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Inter-Ventricular Interaction as a Possible Mechanism for the presence of a Bi-phasic Systolic Velocity Profile in Normal Left Ventricular Free Walls.
  1. Maciej Marciniak (mmarcini{at}sgul.ac.uk)
  1. Department of Cardiology, St.George's Hospital, University of London, United Kingdom
    1. Bart Bijnens
    1. Medical School and Faculty of Electronic Engineering, University of Zagreb, Croatia
      1. Aigul Baltabaeva
      1. Department of Cardiology, St.George's Hospital, University of London, United Kingdom
        1. Anna Marciniak
        1. Department of Cardiology, St.George's Hospital, University of London, United Kingdom
          1. Chirine Parsai
          1. Department of Cardiology, St.George's Hospital, University of London, United Kingdom
            1. Piet Claus
            1. University of Leuven, Belgium, Belgium
              1. George R Sutherland (george.sutherland{at}stgeorges.nhs.uk)
              1. Department of Cardiology, St.George's Hospital, University of London, United Kingdom

                Abstract

                Background In normal subjects, systolic longitudinal regional velocity profiles (SVP) (measured both based on Pulsed or Tissue Doppler) have a non-uniform pattern. SVP from the right ventricle (RV), the septal (Sep) and the inferior wall are similar in shape and tend to be mono-phasic. Their shape differs markedly from the lateral (LW), the posterior and the anterior wall, which are bi-phasic. We studied the hypothesis that the double peaked SVP in the left ventricular free walls are caused by inter-ventricular interaction. This might have additional implication in understanding the measurements of the timing of SVP maxima in pathology, as for example used to determine intra-ventricular dyssynchrony in heart failure.

                Methods and Results 38 healthy individuals underwent a standard echo examination and a tissue Doppler study. SVP from the RV, Sep and LW basal segments were acquired in an apical 4-chamber view. The amplitude and timing of the peak velocities were measured. If a double peak was present, the amplitude and timing of the dip was calculated.<BR> RV and Sep had a single systolic velocity peak, while the LW had two peaks with a clear dip between both peaks. The first peak in the LW was the earliest event in the cycle (119±19ms) followed by the peak Sep (123±20ms; p=0.34). Peak RV velocity occurred at the same time as the dip in the LW (200±30 vs 203±30ms respectively; p=0.53).

                Conclusions Our study suggests that the bi-phasic SVP in the free walls are likely caused by inter-ventricular interaction. Therefore the use of timing of maxima on SVP should be used with great caution when looking for intra-ventricular dyssynchrony as the peaks are influenced by RV function.

                • cardiac resynchronization therapy
                • echocardiography
                • tissue velocity imaging

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