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260 GRADUATION FROM CPAP: IS WHAT PATIENTS WANT REALLY POSSIBLE?
S70
Abstracts of 3rd International Congress of the Association of Sleep Medicine (WASM) / Sleep Medicine 10, Suppl. 2 (2009) S1–S83
changes may exceed the normal range and, when associated with other factors, constitute pathology, i.e., sleep apnea. The pathophysiology underlying apnea is not completely known, and we hypothesize that cortical electrical activity may be somehow involved. The question is: Is there a possibility that the EEG exhibits changes prior to the apnea signs, or are the EEG changes a consequence of sleep apnea? Methods: Five patients were studied with conventional polysomnographic recordings (PSG). The EEG power (Fast Fourier Transform, FFT) of the different sleep stages was analyzed studying the delta (δ, 0.5-2.5 c/s), theta (θ, 3-7 c/s), alpha (α, 8-12 c/s) and beta (β, >12 c/s) brain rhythms separately. A 2 s temporal window for each sleep stage power analysis was used. Temporal windows were considered for study in three different situations: a) during sleep epochs without apnea (control recording), b) during sleep with apnea and, c) immediately prior to the apnea episodes. The statistical analysis of the different situations was carried out with the Student’s t-test. Results and Discussion: Statistically significant increments were found in the power spectra of delta and theta waves (FFT) during periods of sleep stages I and II as well as paradoxical sleep with apnea, while non-significant changes in the power of the alpha and beta rhythms were observed. Additionally, the EEG power showed no differences between “control” temporal windows and the windows immediately previous to the apnea episodes. The temporal correlation between changes in delta and theta power and apneas could correspond to functional cortical organization shifts, which may be part of a general warning network to resume waking and bring the apnea episode to an end. It is still a question whether the EEG changes are a consequence or a sign of the beginning of apnea.
259
SLEEP EVALUATION IN PATIENTS WITH MUCOPOLYSACCHARIDOSIS TYPE VI
A. John 1 , S. Fagondes 1 , I. Schwartz 2 , A.C. Azevedo 2 , P. Barrios 3 , P. Dalcin 4 , S.M. Barreto 4 , R. Giugliani 2 . 1 Sleep disorder center, Pulmonology Service Hospital de Clínicas de Porto Alegre; 2 Medical Genetics Service - Hospital de Clínicas de Porto Alegre; 3 Cardiology Service - Hospital de Clínicas de Porto Alegre; 4 Pulmonology Service - Hospital de Clínicas de Porto Alegre Introduction: Mucopolysaccharidosis type VI (MPS VI) is a lysosomal storage disease affecting an enzyme responsible for the degradation of glycosaminoglycans (GAGs). Partially degraded GAGs accumulate in the upper airways and may cause obstructive sleep apnea (OSA). Objectives: To determine the prevalence of OSA in a group of MPS VI patients who had no previous treatment and to determine the association of OSA with clinical and echocardiographic findings. Methods: Twenty-eight patients, aged 4 years or older with biochemical confirmation of MPS VI, were included. Fourteen of the patients were boys and the mean age was 98.5 months. Clinical history, physical examination, transthoracic echocardiogram, and overnight polysomnography (PSG) results were collected. Results: The most frequent clinical signs during sleep were snoring and witnessed apnea. Physical examination revealed that 78.6% had macroglossia and 82.1% pectus carinatum. Nine patients had undergone adenotonsillectomy or adenoidectomy. Polysomnography results showed that 23 out of 27 patients (85.1%) had OSA. Mean apnea-hypopnea index (AHI) was 19.8±26.3 events/hour; mean oxygen saturation (SpO2) was 93.3±5%, mean nadir SpO2 was 80.3±10%. Echocardiogram showed evidence of pulmonary hypertension (PH) in 14 subjects. Lower mean SpO2 and nadir SpO2 were positively associated with PH (p=0.037 for mean; p=0.007 for nadir). Witnessed apnea was the most important predictor of PH in this sample (p=0.016; OR 9.9; CI 1.5 to 63.7). Clinical signs suggestive of respiratory abnormalities during sleep were not significantly correlated with the PSG results. Conclusion: The prevalence of OSA in patients with MPS VI is elevated, and the level of desaturation was positively correlated with PH.
260
GRADUATION FROM CPAP: IS WHAT PATIENTS WANT REALLY POSSIBLE?
M. Kawai 1 , S. Fujii 2 , K. Yamamoto 2 , S. Koike 2 . 1 The Methodist Hospital; Toyohashi Mates Sleep Center
2
Introduction: Only limited data is available on how frequently patients are interested in discontinuation of CPAP or whether it is possible to discontinue CPAP with weight reduction or with other interventions.
