CardiOhio Podcast

Episode 7 - Post-PCI Antiplatelets: A Patient-Centered Focus

Kanny Grewal Season 1 Episode 7

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0:00 | 29:18

Join our special guest,  Dr. Jagadish Khanagavi from the University of Cincinnati, for a practical discussion on the use of anti-platelets following PCI.  We review current guidelines for the choice of agent, duration, and discontinuation of antiplatelet therapy, with special focus on patient-centered  decision-making. We also address the need to interrupt anticoagulation on an urgent basis, and the use of concomitant anticoagulation. This is a practical discussion with real world practice tips.  Please subscribe to receive updated episodes automatically! More information at https://www.ohioacc.org/cardiohio-podcast/.  

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Kanny

This is the cardio Ohio podcast, the presentation of the Ohio chapter of the American college of cardiology. This is canny gray wall president of the Ohio chapter and host for today's discussion. Further information about this podcast, including speaker biographies, as well as references are available@ohioacc.org. The podcast will also be available for download wherever you access podcasts, and we encourage you to subscribe, to receive updates on future sessions And now for today's discussion Welcome back to the cardio Ohio podcast. This is can Greyal your co-host today. I'd also like to welcome again, my reliable co-host Ben Allen cherry from the north coast of Ohio. Ben, how are you doing?

Ben

I'm doing great today. Can I'm I'm excited to delve into the world of intervention and, learn more about optimal D a P T practices.

Kanny

Yeah, absolutely. And, and in that regard, we are very fortunate to welcome Dr. JDI. Kaga now he's currently the assistant professor of internal medicine at the, university of Cincinnati college of medicine. He practices at university there as well. Jadi show welcome. And. For our first question, we just thought you could kind of introduce yourself and talk a little about like what personally led you to your career in interventional cardiology and also how you arrived in Cincinnati.

Jagadish

Good evening, Kenny. Thank you so much for, inviting me to. Be part of this, cardio Ohio podcast, in terms of my career goals of being an interventional cardiologist, I think a lot of credit goes to my mentors at rush university, as well as cook county hospital, where I trained both those hospitals were very geared towards interventional cardiology. and yeah, I think just a natural gravitation towards the field

Ben

And your, reputation and your impact on your fellows at Cincinnati precedes you because several of them recommended you. And, and we're excited to hear what

Jagadish

you have to say. Thanks so much, Ben. I look forward.

Kanny

So, JDI, Ben and I were both, noninvasive cardiologists, we're all, all of us are busy clinicians. You yourself see a lot of patients, both in the hospital and the clinic. And of course you're very busy in the interventional lab. Obviously a majority of patients who have Corona disease, even those who require intervention ultimately are followed by general cardiologists. For our podcast today, we have an audience of general cardiologists. We have sub-specialists in, in all the various areas. We have a lot of advanced practice practitioners in cardiology and, fellows in training as well. So pretty broad audience, most of whom are not interventional specialists. So we really appreciate your perspective today on what is a very, very practical topic that I think all of us in every area of cardiology have to dress every day, which. The type, the duration of antiplatelet therapy after cardiac intervention and how to address specific situations when it may need to be discontinued modified or extended. we wanted to start by just asking you in, in routine patients who have. Percutaneous intervention, whether it's part of an acute coronary syndrome or simply somebody with chronic stable disease, what, what are the key factors that help you decide the initial antiplatelet therapy in terms of when you might pick a more potent agent versus the more, you know, traditional route of, of using Clery and aspirin? Right,

Jagadish

Kenny, I think, it's a very important, primary question to answer. And I think in the last 10 years, there has been so much of very good trial data, which has actually now made us maker our, what used to be expert opinion decisions with a lot more data per se, and kind of elaborate that as we discussed this other subtopics in this, but. This question of which initial oral P two Y one, two inhibitor to choose has some clarity, at least when it comes to, if we look at the clinical scenario where we end up choosing it. So electro PCI for a stable clinic, heart disease, patient. the strongest data. All the data exists mostly for Clore. And if we have an acute coronary syndrome patient, then we have all three of our oral and, P two I two inhibitors, which is Clore prosor and TACA. And. The recent data, definitely, which is what all the guidelines, both European and American guidelines kind of, pretty give clear indication is to choose TACA or pro grow with some caveats to pro grow with based on clinical situations over proper or grow. So I think the first distinction to make is the P C S done for stable ischemic heart disease versus ACS. And if it's a stable ischemic heart, use clod. If it is acute current syndrome preference for TA and VIR, overlo more sot because it has lesser restrictions. you an example, like if you had a patient with prior stroke, you're restricted from not being able to use If you have a patient, who's got a GFR which is low, or if you. Patient who is low body weight. So the certain restrictions which would come with PR, but nonetheless, there is also some good data saying that pro for the right patient does equally good. So basically they have much more ischemic benefit, less 10th thrombosis, less nonrelated ischemic events as well.

