title: Deep echo attenuation without calcification increases the risk of periprocedural myonecrosis after elective percutaneous coronary intervention in patients with coronary artery disease.
abstract: OBJECTIVE
  To investigate the clinical factors, including intravascular ultrasound (IVUS) findings, associated with percutaneous coronary intervention (PCI)-related periprocedural myonecrosis (PM) in patients with stable coronary artery disease (CAD).
  
  
  METHODS
  The study included 46 patients (mean age 65±2 y, 37 men) with stable CAD who underwent elective PCI using IVUS and a Doppler flow guidewire. In addition to routine IVUS measurements, the presence of deep echo attenuation (DEA) without calcification was assessed. The sum of all high-intensity transient signals (HITS) after a balloon deflation procedure was calculated using a Doppler flow guidewire. PM was defined as an elevation in troponin T to >0.03 ng/mL 24-hour after PCI. Patients were divided into 2 groups on the basis of the presence or absence of PM.
  
  
  RESULTS
  PM was identified in 17 patients (37%). Estimated glomerular filtration ratio was lower in the PM group (p=0.021). Target vessel distribution was different between the groups (p=0.004). Positive remodeling and DEA, as observed on IVUS, were more common in the PM group (p=0.03 and p<0.0001, respectively). The total number of HITS was higher in the PM group (p=0.003). Logistic regression analysis demonstrated that the presence of DEA (p=0.003) was the sole factor associated with the occurrence of PM.
  
  
  CONCLUSIONS
  These results demonstrated that DEA is an important factor associated with PM in patients who underwent an elective PCI. Therefore, IVUS to determine the presence of DEA should be performed before PCI.
authors.affiliation: Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical Sciences, Japan.
authors.forename: Naoya
authors.initials: N
authors.lastname: Mitsuba
authors.forename: Hiroki
authors.initials: H
authors.lastname: Teragawa
authors.forename: Takaki
authors.initials: T
authors.lastname: Hata
authors.forename: Kenji
authors.initials: K
authors.lastname: Nishioka
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Fujii
authors.forename: Shinsuke
authors.initials: S
authors.lastname: Mikami
authors.forename: Noritaka
authors.initials: N
authors.lastname: Fujimura
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Maruhashi
authors.forename: Satoshi
authors.initials: S
authors.lastname: Kurisu
authors.forename: Yasuki
authors.initials: Y
authors.lastname: Kihara
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D002114:Calcinosis / Q000000981:diagnostic imaging; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood / Q000000981:diagnostic imaging* / Q000473:pathology / Q000628:therapy*; D052279:Creatine Kinase, MB Form / Q000097:blood; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009336:Necrosis; D011379:Prognosis; D012307:Risk Factors; D020107:Troponin T / Q000097:blood; D018084:Ultrasonography, Interventional
chemical_list: D015415:Biomarkers; D020107:Troponin T; D002097:C-Reactive Protein; D052279:Creatine Kinase, MB Form