title: Increased apolipoprotein deposits in early atherosclerotic lesions distinguish symptomatic from asymptomatic patients.
abstract: OBJECTIVE
  Apolipoprotein E (apoE) and apolipoprotein B100 (apoB) are both involved in receptor-mediated uptake of atherogenic lipoproteins by the liver. Inefficient hepatic clearance of these lipoproteins leads to symptomatic atherosclerosis. Using arterial tissue microarrays, we tested the hypothesis that apoE and apoB accumulation in the arterial wall discriminates between patients with symptomatic atherosclerosis and patients who never experienced cardiovascular events.
  
  
  RESULTS
  In a postmortem study involving 49 patients (22 patients with symptomatic atherosclerosis), we quantified apolipoprotein deposits in arterial rings obtained from the left main coronary, the common carotid, the common iliac, and the renal artery applying tissue microarray technology and semiquantitative immunohistochemistry. In early atherosclerotic lesions, even before atheroma appeared, symptomatic patients had significantly more arterial apoE and apoB deposits than patients without cardiovascular events (P<0.001). Among the symptomatic patients, those without diabetes had more intense apolipoprotein deposits than diabetics. Large amounts of apoE and apoB were found in advanced atherosclerotic lesions, regardless of the activity of the disease.
  
  
  CONCLUSIONS
  Increased apolipoprotein deposits are an early sign of symptomatic atherosclerosis. They may reflect either enhanced retention of atherogenic lipoproteins or impaired local apolipoprotein degradation. The arterial lipoprotein turnover may be different in diabetic patients.
authors.affiliation: Department of Medicine, University Hospital Bruderholz, Bruderholz, Switzerland.
authors.forename: Moritz
authors.initials: M
authors.lastname: Wyler von Ballmoos
authors.forename: Denise
authors.initials: D
authors.lastname: Dubler
authors.forename: Martina
authors.initials: M
authors.lastname: Mirlacher
authors.forename: Gieri
authors.initials: G
authors.lastname: Cathomas
authors.forename: Jürgen
authors.initials: J
authors.lastname: Muser
authors.forename: Barbara C
authors.initials: BC
authors.lastname: Biedermann
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D053299:Apolipoprotein B-100; D001055:Apolipoproteins B / Q000378:metabolism*; D001057:Apolipoproteins E / Q000378:metabolism*; D050197:Atherosclerosis / Q000378:metabolism* / Q000473:pathology*; D015415:Biomarkers / Q000378:metabolism; D017536:Carotid Artery, Common / Q000378:metabolism / Q000473:pathology; D003331:Coronary Vessels / Q000378:metabolism / Q000473:pathology; D018450:Disease Progression; D005260:Female; D006801:Humans; D007083:Iliac Artery / Q000378:metabolism / Q000473:pathology; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D015588:Observer Variation; D012077:Renal Artery / Q000378:metabolism / Q000473:pathology; D012720:Severity of Illness Index; D013194:Staining and Labeling
chemical_list: D053299:Apolipoprotein B-100; D001055:Apolipoproteins B; D001057:Apolipoproteins E; D015415:Biomarkers