Ben

And I think you bring up a good point Jugg about that. about the duration. So just for the fellows and trainees listening, the 2021, guidelines that are endorsed by ACC a H a N sky. Kind of have that same flow chart. You're talking about immediate distinction between stable, human heart disease and acute coronary syndrome. And you, you briefly touched on the choice of antiplatelet therapy. Now we kind of wanna talk about the duration, you know, when you're deciding this first, we always balance bleeding risk. Et cetera. And, and in all the trials they use different sort of gauges of bleeding risk. What are you actually using in your practice regardless if it's ACS or stable scheming, heart disease, are you using a particular risk score or are you, are you taking just a, a general gestalt on history and, and some of the patients characteristics, how are you deciding the bleeding risk in the patients you

Jagadish

treat clinically? I think that's an excellent question, Ben. I. Okay. Generally, it's pretty obvious sometimes with the patient clinical history or of certain findings, which kind of give us an idea. But recently we have had some amount of data that supports this, especially with the bleeding research council or, are B a R C. We have now some data to kind. Classify patients into high breeding risk. having said that in routine clinical use, it's quite, it's a quite an extensive list. It's almost like a grade score, right? Which we use to stratify patients into end stem to who needs early invasive management. Similarly, this high bleeding risk classification has almost like 20 clinical parameters, which go into it to kind of give you, so the general concept I'll tell you basically is. If you have one major bleeding risk criteria or two minor bleeding risk criteria and all of these criteria, which go into it are clinical and make very intuitive sense, which is basically like say somebody had a history of TRAC hemorrhage in the last six months or history of stroke in the last six months or history of thrombocytopenia. All these would be like considered major risk factors. So if you had one major criteria, You would consider that as a high beating risk patient. So I think by clinical Al when you kind of evaluate the patient, you already have a pretty good sense, but if you want to objectively quantify it, there are tools like, like, like what I was saying based on, some of the data sets mostly of some of it were developed in Europe. There's also something called a precision tap score. Uses five clinical factors, which again, developed in Europe used pretty commonly over there, routine clinical practice from my, from my side, I would say most often it is knowing this in the background, knowing all of these risk factors. And looking at the patient when you're looking at all the clinical risk factors, if you see obvious red flags, which, you know, like say, you know, that the patient has like a cancer, which is gonna be operated on within, or need to be operated around a month or a couple of months, then by definition, it's one of the major criteria for high leading risk. So not necessarily using these tools, but being aware of all of these risk factors and kind of thinking about it. And this is what all those recent, data has shown us that being able to recognize and having the options as with the new newer generation stems of shortening, the duration of tap makes you more aware of, okay, this is how I'm gonna define a high bleeding of this patient. Yeah, I think

Ben

that's helpful. we'll also include in the show notes that precision, that precise depth score and encourage everyone to kind of play around with it. you can kind of see how your, the high risk bleeding can change with little parameters such as hemoglobin change, et cetera. Yep. and so I, that's a, that's good to know that that's more of a gestalt thing, especially as you get more used to it. Just one more question to piggyback before we change our topic. There are sometimes where you may want to extend. The duration of dual antiplatelet therapy after an intervention, stent characteristics, other disease, the, the placement of the stent, if it was well opposed, et cetera, can you just give us a, an example of a recent patient where you thought maybe we'll extend therapy of dual, of dual antiplatelet therapy after an intervention?

Jagadish

I think one of the very easy things to kind of make sense of this is I think the patients whom we consider a long, longer duration of dual antiplatelet therapy is very clearly low bleeding risk patient with a high ischemic risk. And one of the commonest examples I can tell you is say somebody, you did a left main PCI. And let's see for whatever, the reason the patient didn't go for bypass graft surgery ended up getting a left main PCI, and you have so much MyCard at risk that, and if they are truly low bleeding risk, you could define that with a. You could use adapt trial data for that. If you have a favorable adapt score, which is greater than equal to two, the, then that's a patient whom you would consider definitely extending an antiplatelet beyond 12 months. another example I could give is somebody, if you did a SPHS vein graft intervention, if they. If they happen to be a younger patient and otherwise, even if they're not younger, but a low bleeding risk profile. Yes. That's another patient whom you know that you're gonna have high ischemic events just by the nature of how SPH vein graft intervention results are. We still know that these patients will have more events per se, just from get go. Those are a couple of things, which I think I can actively like easily think of which I would continue long term.

