title: Transmural distribution of three-dimensional systolic strains in stunned myocardium.
abstract: BACKGROUND
  Regional function in stunned myocardium is usually thought to be more depressed in the endocardium than the epicardium. This has been attributed to the greater loss of blood flow at the endocardium during ischemia.
  
  
  RESULTS
  We measured transmural distributions of 3D systolic strains relative to local myofiber axes in open-chest anesthetized dogs before 15 minutes of left anterior descending coronary artery occlusion and during 2 hours of reperfusion. During ischemia, regional myocardial blood flow was reduced 84% at the endocardium and 32% at the epicardium (P<0.005, n=7), but changes in end-systolic fiber length from baseline were transmurally uniform. Relative to baseline, radial segments in stunned tissue were significantly thinner at the endocardium than the epicardium at end systole (24+/-5% versus 16+/-3%; P<0.05, n=8), consistent with previous reports. Unlike radial and cross-fiber segments, however, the increase of end-systolic fiber lengths in stunned myocardium had no significant transmural gradient (23+/-8% epicardium versus 21+/-4% endocardium). We also observed significant 3D diastolic dysfunction in the ischemic-reperfused region transmurally.
  
  
  CONCLUSIONS
  Myocardial ischemia/reperfusion in the dog results in a significant transmural gradient of dysfunction between epicardial and endocardial layers in radial and cross-fiber segments, but not for fiber segments, despite a gradient in blood flow reduction during ischemia. Perhaps systolic fiber dysfunction rather than the degree of perfusion deficit during the preceding ischemic period may be the main determinant of myocardial dysfunction during reperfusion.
authors.affiliation: Department of Bioengineering, The Whitaker Institute for Biomedical Engineering, University of California San Diego, La Jolla, California, USA.
authors.forename: R
authors.initials: R
authors.lastname: Mazhari
authors.forename: J H
authors.initials: JH
authors.lastname: Omens
authors.forename: R S
authors.initials: RS
authors.lastname: Pavelec
authors.forename: J W
authors.initials: JW
authors.lastname: Covell
authors.forename: A D
authors.initials: AD
authors.lastname: McCulloch
mesh_terms: D000818:Animals; D001783:Blood Flow Velocity; D002316:Cardiotonic Agents / Q000494:pharmacology; D003326:Coronary Circulation; D003327:Coronary Disease / Q000503:physiopathology; D003971:Diastole; D004195:Disease Models, Animal; D004280:Dobutamine / Q000494:pharmacology; D004285:Dogs; D004699:Endocardium / Q000187:drug effects / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects; D009200:Myocardial Contraction / Q000187:drug effects; D015425:Myocardial Reperfusion; D017682:Myocardial Stunning / Q000503:physiopathology*; D009210:Myofibrils / Q000187:drug effects / Q000473:pathology; D010496:Pericardium / Q000187:drug effects / Q000503:physiopathology; D013314:Stress, Mechanical; D013599:Systole; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D002316:Cardiotonic Agents; D004280:Dobutamine