title: Intravascular ultrasound assessment of ulcerated ruptured plaques: a comparison of culprit and nonculprit lesions of patients with acute coronary syndromes and lesions in patients without acute coronary syndromes.
abstract: BACKGROUND
  It is not clear why some plaque ruptures lead to acute coronary syndromes (ACS) but others do not.
  
  
  RESULTS
  We analyzed 80 plaque ruptures in 74 patients and compared culprit lesions of ACS patients with nonculprit lesions of ACS patients and lesions of non-ACS patients; both culprit and nonculprit plaque ruptures were studied in 6 of 54 ACS patients. Intravascular ultrasound findings suggesting thrombus were observed more frequently in culprit lesions of ACS patients (n=35) compared with nonculprit lesions of ACS patients (n=19) and lesions of non-ACS patients (n=26): 60% versus 32% versus 8% (P<0.001). At the minimal lumen site, smaller lumen areas (3.3+/-1.5 versus 5.4+/-2.6 versus 6.1+/-2.0 mm2, P<0.001) and greater area stenosis (61+/-15% versus 50+/-14% versus 46+/-18%, P=0.002) and plaque burden (80+/-8% versus 71+/-8% versus 69+/-10%, P<0.001) were observed in culprit lesions of ACS patients compared with nonculprit lesions of ACS patients and lesions of non-ACS patients. Lesions were longer (18.7+/-6.4 versus 154.9+/-6.1 versus 12.0+/-4.9 mm, P<0.001) and rupture site remodeling indices were greater (1.26+/-0.21 versus 1.24+/-0.21 versus 1.09+/-0.05, P=0.002). Independent predictors of culprit plaque ruptures in ACS patients were smaller minimum lumen areas (P=0.02) and presence of thrombus (P=0.01).
  
  
  CONCLUSIONS
  Ruptured plaques in culprit lesions of ACS patients have smaller lumens; greater plaque burdens, area stenosis, and remodeling indices; and more thrombus. Plaque rupture itself does not lead to symptoms. The association of plaque rupture with a smaller lumen area and/or thrombus formation causes lumen compromise and leads to symptoms.
authors: Cardiovascular Research Foundation, Lenox Hill Heart and Vascular Institute, 130 East 77th St, 9th Floor, New York, NY 10021, USA.
authors: Kenichi
authors: K
authors: Fujii
authors: Yoshio
authors: Y
authors: Kobayashi
authors: Gary S
authors: GS
authors: Mintz
authors: Hideo
authors: H
authors: Takebayashi
authors: George
authors: G
authors: Dangas
authors: Issam
authors: I
authors: Moussa
authors: Roxana
authors: R
authors: Mehran
authors: Alexandra J
authors: AJ
authors: Lansky
authors: Edward
authors: E
authors: Kreps
authors: Michael
authors: M
authors: Collins
authors: Antonio
authors: A
authors: Colombo
authors: Gregg W
authors: GW
authors: Stone
authors: Martin B
authors: MB
authors: Leon
authors: Jeffrey W
authors: JW
authors: Moses
mesh_terms: D000208:Acute Disease; D001161:Arteriosclerosis / Q000145:classification / Q000150:complications / Q000000981:diagnostic imaging*; D003327:Coronary Disease / Q000000981:diagnostic imaging* / Q000209:etiology; D005260:Female; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D012422:Rupture, Spontaneous / Q000150:complications / Q000000981:diagnostic imaging; D013927:Thrombosis / Q000150:complications / Q000000981:diagnostic imaging*; D018084:Ultrasonography, Interventional; D014654:Vascular Patency