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Although longitudinally directed fibres—situated mainly in the subepicardium and subendocardium regions of the left and right ventricular free walls and the papillary muscles—comprise only a small proportion of the total ventricular myocardial mass, they play a major role in the maintenance of normal ejection fraction and in determining atrioventricular interactions.1 Not surprisingly, therefore, loss of longitudinal fibre function leads to characteristic disturbances.
Longitudinal function is always reduced when ventricular cavity size is increased, in addition ejection fraction is reduced and may be absent.2 3 This relation is consistent enough for long axis amplitude, or its equivalent, the amplitude of atrioventricular ring motion, to be used as an index of ejection fraction.4It applies not only to the left ventricle, where it can be shown to relate to prognosis but also to the right, where it provides a simple method of assessing right ventricular function.5 When overall long axis amplitude is low, peak shortening and lengthening rates are reduced. In restrictive left ventricular disease, long axis amplitude is low even when cavity size is normal at end diastole, although the effects of this reduction are apparent in a reduced amplitude of wall thickening and thus of shortening fraction.6 After mitral valve replacement, long axis amplitude is strikingly reduced; this does not occur with mitral valve repair or mild mitral stenosis,7 nor is it a consistent effect of cardiopulmonary bypass done for other reasons, and so is likely to be the result of loss of papillary muscle function. Although shortening fraction is frequently normal in such patients, normal wall thickening is associated with an exaggerated amplitude of epicardial motion, possibly to compensate for loss of the component owing to long axis shortening.
Regional reduction in the extent and velocity of long axis shortening is common after …
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