title: Myocardial performance is reduced immediately prior to ventricular ectopy.
abstract: BACKGROUND
  We recently demonstrated local voltage potentials indicating conduction impairment and block in the sinus beats preceding ventricular premature beats (VPBs) originating in the ventricular outflow tracts.
  
  
  OBJECTIVE
  The purpose of this study was to test the hypothesis that impairment of impulse conduction would also lead to changes in the contractile performance of sinus beats preceding ventricular ectopy using Tissue Doppler echocardiography.
  
  
  METHODS
  Twenty-three consecutive patients with VPBs were examined in the apical 4-chamber view with a frame rate of 150 Hz (GE VIVID VII). Eleven patients had no structural heart disease, 5 had dilated cardiomyopathy, 4 had ischemic heart disease, 2 had arrhythmogenic right ventricular dysplasia, and 1 had aortic stenosis. The ectopy originated in the ventricular outflow tracts in 15 patients and in the left ventricle 8. Eleven of the patients underwent radiofrequency ablation of the VPBs.
  
  
  RESULTS
  Tissue Doppler imaging demonstrated a highly statistically significant decrease in myocardial performance in the last sinus beat before the VPB compared to earlier sinus beats. Thus, ejection time (time to peak end-systolic contraction) and peak systolic velocity shortened significantly (P <.001 for both) with a subsequent reduction in systolic shortening (end-systolic displacement; P <.001).
  
  
  CONCLUSIONS
  Ventricular ectopy is preceded by a significant decrease in myocardial performance in the last sinus beat preceding VPBs as observed in consecutive patients with a broad variety of heart conditions pointing to a mutual underlying electrical mechanism (ie, localized conduction block confined to an area surrounding the ectopic pacemaker).
authors.affiliation: Cardiology Department P, Gentofte University Hospital, Copenhagen, Denmark. pebt@geh.regionh.dk
authors.forename: Poul Erik Bloch
authors.initials: PE
authors.lastname: Thomsen
authors.forename: Thomas Fritz
authors.initials: TF
authors.lastname: Hansen
authors.forename: Christian
authors.initials: C
authors.lastname: Jons
authors.forename: Thue
authors.initials: T
authors.lastname: Olsen
authors.forename: Arne
authors.initials: A
authors.lastname: Johannessen
authors.forename: Knud
authors.initials: K
authors.lastname: Særmark
authors.forename: Scott
authors.initials: S
authors.lastname: McNitt
authors.forename: Mark
authors.initials: M
authors.lastname: Haigney
authors.forename: Peter
authors.initials: P
authors.lastname: Sogaard
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002311:Cardiomyopathy, Dilated / Q000503:physiopathology*; D015150:Echocardiography, Doppler; D004553:Electric Conductivity; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology*; D017202:Myocardial Ischemia / Q000503:physiopathology*; D018879:Ventricular Premature Complexes / Q000503:physiopathology*; D055815:Young Adult