Meeting News

Lp(a) has strong effect on CVD risk

Patrick M. Moriarty

CHICAGO — Lipoprotein(a) has been shown to be an independent, causal and genetic risk factor for CVD, with higher prevalence in patients of African, South Asian, Asian and Oceanic ancestry, according to a presentation at the Cardiometabolic Health Congress.

During his presentation, Patrick M. Moriarty, MD, FACC, FACP, professor of medicine and director of clinical pharmacology and the Atherosclerosis/Lipoprotein-Apheresis Center at the University of Kansas Medical Center, highlighted several key updates in treatment of Lp(a).

“Well, what’s the big deal? The big deal is, a lot of people have this,” Moriarty said. “There’s always been this snafu I get from clinicians when I talk about this, that they can’t measure Lp(a); no one covers it; there’s no ICD-10 coding; and that it costs so much. Believe it or not, it doesn’t cost a lot. There are two ICD-10 codes for it — E78.41 Elevated Lp(a) and Z83.430 Family History of Elevated Lp(a) — and the American Heart Association/American College of Cardiology guidelines that came out last year said that if you have a patient with high CV risk, which I think most of your patients do, you should measure their Lp(a) to see if they have further risk.”

Genetic association with Lp(a )

According to the presentation, Lp(a) levels greater than 50 mg/dL appear to contribute to a higher risk for heart disease, with several ethnicities being more genetically predisposed to this risk factor.

“There’s a genetic association to this,” Moriarty said in his presentation. “It seems as though it’s highly prevalent and African Americans, up to 30% or more. In Asian countries, India for example, has a high percentage, but Asians such as Chinese and so forth, have a very low correlation to high Lp(a) in the genetics.”

In addition, Moriarty also presented findings on potential treatment methods for Lp(a) and their efficacy, including that:

  • A low-fat diet raises Lp(a) levels, regardless of vegetable consumption.
  • Physical activity has little effect on Lp(a) levels.
  • Niacin therapy reduces Lp(a) and oxidized phospholipid levels but has not demonstrated, in clinical trials, its ability to lower CVD events.
  • Hormone therapy lowers Lp(a) levels and CVD.

“Lp(a) usually stays the same throughout your life span because diet, exercise and weight reduction has no effect,” Moriarty said. “It doesn’t change dramatically except in postmenopausal women because they lose estrogen and, therefore, inhibition by estrogen is lost. In women, as they age, their Lp(a) can go up, unlike men. In fact, elderly women have a higher risk for association with high Lp(a) than men do, which we think is partially related to the elevation at that mark.”

What could be done

“The problem is, if you have a high Lp(a), a PCSK9 inhibitor can lower it by about 15%, but when your Lp(a) is lower, it’s about 30%,” Moriarty said during his presentation. “You would think it would be the opposite, but it isn’t. It’s still beneficial.”

In addition, Moriarty added that in his own clinic, he treats patients with high Lp(a) and CVD using apheresis.

“Apheresis in the U.S. has been approved mainly for LDL, homozygous familial hypercholesterolemia with LDLs over 500 mg/dL, heterozygous familial hypercholesterolemia with LDL over 200 mg/dL with CVD and functional heterozygous familial hypercholesterolemia with LDLs greater than 100 mg/dL,” Moriarty said. “Recently they lowered the level of LDL to 100 mg/dL with ongoing CVD despite aggressive medical management, but the American Society for Apheresis came out with their 2019 guidelines and they recommend using lipid apheresis for patients with Lp(a) greater than 50 mg/dL with ongoing CVD and normal LDLs.” by Scott Buzby

Reference:

Moriarty PM. Update on Lipoprotein(a). Presented at: Cardiometabolic Health Congress; Oct. 10-13, 2019; Chicago.

Disclosure: Moriarty reports he received fees/funding from Academic CME, Akcea, Amarin, Amgen, Eli Lilly, Esperion, FH Foundation, Ionis, Kaneka, Kowa, the National Lipid Association, Novartis, Regeneron, RegenXBio, Renew and Sanofi.

