Transcription
I will give today technical tips regarding STEMI primary PCI. There are many ways of approaching the technical details of primary PCI, but I will give you my personal approach.
First, regarding access, I overwhelmingly favor radial access. Radial access has shown mortality improvement, particularly in STEMI, more so than non-STEMI or stable CAD. One question that comes up is whether you should go directly with a guiding catheter for the culprit. For example, in anterior MI, should you start directly with a left coronary guide catheter, or should you do a right coronary inogram then go with the left coronary guide catheter? In anterior AMI, I start directly with a left guide catheter; then I do the R-COGRAM at the end, after finishing my primary PCI.
The guide catheter that I start with is IARI Left 4 or CLS or EBU 3.5. And I choose larger numbers in patients who I know have dilated aorta or tall, old patients. For example, over 5'11" old patients, I may choose 4.5 IARI or CLS EBU 4. The reason I use a larger arm with IARI in general versus the EBU CLS is that IARI Left is a less supportive guiding catheter. For that reason, I always try to engage IARI Left from below, loop it onto the aortic valve and the opposite aortic wall, and loop it from below. And for that reason, I need a longer arm. On the other hand, the EBU and CLS systems are more supportive, and therefore you can get good support engaging the catheter from above or approaching your engagement from above or approaching it from below. And when I approach it from above, a 3.5 size is enough. When I approach it from below, I would need a longer size, such as 3.75 to 4. I have explained those in detail in prior talks, the left coronary engagement talks, and I suggest you review those.
Another note is that for the IARI Left, you can engage it from above; however, even if you engage it from above, you need to push it and loop it from below and give it a power position to get the support from an IARI Left guide. This is what we call the power position with an IARI Left guide. This is an illustration of an engagement with an IARI Left guide. Here we had already jumped from the right CP to the left cusp. We came below the coronary left coronary; we tried to engage from above by pulling the catheter and going in with a clock maneuver; it didn't work, so we pushed it back and engaged from below. And you can see how we engaged; this is a perfect power position, looped on the opposite aortic wall and on the aortic valve. Now, had we been able to engage by simple pull, engage it from above by simple pull with a clock, even if you engage from above, you push the catheter to give it a power position and get the support from an IARI Left. This is not necessary with an EBU/CLS system; engaging from above gives you good support; it's a more sturdy, stiff, and robust catheter, and that's why I usually start with a smaller arm within EBU system than with an IARI Left.
Now, how do I approach inferior MI and posterolateral MI? In inferior MI, the culprit is the RCA 75% of the time and the left circumflex 25% of the time, meaning you don't need to have a dominant left circumflex for it to give you an inferior MI. An infarct involving a low obtuse marginal branch can give you inferior ST elevation even if the PDA is not involved, even if the left circumflex doesn't give a PDA. The way I approach those cases, unlike anterior MI, in those cases I try to do a full inogram before I perform PCI of the culprit. And the way I do it, I start with the inogram of the less likely culprit artery. For example, if I suspect RCA culprit, I start with an inogram of the left coronary artery, left circumflex; then I go with a guiding catheter for the RCA, and I do usually use in those cases IARI Left 4. So I go with an IARI Left 4. I engage the left coronary artery if I think that's not the culprit with the IARI Left 4; then I disengage and I flip it and I try to engage the right coronary artery with the same IARI Left 4, and I do PCI of the RCA with that same IARI Left 4. So I use one guide catheter to do inogram of the left and to do intervention of the right, or vice versa, to do inogram of the right and to do PCI of the left circumflex in an inferior MI. This way I limit my catheter exchanges. The important idea here is that IARI Left is a great left coronary guide, but also it is an excellent right coronary guiding catheter, and if you're good at using it, that can save you a lot of time. This is, for example, a case where we use the IARI Left to engage the left coronary artery, but you also use the IARI Left to engage the right coronary artery. So again, the IARI Left—not right—the IARI Left is a great guide for the RCA as well, not just the left coronary artery. And the way I would use it to engage the RCA is kind of the same way I would use it—J-KIN Right. We go, we touch the right coronary cusp, we pull with a clockwise maneuver and engage. You need to keep a pull tension on that IARI Left because it tends to point up, so as you're pulling and clocking, you need to pull typically more than you would pull when you're engaging with a J-KIN Right catheter.
