title: Impact of atherosclerotic plaque composition on coronary microembolization during percutaneous coronary interventions.
abstract: BACKGROUND
  Cardiac marker release after percutaneous coronary interventions (PCI) reflects myocardial necrosis which is usually the result of periprocedural (micro)embolization of atherothrombotic debris and associated with impaired left ventricular function and adverse outcome.
  
  
  METHODS
  In this prospective study, we examined 55 patients treated by direct stenting of single de-novo lesions to assess the relationship between plaque composition, as determined by preinterventional intravascular ultrasound (IVUS) with radiofrequency data (IVUS-RF) analysis (so-called Virtual Histology) versus coronary microembolization, as determined by serial measurement of cardiac markers. IVUS was performed with an electronic system and 20-MHz IVUS catheters. Serum creatine kinase (CK) and cardiac troponin I (CTnI) were determined before PCI and after 6, 12, and 24 hours.
  
  
  RESULTS
  Plaques had a volume of 99 +/- 63 mm(3) and were composed of fibrous (61 +/- 9%) and fibro-fatty tissue (27 +/- 12%), dense calcium (4 +/- 3%), and necrotic core (NC) (8 +/- 6%). NC volume per se, volume per 10 mm of segment length, and volume % were correlated (r = 0.64, 0.66, and 0.52 respectively; all P < 0.01) with the maximum increase in cardiac markers (CK 55.4 +/- 55.7 U/l; CTnI 0.49 +/- 0.68 ng/ml). Patients in the 4th quartile of NC volume (>10.8 mm(3)) had a particularly high increase in markers (P < 0.001). In contrast, total plaque volume and plaque components other than NC had no relation with cardiac markers (ns).
  
  
  CONCLUSIONS
  Patients with large NC in culprit lesions may experience more myocardial injury from peri-interventional microembolization. IVUS-RF assessment before PCI has the potential to identify lesions at particular high risk which may help to tailor PCI.
authors.affiliation: Dept. of Cardiology, West German Heart Center, University of Duisburg-Essen, Hufelandstrasse 55, 45122, Essen, Germany. dirk.boese@uk-essen.de
authors.forename: Dirk
authors.initials: D
authors.lastname: Böse
authors.forename: Clemens
authors.initials: C
authors.lastname: von Birgelen
authors.forename: Xiu Ying
authors.initials: XY
authors.lastname: Zhou
authors.forename: Axel
authors.initials: A
authors.lastname: Schmermund
authors.forename: Sebastian
authors.initials: S
authors.lastname: Philipp
authors.forename: Stefan
authors.initials: S
authors.lastname: Sack
authors.forename: Thomas
authors.initials: T
authors.lastname: Konorza
authors.forename: Stefan
authors.initials: S
authors.lastname: Möhlenkamp
authors.forename: Kirsten
authors.initials: K
authors.lastname: Leineweber
authors.forename: Petra
authors.initials: P
authors.lastname: Kleinbongard
authors.forename: William
authors.initials: W
authors.lastname: Wijns
authors.forename: Gerd
authors.initials: G
authors.lastname: Heusch
authors.forename: Raimund
authors.initials: R
authors.lastname: Erbel
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000379:methods*; D003324:Coronary Artery Disease / Q000097:blood / Q000000981:diagnostic imaging / Q000473:pathology*; D054059:Coronary Occlusion / Q000097:blood / Q000000981:diagnostic imaging / Q000473:pathology*; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000473:pathology*; D003402:Creatine Kinase / Q000097:blood; D004617:Embolism / Q000097:blood / Q000000981:diagnostic imaging / Q000473:pathology*; D005260:Female; D006801:Humans; D015994:Incidence; D008297:Male; D008875:Middle Aged; D009336:Necrosis / Q000097:blood / Q000000981:diagnostic imaging / Q000473:pathology; D011446:Prospective Studies; D012720:Severity of Illness Index; D015607:Stents; D019210:Troponin I / Q000097:blood; D018084:Ultrasonography, Interventional
chemical_list: D019210:Troponin I; D003402:Creatine Kinase