Introduction: 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.
Aim: To demonstrate that ventricular-arterial uncoupling is frequently present in the development of LV hypertrophy (H) and diastolic dysfunction (DD) in hypertension (HBP).
Methods: 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.
Results: 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/m 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/m, 91.4 ± 22.2 g-min/m, and 57 ± 14.6 dynes/cm in quartile 1, and 33.5 ± 6.6 cc/m, 65.5 ± 15.2 g-min/m, and 77.8 ± 17.1 dynes/cm, in quartile 4, respectively (p < 0.001). Peripheral resistance index was 3349 ± 1072 and 4410 ± 1143 dynes*s/cm-5/m 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).
Conclusions: 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.
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