BACKGROUND: The diabetic heart exhibits increased left ventricular (LV) mass and reduced ventricular function. However, this relationship has not been studied in patients with aortic stenosis (AS), a disease process that causes LV hypertrophy and dysfunction through a distinct mechanism of pressure overload. The aim of this study was to determine how diabetes mellitus (DM) affects LV remodeling and function in patients with severe AS. METHODS AND RESULTS: Echocardiography was performed on 114 patients with severe AS (mean aortic valve area [AVA], 0.6 cm(2)) and included measures of LV remodeling and function. Multivariable linear regression models investigated the independent effect of DM on these aspects of LV structure and function. Compared to patients without diabetes (n=60), those with diabetes (n=54) had increased LV mass and LV end-systolic and end-diastolic dimensions, and decreased LV ejection fraction (EF) and longitudinal systolic strain (all P<0.01). In multivariable analyses adjusting for age, sex, systolic blood pressure, AVA, body surface area, and coronary disease, DM was an independent predictor of increased LV mass (β=26 g, P=0.01), LV end-systolic dimension (β=0.5 cm, P=0.008), and LV end-diastolic dimension (β=0.3 cm, P=0.025). After also adjusting for LV mass, DM was associated with reduced longitudinal systolic strain (β=1.9%, P=0.023) and a trend toward reduced EF (β=-5%, P=0.09). Among patients with diabetes, insulin use (as a marker of disease severity) was associated with larger LV end-systolic dimension and worse LV function. LV mass was a strong predictor of reduced EF and systolic strain (both P<0.001). CONCLUSIONS: DM has an additive adverse effect on hypertrophic remodeling (increased LV mass and larger cavity dimensions) and is associated with reduced systolic function in patients with AS beyond known factors of pressure overload.
BACKGROUND: The diabetic heart exhibits increased left ventricular (LV) mass and reduced ventricular function. However, this relationship has not been studied in patients with aortic stenosis (AS), a disease process that causes LV hypertrophy and dysfunction through a distinct mechanism of pressure overload. The aim of this study was to determine how diabetes mellitus (DM) affects LV remodeling and function in patients with severe AS. METHODS AND RESULTS: Echocardiography was performed on 114 patients with severe AS (mean aortic valve area [AVA], 0.6 cm(2)) and included measures of LV remodeling and function. Multivariable linear regression models investigated the independent effect of DM on these aspects of LV structure and function. Compared to patients without diabetes (n=60), those with diabetes (n=54) had increased LV mass and LV end-systolic and end-diastolic dimensions, and decreased LV ejection fraction (EF) and longitudinal systolic strain (all P<0.01). In multivariable analyses adjusting for age, sex, systolic blood pressure, AVA, body surface area, and coronary disease, DM was an independent predictor of increased LV mass (β=26 g, P=0.01), LV end-systolic dimension (β=0.5 cm, P=0.008), and LV end-diastolic dimension (β=0.3 cm, P=0.025). After also adjusting for LV mass, DM was associated with reduced longitudinal systolic strain (β=1.9%, P=0.023) and a trend toward reduced EF (β=-5%, P=0.09). Among patients with diabetes, insulin use (as a marker of disease severity) was associated with larger LV end-systolic dimension and worse LV function. LV mass was a strong predictor of reduced EF and systolic strain (both P<0.001). CONCLUSIONS:DM has an additive adverse effect on hypertrophic remodeling (increased LV mass and larger cavity dimensions) and is associated with reduced systolic function in patients with AS beyond known factors of pressure overload.
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