MANDEEP SINGH: Hi, everyone. Good afternoon. My name is Mandeep 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 we'll talk about mechanical complications in patients with acute myocardial infarction.
It is my distinct pleasure and honor actually, to introduce to you Jeff Geske, who's been recently promoted to a position of full professor. Congratulations. And he needs no introduction. He has co-anchored our CV Board Review course for as long as I remember, and actually helped me pass those with flying colors. And he teaches medical students very passionately.
He is leading the research in HOCM patients, does Echoes. I don't know what else he does, but he does a lot of things. And above all, I think he's a great educator. I think that's his suffix, I would say, if I have to say-- Dr. Geske, the educator. So with those words, let me pass it on to Dr. Geske, who will talk about the mechanical complications in patients with acute myocardial infarction. Dr. Geske, good afternoon.
JEFF GESKE: Well, thank you so much, Mandeep, for the kind introduction. I appreciate that, and I'm looking forward to speaking with our web audience. I look forward to your questions at the conclusion of the presentation. And speaking about mechanical complications in patients with acute MI, 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 MI. 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 are oftentimes 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 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 MR, 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 papillary 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 pseudoaneurysm. But let's first dive into the unrputured complications and talk about profound LV failure. When we say profound LV failure, we're really referring to cardiogenic shock in the setting of acute MI.
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 an agreed-upon definition that we can think of. The hemodynamic 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 pulmonary capillary wedge pressure, our left atrial pressures as the heart begins to back up. In the setting of acute MI, really, we're thinking about extensive myocardial infarction as the number one cause of cardiogenic shock. Many times this will be an in anterior distribution but not always.
Just knowing that the LAD supplies so much out of the myocardium. You need about 40% of the myocardial 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 myocardial loss is enough to do that. There are some non-infarct causes-- pulmonary embolism, aortic dissection with acute AR, apical 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 germane during this talk, to mention that there are non-infarct causes. 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 myocardium.
It takes less incremental loss to get to that 40% threshold that causes profound LV failure. This happens most commonly in those with multivessel disease or left main disease. Again, thinking about the myocardial territory that's supplied. But this last one at first caught me off guard-- early use of beta blockers in large infarcts, because I generally think of beta blockade as being a good idea. This ends up being supportive.
It's so much a part of the chronic care of patients with CAD. So what is the data that goes into early use of beta blockers in large infarcts 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 MI, and it randomized them into patients receiving protocolized high dose metoprolol versus placebo.
And I think if you just see metoprolol versus placebo, then that's fine. But the devil is in the details here, because the metoprolol group received 5 milligrams IV every two to three minutes so long as their systolic blood pressure was not below the 90s, or they weren't profoundly bradycardic. And then immediately thereafter, began loading with 50 milligrams of oral metoprolol every six hours, such that within the first 24 hours in a patient who may have been beta blocker naive, they've received 200 milligrams of metoprolol.
Well, what happens when you bury someone in a mountain full of metoprolol? Well, you do decrease reinfarction and ventricular fibrillation, but we also saw that in the first one to two days, you have a lot more cardiogenic shock. The person already has an insult going on, and then if you load them up with a high dose protocolized beta blocker, you end up with trouble. So my take-home point from that is to avoid high dose, particularly IV beta blockers in acute MI, when you're doing it in a protocolized fashion.
That doesn't mean you couldn't give beta blockers in acute MI, 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 myocardial infarction, it accounts for a disproportionate amount of the mortality. And so should we be treating those patients more aggressively? Should we be emergently revascularizing patients who present in LV failure, either with PCI or emergent CABG?
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. SHOCK trial looked at 300 patients who had STEMI and presented with cardiogenic shock, and it split them half and half between medical stabilization, which actually could include fibrinolysis-- 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 PCI and CABG.
And what did we learn from the SHOCK trial? We learned that there was initially no mortality benefits 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 revascularized 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 MI, you should pursue revascularization within the first 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 PCI or CABG should be considered for patients presenting with cardiogenic shock in the setting of acute MI, particularly if they're less than 75 years of age.
