Left Ventricular Twist and Ventricular–Arterial Coupling in Hypertensive Patients

BACKGROUND: Left ventricular (LV) twist is usually influenced by LV hypertrophy resulting from hypertension or vascular stiffness. Vascular stiffness would increase arterial elastance (Ea), whereas LV end-systolic stiffness (Ees) could be influenced by LV hypertrophy. Therefore, in hypertensive patients, we assessed the extent to which ventricular-arterial coupling (VAC; Ea/Ees) affects LV twist, which may be a compensatory mechanism for systolic dysfunction. METHODS: Hypertensive patients (n = 128) and healthy controls (n = 40) underwent conventional and speckle tracking echocardiography including LV twist. Ea and Ees were estimated noninvasively by echocardiography. Patients were divided into 3 tertiles according to the twist angle. Univariate and multivariate regression analyses were performed to test the influence of VAC on twist. RESULTS: Patients in the lowest LV twist tertile had larger LV end-systolic volume, lower ejection fraction, lesser mid-wall fractional shortening (MWFS), and higher LV mass index (LVMI), compared to those with the highest tertile. They showed the lower septal tissue Doppler velocity, and global longitudinal and circumferential strain. With regard to VAC, Ea was similar among 3 groups, but Ees was significantly decreased in patient with lower tertile, resulting in increased VAC (1.1 ± 0.2 vs. 0.9 ± 0.1 vs. 0.7 ± 0.1, P < 0.001). While LV twist showed significant correlations with Ees, MWFS, and LVMI, VAC (β = -14.92, P < 0.001) was most associated with twist in a multivariate analysis. CONCLUSIONS: LV twist was significantly associated with VAC in accordance with LV function; LV twist and VAC decreased progressively as LV systolic function deteriorated, while being enhanced during the well-compensated phase.