title: Altered myocardial shear strains are associated with chronic ischemic mitral regurgitation.
abstract: BACKGROUND
  Ischemic mitral regurgitation (IMR) limits life expectancy and can lead to postinfarction global left ventricular (LV) dilatation and remodeling, the pathogenesis of which is not completely known. We tested the hypothesis that IMR perturbs adjacent myocardial LV systolic strains.
  
  
  METHODS
  Thirteen sheep had three columns of miniature beads inserted across the lateral LV wall, with additional epicardial markers silhouetting the ventricle. One week later posterolateral infarction was created. Seven weeks thereafter, the animals were divided into two groups according to severity of IMR (< or = 1+, n = 7, IMR[-] vs > or = 2+, n = 6, IMR[+]). Four dimensional marker coordinates and quantitative histology were used to calculate ventricular volumes, transmural myocardial systolic strains, and systolic fiber shortening.
  
  
  RESULTS
  Seven weeks after infarction, end-diastolic (ED) volume increased similarly in both groups, end-systolic (ES) E13 (circumferential-radial) shear increased in both groups, but more so in IMR(+) than IMR(-) (+0.12 vs 0.04, p < 0.005), and E12 (circumferential-longitudinal) shear increased in IMR(-) but not IMR(+) (+0.04 vs -0.01, p < 0.005). There were no significant differences in ED or ES remodeling strains or systolic fiber shortening between IMR(-) and IMR(+).
  
  
  CONCLUSIONS
  An equivalent increase in LV end-diastolic (ED) volume in both groups, coupled with unchanged ED and end-systolic remodeling strains as well as systolic circumferential, longitudinal, and radial strains, argue against a global LV or regional myocardial geometric basis for the cardiomyopathy associated with IMR. Further, similar systolic fiber shortening in both groups militates against an intracellular (cardiomyocyte) mechanism. The differences in subepicardial E12 and E13 shears, however, suggest a causal role of altered interfiber (cytoskeleton and extracellular-matrix) interactions.
authors.affiliation: Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, California 94305-5247, USA.
authors.forename: Tom C
authors.initials: TC
authors.lastname: Nguyen
authors.forename: Allen
authors.initials: A
authors.lastname: Cheng
authors.forename: Frank
authors.initials: F
authors.lastname: Langer
authors.forename: Filiberto
authors.initials: F
authors.lastname: Rodriguez
authors.forename: Robert A
authors.initials: RA
authors.lastname: Oakes
authors.forename: Akinobu
authors.initials: A
authors.lastname: Itoh
authors.forename: Daniel B
authors.initials: DB
authors.lastname: Ennis
authors.forename: David
authors.initials: D
authors.lastname: Liang
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; D002908:Chronic Disease; D005109:Extracellular Matrix / Q000378:metabolism; D008944:Mitral Valve Insufficiency / Q000503:physiopathology*; D017202:Myocardial Ischemia / Q000150:complications*; D012756:Sheep; D013314:Stress, Mechanical; D013599:Systole; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling