Expert Perspectives on Managing Polyvascular Disease and Coronary Artery Disease - Episode 1
Drs Marc Bonaca and Manesh Patel provide an overview of Polyvascular Disease and prevalence of coronary artery disease and peripheral artery disease.
Deepak Bhatt, MD, MPH: Hello, and welcome to this HCPLive® Peer Exchange titled “Expert Perspectives on Managing Polyvascular Disease and Coronary Artery Disease.” I’m Dr Deepak Bhatt from Brigham Women’s Hospital and Harvard Medical School in Boston, Massachusetts. It’s a real pleasure to be with you today. I’m fortunate to have 5 good friends and distinguished colleagues with me. Let me start with the far end of the table. Dr Manesh Patel is the chief of cardiology at Duke University Medical Center in Morrisville, North Carolina. Welcome, Manesh.
Manesh Patel, MD: Thanks.
Deepak Bhatt, MD, MPH: I’ll move on to Dr Amy Pollak, who is the director of cardiac subspecialties at the Mayo Clinic in Jacksonville, Florida. It’s great to have you here.
Amy Pollak, MD: Thank you.
Deepak Bhatt, MD, MPH: Dr Marc Bonaca is a professor of medicine and the director of vascular research at the University of Colorado in Aurora, Colorado. Welcome, Marc.
Marc P. Bonaca, MD, MPH: Thank you.
Deepak Bhatt, MD, MPH: Dr Sahil Parikh is an associate professor at Columbia University [College of Physicians and Surgeons in New York, New York]. Dr Eric Secemsky is the director of vascular intervention at Beth Israel Deaconess Medical Center in Boston, Massachusetts. Today, we’re going to discuss treatment of polyvascular disease, in particular coronary artery disease and associated conditions such as peripheral artery disease [PAD], cerebrovascular disease, etc. We’re going to talk about dual-antiplatelet therapy in that context. We’re going to talk about dual-pathway inhibition in that context. For anyone not familiar with that term, we’re going to explain exactly what that means. We’re also going to share what we consider to be the optimal duration of that—a very controversial topic—and the rationale for switching between different forms of therapy. De-escalation for single antiplatelet therapy, escalation from single antiplatelet therapy to dual antiplatelet therapy, where does dual pathway inhibition fit into that. There are lots of different, sometimes overlapping, topics that will hopefully shed light on and inform your clinical practices.
With that, let’s get started with our first topic, which is a discussion of polyvascular disease and coronary artery disease. I’ll turn to Dr Bonaca and ask, what exactly is polyvascular disease? I imagine many people in our audience haven’t heard the term. Before we talk about what we do with it, maybe it would be good to say what it is.
Marc P. Bonaca, MD, MPH: Thank you. This is such an important topic, and it’s emerged in the last 10 to 15 years. Deepak, I learned the term from you from the REACH [Reduction of Atherothrombosis for Continued Health] Registry. Although we know there are different manifestations of atherosclerosis—coronary, cerebrovascular, and peripheral—and that those patients are all high-risk, they share an underlying pathobiology. There are a group of patients who manifest symptoms in multiple vascular territories. They have coronary disease and peripheral disease, or cerebrovascular disease and coronary disease. They’re at extremely high risk. No matter what data set you look at, it’s been recapitulated many times from your initial work that after you adjust for all the other differences, they’re at 50% to 80% higher risk of having bad things happen, like atherothrombotic events. They’re really emerging as a unique population of patients who are at extreme risk of irreversible harm events of the heart, limb, and brain. Some of that depends on where they manifest symptoms, but they’re all extremely high risk.
Deepak Bhatt, MD, MPH: Those are really valuable points for the audience, that polyvascular disease and its identifications are important for those patients who are high risk. Later, we’ll get to what we can do about that. Manesh, is it fair to lump all those things together? For coronary artery disease and peripheral artery disease—I’m going to throw in cerebrovascular disease—are they more of the same? Or are they different beasts?
Manesh Patel, MD: That’s a great question. That’s something we’ve been trying to understand even better. Our understanding of the biology is that atherosclerosis, as we’ve often used the term, is an inflammatory atherothrombotic event. In all these different vascular beds, patients will have downstream events. But we’ve learned that some of our patients with PAD who haven’t had coronary events probably have an overexpression of atherosclerosis in their lower extremity. When we did some of the PAD studies that many in this group have been involved with, we saw that concerning coronary disease, we often think of it as the same disease. I like to think of it as different phenotypic manifestations of the same disease. But if you see a patient in clinic who’s 65, 70 years old with peripheral vascular disease and they haven’t had a coronary event, that doesn’t mean they don’t have coronary atherosclerosis. It means they’re expressing that risk in their lower extremities much as somebody might do with stroke.
Why do they have it in different beds? That’s an unusual question that I don’t think we know the answer to. We know that atherosclerosis starts in the lower extremities, in the iliacs. There’s wonderful work by Dr Val Fuster and others that starts to show us the natural disease course. On average, for the clinicians and people I see in clinic, I think about polyvascular disease as how many places is this really important manifestation happening. Is it in the legs? Is it in the brain? Is it in the carotids? I’ll even go further. Is it in the kidney? Do they have diabetes? Do they have multivessel coronary disease? All these are risk factors. One might say polyvascular is usually used for vascular beds. We don’t think about the kidney and atherosclerosis as much. We don’t use diabetes as a marker as much. But I’d be thinking about my patient who has those conditions also as polyvascular.
Deepak Bhatt, MD, MPH: Those are some insightful comments. Diabetes, for sure. That definitely amplifies risk even beyond the presence of polyvascular disease. Your comment about the kidney is very interesting. Polyvascular disease was initially defined in the REACH Registry. But concerning kidney, why shouldn’t that count? Dr Eugene Braunwald made that point in an analysis from the SAVOR-TIMI 53 trial. Your current faculty member Dr Tony Gutierrez looked at that as an additional vascular bed. It’s not the traditional coronary peripheral, cerebral. What if they do have microalbuminuria, macroalbuminuria? Does that count as an additional risk amplifier, as you’re rightly suggesting? Yes, indeed it does. That’s a really good point.
Transcript Edited for Clarity