Objetivos: Determinar o tempo de espera para o diagnóstico e início do tratamento da síndrome da apneia obstrutiva do sono (SAOS) em hospital público brasileiro. Desenho do estudo: Estudo transversal. Métodos: Foi avaliada, com um questionário específico, uma amostra de conveniência composta por 68 pacientes com síndrome da apneia obstrutiva do sono (SAOS), com indicação de tratamento com pressão positiva em vias aéreas (PAP) e que utilizaram o aparelho durante acompanhamento ambulatorial, no período de janeiro de 2005 a dezembro de 2009. Foram excluídos os pacientes menores de 18 anos, incapazes de responder ao questionário ou que se negaram a participar. Resultados: Dos pacientes avaliados, a maioria era de homens (62%), com média de idade de 54,4 (+ 10,7) anos e obesos (IMC médio 33,7 + 7,1 Kg/m2); 76% eram hipertensos, 22% portadores de diabete melito e igual número de doença arterial coronariana; 10% destes apresentavam hipoventilação associada. A mediana do tempo entre a primeira consulta médica e a realização da PSG diagnóstica foi de 8,3 (intervalos interquartis [IQ] 3,3-14,3) meses e a mediana do tempo da indicação da PAP até a aquisição do aparelho foi de 10,5 (IQ 3,1-16,7) meses. Sessenta e quatro pacientes (94%) eram usuários de CPAP e 4 usuários de bilevel (6%). A maioria dos aparelhos (57%) foi obtida de forma gratuita por meio da rede pública de saúde. Conclusão: O presente estudo evidenciou a demora excessiva para diagnóstico e tratamento dos pacientes portadores de SAOS em atendimento em um hospital público de referência no Brasil. / Objectives: To determine the waiting time for the diagnosis and beginning of treatment of syndrome of obstructive sleep apnea (OSA) in Brazilian public hospital. Study design: cross-sectional study Methods: A convenience sample composed of 68 patients with syndrome of obstructive sleep apnea (OSA) was assessed through a specific questionnaire. All patients were indicated a treatment with positive airway pressure (PAP) and that used the unit during de period between January 2005 and December 2009. Patients who were under 18 years old, who were uncapable of answering the questionnaire or who refused to answer were excluded. Results: Among the patients, the majority were men (62%), with an average age of 54.4 (+10.7) years and obese (mean BMI 33.7 + 7.1 kg/m2); 76% were hypertensive, 22% diabetes mellitus patients and an equal number with coronary artery disease, 10% of them had associated hypoventilation. The average time between the first medical consultation and the implementation of diagnostic PSG was 8.3 (interquartile range [IQ] 3.3 to 14.3) months and the average time indication of the PAP until the purchase of the equipment was 10,5 (CI 3.1 to 16.7) months. Sixty-four patients (94%) were users of CPAP and 4 were users of bilevel (6%). Most appliances (57%) were obtained free of charge through the public health system. Conclusion: The present study demonstrated the excessive delay to diagnosis and treatment of patients with OSAS in attendance at a public hospital of reference in Brazil.

Ng, Mei. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves xvi-xlviii). / Abstracts in English and Chinese. / ACKNOWLEDGEMENTS --- p.i / ABSTRACT / In English --- p.ii / In Chinese --- p.iv / LIST OF TABLES --- p.vi / LIST OF FIGURE --- p.viii / ABBREVIATIONS / For Units --- p.ix / For Prefixes of the International System of Units --- p.ix / For Terms Commonly Used --- p.X / Chapter CHAPTER 1 --- Overview of Childhood Obstructive Sleep Apnoea Syndrome (OSAS) / Chapter 1.1 --- Prevalence --- p.1 / Chapter 1.2 --- Clinical Features --- p.3 / Chapter 1.3 --- Definitions and Cutoffs --- p.4 / Chapter 1.4 --- Pathophysiology --- p.6 / Chapter 1.5 --- Risk Factors / Chapter 1.5.1 --- Gender --- p.8 / Chapter 1.5.2 --- Obesity --- p.9 / Chapter 1.5.3 --- Adenotonsillar Hypertrophy --- p.10 / Chapter 1.5.4 --- Genetic --- p.11 / Chapter 1.5.5 --- Atopic Diseases --- p.12 / Chapter 1.6 --- Complications / Chapter 