Journal
INTERNATIONAL JOURNAL OF CLINICAL PRACTICE
Volume 75, Issue 12, Pages -Publisher
WILEY-HINDAWI
DOI: 10.1111/ijcp.14952
Keywords
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Funding
- Universita degli Studi di Bari Aldo Moro within the CRUI-CARE Agreement
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This study evaluated cardiovascular risk in 185 OSA patients, finding a strong association between cardiovascular risk and obesity, but a weak relationship with AHI values. Obese individuals had higher scores in the Epworth Questionnaire and Charlson Co-morbidity Index compared to other sub-groups. Further studies are needed to explore the role of inflammation from obesity in increasing cardiovascular risk in OSA patients.
Background Obstructive sleep apnea (OSA) is a worldwide increasing syndrome, which, by promoting endothelial dysfunction, contributes to extend the cardiovascular risk. We evaluated the cardiovascular risk in a group of OSA patients. Methods A total of 185 OSA subjects (19 normal weight, 57 overweight, 109 obese), who entered the Ambulatory of Sleep Disorders of the Institute of Respiratory Diseases of the University of Bari, during 1 year, were enrolled in the study. We assessed anthropometric features, polysomnographic findings, cardiovascular risk factors, smoking habit, Pulmonary Function Test, Arterial Blood Gas Analysis, Epworth Questionnaire, and Charlson Co-morbidities Index (CCI). Subjects were divided into three groups, according to their BMI: individuals with BMI >= 30 kg/m(2) (Group 1 n = 109, mean age 61 +/- 1; 74.3% men), individuals with BMI ranging from 25.0 to 29.9 kg/m(2) defined as overweight subjects (Group 2 n = 57, mean age 58.8 +/- 1.4; 77% men), and subjects with a BMI ranging from 18.5 to 24.9 kg/m(2) defined as normal weight subjects (Group 3 n = 19, mean age 54.2 +/- 2.3; 64,2% men). Results In the whole population, the percentage cardiovascular risk was weakly related with BMI (r = 0.33; P < .001), but not with AHI. The cardiovascular risk was strictly related to the obesity (P < .00002), while the Epworth Questionnaire score and the Charlson Co-morbidity Index were respectively statistically higher in the group of obese individuals (P = .004, P = .0002) than in the other two sub-groups. When AHI values were stratified in tertiles, the percentage cardiovascular risk did not vary with increasing AHI values (Figure 2). Conclusions Further studies are required to investigate the pivotal role of inflammation resulting from obesity, and underlying increased cardiovascular risk in OSA patients.
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