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Obstructive sleep apnea severity is associated with left ventricular mass independent of other cardiovascular risk factors in morbid obesity.
Journal of Clinical Sleep Medicine : JCSM : Official Publication of the American Academy of Sleep Medicine 2013 November 16
OBJECTIVE: To evaluate the relation between obstructive sleep apnea (OSA) and left ventricular mass (LVM) in morbid obesity and the influence of gender, menopausal status, anthropometry, body composition, hypertension, and other cardiovascular risk factors in this relationship.
DESIGN: Cross-sectional descriptive study.
METHODS: Polysomnographic and echocardiographic studies were performed in a cohort of 242 patients (86 men, 100 premenopausal (PreM) and 56 postmenopausal (PostM) women), with grade II obesity and above (BMI: 43.7 ± 0.4 kg/m(2)) to investigate OSA and LVM respectively. Anthropometry, body composition, glucose tolerance, and blood pressure were also recorded.
RESULTS: OSA to different degrees was diagnosed in 76.2% of the patients (n: 166), its prevalence being 90.9% (n: 70) for men, and 76% (n: 38) and 63.8% (n: 58) for PostM and PreM women, respectively (p < 0.01). LVM excess was greatest for PostM women (90.2%), followed by men (81.9%) and PreM females (69.6%) (p < 0.01). LVM values increased in accordance to OSA severity (absence, 193.7 ± 6.9 g; mild, 192.6 ± 7.8 g; moderate, 240.5 ± 12.5 g; severe, 273.6 ± 14.6 g; p < 0.01). LVM magnitude correlated with the menopausal state, age, central adiposity, hypertension (HT), type 2 diabetes (DM), desaturation index (DI), and apnea-hypopnea index (AHI) (r = 0.41; p < 0.01). The relationship between LVM and AHI persisted in the multivariate analysis (β = 0.25; p < 0.05) after adjusting for age, gender, menopausal state, BMI, waist circumference, neck circumference, DI, fasting plasma glucose, DM, and HT. But if tobacco habits are included, the statistical difference disappears (β = 0.22; p = 0.06).
CONCLUSIONS: Morbid obesity is frequently associated with abnormal LVM, particularly in patients with OSA; this association is independent of HT, BMI, body composition, and other clinical factors, supporting a direct role of OSA on LVM in morbid obesity. This suggests that OSA and LVM might be taken as predictors of the cardiovascular risk in these patients.
DESIGN: Cross-sectional descriptive study.
METHODS: Polysomnographic and echocardiographic studies were performed in a cohort of 242 patients (86 men, 100 premenopausal (PreM) and 56 postmenopausal (PostM) women), with grade II obesity and above (BMI: 43.7 ± 0.4 kg/m(2)) to investigate OSA and LVM respectively. Anthropometry, body composition, glucose tolerance, and blood pressure were also recorded.
RESULTS: OSA to different degrees was diagnosed in 76.2% of the patients (n: 166), its prevalence being 90.9% (n: 70) for men, and 76% (n: 38) and 63.8% (n: 58) for PostM and PreM women, respectively (p < 0.01). LVM excess was greatest for PostM women (90.2%), followed by men (81.9%) and PreM females (69.6%) (p < 0.01). LVM values increased in accordance to OSA severity (absence, 193.7 ± 6.9 g; mild, 192.6 ± 7.8 g; moderate, 240.5 ± 12.5 g; severe, 273.6 ± 14.6 g; p < 0.01). LVM magnitude correlated with the menopausal state, age, central adiposity, hypertension (HT), type 2 diabetes (DM), desaturation index (DI), and apnea-hypopnea index (AHI) (r = 0.41; p < 0.01). The relationship between LVM and AHI persisted in the multivariate analysis (β = 0.25; p < 0.05) after adjusting for age, gender, menopausal state, BMI, waist circumference, neck circumference, DI, fasting plasma glucose, DM, and HT. But if tobacco habits are included, the statistical difference disappears (β = 0.22; p = 0.06).
CONCLUSIONS: Morbid obesity is frequently associated with abnormal LVM, particularly in patients with OSA; this association is independent of HT, BMI, body composition, and other clinical factors, supporting a direct role of OSA on LVM in morbid obesity. This suggests that OSA and LVM might be taken as predictors of the cardiovascular risk in these patients.
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