Transcription
So, it's truly a pleasure to be here. Um, I remember when I started, I was much younger. Time evolves, and lots of people get older; some of us are even maybe elderly. But there's one person, like, uh, Jean, and Dr. Kim and Dr. Ryner, who keep getting younger. That's very kind. Okay, so let me start by talking about the complication of acute AMI. There are, uh, really four types, or three types, hemodynamic disturbances, of which there are four types: LV failure with or without RV failure, RV failure predominantly, cardiogenic shock, and mechanical complications. I'll be spending most of the time on mechanical complications because, really, these are, although the most infrequent, these are the most threatful. So they have the higher mortality and morbidity. Uh, I may not be—have may not have the time to touch on arrhythmic complications, but it's all in your slides, and I hope to be able to touch on some of the pericardial complications, which now are extremely infrequent.
So let me start by telling you that there are three types of major mechanical complications complicating acute AMI, and here we're promptly talking about ST elevation myocardial infarction. There's LV free wall rupture, VSD, or interventricular septal rupture, and development of mitral regurgitation. The mainstay treatment for these is surgical repair, plus or minus surgical revascularization when needed. So, um, the occurrence, or the incidence of these mechanical complications, are extremely rare or very infrequent; they are less than 1%. So, in the relatively contemporary—or maybe now it's a decade old actually—APEX AMI study from 2004 to 2006, the mechanical complications incidence was less than 1%; it was 0.91%. And, uh, if you do not have a mechanical complication complicated acute MI, your survival is 96% plus at 90 days. However, if you have any of the three complications, your survival will go down to an average of 60–70%. Highest mortality at 90 days is for free wall—is for ACMR actually, 73%, then for free wall rupture, then for VSD. So very infrequent, but high mortality and morbidity.
Let's start with the LV free wall rupture. The risk factors for this is no prior angina or big MI, with usually transmural, full-thickness MI, and phasic therapy in the old days accelerated the occurrence and the time of onset of LV free wall rupture. But with primary PCI, you've got reduced incidence. And other risk factors include include anterior location, age, and female sex. Now, the timing: usually 50% occur within the first five days, and nearly almost of them occur within the first two weeks. And the timing is really bimodal. So you have an early phase within less than 72 hours, and then the rest occur late, more than four days, but really less than two weeks. And it commonly affects the anterior and the lateral walls of the LV, usually near the junction of the infarcted and normal myocardium. So the clinical presentation is threefold: could be sudden cardiac death, hemopericardium leading to tamponade and death, and very infrequently you have incomplete rupture with indolent course. And the diagnostic modality of choice is by echocardiogram. Um, and if you diagnose hemopericardium, you want to do what you call controlled pericardiocentesis, whereby you do pericardiocentesis to maintain some arterial blood pressure, but not to exsanguinate the patient. So it's—you do frequent taps or frequent withdrawal of blood, and then you go for immediate surgery. And, of course, in the interim, you do hemodynamic stabilization before going to surgery.
Now, VSD is the second mechanical complication. Its incidence is half that of free wall rupture, but it has, really, at least in the APEX AMI, double the mortality. And it has the same timing, uh, with bimodal timing, occurring either early on or after 3 to 5 days, but certainly before two weeks. The risk factors are very similar, but it usually affects patients with MI affecting a single large coronary artery, especially a wrap-around LAD. So LAD that reaches the apex and rounds and wraps to the mid-inferior wall. And at that time, you have an apical VSD complicating a large transmural wrap-around LAD. Um, and it can occur equally in the anterior and non-anterior MI. Uh, if it's happening with anterior MI, it usually affects the apex; if it's happening in the—with the inferior MI, it's usually at the base of the inferior wall. And usually it develops at the margin of the necrotic and non-necrotic myocardium. And the clinical manifestations are usually hypotension, biventricular failure, predominantly right-sided, and you hear often a loud harsh holosystolic murmur with a palpable thrill, RV lift, and very hyperdynamic precordium. If you do a right heart cath, you usually see giant V waves and an echocardiogram is usually the mainstay for diagnosis, and you need to proceed with surgical repair.