Objectives: To identify the actual prevalence of interest in discontinuation of CPAP treatment and to analyze whether it is possible to discontinue CPAP treatment. Methods: We gathered questions from patients currently on CPAP treatment. They were requested to ask any questions they were most interested in. Subsequently retrospective reviews of medical charts were performed in all patients diagnosed as OSA who underwent polysomnogram (PSG) and CPAP titration in Toyohashi Mates clinic, Toyohashi, Japan from September 2001 to November 2008. After initial CPAP titration, follow-up PSG was performed when the patients requested to be reexamined in order to determine whether CPAP was able to be discontinued. Results: Among 106 patients who responded, the most frequent question (31 patients) was related to whether or how they can discontinue the usage of CPAP. We identified a total of 1,459 patients who were followed in our clinic after introduction of CPAP treatment. 1,246 were men and 213 were women. Average age, average AHI, mean BMI and mean follow-up period were 51.4 years, 52.0, 26.8 kg/m2 and 571.8 days. In 28 patients, CPAP treatment was discontinued due to improvement of AHI to less than 20 in the follow-up studies, because CPAP treatment is not approved by the Japanese national insurance system if AHI is less than 20. CPAP was discontinued in 6 patients without OA or surgery (group 1). 16 patients required oral appliances (OA) (group 2) and 6 patients required surgical interventions (tonsillectomy or uvulopalatopharyngoplasty) (group 3). Average BMI change in group 1, 2, and 3 was -1.71, -0.49 and -1.16, respectively. Average ESS was 5, 10.4 and 10.33. Average AHI was 11.5, 8.44 and 9.66. Compared with average BMI change, ESS and AHI in patients currently on CPAP (-0.12, 5.25 and 3.89), BMI was more reduced in group 1 (p=0.018), ESS was higher in group 2 and 3 but not in group 1, and AHI was higher in all groups, with statistical significance. Conclusion: Even though many patients are interested, discontinuation of CPAP treatment without intervention seems possible only in a small group of patients with significant weight reduction or alternative treatment with OA or surgery. In our patients, ESS did not decrease after discontinuation of CPAP treatment, though AHI scores rose.
261
THE RELATIONSHIP BETWEN SLEEP APNEA AND CORONARY ARTERY DISEASE RISK FACTORS
C. Klein 1 , F.S. Hackenhaar 1 , F.M. Suris 1 , T.M. Machado 1 , M.S. Benfatto 1 , D. Massierer 2 , M.V. Wainstein 2 , S.C. Gonçalves 2 , F.D. Fuchs 2 , D. Martinez 2 . 1 Departamento de Biofísica, PPG em Biologia Celular e Molecular, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brasil; 2 Cardiology Division, Hospital de Clinicas de Porto Alegre, Brazil Introduction: Sleep apnea is associated with coronary artery disease. The risk factors for both conditions, however, are similar and may confound the analyses. Investigations of the lipid profile are routine in the adult population, even without symptoms or suspected cardiac ailment. Sleep apnea remains underdiagnosed in spite of clear clinical manifestations. Objectives: To verify the association between sleep apnea and coronary artery disease (CAD) adjusting for other CAD risk factors. Methods: We included patients who underwent diagnostic or therapeutic coronariography and portable type III polysomnography. The severity of SA was determined by the apnea-hypopnea index (AHI). We measured classic CAD risk factors such as fasting glucose; total, HDL, and LDL cholesterols; triglycerides, uric acid, and C-reactive protein. We excluded patients older than 65 years, with body mass index (BMI) higher than 40 kg/m2 , diabetes, or smoking history in the last year. Results: Of 56 patients, 28 had AHI > 15 and 9.2 times higher risk of CAD (95% confidence interval: 2.7-31.0) in comparison to the 28 patients with IAH < 15 (p=0.031). Patients without CAD (n=30), when compared with CAD cases (n=26), showed respectively: AHI, 11±11/h vs. 23±14/h (p=0.001); age, 51±7 vs. 57±6 years (p=0.003); and HDL cholesterol, 51±13 vs. 40±12 mg/dL (p=0.003). The CAD and non-CAD groups did not differ in terms of BMI, glucose, total cholesterol, LDL cholesterol, triglycerides, uric acid or Creactive protein. In a binary logistic regression stepwise model to predict CAD, controlling for the above risk factors, the only variable entered in the model was AHI (odds ratio = 2; 1.3-3.1). Increase of one AHI unit (1 AH/hour) raises the risk of CAD 3 to 17%. Conclusion: These results, from a sample without smokers, morbidly obese or diabetic patients, support the involvement of sleep apnea as the main risk factor for coronary artery disease. The results suggest that assessing the AHI should be part of the clinical investigation for coronariopathy.
