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Ever since the time of Vesalius and Harvey,1 it has been recognised that the fall in cavity volume with left ventricular systole involves longitudinal as well as circumferential shortening, although the latter plays the dominant role. This asymmetry is reflected in myocardial structure—most of the left ventricular fibres are arranged circumferentially, particularly in the mid-wall and the base of the ventricle, however, with the progressive change in fibre angle across the wall, longitudinally directed fibres are found in the subendocardial and subepicardial free wall (fig 1) as well as in the papillary muscles.2
In view of the preponderance of circumferential fibres, it seems logical to deduce underlying myocardial function from the extent and velocity of their shortening3; however, the picture of the underlying function reached from observing changes in left ventricular minor axis is at first sight surprising. Normal dimensions fall by 25–40% during ejection, while the normally loaded sarcomere shortens by only 10–12%.4 Furthermore, this remarkable fall in minor axis is the result of thickening of the posterior wall to an extent much greater than would be expected from simultaneous inward movement of the epicardium.5 This apparent increase in myocardial mass that must underlie the observed extent of thickening can only be explained by concurrent shortening, and thus transverse thickening, of the longitudinally directed fibres. Without this longitudinal component, normal sarcomere shortening would lead to a shortening fraction of 12% and an ejection fraction of less than 30%. Thus, even normal changes in minor axis with ejection can be explained only on the basis of the combined action of the circumferential and longitudinal fibres.6 This …
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