Should we be using balloon pumps? Knowing that this has high mortality, should we protocolize use of balloon pumps in patients with profound LV failure? Is there evidence for that? That was the SHOCK 2 trial. And SHOCK 2 looked at 600 patients with non-rupture cardiogenic shock, and protocolized them to receive balloon pump or not, and found that protocolized use of balloon pumps had no mortality benefit at 30 days or 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 it as a first line agent, and the patient is not responding, then it's Class IIa to still use it. This is 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 Impella can provide very high level support, and this can actually be placed even subclavian. This provides up to 5 liters of continuous support, can be kept in place for some time-- up to 60 days-- and can really serve to stabilize patients as a bridge to LVAD or transplant. So I wonder if some of the recommendation guideline differences there actually relate to alternative mechanical support.
This can be a very challenging decision to make, when to proceed with mechanical support. I'm always glad to have my colleagues in the Cath Lab, 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 MI?
Thankfully, RV infarct occurs in the minority of infarcts, about 10%, and is much more common in inferior STEMIs, likely because this is stemming from RCA coronary distribution. Oftentimes occurs in a proximal RCA lesion. Think about the RV branches coming off high on the RCA to supply right ventricular myocardium. How we diagnose this, we look for 1 millimeter STE elevation in leads V1, and then placement of right-sided leads. So lead V4R is another place to look.
Recall right-sided leads aren't done unless you ask for them. So if you're suspicious of a right-sided infarct, an RV infarct, make sure that you pursue right-sided leads, because this is really the most sensitive ECG marker for RV injury. What does that look like? Here we have an example of an RV infarct. You can see here circled ST elevations in V1.
And then I've just had to relabel V4, V5, V6 as the R 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 hypokinesis. 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 infarct.
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 preload goes down, and as the LV preload goes down, we slide down our Starling curve, our LV stroke volume goes down. And therefore, we have a total decrease in cardiac output, both RV and LV output.
Now as the RV 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 confine, and can squish that underfilled LV, further decreasing LV filling. There's a classic triad of symptoms and presentation of RV infarct. And I think it's important to recognize this. A classic triad of hypotension, clear lung fields, and elevated JVP. 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 ECG criteria, that Echo that we looked at, or you're just suspecting it based on the clinical triad 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 ovale 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 reperfusion. That's a theme that we saw in LV infarct, in profound LV infarct. Same thing here. Prompt reperfusion is key.
In addition, we want to maintain RV preload. Now this can actually seem counterintuitive in the setting of an RV infarct. You can develop jugular venous distension, because blood is backing up, RA pressure is increasing. But despite an elevated JVP, we actually want to give these patients fluids, because their LV is so underfilled-- their LV preload is low-- that giving additional fluids actually supports the RV and LV function.
You may require inotropes in these patients. And they can really escalate quickly from being very sick. You may need to restore AV synchrony if they go into atrial fibrillation. And avoid hypoxia. Now we learned of 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 afterload, 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 reperfusion, think about whether this patient deserves mechanical support, as there are options out there. I've shown two here, one being the ProtekDuo, the other being the RV Impella. These are things that may be needed to support these patients as you're pursuing IV fluid resuscitation, coronary revascularization, treatment of hypoxia, all of these different things in concert.
Let's next move on to LV aneurysm. LV aneurysm occurs in less than 5% of STEMIs. It's very infrequent. Tends to be in patients with anterior infarct and a decrease incidence, now that we have more timely reperfusion. 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 myocardium, and will have a broad-based neck. [LAUGHS]
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 MRI example of a true aneurysm shown here in the same distribution of that illustration that we looked at, a basal inferior distribution. While these don't rupture, they can be associated with significant arrhythmias.
You can get thrombus formation in these. There can be other complications, but they do not rupture. Let's talk about ischemic mitral regurgitation. Now ischemic mitral regurgitation is the consequence of LV remodeling. Now acutely, this can occur because of ischemia to the papillary muscles, whereby you can have retraction of that mitral subvalvular 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 tents that mitral leaflet by pulling on that subvalvular apparatus. Here's 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 akinesis. There posterior mitral leaflet has become tethered, and anterior mitral leaflet override has occurred, which results in an eccentric posteriorly directed mitral 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 reperfusion. You may need to use diuretics in these patients with pulmonary edema. And afterload reduction allows for additional forward flow. It makes the path of least resistance for blood to go forward, as opposed to injecting retrograde into the left atrium and into the lungs.
