Inflammation
Angioplasty acutely raises Lp(a) by 64% and oxidized phospholipids by 36%, a mechanistic study of 141 patients (Circulation 2004)
Original title: Percutaneous coronary intervention results in acute increases in oxidized phospholipids and lipoprotein(a): short-term and long-term immunologic responses to oxidized low-density lipoprotein
This study measured oxidized LDL (via antibody E06), Lp(a), and related immune markers before and after percutaneous coronary intervention (PCI) in 141 patients with stable angina, sampled serially from before PCI through 6 months. OxLDL-E06 and Lp(a) significantly increased immediately after PCI, by 36% (P<0.0001) and 64% (P<0.0001) respectively, returning to baseline by 6 hours; nearly all E06-detected oxidized phospholipids were bound to Lp(a) at all time points except immediately post-PCI, and OxLDL-E06 and Lp(a) were strongly correlated (r=0.68, P<0.0001). Autoantibodies to oxidized LDL decreased while apoB immune complexes increased after PCI, both returning to baseline by 6 hours, while IgM autoantibodies peaked at 1 month and IgG autoantibodies rose steadily over 6 months. The findings show PCI acutely raises Lp(a) and oxidized phospholipids, with oxidized phospholipids transferring to Lp(a), suggesting Lp(a) may play a protective innate immune role acutely, while chronically elevated Lp(a) may instead be atherogenic as a carrier of pro-inflammatory oxidation products.
Original abstract
Background: This study was performed to assess whether oxidized low-density lipoprotein (OxLDL) levels are elevated after percutaneous coronary intervention (PCI).
Methods And Results: Patients (n=141) with stable angina pectoris undergoing PCI had serial venous blood samples drawn before PCI, after PCI, and at 6 and 24 hours, 3 days, 1 week, and 1, 3, and 6 months. Plasma levels of OxLDL-E06, a measure of oxidized phospholipid (OxPL) content on apolipoprotein B-100 detected by antibody E06, lipoprotein(a) [Lp(a)], autoantibodies to malondialdehyde (MDA)-LDL and copper-oxidized LDL (Cu-OxLDL), and apolipoprotein B-100-immune complexes (apoB-IC) were measured. OxLDL-E06 and Lp(a) levels significantly increased immediately after PCI by 36% (P<0.0001) and 64% (P<0.0001), respectively, and returned to baseline by 6 hours. In vitro immunoprecipitation of Lp(a) from selected plasma samples showed that almost all of the OxPL detected by E06 was bound to Lp(a) at all time points, except in the post-PCI sample, suggesting independent release and subsequent reassociation of OxPL with Lp(a) by 6 hours. Strong correlations were noted between OxLDL-E06 and Lp(a) (r=0.68, P<0.0001). MDA-LDL and Cu-OxLDL autoantibodies decreased, whereas apoB-IC levels increased after PCI, but both returned to baseline by 6 hours. Subsequently, IgM autoantibodies increased and peaked at 1 month and then returned to baseline, whereas IgG autoantibodies increased steadily over 6 months.
Conclusions: PCI results in acute plasma increases of Lp(a) and OxPL and results in short-term and long-term immunologic responses to OxLDL. OxPL that are released or generated during PCI are transferred to Lp(a), suggesting that Lp(a) may contribute acutely to a protective innate immune response. In settings of enhanced oxidative stress and chronically elevated Lp(a) levels, the atherogenicity of Lp(a) may stem from its capacity as a carrier of proinflammatory oxidation byproducts.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.