title: Relationships of elevated systemic pentraxin-3 levels with high-risk coronary plaque components and impaired myocardial perfusion after percutaneous coronary intervention in patients with ST-elevation acute myocardial infarction.
abstract: BACKGROUND
  We aimed to assess the relationships of pentraxin-3 (PTX3) with coronary plaque components and myocardial perfusion after percutaneous coronary intervention (PCI) in order to clarify the mechanisms underlying the prognostic function of PTX3 in ST-elevation acute myocardial infarction (STEMI) patients.
  
  
  RESULTS
  We enrolled 75 STEMI patients who underwent pre-PCI virtual histology (VH)-intravascular ultrasound. Relationships of the systemic pre-PCI PTX3 level with coronary plaque components and post-PCI myocardial blush grade (MBG) were evaluated. Lesions with elevated pre-PCI PTX3 (median ≥3.79ng/ml) had higher frequencies of VH-derived thin-cap fibroatheroma (65.8% vs. 24.3%, P<0.0001), plaque rupture (63.2% vs. 24.3%, P=0.001), and post-PCI MBG (0-1) (65.8% vs. 40.5%, P=0.03) than those with PTX3 <3.79ng/ml. In multivariate analysis, pre-PCI PTX3 level was independently related to post-PCI MBG (0-1) (odds ratio, 11.385; 95% confidence interval (CI), 1.346-96.289; P=0.026). At 9-month follow-up, cardiac event-free survival was poorer for patients with post-PCI MBG (0-1) (log-rank test χ(2)=8.6; P=0.003). Cox proportional-hazards analysis showed post-PCI MBG (0-1) (hazard ratio, 4.109; 95% CI, 1.372-12.309; P=0.012) and Killip class >2 on admission (hazard ratio, 5.356; 95% CI, 1.409-20.359; P=0.014) as independent predictors of adverse cardiac events during follow-up.
  
  
  CONCLUSIONS
  Systemic pre-PCI PTX3 was associated with high-risk plaque components and impaired post-PCI myocardial perfusion. Thus, PTX3 may be a reliable predictor of outcome in STEMI patients.
authors.affiliation: Cardiovascular Center, Yokosuka Kyosai Hospital.
authors.forename: Shigeki
authors.initials: S
authors.lastname: Kimura
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Inagaki
authors.forename: Go
authors.initials: G
authors.lastname: Haraguchi
authors.forename: Tomoyo
authors.initials: T
authors.lastname: Sugiyama
authors.forename: Toru
authors.initials: T
authors.lastname: Miyazaki
authors.forename: Yu
authors.initials: Y
authors.lastname: Hatano
authors.forename: Shunji
authors.initials: S
authors.lastname: Yoshikawa
authors.forename: Takashi
authors.initials: T
authors.lastname: Ashikaga
authors.forename: Mitsuaki
authors.initials: M
authors.lastname: Isobe
mesh_terms: D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism*; D003324:Coronary Artery Disease / Q000097:blood / Q000401:mortality / Q000601:surgery; D018572:Disease-Free Survival; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000401:mortality / Q000601:surgery; D062645:Percutaneous Coronary Intervention; D010477:Perfusion; D058226:Plaque, Atherosclerotic / Q000097:blood / Q000401:mortality / Q000601:surgery; D000683:Serum Amyloid P-Component / Q000378:metabolism*; D015996:Survival Rate; D000099153:Pentraxins
chemical_list: D002097:C-Reactive Protein; D000683:Serum Amyloid P-Component; D000099153:Pentraxins