Non-invasive assessment of end-systolic pressure-length and stress-shortening relationships in normal individuals: significance of different loading conditions induced by methoxamine and angiotensin II

Abstract

To evaluate whether the end-systolic pressure-dimension and stress-shortening relations are influenced by the drugs used for their assessment, we analysed the effects of angiotensin II (N = 30) and methoxamine (N = 10) in normal individuals. Serial measurements of left ventricular dimensions and wall thickness were performed by M-mode echocardiography; the end-systolic pressure was assessed by indirect, calibrated carotid pulse tracings. The end-diastolic dimension, which reflects preload, remained unchanged during the afterload challenge using angiotensin II, but increased significantly using methoxamine (P less than 0.001). Significant differences due to the agent used were observed for the end-systolic pressure-dimension relationship (P less than 0.002), the relation between end-systolic wall stress and fractional shortening (P less than 0.0002), and the relation between end-systolic wall stress and mean fibre shortening velocity (P less than 0.02). The extrapolated end-systolic dimension D0 at zero end-systolic pressure was significantly shifted to the left when using angiotensin II (P less than 0.02); this is considered to be due to its negligible effect on preload. Our data suggest that the assessment of the end-systolic pressure-dimension and stress-shortening relationships depends significantly on drug specific effects and the variation of preload during the afterload challenge. Based on these results, the use of angiotensin II is emphasized for the assessment of the end-systolic pressure-dimension and stress-shortening relationships.