P418 CARDIOMETABOLIC ALTERATIONS IN OBESE PATIENTS WITH OBSTRUCTIVE SLEEP APNEA SYNDROME

Abstract Background Obesity and Obstructive Sleep Apnea Syndrome (OSAS) has been recognized as two of the major cardiac risk factors and they often coexist in one patient. OSAS increase the risk of as myocardial infarction, heart failure and arrhythmias. On the other hand, obesity is and independent predictor of cardiovascular mortality since it causes insulin resistance, dyslipidemia, sympathetic hyperactivation, chronic inflammation and endothelial dysfunction. Aim To evaluate cardiometabolic profile, echocardiographic alterations and the presence of arrhythmias in obese patients with Obstructive Sleep Apnea Syndrome and non obese patients. Patients and Methods 67 obese patients (37 male/30 female) and 52 non obese patients (40 male/12 female) were enrolled. All subjects underwent anthropometrical evaluation and a venous blood sample for biochemical and hormonal determinations including fasting plasma glucose, fasting plasma insulin, Hba1c and OGTT to 5 hours. The insulin resistance was evaluated by HOMA–IR. All the patients underwent echocardiographic examination, polysomnographic evaluation, in order to diagnose the OSAS, and a simultaneous 12–lead Holter ECG to evaluate the presence of nocturnal arrhythmias. Results As expected, we found a better antropometrics profile in non obese patients. Obese patients display a severe OSAS compared to non–obese patient as shown by higher values of AHI (26.37 ±24.95 vs 16.58 ±14.07; P < 0.05), TC90 (19.61 ±24.45 vs 8.63 ±17.80; P < 0.05) and ODI (40.55 ±27.41 vs 21.06 ±22.78; P < 0,05). In obese patients we also found a significant reduction of both ejection fraction (55.54 ±7.97 vs 66.52 ±8.95; P < 0.05) and A–wave (0.75 ±0.17 vs 0.83 ±0.19; P < 0.05). In 20% of obese patients, 12–lead Holter ECG showed the presence of cardiac pause > 3 sec during apnea. In obese population alone we demonstrated a significant negative correlation between AHI and E–wave (r= –0.3; P = 0.04) and a positive correlation with interventricular septum (r = 0.38; P = 0.01) and left ventricular mass (r = 0.32; P = 0.02). Post–hoc analysis shown how these findings maintained statistical significance even when the obese patients were stratified in subgroups according to the severity of OSAS. Conclusions Our data, even if preliminary, seem to indicate that OSAS is not only linked to obesity but it also acts as a negative factor on the cardiometabolic risk.