Abstracts of 3rd International Congress of the Association of Sleep Medicine (WASM) / Sleep Medicine 10, Suppl. 2 (2009) S1–S83
changes may exceed the normal range and, when associated with other factors, constitute pathology, i.e., sleep apnea. The pathophysiology underlying apnea is not completely known, and we hypothesize that cortical electrical activity may be somehow involved. The question is: Is there a possibility that the EEG exhibits changes prior to the apnea signs, or are the EEG changes a consequence of sleep apnea? Methods: Five patients were studied with conventional polysomnographic recordings (PSG). The EEG power (Fast Fourier Transform, FFT) of the different sleep stages was analyzed studying the delta (δ, 0.5-2.5 c/s), theta (θ, 3-7 c/s), alpha (α, 8-12 c/s) and beta (β, >12 c/s) brain rhythms separately. A 2 s temporal window for each sleep stage power analysis was used. Temporal windows were considered for study in three different situations: a) during sleep epochs without apnea (control recording), b) during sleep with apnea and, c) immediately prior to the apnea episodes. The statistical analysis of the different situations was carried out with the Student’s t-test. Results and Discussion: Statistically significant increments were found in the power spectra of delta and theta waves (FFT) during periods of sleep stages I and II as well as paradoxical sleep with apnea, while non-significant changes in the power of the alpha and beta rhythms were observed. Additionally, the EEG power showed no differences between “control” temporal windows and the windows immediately previous to the apnea episodes. The temporal correlation between changes in delta and theta power and apneas could correspond to functional cortical organization shifts, which may be part of a general warning network to resume waking and bring the apnea episode to an end. It is still a question whether the EEG changes are a consequence or a sign of the beginning of apnea.
259
SLEEP EVALUATION IN PATIENTS WITH MUCOPOLYSACCHARIDOSIS TYPE VI
A. John 1 , S. Fagondes 1 , I. Schwartz 2 , A.C. Azevedo 2 , P. Barrios 3 , P. Dalcin 4 , S.M. Barreto 4 , R. Giugliani 2 . 1 Sleep disorder center, Pulmonology Service Hospital de Clínicas de Porto Alegre; 2 Medical Genetics Service - Hospital de Clínicas de Porto Alegre; 3 Cardiology Service - Hospital de Clínicas de Porto Alegre; 4 Pulmonology Service - Hospital de Clínicas de Porto Alegre Introduction: Mucopolysaccharidosis type VI (MPS VI) is a lysosomal storage disease affecting an enzyme responsible for the degradation of glycosaminoglycans (GAGs). Partially degraded GAGs accumulate in the upper airways and may cause obstructive sleep apnea (OSA). Objectives: To determine the prevalence of OSA in a group of MPS VI patients who had no previous treatment and to determine the association of OSA with clinical and echocardiographic findings. Methods: Twenty-eight patients, aged 4 years or older with biochemical confirmation of MPS VI, were included. Fourteen of the patients were boys and the mean age was 98.5 months. Clinical history, physical examination, transthoracic echocardiogram, and overnight polysomnography (PSG) results were collected. Results: The most frequent clinical signs during sleep were snoring and witnessed apnea. Physical examination revealed that 78.6% had macroglossia and 82.1% pectus carinatum. Nine patients had undergone adenotonsillectomy or adenoidectomy. Polysomnography results showed that 23 out of 27 patients (85.1%) had OSA. Mean apnea-hypopnea index (AHI) was 19.8±26.3 events/hour; mean oxygen saturation (SpO2) was 93.3±5%, mean nadir SpO2 was 80.3±10%. Echocardiogram showed evidence of pulmonary hypertension (PH) in 14 subjects. Lower mean SpO2 and nadir SpO2 were positively associated with PH (p=0.037 for mean; p=0.007 for nadir). Witnessed apnea was the most important predictor of PH in this sample (p=0.016; OR 9.9; CI 1.5 to 63.7). Clinical signs suggestive of respiratory abnormalities during sleep were not significantly correlated with the PSG results. Conclusion: The prevalence of OSA in patients with MPS VI is elevated, and the level of desaturation was positively correlated with PH.
260
GRADUATION FROM CPAP: IS WHAT PATIENTS WANT REALLY POSSIBLE?
M. Kawai 1 , S. Fujii 2 , K. Yamamoto 2 , S. Koike 2 . 1 The Methodist Hospital; Toyohashi Mates Sleep Center
2
Introduction: Only limited data is available on how frequently patients are interested in discontinuation of CPAP or whether it is possible to discontinue CPAP with weight reduction or with other interventions.
