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.
BACKGROUND
This study was performed to assess whether oxidized low-density lipoprotein (OxLDL) levels are elevated after percutaneous coronary intervention (PCI).


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.
Tsimikas
Sotirios
S
Vascular Medicine Program, Department of Medicine, University of California San Diego, 9500 Gilman Drive, BSB 1080, La Jolla, CA 92093-0682, USA. stsimikas@ucsd.edu
Lau
Herbert K
HK
Han
Kyoo-Rok
KR
Shortal
Brian
B
Miller
Elizabeth R
ER
Segev
Amit
A
Curtiss
Linda K
LK
Witztum
Joseph L
JL
Strauss
Bradley H
BH
D000787:Angina Pectoris / Q000097:blood / Q000276:immunology / Q000601:surgery*; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D053299:Apolipoprotein B-100; D001055:Apolipoproteins B / Q000097:blood / Q000276:immunology; D001323:Autoantibodies / Q000097:blood* / Q000276:immunology; D001324:Autoantigens / Q000097:blood* / Q000276:immunology; D002404:Catheterization; D015331:Cohort Studies; D023903:Coronary Restenosis / Q000517:prevention & control / Q000601:surgery; D000939:Epitopes / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D007075:Immunoglobulin M / Q000097:blood; D017270:Lipoprotein(a) / Q000097:blood* / Q000276:immunology; D008077:Lipoproteins, LDL / Q000097:blood* / Q000276:immunology; D008315:Malondialdehyde / Q000276:immunology; D010084:Oxidation-Reduction; D010743:Phospholipids / Q000097:blood* / Q000276:immunology; D011446:Prospective Studies; D015607:Stents
D053299:Apolipoprotein B-100; D001055:Apolipoproteins B; D001323:Autoantibodies; D001324:Autoantigens; D000939:Epitopes; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D017270:Lipoprotein(a); D008077:Lipoproteins, LDL; D010743:Phospholipids; C099252:oxidized low density lipoprotein; D008315:Malondialdehyde