Kanny

And one question just to clarify Jadi yep. You know, when you talk about extending therapy, I know in the DAP trial they use dual therapy, but I also know there have been trials of Plavix like monotherapy, in patients beyond 12 months. Is, is there any consensus now on what patient may benefit from which of those, or is it also still kind of tailored to their characteristics?

Jagadish

I think the dual antiplatelet therapy has more data from trials and, but having said. the way I would think about it is what all the shorter duration trials have shown is that this more potent, especially VIR single antiplatelet therapies equally good, compared to adding edition on aspirin on top of it. So you could make a case that say beyond. Beyond a year. If you wanted to consider a single antiplatelet therapy, you could drop the aspirin instead of dropping the P two Y one two in a better. And with the, the data we have, it makes intuitive sense to continue, single antiplatelet, which. Plavix probably rather than tra or talar, because they're so patent and you don't really have that much of, ischemic burden one year out. so I would say it, it makes a lot of clinical sense. Say if you wanted to give somebody a protection, the Plavix, the only clinical reason not to do it as obviously patients tend to have reasons to stop Plax for say like a dental. Procedure mind, minor surgery or something like that. And those are the things again, where clinically you, you have to be vigilant of that because if you're extending the duration of the antiplatelets, you will continue to have. multiple visits or phone calls or clinical questions being raised about, okay, what do we do with your colonoscopy now? What are you gonna do with your dental extraction? So I think that is only caveat about when you consider single antiplatelet longer term.

Ben

And Ja you bring up a great point and this is something that we as fellows deal with a lot, especially as pre-op testing, we sometimes see these patients on. On Plavix monotherapy and they either had it stopped and had an ischemic event, pre colonoscopy or something. This is not meant to be a trap question or anything, but just a clinical vignette for you. If you have a patient like that, who had an event greater than one year ago and they're on Plavix monotherapy. Do do you, what do you suggest that patient to do? Do they switch to aspirin and they do the procedure on aspirin? Or do you have a conversation with the proceduralists that consider doing this on Plavix? How does that actually work out in the real world?

Jagadish

I think the data for safely interrupting an antiplatelet is pretty strong after even like three to six months. although there is some data actually, like research papers, which actually quantify the amount of dealing risk with antiplatelets with different kinds of surgeries. What I find in little practices, surgeons prefer to operate on aspirin and not on any other antiplatelet. So I would, if the patient has not had, If, PCI or an ischemic event in the last three to six months, I would just switch them to aspirin to just help them get through the surgery, for that amount of time.

Kanny

And since we're already talking a little bit about, unexpected discontinuation of therapy, I think the other topic, you know, we certainly want your input on is the patients who come in with more serious. You know, bleeding events early in the post PCI course, maybe, maybe they just have an upper GI bleed or maybe they have a, you know, a CNS event and they need urgent neurosurgery. I know. the risk is not continuous, right from the time of the intervention, it does drop off after certain periods of time. So ju D do you feel like you have a better sense of the timeframe when the risk starts to become acceptable? say both ACS or non ACS, if the patient is not coming in a period of months afterwards and requiring, you know, major surgery, that's unexpected.

