The Role of Factor Xa Inhibitors in the Management of CAD/PAD - Episode 3
Deepak L. Bhatt, MD, MPH: I can imagine though, if you’re a primary care physician [PCP] on the front lines, you just said a lot of stuff: you said CRP [C-reactive protein]; you said CAC, that’s coronary artery calcium; and LPa [lipoprotein-little-a], which perhaps not everyone measures, but the most recent European guidelines actually said everybody should have it measured once in their life. So what do you think? You’re a chief of cardiology, you’ve had to provide some guidance to a health care system. How do you deal with that? What should the primary care physician be responsible for monitoring and measuring, and when would you refer along this continuum of risk? Not the easy stuff, such as if somebody has got angina climbing up a flight of stairs, obviously that will prompt a referral to the cardiologist, or if someone has a heart attack, heart failure, not the easy stuff. But more in this continuum of risk short of actual ischemic events.
Manesh Patel, MD: As you said, this is not so straightforward. We’ve made messages that are sometimes complicated, right? We’ve said, oh, it’s not the LDL [low-density lipoprotein], it is the LDL, it’s the drug, right? So we’ve not made it easy for people to follow all the time.
Deepak L. Bhatt, MD, MPH: Same with LPa. Now it’s in, but at a prior time.
Manesh Patel, MD: Calcium scoring, don’t do it. I think one way to think about it is, as you said, it’s a continuum of risk so just start with what’s the best way of figuring out the patient’s risk? And so what we tell people, much like the guidelines, is—and it is sort of artificial to start with events—for those who haven’t had events, we’re going to ask you to calculate the ASCVD risk score or the atherosclerotic cardiovascular disease risk score that the guidelines recommend, and now I think in practice are pretty well known, which try to project what your 10-year risk is of having a cardiovascular or heart disease event, stroke, heart attack, or death due to heart disease. And in that group what we tend to say is if you get high risk, you get a 7.5%, 10%, you’re going to be treating. If you’re low risk, let’s say 5% or less, we’re going to be doing a variety of lifestyle modifications and potentially getting you to a goal of let’s say an LDL that is not as low as I described before, where that 70 mg/dL cut point is for the high risk.
Where the tests you described are important, often this is where you might get a referral. Because outside of ordering LPa, you wanted a calcium score, you wanted to act on that, you’re trying to convince the patient to take a statin or do something else in their life. There I think in a lot of health systems beyond, and the referral may not be to a cardiologist, it may be to a dietitian or it may be to a pharmacist. It’s a variety of places you’re going to try to build that system. But between that intermediate risk, which actually I think is unfortunately the majority of people in the United States and growing, those who are at risk to have cardiovascular disease and probably need to be treated might need 1 more piece of data to make them think they need to be treated, whether it’s a scan or their heart, a lipid level, or a sub-particle that tells you, oh, I’m at high risk, an inflammatory marker.
Vamsi Krishna, MD: So back to the point of what does primary care come back to. I think our guidelines sometimes do us a disservice when it comes to LDL cutoffs. And so what I mean by this is that NLA [National Lipid Association], ACC [American College of Cardiology], and AHA [American Heart Association] may all have different cutoff points.
Deepak L. Bhatt, MD, MPH: There are all the endocrinology guidelines. There are different sets there.
Vamsi Krishna, MD: Absolutely. So then now as a primary care physician, you’re seeing, let’s say, someone who has diabetes, is 60 years old, has CKD [chronic kidney disease] stage III and hypertension, and they’re coming in just for an annual follow-up. You have 5, 10 minutes to make this evaluation, how are you really gauging it? But as I tell my PCPs, that’s actually the patient who we want to treat now. If we treat that patient, and in my opinion based on histopathology and what not, if you have an LDL of less than 60 mg/dL, it’s going to be very difficult to form new plaque. And so I am quite aggressive with lipid management, albeit statins or non-statins, and I’m really big in the diet world. And so my point is that we need to do something, and it could be up for debate on how we treat it. Not everyone needs to be treated with statins, but I think that is going to be where we’re going to target primary prevention better. Do you agree with that?
Deepak L. Bhatt, MD, MPH: He said something interesting about LDL. What do you think, John, if the LDL is really well controlled? One could argue about 60 mg/dL as the number, but let’s say the LDL is 30 mg/dL, and it’s been that way for a little while naturally or with pharmacotherapy. The patient is stable. What is the incremental value there of antithrombotic therapy if that LDL has been in that 20 to 30 mg/dL range for the past 3 to 4 years? Maybe even the person did have an ischemic event in the past, but now LDL is controlled, non-smoker, is there still value of stacking antithrombotic therapies?
John Eikelboom, MBBS, MSc, FRCPC: Well, it’s a really good question. I don’t know that we have a definitive answer for it. What we do know is that they’re on that continuum of risk, and if you get the LDL super low, you’re going to drive them down in terms of risk. The lower you are on the risk continuum, the smaller the absolute benefits of stacking risk modifying agents. So I don’t know if I’ve seen anybody with an LDL of 30 mg/dL, but I guess as a hematologist I’m just happy they’re on something. I’m probably more of a primary care provider than you because you’re all dealing with advanced vascular disease. We’ve learned from and will talk later about some of the trials. But if you’ve got really well controlled risk factors, the incremental benefits say of antithrombotic therapy are going to be more modest.
Transcript edited for clarity.