Objectives: To identify the actual prevalence of interest in discontinuation of CPAP treatment and to analyze whether it is possible to discontinue CPAP treatment. Methods: We gathered questions from patients currently on CPAP treatment. They were requested to ask any questions they were most interested in. Subsequently retrospective reviews of medical charts were performed in all patients diagnosed as OSA who underwent polysomnogram (PSG) and CPAP titration in Toyohashi Mates clinic, Toyohashi, Japan from September 2001 to November 2008. After initial CPAP titration, follow-up PSG was performed when the patients requested to be reexamined in order to determine whether CPAP was able to be discontinued. Results: Among 106 patients who responded, the most frequent question (31 patients) was related to whether or how they can discontinue the usage of CPAP. We identified a total of 1,459 patients who were followed in our clinic after introduction of CPAP treatment. 1,246 were men and 213 were women. Average age, average AHI, mean BMI and mean follow-up period were 51.4 years, 52.0, 26.8 kg/m2 and 571.8 days. In 28 patients, CPAP treatment was discontinued due to improvement of AHI to less than 20 in the follow-up studies, because CPAP treatment is not approved by the Japanese national insurance system if AHI is less than 20. CPAP was discontinued in 6 patients without OA or surgery (group 1). 16 patients required oral appliances (OA) (group 2) and 6 patients required surgical interventions (tonsillectomy or uvulopalatopharyngoplasty) (group 3). Average BMI change in group 1, 2, and 3 was -1.71, -0.49 and -1.16, respectively. Average ESS was 5, 10.4 and 10.33. Average AHI was 11.5, 8.44 and 9.66. Compared with average BMI change, ESS and AHI in patients currently on CPAP (-0.12, 5.25 and 3.89), BMI was more reduced in group 1 (p=0.018), ESS was higher in group 2 and 3 but not in group 1, and AHI was higher in all groups, with statistical significance. Conclusion: Even though many patients are interested, discontinuation of CPAP treatment without intervention seems possible only in a small group of patients with significant weight reduction or alternative treatment with OA or surgery. In our patients, ESS did not decrease after discontinuation of CPAP treatment, though AHI scores rose.
261
THE RELATIONSHIP BETWEN SLEEP APNEA AND CORONARY ARTERY DISEASE RISK FACTORS
C. Klein 1 , F.S. Hackenhaar 1 , F.M. Suris 1 , T.M. Machado 1 , M.S. Benfatto 1 , D. Massierer 2 , M.V. Wainstein 2 , S.C. Gonçalves 2 , F.D. Fuchs 2 , D. Martinez 2 . 1 Departamento de Biofísica, PPG em Biologia Celular e Molecular, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brasil; 2 Cardiology Division, Hospital de Clinicas de Porto Alegre, Brazil Introduction: Sleep apnea is associated with coronary artery disease. The risk factors for both conditions, however, are similar and may confound the analyses. Investigations of the lipid profile are routine in the adult population, even without symptoms or suspected cardiac ailment. Sleep apnea remains underdiagnosed in spite of clear clinical manifestations. Objectives: To verify the association between sleep apnea and coronary artery disease (CAD) adjusting for other CAD risk factors. Methods: We included patients who underwent diagnostic or therapeutic coronariography and portable type III polysomnography. The severity of SA was determined by the apnea-hypopnea index (AHI). We measured classic CAD risk factors such as fasting glucose; total, HDL, and LDL cholesterols; triglycerides, uric acid, and C-reactive protein. We excluded patients older than 65 years, with body mass index (BMI) higher than 40 kg/m2 , diabetes, or smoking history in the last year. Results: Of 56 patients, 28 had AHI > 15 and 9.2 times higher risk of CAD (95% confidence interval: 2.7-31.0) in comparison to the 28 patients with IAH < 15 (p=0.031). Patients without CAD (n=30), when compared with CAD cases (n=26), showed respectively: AHI, 11±11/h vs. 23±14/h (p=0.001); age, 51±7 vs. 57±6 years (p=0.003); and HDL cholesterol, 51±13 vs. 40±12 mg/dL (p=0.003). The CAD and non-CAD groups did not differ in terms of BMI, glucose, total cholesterol, LDL cholesterol, triglycerides, uric acid or Creactive protein. In a binary logistic regression stepwise model to predict CAD, controlling for the above risk factors, the only variable entered in the model was AHI (odds ratio = 2; 1.3-3.1). Increase of one AHI unit (1 AH/hour) raises the risk of CAD 3 to 17%. Conclusion: These results, from a sample without smokers, morbidly obese or diabetic patients, support the involvement of sleep apnea as the main risk factor for coronary artery disease. The results suggest that assessing the AHI should be part of the clinical investigation for coronariopathy.