Now, in the past, surgical repair timing used to be controversial. And the old retrospective data, if you waited a few weeks, you get the scar to heal and a better chance of survival when you repair VSD. However, these data are confounded by selection bias; patients who were able to wait for six weeks or more self-selected themselves to be survivors. So nowadays, especially—I mean, if you have cardiogenic shock, you need to proceed immediately. But nowadays, with percutaneous ventricular assist devices, whether it's TandemHeart or Impella, you could stabilize some of these patients, allow a few days for them to heal, and then proceed with surgical repair, hopefully with concomitant CABG because that increases the survival. So this is—now, when was it? Almost eight years ago, I was in Boston; that was my very first case of VSD closure, uh, doing it with my mentor. And at that time, I remember we closed—this is published in European Heart Journal—it's a mid-LAD acute AMI with an apical VSD. We closed it with an intra-aortic balloon pump, going actually from the right-sided approach. Uh, and at that time, I still remember the patient's blood pressure was nearly 40–50 all throughout the procedure, although the procedure was successful; the patient ended up dying, really, because of multi-organ failure. Nowadays, we have real support devices, the percutaneous ventricular assist devices, whether it's Impella CP or TandemHeart. And this is a case we've done three—three years ago now—of an apical VSD supported with a TandemHeart. You could see over here that the TandemHeart cannula is across the interventricular septum, unloading the heart, unloading the heart really proximally or upstream from the left atrium. And then retrogradely, we have—I believe that's a Judkins right 5 French or so—crossing from the left to the right. You could cross also with a balloon flotation catheter with a wire. And then once you cross from the left side to the right side, best to position your wire into the pulmonary artery because it's easier to snare the wire. And then we snare the wire from the pulmonary artery; we use an extra-stiff wire that we snared and externalized in the—from the arterial to the venous side. So we have now a very good rail-to-rail—our device over—and you could see over here from the venous side, antegradely, we came up with the U-delivery sheath across the apical VSD. You always want to protect your wire, um, your stiff wire, with a catheter so that you don't cut the aortic valve or any of the cardiac structures. And we're delivering here the left disc of the Impella VSD device and then the right disc, and the patient did extremely well. So nowadays, the paradigm is really to passivate this patient with percutaneous ventricular assist device, let the scar heal, at which time you could close better. But if they're really, really decompensated and you can't do that, you need to be going as early as you can.
Acute regurgitation is the third complication of acute AMI, and moderate to severe MR can occur with up to 2–3% of all acute AMIs, but in shock patients it's up to 40%. And, of course, the cause of mitral regurgitation could be threefold: ischemic papillary muscle displacement, papillary muscle rupture, or LV dilation from severe LV dysfunction. You hear a holosystolic murmur, but in 50% of the time, if you have equalization of the LV and left atrium, you can hear a very soft murmur or no murmur. So don't—the absence of murmur should not fool you that this is not an acute mitral regurgitation complicated acute AMI. And the papillary muscle rupture may be partial, and it usually affects the posteromedial papillary muscle because of its single blood supply, as opposed to the anterolateral papillary muscle. And the clinical manifestation is very similar to the VSD: acute hypotension, pulmonary edema, hyperactive precordium with a holosystolic murmur, but in 50% of the time it's not very loud; it could be very soft or absent, and giant V waves. And remember, giant V waves are really not pathognomonic, neither sensitive nor specific; they could happen with VSD, with severe heart failure, and they really depend on the left atrial compliance. Diagnosis is usually clinical, of course, with an echocardiogram, and often times—not often times, but in maybe 30–40% of the time—you may need a transesophageal cardiogram to visualize the prolapsing papillary muscle into the left atrium. Remember, the left atrium is the most posterior structure of the heart, and the TEE could visualize it very well. Treatments again, after stabilization and aggressive afterload reduction, emergent surgical intervention is the treatment of choice in these patients, with concomitant CABG if needed. So I ended the mechanical complications. Again, you're going to see very, very few of these, but you need to know how to diagnose them because they're very deadly when they occur.
