Abstracts / Sleep Medicine 7 (2006) S1–S127
S59
Methods and measurements: Twenty-three OSA patients divided into three subgroups: non-obese-OSA (BMI = 27 ± 1.3; AHI = 24.4 ± 18.0; age = 46.0 ± 12.0; n = 7), obese-OSA patients (BMI = 32.8 ± 3.7; AHI = 29.7 ± 16.0; age = 45.3 ± 9.6; n = 9), and obese-OSA with hypertention (OSA/Ht, BMI = 33.4 ± 2.5; AHI = 46.3 ± 15.5; age = 60 ± 7.6; n = 11) were compared with 16 controls (BMI = 26.8 ± 3.1; AHI = 7.2 ± 3.7; age = 45.0 ± 10.0). Intracellular HSP70 and TNF-a expression were determined by flow cytometry in monocytes maintained at 37 °C (basal level) or heat shocked at 43 °C for 30 min followed by a 4 h recovery period (HSinduced). Results: The intensity of basal HSP70 expression was twofold higher in all groups of OSA patients compared to controls and was positively correlated with ODI (r = 0.38, p = 0.03). No significant differences were found among patients regardless of age, BMI, AHI or hypertension. Inversely, HS-induced HSP70 expression was attenuated in OSA as compared to controls (by 30% in nonobese-OSA, 54% in obese-OSA and 55% in OSA/Ht), and was negatively correlated with age (r = 0.41, p < 0.01), BMI (r = 0.56, p < 0.0002) and ODI (r = 0.50, p < 0.002). Basal and induced HSP70 expression calculated across all groups showed a strong negative correlation (r = 0.74, p = 0.00001). Basal TNF-a levels in monocytes prior to exposing them to HS were negatively correlated with induced HSP70 expression (r = 0.43, p < 0.01). Using antibodies which neutralized TNF-a resulted in increased expression of induced HSP70 (530 ± 135 MFI vs. 546 ± 131 MFI, p = 0.03). Conclusions: The basal HSP70 expression reflects a stress response in OSA patients, whereas, the HS-induced response reflects a diminished protection from a subsequent severe stress. Intracellular TNF-a limits HSP70 inducibility and thus may decrease the protection of monocytes from oxidative stress and hypoxia in OSA. Age and obesity can further exacerbate these processes.
CSA). Patients with CHF and CSR-CSA revealed poor prognosis. Therefore the treatment of CSR-CSA has been developed. Recently, CPAP failed to show the mortality benefits in patients with CSR-CSA and CHF. Then, the other devices have been in focus. We firstly reported the efficacy of new adaptive servo-ventilation (ASV) device among Japanese CHF patients with CSR-CSA. Materials and methods: Four chronic CHF patients with moderate to severe sleep apnea which was dominantly consistent with CSR-CSA and was insufficiently treated with conventional positive air way pressure devices including continuous positive air way pressure (CPAP) or bi-level positive airway pressure (bi-level PAP) were undergone one night trial of new ASV device (Heart PAP, manufactured by Respironics). During first trial of this device, polysomnography (PSG) was simultaneously undergone. The improvement of the PSG findings on conventional positive airway pressure devices and on ASV was assessed. Results: On conventional PAP, the apnea–hypopnea index (AHI) and central AHI (CAHI) were significantly reduced (AHI 62.7 ± 10.1 to 17.8 ± 3.3/h, P = 0.02, CAHI 54.5 ± 6.7 to 13.5 ± 1.5, P = 0.02), however, there were moderate residual apnea events. The sleep quality expressed as arousal index, percentage of slow wave sleep (SWS) was moderately improved (ArI 62.0 ± 10.5 to 22.2 ± 5.3 /h, P = 0.03, percentages of SWS 2.6 ± 2.6 to 11.9 ± 4.1%, P = 0.24). On the other hand, both AHI and CAHI were also significantly improved on ASV (AHI 62.7 ± 10.1 to 5.9 ± 2.2 /h, P = 0.0006, CAHI 54.5 ± 6.7 to 5.6 ± 2.3 /h, P = 0.007) and there were less residual apnea events than on conventional PAP. In addition, both ArI and percentage of SWS were significantly improved on ASV (ArI 62.0 ± 10.5 to 18.7 ± 6.2 /h, P = 0.012, percentages of SWS 2.6 ± 2.6 to 19.1 ± 4.8%, P = 0.042). Conclusion: The CSR-CSA among Japanese patients with CHF was sufficiently improved with using this new ASV device.