The more mitral regurgitation that you have post-MI, the worse 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 apical infarct, where we lose our apical contractile function, and we develop compensatory hyperdynamic basal contractile function, which can result in dynamic outflow tract obstruction akin to the pathophysiology of hypertrophic obstructive cardiomyopathy.
Now this results in hypotension, because you lose forward flow out the outflow tract. But interestingly, the treatment differs from all of the other forms of hypotension 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 going to be through transthoracic echocardiogram. And in this hypotensive patient undergoing acute MI, we're actually going to give them a beta blocker.
Remember when we said that could be problematic and actually can promote profound LV failure? But in this case, we have a different mechanism. Even though hypotension is still presenting, beta blocker actually helps to prevent that hyperdynamic basal function. We want to avoid positive inotropes, 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 pathway result of low blood pressure. So think about the mechanism of what's going on with hypotension in the setting of acute MI. Don't use a default treatment for everyone, because the mechanical complications differ from one another. Let's 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 two to five. My pathology colleagues tell me this is when the myocardium kind of looks like mushed peas, as all the granulocytes are distributing within the myocardium, we lose structural integrity of that myocardial wall, and it's ripe for myocardial complications of rupture. We said we can divide these into different groups. Let's start by talking about papillary muscle rupture.
Papillary muscle rupture is important to know, because the papillary muscles are a subendocardial structure. And unlike many of the rupture complications that we'll talk about that only occur really in the setting of transmural infarct, papillary muscle rupture can occur with transmural infarct, STEMI, or actually in the setting of NSTEMI, subendocardial ischemia. We tend to lose flow to the subendocardium first.
So this is an area frequently affected by myocardial infarction. And it tends to be for papillary muscle rupture that it's not symmetric which papillary muscle is involved. This is much more commonly involving the posterior medial papillary muscle. And that really relates to the blood supply, because the posterior medial papillary muscle has a single blood supply from the PDA, whereas the anterolateral papillary muscle splits its blood supply from the LAD in the circumflex.
So in those patients that may actually be undergoing an RV infarct, they could further on end up having papillary muscle rupture, because that RCA tends to provide the PDA in about 70% of people. So in someone with an RCA infarct, 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 injecting less blood out the aorta. So you have this sudden, profound drop in forward stroke volume that can result in cardiogenic shock now our baroreceptor reflex sees this profound decrease in forward flow and can actually increase our systemic vascular resistance in an effort to maintain end organ perfusion, but that actually increases LV afterload, and further causes mitral regurgitation.
A 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 dyspnea and pulmonary edema. They are sitting bolt upright in bed in 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 LA, and you may have a rapid equalization of LV and LA pressures during systolic ejection.
Therefore, you may have no murmur at all. Here's an example of this. We see here this case, we see that the posterior medial papillary muscle is taking a vacation into the left atrium. It's not sticking down in the ventricle. And as one would expect, you can see there is torrential, profound, wide open mitral regurgitation. How much mitral regurgitation? Literally, you could drive a truck through this mitral regurgitation. That's how much there is.
This person is in profound respiratory distress. They are 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 with inotropes, with balloon pump, but rapidly get them to the OR. I would not take this person back to the Cath Lab to redefine the coronaries before taking them to the OR. Time is of the essence, you need to get them there. And although 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 transthoracic echocardiogram at the basal level, and you can see there's loss of continuity of the myocardium at that basal inferoseptum. If we put some color over that area, you can see that there is loss of tissue integrity, and a shunt that has developed at that basal inferoseptum.
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 infarcts tend to be associated with a wraparound LAD, and tend to cause an apical VSD. The other flavor's the one that we just saw. In an inferior infarct, you can develop a basal 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 AV valves, and these can many times have a very serpiginous course. So these patients with VSD will present with hypotension, shock, dyspnea, pain, and a harsh systolic murmur, a harsh systolic murmur frequently accompanied by a thrill. And this harsh, loud, vigorous thrill-associated murmur is a good way to tell us apart of VSD and a papillary muscle rupture.
Remember, papillary muscle ruptures can actually be completely auscultatory 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's sitting bolt upright in respiratory distress, and may even have an absent or very soft murmur, think about acute MR.