Now, I have the time only to go over LV failure and possibly cardiogenic shock, and the rest is going to be in your slides. Whenever you have a heart failure or ventricular—LV failure complicating MI, you've got usually systolic and diastolic dysfunction. And with systolic dysfunction, you have low cardiac output; with diastolic dysfunction, you get venous congestion and pulmonary edema. And please remember, the treatment of choice is not inotropes and vasopressors; if you could unload the hearts with vasodilators and afterload reduction, that's the way to go, especially to minimize increase in myocardial oxygen demands and to avoid arrhythmias. Besides oxygenation and whether endotracheal intubation or mechanical ventilation, after that you need to unload the hearts with diuretics, but avoid excessive diuresis. You'd want to maintain LVEDP at least above 18. Remember, these patients have a shifted Frank-Starling curve, and they need a good LVEDP for their performance. And then you need to—afterload and preload—to use these agents. And the best is really a combination of nitroprusside and nitroglycerin, if possible. Uh, remember, nitroprusside can exacerbate ischemia, and remember it's contraindicated with severe aortic insufficiency. But if you could maintain a systolic blood pressure above 90 and a wedge in the 18–20 range, that's would be your goal. And vasodilators are really recommended whenever you have room in your blood pressure in these patients with heart failure complicating MI. Now, if you don't have—if the patient is hypotensive and you're unable to use vasodilators to unload the hearts, then this is when you use your beta-agonist, dobutamine, uh, to increase your inotropic function, dopamine at a very low dose if needed to complement—dopamine, no more than 5 micrograms or so, to achieve inotropic effect, some vasodilatory effect on the pulmonary circulation, but no more than that. Remember, in 2010, there was a major SHOCK trial paper examining actually norepinephrine versus dopamine, and the subset of patients with cardiogenic shock, dopamine really had a signal of increased harm because of its arrhythmias and increased myocardial oxygen demand. So nowadays, in addition to dobutamine, I try to use norepinephrine, and if needed you could use milrinone; also has inotropic effects, but it's an excellent pulmonary hypertension vasodilator.
I'm going to end by telling you cardiogenic shock is the other major hemodynamic complication; it complicates 6–7%, 6–8%, around 7% of all MIs. The one thing you need to remember is that it doesn't only happen with acute ST elevation MI; it also happens with up to 2–3% of non-ST elevation acute coronary syndrome. And very important to realize that it's—part of its classic paradigm is not only diastolic and systolic myocardial dysfunction, but also a systemic inflammatory syndrome and release of nitric oxide. And that's why at the very end stages, instead of having high SVR, you may have extreme vasodilation and really low SVR. And the SHOCK trial now is historic; it's more than 15 years old, very small study that showed mortality benefits and its secondary endpoint at six months with survival benefit from revascularization. This is something we take now for granted, but that was studied in 1999 by an NHLBI grant, showing that compared to medical therapy, revascularization—of which one-third, by the way, was surgical at that time—improved survival. And the benefit of revascularization at any time you need to proceed with revascularization with cardiogenic shock is evident in every subgroup. Now, early on in the elderly, there was an issue of a signal of harm; we no longer believe this. We know, and we've done one of the systematic reviews actually with one of the Baylor colleagues, showing really at every age group, in appropriately selected patients, you get a survival benefit from revascularizing the patient, irrespective of age. And be aware of iatrogenic shock induced by IV beta-blocker. IV beta-blocker is no longer a cardiac performance measure; it was taken out from the O6 performance measure in the aftermath of a COMET trial, which showed an increased signal of cardiogenic shock that really counterbalanced the beneficial effect of IV beta-blocker in reducing MI and sudden cardiac death. So the shock signal was really major, up to 5%, and we no longer use it in AMI. We're currently revising the performance measures, and I think we should come up with the statements. In 2016, balloon pump works very rarely or very weakly in cardiogenic shock. We have the SHOCK II trial published maybe a year ago now or more, maybe lower-risk shock, but at least at 30-day and 600 patients plus, showing no benefits over primary PCI in ST elevation AMI. So it wouldn't be my first choice to use it; I would use other percutaneous devices, whether it's the Impella or the TandemHeart, mostly the Impella because of its ease of use. Saying that, in high-risk PCI and in patients with refractory ischemia, balloon pump is still very beneficial; it can increase your cardiac output anywhere between 0.5 to 0.9 liters per minute, can increase your coronary perfusion, it's a 7.5 to 8 French, easy to use, and so forth. Again, the SHOCK II trial, recently released, showed no benefit of balloon pump in shock patients caused by acute MI. Now, when I talk about shock, now I've been talking about MI-related shock, but remember 20% of cardiogenic shock is—cause is related to—not predominantly to acute myocardial infarction; is related to other etiologies. Could be mechanical complication or arrhythmia, but also could be venous thromboembolism, cardiac tamponade, and so forth. Just to close, Impella and TandemHeart: we have now the stronger Impella, the Impella CP, that achieves 3.5 liters per minute or more, and this really, I—in—I believe will take over from the TandemHeart that achieves 5 liters or plus per minute. And you usually—we used to think that TandemHeart really is the ultimate; it can close the aortic valve and take over completely the mechanics of the heart. But with the Impella CP, I think you could do a very high-risk PCI and maintain cardiogenic shock patients very, very well. I'm going to stop here because of the sake of time. Thank you for allowing me a few extra minutes; it's a pleasure to be here, and you have the slides in your—in your curriculum. Thank you for your time.