title: Visualization of risk-area myocardium as a high-intensity, hyperenhanced "hot spot" by myocardial contrast echocardiography following coronary reperfusion: quantitative analysis.
abstract: OBJECTIVE
  We examined whether delayed post-injection imaging of a new ultrasound contrast agent (BR-14) could produce prolonged opacification and hyperenhancement of myocardium subjected to coronary occlusion/reperfusion.
  
  
  BACKGROUND
  We hypothesized that ultrasound exposure destroyed BR-14 and eliminated visualization of sustained myocardial opacification from retained microbubbles.
  
  
  METHODS
  We studied eight open-chest dogs with 3 h of left anterior descending coronary artery (LAD) occlusion followed by 3 h of reperfusion. Myocardial contrast echocardiography (MCE) was performed before occlusion and 120 min after the onset of both occlusion and reperfusion. Ultrasound imaging was initiated 15 min after injection. Myocardial blood flow (MBF) was assessed by microspheres.
  
  
  RESULTS
  Pre-occlusion images revealed uniform opacification of left ventricular myocardium greater than that of the cavity, with a mean intensity of the LAD bed of 8.66 +/- 1.38 dB. During occlusion, MCE resulted in the appearance of a perfusion defect in the LAD risk area (intensity 2.08 +/- 1.10 dB). After 120 min of reperfusion, the LAD risk-area myocardium manifested dense opacification of a higher intensity ("hot spot") than baseline (13.7 vs. 8.7 dB), but with reduced MBF consistent with accumulation of a high concentration of microbubbles. Increased MCE intensity was associated with a greater myeloperoxidase score.
  
  
  CONCLUSIONS
  These data establish that contrast opacification by BR-14 may be selectively retained within the perfusion bed of a coronary artery subjected to occlusion/reperfusion. Such opacification exhibits defects with occlusion, manifests hyperenhanced intensity (hot spot) with reperfusion, is associated with the level of myeloperoxidase activity, and conforms to the area of myocardium subjected to altered flow.
authors.affiliation: Division of Cardiology, University of California at San Diego, 92103-8411, USA. ademaria@ucsd.edu
authors.forename: Hideki
authors.initials: H
authors.lastname: Kunichika
authors.forename: Barry
authors.initials: B
authors.lastname: Peters
authors.forename: Bruno
authors.initials: B
authors.lastname: Cotter
authors.forename: Hisashi
authors.initials: H
authors.lastname: Masugata
authors.forename: Naomi
authors.initials: N
authors.lastname: Kunichika
authors.forename: Paul L
authors.initials: PL
authors.lastname: Wolf
authors.forename: Anthony N
authors.initials: AN
authors.lastname: DeMaria
mesh_terms: D000818:Animals; D003287:Contrast Media / Q000008:administration & dosage; D003326:Coronary Circulation / Q000502:physiology*; D004285:Dogs; D004452:Echocardiography; D005466:Fluorocarbons / Q000008:administration & dosage; D007275:Injections, Intravenous; D017202:Myocardial Ischemia / Q000175:diagnosis / Q000000981:diagnostic imaging*; D015425:Myocardial Reperfusion; D010743:Phospholipids / Q000008:administration & dosage
chemical_list: C471302:BR14 contrast agent; D003287:Contrast Media; D005466:Fluorocarbons; D010743:Phospholipids