These patients shunt from left to right. They develop an acute increase in their pulmonary blood flow, therefore. And they have an oxygen step-up in the RV, if we do a cath. Now interestingly, because of that increased flow through the pulmonary 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, a V wave. A V wave's not a great way to tell apart papillary muscle rupture from a VSD.
They actually both can get a V wave. In papillary muscle rupture, the V is from the torrential mitral regurgitation. It's 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 papillary muscle rupture, you get a 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 inaudible murmur-- pulmonary edema. Rapidly progressive-- think about papillary muscle rupture. In a VSD, you're again going to think about emergent surgical repair. These can abruptly expand, and in someone who's more hemodynamically stable, they may become less hemodynamically stable.
But know that in those inferior ones, like the one that we showed, sometimes these can be really technically challenging, and a surgeon may say, no, let's stick with medical management, with stabilization. And that may be 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 percutaneous closure device.
High operative mortality in these patients. Our last of the rupture complications is that of free wall rupture. We'll talk about frank rupture to start. This is a dramatic, often fatal complication. Many times this presents as an elderly woman with her first myocardial infarction that's in the anterior distribution. An elderly woman with her first anterior MI, 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 anterior MI. 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 as death.
This is a frequently fatal event. But if you get a pulseless electrical rest or an unheralded vagal event, you should be thinking about free wall rupture, especially in an elderly woman presenting with her first anterior myocardial infarction. The last part of this, free wall rupture that's contained, this is sometimes called a pseudoaneurysm. I don't love that term, a "pseudoaneurysm," 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-- incomplete rupture, subacute rupture, pseudoaneurysm. And this is where just a single layer of organized thrombus or pericardium is sealing that perforation. This may be a clinically silent event, or it may be someone who has a stuttering chest pain that occurs in that correct two- to five-day window. And if you see a new pericardial effusion in someone who's post-MI, that should raise your suspicion for this.
When you see a pseudoaneurysm, a pseudoaneurysm, 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 pseudoaneurysm. If you look here out at the LV apex in this four-chamber view, you can see that there is flow from the LV apex out into this space, this Echo loose in space out at the apex.
And this is someone who has developed an apical pseudoaneurysm. These can have unpredictable progression to true-- 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, spanning profound LV failure, RV infarct, LV aneurysm, ischemic MR, 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 and the evening, come back for one slide. These are the things I think are really high-yield. Avoid high-dose protocolized IV beta blockers in large acute MI. You've 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 MI, particularly if they're less than 75 years old and they've developed cardiogenic shock, think about early reperfusion. And truthfully, the guidelines would support early reperfusion in all patients, not just those less than 75. RV infarct has that classic triad that we talked about of hypotension, clear lungs, and elevated JVP,
Re-perfuse them in timely fashion. Give them IV fluids. And know that these patients can progress quickly. You may need to give them inotropic 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 arrhythmogenic complications, embolic complications, but they don't rupture, whereas a narrow neck, 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 anterior myocardial infarction, especially in that two- to five-day window where the myocardium looks like smushed beans.
The patient's lying flat and they've got a thrill? VSD. If they're sitting upright in pulmonary edema, think about mitral regurgitation, even if the murmur's not present. And know that a V wave is not the best way to distinguish between acute MR 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 reperfusion. 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.
MANDEEP SINGH: All right. Thanks, Jeff. What a wonderful talk. What a delight. Let me start off from your last half of the presentation from a rupture perspective. Having worked in Cath Lab for now three decades, I think there is complimentary information to be had by doing an LV angiogram if we suspect, for example, a VSD or a papillary muscle rupture, especially if we can't hear an MR murmur.
And then the step up from RA to RV, or RV to PA, I think, is critical information to be had if Echo is not readily available in a patient who has a PEA cardiac arrest. And then Echo may show just pericardial effusion. My question to you is that if you think that this is the kind of approach, if a patient has a cardiac arrest in the field or in the ED, 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 PCI and lytics being given very aggressively? Because all these data that's coming up is not contemporary, it's kind of quite old.
JEFF GESKE: Yeah. And 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 pursued timely reperfusion. And you'll notice the number one treatment for many of these is timely reperfusion. So I think that really serves to emphasize that point.
