title: Intravascular ultrasound analysis of infarct-related and non-infarct-related arteries in patients who presented with an acute myocardial infarction.
abstract: BACKGROUND
  Previous studies have reported diffuse destabilization of atherosclerotic plaques in acute myocardial infarction (AMI).
  
  
  RESULTS
  We used intravascular ultrasound (IVUS) to assess 78 coronary arteries (38 infarct-related arteries [IRAs] with culprit and nonculprit lesions and 40 non-IRAs) from 38 consecutive AMI patients. IVUS analysis included qualitative and quantitative measurements of reference and lesion external elastic membrane (EEM), lumen, and plaque plus media (P&M) area. Positive remodeling was defined as lesion/mean reference EEM >1.0. Culprit lesions were identified by a combination of ECG, wall motion abnormalities (ventriculogram or echocardiogram), scintigraphic perfusion defects, and coronary angiogram. Culprit lesions contained more thrombus (23.7% versus 3.4% in nonculprit IRA plaques and 3.1% in non-IRA plaques; P=0.0011). Culprit lesions were predominantly hypoechoic (63.2% versus 37.9% of nonculprit IRA plaques and 28.1% of non-IRA plaques; P=0.0022). Culprit lesions were longer (17.5+/-10.1, 9.8+/-4.0, and 10.3+/-5.7 mm, respectively; P<0.0001), had larger EEM area (15.0+/-6.0, 11.5+/-5.7, and 12.6+/-5.6 mm2, respectively; P=0.0353) and P&M area (13.0+/-6.0, 7.5+/-3.7, 9.3+/-4.3 mm2, respectively; P<0.0001), smaller lumens (2.0+/-0.9, 4.1+/-3.1, and 3.4+/-2.5 mm2, respectively; P=0.0009), and more positive remodeling (79.4%, 59.0%, and 50.8%, respectively; P=0.0155). The frequency of plaque rupture/dissection was greater in culprit, nonculprit IRA, and non-IRA plaques in AMI patients than in a control group of chronic stable angina patients with multivessel IVUS imaging.
  
  
  CONCLUSIONS
  Culprit plaques have more markers of instability (thrombus, positive remodeling, and large plaque mass); however, these markers of instability are not typically found elsewhere. This suggests that the vascular event in AMI patients is determined by local pre-event lesion morphologies.
authors.affiliation: Cardiovascular Research Institute, Washington Hospital Center, 110 Irving St NW, Suite 4B-1, Washington, DC 20010, USA.
authors.forename: Jun-ichi
authors.initials: J
authors.lastname: Kotani
authors.forename: Gary S
authors.initials: GS
authors.lastname: Mintz
authors.forename: Marco T
authors.initials: MT
authors.lastname: Castagna
authors.forename: Ellen
authors.initials: E
authors.lastname: Pinnow
authors.forename: Chalak O
authors.initials: CO
authors.lastname: Berzingi
authors.forename: Anh B
authors.initials: AB
authors.lastname: Bui
authors.forename: Augusto D
authors.initials: AD
authors.lastname: Pichard
authors.forename: Lowell F
authors.initials: LF
authors.lastname: Satler
authors.forename: William O
authors.initials: WO
authors.lastname: Suddath
authors.forename: Ron
authors.initials: R
authors.lastname: Waksman
authors.forename: John R
authors.initials: JR
authors.lastname: Laird
authors.forename: Kenneth M
authors.initials: KM
authors.lastname: Kent
authors.forename: Neil J
authors.initials: NJ
authors.lastname: Weissman
mesh_terms: D000787:Angina Pectoris / Q000150:complications / Q000000981:diagnostic imaging; D001161:Arteriosclerosis / Q000145:classification* / Q000150:complications / Q000000981:diagnostic imaging*; D017023:Coronary Angiography; D003331:Coronary Vessels / Q000000981:diagnostic imaging*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000000981:diagnostic imaging* / Q000209:etiology / Q000628:therapy; D018084:Ultrasonography, Interventional