doi:10.1016/j.sleep.2006.07.144
doi:10.1016/j.sleep.2006.07.145
P336 The experience of using new adaptive servo-ventilation device for treating Cheyne-Stokes respiration with central sleep apnea among Japanese patients with congestive heart failure Koji Narui 1, Takatoshi Kasai 1, Tomotaka Dohi 2
P337 Carotid artery stenosis and night breathing Karel Sonka 1, Zilla Onkova 2, Kate Svatova 1, Miroslav Kalina 2, Pavel Ebesta 2
1
Toranomon Hospital, Sleep Center, Tokyo, Japan Tranomon Hospital, Cardiovascular Center, Tokyo, Japan
2
Objectives: Several studies have shown that patients with congestive heart failure (CHF) often complicated Cheyne-Stokes respiration with central sleep apnea (CSR-
1
Charles University, 1st Med Faculty, Prague, Czech Republic 2 Hospital Na Homolce, Department of Neurology, Prague, Czech Republic Objectives: To evaluate sleep-related breathing disturbances (SBD) in patients suffering from carotid artery stenosis. SBD are closely related to cardiovascular morbidity. SBD is a risk factor for atherogenesis and for
S60
Abstracts / Sleep Medicine 7 (2006) S1–S127
stroke. According to some studies, however, impaired cerebral perfusion can induce sleep apnea. Design: Prospective clinical study in a specialised hospital setting. Methods and measurements: Consecutive patients indicated for endarterectomy because of major carotid stenosis were examined clinically and by means of unattended polygraphy (respiratory flow, chest and abdomen respiratory movements, oxygen saturation, respiratory noises, and leg movements). The patients had at the time of examination no residual neurological symptoms and no other vascular disorder (except coronary stenosis and hypertension). Results: Thirteen patients (5 women, 8 men, mean age 64.5 ± SD = 10.1 years) were examined. Six patients had undergone a transitory ischaemic attack (at least 5 weeks before polygraphy), 5 had no history of neurological symptoms, and 2 had in the past a stroke without any sequels. The mean Apnoea/Hypopnoea Index (AHI) was 12.7 ± 13.5, mean Oxygen Desaturation Index (ODI – number of oxygen saturation drops of 3% and more) 20.0 ± 16.5 and mean oxygen saturation 93.8 ± 2.0%. Mean time of saturation below 90% was 6.8% ± 18.0. Nine patients (69%) had AHI P 5. Two patients experienced SBD mainly in the supine position, central apnoeas were found in two patients. The polygraphic recording was repeated one month after endarterectomy in 8 patients and a non significantly lower AHI was found: 6.9 ± 6.1. Conclusions: The large number of patients meeting the criteria of AHI P 5 suggests a relationship between carotid artery stenosis and SBD. Supported by Ministry of Education grants ME 701 and 0021620816. doi:10.1016/j.sleep.2006.07.146
P338 Effect of a 1-year treatment with sibutramine on blood pressure in obese at risk patients with obstructive sleep apnea Sara Croteau, Annie Ferland, Paul Poirier, Diane Page, Fre´de´ric Se´rie`s Centre de recherche de l’Hoˆpital Laval, Institut universitaire de cardiologie et de pneumologie de l’Universite´ Laval, Sainte-Foy, Que., Canada Objectives: To assess the effects of sibutramine on systolic (SBP) and diastolic blood pressure (DBP) in patients with obstructive sleep apnea syndrome (OSAS). Methods and measurements: Twenty-two patients with a body mass index (BMI) P 30 kg/m2, with OSAS and well-controlled hypertension or normotension were recruited. Subjects received a sibutramine treatment (10 or 15 mg daily) for 1-year, associated with a personalized
dietary and physical exercise recommendations. Ambulatory blood pressure monitoring (ABPM) was performed before and after the 1-year treatment of sibutramine. Results: After 1-year of sibutramine treatment, subjects lost 5.4 ± 1.4 kg (mean ± SEM, P < 0.001). Reduction in waist circumference (116 ± 2 vs. 108 ± 3 cm, P < 0.001) and body mass index (35.1 ± 1.9 vs. 33.4 ± 1.9 kg/m2, P < 0.001) were also observed. At baseline, 11 subjects met the metabolic syndrome criteria compared to 9 subjects following the 1-year treatment. ABPM data showed that mean SBP and DBP were not significantly different after treatment in comparison with baseline (133 ± 2 vs. 132 ± 2 mmHg for SBP and 82 ± 1 vs. 84 ± 2 mmHg for DBP). No significant difference was also observed in day-time and nighttime mean SBP and DSB, and mean heart rate (HR). Conclusion: A 1-year sibutramine treatment did not change SBP and DBP, and had no effect on HR in obese OSAS patients with or without the metabolic syndrome. The associated impact of weight loss on SBP and DBP observed following a 1-year treatment of sibutramine might have attenuated by the potential hypertensive effect of sibutramine per se. Supported by Abbott laboratories doi:10.1016/j.sleep.2006.07.147
P339 Impact of sibutramine on cardiac autonomic nervous system in obese patients with obstructive sleep apnea syndrome Annie Ferland, Sara Croteau, Fre´de´ric Se´rie`s, Diane Page, Paul Poirier Centre de recherche de l’Hoˆpital Laval, Institut universitaire de cardiologie et de pneumologie de l’Universite´ Laval, Sainte-Foy, Que., Canada Objectives: To investigate the impact of sibutramine-induced weight loss on cardiovascular autonomic function in obese patients with obstructive sleep apnea syndrome (OSAS). Methods and measurements: Twenty-two obese subjects (BMI of 35.1 ± 1.9 kg/m2) with OSAS underwent a 1year sibutramine treatment (10 or 15 mg) combined with dietary and physical exercise recommendations. Heart rate variability (HRV) was derived from a 24-h Holter monitoring, performed at two occasions (baseline and after 1 year). Using frequency domains, power in the very-low frequency (VLF), low frequency (LF), LF/high frequency (HF) was calculated. Using time domains, the mean NN, the SDNN, the SDANN, the rMSSD and the pNN50 indices were determined. Results: After a 1-year treatment of sibutramine, there were a 5% decrease in weight, a 7% reduction in waist circumference and an increase of HDL-cholesterol levels