Here is a new paper for the lipid nerds from the Balance and ESSENCE trials: Lp(a) is genetically determined—but can change due to metabolic factors. In genetically confirmed FCS, Lp(a) is markedly suppressed, especially in those with small apo(a) isoforms genetically programmed for high Lp(a). Why? Likely the absence of normal LPL-mediated lipolysis/remodeling in a chylomicron-dominant state, altering the apoB-100 particles available for Lp(a) assembly. And the OxPL story (@OxPL_apoB) is striking: OxPL-apo(a) falls disproportionately, with a ~70% lower OxPL-apo(a)/OxPL-apoB ratio—evidence that OxPL partitioning shifts away from Lp(a). jlr.org/article/S0022-2275(2…

Lp(a) carries biologically active oxidized phospholipids (OxPL). New research links its OxPL cargo to platelet hyperactivation through CD36, connecting Lp(a) biology to thrombosis and highlighting the importance of what the particle carries. Lp(a) may be more involved in platelet function that previously appreciated, see our review on this also. ncbi.nlm.nih.gov/pubmed/3793… doi.org/10.1161/CIRCRESAHA.1…

We have a new paper today that links Lp(a) with triglycerides in patients with moderate hypertriglyceridemia (TG 150-500). Using our new methods we developed @UCSDCardiology Lp(a) becomes TG- and cholesterol-enriched. ApoC-III inhibition reduced Lp(a)-TG and Lp(a)-C by ~60–70% without lowering Lp(a) particle number, revealing pharmacologically modifiable Lp(a) heterogeneity. We now need to see how Lp(a)-C and Lp(a)-TG correlate with CV outcomes. sciencedirect.com/science/ar…