, if you if you think about it trump symbolism if you have a trump Asus record in trump embolism. Arrhythmia. You mentioned intractable heart failure in a patient who's otherwise, you know, has as a good life expectancy. You don't want to send the patient for surgery if they have a lot of co mobility's they're elderly and so you're right. I mean the treatment for true aneurysm needs to be individualist based on so many factors other than what the complications the true aneurysm can bring to the patient. Yeah and and differentiating true versus false is quite important in that regard because the presence of a false aneurysm you should think about unreliable, unpredictable sudden catastrophic progression of rupture versus true aneurysm. I think that you're really making that longer term planning as you said. Intractable heart failure, a arrhythmias, throttle anabolic risk management. I think I think there's a different pace to to that decision making and also some different things to consider. Yeah. Yeah. Perfect. So um I have a question uh from from me and then we have a follow up audience questions. So my question is now you said about ischemic M. R. Right. So ischemic M. R. Short term and long term. How would you classify ischemic M. R. Would it be a primary M. R. Or when the LV remodeling happens. Is it a secondary EMR or is it a combination of the two? How would you classify an M. R. Related to ischemia? Yeah that's a that's a good question. And we've seen in the 2020 valve guidelines some uh evolution or kind of development of our terminology for for discussing M. R. You know it's not really the leaflets fault in the setting of ischemic M. R. Okay this is really dealing with the sabah valvular apparatus whether it's a skeptic retraction of papillary muscles or whether longer term it relates to adverse or undesired LV remodeling. So in that regard I would think of this more along the lines of a secondary or non primary uh might trigger agitation. Um Now I think there can be overlaps between things but in general I would think of it in that regard. Um as opposed to a rupture based might trigger vegetation. There's really not role for things like mitral clip or per catania's mitral valve repair in uh in pathway muscle rupture or but I've seen used before in ischemic mitral regurgitation uh trans catheter approaches. I think once again having that that multidisciplinary team involved getting a surgeon involved because a surgeon would be a part of that discussion figuring out patient surgical risk. Uh and the and the best approach to to the mitral valve issue is important. Yeah. Yeah. So the question from the audience is a good one which is how would you then differentiate in ischemic M. R. From a ruptured popularly muscle when both of them can present similarly it's not like one of those dramatic echoes that you've shown but they can be less dramatic. Right? So they can just to record for example or the sub value apparatus is intact but but it is his chemical. So how would you then differentiate the two? That's a one? And the follow up question to that is how would you then manage? In other words is it always that ischemic mmr proceeds popularly muscle rupture. Do you have any insight to that or not? So I think the question really brings about the important point that imaging is key to differentiate these two. They both present with them are they both could have a murmur of M. R. And recognizing the underlying mechanism will define our treatment pathways. So and someone with ischemic M. R. We're looking for retraction of the sub valvular apparatus. We're looking for retraction of the papery muscles. We're looking for regionals that alter our closure anatomy for rupture syndromes. I would say in the setting of acute M. I. We're really talking about popular muscle rupture. Not not as much chordal rupture, chordal rupture I think of more as a complication of something like you know Microsoft prolapse repetitive wear and tear. But papery muscle rupture would be mechanical complication. Um If you're unsure based on trans drastic imaging because there's a confusing jet or because image quality is suboptimal or because the there's multiple jets then I think that this is a reason to proceed with trans esophageal echocardiogram. I think that you need to know the mechanism because a patient with popular muscle rupture. Even partial pepper and muscle rupture as the mechanism of significant regurgitation that's really a surgical issue. It's a structural mechanical issue and no amount of revascularization and medical therapy is going to unruptured it. Whereas someone who has ischemic mitral regurgitation. Uh Timely revascularization may be helpful. Uh and I think that recognizing that revascularization can improve my credit function. Can uh medical medical therapy can can result in reverse remodeling. That that there is a different general approach that can be taken and and there is some overlap again in a patient that has pectoral muscle rupture, they may have in addition elements of ischemic mitral regurgitation that have occurred because initially the peppery muscle was a systemic began to get retracted and then tore. So you have mixed mechanism. But once you've invoked a rupture as a as a part of this, we really transition from to a lot more surgical consideration. So if you have a significant M. R. In the setting of even though you are not able to demonstrate a lack of integrity of the mitral valve apparatus, do you routinely go for transits of eagle echocardiogram just to prove or disprove, I would not say that we do that in every patient. I think that you need to look at your images. I think defining a mechanism for my true regurgitation has equal priority to the severity of regurgitation. And so a report that just says severe M. R. But doesn't tell you why or how is not is not as helpful as it should be. And so I think engaging the imaging group in in that discussion. Looking at your own images is important if it's very clear that there's inter leaflet override because of retracted some value apparatus. And that is the mechanism I don't