title: Transmural left ventricular shear strain alterations adjacent to and remote from infarcted myocardium.
abstract: OBJECTIVE
  In some patients, dysfunction in a localized infarct region spreads throughout the left ventricle to aggravate mitral regurgitation and produce deleterious global left ventricular (LV) remodeling. Alterations in transmural strains could be a trigger for this process, as these changes can produce apoptosis and extracellular matrix disruption. The hypothesis was tested that localized infarction perturbs transmural strain patterns not only in adjacent regions but also at remote sites.
  
  
  METHODS
  Transmural radiopaque beadsets were inserted surgically into the anterior basal and lateral equatorial LV walls of 25 sheep; additional markers were used to silhouette the left ventricle. One week thereafter, 10 sheep had posterior wall infarction from (obtuse marginal occlusion, INFARCT) and 15 had no infarction (SHAM). Four-dimensional marker dynamics were studied with biplane videofluoroscopy eight weeks later. Fractional area shrinkage, LV volumes and transmural circumferential, longitudinal and radial systolic strains were analyzed.
  
  
  RESULTS
  Compared to SHAM, INFARCT greatly increased longitudinal-radial shear (mid-wall: 0.07 +/- 0.07 versus 0.14 +/- 0.06; subendocardium: 0.03 +/- 0.07 versus 0.20 +/- 0.08) in the inner half of the lateral LV wall and increased circumferential-radial shear (mid-wall: 0.03 +/- 0.05 versus 0.10 +/- 0.04; subepicardium: 0.02 +/- 0.05 versus 0.12 +/- 0.10) increased in the outer half of the LATERAL wall. In the ANTERIOR wall, INFARCT also increased longitudinal-radial shear (midwall: 0.01 +/- 0.05 versus 0.12 +/- 0.04; subendocardium: 0.04 +/- 0.09 versus 0.25 +/- 0.20) in the inner layers.
  
  
  CONCLUSIONS
  Increased transmural shear strains were found not only in an adjacent region, but also at a site remote from a localized infarction. This perturbation could trigger remodeling processes that promote the progression of ischemic cardiomyopathy. A better understanding of this process is important for the future development of surgical therapies to reverse destructive LV remodeling.
authors.affiliation: Department of Cardiovascular and Thoracic Surgery, Stanford University School of Medicine, Stanford, California 94305-5247, USA.
authors.forename: Allen
authors.initials: A
authors.lastname: Cheng
authors.forename: Frank
authors.initials: F
authors.lastname: Langer
authors.forename: Tom C
authors.initials: TC
authors.lastname: Nguyen
authors.forename: Marcin
authors.initials: M
authors.lastname: Malinowski
authors.forename: Daniel B
authors.initials: DB
authors.lastname: Ennis
authors.forename: George T
authors.initials: GT
authors.lastname: Daughters
authors.forename: Neil B
authors.initials: NB
authors.lastname: Ingels
authors.forename: D Craig
authors.initials: DC
authors.lastname: Miller
mesh_terms: D000818:Animals; D017023:Coronary Angiography; D004195:Disease Models, Animal; D006352:Heart Ventricles / Q000503:physiopathology*; D009200:Myocardial Contraction / Q000502:physiology; D009203:Myocardial Infarction / Q000150:complications* / Q000000981:diagnostic imaging / Q000503:physiopathology; D012756:Sheep; D013314:Stress, Mechanical; D018487:Ventricular Dysfunction, Left / Q000209:etiology* / Q000503:physiopathology; D020257:Ventricular Remodeling / Q000502:physiology*