Now, IARI Left is a great right coronary guiding catheter, and the beauty of it is its versatility. For the right coronary artery, you could use it as a J-KIN Right catheter, but you can also use it as an Amplatz Left configuration. So what you do in this case, you engage, then you push it to give it an Amplatz Left morphology and to give it support from the opposite aortic wall and sometimes from the aortic valve cusp. This is what we call the power position, and you can dance between those two morphologies. You can push it to get the support to advance your stent and distal devices, and you can pull it if you want to stent proximally and give it a JR4 shape, so it can be very supportive and be used like an Amplatz Left. On the other hand, it could be pulled back slightly counter-clocked and allowed to maneuver and place devices in the ostium.
Now, why don't I go straight with a guiding catheter in the case of inferior MI, and why do I do a full inogram? There are two reasons for me to do that. One, it is difficult to ascertain RCA versus left circumflex by EKG, although I will give you criteria to help you distinguish. But two, even when I'm certain it's an RCA culprit, I don't go straight with the guide for the RCA because I like to image the left before fixing the RCA. When the culprit is RCA, I still need to know whether the patient has a critical 90% left main or LM and left circumflex disease and whether he will need CABG soon. And if I deem it that the patient has critical left disease and he needs CABG, I may just try to balloon the right coronary artery, the infarct, and reestablish flow and refer the patient for CABG within few days. So those are the two reasons why I try to do a full inogram in an inferior infarct. I shoot what I expect to be non-culprit first; then I engage the culprit with my guide and I try to fix it, and ideally both those are done with—in my case—with one catheter, IARI Left 4.
Now, how to distinguish inferior infarct from RCA versus left circumflex? When you have an inferior MI, the vector of injury is actually a bit different between the RCA and the left circumflex. The vector of injury in the case of RCA looks toward the right, whereas the vector of injury in case of left circumflex looks toward the left. And those differences in the vector of injury translate into some difference in EKG features. In particular, there are four differences between the RCA and left circumflex infarct. One easy one is the lateral leads. So if you have ST depression in both leads I and aVL, it is an RCA infarct. If you have ST elevation in both I and aVL, it is left circumflex infarct. The problem is that not uncommonly you have discrepant findings between I and aVL. In particular, you can have ST elevation in I and ST depression in aVL, and in this case it's inconclusive whether the infarct is RCA or left circumflex. The vector in this case is almost vertical in the middle, so we can end up with ST elevation in I and ST depression in aVL with both RCA and left circumflex. Okay. Now, another feature that we use is aVR. Left circumflex injury is completely opposite to aVR, so if you have pronounced ST depression in aVR, it's highly, highly likely that you have left circumflex infarct. However, if you have borderline ST depression around 1 mm or mild ST depression, then it is difficult to tell. So but pronounced ST depression tells you the infarct is in left circumflex. A third and extremely important feature is RV infarct. So if you have ST elevation in lead V1 or in the right-sided lead V4, this implies RV infarct, and this implies definitely RCA. This is a very specific finding for RCA. Keep in mind you don't need to do right-sided leads. ST elevation in V1 plus or minus V2 in a patient with inferior infarct, this is an RV infarct, and this tells you it is an RCA, not left circumflex.
