Management of Patients With ASCVD and Hypercholesterolemia

EP: 1.Prevalence and Risk Factors for ASCVD Associated With Hypercholesterolemia

EP: 2.Impact of Comorbidities on Atherosclerosis

Now Viewing

EP: 3.Management of Patients With ASCVD and Hypercholesterolemia

EP: 4.Utilizing Guideline Recommendations for ASCVD and Hypercholesterolemia Management

EP: 5.DCRM Practice Recommendations for ASCVD and Metabolic Diseases

EP: 6.Implementing Lifestyle Modifications for ASCVD and Hypercholesterolemia Management

EP: 7.Managing ASCVD and Hypercholesterolemia: Statins, Ezetimibe, and PCSK9 Inhibitors

EP: 8.Bempedoic Acid to Manage ASCVD and Hypercholesterolemia

EP: 9.Older Agents to Manage ASCVD and Hypercholesterolemia

EP: 10.Role of Icosapent Ethyl in Managing ASCVD and Other Lipid Disorders

EP: 11.ASCVD and Hypercholesterolemia: Combination Therapy and Statin Intolerance

EP: 12.Safety and Efficacy of Bempedoic Acid for ASCVD and Hypercholesterolemia

EP: 13.ASCVD and Hypercholesterolemia: Patient Selection for Bempedoic Acid

EP: 14.Emerging Agents for Treatment of Hypercholesterolemia and ASCVD

EP: 15.Future Directions for the Treatment of ASCVD and Hypercholesterolemia

Yehuda Handelsman, MD: Let’s discuss managing patients, and see how our management has evolved and changed over the years. Let’s start with you, Christie, because you mentioned your times as an intern.

Christie Ballantyne, MD: The reason I ended up going into preventive cardiology was because I was frustrated, working at Parkland Hospital, in Dallas, Texas, and seeing people come in who had diabetes, hyperlipidemia, hypertension, and they’d have a stroke, infarct, lose a toe, then a foot, and then go blind. I thought, we’ve got to do something better than just treating the symptoms, palliation. High cholesterol was 300 mg/dL, and high blood pressure was your age plus 100 systolic, so if you were 75 years old, it was 175. High glucose, if it was over 300 mg/dL, and had polyuria, polydipsia, or polyphagia, that was poor control. It’s dramatically changed, the concept of what we can do in prevention. I emphasize what we can do, not necessarily what we are doing, as those are different things, but particularly for lipids and cholesterol, it’s unbelievable what we have the ability to do now.

Erin D. Michos, MD, MHS: We have new tools in the tool kit. For lipids, it used to just be statins. Now we have all these other agents, esketamine, PCSK9 inhibitors, inclisiran, bempedoic acid, and more tools than we ever did before. It gives more flexible options for patients who have been intolerant to statins, although most patients can tolerate statins on a rechallenge. We have more therapies, but we’re underutilizing them, and we’re not using combination therapy up front. We have other prevention agents that are outside of the lipid field, with SGLT2 inhibitors and GLP-1 receptor agonists that I consider as prevention agents. Now we’re moving beyond just patients with type 2 diabetes; we know that SGLT2 inhibitors can be used as treatment for patients with heart failure and kidney disease. We are in a new era, it’s an exciting time to be a preventive cardiologist.

Yehuda Handelsman, MD: In your practice, Matt, have you seen a change in how you approach your patients?

Matthew J. Budoff, MD: To Erin’s point, a lot more upfront, dual therapy, more than just saying, “OK, you’re on a high potency statin, that’s enough,” and walking away from an LDL [low-density lipoprotein] that might be too high. Now we have, as she said, all these great tools in the tool chest, and I’m starting to get more people on therapy earlier, hopefully avoiding a lot of these complications that Christie discussed.

Yehuda Handelsman, MD: We are in a time right now where there is a paradigm shift in the management. We used to do just traditional cardiovascular risk control, the lipids, blood pressure, glucose, and now we’re getting more combination therapy, which we are seeing in blood pressure and glucose, and now we start seeing it also in lipids. We’re getting into an era in which we prevent the next event, we give the SGLT2, GLP-1, PCSK9, and we prevent the next event. We must do a short-term, immediate, let’s prevent the next event, and then continue the long-term risk control, because otherwise, we are going to lose what we do right now. But it’s a very exciting era. Paul.

Paul S. Jellinger, MD, MACE: The level of LDL gets all the attention as a causative agent for atherosclerosis, and rightfully so, but the other important point is the duration of LDL elevation, lifetime exposure. You can have an LDL of 120 and 130 mg/dL, but for an entire lifetime that may be pathogenic, while an LDL of 180 mg/dL for a short period may be less so. Starting early is a key. We talked about when do we start, and duration of LDL exposure is critical and often overlooked. I don’t think we start patients early enough on LDL-lowering therapy. And the introduction of the statins is marvelous. I don’t think a class of drugs has done more to save lives than statins has in the last number of years, but it also allowed us to do clinical trials that brought LDL down to levels we couldn’t do before, and to show that the lower the LDL, the better.

Yehuda Handelsman, MD: It’s very interesting. Christie, I’ll remind you, about 8 years ago, we were involved in a lower LDL project with the ACC [American College of Cardiology]. I had a question about patients with HeFH, heterozygous familial hypercholesterolemia, was it something genetic that would predispose them to heart disease, or is it the exposure to LDL? The answer you and others gave was it is exposure to LDL. My question was, HeFH, let’s say with an LDL of 190 or 200 mg/dL. What if you have LDL of 170 mg/dL? Are you not exposed to that, just another 5 years later, what do you think?

Christie Ballantyne, MD: If you go back to the concept of the integral, the area under the curve [AUC], I think it is important. But I like to explain to patients that it’s multiplicative with other risk factors. You have the AUC of the cholesterol, but also, what’s the blood pressure during that exposure period? Did they smoke cigarettes, other genetic factors from the family, obesity, diabetes? They might have an LDL of 160 md/dL, but they have 4 other problems. Two to the fourth, that’s a lot different than 4 times, 1 times 1 times 1. That’s the whole patient approach, which is critical right now. If you’re going to be effective, you must start early, but you must treat everything.

Yehuda Handelsman, MD: Because LDL is not the same for everybody, it’s not created equal. The higher the risk of the patient, the more damage your LDL will do, and therefore you can bring things down.

Paul S. Jellinger, MD, MACE: I like to call that global risk, I think that’s the best term, and we need to look at everything.

Transcript Edited for Clarity