RELATION OF HEMODYNAMIC VOLUME LOAD TO ARTERIAL AND CARDIAC SIZE

Citation
Ec. Jones et al., RELATION OF HEMODYNAMIC VOLUME LOAD TO ARTERIAL AND CARDIAC SIZE, Journal of the American College of Cardiology, 29(6), 1997, pp. 1303-1310
Citations number
53
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
07351097
Volume
29
Issue
6
Year of publication
1997
Pages
1303 - 1310
Database
ISI
SICI code
0735-1097(1997)29:6<1303:ROHVLT>2.0.ZU;2-#
Abstract
Objectives. This study sought to assess the relation of Doppler stroke volume (SV) to cardiac and carotid artery size and to determine wheth er volume load accounts for the parallelism between the two. Backgroun d. It has been suggested that altered hemodynamic volume load can modi fy the degree and pattern of left ventricular (LV) hypertrophy from th at predicted from blood pressure (BP) alone. Methods. We related Doppl er echocardiographic SV in 342 normotensive or unmedicated asymptomati c hypertensive adults to echocardiographic LV mass, LV internal dimens ion (LVID), wall thickness, carotid ultrasound arterial lumen diameter , intimal-medial thickness (IMT) and cross-sectional area (CSA). Resul ts. SV was positively related to LV mass (r = 0.42), LVID (r = 0.45), ventricular wall thickness (r = 0.20 to 0.29) and carotid diameter (r = 0.23, all p < 0.0001); CSA (r = 0.17, p < 0.002); and IMT (r = 0.12, p 0.03). In multivariate analyses controlling for awake ambulatory BP and the circumferential end-systolic stress/end systolic volume index ratio, SV remained an independent predictor of LV mass and chamber si ze (both p < 0.0001) but not LV wall thickness. SV also predicted caro tid diameter (p < 0.0002), CSA (p = 0.001) and, to a lesser degree, IM T (p = 0.02) after controlling for mean awake BP and age. In additiona l analyses, LV and carotid dimensions were significantly interrelated independent of SV. Conclusions. SV measured by invasively validated Do ppler echocardiography is associated with LV and carotid artery enlarg ement and eccentric hypertrophy, independent of arterial pressure, LV contractility, age and body size; however, SV and other variables do n ot account for the previously documented parallelism between cardiac a nd arterial structure. (C) 1997 by the American College of Cardiology.