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Age, sex, and hypertension-related remodeling influences left ventricular torsion assessed by tagged cardiac magnetic resonance in asymptomatic individuals: the multi-ethnic study of atherosclerosis.

 Yoneyama, Kihei ; Gjesdal, Ola ; Lima, Joao ; Bluemke, David A ; McClelland, Robyn L ; Liu, Chia-Ying ; Gomes, Antoinette S ; Hundley, W. Gregory ; Wu, Colin O ; Choi, Eui-Young 
 Circulation, Vol.126(21) : 2481~2490, 2012 
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BACKGROUND: The aim of the present study was to evaluate how torsion is influenced by left ventricular (LV) remodeling associated with age, sex, and hypertension in a large community-based population. METHODS AND RESULTS: Myocardial shortening and torsion were assessed by tagged cardiac magnetic resonance in 1478 participants without clinically apparent cardiovascular disease in the Multi-Ethnic Study of Atherosclerosis (MESA). Torsion was defined as the difference between apical and basal rotation divided by slice distance. In multivariable linear regression models, older age was associated with lower stroke volume (-3.6 mL per decade; P<0.001) and higher LV mass-to-volume ratio (0.03 g/mL per decade; P<0.001), along with lower circumferential shortening (-0.17% per decade; P<0.05). Torsion, however, was greater at older ages (0.14° per decade; P<0.001) and in women (0.37°/cm versus men; P<0.001). Hypertensive participants had higher LV mass and LV mass-to-volume ratio (15.5 g and 0.07 g/mL, respectively; P<0.001 for both). Circumferential shortening was lower in hypertensive (-0.42%; P<0.01), whereas torsion was higher after adjustment for age and sex (0.17°/cm; P<0.05). CONCLUSIONS: Older age is associated with lower LV volumes and greater relative wall thickness and is accompanied by lower circumferential myocardial shortening, whereas torsion is greater with older age. Hypertensive individuals have greater LV volumes and relative wall thickness and lower circumferential shortening. Torsion, however, is greater in hypertension independently of age and sex. Torsion may therefore represent a compensatory mechanism to maintain an adequate stroke volume and cardiac output in the face of the progressively reduced LV volumes and myocardial shortening associated with hypertension and aging.
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