1.6.1 --- Neurobehavioural Deficits --- p.13 / Chapter 1.6.2 --- Growth Defects --- p.14 / Chapter 1.6.3 --- Metabolic Disorders --- p.16 / Chapter 1.6.4 --- Systemic inflammation --- p.17 / Chapter 1.6.5 --- Cardiovascular Consequences --- p.19 / Chapter 1.7 --- Diagnosis --- p.20 / Chapter 1.8 --- Treatment / Chapter 1.8.1 --- Surgical Treatment --- p.22 / Chapter 1.8.2 --- Continuous Positive Airway Pressure (CPAP) --- p.24 / Chapter 1.8.3 --- Corticosteroids --- p.24 / Chapter 1.8.4 --- Leukotriene Receptor Antagonist --- p.25 / Chapter 1.8.5 --- Oral Appliances --- p.26 / Chapter 1.8.6 --- Weight Control --- p.27 / Chapter CHAPTER 2 --- OSAS and Cardiovascular Complications in Adults / Chapter 2.1 --- Mechanism / Chapter 2.1.1 --- Acute Cardiovascular Responses --- p.28 / Chapter 2.1.2 --- Chronic Cardiovascular Responses --- p.29 / Chapter 2.2 --- Hypertension / Chapter 2.2.1 --- Epidemiological and Clinical Data --- p.31 / Chapter 2.2.2 --- Characteristics --- p.32 / Chapter 2.2.3 --- Mechanisms --- p.33 / Chapter 2.2.4 --- Treatment --- p.34 / Chapter 2.3 --- Heart Failure --- p.35 / Chapter 2.4 --- Stroke --- p.37 / Chapter 2.5 --- Cardiac Arrhythmias --- p.39 / Chapter 2.6 --- Myocardial Ischemia and Vascular Disease --- p.41 / Chapter 2.7 --- Pulmonary Hypertension --- p.43 / Chapter CHAPTER 3 --- OSAS and cardiovascular complication in children / Chapter 3.1 --- Blood Pressure --- p.45 / Chapter 3.2 --- Ventricular Hypertrophy and Dysfunctions --- p.48 / Chapter 3.3 --- Heart Rate Variability --- p.50 / Chapter 3.4 --- Arterial Tone --- p.51 / Chapter 3.5 --- Endothelial Function --- p.51 / Chapter CHAPTER 4 --- Longitudinal follow-up study of children with OSAS - a cardiovascular perspective / Chapter 4.1 --- Introduction --- p.53 / Chapter 4.2 --- Methods / Chapter 4.2.1 --- Subjects and Study Design --- p.57 / Chapter 4.2.2 --- Polysomnography --- p.59 / Chapter 4.2.3 --- Ambulatory Blood Pressure Measurement --- p.61 / Chapter 4.2.4 --- Statistical Analysis --- p.62 / Chapter 4.3 --- Results / Chapter 4.3.1 --- Subject Characteristics --- p.64 / Chapter 4.3.2 --- Blood Pressure During Wakefulness --- p.71 / Chapter 4.3.3 --- Blood Pressure During Sleep --- p.76 / Chapter 4.3.4 --- Nocturnal Blood Pressure Dipping --- p.83 / Chapter 4.3.5 --- Blood Profile --- p.86 / Chapter 4.4 --- Discussion --- p.87 / Chapter 4.5 --- Conclusion --- p.99 / Reference List --- p.xvi

Leung, Kin Ling. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 133-162). / Abstracts in English and Chinese. / CONTENTS --- p.i / ACKNOWLEDGEMENTS --- p.ii / ABBREVIATIONS --- p.iii / ABSTRACT --- p.vi / 論文摘要 --- p.ix / Chapter CHAPTER 1 --- INTRODUCTION --- p.1 / Chapter 1.1 --- Obstructive sleep apnea syndrome --- p.1 / Chapter 1.1.1 --- Symptoms of OSA --- p.2 / Chapter 1.1.2 --- Causes of OSA --- p.5 / Chapter 1.1.3 --- Complications of OSA --- p.6 / Chapter 1.1.4 --- Episodic hypoxia profile --- p.9 / Chapter 1.2 --- Hippocampus --- p.12 / Chapter 1.2.1 --- General structure of hippocampus --- p.12 / Chapter 1.2.2 --- The neuronal circuitry of hippocampus --- p.17 / Chapter 1.2.3 --- Cell types of hippocampus --- p.21 / Chapter 1.2.4 --- Functions of hippocampus --- p.24 / Chapter 1.3 --- Memory Formation and long term potentiation --- p.27 / Chapter 1.4 --- Neurotrophins --- p.33 / Chapter 1.5 --- Brain-derived neurotrophic factor (BDNF) --- p.38 / Chapter 1.5.1 --- Molecular characteristics of BDNF --- p.38 / Chapter 1.5.3 --- Functions of BDNF --- p.46 / Chapter 1.5.4 --- BDNF and neuronal plasticity --- p.46 / Chapter 1.6 --- Tissue plasminogen activator - plasmin system --- p.51 / Chapter 1.6.1 --- Molecular characteristics of tissue plasminogen activator - plasmin system --- p.51 / Chapter 1.6.2 --- Functions of tissue plasminogen activator - plasmin system --- p.54 / Chapter 1.7 --- Aim of the study --- p.59 / Chapter CHAPTER 2 --- MATERIALS AND METHODS --- p.61 / Chapter 2.1 --- Animal model of obstructive sleep apnea --- p.61 / Chapter 2.1.1 --- Intermittent hypoxia --- p.61 / Chapter 2.2 --- Electrophysiological recordings --- p.65 / Chapter 2.2.1 --- Preparation of brain slices --- p.65 / Chapter 2.2.1 --- Visualization of hippocampus CA1 Neurons --- p.66 / Chapter 2.2.3 --- Patch-clamp recordings --- p.66 / Chapter 2.3 --- Protein analysis - ELISA --- p.71 / Chapter 2.3.1 --- Isolation of mouse hippocampus total protein --- p.71 / Chapter 2.3.2 --- ELISA --- p.72 / Chapter 2.3 --- Protein analysis (II) - Western blot --- p.74 / Chapter 2.4.1 --- Isolation of mouse hippocampus total protein --- p.74 / Chapter 2.4.2 --- Western blot analysis --- p.75 / Chapter 2.5 --- Data analysis --- p.78 / Chapter CHAPTER 3 --- RESULTS --- p.79 / Chapter 3.1 --- Effect of intermittent hypoxia on passive and active properties of hippocampal CA1 neurons --- p.79 / Chapter 3.1.1 --- Passive properties --- p.79 / Chapter 3.1.2 --- Membrane excitability --- p.83 / Chapter 3.1.3 --- Action potential characteristics --- p.93 / Chapter 3.2 --- Effect of intermittent hypoxia on the expression of BDNF and related proteins --- p.104 / Chapter 3.2.1 --- "Levels of total BDNF, NGF, NT-3 and NT-4/5" --- p.104 / Chapter 3.2.2 --- Recovery study of the expression of BDNF after IH treatment --- p.110 / Chapter 3.2.3 --- Differential effect of IH on pro-BDNF and mature BDNF --- p.114 / Chapter 3.2.4 --- "Expressions of tissue plasminogen activator, plasmin and plasminogen" --- p.117 / Chapter Chapter 4 --- Discussion --- p.121 / Chapter 4.1 --- Changes in neuronal excitability of CA1 neurons under intermittent hypoxia --- p.121 / Chapter 4.2 --- Intermittent hypoxia-induced changes in BDNF level --- p.127 / Chapter 4.3 --- Conclusion --- p.130 / REFERENCES --- p.133

Au, Chun Ting. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves xxvii-lv). / Abstracts in English and Chinese. / ACKNOWLEDGEMENTS --- p.i / ABSTRACT / In English --- p.ii / In Chinese --- p.v / LIST OF TABLES --- p.vii / ABBREVIATIONS / For Units --- p.ix / For Prefixes of the international system of units --- p.ix / For Terms commonly used in the report --- p.x / STATEMENT OF WORK DONE --- p.xvi / Chapter CHAPTER 1 --- Overview of Childhood Obstructive Sleep Apnea Syndrome (OSAS) / Chapter 1.1. --- Clinical Features of Childhood OSAS --- p.1 / Chapter 1.2. --- Definition of Childhood OSAS --- p.2 / Chapter 1.3. --- Prevalence of Childhood OSAS --- p.3 / Chapter 1.4. --- Pathophysiology --- p.4 / Chapter 1.5. --- Risk Factors --- p.6 / Chapter 1.6. --- Diagnosis --- p.10 / Chapter 1.7. --- Treatment / Chapter 1.7.1. --- Tonsillectomy and Adenoidectomy (T&A) --- p.12 / Chapter 1.7.2. --- Continuous Positive Airway Pressure (CPAP) --- p.14 / Chapter 1.7.3. --- Corticosteroids --- p.15 / Chapter 1.7.4. --- Leukotriene Receptor Antagonist --- p.16 / Chapter 1.8. --- Complications of Childhood OSAS / Chapter 1.8.1. --- Growth Failure --- p.17 / Chapter 1.8.2. --- Neurocognitive Abnormalities --- p.19 / Chapter 1.8.3. --- Cardiovascular Abnormalities --- p.20 / Chapter CHAPTER 2 --- Cardiovascular Complications of OSAS in Adults (Literature Review) / Chapter 2.1. --- Acute Effects of OSAS on Cardiovascular System --- p.21 / Chapter 2.2. --- Chronic Effects of OSAS on Cardiovascular System --- p.23 / Chapter 2.3. --- Hypertension --- p.24 / Chapter 2.4. --- Heart Failure --- p.28 / Chapter 2.5. --- Pulmonary Hypertension --- p.30 / Chapter 2.6. --- Arrhythmias --- p.31 / Chapter 2.7. --- Cardiac Ischemia and Vascular Disease --- p.33 / Chapter 2.8. --- Stroke --- p.34 / Chapter CHAPTER 3 --- Cardiovascular Complications of Childhood OSAS (Literature Review) / Chapter 3.1. --- Blood Pressure --- p.37 / Chapter 3.2. --- Ventricular Structure and Function --- p.40 / Chapter 3.3. --- Arterial Distensibility --- p.42 / Chapter 3.4. --- Heart Rate Variability --- p.42 / Chapter CHAPTER 4 --- Ambulatory Blood Pressure in Children with OSAS / Chapter 4.1. --- Introduction --- p.44 / Chapter 4.2. --- Methods / Chapter 4.2.1. --- Subjects and Study Design --- p.46 / Chapter 4.2.2. --- Polysomnography (PSG) --- p.47 / Chapter 4.2.3. --- Ambulatory Blood Pressure Measurement (ABPM) --- p.49 / Chapter 4.2.4. --- Statistical Analysis --- p.50 / Chapter 4.3. --- Results / Chapter 4.3.1. --- Subject Characteristics --- p.52 / Chapter 4.3.2. --- Blood Pressure during Wakefulness --- p.55 / Chapter 4.3.3. --- Blood Pressure during Sleep --- p.57 / Chapter 4.4. --- Discussion --- p.62 / Chapter 4.5. --- Conclusion --- p.70 / Chapter CHAPTER 5 --- Cardiac Remodeling and Dysfunction in Children with OSAS / Chapter 5.1. --- Introduction --- p.71 / Chapter 5.2. --- Methods / Chapter 5.2.1. --- Subjects and Study Design --- p.72 / Chapter 5.2.2. --- Polysomnography (PSG) --- p.74 / Chapter 5.2.3. --- Conventional Echocardiography --- p.75 / Chapter 5.2.4. --- Tissue Doppler Imaging --- p.76 / Chapter 5.2.5. --- Statistical Analysis --- p.77 / Chapter 5.3. --- Results / Chapter 5.3.1. --- Study Population --- p.79 / Chapter 5.3.2. --- Polysomnographic Findings --- p.79 / Chapter 5.3.3. --- Echocardiographic Findings / Chapter 5.3.3.1. --- Right Ventricle --- p.81 / Chapter 5.3.3.2. --- Left Ventricle --- p.83 / Chapter 5.3.4. --- Treatment Effect --- p.86 / Chapter 5.4. --- Discussion --- p.90 / Chapter 5.5. --- Conclusion --- p.95 / Chapter CHAPTER 6 --- Conclusion --- p.96 / APPENDIX I Hong Kong Children Sleep Questionnaire (Chinese) --- p.xvii / APPENDIX II Hong Kong Children Sleep Questionnaire (English) --- p.xxii / REFERENCES --- p.xxvii

INTRODUÇÃO: A apnéia obstrutiva do sono é uma doença altamente prevalente na população adulta e associada à morbidade significante. A polissonografia noturna é o método padrão ouro para o diagnóstico de apnéia obstrutiva do sono. Entretanto seu custo é elevado e a disponibilidade de leitos para polissonografia é muito inferior a demanda. Por esta razão, estratégias para otimizar o diagnóstico de apnéia obstrutiva do sono são urgentes e necessárias. O objetivo deste estudo foi o de comparar um exame diurno de polissonografia, de curta duração e através de sono induzido por benzodiazepínico com a polissonografia noturna para o diagnóstico de apnéia obstrutiva do sono. MÉTODOS: Foram estudamos 40 pacientes divididos em dois grupos baseados no resultado da polissonografia noturna (Índice de Apnéia e Hipopnéia = 15 eventos/hora). Os dezoito Indivíduos portadores de apnéia obstrutiva do sono (id= 46 + 9 anos) e os vinte e dois controles (id= 38 + 10 anos) foram submetidos a uma polissonografia diurna, de curta duração, com indução de sono através de infusão intravenosa lenta de midazolam. RESULTADOS: O sono induzido foi obtido em todos indivíduos. O tempo total de sono foi de 41,5 + 18,9 minutos. A maioria dos eventos respiratórios durante o sono induzido forma obstrutivos e similares aos observados durante a polissonografia noturna. Não houve diferença estatisticamente significativa entre o índice de apnéia e hipopnéia bem como com a saturação mínima de oxigênio obtido pela polissonografia noturna e com sono induzido nos grupos estudados (p>0,05). Reunindo os dois grupos, o índice de apnéia e hipopnéia e a menor saturação de oxigênio obtidos pelos dois métodos tiveram correlação significativa (r=0,67 e r=0,77, respectivamente). A sensibilidade e especificidade para o diagnóstico de apnéia obstrutiva do sono através do sono induzido foi 0,83 e 0,72 respectivamente. Nenhuma complicação foi observada durante o sono induzido. CONCLUSÃO: A polissonografia com sono induzido é um método rápido e seguro que pode ser uma alternativa a polissonografia noturna para o diagnóstico de apnéia obstrutiva do sono. / Polysomnography is the gold standard method for diagnosing obstructive sleep apnea. However, the gap between demand and capacity in performig polysomnography is a major healthcare problem. We sought to compare a short day-time induced sleep with full overnight standard PSG (full PSG) monitoring for the diagnosis of obstructive sleep apnea. We studied 40 patients classified into subjects