Ps. Saba et al., Impact of arterial elastance as a measure of vascular load on left ventricular geometry in hypertension, J HYPERTENS, 17(7), 1999, pp. 1007-1015
Citations number
47
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Objective Effective arterial elastance (E-a), integrating the pulsatile com
ponent of left ventricular (LV) afterload, is an estimate of aortic input i
mpedance. We evaluated relationships of E-a with left ventricular anatomy a
nd function in essential hypertension,
Design A cross-sectional analysis in 81 normotensive and 174 untreated hype
rtensive individuals enrolled in a referral hypertension centre,
Methods Using echocardiography we determined left ventricular mass index (L
VMI), relative wall thickness (RWT), stroke volume (SV), endocardial (FS,)
and midwall (FS,) fractional shortening and total peripheral resistance (TP
R), Carotid pressure waveforms were obtained by arterial tonometry, and end
-systolic pressure (P-es) was measured at the dicrotic notch. E-a index (Ea
I) was calculated as P-es/(SV index); LV elastance (E-es) was estimated as
P-es/LV end-systolic volume, and ventriculoarterial coupling was evaluated
by the E-a/E-es ratio.
Results EaI was higher in hypertensives than in normotensives (3.02 +/- 0.6
3 versus 2.40 +/- 0.52 mmHg/l per m(2); P< 0.0001). Using the 95% upper con
fidence limit in normotensives, hypertensives were divided in two groups wi
th normal or elevated EaI. The 38 hypertensives with elevated EaI had highe
r RWT(0.41 +/- 0.06 versus 0.37 +/- 0.05), lower LVMI (87.5 +/- 18.5 versus
96.8 +/- 19.3 g/m(2)), higher TPR (2247 +/- 408 versus 1658 +/- 371 dynes/
cm s(-5)) and lower FSe and FSm (35 +/- 5 versus 39 +/- 5 and 16 +/- 2 vers
us 18 +/- 2%; all P< 0.05) than patients with normal EaI. E-a/E-es ratio wa
s increased and cardiac output was reduced in hypertensives with elevated
Conclusions High values of EaI identify a minority of hypertensive patients
characterized by elevated TPR, left ventricular concentric remodelling, de
pressed left ventricular systolic function and impaired ventriculoarterial
coupling. J Hypertens 1999, 17:1007-1015 (C) Lippincott Williams & Wilkins.