Abstract 18623: Evaluation of Left Ventricular Geometry Changes in Patients with Tight Aortic Stenosis Using Multi-detector Computed Tomography
Background: Although aortic stenosis (AS) is a prototype of left ventricular hypertrophy (LVH) due to pressure overloading, patterns of LV geometric changes in patients with tight AS and their potential impact remain to be established.
Methods: LV mass index (LVMI), LV end-diastolic volume (LVEDV) and regional LV wall thickness in 16 segments were measured in 147 patients with tight AS (indexed aortic valve area [AVA] < 0.6 cm2/m2) using multi-detector computed tomography and compared with those of 32 normal controls. LVH was defined as LVMI >95th percentile of normal controls and LV remodeling as increased LVM/LVEDV with normal range of LVMI. Asymmetric remodeling or hypertrophy were used for patients with septal wall thickness >1.5 fold compared to the opposite segment. Patients with increased LVMI but normal range of LVM/LVEDV were classified to have eccentric LVH and those with eccentric LVH and decreased LV systolic function were defined to have de-compensation.
Results: AS patients with mean indexed AVA of 0.36 ± 0.08 cm2/m2 showed 7 different patterns of LV geometry including normal LV geometry (n=44), remodeling (n=7), asymmetric remodeling (n=7), concentric hypertrophy (n=16), asymmetric hypertrophy (n=23), eccentric hypertrophy (n=38), and de-compensation (n=12). Peak transaortic velocity (r=0.31, p<0.001) and E/E’ (r=0.29, p<0.001) showed positive correlation with LVMI: compared to other groups, patients with LVH (concentric or asymmetric or eccentric) showed higher peak velocity and E/E’ with smaller AVA (all, p<0.001). Despite similar AVA and mean pressure gradient, patients with E/E’ ≥ 15 (n=110) showed different LV remodeling patterns (p=0.028) with higher LVMI (97.8 ± 21.1 vs 86.4 ± 20.2 g/m2, p=0.005).
Conclusions: Various remodeling patterns of LV geometry were observed in tight AS and individual variation in LVH severity under similar LV pressure overloading could explain different severity of diastolic dysfunction.
Author Disclosures: J. Jang: None. D. Yang: None. S. Cheon: None. H. Park: None. M. Kim: None. H. Choi: None. H. Choi: None. J. Roh: None. B. Sun: None. J. Kang: None. D. Kim: None. J. Song: None. D. Kang: None. J. Song: None.
- © 2014 by American Heart Association, Inc.