with obstructive sleep apnea (n=18, age= 46.8 + 9.1yr) and controls (n=22, age= 38.5 + 10,7yr) groups, based on the results of a full polysomnography (apnea-hypopnea index >= 15 events/hour). All subjects underwent a short day-time polysomnography. Sleep was induced by slow intravenous drip infusion of midazolam and achived in all subjects. Total time of induced sleep was 41.5 ± 18.9 min. The majority of the respiratory events during induced sleep were obstructive and similar to that observed during full polysomnography. There was no difference between apnea-hypopnea index obtained by full and short polysomnography in obstructive sleep apnea and control groups (p>0,05). The same occured to lowest O2 saturation. Taken all together, apnea-hypopnea index and lowest O2 saturation during short polysomnography correlated well with full polysomnography (r=0,67 and r=0,77, respectively). Sensitivity and specificity for the diagnosis of obstructive sleep apnea by induced sleep was 0,83 and 0,72, respectively. No complications were observed. Induced sleep PSG by midazolan is a short and safe study that may represent an alternative for full polysomnography in the diagnosis of obstructive sleep apnea.

Introdução: É comum a associação entre apnéia do sono e a doença arterial coronária (DAC), devido a fatores predisponentes comuns como sexo masculino e obesidade. Entretanto, ainda não existe uma definição objetiva da relação entre apnéia e DAC. Objetivo: Avaliar se os episódios de isquemia miocárdica, a variabilidade da freqüência cardíaca (VFC) e as arritmias cardíacas de portadores de DAC sofrem alteração na presença da apnéia do sono. Métodos: Cinqüenta e três pacientes portadores de DAC foram submetidos à monitorização eletrocardiográfica ambulatorial de 48 horas e ao estudo do sono na primeira noite da monitorização. Os pacientes foram divididos de acordo com o índice de apnéia e hipopnéia (IAH) em: grupo Controle (IAH<=15) e grupo Apnéia (IAH>15). Os grupos foram comparados quanto à isquemia miocárdica, VFC e arritmias cardíacas ocorridas no período da vigília e do sono. Uma subanálise apenas com pacientes portadores de apnéia grave (IAH>30 - grupo Ap-Grave) foi realizada e comparada ao grupo Controle. A análise estatística foi realizada utilizando-se o teste de Mann-Whitney, teste de Fisher e teste T de student. Resultados: Não foram observadas diferenças nas características clínicas básicas entre os grupos, exceto pelos níveis de pressão arterial mais elevada no grupo Ap-Grave (p<0,05). Nenhum dos pacientes despertou por angina noturna; 75% foram submetidos a cateterismo cardíaco, sem diferença quanto à gravidade da DAC e aos valores da fração de ejeção. Foi registrada isquemia em 39 (73,58%) pacientes, com carga isquêmica de 2892,26 minutos na vigília e 1186 no sono. Na vigília, foi menor a duração dos episódios isquêmicos no grupo Ap- Grave (p<0,05); no período do sono não houve diferença entre os grupos. Não houve diferença nas medidas da VFC e arritmias entre os grupos. Não foram registradas pausas >2 segundos, fibrilação ou flutter atrial, ou qualquer tipo de bloqueio atrioventricular. Conclusão: A apnéia do sono não apresentou relação direta com isquemia miocárdica, variabilidade da freqüência cardíaca e arritmias cardíacas em pacientes portadores de DAC. / Introduction: It is common to associate obstructive sleep apnea (OSA) with coronary artery disease (CAD) given the common predisposing factors; however, there are still controversies on the influence of OSA in the progression of CAD. Objective: To assess if OSA causes any changes in myocardial ischemia episodes, heart rate variability (HRV) and cardiac arrhythmias in patients with CAD. Methods: Fifty-three people with CAD were submitted to ambulatory electrocardiographic monitoring and to polysomnography) simultaneously and divided according to the apnea-hypopnea index (AHI) into two groups: Control (AHI<=15) and Apnea (AHI>15). A sub analysis including only people with severe apnea (AHI>30) was done and compared with the control group. Results: Differences in the basic clinical characteristics between the groups were not found, except for higher blood pressure levels in the Severe Apnea Group (p<0.05). None of the patients woke up because of nocturnal angina. The groups did not differ in relation to the extension of coronary artery disease and ejection fraction values. Myocardial ischemia was recorded in 39 (73.58%) patients. The total ischemic burden was 2892.26 minutes while awake and 1186 minutes while asleep; the groups did not differ during sleep. There was also no significant difference in HRV and arrhythmia measurements between the groups. Pauses >2 seconds, fibrillation or atrial flutter or any type of atrioventricular blocks were not registered. Conclusion: OSA did not present a direct relationship with myocardial ischemia, heart rate variability and arrhythmias in patients with CAD.

Objetivos: Determinar o tempo de espera para o diagnóstico e início do tratamento da síndrome da apneia obstrutiva do sono (SAOS) em hospital público brasileiro. Desenho do estudo: Estudo transversal. Métodos: Foi avaliada, com um questionário específico, uma amostra de conveniência composta por 68 pacientes com síndrome da apneia obstrutiva do sono (SAOS), com indicação de tratamento com pressão positiva em vias aéreas (PAP) e que utilizaram o aparelho durante acompanhamento ambulatorial, no período de janeiro de 2005 a dezembro de 2009. Foram excluídos os pacientes menores de 18 anos, incapazes de responder ao questionário ou que se negaram a participar. Resultados: Dos pacientes avaliados, a maioria era de homens (62%), com média de idade de 54,4 (+ 10,7) anos e obesos (IMC médio 33,7 + 7,1 Kg/m2); 76% eram hipertensos, 22% portadores de diabete melito e igual número de doença arterial coronariana; 10% destes apresentavam hipoventilação associada. A mediana do tempo entre a primeira consulta médica e a realização da PSG diagnóstica foi de 8,3 (intervalos interquartis [IQ] 3,3-14,3) meses e a mediana do tempo da indicação da PAP até a aquisição do aparelho foi de 10,5 (IQ 3,1-16,7) meses. Sessenta e quatro pacientes (94%) eram usuários de CPAP e 4 usuários de bilevel (6%). A maioria dos aparelhos (57%) foi obtida de forma gratuita por meio da rede pública de saúde. Conclusão: O presente estudo evidenciou a demora excessiva para diagnóstico e tratamento dos pacientes portadores de SAOS em atendimento em um hospital público de referência no Brasil. / Objectives: To determine the waiting time for the diagnosis and beginning of treatment of syndrome of obstructive sleep apnea (OSA) in Brazilian public hospital. Study design: cross-sectional study Methods: A convenience sample composed of 68 patients with syndrome of obstructive sleep apnea (OSA) was assessed through a specific questionnaire. All patients were indicated a treatment with positive airway pressure (PAP) and that used the unit during de period between January 2005 and December 2009. Patients who were under 18 years old, who were uncapable of answering the questionnaire or who refused to answer were excluded. Results: Among the patients, the majority were men (62%), with an average age of 54.4 (+10.7) years and obese (mean BMI 33.7 + 7.1 kg/m2); 76% were hypertensive, 22% diabetes mellitus patients and an equal number with coronary artery disease, 10% of them had associated hypoventilation. The average time between the first medical consultation and the implementation of diagnostic PSG was 8.3 (interquartile range [IQ] 3.3 to 14.3) months and the average time indication of the PAP until the purchase of the equipment was 10,5 (CI 3.1 to 16.7) months. Sixty-four patients (94%) were users of CPAP and 4 were users of bilevel (6%). Most appliances (57%) were obtained free of charge through the public health system. Conclusion: The present study demonstrated the excessive delay to diagnosis and treatment of patients with OSAS in attendance at a public hospital of reference in Brazil.

