Goddamn, this is a disappointment. Everyone thought (and probably still thinks) Lp(a) was/is causal. There is a very "neat" story about how the shorter LPA genes (with fewer Kringle repeats) leaves the Lp(a) cholesterol particle's surface exposed, and the shorter genes over-expressed their products. Although I don't think anyone demonstrated the specific damage mechanism, it sure seemed like that could be a smoking gun.
That said, I look forward to seeing the actual data. Since they enrolled patients with previous coronary events, the damage may have already been done, and lowering Lp(a) levels might not do much in that case. Still, it was hoped that the damage would stop accumulating, leading to noticeably fewer events.
Beautiful theories once again murdered by ugly facts.
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Goddamn, this is a disappointment. Everyone thought (and probably still thinks) Lp(a) was/is causal. There is a very "neat" story about how the shorter LPA genes (with fewer Kringle repeats) leaves the Lp(a) cholesterol particle's surface exposed, and the shorter genes over-expressed their products. Although I don't think anyone demonstrated the specific damage mechanism, it sure seemed like that could be a smoking gun.
That said, I look forward to seeing the actual data. Since they enrolled patients with previous coronary events, the damage may have already been done, and lowering Lp(a) levels might not do much in that case. Still, it was hoped that the damage would stop accumulating, leading to noticeably fewer events.
Beautiful theories once again murdered by ugly facts.