Early diastolic rapid wall thinning is a key physiological process dependent on regional fiber arrangement that determines left ventricular filling, and its impairment contributes to diastolic dysfunction in various cardiac diseases.
Continuous measurement of posterior left ventricular wall thickness on one or two-dimensional echocardiograms or left ventriculograms has demonstrated an early diastolic period of rapid thinning at a peak rate of 10 ± 1.7 cm/s, significantly greater than the peak thickening rate during systole. In normal subjects, this period ends abruptly, and is coterminous with rapid filling. Thinning rates are greatest at the level of the tips of the papillary muscles, and are significantly lower towards the mitral ring. In patients with ischaemic heart disease, mitral valve opening may be delayed until rapid thinning is complete, showing that it is not a function of left ventricular filling, and therefore likely to be a manifestation of relaxation itself. Thinning rate is reduced in patients with left ventricular hypertrophy due to hypertension, aortic stenosis or hypertrophic cardiomyopathy, when it is associated with a corresponding reduction in the peak rate of dimension increase. It persists when the cause of the hypertrophy is removed as after resection of coarctation of the aorta, even if wall thickness returns to normal. Variation in peak rapid thinning rate with position in the cavity appears to underly abnormal filling patterns in pure mitral regurgitation, and determines the distribution of abnormal wall movement during isovolumic relaxation in patients with coronary artery disease. This distribution also correlates with fibre orientation in normal human hearts as demonstrated by dissection. The period of rapid thinning is associated with intraventricular pressure gradients. It is also exactly synchronous with the early diastolic period when calculated wall stress remains constant in spite of increasing cavity size, an effect that has previously been attributed to viscosity. We conclude that rapid early diastolic wall thinning depends on the integrity of regional fibre arrangement, and is a major determinant of the rate and pattern of the rapid phase of left ventricular filling in normals. Its loss causes disturbances of wall movement during relaxation and filling in disease.
Gibson et al. (Wed,) studied this question.