title: The role of oxidized phospholipids, lipoprotein (a) and biomarkers of oxidized lipoproteins in chronically occluded coronary arteries in sudden cardiac death and following successful percutaneous revascularization.
abstract: OBJECTIVE
  OxPL are pro-inflammatory and may mediate atherogenesis, thrombosis and endothelial dysfunction. We studied the histological presence and temporal increases in oxidized phospholipids on apolipoprotein B-100 particles (OxPL/apoB), lipoprotein (a) [Lp(a)] and biomarkers of oxidized lipoproteins in subjects with chronic total coronary occlusions (CTO) with sudden cardiac death (SCD) and following percutaneous coronary intervention (PCI).
  
  
  METHODS
  Eight subjects with SCD and CTO and 33 patients with successful PCI of CTO were included. Blood samples were drawn before PCI, immediately post-PCI, at 6 and 24 h, at 3 days and at 1 week. Plasma levels of OxPL/apoB, Lp(a), IgG and IgM autoantibodies to malondialdehyde (MDA) low-density lipoprotein and apoB-immune complexes were measured in all samples and compared with previous data from 141 patients undergoing PCI of non-CTO vessels.
  
  
  RESULTS
  Immunohistochemistry of coronary CTOs revealed OxPL and MDA-like epitopes, particularly in areas of recanalized and organized thrombus and neovascularization. Following PCI, OxPL/apoB and Lp(a) levels, expressed as percent change from baseline levels before PCI, rose gradually and progressively over the next 7 days. In contrast, levels of OxPL/apoB and Lp(a) in non-CTO vessels rose immediately post PCI and then dropped rapidly to baseline within 24 h.
  
  
  CONCLUSIONS
  CTOs contain immunohistological evidence of OxPL and MDA-like epitopes. Successful PCI of CTOs results in a slower increase in OxPL/apoB and Lp(a) but higher increase in IgM immune complexes compared to non-CTO vessels. Pro-inflammatory oxidation-specific epitopes may impact development of CTOs and affect outcomes following PCI that can be evaluated in larger clinical trials.
authors.affiliation: Schulich Heart Center, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada M4N 3M5.
authors.forename: Paul
authors.initials: P
authors.lastname: Fefer
authors.forename: Sotirios
authors.initials: S
authors.lastname: Tsimikas
authors.forename: Amit
authors.initials: A
authors.lastname: Segev
authors.forename: John
authors.initials: J
authors.lastname: Sparkes
authors.forename: Fumiyuki
authors.initials: F
authors.lastname: Otsuka
authors.forename: Fumiyuki
authors.initials: F
authors.lastname: Otsuma
authors.forename: Frank
authors.initials: F
authors.lastname: Kolodgie
authors.forename: Renu
authors.initials: R
authors.lastname: Virmani
authors.forename: Joseph
authors.initials: J
authors.lastname: Juliano
authors.forename: Thierry
authors.initials: T
authors.lastname: Charron
authors.forename: Bradley H
authors.initials: BH
authors.lastname: Strauss
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D053299:Apolipoprotein B-100 / Q000097:blood* / Q000276:immunology; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein; D003324:Coronary Artery Disease / Q000097:blood* / Q000401:mortality / Q000628:therapy; D016757:Death, Sudden, Cardiac / Q000209:etiology*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D017270:Lipoprotein(a) / Q000097:blood* / Q000276:immunology; D008077:Lipoproteins, LDL / Q000097:blood*; D008297:Male; D008315:Malondialdehyde / Q000031:analogs & derivatives* / Q000097:blood; D008875:Middle Aged; D010743:Phospholipids / Q000097:blood* / Q000276:immunology
chemical_list: D053299:Apolipoprotein B-100; D015415:Biomarkers; D017270:Lipoprotein(a); D008077:Lipoproteins, LDL; D010743:Phospholipids; C569869:malondialdehyde-low density lipoprotein, human; C099252:oxidized low density lipoprotein; D008315:Malondialdehyde; D002097:C-Reactive Protein