Now, what confuses those EKG features and the picture furthermore is that sometimes you have an RCA culprit with a left circumflex CTO or vice versa, and in those cases you can have left circumflex EKG criteria even with an RCA infarct and vice versa. So whenever you have that situation, how can you tell which one is the culprit? Is it the RCA or the left circumflex? So one, the EKG features remain useful, although less so, and there is more overlap in those features. Two, collaterals. Having grade three collaterals to one artery implies that this one artery is likely the CTO while the other one is likely the culprit. So grade three collaterals mean robust collaterals wherein you see reconstitution of the major epicardial vessel. Those collaterals take at least two weeks to form based on some data; however, occasionally you can have them in an acute infarct if it was preceded by a chronic 90-95% stenosis. So grade three collaterals do not absolutely tell you this is a CTO; it can be the acute culprit, but it makes it much more likely. In a patient with two occlusions, it makes it much more likely to be the CTO rather than the culprit. Another feature, an angiographic feature, is a round filling defect or contrast stain. Either one of those two implies clot, fresh clot, and it implies that this is likely the culprit. In case your artery is fully occluded, the round filling defect will appear like a luminal concavity, a concavity of that lumen on this side, and the D-stain is another feature also of fresh thrombus. Now, if the occlusion is not complete, having what we call an eccentric, irregular, subtotal occlusion with an overhanging edges and reduced flow implies this is an unstable stenosis. So this is the stenosis; it's not hourglass; it's sharp at the edges, has acute angles at the edges, not hourglass, and it's irregular, eccentric with reduced flow. This is particularly useful in non-STEMI to tell this is an unstable plaque in non-STEMI, but it may be used in STEMI as well when flow is not completely occluded. So those features help you tell which one is an acute stenosis. The last thing is if you cannot figure—figure it out—you suspect the RCA is the culprit, you try to wire it, but if you're unable to cross it with a simple polymer wires—so let's say you don't cross it with the Workhorse wire, BMW wire—you try a soft polymer wire such as Whisper wire, and you still cannot cross it within a couple of minutes, then you start suspecting this is maybe the CTO and the other vessel is potentially the culprit. So those are the four features I use when I have occlusion of both arteries.
Now, how about patients with grafts? In graft PCI patients, I generally do a full diagnostic inogram before PCI. If I suspect vein graft occlusion—for example, the patient has inferior infarct and I suspect occlusion of a vein graft to RCA—I generally save that vein graft for last and I engage it with a guiding catheter to save one step.
Now, what access do I use? We frequently use femoral approach; however, I do consider left radial approach in specific cases when the graft anatomy is known, especially if the graft anatomy is known plus one of those two additional features: I have access to a prior venous graft inogram and I can see where those grafts are located on the aorta, or I don't have access to a prior inogram or the patient never had a graft inogram, but I know that he has one or no left vein graft and the left vein graft is not suspected to be the culprit. Remember, left vein graft is the most difficult artery to engage in a patient with a graft. It is high, and you have to engage it after a sharp bend. You tend to get the least support, and you need difficult maneuvering to engage it. On the other hand, right vein graft is low and it's easier to engage it as it better embraces the curvature of the aorta. As I explained in my graft talk, I suggest you review that. I explained engagement.
How about wiring? I start with a Workhorse non-polymer wire such as BMW wire or Samurai wire. The maneuver I use is the spin technique. I get the wire to the occlusion side and I spin it—one to two spins in each direction. I make it sit around that occlusion with a very mild and gentle push. I focus on spinning the wire around this occlusion site, let the wire itself find microchannels and slip into them. So I spin it around—one to two spins in every direction—one to two this way, one to two that way, while sitting at that occlusion site, and I let the wire find the channel. Once it finds it, you will see it give—give in—and cross the lesion. And once this happens, you'll spin it further more through the lesion to get past it. You need to be able to recognize that giving in, falling of the wire. Avoid wire buckling at any time. Wire buckling means you're pushing too much on that wire; you should not push hard; it should mainly be a spin with a mild push. If you buckle, you risk dissecting, and in that case it will be very hard to redirect your wire into the true thrombus and the true intima.
