Evidence of left ventricular wall movement actively decelerting aortic

Abstract

Efficient function of the left ventricle (LV) is achieved by coherent behaviour of its circumferential and longitudinal myocardial components. Little was known about the direct association between the long and minor axis velocities and the overall haemodynamics generated by ventricular systolic function such as aortic waves. The forward running expansion wave (FEW) during late systole contains important information about the condition of the LV and its interaction with the arterial system. The aim of this thesis was to underpin the mechanics and timing of the LV wall velocities, which are associated with the deceleration of flow. Both invasive and noninvasive data have been analysed in canines and humans and the following conclusions can be drawn. LV long axis peak shortening velocity lags consistently behind the minor axis, representing a degree of normal asynchrony. The FEW is seen to have a slow onset before a rapid increase in energy. The slow onset corresponds with the time that the long axis reaches its peak velocity of shortening. After both axes reach their respective maximum shortening velocity they continue to contract, although at a slow steady velocity until late ejection when there is a sudden simultaneous change of shortening velocity of both axes. This time corresponds with peak aortic pressure and the rapid increase in energy of the FEW. The time that the minor axis reaches its maximum velocity of shortening interestingly coincides with the arrival of the reflected wave at the LV during mid-systole. During canine aortic manipulation through the introduction of total occlusions along the aorta, the sequence of events observed in control conditions remains unchanged. In humans both LV wall movement and carotid wave intensity can be measured successfully using non-invasive methods. The FEW is generated when the last long axis segment begins to slow. The minor axis begins to slow before this time and corresponds to the time of peak aortic flow.