title: Hypercholesterolemia and hypoadiponectinemia are associated with necrotic core-rich coronary plaque.
abstract: BACKGROUND
  Hypercholesterolemia is a risk factor for coronary artery disease and closely linked to unstable plaque. Hypoadiponectinemia is frequently observed in patients with metabolic syndrome complicated with macroangiopathy and predicts poor clinical outcome. Spectral analysis of intravascular ultrasonography radiofrequency (IVUS-Virtual Histology [VH]) allows quantitative analysis of plaque composition. The purpose of this study was to verify the effects of low-density lipoprotein (LDL) cholesterol level on plaque morphology, and test the hypothesis that adiponectin influences coronary plaque volume and composition.
  
  
  METHODS
  Preintervention IVUS-VH using a continuous pullback was performed in 92 coronary vessels in 92 patients with coronary artery disease. The morphological distribution of plaque was evaluated prospectively in a 60-mm segment of coronary vessels containing the culprit lesion.
  
  
  RESULTS
  Serum LDL cholesterol levels correlated positively with necrotic core volume (r = 0.217, P = 0.037) and percent necrotic core tissue (r = 0.308, P = 0.003), while plasma adiponectin levels correlated negatively with plaque volume (r = -0.297, P = 0.004) and necrotic core volume (r = -0.306, P = 0.003). Multiple regression analyses showed close association between necrotic core volume and statin-use (β = -21.68, P = 0.004) and adiponectin levels (β = -31.25, P = 0.038), and that percent necrotic core tissue was influenced by statin-use (β = -4.595, P = 0.026) and LDL cholesterol levels (β = 0.092, P = 0.031).
  
  
  CONCLUSIONS
  Adiponectin is closely linked to coronary plaque volume. Hypercholesterolemia and hypoadiponectinemia correlate with necrotic core lesions and may contribute to increased risk of coronary plaque vulnerability. Statins can affectively prevent necrotic core plaque formation associated with hypercholesterolemia and hypoadiponectinemia.
authors.affiliation: Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan. kojimas@kumamoto-u.ac.jp
authors.forename: Shinobu
authors.initials: S
authors.lastname: Kojima
authors.forename: Sunao
authors.initials: S
authors.lastname: Kojima
authors.forename: Hidetomo
authors.initials: H
authors.lastname: Maruyoshi
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Nagayoshi
authors.forename: Koichi
authors.initials: K
authors.lastname: Kaikita
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Sumida
authors.forename: Seigo
authors.initials: S
authors.lastname: Sugiyama
authors.forename: Tohru
authors.initials: T
authors.lastname: Funahashi
authors.forename: Hisao
authors.initials: H
authors.lastname: Ogawa
mesh_terms: D052242:Adiponectin / Q000097:blood* / Q000172:deficiency*; D000368:Aged; D015415:Biomarkers / Q000097:blood; D003324:Coronary Artery Disease / Q000097:blood* / Q000473:pathology*; D005260:Female; D006801:Humans; D006937:Hypercholesterolemia / Q000097:blood* / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D009336:Necrosis; D058226:Plaque, Atherosclerotic / Q000097:blood* / Q000473:pathology*; D011446:Prospective Studies
chemical_list: D052242:Adiponectin; D015415:Biomarkers