And 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 reperfusion. That should raise your radar to suggest that these patients may be at higher risk for such mechanical complications.
As far as your question regarding kind of triage of patients presenting with out-of-hospital arrest and things, I do think that there is some individual care that needs to be occurring there. If you're having a patient that is having ST elevation on their resuscitated rhythm, then I think that timely reperfusion is really of the essence. We didn't get into this talk into going through targeted temperature management, and some of the ways that has improved outcomes in out-of-hospital arrest, but I do think that especially if the clinical suspicion is high for ACS and for that as the cause of an out-of-hospital arrest, then getting them to the Cath Lab without delay is very important.
I do think as well that Echo serves a very key role in diagnosing, confirming, and following these patients. And this will depend on the availability and access to Echo, but I will say I'm very proud of our ICU group 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 physicians in our ICU are very facile at obtaining a quick Echo image that can help to confirm LV function, that can look for that new effusion.
But I think too, as you pointed out, if you are in the Cath Lab and you have someone who's critically ill, and they've just had a PA arrest or their hemodynamics are unstable, and you're concerned for a mechanical complication, then getting information expeditiously, whether it's an LV gram, 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 a transthoracic echocardiogram, whether it's the LV gram, whether it's the hemodynamics to support this, are important. But know that some of these can look alike. And I emphasized that a little bit when we talked about comparing dynamic outflow tract obstruction and cardiogenic shock, two 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've differentiated between these conditions, because the management can really differ. And expeditiously figuring that out is important, as hemodynamics, clinical stability can rapidly change in these patients.
MANDEEP SINGH: 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 theme that, don't start beta blockers just before sending the patient for noncardiac 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 theme 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 a priority. 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 Takotsubo cardiomyopathy presenting with ACS, versus the scenario that you described? In terms of LVOT obstruction and hypertension.
JEFF GESKE: Yeah, so I think that Takotsubo associated dynamic outflow tract obstruction and apical MI-associated dynamic outflow tract obstruction, the hemodynamics and physiology are the same. And the two scenarios can look, honestly, very similar in Echo as well. You need that cath to know, do we have an LAD occlusion here that's caused an apical infarct? Do we have a 99% stuttering lesion in the LAD? Or is this a Takotsubo?
But from the standpoint of dynamic outflow tract obstruction mediated hypotension, I think that we're really talking about the same pathophysiology there.
MANDEEP SINGH: Yeah. So regardless, if you have hypotension, and you're suspecting Takotsubo or apical infarct, a true plaque rupture, and you have hypotension, treat them the same way. Do not get bothered about whether it's Takotsubo or it's a true plaque rupture. The management is pretty similar.
JEFF GESKE: Absolutely. And I think if you're wondering between those two conditions-- not because of the presence of the dynamic outflow tract obstruction, but the clinical scenario is unclear if this is a Takotsubo or if this is an apical infarct, you need to err on the side of defining the coronaries and determining the direct invasive coronary angiography, what's going on. And I think that's really important, because absent that, Echo findings are really not going to tell you if this is an apical infarct or a Takotsubo. And the management's going to differ.
MANDEEP SINGH: I think that's the key point, which is if we suspect Takotsubo, 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 Takotsubo or not, because almost 90% of ACS are plaque ruptures and not Takotsubos.
JEFF GESKE: Yeah. And you might have a clinical scenario that doesn't involve coronary angiogram, but it's more the exception than the rule. If you have someone who has well-defined coronaries, maybe they just had a CTA of their chest because the clinical scenario was 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. There are scenarios where you may not go forward with coronary angiogram, but I think the default needs to be to define the coronaries.
MANDEEP SINGH: Exactly. So 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? If you find a true aneurysm, what are your guidelines in terms of innovative management versus sending them for repair of true aneurysm?
JEFF GESKE: Yeah, that's a good question. I think that 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. I would really want to know a lot more about the scenario, because if you have a large pseudoaneurysm that's profoundly affecting LV function, I think that there's some benefit to focusing on LV function therapies, beta blockers, ACE inhibitors. But the presence of a true aneurysm, somewhat, the horse has left the barn, and you've got some irreversible damage there.