Another idea regarding the shape of the wire: normally the sharpness of my wire depends on the sharpness of the branch I'm trying to reach, including potentially the LAD or left circumflex of the left main, and the length of my wire tip depends on the size of the main branch. Specifically in STEMI, if I can, I try to keep my—uh—shape, my angle somewhat shallow and somewhat short to avoid that wire from drilling around the edges, to stay centered and try to find microchannels inside the center of that thrombus. Now, if the left main angle into the LAD or left circumflex culprit is sharp, I may have to put a sharp and long tip, but in general I try to favor a shallower and smaller tip. Another important idea is that the wire tip must be moving freely past the occlusion. So you spin it around, you fall into the occlusion site and the thrombus, you get past it. Now, the wire must move freely. This is how you know you crossed the true thrombus; you did not get behind it into the sub-adventitia. So it must move freely past the occlusion site. This is an illustration of that spinning I'm describing. There is an occlusion of the LAD here. So here the fellow is spinning it around, spinning it; he buckled at one point, immediately pulled back. So look here, he buckled, he immediately pulled back—no buckling, we don't want that. Buckle that J-shaped to the wire; then he kept spinning again; he crossed. Now he crossed; you—he felt the wire give in; he crossed in the septal initially; then he redirected it in the LAD and—not that—past the occlusion the wire moves very freely, and that's how you know you are in the true lumen of the vessel distally, even without any contrast injection, even without any flow. Keep in mind at this stage we have no flow; it's all based on feeling of the wire. It is okay to go into a branch initially. Let's say here he fell into the septal branch and he could not redirect it into the main LAD; it's okay to get a balloon, obtain a flow; then once you have flow, you know exactly how to redirect your wire into the main LAD. So initially, after you cross the occlusion, it's okay if your wire falls into septal or diagonal; it's okay to get a small balloon, establish flow, then redirect your wire. The key is that your wire, even if it is in a branch, it's moving freely, and you need to know how your arteries look in your standard views. That's how the fellow was able to tell this is a septal, not the main LAD, and that's how he was able to redirect it into the main LAD in this shallow, aro-cranial view. If after 1 minute of spinning the Workhorse wire there is no success in crossing the lesion, this is when I switch to soft polymer wire such as Whisper or Fielder FC wire. Or occasionally, if the polymer wire is still not crossing the occlusion, I use polymer wire with over-the-wire microcatheter support, especially in late presenters, more than 12-24 hours, where thrombus becomes organized and more difficult to cross. You may also need that in patients whose occlusion is past a large branch; the wire may tend to prolapse into that side branch, so having the support of a microcatheter here may help you across the thrombus. Rarely you may need to put a wire on the side branch and use a dual-lumen catheter, but this is rarely needed. Most often you just need a polymer wire that is less likely to prolapse and sometimes a polymer wire with a microcatheter support.
Now, after wiring the occlusion, we do balloon dilation, usually downsized about half mm compared to the proximal reference. Angiographically, I use a standard compliant balloon which has a lower profile than a non-compliant balloon. Then, if needed, I may readjust my wire position. If it was in a diagonal or septal or small branch, I readjust it into the main vessel; then I stent. I try to stent all severe disease that is obstructive, more than 70%, so not just where the 100% occlusion was, but also if beside the 100% occlusion there is another area that has 80% stenosis in that same culprit artery, I try to stent it unless it is in a very distal portion of the vessel or a small portion of the vessel or if it is a branch stenosis of the culprit artery; those I try to leave them alone. I don't always post-dilate. It's well known that post-dilatation it creates further cheese-cratering effect of the stent; it squeezes more clot through the cells of the stent and it can create more dis-semination. So if my result is good angiographically, I try not to post-dilate. And we use that balloon, that first balloon dilatation, we use it to kind of size the vessel in terms of diameter as well as length.
