title: Impact of coronary plaque composition on cardiac troponin elevation after percutaneous coronary intervention in stable angina pectoris: a computed tomography analysis.
abstract: OBJECTIVE
  The authors used multidetector computed tomography (MDCT) to study the relation between culprit plaque characteristics and cardiac troponin T (cTnT) elevation after percutaneous coronary intervention (PCI).
  
  
  BACKGROUND
  Percutaneous coronary intervention is often complicated by post-procedural myocardial necrosis manifested by elevated cardiac biomarkers.
  
  
  METHODS
  Stable angina patients (n = 107) with normal pre-PCI cTnT levels underwent 64-slice MDCT before PCI to evaluate plaque characteristics of culprit lesions. Patients were divided into 2 groups according to presence (group I, n = 36) or absence (group II, n = 71) of post-PCI cTnT elevation ≥3 times the upper limit of normal (0.010 ng/ml) at 24 h after PCI.
  
  
  RESULTS
  Computed tomography attenuation values were significantly lower in group I than in group II (43.0 [26.5 to 75.7] HU vs. 94.0 [65.0 to 109.0] HU, p < 0.001). Remodeling index was significantly greater in group I than in group II (1.20 ± 0.18 vs. 1.04 ± 0.15, p < 0.001). Spotty calcification was observed significantly more frequently in group I than in group II (50% vs. 11%, p < 0.001). Multivariate analysis showed presence of positive remodeling (remodeling index >1.05; odds ratio: 4.54; 95% confidence interval: 1.36 to 15.9; p = 0.014) and spotty calcification (odds ratio: 4.27; 95% confidence interval: 1.30 to 14.8; p = 0.016) were statistically significant independent predictors for cTnT elevation. For prediction of cTnT elevation, the presence of all 3 variables (CT attenuation value <55 HU; remodeling index >1.05, and spotty calcification) showed a high positive predictive value of 94%, and their absence showed a high negative predictive value of 90%.
  
  
  CONCLUSIONS
  MDCT may be useful in detecting which lesions are at high risk for myocardial necrosis after PCI.
authors.affiliation: Cardiovascular Division, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Watabe
authors.forename: Akira
authors.initials: A
authors.lastname: Sato
authors.forename: Daiki
authors.initials: D
authors.lastname: Akiyama
authors.forename: Yuki
authors.initials: Y
authors.lastname: Kakefuda
authors.forename: Toru
authors.initials: T
authors.lastname: Adachi
authors.forename: Eiji
authors.initials: E
authors.lastname: Ojima
authors.forename: Tomoya
authors.initials: T
authors.lastname: Hoshi
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Murakoshi
authors.forename: Tomoko
authors.initials: T
authors.lastname: Ishizu
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Seo
authors.forename: Kazutaka
authors.initials: K
authors.lastname: Aonuma
mesh_terms: D000368:Aged; D060050:Angina, Stable / Q000097:blood* / Q000601:surgery*; D015906:Angioplasty, Balloon, Coronary; D003324:Coronary Artery Disease / Q000097:blood* / Q000601:surgery*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D058226:Plaque, Atherosclerotic / Q000097:blood* / Q000000981:diagnostic imaging*; D014057:Tomography, X-Ray Computed; D020107:Troponin T / Q000097:blood*
chemical_list: D020107:Troponin T