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A few more details on the FOURIER Lp(a) paper ncbi.nlm.nih.gov/pubmed/30586750:
1-33% of pts had Lp(a) >120 nmol/L (>50 mg/gL)
2- The median % Lp(a) eduction was 27%, but only 16% in 4th highest quartile, thus the higher the Lp(a) the less effective PCSK9i is in lowering it,
1-33% of pts had Lp(a) >120 nmol/L (>50 mg/gL)
2- The median % Lp(a) eduction was 27%, but only 16% in 4th highest quartile, thus the higher the Lp(a) the less effective PCSK9i is in lowering it,
3-each doubling of Lp(a) was associated with 8% higher risk for CVD
4- The pts benefited irrespective of LDL-C levels. A along with our recent Lancet paper, it puts to end the 20-yr old faulty hypothesis that one does not need to worry about Lp(a) when LDL-C is controlled
4- The pts benefited irrespective of LDL-C levels. A along with our recent Lancet paper, it puts to end the 20-yr old faulty hypothesis that one does not need to worry about Lp(a) when LDL-C is controlled
5- the pts that benefited the most were those with highest Lp(a), despite getting a less effective Lp(a) lowering
6- lowering Lp(a) by 37 nmol/L (~15 mg/dL) is predicted to lead to a 20% RRR, similar to ODYSSEY ACC presentation,
6- lowering Lp(a) by 37 nmol/L (~15 mg/dL) is predicted to lead to a 20% RRR, similar to ODYSSEY ACC presentation,
7- This is very different than the Burgess paper ncbi.nlm.nih.gov/pubmed/2992609… mendelian randomization in primary prevention cohorts suggesting a 100 mg/dL is needed to lower RRR 20%. This is might be comparing apples to oranges as FOURIER and ODYSSEY had secondary prevention cohorts.
8- These are hypothesis generating sub-studies and we do need the outcomes trial. If FOURIER and ODYSSEY RRR are accurate the Phase 3 ASO trial should be highly positive as it can lower Lp(a) ~200 nmol/L or 80 mg/dL.
9- Should be an exciting and hopeful next few yrs for all.
9- Should be an exciting and hopeful next few yrs for all.
