My Lp(a) is 76 nmol/l, high according to my doctor. LDL 88, ApoB 85, HbA1C 4.9, HS-CRP .4, fasting insulin 4, normal BP, etc. My physician is super fixated on the Lp(a), which is one “number” above normal and is recommending a statin and a CAC. I viewed it as information and motivation to keep other numbers as they are. I am not interested in a CAC or statin. Hopefully, I am not wrong, but it seems like a further reduction in LDL would not really decrease my risk of heart disease or a cardiac event in a meaningful way. I eat a high fiber, low saturated fat diet, and I move my body daily.
Thank you for sharing your perspective. I think you’ve identified the central question: would further LDL lowering offer enough benefit to matter to you?
This is where studies of calcium scoring offer useful context. In MESA, researchers found that people with elevated Lp(a) and a calcium score of zero had relatively low cardiovascular risk over about 10 years, while those with elevated Lp(a) and scores of 100 or higher had substantially higher risk. That doesn’t mean your Lp(a) falls into the same category studied, but it illustrates how similar bloodwork can sit within very different risk pictures.
The value of CAC in that discussion isn’t necessarily to make the case for medication—it can help clarify the underlying risk when the benefit of treatment is uncertain. That’s the decision-making role I hoped to highlight.
In response to the question: what to do about an elevated lipoprotein(a), I felt it appropriate to share some real world experience of how Lipoprotein(a) is assessed and dealth with. As you will see its not a one size fits all approach.
The contrast between a high Lp(a) with a zero calcium score and a similar result with established coronary disease is the part I keep coming back to. A concentration in mg/dL also hides apo(a) size, and the apoB beside it often says more about LDL particle burden than the Lp(a) number alone. When you look at the HORIZON miss, do you read it as a failure to lower events, or as a failure of the population to have enough residual risk for the drug to move?
The latter given we already are treating this population appropriately. I also suspect the study popuation was "tainted" with low risk high lp-a patients ... the isoforms of large size but low particle number
That makes sense. With LDL-C and apoB already well treated in most of the trial, the absolute event rate left to move was small. A mg/dL cutoff can also pull in large-isoform patients whose particle count in nmol/L is lower than the mass suggests, which would dilute any effect. Since pelacarsen is still investigational, I would read HORIZON as a question about who to select for Lp(a) lowering rather than a verdict on the target itself.
My Lp(a) is 76 nmol/l, high according to my doctor. LDL 88, ApoB 85, HbA1C 4.9, HS-CRP .4, fasting insulin 4, normal BP, etc. My physician is super fixated on the Lp(a), which is one “number” above normal and is recommending a statin and a CAC. I viewed it as information and motivation to keep other numbers as they are. I am not interested in a CAC or statin. Hopefully, I am not wrong, but it seems like a further reduction in LDL would not really decrease my risk of heart disease or a cardiac event in a meaningful way. I eat a high fiber, low saturated fat diet, and I move my body daily.
Thank you for sharing your perspective. I think you’ve identified the central question: would further LDL lowering offer enough benefit to matter to you?
This is where studies of calcium scoring offer useful context. In MESA, researchers found that people with elevated Lp(a) and a calcium score of zero had relatively low cardiovascular risk over about 10 years, while those with elevated Lp(a) and scores of 100 or higher had substantially higher risk. That doesn’t mean your Lp(a) falls into the same category studied, but it illustrates how similar bloodwork can sit within very different risk pictures.
(https://pmc.ncbi.nlm.nih.gov/articles/PMC10966924/)
The value of CAC in that discussion isn’t necessarily to make the case for medication—it can help clarify the underlying risk when the benefit of treatment is uncertain. That’s the decision-making role I hoped to highlight.
https://www.acc.org/latest-in-cardiology/articles/2021/10/12/12/46/new-evidence-supporting-selective-use-of-coronary-artery-calcium-scoring
In response to the question: what to do about an elevated lipoprotein(a), I felt it appropriate to share some real world experience of how Lipoprotein(a) is assessed and dealth with. As you will see its not a one size fits all approach.
The contrast between a high Lp(a) with a zero calcium score and a similar result with established coronary disease is the part I keep coming back to. A concentration in mg/dL also hides apo(a) size, and the apoB beside it often says more about LDL particle burden than the Lp(a) number alone. When you look at the HORIZON miss, do you read it as a failure to lower events, or as a failure of the population to have enough residual risk for the drug to move?
The latter given we already are treating this population appropriately. I also suspect the study popuation was "tainted" with low risk high lp-a patients ... the isoforms of large size but low particle number
That makes sense. With LDL-C and apoB already well treated in most of the trial, the absolute event rate left to move was small. A mg/dL cutoff can also pull in large-isoform patients whose particle count in nmol/L is lower than the mass suggests, which would dilute any effect. Since pelacarsen is still investigational, I would read HORIZON as a question about who to select for Lp(a) lowering rather than a verdict on the target itself.