ObjectiveEffective arterial elastance (Ea), integrating the pulsatile component of left ventricular (LV) afterload, is an estimate of aortic input impedance. We evaluated relationships of Eawith left ventricular anatomy and function in essential hypertension.DesignA cross-sectional analysis in 81 normotensive and 174 untreated hypertensive individuals enrolled in a referral hypertension centre.MethodsUsing echocardiography we determined left ventricular mass index (LVMI), relative wall thickness (RWT), stroke volume (SV), endocardial (FSe) and midwall (FSm) fractional shortening and total peripheral resistance (TPR). Carotid pressure waveforms were obtained by arterial tonometry, and end-systolic pressure (Pes) was measured at the dicrotic notch. Eaindex (EaI) was calculated as Pes/(SV index); LV elastance (Ees) was estimated as Pes/LV end-systolic volume, and ventriculoarterial coupling was evaluated by the Ea/Eesratio.ResultsEaI was higher in hypertensives than in normotensives (3.02 ± 0.63 versus 2.40 ± 0.52 mmHg/l per m2;P< 0.0001). Using the 95% upper confidence limit in normotensives, hypertensives were divided in two groups with normal or elevated EaI. The 38 hypertensives with elevated EaI had higher RWT (0.41 ± 0.06 versus 0.37 ± 0.05), lower LVMI (87.5 ± 18.5 versus 96.8 ± 19.3 g/m2), higher TPR (2247 ± 408 versus 1658 ± 371 dynes/cm s−5) and lower FSeand FSm(35 ± 5 versus 39 ± 5 and 16 ± 2 versus 18 ± 2%; allP< 0.05) than patients with normal EaI. Ea/Eesratio was increased and cardiac output was reduced in hypertensives with elevated EaI.ConclusionsHigh values of EaI identify a minority of hypertensive patients characterized by elevated TPR, left ventricular concentric remodelling, depressed left ventricular systolic function and impaired ventriculoarterial coupling.