Jagadish

Yeah, I think Ken that's a very, can, that's a very important question, to answer actually, and I'll kind of profess it this way. I've not used a bare metal stent in. Four years, since like, since I've started working as an attending. And the reason for that, like I still remember, using a couple of bare metal STS probably through my interventional year. And that reason used to be because of you would use a bare metal stand in a patient who has a surgery coming up, or it's a higher bleeding. The reason that has happened, where we have not, we are using DS on pretty much everybody is we know that DS is much better. That's kind of very well proven. And now we have the options of getting patients through with. Bridging therapies with IV cannular that has been such a big help to intervention cardiologists, because we always encounter these patients who say have some kind of surgery coming up and then they get a pre-op and then we, we find a critical lesion and we need to optimize those patients for their surgery. And we then put a Stentin and then they need to go for the surgery. So set. New expert consists opinion is that if you're gonna operate on less than three months, then there is a lot of favor in bridging those patients with IV anti antiplatelets. now with cannular, there's pretty much a very good, algorithm for it. which most institutions use, we certainly do, it's a loader can load rep. We just kind of start. On the day when you interrupt the antiplatelet. so say if it is Plavix, you would stop the Plavix five days prior to the procedure plan procedure, and start the patient inpatient on IV cannular at 0.75. And. Like you could even prepone the surgery say by like Ben was asking about, looking at plate reactivity essays. Some, some of our surgeons do that. They will try to see if the Plavix is still active. Once the P 2, 1, 2 levels go up, they. See that the platelet activity has gone down and they will, they may even operate a little sooner, but at least you have this opportunity where you can bridge the patient. So the data is definitely where, where most people are now thinking of as less than three months after deses consider bridging after three months with all of the short adapt trials. Now, actually even the guidelines. You can drop the second antiplatelet, say in the case of a stable ischemic heart disease patient, which should, what a pre-op patient would've been. You can stop after three months, this, this antiplatelet, and just continue aspirin. So that is prob that's been my practice where I have a cutoff, like three months. For bridging until after that, just basically have them stop the antiplatelet as minimum as they can.

Kanny

And that, three month window would be relevant for both ACS or non ACS is something we

Jagadish

can remember. Oh, ACS. Yes. That's the only distinction ACS, unless the surgery is is critical. I would probably extend the bridging until six months, especially if it is a high ischemic burden patient or a high ischemic risk. so you would probably stretch bridging until six months,

Kanny

yeah. That's that's I think that's something us non interventionalists are less familiar with, but it sounds like it's, becoming the consensus in that population In our last five or 10 minutes. we just wanted to touch on really two brief topics. the first is, you know, concomitant OACs cuz obviously this is a very common clinical dilemma, the patient who has atrial fibrillation, or maybe a history, pulmonary embolic disease, and now needs PCI. I think that's evolved as well in the last few years. To kind of, more of a standard approach, but we just wanted to get your thoughts about, you know, the patient who clearly has an indication for an OAC. How do we approach both the, per procedural antiplatelet therapy? And then how do we approach, the post PCI type and duration of therapy?

Jagadish

I think the way, you, you split it very nicely, actually what to do very procedural as well as long term I'll first address. very procedural part of it. I think that we are basically talking about a patient who is on anti anticoagulation for, for AF. Let's say and now needs a cat and subsequently a PCI. So when do we hold his Zerto? Or when do you hold his, apixaban so the consensus is 24 to 48 hours. Why do I give that window? So if you are convinced that you're gonna do a good radi. access radi, PCI. Then you could get away with holding a apixaban for a day, but sometimes 10% of the time you have to switch to femoral. And the data for that is around 48 hours. So my standard practice has been 48 hours. And the similar things, with, INR targets for Coumadin. the sky consensus for that for best practices is INR of less than 1.8. Again, a lot of us say, if we are doing it for somebody who say has a mechanical valve and is in Coumadin and we are trying to kind of not interrupt them too much and also add ox on top, then we will try to work as much radial as we can and try to keep them on the lower target around. So I will do a case with say, mechanical ATIC valve with an IR of two. rather than a 1.8. So there is some amount of leniency and we, if we go femoral, we also try to use closure devices so that the risk of bleeding is a little less. So that's one aspect of it as to how, and we resume basically the, or anticoagulant. The same night, most of the times, or the next day morning, if as long as there is no exercise bleeding and there is good hemostasis. So that's the very part of how, we are doing, the anticoagulation part. And the next question is what antiplatelet do you add now? This patient has gotten a stent during that CA what antiplatelet do you are? The consensus, almost a consensus is to use flax or than more potent because you already have an anticoagulant which is gonna reduce your ischemic risk of stent thrombosis or another ischemic event and you ischemic event. So you really need an antiplatelet to just get you good epithelization of the stent and not cause like give you more additional, reduction in this ischemic burden. triple therapy is pretty much now confined only to acute Corona syndrome. And even in there, it is probably most people, most of us do one week. If, if you have a really high ischemic burden patient and you say again, the same example, like a left main PCI in an ACS or a S vein graft AC ACS, I would use aspirin for a month. Not, not longer than that. So I would use. I would use a apixaban CLX and an aspirin from anywhere from a week to a month. And on some patients who are stable, ischemic heart disease, and it's a type, a lesion and a straightforward, no non verification PCI. The, the only aspirin they get is on the day of the procedure, the 3 25 loading doors on the day. When the stent goes in and they get the apixaban in the night, they go with apixaban and Plavix. Yeah, Julie,

Ben

that's, that's helpful to, to hear that some of those stent characteristics, location extent of other disease helps dictate not only the duration, but also the intensity of antiplatelet and anticoagulant therapy. To bring up just a point about this now, as fell as we sometimes see platelet reactivity testing. And you talked about the, the commercial verified now system, just, just from your practice, not, there's not uniform usage of this, especially after giving an antiplatelet to see. You know how the patient would respond from a platelet reactivity point of view. When are you actually using this? And you can, you know, you can just give clinical situations when you're using platelet reactivity testing, in your daily practice.

