CVD Real-World Case Scenario 3



Deepak Bhatt, MD, MPH: Let's move onto the final of our 3 cases. Let's go ahead to you, Brett. The case is a 66-year-old man with hypertension, arthralgias and arthritis. He presents with a lipid panel that was taken before and after being on atorvastatin 10 mg a day and fenofibrate of 145 mg. His trigs [triglyceride] levels were reduced from 592 to 217 mg/dL, the non-HDL [high-density lipoprotein] from 228 to 175 mg/dL, and total cholesterol from 232 to 158 mg/dL. What would you go ahead and do with this person?

Brett Nowlan, MD, FACC, RPVI: Got it. I know my colleagues here tonight do what I’m about to describe first, but it always bears repeating and emphasizing. I want to make sure that he is not on any offending medications such as steroids that might be causing these numbers. I really would want to check his thyroid function, his liver and renal function, urinalysis, and make sure there is not another primary condition going on that’s driving these numbers.

Certainly in all of my patients, I take a diet history. I’m very diet obsessed with my patients, and inevitably with his triglycerides the way that they are, I'm going to yell at him about excessive refined carbohydrates, and I would also want to check his alcohol intake. That's going to be very important for all of our patients, but I know my colleagues here tonight do that. Having said that, this gentleman has mixed dyslipidemia, possibly familial combined hyperlipidemia. His non-HDL cholesterol is very high.

If you look at the comparison between his total cholesterol and is non-HDL cholesterol, that would actually suggest that his HDL is extremely low. If you assume the rest of his risk factors are perfect, which I'm sure they are not, and you did a risk evaluation or a 10-year risk, you would certainly be above 20% risk. That would potentially warrant high intensity statin therapy. You also may have some risk enhancers there. We've got persistent triglycerides, and he's got aches and pains. Does he have a chronic inflammatory condition like rheumatoid arthritis? There is a strong suspicion for hyperinsulinemia in this man, based on his numbers, so metabolic syndrome, prediabetes, or type 2 diabetes. So on the blush of it, he is high risk.

As I said, the way that I like to approach patients is a plaque-driven phenomenon because I certainly would want to optimize his medications. But depending on how far I would go, I would like to be guided by presence or absence or degree of plaque with a calcium scan. I tend to evaluate most of my patients in that context and interpret their lipid numbers within that context. As I said, if you did not have that available to you, it's certainly reasonable to increase this gentleman’s statin dose because he is high risk.

When it comes to that fenofibrate, I'm definitely less enthusiastic about that. I understand why it may have been done. When he first presented, his triglycerides were above 500 mg/dL, and certainly some guidelines recommend that then being your first issue to address in a mixed dyslipidemia. However, we have better stuff available. If you look at the ACCORD-Lipid, it was a cardiovascular outcome trial that did look specifically at fenofibrate. Adding to a statin, there was really no cardiovascular benefit. If you drilled down into the subgroups and you looked at those people with high triglycerides and low HDL, they came close, but they didn't quite make it.

However, if you look at what we have available today, icosapent ethyl, we know that that is very effective at lowering triglycerides. That was studied in the MARINE trial. Certainly in that trial, if you had triglycerides over 500 mg/dL, and you used icosapent ethyl at 4 g per day, you would lower your triglycerides by about 33%. Of course we now have data in a different pool of patients, but I can't see why they wouldn't also get that benefit. We know that there is ASCVD [atherosclerotic cardiovascular disease] event reduction with that medication.

If I had to meet this gentleman, I think I would clean up his regimen, and this is what I spend a lot of time doing in my office, in that I would take him off the fenofibrate. I think I would put him on icosapent ethyl 4 g per day and combine that with statin therapy and then recheck. There is a little caveat in this particular case, this gentleman already has aches and pains, and so I would want to be a little bit gentle with him with the statin that I use. As I like to tell people, the only benefit you get from statins is the statin that you take.

