Background: The influence of obesity on the cardiac geometry is less clear. Our objective was to determine if body mass index (BMI) was an independent predictor of left atrial enlargement (LAE) relative to LV thicknes...Background: The influence of obesity on the cardiac geometry is less clear. Our objective was to determine if body mass index (BMI) was an independent predictor of left atrial enlargement (LAE) relative to LV thickness, dimension and function. Methods: Retrospective analysis of 90 consecutive patients with available echocardiographic data was performed. Patients were categorized into those with LAE (defined as >4.0 cm in transverse dimension by M-mode, n = 36) and those with normal LA size (n = 54). The clinical and echocardiographic variables were compared between the two groups. Results: Compared to patients with normal LA size, patients with LAE had significantly higher BMI (32 ± 8 vsi ± 8, p = 0.006), greater LV thickness, increased LV cavity dimension, and depressed LV systolic function. BMI was a strong and independent predictor of LAE. Left ventricular thickness and LV end-diastolic (LVED) dimension were other independent predictors of LAE. After adjusting for the significant effects of LV thickness and LV diameter, every unit increase in BMI resulted in an 8% increase in the odds of having LAE. Conclusions: 1) Higher BMI is an independent predictor of LAE. 2) Presence of LV enlargement and LV systolic dysfunction in these patients suggests that in the face of higher BMI, cardiac workload may exceed the compensatory LV hypertrophy and 3) LAE may be a consequence of the greater force developed by the LA to fill the LV.展开更多
文摘Background: The influence of obesity on the cardiac geometry is less clear. Our objective was to determine if body mass index (BMI) was an independent predictor of left atrial enlargement (LAE) relative to LV thickness, dimension and function. Methods: Retrospective analysis of 90 consecutive patients with available echocardiographic data was performed. Patients were categorized into those with LAE (defined as >4.0 cm in transverse dimension by M-mode, n = 36) and those with normal LA size (n = 54). The clinical and echocardiographic variables were compared between the two groups. Results: Compared to patients with normal LA size, patients with LAE had significantly higher BMI (32 ± 8 vsi ± 8, p = 0.006), greater LV thickness, increased LV cavity dimension, and depressed LV systolic function. BMI was a strong and independent predictor of LAE. Left ventricular thickness and LV end-diastolic (LVED) dimension were other independent predictors of LAE. After adjusting for the significant effects of LV thickness and LV diameter, every unit increase in BMI resulted in an 8% increase in the odds of having LAE. Conclusions: 1) Higher BMI is an independent predictor of LAE. 2) Presence of LV enlargement and LV systolic dysfunction in these patients suggests that in the face of higher BMI, cardiac workload may exceed the compensatory LV hypertrophy and 3) LAE may be a consequence of the greater force developed by the LA to fill the LV.