When the occlusion is at bifurcation, I try to use the provisional strategy, one-stent strategy. I try to avoid bifurcation two-stent strategy in this highly thrombotic state. There is no data on one-stent versus two-stent strategy in STEMI. Almost all of the one-stent versus two-stent bifurcation trials excluded STEMI patients except for a small subgroup of DK CRUSH II trial, so there is no data, but I would expect a two-strategy in this highly thrombotic state to cause more complication, more thrombotic complications. So I focus on stenting the main branch and ballooning the side branch using provisional strategy. Keep in mind that bifurcation disease in STEMI—like say you have an occlusion and you have a severe diagonal stenosis next to the occlusion—keep in mind that that's bifurcation disease and that diagonal disease is frequently thrombotic and side branch occlusion is frequently thrombotic; hence it may be alleviated with using glycoprotein IIb/IIIa inhibitor. So rather than maneuvering the side branch, you know you can wire it, potentially balloon it, but definitely try to avoid stenting it and try to rely on IIb/IIIa inhibitors. Sometimes if it is 90% stenotic the side branch and it looks like a thrombus, I try to even not balloon the side branch; I just give IIb/IIIa inhibitors along with stenting the main branch.
Now, how about additional thrombus treatment?
In patient with heavy thrombus burden, such as long thrombus and/or distal imoli and/or large side branch emboli, like I just described, particularly assessed after initial ballooning. After you initially balloon, you can better assess the thrombotic burden. So if you see a heavy thrombus burden and the patient age is less than 70-75, especially if you're using radial axis, if you have those three conditions, especially the first two, then consider IIb/IIIa inhibitors, which are used in 20% of STEMI trials and registries. The IIb/IIIa inhibitor eptifibatide may be administered intravenously or intracoronary. Try to administer it intracoronary distally via dual lumen catheter, such as a TwinPass catheter.
In patients with a slow coronary flow, as I explained in my STEMI part two talk, avoid routine mechanical suction thrombectomy in STEMI. It's given in class three in the ACC guidelines based on the large TOTAL trial, where routine mechanical thrombectomy in STEMI increased the stroke risk. However, you may selectively use mechanical thrombectomy, particularly the Pombo catheter, which is popular in the US, in heavy long thrombus burden, especially if the patient has high bleeding risk and is not a candidate for IIb/IIIa inhibitor, such as age over 75 and femoral access. The Pombo device is a suction catheter; it's a monorail suction catheter attached to a continuous vacuum suction motor. So this allows for a more robust and more consistent suction power during the procedure rather than a syringe suction with the old devices. So it is more effective than the old devices and in reducing the clot burden and maybe in decreasing the risk of retrograde embolization in the aorta and a stroke. However, there is no large trial of Pombo, and there is actually no large data of Pombo, so be careful, and I would reserve it for cases where I cannot use IIb/IIIa with heavy thrombus burden.
Another adjunctive treatment is local intracoronary vasodilator and/or local distal IIb/IIIa inhibitors for slow flow TIMI 1 or TIMI 2 flow, despite a resolution of epicardial stenosis. This is done via distal dual lumen catheter. Consider IVUS or OCT as in all PCIs. However, major imaging trials did not include acute STEMI, and beware of excessive post-dilatation in STEMI because excessive post-dilatation causes cheese crater effect and squeezing of clot from behind the stent into the stent lumen and distal embolization. Keep in mind that IVUS and OCT generally make you want to post-dilate and make you want to further expand your stent, so you know that's why I don't universally use IVUS and OCT in STEMI, and I may feel content with just angiographic assessment.
Now, how about the LV? I do small volume LV gram in a patient with shock, especially shock with inferior AMI, where you have to absolutely rule out mechanical complication. In those cases, I actually start with an LVR. Inferior AMI with shock, I may either do a quick bedside echo before a catheterization, or if we haven't done that, I would start with a small volume LVR to rule out mechanical complications. I do LVDP in all patients, for example, with the same IARI left catheter in stable patients. I do it at the end of the case after I finish my PCI and my angiogram. I would do it early on if the patient is unstable or if he is hypoxemic to decide about support and about diuresis. And like I said, if the patient is unstable or hypoxemic with an inferior MI, I would favor starting with not just LVDP but an LVR before I do my PCI and my uh full coronary angiogram.
