title: Alterations in left ventricular torsion in tachycardia-induced dilated cardiomyopathy.
abstract: OBJECTIVE
  Left ventricular torsion reduces transmural systolic gradients of fiber strain, and torsional recoil in early diastole is thought to enhance left ventricular filling. Left ventricular remodeling in dilated cardiomyopathy may result in changes in torsion dynamics, but these effects are not yet characterized. Tachycardia-induced cardiomyopathy is accompanied by systolic and diastolic heart failure and left ventricular remodeling. We hypothesized that cardiomyopathy would alter systolic and diastolic left ventricular torsion mechanics, and this hypothesis was tested by studying sheep before and after the development of tachycardia-induced cardiomyopathy.
  
  
  METHODS
  Implanted miniature radiopaque markers were used in 8 sheep to measure left ventricular geometry and function, maximal torsional deformation, and early diastolic recoil before and after rapid ventricular pacing was used to create tachycardia-induced cardiomyopathy.
  
  
  RESULTS
  All animals had significant heart failure with ventricular dilatation and remodeling. With tachycardia-induced cardiomyopathy, maximum torsion relative to control conditions decreased (1.69 degrees +/- 0.61 degrees vs 4.25 degrees +/- 2.33 degrees ), and early diastolic recoil was completely abolished (0.53 degrees +/- 1.19 degrees vs -1.17 degrees +/- 0.94 degrees ).
  
  
  CONCLUSIONS
  Cardiomyopathy is accompanied by decreased and delayed systolic left ventricular torsional deformation and loss of early diastolic recoil, which may contribute to left ventricular dysfunction by increasing systolic transmural strain gradients and impairing diastolic filling. Analysis of left ventricular torsion with radiofrequency-tagging magnetic resonance imaging should be explored to elucidate the role of torsion in patients with cardiomyopathy.
authors.affiliation: Department of Cardiovascular and Thoracic Surgery, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, CA 94305-5247, USA.
authors.forename: Frederick A
authors.initials: FA
authors.lastname: Tibayan
authors.forename: David T M
authors.initials: DT
authors.lastname: Lai
authors.forename: Tomasz A
authors.initials: TA
authors.lastname: Timek
authors.forename: Paul
authors.initials: P
authors.lastname: Dagum
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; D002304:Cardiac Pacing, Artificial; D002311:Cardiomyopathy, Dilated / Q000209:etiology / Q000503:physiopathology*; D006439:Hemodynamics / Q000502:physiology; D009200:Myocardial Contraction / Q000502:physiology; D012756:Sheep; D013610:Tachycardia / Q000503:physiopathology; D014102:Torsion Abnormality; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*; D020257:Ventricular Remodeling / Q000502:physiology