Mechanisms of Left Atrial Enlargement in Obesity

Left atrial (LA) enlargement is common in obesity. We sought to determine the influence of ventricular (LV) remodeling on LA size in obesity. We studied 50 otherwise healthy obese subjects (body mass index 37.2 ± 4.6 kg/m2, 50 ± 6 years) and 58 age and gender-matched nonobese controls (body mass index 26.2 ± 2.9 kg/m2, 52 ± 5 years). Diastolic function, relative wall thickness (RWT), and LV mass were assessed using echocardiography. LA and LV volume was measured by 3D-echocardiography. Primary outcome was the ratio of LA volume indexed to LV volume in obese and control subjects. Obese subjects had substantially larger LA volumes compared with control subjects (61.0 ± 16.9 vs 38.9 ± 9.2 ml, p < 0.0001). When scaled to body size or lean mass, differences in LA size persisted. However, when indexed to LV end-diastolic volume, LA volumes between control and obese subjects were comparable (obese vs controls: 0.44 ± 0.15 vs 0.42 ± 0.10, p = 0.46). A small subset of obese subjects (26%) had LA volume markedly out of proportion to LV volume (LA/LV volume ratio ≥0.5) and displayed concentric LV remodeling with larger RWT and LV mass compared with obese subjects with LA/LV <0.5 (RWT: 0.46 ± 0.09 vs 0.36 ± 0.06, p < 0.0001; LV mass: 79 ± 18 vs 62 ± 13 g/m2 p < 0.01). In conclusion, LA enlargement in patients with obesity generally occurs commensurate with LV enlargement and parallels eccentric LV remodeling. LA enlargement out of proportion to LV size is associated with increased RWT and mass. This unique signature may identify obese subjects with pathologic LA remodeling. Left atrial (LA) enlargement is common in obesity. We sought to determine the influence of ventricular (LV) remodeling on LA size in obesity. We studied 50 otherwise healthy obese subjects (body mass index 37.2 ± 4.6 kg/m2, 50 ± 6 years) and 58 age and gender-matched nonobese controls (body mass index 26.2 ± 2.9 kg/m2, 52 ± 5 years). Diastolic function, relative wall thickness (RWT), and LV mass were assessed using echocardiography. LA and LV volume was measured by 3D-echocardiography. Primary outcome was the ratio of LA volume indexed to LV volume in obese and control subjects. Obese subjects had substantially larger LA volumes compared with control subjects (61.0 ± 16.9 vs 38.9 ± 9.2 ml, p < 0.0001). When scaled to body size or lean mass, differences in LA size persisted. However, when indexed to LV end-diastolic volume, LA volumes between control and obese subjects were comparable (obese vs controls: 0.44 ± 0.15 vs 0.42 ± 0.10, p = 0.46). A small subset of obese subjects (26%) had LA volume markedly out of proportion to LV volume (LA/LV volume ratio ≥0.5) and displayed concentric LV remodeling with larger RWT and LV mass compared with obese subjects with LA/LV <0.5 (RWT: 0.46 ± 0.09 vs 0.36 ± 0.06, p < 0.0001; LV mass: 79 ± 18 vs 62 ± 13 g/m2 p < 0.01). In conclusion, LA enlargement in patients with obesity generally occurs commensurate with LV enlargement and parallels eccentric LV remodeling. LA enlargement out of proportion to LV size is associated with increased RWT and mass. This unique signature may identify obese subjects with pathologic LA remodeling.