Case 1: Antithrombotic Regimen in High-Risk Patient
EP: 1.Role of NOACs in Venous Thromboembolism and COMPASS Trial
EP: 2.COMPASS Trial: Subgroup Analysis and Implications
EP: 3.Rationale and Study Design of the VOYAGER PAD Trial
EP: 4.Case 1: Antithrombotic Regimen in High-Risk Patient
EP: 5.Case 1: Choice of Therapy for Peripheral Artery Disease
EP: 6.Case 1: THEMIS Trial and Subgroup Analysis With Revascularization
EP: 7.Case 2: Triple Antiplatelet Therapy in Patients With Stents
EP: 8.Case 2: Combination of Device and Drug for Patients With Stents
EP: 9.Case 2: Relationship Between LDL and Major Adverse CV Events
Transcript:
Deepak Bhatt, MD, MPH: Let me start with the first case, and hopefully we’ll get through complementary cases. The first case is of a woman with an age in the mid-70s. She has a history of hypertension, dyslipidemia, and type 2 diabetes. I’m sure you all see many patients with that conglomeration of risk factors. They often go together. She also has a history of smoking 50 pack-years, though she quit a year ago, so good for her.
Her lipid profile shows the LDL [low-density lipoprotein] is 128 mg/dL, the triglycerides are 110 mg/dL, her hemoglobin A1C [glycated hemoglobin] is 7.5%, and the creatinine is 1.3 mg/dL. She is on the following medicines: Aspirin, 81 mg a day; metformin, 1000 mg twice a day; and atorvastatin, 20 mg a day. She has claudication, but she reports that her claudication has gotten better since she stopped smoking a year ago, and at the time when she presented with claudication, she was also started on a walking program.
Marc Cohen, we’ll start with you. You care for a lot of patients. What is your initial impression of this patient? What would you do with her with respect to her antithrombotic regimen? Would you just continue aspirin? Would you switch her to clopidogrel? Would you switch her to aspirin plus clopidogrel? Would you switch her to the COMPASS trial regimen? We’ll start with that.
Marc Cohen, MD: First and foremost, I would dichotomize my approach to her. Her treatment for her lipid risk is woefully inadequate, and I would also apply the same terminology to her antithrombotic regimen. That’s woefully inadequate. I see her as being a very high-risk patient. I can begin to imagine, forgetting about her claudication, what her aorta looks like as another target organ, which is very diseased and for which we need to treat to prevent thromboembolic events from all the plaque that’s up and down her aorta. I would attack her on 2 fronts: 1 would be very aggressive, maybe including PCSK9 inhibitors. Dr Bonaca, who is part of this group, has some exciting data from his PCSK9 trials regarding how lipid management can reduce limb ischemia, as well as how the COMPASS trial strategy can reduce limb ischemia.
Deepak Bhatt, MD, MPH: Those are useful ways of looking at this sort of patient. Kelley, I’ll turn to you next. What are your thoughts about her management, whether it pertains to the antithrombotic regimen, the lipid regimen, or any other aspect you might want to comment on?
Kelley Branch, MD, MS: I would echo Marc Cohen’s comments that the lipids need to be addressed, not really first and foremost but in parallel with atorvastatin 20-mg dose. Unless there’s a reason why she was not tolerating it, it should be maximized. I’m then thinking about additional therapy on top of that, either ezetimibe or PCSK9. In addition, the patient is diabetic. Hemoglobin A1C is not under good control, so we can consider other medications that are beneficial—antidiabetic medications, but they have really become cardiovascular medications that happen to treat diabetes as well. It’s the SGLT2 inhibitors and GLP1s. They’re not all exactly equal. There are GLP1s that seem to have cardiovascular benefit and some that don’t. SGLT2s are pretty much a class effect, so I’d consider those.
Thinking about the antithrombotic therapy, it’s also important to make sure that we know what we’re dealing with. We don’t have objective evidence that this is peripheral arterial disease [PAD], although there’s definitely claudication, so there are symptoms suggestive of that. I’d like to make sure that the patient has peripheral arterial disease. If so, then my mind changes dramatically. I need to be more aggressive in this patient because if you have enough atherosclerosis to create PAD, you have enough atherosclerosis to be at higher risk of stroke, MI [myocardial infarction], cardiovascular death, all causes of mortality, all those things. We need more information to make sure this is PAD-associated claudication, then we need to intensify therapy to make sure we reduce the risk as much as we can.
Deepak Bhatt, MD, MPH: That’s good. I’m glad you mentioned the “diabetes” drugs as well because you’re quite right. Those have moved outside just diabetes to being cardiovascular risk-reducing drugs, whether it’s heart failure, kidney-related risk, or atherosclerotic risk, depending on the SGLT2 inhibitor or GLP1 agonist. That’s important to be in the comfort zone of cardiologists and primary care physicians. Obviously, of course, endocrinologists are already comfortable with those classes of drugs.
Transcript Edited for Clarity
