title: Detection and quantification of embolic particles during percutaneous coronary intervention to stable plaque: it correlates to coronary flow dynamics and myocardial damage.
abstract: OBJECTIVE
  We detected embolic particles liberated from plaque during percutaneous coronary intervention (PCI) as high-intensity transient signals (HITS) with a Doppler guidewire and studied their impact on coronary flow dynamics and the myocardium in patients with stable angina pectoris.
  
  
  BACKGROUND
  These embolic particles during PCI may cause myocardial injury. However, this was difficult to confirm because it was impossible to detect embolic particles.
  
  
  METHODS
  We performed balloon angioplasty followed by stenting in 31 patients while monitoring coronary flow velocity. After PCI, we measured average peak velocity at baseline and after infusion of adenosine 5'-triphosphate to calculate coronary flow velocity reserve (CFVR) and coronary resistance index (CRI). In patients with PCI to the left coronary artery (n = 21), we calculated relative CFVR as the ratio of CFVR in the target vessel to that in the reference vessel. We measured cardiac troponin T (cTnT) the day after PCI.
  
  
  RESULTS
  HITS were detected in 27 (87%) of 31 patients and the majority were observed after stenting. The total number of HITS was correlated with CRI (r = 0.36, P = 0.049) or relative CFVR (r = 0.65, P = 0.0036) but not with CFVR (r = 0.048, P = 0.82). Thirteen patients showed elevated cTnT (range, 0.05-0.31 ng/ml) and the total number of HITS was greater in those with elevated cTnT than in those without elevated cTnT (24 +/- 9 vs. 10 +/- 7, P = 0.0007).
  
  
  CONCLUSIONS
  Embolic particles are frequently observed during PCI to stable plaque and the majority are liberated after stenting. There appears to be a quantitative relationship between amounts of HITS and coronary microvessel dysfunction and minor myocardial injury.
authors.affiliation: Division of Cardiology, Sakurabashi Watanabe Hospital, 2-4-32 Umeda, Kita-ku, Osaka 530-0001, Japan.
authors.forename: Atsunori
authors.initials: A
authors.lastname: Okamura
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ito
authors.forename: Katsuomi
authors.initials: K
authors.lastname: Iwakura
authors.forename: Shigeo
authors.initials: S
authors.lastname: Kawano
authors.forename: Toshiya
authors.initials: T
authors.lastname: Kurotobi
authors.forename: Motoo
authors.initials: M
authors.lastname: Date
authors.forename: Koichi
authors.initials: K
authors.lastname: Inoue
authors.forename: Toshio
authors.initials: T
authors.lastname: Ogihara
authors.forename: Kenshi
authors.initials: K
authors.lastname: Fujii
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D015906:Angioplasty, Balloon, Coronary; D015415:Biomarkers / Q000097:blood; D001783:Blood Flow Velocity; D019917:Blood Vessel Prosthesis Implantation; D017023:Coronary Angiography; D003326:Coronary Circulation; D052279:Creatine Kinase, MB Form / Q000097:blood; D015150:Echocardiography, Doppler; D004617:Embolism / Q000150:complications / Q000175:diagnosis* / Q000000981:diagnostic imaging / Q000503:physiopathology*; D005260:Female; D006801:Humans; D007432:Intraoperative Period; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000628:therapy*; D011446:Prospective Studies; D012107:Research Design; D012815:Signal Processing, Computer-Assisted; D015607:Stents; D016896:Treatment Outcome; D020107:Troponin T / Q000097:blood; D014655:Vascular Resistance
chemical_list: D015415:Biomarkers; D020107:Troponin T; D052279:Creatine Kinase, MB Form