Ventricular-Arterial Uncoupling and Hypertension Mediated Diastolic Dysfunction.

Abstract

The increase in the pulsatile component of left ventricle afterload is suspected to cause a mismatch between the left ventricle (LV) and the vascular tree. Todemonstrate that ventricular-arterial uncoupling is frequently present in the development of LV hypertrophy (H) and diastolic dysfunction (DD) in hypertension (HBP). Observational study, HBP patients with ejection fraction >54%. Conventional 2D echocardiography and tissue Doppler performed following imaging guidelines. LV end systolic elastance (Ees), the effective arterial elastance (Ea), and ventricular-arterial coupling (VAC) measured by Chen single beat method. 288 patients, mean age 56.3±12.5 years and 168 patients (58.3%) males. Mean LV mass index was 87.2±20.4 grs/m2 and frequency of LVH 20.1% (58 patients). The mean VAC was 0.54±9.23. LV Stroke volume, stroke work and systolic stress were 46.2±10.3 cc/m2, 91.4±22.2 g-min/m2, and 57±14.6 dynes/cm2 in quartile 1, and 33.5±6.6 cc/m2, 65.5±15.2 g-min/m2, and 77.8±17.1 dynes/cm2, in quartile 4, respectively (p<0.001). Peripheral resistance index was 3349±1072 and 4410±1143 dynes*s/cm-5/m2 quartiles 1 vs. 4 (p<0.005). The frequency of LVH was 31.9% in quartile 1 and 11.3% in quartile 4 (p<0.005) and LVH or DD was 37.5% and 12.7%, respectively (p<0.001). Stroke volume and stroke work were significantly increased while systolic stress and peripheral resistance index were significantly reduced in patients with worst VAC. Ventricular-arterial uncoupling is mostly caused by an increase in Ees rather than by an elevation of Ea. LVH or DD are more frequent in the worst cases of ventricular-arterial uncoupling.