lowest LDL without using a PCSK9 inhibitor?

Lp(a) additive risk is linear with Lp(a) level (higher levels = higher risk). The hazard ratio at 140 nmol/L is 1.3-1.5 (30-50% increased risk) depending on what study we're looking at. The researchers gave us a handy dandy table to tell us how much we need to lower LDL to mitigate the risk of elevated Lp(a):

Lp(a) (nmol/L)Δ Lp(a) vs median (nmol/L)Lp(a) percentileHR for MCVE due to ↑Lp(a)LDL‑C reduction starting age 30 y (mg/dL)40 y (mg/dL)50 y (mg/dL)60 y (mg/dL)
320300992.56≈46≈54≈66≈89
27025097.52.19≈39≈46≈58≈73
22020093.51.87≈31≈35≈46≈58
170150901.60≈23≈27≈35≈43
12010082.51.37≈15≈19≈23≈31
7050751.17≈8≈8≈12≈15
20ref.50ref.ref.ref.ref.ref.
If I’m reading this right, my LPA is 144 nmol/l. This chart is saying I should be at 15mg/dL LDL? Or am I reading this wrong?
 
the important thing is that your LDL is already so low, so congratulations, therapy was clearly successful!
Thanks, I appreciate it.
It's taken many years to get to this point. I still can't believe I'm tolerating therapy so well after trying literally every other drug on market. Even Nexletol caused my CK to go high out of range with severe muscle aches.

How They Work (Mechanism of Action)
  • Leqvio (siRNA): Uses RNA interference (RNAi) to target the liver, preventing it from producing the PCSK9 protein in the first place.
  • Repatha (Monoclonal Antibody): Directly binds to the PCSK9 protein in the bloodstream, blocking it from binding to LDL receptors.
  • Result: Both methods allow more LDL receptors on the surface of liver cells to remain active, which removes more "bad" cholesterol from the blood.
 
Thanks, I appreciate it.
It's taken many years to get to this point. I still can't believe I'm tolerating therapy so well after trying literally every other drug on market. Even Nexletol caused my CK to go high out of range with severe muscle aches.

How They Work (Mechanism of Action)
  • Leqvio (siRNA): Uses RNA interference (RNAi) to target the liver, preventing it from producing the PCSK9 protein in the first place.
  • Repatha (Monoclonal Antibody): Directly binds to the PCSK9 protein in the bloodstream, blocking it from binding to LDL receptors.
  • Result: Both methods allow more LDL receptors on the surface of liver cells to remain active, which removes more "bad" cholesterol from the blood.

I’m familiar with the intolerance to the other 3, but what was the issue with Repatha?
 

Sponsors

Back
Top