Now, how about STEMI with pre-shock and shock? How to approach that? I would do radial access if the patient is in pre-shock or shock on small IO pressor doses, such as a shock stage C. If severe shock on high ion oppressor doses—this, the shock stages D and E—then I would favor femoral access simply because in those patients the radial artery will be small and will be difficult to access and it will be difficult to maneuver your catheters. Femoral access has two advantages in shock patients, particularly again severe shock: one, the radial artery is small and difficult to access and maneuver in those patients; another possible advantage is if LV support is placed at the end of PCI in mild shock that deteriorates during PCI, that same femoral access may be used to put your balloon pump or your Impella. But this is unpredictable. I would not do femoral access saying that, okay, I'll do femoral access because at the end of the case I want to put balloon pump or Impella. This is unpredictable. I make an upfront decision at the beginning of the case. If he's a stage D or E, I think he needs a support device; I will put it upfront. I will do femoral access for the Impella and balloon pump and femoral access for my PCI. Uh, sometimes you can use the same access for Impella and and for your PCI, the single access through the 14 French Impella sheath, particularly in patients who are not very tall. Conversely, if I decide that the patient doesn't need a support device, I want to go with my PCI, then I would favor going radial in that case, and if the patient deteriorates then I would put a support device at the end, but there's a good chance that the patient is not going to deteriorate and I will not need to do any femoral access on that patient.
Now, if the patient is in distress when they are in pre-shock and shock, the patient is in distress and in moving around; it's a problem for usually for both radial and femoral, so that by itself is not an incentive for me to go femoral rather than radial. Those those are the ideas I use to decide. Now, if you need a support device before PCI and a patient was very unstable, then you can use femoral access for the support device; you can use radial access as your second access for PCI to spare you from a second femoral access. But again, those patients usually have severe shock, and radial access is difficult because of the radial being small.
Now, if the patient is hypoxemic, I would give him IV Lasix in the ER even before I bring him to the cath lab. If no quick improvement, I would consider intubation before primary PCI, whether in the ER preferably or in the cath lab, especially if the blood pressure is borderline, to avoid worsening hemodynamics during PCI and the need for rush intubation. So hypoxemic and in distress, I would give him IV Lasix. If he doesn't quickly improve in the ER or at the latest by the time he gets to the cath lab, I would consider intubating before primary PCI to avoid worsening hemodynamics and rush intubation during PCI. If it is shock stage C on one in oppressor small or medium dose, I would start my case with an LVDP and IV Lasix, which I might have given in the emergency room. If the patient is hypoxemic, then I do primary PCI before considering any LV support, as I explained here. For shock stage C, I consider LV support at the end of the procedure depending on how hemodynamics evolve, but the answer is most often not, based on that IABP SHOCK II trial and based on the ESC guidelines. So most often not versus occasionally balloon pump versus occasionally Impella CP. If you have severe LV shock, stage D or E, those are the cases where I start with intubation and then LV support, usually Impella CP plus or minus VA ECMO for institutions where you can do that expeditiously. But typically you would start with an Impella CP, then you do primary PCI. So be careful with that sequence and don't forget the idea of intubation before PCI in patients who are hypoxemic and who do not improve quickly and intubation probably before LV support device in patients with advanced shock.
These are the guidelines regarding balloon pump: The ESC guidelines recommend against placing a balloon pump in patients with cardiogenic shock and no mechanical complication. This is based on IABP SHOCK II trial. Interestingly, most patients in IABP SHOCK II trial were on norepinephrine with a median dose of 3 mcg per kilogram per minute, and the uh range was 0.1 to 1.2, and most frequently they were also on dobutamine. So they were on double therapy, and the lactic acid was 4 with a range between 2 to 8. So a lot of the patients in IABP SHOCK II trial were stage C, but also a good proportion of patients were were probably shock stage D, and 45% of patients had cardiac arrest pre-PCI. Yet no benefit of IABP. Again, this goes to my idea that in shock stage C, I try not to put a support device; there is no evidence that the support device is better than small to medium ion oppressor dose, as has been the case in IABP SHOCK II trial.
