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Effect of Obesity on Left Ventricular Mass: Results from 320 Multi-Slices Computed Tomography.
Journal of the Medical Association of Thailand 2017 Februrary
Objective: To determine effects of obesity and gender on left ventricular mass in normotensive and hypertensive Thai patients using 320-slice cardiac computed tomography (CT).
Material and Method: Left ventricular mass (LVM) obtained from 320-slice coronary CT angiogram was compared in 597 normotensive subjects (175 men [65 obese] and 422 women [133 obese], aged 55±7 years) and 483 hypertensive patients (180 men [104 obese] and 303 women [170 obese], aged 60±7 years). Obesity in Asian population was defined by body mass index (BMI) ≥ 25 kg/m2 in both genders. LV mass was normalized for body surface area (BSA)and height2.7.
Results: The upper normal limit of LVM/ height2.7 developed from 244 (197 women, 47 men) low risk subjects (non-smoking normal-weight adults free from hypertension, diabetes, coronary artery disease & dyslipidemia) was lower than the established criteria for left ventricular hypertrophy (LVH) (31 versus 44 g/m2.7 in women; 36 versus 48 g/m2.7 in men). There is statistical difference between men and women in all groups of analysis. Among both hypertensive and normotensive subjects, the prevalence of LVH and LVM/height2.7 are higher in the obese group than normal-weight group in both genders (LVM/height2.7p<0.001; prevalence of LVH – obese versus normal-weight hypertension: 58% versus 34% in women, 43% versus 14% in men; obese versus normal-weight normotension: 35% versus 16% in women, 40% versus 15% in men). The same differences between obese and normal-weight groups were also present when normalizing LVM for height but not with LVM/BSA. Logistic regression analysis revealed that systolic blood pressure and BMI were the main predictors of LVH in the entire population (p<0.001 in both genders). Equations for predicting LVH in men and women were: Risk of LVH = 1/(l+e-w) where w is as follows: w (men) = 0.02* systolic pressure + 0.25*BMI – 9.86, w (women) = 0.03* systolic pressure + 0.17*BMI – 8.82.
Conclusion: Obesity is an independent stimulus to increase LVM in normo-tensive subjects, and its effect is additive in hypertensive patients. Gender and obesity affect LVM and prevalence of LVH.
Material and Method: Left ventricular mass (LVM) obtained from 320-slice coronary CT angiogram was compared in 597 normotensive subjects (175 men [65 obese] and 422 women [133 obese], aged 55±7 years) and 483 hypertensive patients (180 men [104 obese] and 303 women [170 obese], aged 60±7 years). Obesity in Asian population was defined by body mass index (BMI) ≥ 25 kg/m2 in both genders. LV mass was normalized for body surface area (BSA)and height2.7.
Results: The upper normal limit of LVM/ height2.7 developed from 244 (197 women, 47 men) low risk subjects (non-smoking normal-weight adults free from hypertension, diabetes, coronary artery disease & dyslipidemia) was lower than the established criteria for left ventricular hypertrophy (LVH) (31 versus 44 g/m2.7 in women; 36 versus 48 g/m2.7 in men). There is statistical difference between men and women in all groups of analysis. Among both hypertensive and normotensive subjects, the prevalence of LVH and LVM/height2.7 are higher in the obese group than normal-weight group in both genders (LVM/height2.7p<0.001; prevalence of LVH – obese versus normal-weight hypertension: 58% versus 34% in women, 43% versus 14% in men; obese versus normal-weight normotension: 35% versus 16% in women, 40% versus 15% in men). The same differences between obese and normal-weight groups were also present when normalizing LVM for height but not with LVM/BSA. Logistic regression analysis revealed that systolic blood pressure and BMI were the main predictors of LVH in the entire population (p<0.001 in both genders). Equations for predicting LVH in men and women were: Risk of LVH = 1/(l+e-w) where w is as follows: w (men) = 0.02* systolic pressure + 0.25*BMI – 9.86, w (women) = 0.03* systolic pressure + 0.17*BMI – 8.82.
Conclusion: Obesity is an independent stimulus to increase LVM in normo-tensive subjects, and its effect is additive in hypertensive patients. Gender and obesity affect LVM and prevalence of LVH.
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