I think the time that we've seen the most aggressive management, and I think appropriately so, is when there's been arrhythmia associated with this. True aneurysm can be a nidus for ventricular arrhythmias, and I've seen cases where we've gone in and done ventricular ablations, but also where we've gone in and done aneurysmectomy and patching, because of the presence of ventricular arrhythmias associated with that true aneurysm. I think as well.
MANDEEP SINGH: The key selection is the key, right? If you think about it, thromboembolism, if you have a thrombus, a recurrent thromboembolism, arrhythmia you mentioned, intractable heart failure in a patient who's otherwise-- has as a good life expectancy, you don't want to send the patient for surgery if they have a lot of comorbidities, they're elderly. And so you're right, the treatment for true aneurysm needs to be individualized based on so many factors other than what the complications, the true aneurysm can bring to the patient.
JEFF GESKE: Yeah, 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, arrhythmias, thromboembolic risk management. I think there's a different pace to that decision-making, and also some different things to consider.
MANDEEP SINGH: Yeah. Perfect. So I have a question from me, and then we have a follow-up audience question. So my question is, now you said about ischemic MR, right, so ischemic MR, short-term and long-term, how would you classify ischemic MR? Would it be a primary MR? Or when the LV remodeling happens, is it a secondary MR, or is it a combination of the two? How would you classify an MR related to ischemia or ACS?
JEFF GESKE: Yeah, that's a good question, and we've seen in the 2020 valve guidelines some evolution or kind of development of our terminology for discussing MR. It's not really the leaflets' fault in the setting of ischemic MR, OK? This is really dealing with the subvalvular apparatus, whether it's ischemic 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 mitral regurgitation.
Now I think there can be overlaps between things. But in general, I would think of it in that regard. As opposed to a rupture-based mitral regurgitation, there's really not role for things like MitraClip or percutaneous mitral valve repair in papillary muscle rupture. But I've seen used before in ischemic mitral regurgitation transcatheter approaches. I think once again, having that multidisciplinary team involved, getting a surgeon involved, because a surgeon would be a part of that discussion, figuring out patient surgical risk, and the best approach to the mitral valve issues is important.
MANDEEP SINGH: Yeah. So the question from the audience is a good one, which is, how would you then differentiate an ischemic MR from a ruptured papillary muscle, when both of them can present similarly. It's not like one of those dramatic Echos that you've shown, but they can be less dramatic, right? So they can just-- tore a cord, for example. Or the subvalvular apparatus is intact, but it is ischemic.
So how would you then differentiate the two? That's one. And the follow-up question to that is, how would you then manage? In other words, is it always that ischemic MR precedes papillary muscle rupture? Do you have any insight to that or not?
JEFF GESKE: So I think the question really brings about the important point that imaging is key to differentiate these two. They both present with MR. They both could have the murmur of MR. And recognizing the underlying mechanism will define our treatment pathway. So in someone with ischemic MR, we're looking for retraction of the subvalvular apparatus. We're looking for retraction of the papillary muscles. We're looking for regionals that alter our closure anatomy.
For rupture syndromes, I would say in the setting of acute MI, we're really talking about papillary muscle rupture, not as much chordal rupture. Chordal rupture I think of more as a complication of something like mitral valve prolapse, repetitive wear and tear. But papillary muscle rupture would be a mechanical complication. If you're unsure based on transthoracic imaging, because there's a confusing jet or because image quality is suboptimal, or because there's multiple jets, then I think that this is a reason to proceed with transesophageal echocardiogram.
I think that you need to know the mechanism, because a patient with papillary muscle rupture, even partial papillary muscle rupture, has the mechanism of significant regurgitation papillary, that's really a surgical issue. It's a structural, mechanical issue, and no amount of revascularization and medical therapy is going to un-rupture it. Whereas someone who has ischemic mitral regurgitation, timely revascularization may be helpful.
And I think that recognizing that revascularization can improve myocardial function and medical therapy can result in reverse remodeling, that there is a different general approach that can be taken. And there is some overlap. Again, in a patient that has papillary muscle rupture, they may have in addition, elements of ischemic mitral regurgitation that have occurred because initially, the papillary muscle was ischemic, it began to get retracted, and then it tore, So you have mixed mechanism. But once you've invoked a rupture as a part of this, we really transition to a lot more surgical consideration.