Another idea for RV shock: Here is how I handle RV shock in a patient with inferior AMI. I bring them to the cath lab for PCI emergently, and and I do the first two ideas simultaneously: to bringing them to the cath lab and to PCI: one, fluid administration until a RA pressure of 10 to 14 mm of mercury, which corresponds to a JVP of around 15 cm of water. Basically, I give them 500 mL at a time while assessing JVP and hemodynamic blood pressure, pulse pressure response to each bolus. The idea of that RA pressure 10 to 14 mm of mercury came from an old but excellent study; the best stroke volume in that study was seen when RA pressure was 10 to 14 mm of mercury, which is around 13 to 16 cm of water. Beyond that point, if you give more volume, the stroke volume will actually decline because once the RV dilates, fluid administration will worsen ventricular interdependence, further reduce LV output and increase transp agitation. That's why in RV infarct with inferior infarct, the first treatment is careful fluid administration, 500 mL boluses at a time while monitoring JVP and the blood pressure response. Beside that, almost simultaneously, if there is no quick improvement with a first bolus, I would start inotropic therapy, small dose of dobutamine or IV epinephrine. The third-line treatment is balloon pump. Now, balloon pump unloads the left ventricle; however, it may improve RV shock indirectly when RV failure is partly aggravated by pulmonary hypertension and LV failure, then balloon pump will help RV shock. So it will help patients with biventricular shock, but also it will help RV shock by improving diastolic right coronary flow and RV perfusion. So that that's why balloon pump is a third-line treatment. If PCI and those two don't stabilize the patient, by the end of your PCI the patient is still not stable on a small to medium dose of inotropic therapy, I would consider balloon pump.
Another important key idea that a lot of cardiologists don't know is that AV synchrony is extremely important in RV shock, even more than in LV shock. So if you have somebody with AV block or he doesn't have a block but he has accelerated junctional rhythm with lack of AV synchrony, put temporary pacer leads in both RA and RV and synchronously pace the RA and RV. If you have a fib, try to get him out of a fib, potentially using amiodarone. You don't want to sedate and to in order to DC cardiovert; you may want to try to pharmacologically cardiovert to avoid the sedation that you need with DC cardioversion. Here's the idea about the importance of the atrial kick in RV shock: In in the low pressure RV system, when the RV is massively stunned, the RA contraction can actually take over and fill not just the RV, fill the PA; it becomes a major contributor to the RV stroke volume and PA pressure generation. This is from a Circulation paper from Dr. Goldstein. So the failing ventricles, especially the RV, become disproportionately dependent on the atrial boost contraction and contribution to the filling and output. So that's why it's so important to preserve it. So if you have somebody with complete AV block and uh RV shock, don't just pace the right ventricle; put a lead in the atrium and the ventricle and pace synchronously the atrium and the ventricle, or try to do RV pacing that tracks the sinus P wave. Those patients you need a higher rate anyway, so it's good to pace both the atrium and the ventricle at a rate about 100 beats per minute, 110 beats per minute. If they are in accelerated junctional rhythm, then you try to pace the right atrium and right ventricle at a rate usually faster just to ensure AV sequential pacing. Now, of course, like I explained last time, if you have complete AV block but the patient doesn't have shock, then you know you may not even need to pace the patient at all. I'm specifically talking about RV shock. I can't tell you how many times I see a patient with RV shock and accelerated junctional rhythm of 80-90 beats per minute; he flips spontaneously into sinus rhythm automatically; his pulse pressure rises by 20 mm of mercury. I've seen that case scenario so many times that that again shows you the importance of AV synchrony. The fifth line of treatment in those patients is eventually, if they don't stabilize with all those, eventually you do right-sided Impella and/or VA ECMO. Those are reserved for RV shock refractory to all the prior measures.
