title: Enhanced Impact of Cholesterol Absorption Marker on New Atherosclerotic Lesion Progression After Coronary Intervention During Statin Therapy.
abstract: OBJECTIVE
  Clinical trials suggest that residual risks remain for coronary artery disease (CAD) during low-density lipoprotein cholesterol (LDL-C) lowering therapy. We aimed to investigate the role of exogenous lipids in the prognosis of CAD after percutaneous coronary intervention (PCI).
  
  
  METHODS
  A total of 145 patients with CAD, who underwent elective PCI, and 82 non-CAD (control) patients were enrolled in this study. CAD patients underwent follow-up coronary angiography 6-9 months after PCI, and were classified into three groups: 1) patients who showed in-stent restenosis (ISR) in the original stented segment, 2) patients with other non-target coronary atherosclerotic lesions (de novo), and 3) patients with neither ISR nor a de novo lesion. Biochemical analyses were performed on fasting serum samples at the time of follow-up coronary angiography.
  
  
  RESULTS
  Despite the controlled serum LDL-C levels, CAD patients with statin showed elevated cholesterol absorption marker campesterol/total cholesterol (TC), synthesis marker lathosterol/TC, campesterol/lathosterol ratio, and apolipoprotein B48 (apoB48) concentration compared with non-CAD patients. The high campesterol/TC, campesterol/lathosterol ratio, and apoB48 concentration were associated with de novo lesion progression after PCI. In stepwise multivariate logistic regression analysis, campesterol/TC and apoB48 concentrations were independent risk factors for de novo lesion progression in statin-treated CAD patients after PCI.
  
  
  CONCLUSIONS
  The increase of cholesterol absorption marker and apoB48 concentration may lead to the progression of de novo lesions, and these markers may represent a residual risk during statin treatment after PCI.
authors.affiliation: Division of Cardiovascular Medicine, Kobe University Graduate School of Medicine.
authors.forename: Kenta
authors.initials: K
authors.lastname: Mori
authors.forename: Tatsuro
authors.initials: T
authors.lastname: Ishida
authors.forename: Shigeyasu
authors.initials: S
authors.lastname: Tsuda
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Oshita
authors.forename: Masakazu
authors.initials: M
authors.lastname: Shinohara
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Hara
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Irino
authors.forename: Ryuji
authors.initials: R
authors.lastname: Toh
authors.forename: Ken-Ichi
authors.initials: KI
authors.lastname: Hirata
mesh_terms: D000368:Aged; D000924:Anticholesteremic Agents / Q000009:adverse effects*; D053283:Apolipoprotein B-48 / Q000378:metabolism*; D015415:Biomarkers / Q000378:metabolism; D016022:Case-Control Studies; D002784:Cholesterol / Q000378:metabolism*; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007408:Intestinal Absorption / Q000187:drug effects*; D008297:Male; D008875:Middle Aged; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects*; D011379:Prognosis; D012307:Risk Factors
chemical_list: D000924:Anticholesteremic Agents; D053283:Apolipoprotein B-48; D015415:Biomarkers; D002784:Cholesterol