MANDEEP SINGH: So if you have a significant MR in the setting of ACS, even though you are not able to demonstrate lack of integrity of the mitral valve apparatus, do you routinely go for transesophageal echocardiogram just to prove or disprove?
JEFF GESKE: 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 mitral regurgitation has equal priority to the severity of regurgitation. And so a report that just says, severe MR, but doesn't tell you why or how is not as helpful as it should be. And so I think engaging the imaging group in that discussion, looking at your own images, is important.
If it's very clear that there's anterior leaflet override because of a retracted subvalvular apparatus and that is the mechanism, I don't send all of those patients for transesophageal imaging, no. If there's uncertainty or suspicion, but not enough to confirm, you bring the surgeon out and you say, look, I think that's what it is, and they say, yeah, but we can't tell good enough, then additional imaging is important. And that's not something that you wait for the next day to decide.
If you suspect a papillary muscle rupture and you have suboptimal transthoracic images, you've got to get the TEE in. And maybe that's a TE that's done in the OR suite as you're getting ready for sternotomy, but things have to move fast, because once the ruptures have occurred, the clock is really ticking.
MANDEEP SINGH: Yeah. Very nice. The SHOCK trial is quite old, and we still quote it because there is no other trial that we can lean back on that confirms our contemporary practice. But even though it was an old trial, it still stands true. Maybe it was very slow in enrollment, but over time, we haven't done much in terms of improving outcomes of patients who present with shock.
Even more recently, when you compare small studies comparing Impella versus balloon pump, not much difference could be generated. Maybe with a small sample size, maybe Impella is not a whole lot superior to balloon pump. Intuitively, it seems to me that Impella should work better than balloon pump if there is some LV contractility left. But we are just stagnant in terms of some innovative aspects. Even reducing inflammation, those trials have been negative. What do you think should be our next approach in terms of improving management of these patients who are so sick?
JEFF GESKE: Yeah, you've asked a very challenging question, because I share your sentiment. Whenever I put together a talk on mechanical complications, I always do a literature search to try and find that one breakthrough paper that's really going to shift the landscape. And then I end up citing the SHOCK trial. And I think that one thing that maybe 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 I think recognizing ACS and pursuing timely revascularization is the key. That's why we've seen less and less development of many of these mechanical complications. So once you have a patient who has the complication-- again, we're kind of outside of the answer that I just gave. I don't know the answer, because as you said, trials that have looked at immunosuppressants for shutting down inflammation have come up blank.
And 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 it may be tough, just given how sick these patients are, how rapidly things can progress, to ever find that key answer. I share your thought that one of the areas of support that has evolved the most recently is in percutaneous support.
And it may be that as we go from Impella to things like biventricular support, using a ProtekDuo and an Impella at the same time, and someone who's presenting with biventricular systolic function. I think reaching for those additional tools early and having the resources 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.
MANDEEP SINGH: Yeah, we have a very robust ECMO team who can present at a very short notice if we have an eligible patient. But I think there is a conflict-- there are two competing themes that are going on. One is we have improved time to reperfusion with very good 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 theme here is that patients who are getting into shock are older than what initially the enrolled patients were in SHOCK trial, with a lot more now comorbidities, advanced age, that even though we have made advances towards rapidity in terms of reperfusion, we are dealing with older and sicker patients. So we haven't made too much inroads into improving their outcomes.
JEFF GESKE: And I agree fully. I think that as we've reduced the number of young patients that come to this outcome by timely reperfusion, we're left with a sicker pool entering into a high mortality state. And how we bring them back from the brink of cardiovascular compromises is very challenging. I think ECMO is a wonderful resource, and certainly one that the current state of medical affairs has resulted in having challenging availability at times. So I think that also offers unique challenges moving forward.
MANDEEP SINGH: Yeah. No, I think it's been a wonderful hour of presentation and discussion with you, Jeff. Any last-minute pearls for the audience that you want to share with us?
JEFF GESKE: Yeah, I think 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 MI setting, if they're hypotensive, if they're in that two- to five-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 incidence of these complications go down with timely reperfusion, 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 patient. 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.
MANDEEP SINGH: All right. Thanks, Jeff, for all your insight. Thank you so much, and have a wonderful afternoon. Goodbye now.