I want to talk about one more idea that I discussed under my talk STEMI part one, but I want to provide an update based on the newly published BIOVASC trial. So multivessel CAD in STEMI: when to treat the non-culprit artery in the same setting or electively? So I described in the past the large COMPLETE trial, which showed that PCI of the non-culprit artery versus leaving it alone reduces MI risk. Non-culprit artery in that study was performed as a separate procedure before discharge or within six weeks of discharge. And other studies, these two here, have performed non-culprit PCI in the same procedure and showed that it was beneficial versus no PCI at all, but there was no trial that compared non-culprit PCI in the same procedure versus non-culprit PCI later on. Finally, we have such a trial. It was presented at ACC and published in Lancet; it's the BIOVASC trial. It's the only study that compares non-culprit PCI in the same setting as culprit PCI versus separate setting. So they took STEMI patients but also non-STEMI; actually, close to 60% of patients in that study were non-STEMI, and they showed that doing non-culprit PCI in the same setting as culprit PCI is non-inferior to staged PCI, and in fact, doing it in the same setting was associated with numerically less myocardial infection; no difference in mortality. So there was numerical superiority of immediate multivessel PCI versus a staged non-culprit PCI, particularly on subgroup analysis, particularly in non-STEMI, in patients with normal renal function and in patients with a total contrast use less than 220 mL. Interestingly, most of the reduction events occurred very quickly in the first month after MI; in fact, recurrent MI was reduced in that waiting period between the culprit and non-culprit PCI. And here are the two key messages from that: One, try to do multivessel PCI in the same setting in non-STEMI if you can, because another study published in Circulation and using MRI has shown that we misidentify the culprit artery in non-STEMI in 30 to 35% of patients, particularly because in non-STEMI the EKG does not localize ischemia. And number two, if you do staged non-culprit PCI, try to do it before hospital discharge, since most non-culprit related MI's were occurring in that waiting period.
And here is a summary of my approach in light of that new trial: So consider non-culprit PCI in the same setting if non-culprit PCI is expected to be simple, definitely not more complex or or longer than culprit PCI; that makes common sense. Number two, the culprit PCI has not been too complex or too long, and you expect the total contrast use to be less than 150 mL. Three, the patient is very stable. As from the spirit of CULPRIT-SHOCK trial, we should avoid multivessel PCI in any tenuous patient, even if he's not in shock; if he's in heart failure, if he's hypoxic, agitated, if he's in pre-shock, if he has borderline hemodynamics, you should avoid multivessel PCI and get out as quickly as you can; that's the spirit of CULPRIT-SHOCK trial. Also, I would consider non-culprit PCI in the same setting if additionally the renal function is normal, and I would also account for operator and staff fatigue and off hours. If you're doing your procedure at 2 a.m. and tomorrow you have a long clinic day, well, maybe I don't want to expend my procedure another hour, and that's perfectly reasonable; it's perfectly appropriate to do non-culprit PCI electively, preferably before discharge. So if staging non-culprit stenosis, try to do it before discharge; try to do culprit and non-culprit in the same setting if you have those features, especially in non-STEMI, as I described. The non-culprit stenosis must be over 70% to consider fixing it in any setting, same setting or later setting; it must be a major artery, particularly proximal or mid-vessel supplying a major territory. Lesions that are 50 to 70% stented based on IFR or FFR were very rare in COMPLETE and BIOVASC trial; they were less than 1% in COMPLETE trial and they were less than 15% in BIOVASC trial. So basically, focus on treating over 70% using angiographic guidance, not FFR or IFR guidance, although you can use that for non-culprit arteries, but overwhelmingly those trials relied on angiographic stenosis over 70%.