Avaliou-se a arquitetura do sono e distúrbios respiratórios do sono (DRS) em crianças (6 a 12 meses) portadoras de doenças cardíacas congênitas (DCC) sem (DCC-NH) e com presença hipoxemia (DCC-H) durante a vigília. Foram estudadas 21 crianças através de polissonografia noturna (7 DCC-NH, 7 DCC-H e 7 controles). O índice de distúrbios respiratórios (eventos/hora de sono) foi de 2,2, 2,5 e 0,7 nos grupos DCC-NH, DCC-H e controle, respectivamente, p < 0,05. A saturação de oxigênio mínima foi de 79%, 73% e 90% nos grupos DCC-NH, DCC-H e controle, respetivamente, p < 0,05. Apesar do alto índice de DRS nas crianças com DCC, a arquitetura do sono mostrou-se preservada / This study has investigated the sleep architecture and sleep breathing disorders (SBD) in infants (6 to 12 months) with congenital cardiac disease (CCD). Nocturnal polysomnography was performed in 21 infants: 7 non-hypoxemic, 7 hypoxemic and 7 healthy infants (control group). The respiratory disturbance index (events/hour) was 2.2, 2.5 and 0.7 in the non-hypoxemic, hypoxemic and control group (p < 0.05). The minimum oxygen saturation was 79% for the non-hypoxemic group, 73% for the hypoxemic group and 90% for the control group. Despite the high respiratory disturbance index the sleep architecture was preserved in infants with CCD

Objetivos: Determinar o tempo de espera para o diagnóstico e início do tratamento da síndrome da apneia obstrutiva do sono (SAOS) em hospital público brasileiro. Desenho do estudo: Estudo transversal. Métodos: Foi avaliada, com um questionário específico, uma amostra de conveniência composta por 68 pacientes com síndrome da apneia obstrutiva do sono (SAOS), com indicação de tratamento com pressão positiva em vias aéreas (PAP) e que utilizaram o aparelho durante acompanhamento ambulatorial, no período de janeiro de 2005 a dezembro de 2009. Foram excluídos os pacientes menores de 18 anos, incapazes de responder ao questionário ou que se negaram a participar. Resultados: Dos pacientes avaliados, a maioria era de homens (62%), com média de idade de 54,4 (+ 10,7) anos e obesos (IMC médio 33,7 + 7,1 Kg/m2); 76% eram hipertensos, 22% portadores de diabete melito e igual número de doença arterial coronariana; 10% destes apresentavam hipoventilação associada. A mediana do tempo entre a primeira consulta médica e a realização da PSG diagnóstica foi de 8,3 (intervalos interquartis [IQ] 3,3-14,3) meses e a mediana do tempo da indicação da PAP até a aquisição do aparelho foi de 10,5 (IQ 3,1-16,7) meses. Sessenta e quatro pacientes (94%) eram usuários de CPAP e 4 usuários de bilevel (6%). A maioria dos aparelhos (57%) foi obtida de forma gratuita por meio da rede pública de saúde. Conclusão: O presente estudo evidenciou a demora excessiva para diagnóstico e tratamento dos pacientes portadores de SAOS em atendimento em um hospital público de referência no Brasil. / Objectives: To determine the waiting time for the diagnosis and beginning of treatment of syndrome of obstructive sleep apnea (OSA) in Brazilian public hospital. Study design: cross-sectional study Methods: A convenience sample composed of 68 patients with syndrome of obstructive sleep apnea (OSA) was assessed through a specific questionnaire. All patients were indicated a treatment with positive airway pressure (PAP) and that used the unit during de period between January 2005 and December 2009. Patients who were under 18 years old, who were uncapable of answering the questionnaire or who refused to answer were excluded. Results: Among the patients, the majority were men (62%), with an average age of 54.4 (+10.7) years and obese (mean BMI 33.7 + 7.1 kg/m2); 76% were hypertensive, 22% diabetes mellitus patients and an equal number with coronary artery disease, 10% of them had associated hypoventilation. The average time between the first medical consultation and the implementation of diagnostic PSG was 8.3 (interquartile range [IQ] 3.3 to 14.3) months and the average time indication of the PAP until the purchase of the equipment was 10,5 (CI 3.1 to 16.7) months. Sixty-four patients (94%) were users of CPAP and 4 were users of bilevel (6%). Most appliances (57%) were obtained free of charge through the public health system. Conclusion: The present study demonstrated the excessive delay to diagnosis and treatment of patients with OSAS in attendance at a public hospital of reference in Brazil.

