Lipoprotein(a) and oxidized phospholipids are associated with myocardial inflammation after acute myocardial infarction.

Localized myocardial inflammation after acute myocardial infarction (MI) is regulated by innate immune pathways. Oxidized phospholipids (OxPLs) carried on lipoprotein(a) (Lp(a)) are proinflammatory, but their association with myocardial inflammation during the early post-MI period has not been described. Here we study patients enrolled in a randomized, double-blind trial of in-hospital PCSK9 inhibition versus placebo, in whom this treatment decreased myocardial inflammation after MI. We analyze plasma levels of OxPLs on apolipoprotein B-100 containing lipoproteins (OxPL-apoB), OxPLs on apolipoprotein(a) (OxPL-apo(a)), and Lp(a) during hospital admission and at 30 days, and paired [18F]-fluorodeoxyglucose positron emission tomography of myocardial inflammatory activity. Higher levels of OxPL-apoB, OxPL-apo(a) and Lp(a) at 30 days were associated with greater myocardial inflammatory activity; changes in Lp(a) and OxPL-apoB from baseline to 30 days were positively correlated with the change in myocardial [18F]-fluorodeoxyglucose uptake. These findings demonstrate that Lp(a) and OxPL are associated with persistent myocardial inflammation after an acute MI.