Relation of left ventricular longitudinal and circumferential shortening to ejection fraction in the presence or in the absence of mild hypertension.
Academic Article
Overview
abstract
OBJECTIVES: To study left ventricular longitudinal shortening in arterial hypertension and the relative contribution of longitudinal and circumferential fiber shortening to ventricular ejection. METHODS: Two-dimensional and M-mode echocardiograms were obtained for 50 normotensive subjects (aged 49 +/- 12 years) and 50 never-treated mild hypertensive patients (aged 49 +/- 11 years), to measure the minor-axis endocardial and midwall shortening, long-axis shortening and ejection fraction. RESULTS: The midwall shortening was lower in hypertensive than it was in normotensive subjects (P < 0.001) and was related inversely to the circumferential wall stress for both groups (P < 0.04 and 0.0001, respectively). The long-axis shortening in hypertensive patients (22.2 +/- 4.2%) and in normotensives (23.6 +/- 5.4%) was not statistically different, and was not related either to the meridional or to the circumferential wall stress. The ejection fraction was also similar for the two groups (68.2 +/- 6.3 versus 68.6 +/- 5.6%). Both for normotensive and for hypertensive subjects, the ejection fraction was influenced mainly by the midwall shortening (61 and 40% of the variance for normal and hypertensive individuals, respectively), with a minor contribution from the long-axis shortening, which was 7% for normotensive subjects and 18% for hypertensive patients, a statistically significant difference (P < 0.001). The combined effect of midwall and longitudinal shortenings on the ejection fraction was regulated by the relative wall thickness, and was maximal for hypertensive patients with an ejection fraction greater than that predicted by the midwall shortening. CONCLUSIONS: Left ventricular ejection is produced principally by circumferential shortening and is related independently to the relative wall thickness. In the presence of arterial hypertension and an altered cardiac load, longitudinal shortening becomes an important mechanism by which to augment ejection, thereby offsetting the reduction in midwall shortening.
