title: Comparison of tissue characteristics between acute coronary syndrome and stable angina pectoris. An integrated backscatter intravascular ultrasound analysis of culprit and non-culprit lesions.
abstract: BACKGROUND
  Patients with acute coronary syndrome (ACS) have multiple complex coronary plaques associated with plaque vulnerability. The present study assessed the tissue characteristics of coronary plaques between ACS and stable angina pectoris (SAP) of culprit and non-culprit lesions using integrated backscatter intravascular ultrasound (IB-IVUS).
  
  
  RESULTS
  IVUS was performed in 165 patients (40 patients with ACS) with 225 culprit (65 lesions in ACS) and 171 non-culprit lesions (42 lesions in ACS). The percentage of fibrous area (fibrous area/plaque area, %FIB) and the percentage of lipid area (lipid area/plaque area, %LIP) at the segment with minimal luminal area were calculated using IB-IVUS system. Culprit and non-culprit lesions with ACS showed a significant increase in %LIP (38±18 vs. 30±15%, P=0.002, and 38±21 vs. 32±17%, P=0.03, respectively) and a significant decrease in %FIB (59±15 vs. 63±12 %, P=0.04, and 57±18 vs. 62±14%, P=0.04, respectively) compared to those with SAP. On logistic regression analysis, not only culprit lesions but also non-culprit lesions with ACS patients were significantly associated with the lipid-rich plaque.
  
  
  CONCLUSIONS
  Non-culprit coronary lesions with ACS patients are associated with the lipid-rich plaque, suggesting the extensive development of plaques instability in these patients.
authors.affiliation: Department of Cardiology, Chubu-Rosai Hospital, Nagoya, Japan.
authors.forename: Hirohiko
authors.initials: H
authors.lastname: Ando
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Amano
authors.forename: Tatsuaki
authors.initials: T
authors.lastname: Matsubara
authors.forename: Tadayuki
authors.initials: T
authors.lastname: Uetani
authors.forename: Michio
authors.initials: M
authors.lastname: Nanki
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Marui
authors.forename: Masataka
authors.initials: M
authors.lastname: Kato
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Yoshida
authors.forename: Kiminobu
authors.initials: K
authors.lastname: Yokoi
authors.forename: Soichiro
authors.initials: S
authors.lastname: Kumagai
authors.forename: Satoshi
authors.initials: S
authors.lastname: Isobe
authors.forename: Hideki
authors.initials: H
authors.lastname: Ishii
authors.forename: Hideo
authors.initials: H
authors.lastname: Izawa
authors.forename: Toyoaki
authors.initials: T
authors.lastname: Murohara
mesh_terms: D054058:Acute Coronary Syndrome / Q000000981:diagnostic imaging* / Q000473:pathology / Q000628:therapy; D000368:Aged; D000787:Angina Pectoris / Q000000981:diagnostic imaging* / Q000473:pathology / Q000628:therapy; D000789:Angina, Unstable / Q000000981:diagnostic imaging* / Q000473:pathology / Q000628:therapy; D015906:Angioplasty, Balloon, Coronary; D002114:Calcinosis / Q000000981:diagnostic imaging / Q000473:pathology; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000473:pathology; D005260:Female; D005355:Fibrosis; D006801:Humans; D008055:Lipids / Q000032:analysis; D008297:Male; D008875:Middle Aged; D058226:Plaque, Atherosclerotic / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology; D012422:Rupture, Spontaneous; D016037:Single-Blind Method; D018084:Ultrasonography, Interventional / Q000379:methods*
chemical_list: D008055:Lipids