Starting Combination Therapy Early


The panelists discuss how and when to use combination therapy in patients with hyperlipidemia.

Keith C. Ferdinand, MD, FACC, FAHA, FNLA: Dr Ballantyne, I’m a hypertension specialist. We start combination therapy in most middle-aged and older patients, especially higher risk patients. I think I’ve heard you speak about combining different medications from different classes. Do you want to address that?

Christie M. Ballantyne, MD, FACC: When I first trained, I was in Dallas, [Texas], and we had Norman Kaplan, [MD]. He’s a hypertension guru. Hydrochlorothiazide 25 mg, then 50 [mg], then 50 [mg] twice a day. People said that [was] crazy. We would dose [titrate] up clonidine and Aldomet [methyldopa] until someone had [adverse] effects [AEs]. Why do we go all the way to the top? What ends up happening is [AEs] are quite flat until the highest dose—and they’re still low—but the highest dose is the highest dose because you had more [AEs], [and] the dose after that had too many [AEs]. Rosuvastatin 80 mg didn’t get approved because there [were] too [many] muscle problems, and patients know that’s the highest dose. Aren’t there more [AEs] with that dose? Six percent further reduction—I can add ezetimibe when I [want] that. I’m still on a high-intensity statin; it could be 40 mg of atorvastatin or 20 mg [of] rosuvastatin, add ezetimibe, now I get a much bigger reduction. They didn’t change their statin dose, so they’re not going to complain of more muscle symptoms. Then if I need to, I can still increase the statin afterward. Why don’t we do that instead? Like in hypertension, you’re adding to the top dose. You just hit them hard with a good dose, then add the second drug. I’ve been doing this for years, and we have some real-world evidence studies that have shown that approach gives better LDL [low-density lipoprotein] [lowering results] and equally good event reduction, with better adherence. There’s more than 1 way to skin a cat. That’s kind of an ugly expression. I’m not sure we ever even said that.

Keith C. Ferdinand, MD, FACC, FAHA, FNLA: We shouldn’t be skinning cats.

Christie M. Ballantyne, MD, FACC: We don’t want to skin cats, but there’s more than 1 way to get [to] the goal. How about that?

Erin D. Michos, MD, MHS: I do want to emphasize—I mentioned earlier in the program about these new thresholds for clinical ASCVD [atherosclerotic cardiovascular disease] at very high risks—we want to get to an LDL threshold less than 55 mg/dL. It’s often very hard to get there with single agents alone. You have to be thinking about combination therapy right out of the box. You know the patient’s starting LDL [level], and you want to reduce it by 50% and get to below these thresholds. I just went over the expected LDL reduction for each of these agents. If you know where you’re starting and where you need to go, you should often be thinking, “I’m going to need 2 agents to get to below these thresholds.” Just like with blood pressure; if somebody comes in and their blood pressure is—like Christie already mentioned—above 160 mm Hg, we’re going to be thinking about combination therapy right at the get-go. The problem with the sequential wait and follow [is] maybe they don’t come back for 6 months to a year, then it takes so much longer [to treat]. It’s part of that inertia of getting [patients] to [the] goal. Whereas, if you’re more intensive up front, we can get patients to [the] goal faster.

Payal Kohli, MD, FACC: I think the point is the urgency to treat, because if you are waiting, you’re leaving that endotoxin unchecked.

Mary McGowan, MD, FNLA: The really important thing is to level set with the patient from the get-go. We do it all the time with familial hypercholesterolemia [FH]. We’ll say, “Your LDL [level] is 240 mg/dL. It’s very likely you’re going to need 2, maybe 3, agents to get to [the] goal. We’re going to be here with you to get you there, and we’re going to do it rapidly.” I think it’s the interaction with the patient, [stating] this is the situation here. And it’s not just us thinking [that] this person is going to need 2 agents. It’s letting the patient know so they don’t feel like a failure. They don’t feel like they have not gotten to where they should be with just a single agent.

Keith C. Ferdinand, MD, FACC, FAHA, FNLA: Dr McGowan, they used to teach us old medicine in medical school a long time ago, but what they taught us was important. The only diagnosis you will never make is the one you don’t think about. This idea that [FH] is somehow really rare…it’s probably because you’re not looking.

Mary McGowan, MD, FNLA: That’s absolutely true. I give grand rounds at [the Geisel School of Medicine at Dartmouth] in medicine and in pediatrics, and I always bring a patient with me because they can [provide] the response to the physician. [In] pediatric grand rounds, we’re talking to a pediatrician at the end who’s had lots of questions with a patient who has 3 children with FH. She has FH [and] her mother had FH. So this physician says, “I think I’ve only had 1 or 2 kids in my entire career with FH.” My patient, Lisa, says, “With all due respect, that’s because you’re not checking.” Let them do the heavy work and really educate people. One in 250 [individuals] has FH. It’s a very common disorder. Where I live in New Hampshire, where we have a founder effect with French Canadians, it’s probably closer to 1 in 180 [individuals].

Keith C. Ferdinand, MD, FACC, FAHA, FNLA: If you can recall, a lot of those [individuals] came around the horn to Louisiana, and some of them from Louisiana went over to Houston, [Texas], so it’s not rare.

Mary McGowan, MD, FNLA: Yes, they came to visit….You got them.

Keith C. Ferdinand, MD, FACC, FAHA, FNLA: It’s not rare.

Transcript Edited for Clarity

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