#210 - Lp(a) and its impact on heart disease | Benoît Arsenault, Ph.D.

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Jun 13, 2022

Benoît Arsenault, a leading researcher from Laval University, dives deep into the genetics of Lp(a), a crucial factor in heart disease. He discusses how Lp(a) is inherited and its significant role in cardiovascular risk. The conversation highlights the challenges of measuring Lp(a) levels and the emerging treatments like antisense oligonucleotides. Benoît also explains why traditional statins don’t adequately address Lp(a) and underscores the importance of identifying this genetic marker for better heart health outcomes.

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INSIGHT

Lp(a) Atherogenicity

Lp(a)'s atherogenicity stems from its LDL component, oxidized phospholipids, and sequence homology with plasminogen.
The oxidized phospholipids carried by Lp(a) contribute to inflammation, thrombosis, and calcification.

ADVICE

Aortic Valve Assessment

Regularly assess the aortic valve in patients with elevated Lp(a) using echocardiogram or cardiac MRI.
Early intervention in aortic stenosis leads to better outcomes, making early detection crucial.

INSIGHT

Lp(a) and Aortic Stenosis

Lp(a) is a strong initiator and accelerator of aortic valve stenosis, especially in younger patients.
Sodium fluoride PET-CT can detect metabolic changes in the aortic valve even before calcification.

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Benoît Arsenault is a research scientist focused on understanding how lifestyle and genetic factors contribute to cardiovascular disease risk. In this episode, the discussion casts a spotlight on Lp(a)—the single most important genetically-inherited trait when it comes to atherosclerotic cardiovascular disease (ASCVD) risk. Benoît explains the biology of Lp(a), how it's inherited, the importance of measuring Lp(a) levels, and the diseases most associated with high Lp(a). He dives into data on the possible treatments for lowering Lp(a) such niacin, statins, and PCSK9 inhibitors, as well as the most exciting new potential therapeutic—antisense oligonucleotides.

We discuss:

How Benoît came to study Lp(a)—a new marker for cardiovascular risk [3:15];
The relationship between Lp(a) and CVD risk [6:45];
What genome-wide association studies (GWAS) revealed about Lp(a) [16:00];
Clinical tests to measure Lp(a) [22:00];
The biology of Lp(a) [25:45];
How statins lower LDL-cholesterol and why this doesn't work for an Lp(a) [29:15];
The structure of LDL-p and Lp(a) and what makes Lp(a) more atherogenic than an equivalent LDL particle [34:00];
The role of Lp(a) in aortic valve disease [42:45];
How greater numbers of Lp(a) particles are associated with increased risk of disease [48:00];
The genetics and inheritance of Lp(a) and how and when to measure Lp(a) levels [52:00];
Niacin and other proposed therapies to lower Lp(a), apoB, and CVD risk [1:00:45];
Why awareness of Lp(a) among physicians remains low despite the importance of managing risk factors for ASCVD [1:14:00];
The variability of disease in patients with high Lp(a) [1:19:00];
Diseases most associated with high Lp(a) [1:26:30];
The biology of PCSK9 protein, familial hypercholesterolemia, and the case for inhibiting PCSK9 [1:35:00];
The variability in PCSK9 inhibitors' ability to lower Lp(a) and why we need more research on individuals with high levels of Lp(a) [1:50:30];
Peter's approach to managing patients with high Lp(a), and Benoît's personal approach to managing his risk [1:54:45];
Antisense oligonucleotides—a potential new therapeutic for Lp(a) [1:57:15]; and
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