If I came out of the gates and blasted at him with high intensity statin therapy and his aches got worse, I may lose him and the therapeutic relationship that we have. I think if I were to continue him on atorvastatin 10 mg per day, we know that that has about a 20% triglyceride reduction. It has about a 35% reduction in non-HDL cholesterol. If you combine that with the EPA [eicosapentaenoic acid] 4 g per day, it gives you a non-HDL reduction of about 18% and triglyceride reduction about 33%, so that combination is actually lowering your non-HDL by 55% as well as your triglycerides by 55%.

That's a very good start in terms of risk modification. To clarify whether I should actually move on to a third-line agent, which I think is certainly possible in this gentleman because he has a very high non-HDL, I would want to be plaque driven. So I would do a coronary calcium scan in him and evaluate plaque. Certainly if he has an Agatston score of 0, then I would not feel compelled to go further. This is because if the Agatston score is positive, and obviously the higher it is the more abnormal it is, then I might be compelled to move on to add-on therapies like ezetimibe or a PCSK9 inhibitor.

Deepak Bhatt, MD, MPH: In your practice, has that approach worked? I don't mean clinically, but let's say this person, I guess most people would bin him as primary prevention. But do you think the PCSK9 inhibitor approvals are a bit easier if you've proven that there is actually plaque there?

Brett Nowlan, MD, FACC, RPVI: Absolutely, no question about it. I'm actually very careful about tracking my own numbers of PCSK9 approvals, and right now it's at 98%. In other words, 98% of patients for whom I request PCSK9 inhibitors are approved. The only thing that I'm very slavish about doing when I want to use a PCSK9 inhibitor is to perform plaque testing. The heavy lifter there that I use is the calcium scan.

But certainly I use other things like carotid ultrasounds and measuring intima-media thickness and ABI [ankle-brachial index] tests. This is because I think if you use a plaque-driven approach, firstly it reassures you that you are using these agents appropriately and cost-effectively, it makes patients much more likely to engage in the therapy that you're offering them. And I have found from the insurance payers it gives me a much higher chance of success of that script, if I can label them as having plaque, which clearly you can do with these studies.

Deepak Bhatt, MD, MPH: Yes, 98%—it's hard to beat that. That's quite impressive. Matt, I'm curious what your thoughts are with this concept of using imaging to enhance risk stratification, here, to guide therapy ultimately. First, perhaps you can talk about just with coronary calcium specifically, but then whether you think there is a role of going beyond that in the primary prevention patient.

Matthew J. Budoff, MD, FACC, FAHA: I agree with Dr Nowlan, as far as plaque-driven, I think it really helps us in cases like this especially in primary prevention, where we just don't know what their underlying cardiovascular risk is. We know that it dramatically drops the number needed to treat. If we look at population-based studies like the MESA study, the Multi-Ethnic Study of Atherosclerosis. We can drop the number needed to treat from something like 500 patients to maybe 20 by having an elevated calcium score. While I can't claim 98% success with my PCSK9 approvals, a high calcium score does help drive approval rates in my practice.

I think I would agree with that, especially in a patient like this, who doesn't have any overt risks that would automatically put him at secondary prevention targets. I have to say I might try atorvastatin 80 mg in him and see if he tolerates it. I agree he has to take it to benefit from it, but my experience is once they're already on a lower dose of the statin that they tend to tolerate that same statin at higher doses more frequently than not. You can always back off again, but I think that would get additional LDL [low-density lipoprotein] lowering and certainly additional triglyceride lowering as well, along with the icosapent ethyl.

Deepak Bhatt, MD, MPH: Well, that's a terrific discussion of 3 challenging real-world cases, lots of real-world experience on this panel. I think it illustrates just how much we can do for patients. Even though people are coming in stable, not necessarily with a complaint, that doesn't mean there aren’t things we can or should do to further reduce their cardiovascular risk. I think that's the challenging thing about patients who aren't coming in with a specific symptom. It's easy just to say, “Don't rock the boat, they're not complaining. Get them out of the office.” But in fact, there is a lot we can and should do with multiple advances that have occurred in cardiovascular prevention and risk reduction.

Transcript Edited for Clarity

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