title: Strain rate acceleration yields a better index for evaluating left ventricular contractile function as compared with tissue velocity acceleration during isovolumic contraction time: an in vivo study.
abstract: OBJECTIVE
  Our study aimed to investigate whether strain rate acceleration (SRA) during isovolumic contraction time (IVCT) could serve as a sensitive indicator of myocardial function.
  
  
  METHODS
  A total of 8 sheep underwent occlusion of left anterior descending coronary artery or diagonal branches and 2 sheep underwent left circumflex coronary artery occlusion to create septal, apical, or basal segment myocardial ischemia 19 to 27 weeks before the study. Baseline, volume-loading, dobutamine, and metoprolol infusion were used to produce 4 hemodynamic stages for each sheep. Doppler tissue imaging was acquired using a 5-MHz probe (GE/VingMed Vivid Five, GE Medical Systems, Milwaukee, Wis) on open-chest animals using the liver as a standoff at the apex. Using software (EchoPac, GE Medical Systems), SRA during IVCT was calculated and compared with tissue velocity acceleration (TVA) during IVCT from areas located in the normal and ischemic zones. Also, invasively monitored left ventricle dP/dt was measured as reference contractile function.
  
  
  RESULTS
  Both TVA and SRA during IVCT showed higher values for normal tissue than for ischemic area (P <.0001). SRA for normal wall segments changed significantly during the 4 stages (P =.01) with corresponding changes on high-fidelity left ventricular pressure catheters (r = 0.92). TVA over normal segments showed no significant change (P =.29) in the 4 hemodynamic stages. Both TVA and SRA of the ischemic segments showed no significant change with pharmacologic maneuvers or loading conditions.
  
  
  CONCLUSIONS
  SRA and TVA during IVCT are both useful indicators for detecting abnormal heart wall motion. However, SRA tends to be more sensitive than TVA for differentiating the response to stress conditions.
authors.affiliation: Clinical Care Center for Congenital Heart Disease, Oregon Health and Science University, Portland 97239, uSA.
authors.forename: Xiaokui
authors.initials: X
authors.lastname: Li
authors.forename: Michael
authors.initials: M
authors.lastname: Jones
authors.forename: Hui-Fang
authors.initials: HF
authors.lastname: Wang
authors.forename: Crispin H
authors.initials: CH
authors.lastname: Davies
authors.forename: Julia C
authors.initials: JC
authors.lastname: Swanson
authors.forename: Ikuo
authors.initials: I
authors.lastname: Hashimoto
authors.forename: Rosemary A
authors.initials: RA
authors.lastname: Rusk
authors.forename: Sebastian T
authors.initials: ST
authors.lastname: Schindera
authors.forename: Brent J
authors.initials: BJ
authors.lastname: Barber
authors.forename: David J
authors.initials: DJ
authors.lastname: Sahn
mesh_terms: D000818:Animals; D002302:Cardiac Output; D002316:Cardiotonic Agents; D004280:Dobutamine; D015150:Echocardiography, Doppler; D006352:Heart Ventricles / Q000000981:diagnostic imaging; D008790:Metoprolol; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000000981:diagnostic imaging* / Q000503:physiopathology; D012756:Sheep; D016277:Ventricular Function, Left
chemical_list: D002316:Cardiotonic Agents; D004280:Dobutamine; D008790:Metoprolol