title: Effect of pharmacologic increases in afterload on left ventricular rotation and strain in a rabbit model.
abstract: BACKGROUND
  Assessment of left ventricular rotational mechanics and myocardial deformation may provide new insight into both systolic and diastolic function. However, the effects of increasing afterload on these measures of cardiac function are poorly understood. The aim of this study was to identify the changes in left ventricular function and rotational mechanics during increasing pharmacologic afterload.
  
  
  METHODS
  In 14 anesthetized rabbits, two-dimensional speckle-tracking echocardiographic images and left ventricular pressure-volume loops were acquired at baseline and during norepinephrine, phenylephrine, and vasopressin infusion at increasing doses. Maximal ventricular elastance, arterial elastance, ventricular-arterial coupling, dP/dt, the time constant of relaxation, and other hemodynamic parameters were determined.
  
  
  RESULTS
  An increase in dP/dtmax with norepinephrine and phenylephrine and a decrease with vasopressin at escalating doses were detected. Ventricular-arterial coupling was preserved with norepinephrine and phenylephrine but decreased with vasopressin (P < .05). Apical rotation, rotational rate, and strain were preserved during the norepinephrine and phenylephrine infusions but were reduced with vasopressin (P < .05). Apical rotation and circumferential strain were significantly correlated with both ventricular-arterial coupling (r = 0.84 and r = 0.81) and dP/dtmax (r = -0.81 and r = -0.77). High-dose vasopressin decreased the diastolic time constant of relaxation and dP/dtmin while reducing apical untwisting rate.
  
  
  CONCLUSIONS
  Pharmacologic increases in afterload with vasopressin resulted in greater derangements in ventricular-arterial coupling and cardiac performance compared with norepinephrine and phenylephrine. Rotation and strain correlated well with invasively determined measures and can be used to assess afterload-induced alteration in cardiac function.
authors.affiliation: Department of Anesthesiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095, USA.
authors.forename: Jonathan K
authors.initials: JK
authors.lastname: Ho
authors.forename: Wei
authors.initials: W
authors.lastname: Zhou
authors.forename: Muhammad
authors.initials: M
authors.lastname: Ashraf
authors.forename: Madhav
authors.initials: M
authors.lastname: Swaminathan
authors.forename: David
authors.initials: D
authors.lastname: Sahn
authors.forename: Aman
authors.initials: A
authors.lastname: Mahajan
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D004452:Echocardiography / Q000379:methods*; D006439:Hemodynamics / Q000187:drug effects; D016014:Linear Models; D009638:Norepinephrine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011817:Rabbits; D015203:Reproducibility of Results; D012399:Rotation; D014667:Vasopressins / Q000494:pharmacology; D016277:Ventricular Function, Left / Q000187:drug effects*
chemical_list: D014667:Vasopressins; D010656:Phenylephrine; D009638:Norepinephrine