title: Evaluation of left ventricular dyssynchrony by onset of active myocardial force generation: a novel method that differentiates between electrical and mechanical etiologies.
abstract: BACKGROUND
  Better clinical tools for measuring left ventricular electrical dyssynchrony are needed. The present study investigates if onset of active myocardial force generation (AFG) may serve as a measure of electrical dyssynchrony.
  
  
  RESULTS
  In anesthetized dogs, we evaluated left ventricular mechanical dyssynchrony by 2 different approaches. First, we measured timing of peak myocardial shortening velocity and strain. Second, we measured the first sign of tension development by onset AFG as defined by the myocardial pressure-segment length loop upward shift from its passive-elastic state. Electrical dyssynchrony was measured by intramyocardial electromyograms (IM-EMG). Dyssynchrony was quantified as peak intersegment time difference and as standard deviation of timing for 6 to 8 myocardial segments. During baseline, reduced preload and myocardial ischemia shortening velocity and strain indicated segmental mechanical heterogeneity, whereas onset AFG and onset R in IM-EMG indicated synchronous activation of all segments. After induction of left bundle-branch block, all methods indicated dyssynchrony. Peak intersegment time difference for shortening velocity and strain showed weak correlations (r=0.17 and 0.16) and weak agreements (mean differences, -48+/-27 ms and -28+/-27 ms, respectively) with IM-EMG. Onset AFG by pressure-segment length loops, however, correlated well with IM-EMG (r=0.93), and agreement was good (mean difference, -0.6+/-6.8 ms). Results were similar for standard deviation of timing. Onset AFG from pressure-strain analysis by echocardiography showed accuracy similar to sonomicrometry.
  
  
  CONCLUSIONS
  Onset AFG was an accurate marker of myocardial electrical activation and was superior to shortening velocity and strain. Identification of electrical dyssynchrony by onset AFG may be feasible clinically using left ventricular pressure-strain analysis.
authors.affiliation: University of Oslo, Medical Faculty and Institute for Surgical Research and Department of Cardiology, Rikshospitalet, Oslo University Hospital, Norway.
authors.forename: Kristoffer
authors.initials: K
authors.lastname: Russell
authors.forename: Anders
authors.initials: A
authors.lastname: Opdahl
authors.forename: Espen W
authors.initials: EW
authors.lastname: Remme
authors.forename: Ola
authors.initials: O
authors.lastname: Gjesdal
authors.forename: Helge
authors.initials: H
authors.lastname: Skulstad
authors.forename: Erik
authors.initials: E
authors.lastname: Kongsgaard
authors.forename: Thor
authors.initials: T
authors.lastname: Edvardsen
authors.forename: Otto A
authors.initials: OA
authors.lastname: Smiseth
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D002037:Bundle-Branch Block / Q000000981:diagnostic imaging / Q000503:physiopathology*; D002304:Cardiac Pacing, Artificial; D004195:Disease Models, Animal; D004285:Dogs; D004452:Echocardiography; D004567:Electrodes, Implanted; D004576:Electromyography; D016018:Least-Squares Analysis; D009200:Myocardial Contraction / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000503:physiopathology*