Growing Role of Lp(a) in Cardiovascular Risk Assessment

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madman

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* Lp(a), a low-density lipoprotein (LDL)-like particle with an apo(a) attached to apoB molecule, is now recognized as a potent genetic risk factor, with levels above 50 mg/dL (125 nmol/L) linked to cardiovascular complications, including myocardial infarction, stroke, aortic stenosis progression, and cardiovascular death. Wong emphasized that Lp(a) may be up to six times more atherogenic than LDL cholesterol (LDL-C)



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Nathan D. Wong, MPH, PhD discusses the evolution of Lp(a) in risk assessment, given its role as a genetic risk factor for cardiovascular complications.




In this expert discussion at the 22nd Annual World Congress Insulin Resistance Diabetes & Cardiovascular Disease (WCIRDC), Nathan D. Wong, MPH, PhD, a professor of medicine and director of the Heart Disease Prevention Program at the University of California, Irvine, discussed the growing excitement surrounding lipoprotein(a) [Lp(a)] and its role in cardiovascular disease prevention.

Lp(a), a low-density lipoprotein (LDL)-like particle with an apo(a) attached to apoB molecule, is now recognized as a potent genetic risk factor, with levels above 50 mg/dL (125 nmol/L) linked to cardiovascular complications, including myocardial infarction, stroke, aortic stenosis progression, and cardiovascular death. Wong emphasized that Lp(a) may be up to six times more atherogenic than LDL cholesterol (LDL-C), underscoring the urgent need for increased awareness and screening.

Despite its clinical significance, Wong noted fewer than 1% of individuals are currently tested for Lp(a). He highlighted recommendations from the National Lipid Association (NLA) advocating for universal, once-in-a-lifetime testing for all adults, indicating screening not only enhances risk stratification—potentially reclassifying patient risk scores—but also increases initiation of lipid-lowering therapies, including statins and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, in high-risk individuals.

At his institution at UC Irvine, Wong noted the implementation of best practice advisory alerts in electronic health records (EHRs) as one method to improve screening rates, particularly in patients with atherosclerotic cardiovascular disease (ASCVD), aortic stenosis, or elevated LDL-C.


Wong expressed excitement about the therapeutic pipeline for Lp(a), including the highly anticipated Lp(a)HORIZON trial of pelacarsen, the first cardiovascular outcomes trial targeting Lp(a), set to read out in 2025. Emerging therapies like siRNA agents and oral Lp(a)-lowering medications promise up to 80-100% reductions in Lp(a) levels. Wong stressed that while these advancements hold promise, clinicians must act now to reduce overall cardiovascular risk through intensive LDL-lowering, blood pressure control, and diabetes management in patients with elevated Lp(a).
 
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Defy Medical TRT clinic doctor
* highly anticipated Lp(a) HORIZON trial of pelacarsen, the first cardiovascular outcomes trial targeting Lp(a), set to read out in 2025
 

 
* Lp(a), a low-density lipoprotein (LDL)-like particle with an apo(a) attached to apoB molecule, is now recognized as a potent genetic risk factor, with levels above 50 mg/dL (125 nmol/L) linked to cardiovascular complications, including myocardial infarction, stroke, aortic stenosis progression, and cardiovascular death. Wong emphasized that Lp(a) may be up to six times more atherogenic than LDL cholesterol (LDL-C)



View attachment 49473




Nathan D. Wong, MPH, PhD discusses the evolution of Lp(a) in risk assessment, given its role as a genetic risk factor for cardiovascular complications.




In this expert discussion at the 22nd Annual World Congress Insulin Resistance Diabetes & Cardiovascular Disease (WCIRDC), Nathan D. Wong, MPH, PhD, a professor of medicine and director of the Heart Disease Prevention Program at the University of California, Irvine, discussed the growing excitement surrounding lipoprotein(a) [Lp(a)] and its role in cardiovascular disease prevention.

Lp(a), a low-density lipoprotein (LDL)-like particle with an apo(a) attached to apoB molecule, is now recognized as a potent genetic risk factor, with levels above 50 mg/dL (125 nmol/L) linked to cardiovascular complications, including myocardial infarction, stroke, aortic stenosis progression, and cardiovascular death. Wong emphasized that Lp(a) may be up to six times more atherogenic than LDL cholesterol (LDL-C), underscoring the urgent need for increased awareness and screening.

Despite its clinical significance, Wong noted fewer than 1% of individuals are currently tested for Lp(a). He highlighted recommendations from the National Lipid Association (NLA) advocating for universal, once-in-a-lifetime testing for all adults, indicating screening not only enhances risk stratification—potentially reclassifying patient risk scores—but also increases initiation of lipid-lowering therapies, including statins and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, in high-risk individuals.

At his institution at UC Irvine, Wong noted the implementation of best practice advisory alerts in electronic health records (EHRs) as one method to improve screening rates, particularly in patients with atherosclerotic cardiovascular disease (ASCVD), aortic stenosis, or elevated LDL-C.


Wong expressed excitement about the therapeutic pipeline for Lp(a), including the highly anticipated Lp(a)HORIZON trial of pelacarsen, the first cardiovascular outcomes trial targeting Lp(a), set to read out in 2025. Emerging therapies like siRNA agents and oral Lp(a)-lowering medications promise up to 80-100% reductions in Lp(a) levels. Wong stressed that while these advancements hold promise, clinicians must act now to reduce overall cardiovascular risk through intensive LDL-lowering, blood pressure control, and diabetes management in patients with elevated Lp(a).
As I have posted previously my wife has a Lp(a) level of around 70. Other studies I have read called levels of sub 30 to be healthy. This is a genetic issue and remains constant throughout one's life. It is inherited. She had a CAC score done and it was 1500+. Her father dropped dead of a massive coronary at 70 and her brother had a stroke at 68.
If the CAC score or Lp(a) is bad likely the other is also.
 
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Unfortunately, none of the studies I have seen assessing the risk of Lp(a) have assessed people with high levels who have truly heart-healthy practices such as low fasting insulin, healthy nitric oxide levels, avoidance of seed oils, low inflammation, sensible sun exposure, heart-healthy micronutrient status, etc. As with many other things, a risk factor is not necessarily a true risk if other factors are healthy.
 
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