Jagadish

I think Ben I've seen like a lot less use of it compared to like say six years ago, but definitely one of the easiest examples is patients who. Or waiting for Corona artery, artery bypass graft surgery during the cardiovascular ICU. And unfortunately they had an AC C event. So they got loaded with pro Plavix. One of those two Mets in the ER, and we found that they have surgical anatomy and they didn't get PCN waiting for surgery. That's when I think like you're trying to balance, like not having to have them in the, sitting in the unit for five days. Especially with Plavix. There is variability of response. You will see some patients that platelet reactivity assays numbers go up very nicely within like two to three days. So they don't, the surgeons don't have to wait for the recommended five to seven days. So that's one example of where I'd use in terms of efficacy testing. I don't ne normally do it on anybody, because of, I know that some of the patients would with just fit because Plavix being. pro drug. Sometimes you may not see the assay and there is biological variability about how the me, how effective medication is, but clinically it does not born out. So I really don't use it in those clinic. Like just check efficacy in any patient at all.

Ben

Got it. Yeah, that, that, it's a bit complex of when we see it in, in real practice. and I know there's a recent publication of. Of a small trial with a ULAR reversal agent. So it might even be used less. but, that that's very helpful. Thanks.

Kanny

Well, Jaha, we're coming up against our time, but I, I really think we covered a lot of very practical topics I've been taking some notes, just listening to all your, insight. And, it really sounds like the, the theme now is, you know, a patient-centered approach that we're not just following formulas for duration or type of drug, but that we're really focusing. On each patient, both for the initial choice of the agent, but also for duration, whether we decide to extend it in the higher risk patients or shorten it for the higher bleeding risk patients. and I'm, am I correct to say also that you're saying judicious use of bleeding scores combined with, you know, your clinical gestalt is, is, is the best approach to assess risk and, you know, you've given us some advice about. Interrupting therapy as well, either because they have concomitant OACs or because, patients who need to undergo interruption for surgery. But I really think that that's, it's been very insightful. Do you have any other final, wrap up comments or any other, related topics you wanted to address before we wrap things up?

Jagadish

Can I think you summarized it? Well, what I like, what I would say is basically you've gone from. The newer earth we have gone from the first generation St where everybody got standard, 12 month of dual antiplatelet therapy towards getting a lot more insight to help us get through clinical situations. And you're absolutely right. Our patient population has continued to become more and more prone to leading like pretty much some data sets say 60% of the patients actually have some or the other clinical factor, which make them a high bleeding risk patient who get, who want to undergo PCI. So. What used to be an expert opinion has now has data to substantiate, and obviously try to be mindful of both trying to address the ischemic burden as well as address the bleeding risk. And that has truly come about because of the second generation St. And the newer, like bioresorbable polymers, all of these stent technologies where the stent struck thickness is a lot more smaller than before, has allowed trialists to try shorter duration of therapy to, and prove their safety as well as efficacy. So I. It's a very exciting field.

Kanny

Yeah. Well, we, definitely look forward to you continuing to educate us both, in this format and also throughout our other educational activities as this data keeps evolving. I do wanna put a quick plugin for our. Annual meeting, which will be held on October 22nd here in Columbus. We're gonna actually have a very nice, discussion on the new ACCHA guidelines on revascularization in terms of both the surgical and interventional perspective with a bit of a debate between some, excellent experts. so I do hope all of our listeners have a chance to, register for that meeting. It's open now the registration, and it's gonna be our first live meeting in three years. So I really look forward to interacting with everyone, including you J de I know you just be, were elected to the, state of Ohio board. So congratulations on that. And, so thank you, Ben, for your insight, and thanks J de we look forward to getting together grant in the future.

Jagadish

Absolutely. Thank you so much for, inviting me, Kenny. And, thank you, Ben, for your input as well. I really look forward to meeting you both at the annual meeting, you know, in October.

Thank you for joining today's podcast. For more information about the speakers or the topics, please go to Ohio acc.org,