Author/Authors :
Amit Segev، نويسنده , , Bradley H. Strauss، نويسنده , , Joseph L. Witztum، نويسنده , , Herbert K. Lau، نويسنده , , Sotirios Tsimikas، نويسنده ,
Abstract :
Background
This study was performed to assess the relationship between oxidized low-density lipoprotein (OxLDL) and restenosis. OxLDL induces up-regulation of inflammatory genes and cytokines and recruits monocytes to the vessel wall. Elevated levels of monocytes post–percutaneous coronary intervention (PCI) are associated with in-stent restenosis.
Methods and Results
One hundred forty-one patients with stable angina pectoris had serial blood samples drawn before PCI (68% balloon only, 32% stent), immediately post-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 apoB-100 detected by antibody E06 (OxPL/apoB), autoantibodies to malondialdehyde-LDL and copper-oxidized LDL, and apoB-immune complexes were measured in all samples. Quantitative and qualitative coronary angiography was performed with 94% angiographic follow-up. Restenosis was defined as >50% diameter stenosis (%DS). The overall angiographic restenosis rate was 32% (39% in balloon group, 16% in stent group). OxPL/apoB levels rose significantly and OxLDL autoantibody titers decreased immediately post-PCI in patients both with and without restenosis, but there were no significant differences among groups. There was also no relationship of any OxLDL marker to lesion length, %DS, or minimal lumen diameter. No differences were noted in stent versus balloon-treated patients.
Conclusions
Serial measurement of a comprehensive panel of circulating OxLDL markers after uncomplicated PCI for stable angina does not predict restenosis.