send all of those patients for trans esophageal imaging. Note if there's uncertainty or or suspicion but not not enough to confirm you bring the surgeon and say look, I think that's what it is and they say yeah, but we can't tell good enough then then additional imaging is important. And and it's not, it's something that you wait for the next day to decide if you suspect a pepper and muscle rupture and you have sub optimal transfer asic images. You've got to get the T. E. E. N. And maybe that's a T. E. That's done in the O. R. Suite as you're getting ready for stir anatomy. But it's a things have to move fast because once the ruptures have occurred, the clock is really ticking. Yeah. Yeah, very nice. Um The shark trial is quite old, you know, and we're still quoted because there is northern trial that we can lean back on. Um That confirms our contemporary practice, you know, But even though it was an old trial, it still stands true. Maybe the it was very slow in enrollment. Um But over time we haven't done much in terms of improving outcomes of patients who present the shot even more recently when you compare small studies comparing impeller versus balloon pump. Not much difference could be generated. Maybe it was small sample size maybe impala is not whole lot superior to balloon pump. Intuitively it seems to me that impala should work better than balloon pump if there is some LV contacted city left. Um, but we are just stagnant in terms of some innovative aspects, even reducing inflammation. You know, those trials have been negative. What do you think should be our next approach in terms of improving management of these patients? Were so sick? Yeah, I um you've you've asked a very challenging question because I share your sentiment. You know, whenever I put together a talk on mechanical complications, I always, you know, do a literature search to try and find, you know, that one breakthrough paper that's really gonna shift the landscape and then I end up citing this shock trial. Um, and I I think that um 11 thing that maybe is is a bit of dodging the question, but I think gets to the root problem is that timely revascularization before the problem occurs is really crucial. And and I think recognizing a CS and pursuing timely revascularization is the key that why we've seen less and less development of many of these mechanical complications. So does once you have a patient who has the complication, that's I mean, that again, we're kind of outside of the answer that I just gave. I think that I don't know the answer. Um, because as you said, you know, trials that have looked at at immunosuppressants for shutting down inflammation have come up blank and and the even the support trials have led to confusing differences in guidelines. And I think we end up resting on a lot of clinical judgment and and it it may be tough just given how how sick these patients are, how rapidly things can progress to ever find that key answer. I share your thought that um that one of the areas of of support that has evolved the most recently is in particular Tania's support. And it may be that that as we go from uh in Pella to things like bi ventricular support. You know, using protect do an impeller at the same time and someone who's presenting with by ventricular systolic function. I think reaching for those additional tools early and having the resources to to do those early is likely where the next advancements in mortality will come. But that's not based on a lot of data. It's kind of more a general thought. Yeah, we we have a very robust ECMO team who can present a very a very short notice if we have an eligible patient. But I think there is a conflict. There are two competing teams that are going on. One is we have improved time to re perfusion with very good uh ah systems in place. We are very aggressive in shortening the door to balloon time. Early recognition may be a problem. But I think the competing team here is that patients who are getting into shock are older than what initially the enrolled patients were in shock trials with lot more comorbidities advanced age that even though we have made advances towards rapidly in terms of re perfusion, we are dealing with older and sicker patients. So we haven't made too much inroads into improving their outcomes. And and I agree fully. I think that um as we've reduced the number of young patients that come to this outcome by timely re perfusion, we're left with a sicker pool entering into a high mortality state. And how how we bring them back from the brink of of kind of cardiovascular compromise is is very challenging. I think ECMO is a wonderful resource and certainly one that that the current state of medical affairs has resulted in having challenging availability at times. So I think that that also offers unique challenges moving forward. Yeah. Yeah. No, I think it's been a wonderful our of presentation and discussion with you Jeff any last minute pearls for the audience that you want to share with us. Yeah. I I think um these patients are so ill. Right. We've just spent the last few minutes talking about how challenging management is. Once we've reached this outcome of these mechanical complications. So I would encourage you when you have a patient in the acute M. I. Setting if they're hypertensive if they're in that 2 to 5 day window really pay attention for the presence of mechanical complications. Because early recognition confirmation via echocardiography of exam or clinical suspicions and timely prompt treatment are really the things that are going to be able to save your patients. Although we've seen the incidents of these complications go down with timely re perfusion, they remain villains in the space of acute myocardial infarction and only by really being vigilant. Are you going to find these in time to save your patients? So I hope that the tools I've helped outline today as far as categorizing them and the approaches that we've talked about are able to help you in your practice. Alright. Thanks Jeff for for all your insight. Thank you so much and have a wonderful afternoon. Goodbye now.