title: Structural basis of regional dysfunction in acutely ischemic myocardium.
abstract: OBJECTIVE
  Impaired systolic function in the normally perfused myocardium adjacent to an ischemic region - the functional border zone - is thought to result from mechanical interactions across the perfusion boundary. We investigated how segment orientation and vessel involved affect regional strains in the functional border zone and whether altered stresses associated with a step transition in contractility can explain the functional border zone.
  
  
  RESULTS
  Regional epicardial strain distributions were obtained from measured displacements of radiopaque markers in open-chest anesthetized canines, and related to local myofiber angles and blood flows. The functional border zone for fiber strain was significantly narrower than that for cross-fiber strain and significantly wider for left anterior descending (LAD) than left circumflex (LCx) coronary occlusion (1.23 vs. 0.45 cm). A detailed three-dimensional computational model with a one-to-one relation between perfusion and myofilament activation and no transitional zone of intermediate contractility showed close agreement with these observations and significantly elevated stresses in the border zone. Differences between LAD and LCx occlusions in the model were due to differences in left ventricular systolic pressure and not to differences in perfusion boundary or muscle fiber orientation. The border zone was narrower for fiber strain than cross-fiber strain because systolic stiffness is greatest along the muscle fiber direction.
  
  
  CONCLUSIONS
  Abnormal regional mechanics in the acute ischemic border arise from increased wall stresses without a transitional zone of intermediate contractility. Perfusion is more tightly coupled to fiber than cross-fiber strain, and a wider functional border zone of fiber strain during LAD than LCx occlusion is primarily due to higher regional wall stresses rather than anatomic variations.
authors.affiliation: Department of Bioengineering, The Whitaker Institute for Biomedical Engineering, University of California San Diego, 92093-0412, USA.
authors.forename: R
authors.initials: R
authors.lastname: Mazhari
authors.forename: J H
authors.initials: JH
authors.lastname: Omens
authors.forename: J W
authors.initials: JW
authors.lastname: Covell
authors.forename: A D
authors.initials: AD
authors.lastname: McCulloch
mesh_terms: D008841:Actin Cytoskeleton / Q000473:pathology; D000818:Animals; D003198:Computer Simulation; D004285:Dogs; D005260:Female; D006439:Hemodynamics; D008297:Male; D008955:Models, Cardiovascular; D017202:Myocardial Ischemia / Q000097:blood / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D012039:Regional Blood Flow; D012044:Regression Analysis; D013314:Stress, Mechanical; D013599:Systole; D016277:Ventricular Function, Left