Guidelines and Management of Patients With Polyvascular Disease


Expert cardiologists discuss CAD guidelines and approaches to management of patients with polyvascular disease.

Deepak Bhatt, MD, MPH: We’re going to move on to not just identifying polyvascular disease, but what to do about it. I’ll start with you, Amy. What do the guidelines from the ACC [American College of Cardiology] and the AHA [American Heart Association] tell us about managing coronary artery disease [CAD]? A bunch of new guidelines have come out lately at this meeting and at the last meeting. But let’s look at the ones pertaining to coronary artery disease and revascularization and that sort of thing?

Amy Pollak, MD: As you said, a tremendous amount has recently come out with updated guidelines. But a lot of the fundamental parts of how we treat cardiovascular patients haven’t changed. If somebody has stable symptoms, we’re focusing on optimal medical management. We’re trying to tease out patients who are going to be at the highest cardiovascular risks, obviously left main disease if someone is symptomatic or 3-vessel disease and seeking revascularization. We’re strategizing for patients who have very stable symptoms, who don’t have left main or 3-vessel disease for whom we’re doing medical therapy vs individuals who need to go to for revascularization.

The risk factor reduction approaches cannot be underscored in terms of the importance of having individuals on appropriate antiplatelet, whether it’s a layered antithrombotic, lipid lowering with aggressive LDL [low-density lipoprotein], cholesterol lowering using statins and PCSK9 inhibitors, among other therapies. Plus, blood pressure control, blood sugar, tobacco cessation. For all those risk factor reduction approaches, which are critical for patients who have polyvascular disease, they’re even more important. It’s striking that in the REACH [Reduction of Atherothrombosis for Continued Health] Registry, for patients who had had a prior ischemic event in the last 12 months, the risk of a future event over a 4-year period was staggering. It was a 25% for patients who have polyvascular disease, in terms of the mortality associated with these diseases. Patients who had diabetes and vascular disease also had extraordinarily high risk.

We have a large amount of tools to help patients and reduce this risk, but we’re not always using them as intensely as we should. In a diverse population, we haven’t touched much on health equity. There are tremendous health disparities in access to screening, medical care, and medications. We have a lot of work to do for all Americans to have access to these life-saving treatments.

Deepak Bhatt, MD, MPH: That’s a great point. In the national dialogue, there has been a lot of talk about disparities. But we need a lot of action, so that’s very good. Beyond classic disparities based on race and sex, which has come up during the COVID-19 pandemic, there are disparities based on location. Rural care in the United States vs urban care. There are a lot of disparities as well.

Manesh, what are your thoughts? Amy did a good job mentioning therapies like lipid-lowering blood pressure. What about antithrombotictherapy? What’s the role there? And for coronary artery disease?

Manesh Patel, MD: As I started, I suspect that in the future there will be therapies for the inflammatory component, where many are testing. But right now, when somebody comes to clinic, I don’t think about anti-inflammatories for cardiovascular disease. I think about atherothrombosis. Obviously, for the athero part, there’s LDL lowering, and there will be some other agents there. Most people are saying, “Let’s get your LDL down as far as possible to control blood pressure, diabetes.” But as an interventional cardiologist, I grew up in a platelet-centric world, where more antiplatelet therapy was good and less put our patients at risk. Deepak you led some of the most important studies in this space, where we know we could add 1 or 2 agents. We started to understand that 2 is better than 1.

Recently, of course, we now know about dual-pathway inhibition. We talked about that. That’s thinking about the evolution from, let’s say broadly, vitamin K antagonist type of medication. It’s a very specific dose for antithrombotic therapy at the 10A level. We know that for 2.5 mg of rivaroxaban, we’re going to talk about some of those trial data. With aspirin, it might be dual-pathway inhibition. Now when I see the patient with coronary artery disease, the guidelines say to first make sure you treat the athero spot.

Then you have to have some antiplatelet therapy for chronic vascular disease for CAD. It’s usually aspirin and clopidogrel or aspirin. Obviously, we’ve seen those data. Most of our patients with coronary artery disease are getting all that in aspirin. We’re starting to see data about doing dual pathway or dual antiplatelet. Because of our stenting world, we were into dual-antiplatelet therapy [DAPT], but for chronic coronary artery disease we’ve got really good evidence now that dual pathway is a pretty significant improvement in their lifestyle. But that’s a change. To Eric’s point, I have to let go of what I learned for many years and relearn some things or convince my patients that this is the right thing to do.

Deepak Bhatt, MD: Those are valuable points. To amplify the dual-antiplatelet therapy, everyone of the audience is familiar with that. Historically that’s been aspirin and clopidogrel, but then aspirin and clopidogrel aspirin and an anticoagulant. The dual-pathway inhibition specifically is referring to aspirin and what some call vascular dose for rivaroxaban, 2.5 mg twice a day of that particular dose. We have a few different options: antiplatelet monotherapy, dual-antiplatelet therapy, dual-pathway inhibition for the patient with the coronary artery disease. Eric, what about throwing PAD [peripheral artery disease] into the mix? How does that alter considerations toward antithrombotic therapy?

Eric Secemsky, MD: I’m reflecting on the comments that Manesh made. We’ve had a bit of an identity crisis in the cath lab. We spent the late 2000s and early 2010s saying that we need dual-antiplatelet therapy in everybody for a long time. We did the DAPT study, and there’s some benefit. There are also some risks. We spent the last 5 years saying that we could probably get rid of Plavix, ticagrelor, prasugrel earlier on, especially for someone coming to the cath lab for a coronary stent. Now everybody wants to be off therapy earlier. There’s a balance there. It’s about what’s going to give you the best long-term benefit for long-term outcomes. We’re thinking a little less about the procedural side with the stents and more about the patient.

Now you throw on PAD. These patients have substantial risks of morbidity and mortality. We love talking about life and limb and keeping both going for these patients. But most patients, especially when they get more advanced PAD, have risks as high as 50% of dying or losing a leg in 1 year. Now we can do things really well in the cath lab. We can move away from the dual-antiplatelet therapy and think about dual-pathway inhibition a little more. When we think about the thrombotic risk, that’s when we can make the long-term benefit for patients for their limbs, as well as their cardiovascular disease and other processes.

I’ll remind the audience that our PAD population rarely dies from a limb-related event. It’s usually a heart attack or a stroke. That’s what we’re really treating these patients for. We treat their legs for quality of life, making sure they heal, but that’s not what drives their mortality. This focus now is on our safer procedures. We’ve got a better hold on how to keep our stents open, our balloons open. We’ve got to think about the therapy that works on the long-term outcomes for these patients. And it goes back to this thrombotic risk that’s added to their atherosclerotic risk.

Deepak Bhatt, MD, MPH: A lot of valuable points that you made. For the audience, we’ll come back in the next segment with a detailed discussion about dual-antiplatelet therapy, antiplatelet monotherapy, de-escalation strategies, and dual-pathway inhibition. We’ll review all those data in some detail. But before we get to that, Sahil, I’d be interested in your perspective. How do we factor in other things? If the patient has diabetes or chronic kidney disease, how does that affect your decision-making in regard to patients with CAD, CAD and PAD, or just cardiovascular disease?

Sahil Parikh, MD: It heightens my concern. In our practice nowadays, 30% to 35% of patients coming to the cath lab have diabetes. In the PAD population, it’s enriched perhaps 2-fold, particularly the critical limb population that many of us take care of. In those patient populations, it’s clear that either renal disease or diabetes is highly likely to be prevalent. Consequently, it will heighten our concern about their atherothrombotic risk.

Transcript Edited for Clarity

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