Introdução: É comum a associação entre apnéia do sono e a doença arterial coronária (DAC), devido a fatores predisponentes comuns como sexo masculino e obesidade. Entretanto, ainda não existe uma definição objetiva da relação entre apnéia e DAC. Objetivo: Avaliar se os episódios de isquemia miocárdica, a variabilidade da freqüência cardíaca (VFC) e as arritmias cardíacas de portadores de DAC sofrem alteração na presença da apnéia do sono. Métodos: Cinqüenta e três pacientes portadores de DAC foram submetidos à monitorização eletrocardiográfica ambulatorial de 48 horas e ao estudo do sono na primeira noite da monitorização. Os pacientes foram divididos de acordo com o índice de apnéia e hipopnéia (IAH) em: grupo Controle (IAH<=15) e grupo Apnéia (IAH>15). Os grupos foram comparados quanto à isquemia miocárdica, VFC e arritmias cardíacas ocorridas no período da vigília e do sono. Uma subanálise apenas com pacientes portadores de apnéia grave (IAH>30 - grupo Ap-Grave) foi realizada e comparada ao grupo Controle. A análise estatística foi realizada utilizando-se o teste de Mann-Whitney, teste de Fisher e teste T de student. Resultados: Não foram observadas diferenças nas características clínicas básicas entre os grupos, exceto pelos níveis de pressão arterial mais elevada no grupo Ap-Grave (p<0,05). Nenhum dos pacientes despertou por angina noturna; 75% foram submetidos a cateterismo cardíaco, sem diferença quanto à gravidade da DAC e aos valores da fração de ejeção. Foi registrada isquemia em 39 (73,58%) pacientes, com carga isquêmica de 2892,26 minutos na vigília e 1186 no sono. Na vigília, foi menor a duração dos episódios isquêmicos no grupo Ap- Grave (p<0,05); no período do sono não houve diferença entre os grupos. Não houve diferença nas medidas da VFC e arritmias entre os grupos. Não foram registradas pausas >2 segundos, fibrilação ou flutter atrial, ou qualquer tipo de bloqueio atrioventricular. Conclusão: A apnéia do sono não apresentou relação direta com isquemia miocárdica, variabilidade da freqüência cardíaca e arritmias cardíacas em pacientes portadores de DAC. / Introduction: It is common to associate obstructive sleep apnea (OSA) with coronary artery disease (CAD) given the common predisposing factors; however, there are still controversies on the influence of OSA in the progression of CAD. Objective: To assess if OSA causes any changes in myocardial ischemia episodes, heart rate variability (HRV) and cardiac arrhythmias in patients with CAD. Methods: Fifty-three people with CAD were submitted to ambulatory electrocardiographic monitoring and to polysomnography) simultaneously and divided according to the apnea-hypopnea index (AHI) into two groups: Control (AHI<=15) and Apnea (AHI>15). A sub analysis including only people with severe apnea (AHI>30) was done and compared with the control group. Results: Differences in the basic clinical characteristics between the groups were not found, except for higher blood pressure levels in the Severe Apnea Group (p<0.05). None of the patients woke up because of nocturnal angina. The groups did not differ in relation to the extension of coronary artery disease and ejection fraction values. Myocardial ischemia was recorded in 39 (73.58%) patients. The total ischemic burden was 2892.26 minutes while awake and 1186 minutes while asleep; the groups did not differ during sleep. There was also no significant difference in HRV and arrhythmia measurements between the groups. Pauses >2 seconds, fibrillation or atrial flutter or any type of atrioventricular blocks were not registered. Conclusion: OSA did not present a direct relationship with myocardial ischemia, heart rate variability and arrhythmias in patients with CAD.