title: Plasma pentraxin-3 levels are associated with coronary plaque vulnerability and are decreased by statin.
abstract: OBJECTIVE
  Pentraxin 3 (PTX3) is a novel candidate immunoinflammatory marker that has been reported to be associated with cardiometabolic risk factors and to predict adverse outcomes in patients with coronary artery disease. The purpose of this study was to investigate the association between the plasma levels of PTX3 and plaque vulnerability and the effect of the levels using statin in patients with coronary artery disease.
  
  
  METHODS
  We determined the associations among the plasma levels of PTX3 and coronary plaque vulnerability in nonculprit coronary lesions with stenosis as assessed by integrated backscatter intravascular ultrasound (study 1). One hundred and eighteen consecutive patients with stable angina who underwent a percutaneous coronary intervention were enrolled. We also enrolled 53 patients with stable angina, and they were treated either with (n=36) or without (n=17) atorvastatin (10 mg/day) (study 2).
  
  
  RESULTS
  In study 1, although there was no association between the plasma levels of PTX3 and plaque vulnerability in all patients, the level of PTX3 was positively correlated with the percentage of lipid volume and negatively correlated with the percentage of fibrous volume in patients without statin treatment. There were no associations between high-sensitivity C-reactive protein levels and percentage of lipid volume and fibrous volume. Moreover, in study 2, statin therapy for 6-8 months significantly decreased the level of PTX3 in addition to high-sensitivity C-reactive protein.
  
  
  CONCLUSIONS
  The plasma level of PTX3 may be a useful biomarker for predicting the tissue characteristics of coronary plaque using integrated backscatter intravascular ultrasound. Statin therapy may have a beneficial effect with regard to the reduction of PTX3 levels.
authors.affiliation: Department of Cardiology, Fukuoka University School of Medicine, Fukuoka, Japan.
authors.forename: Atsushi
authors.initials: A
authors.lastname: Iwata
authors.forename: Shin-Ichiro
authors.initials: S
authors.lastname: Miura
authors.forename: Tohru
authors.initials: T
authors.lastname: Tanaka
authors.forename: Amane
authors.initials: A
authors.lastname: Ike
authors.forename: Makoto
authors.initials: M
authors.lastname: Sugihara
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Nishikawa
authors.forename: Akira
authors.initials: A
authors.lastname: Kawamura
authors.forename: Keijiro
authors.initials: K
authors.lastname: Saku
mesh_terms: D000368:Aged; D060050:Angina, Stable / Q000097:blood / Q000188:drug therapy; D000069059:Atorvastatin; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy*; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D015536:Down-Regulation; D005260:Female; D005355:Fibrosis; D006442:Glycated Hemoglobin / Q000378:metabolism; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D007564:Japan; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D058226:Plaque, Atherosclerotic; D011237:Predictive Value of Tests; D011758:Pyrroles / Q000627:therapeutic use*; D000683:Serum Amyloid P-Component / Q000378:metabolism*; D013997:Time Factors; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional; D014527:Uric Acid / Q000097:blood; D000099153:Pentraxins
chemical_list: D000069059:Atorvastatin; D015415:Biomarkers; D002097:C-Reactive Protein; D006442:Glycated Hemoglobin; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D011758:Pyrroles; D000683:Serum Amyloid P-Component; D014527:Uric Acid; D000099153:Pentraxins; C517652:hemoglobin A1c protein, human