Contribution of afterload, hypertrophy and geometry to left ventricular ejection fraction in aortic valve stenosis, pure aortic regurgitation and idiopathic dilated cardiomyopathy.

Published

Journal Article

To investigate the relation of left ventricular (LV) afterload, hypertrophy, geometry and systolic pump function, 17 normal persons, 24 patients with aortic stenosis (AS), 20 with aortic regurgitation (AR) and 15 with idiopathic dilated cardiomyopathy (DC) were studied. Two-dimensional echograms were used to assess end-systolic meridional and circumferential stresses and their ratio, LV mass, relative wall thickness (h/R ratio) and the ratio of LV minor axis to length, used as an index of shape. Independently obtained ejection fraction (EF) was used to determine which patients had normal (EF greater than or equal to 55%) and which had depressed (EF less than 55%) pump function. Patients with AS and low EF had similar LV mass (228 vs 215 g) but larger LV cavity (5.6 vs 4.5 cm), lower h/R ratio (0.53 vs 0.73, p less than 0.01), and therefore higher circumferential stress (336 vs 268 kdyne/cm2, p less than 0.05). Compared with normal persons, patients with DC had a lower h/R ratio (0.28 vs 0.38, p less than 0.01), higher circumferential stress (362 vs 215 kdyne/cm2, p less than 0.01) and more uniform stress distribution (meridional to circumferential stress ratio 0.57 vs 0.39, p less than 0.01), implying that meridional stress overestimates effective afterload. Afterload excess and LV shape change may be important to pump function in patients with AS or DC. In contrast, in those with AR, no significant shape differences were noted, although LV mass was higher in those with low EF (279 vs 211 g, p less than 0.05). Depressed pump function may result from impaired myocardial performance in AR without afterload excess.

Full Text

Duke Authors

Cited Authors

  • Douglas, PS; Reichek, N; Hackney, K; Ioli, A; Sutton, MG

Published Date

  • June 1, 1987

Published In

Volume / Issue

  • 59 / 15

Start / End Page

  • 1398 - 1404

PubMed ID

  • 2954456

Pubmed Central ID

  • 2954456

International Standard Serial Number (ISSN)

  • 0002-9149

Digital Object Identifier (DOI)

  • 10.1016/0002-9149(87)90928-3

Language

  • eng

Conference Location

  • United States