title: Mechanical dysfunction in the border zone of an ovine model of left ventricular aneurysm.
abstract: BACKGROUND
  The pathophysiology of regional mechanical dysfunction in the border zone (BZ) region of left ventricular aneurysm was studied in an ovine model using magnetic resonance imaging tissue-tagging and regional deformation analysis.
  
  
  METHODS
  Transmural infarcts were created in adult Dorsett sheep (n = 8) by ligation of the distal homonymous coronary artery and were allowed to mature into left ventricular aneurysms for 8 to 12 weeks. Animals were imaged subsequently using double oblique magnetic resonance imaging with radiofrequency tissue tagging. Short axis slices were selected for analysis that included predominantly the septal component of the aneurysm as well as adjacent BZ regions in the anterior and posterior ventricular walls. Dark grid patterns of magnetic presaturations were placed on the myocardium and tracked as they deformed during the diastolic, isovolumic systolic, and systolic ejection phases of the cardiac cycle. Regional ventricular wall strains were calculated in BZ regions and regions remote from the aneurysm and compared with strains measured in corresponding regions from normal control sheep (n = 6).
  
  
  RESULTS
  Diastolic midwall circumferential strains (fiber extensions) were relatively preserved, but abnormal circumferential lengthening strains were observed in the BZ regions during isovolumic systole. Peak circumferential strains ranged from 0.04 to 0.07 in the BZ regions but averaged -0.05 in the normal hearts (p = 0.002 for the anterior BZ and p = 0.001 for the posterior BZ). Midwall end-systolic fiber strains were depressed in the anterior BZ (-0.03 to -0.09 for the BZ versus -0.11 for the normal heart, p < 0.0001) but not in the posterior BZ (p = 0.19).
  
  
  CONCLUSIONS
  Our data support the theory that the stretching of BZ fibers during isovolumic systole contributed to a reduction in fiber shortening during systolic ejection and thus reduced the overall contribution of these fibers to forward ventricular output.
authors.affiliation: Department of Surgery, Washington University, St. Louis, Missouri, USA.
authors.forename: M J
authors.initials: MJ
authors.lastname: Moulton
authors.forename: S W
authors.initials: SW
authors.lastname: Downing
authors.forename: L L
authors.initials: LL
authors.lastname: Creswell
authors.forename: D S
authors.initials: DS
authors.lastname: Fishman
authors.forename: D M
authors.initials: DM
authors.lastname: Amsterdam
authors.forename: B A
authors.initials: BA
authors.lastname: Szabó
authors.forename: J L
authors.initials: JL
authors.lastname: Cox
authors.forename: M K
authors.initials: MK
authors.lastname: Pasque
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D006322:Heart Aneurysm / Q000473:pathology / Q000503:physiopathology*; D008279:Magnetic Resonance Imaging; D008433:Mathematics; D018485:Muscle Fibers, Skeletal / Q000473:pathology; D009200:Myocardial Contraction; D009206:Myocardium / Q000473:pathology; D012756:Sheep; D013318:Stroke Volume; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*