title: Glycation of apoprotein A-I is associated with coronary artery plaque progression in type 2 diabetic patients.
abstract: OBJECTIVE
  To investigate whether glycation level of apoprotein (apo)A-I is associated with coronary artery disease (CAD) and plaque progression in patients with type 2 diabetes.
  
  
  METHODS
  Among 375 consecutive type 2 diabetic patients undergoing quantitative coronary angiography (QCA) and intravascular ultrasound (IVUS), 82 patients with nonsignificant stenosis (luminal diameter narrowing <30% [group I]) and 190 patients with significant CAD (luminal diameter stenosis ≥70% [group II]) were included for analysis of apoA-I glycation level and serum activity of lecithin: cholesterol acyltransferase (LCAT). The control group had 136 healthy subjects. At the 1-year follow-up, angiography and IVUS were repeated mainly in group II patients for plaque progression assessment.
  
  
  RESULTS
  Relative intensity of apoA-I glycation by densitometry was increased, and serum LCAT activity was decreased stepwise across groups control, I, and II. These two measurements were associated with the number of diseased coronary arteries and extent index in group II. During 1-year follow-up, QCA detected 45 patients with plaque progression in 159 subjects, and IVUS found 38 patients with plaque progression in 127 subjects. Baseline relative intensity of apoA-I glycation was significantly increased in patients with plaque progression compared with those without, with values associated with changes in QCA and IVUS measurements. Multivariable regression analysis revealed that baseline relative intensity of apoA-I glycation was an independent determinant of CAD and plaque progression in type 2 diabetic patients.
  
  
  CONCLUSIONS
  ApoA-I glycation level is associated with the severity of CAD and coronary artery plaque progression in type 2 diabetic patients.
authors.affiliation: Department of Cardiology, Shanghai Rui Jin Hospital, Shanghai, People’s Republic of China.
authors.forename: Li Jin
authors.initials: LJ
authors.lastname: Pu
authors.forename: Lin
authors.initials: L
authors.lastname: Lu
authors.forename: Rui Yan
authors.initials: RY
authors.lastname: Zhang
authors.forename: Run
authors.initials: R
authors.lastname: Du
authors.forename: Ying
authors.initials: Y
authors.lastname: Shen
authors.forename: Qi
authors.initials: Q
authors.lastname: Zhang
authors.forename: Zheng Kun
authors.initials: ZK
authors.lastname: Yang
authors.forename: Qiu Jing
authors.initials: QJ
authors.lastname: Chen
authors.forename: Wei Feng
authors.initials: WF
authors.lastname: Shen
mesh_terms: D016632:Apolipoprotein A-I / Q000378:metabolism*; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000378:metabolism*; D003331:Coronary Vessels / Q000378:metabolism* / Q000473:pathology*; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism* / Q000473:pathology*; D005260:Female; D006031:Glycosylation; D006801:Humans; D008297:Male; D058226:Plaque, Atherosclerotic / Q000378:metabolism*
chemical_list: D016632:Apolipoprotein A-I