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Cardiac imaging and non-invasive testing
Interventricular interaction as a possible mechanism for the presence of a biphasic systolic velocity profile in normal left ventricular free walls
  1. M Marciniak1,
  2. B Bijnens2,3,
  3. A Baltabaeva1,
  4. A Marciniak1,
  5. C Parsai1,
  6. P Claus3,
  7. G R Sutherland1
  1. 1
    Department of Cardiology, St George’s Hospital, University of London, UK
  2. 2
    Medical School and Faculty of Electronic Engineering, University of Zagreb, Croatia
  3. 3
    University of Leuven, Belgium
  1. Professor George R Sutherland, St George’s Hospital, Department of Cardiology, Blackshaw Road, London SW17 0QT, UK; George.Sutherland{at}stgeorges.nhs.uk

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 monophasic. Their shape differs markedly from the lateral wall (LW), the posterior wall and the anterior wall, which are biphasic. We studied the hypothesis that the double-peaked SVP in the left ventricular free walls are caused by interventricular interaction. This might have additional implication in understanding the measurements of the timing of SVP maxima in pathology as, for example, used to determine intraventricular dyssynchrony in heart failure.

Methods: 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 four-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.

Results: 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 (19) ms) followed by the peak Sep (123 (20) ms; p = 0.34). Peak RV velocity occurred at the same time as the dip in the LW (200 (30) vs 203 (30) ms, respectively; p = 0.53).

Conclusion: Our study suggests that the biphasic SVP in the free walls is probably caused by interventricular interaction. Therefore the timing of maxima on SVP should be used with great caution when looking for intraventricular dyssynchrony as the peaks are influenced by RV function.

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Footnotes

  • Competing interests: None.

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