Patrick M. Moriarty

CHICAGO — Lipoprotein(a) has been shown to be an independent, causal and genetic risk factor for CVD, with higher prevalence in patients of African, South Asian, Asian and Oceanic ancestry, according to a presentation at the Cardiometabolic Health Congress.

During his presentation, Patrick M. Moriarty, MD, FACC, FACP, professor of medicine and director of clinical pharmacology and the Atherosclerosis/Lipoprotein-Apheresis Center at the University of Kansas Medical Center, highlighted several key updates in treatment of Lp(a).

“Well, what’s the big deal? The big deal is, a lot of people have this,” Moriarty said. “There’s always been this snafu I get from clinicians when I talk about this, that they can’t measure Lp(a); no one covers it; there’s no ICD-10 coding; and that it costs so much. Believe it or not, it doesn’t cost a lot. There are two ICD-10 codes for it — E78.41 Elevated Lp(a) and Z83.430 Family History of Elevated Lp(a) — and the American Heart Association/American College of Cardiology guidelines that came out last year said that if you have a patient with high CV risk, which I think most of your patients do, you should measure their Lp(a) to see if they have further risk.”

Genetic association with Lp(a )

According to the presentation, Lp(a) levels greater than 50 mg/dL appear to contribute to a higher risk for heart disease, with several ethnicities being more genetically predisposed to this risk factor.

“There’s a genetic association to this,” Moriarty said in his presentation. “It seems as though it’s highly prevalent and African Americans, up to 30% or more. In Asian countries, India for example, has a high percentage, but Asians such as Chinese and so forth, have a very low correlation to high Lp(a) in the genetics.”

In addition, Moriarty also presented findings on potential treatment methods for Lp(a) and their efficacy, including that:

  • A low-fat diet raises Lp(a) levels, regardless of vegetable consumption.
  • Physical activity has little effect on Lp(a) levels.
  • Niacin therapy reduces Lp(a) and oxidized phospholipid levels but has not demonstrated, in clinical trials, its ability to lower CVD events.
  • Hormone therapy lowers Lp(a) levels and CVD.

“Lp(a) usually stays the same throughout your life span because diet, exercise and weight reduction has no effect,” Moriarty said. “It doesn’t change dramatically except in postmenopausal women because they lose estrogen and, therefore, inhibition by estrogen is lost. In women, as they age, their Lp(a) can go up, unlike men. In fact, elderly women have a higher risk for association with high Lp(a) than men do, which we think is partially related to the elevation at that mark.”

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What could be done

“The problem is, if you have a high Lp(a), a PCSK9 inhibitor can lower it by about 15%, but when your Lp(a) is lower, it’s about 30%,” Moriarty said during his presentation. “You would think it would be the opposite, but it isn’t. It’s still beneficial.”

In addition, Moriarty added that in his own clinic, he treats patients with high Lp(a) and CVD using apheresis.

“Apheresis in the U.S. has been approved mainly for LDL, homozygous familial hypercholesterolemia with LDLs over 500 mg/dL, heterozygous familial hypercholesterolemia with LDL over 200 mg/dL with CVD and functional heterozygous familial hypercholesterolemia with LDLs greater than 100 mg/dL,” Moriarty said. “Recently they lowered the level of LDL to 100 mg/dL with ongoing CVD despite aggressive medical management, but the American Society for Apheresis came out with their 2019 guidelines and they recommend using lipid apheresis for patients with Lp(a) greater than 50 mg/dL with ongoing CVD and normal LDLs.” by Scott Buzby

Reference:

Moriarty PM. Update on Lipoprotein(a). Presented at: Cardiometabolic Health Congress; Oct. 10-13, 2019; Chicago.

Disclosure: Moriarty reports he received fees/funding from Academic CME, Akcea, Amarin, Amgen, Eli Lilly, Esperion, FH Foundation, Ionis, Kaneka, Kowa, the National Lipid Association, Novartis, Regeneron, RegenXBio, Renew and Sanofi.

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