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It's estimated to be between 6% and 57% of Lp(a) mass. One can't predict unless it's measured directly.

Glad we have a fan to review our old papers Sam Tsimikas - but you do need to place citations of the sources in all your tweets, otherwise no one will know where they come from and it will diminish their impact. That being said, this is a counterintuitive finding and needs proper

Back to triglycerides for a moment: First demonstration of this phenomenon, quite interesting: Ionis sciencedirect.com/science/articl…

Nice case. You should do a poll.

Interesting, full court press with 8 meds. I initially thought this may have been a case of FCS and possibly apoC-III inhibition. Thanks for sharing and nice job getting TGs down.

Interesting and intriguing, need to wait for details, but maybe using an antibody to bind antibody fragments is too simplistic that depends on a secondary clearance mechanism when the plasma cell factory is churning lots of light chains. I would be curious if stoichiometry of

We have a new Lp(a) paper, led by David Erlinge from PROSPECT 2 using IVUS/NIRS. It shows high Lp(a) associates most with vulnerable plaque characteristics, whereas LDL-C with plaque burden. Lp(a) was measured by our UC San Diego Cardiology assay, the only Lp(a) assay I am aware of that is

This is the placebo group in Odyssey outcomes, >90% were on aspirin. There is ~25% higher MACE in people with high Lp(a). We don't know if the spread in risk would be higher with no aspirin, but we are now testing this in ASPREE. Hope to have some data by late this yr or early

We don't know yet, but hopefully will have an answer in the next year.

This is the results of this poll: It seems knowing the corrected, more true LDL-C will make a difference. Now we have to do another poll on this, next tweet.

New poll: If you could order a directly measured Lp(a)-C and have the lipid panel be defined as TC = LDL-C(corrected), + Lp(a)-C + HDL-C + TG/5, and price was similar to LDL-C, would you use it to guide selection of therapy, and how often?:

Not necessarily. Non-HDL-C comes for free (but has same issue with LDL-C, it contains Lp(a)-C in it). Lp(a) needs to be ordered by separately, but both would be useful. Let's see the poll then we can discuss where Lp(a)-C might be useful. We can add apoB to the discussion.

Results of the other poll: Answer is, High Lp(a)/Lp(a)-C. This is a "clinical pearl". When your patient does not respond as expected to any "LDL-C" lowering drug, check for high Lp(a). The Lp(a)-C is not as responsive to LDL-C lowering drugs and thus LDL-C (per the lab estimate,

Lets do one more poll to round things out for discussion: You have a pt with CAD, family hx CAD (father MI 58) and lipid panel as follows: TC= 170, LDL-C by lab estimate or direct LDL-C = 75, TG = 225 (VLDL= 225/5 = 45), HDL-C = 50 on rosuva 40. What would you order next to

New Lp(a) paper led by Alexander C. Razavi from All of US. Long way to go in getting everyone an Lp(a) test.

Here are the results of this poll. Understanding what the true LDL-C is will become much more relevant as we have Lp(a) and maybe Tg lowering drugs for Tg 150-500 in future. Defining and treating the responsible lipoproteins will be important for individualized care. ApoB is a

Results of other poll, this one did not garner as much interest. This topic is not in clinical mainstream yet and it's in the "early adopter stage", but let's see in 2-3 years with more data. This is being rolled out as a research test in clinical trials if validated to impact

This is a good topic for Sat AM Sam Tsimikas Class. In fact, Lp-PLA2 inhibitors block OxPL from degrading, it was predicted to fail. Pelacarsen lowers OxPL-apoB 88%, and so does olpasiran. But a more direct way is in the works.