title: Structural heterogeneity in the ventricular wall plays a significant role in the initiation of stretch-induced arrhythmias in perfused rabbit right ventricular tissues and whole heart preparations.
abstract: BACKGROUND
  Mechanical stress is known to alter the electrophysiological properties of the myocardium and may trigger fatal arrhythmias when an abnormal load is applied to the heart.
  
  
  OBJECTIVE
  We tested the hypothesis that the structural heterogeneity of the ventricular wall modulates globally applied stretches to create heterogeneous strain distributions that lead to the initiation of arrhythmias.
  
  
  RESULTS
  We applied global stretches to arterially perfused rabbit right ventricular tissue preparations. The distribution of strain (determined by marker tracking) and the transmembrane potential (measured by optical mapping) were simultaneously recorded while accounting for motion artifacts. The 3D structure of the preparations was also examined using a laser displacement meter. To examine whether such observations can be translated to the physiological condition, we performed similar measurements in whole heart preparations while applying volume pulses to the right ventricle. At the tissue level, larger stretches (> or = 20%) caused synchronous excitation of the entire preparation, whereas medium stretches (10% and 15%) induced focal excitation. We found a significant correlation between the local strain and the local thickness, and the probability for focal excitation was highest for medium stretches. In the whole heart preparations, we observed that such focal excitations developed into reentrant arrhythmias.
  
  
  CONCLUSIONS
  Global stretches of intermediate strength, rather than intense stretches, created heterogeneous strain (excitation) distributions in the ventricular wall, which can trigger fatal arrhythmias.
authors.affiliation: Department of Human and Engineered Environmental Studies, Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa, Chiba, Japan.
authors.forename: Kinya
authors.initials: K
authors.lastname: Seo
authors.forename: Masashi
authors.initials: M
authors.lastname: Inagaki
authors.forename: Satoshi
authors.initials: S
authors.lastname: Nishimura
authors.forename: Ichiro
authors.initials: I
authors.lastname: Hidaka
authors.forename: Masaru
authors.initials: M
authors.lastname: Sugimachi
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Hisada
authors.forename: Seiryo
authors.initials: S
authors.lastname: Sugiura
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology*; D006352:Heart Ventricles / Q000473:pathology* / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology*; D010477:Perfusion; D011817:Rabbits; D013312:Stress, Physiological