950 resultados para SLEEP-APNEA SYNDROME


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Purpose: The purpose of this study was to evaluate mouth-breathing and nasal-breathing children prior to surgical intervention and 28 months postoperatively, comparing the occlusal features obtained pre- and postoperatively through orthodontic study costs. Methods: The mouth-breathing (MB) group consists of 33 MB children who underwent surgery and presented a nasal-breathing (NB) pattern after surgery The control group comprised 22 NB children. The orthodontic examinations were accomplished prior to surgery (77) and an average of 28 months postoperatively (T2). Results: At T1, the MB and NB children presented no statistically significant difference in any analyzed occlusal features and measurements. At T2, the MB presented larger overjet comparing to NB children (P<.05). MB and NB groups presented statistically similar results (P>.05) concerning intercanine and intermolor distances, second primary molar terminal plane and canine relationship, overbite, crossbite, and open bite. From T1 to T2, the MB and NB groups showed a statistically significant difference in the molar terminal plane. Conclusion: Neither the breathing pattern nor the surgery had any effect on occlusal features in 3- to 6-year-olds. (Pediatr Dent 2012;34:10842) Received May 14, 2010 vertical bar Last Revision April 11, 2010 vertical bar Accepted April 12, 2010

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Jun JC, Shin MK, Yao Q, Bevans-Fonti S, Poole J, Drager LF, Polotsky VY. Acute hypoxia induces hypertriglyceridemia by decreasing plasma triglyceride clearance in mice. Am J Physiol Endocrinol Metab 303: E377-E388, 2012. First published May 22, 2012; doi:10.1152/ajpendo.00641.2011.-Obstructive sleep apnea (OSA) induces intermittent hypoxia (IH) during sleep and is associated with elevated triglycerides (TG). We previously demonstrated that mice exposed to chronic IH develop elevated TG. We now hypothesize that a single exposure to acute hypoxia also increases TG due to the stimulation of free fatty acid (FFA) mobilization from white adipose tissue (WAT), resulting in increased hepatic TG synthesis and secretion. Male C57BL6/J mice were exposed to FiO(2) = 0.21, 0.17, 0.14, 0.10, or 0.07 for 6 h followed by assessment of plasma and liver TG, glucose, FFA, ketones, glycerol, and catecholamines. Hypoxia dose-dependently increased plasma TG, with levels peaking at FiO(2) = 0.07. Hepatic TG levels also increased with hypoxia, peaking at FiO(2) = 0.10. Plasma catecholamines also increased inversely with FiO(2). Plasma ketones, glycerol, and FFA levels were more variable, with different degrees of hypoxia inducing WAT lipolysis and ketosis. FiO(2) = 0.10 exposure stimulated WAT lipolysis but decreased the rate of hepatic TG secretion. This degree of hypoxia rapidly and reversibly delayed TG clearance while decreasing [H-3]triolein-labeled Intralipid uptake in brown adipose tissue and WAT. Hypoxia decreased adipose tissue lipoprotein lipase (LPL) activity in brown adipose tissue and WAT. In addition, hypoxia decreased the transcription of LPL, peroxisome proliferator-activated receptor-gamma, and fatty acid transporter CD36. We conclude that acute hypoxia increases plasma TG due to decreased tissue uptake, not increased hepatic TG secretion.

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Costa-Silva JH, Zoccal DB, Machado BH. Chronic intermittent hypoxia alters glutamatergic control of sympathetic and respiratory activities in the commissural NTS of rats. Am J Physiol Regul Integr Comp Physiol 302: R785-R793, 2012. First published December 28, 2011; doi:10.1152/ajpregu.00363.2011.-Sympathetic overactivity and altered respiratory control are commonly observed after chronic intermittent hypoxia (CIH) exposure. However, the central mechanisms underlying such neurovegetative dysfunctions remain unclear. Herein, we hypothesized that CIH (6% O-2 every 9 min, 8 h/day, 10 days) in juvenile rats alters glutamatergic transmission in the commissural nucleus tractus solitarius (cNTS), a pivotal site for integration of peripheral chemoreceptor inputs. Using an in situ working heart-brain stem preparation, we found that L-glutamate microinjections (1, 3, and 10 mM) into the cNTS of control rats (n = 8) evoked increases in thoracic sympathetic nerve (tSN) and central vagus nerve (cVN) activities combined with inhibition of phrenic nerve (PN) activity. Besides, the ionotropic glutamatergic receptor antagonism with kynurenic acid (KYN; 250 mM) in the cNTS of control group (n = 7) increased PN burst duration and frequency. In the CIH group (n = 10), the magnitude of L-glutamate-induced cVN excitation was smaller, and the PN inhibitory response was blunted (P < 0.05). In addition, KYN microinjections into the cNTS of CIH rats (n = 9) did not alter PN burst duration and produced smaller increases in its frequency compared with controls. Moreover, KYN microinjections into the cNTS attenuated the sympathoexcitatory response to peripheral chemoreflex activation in control but not in CIH rats (P < 0.05). These functional CIH-induced alterations were accompanied by a significant 10% increase of N-methyl-D-aspartate receptor 1 (NMDAR1) and glutamate receptor 2/3 (GluR2/3) receptor subunit density in the cNTS (n = 3-8, P < 0.05), evaluated by Western blot analysis. These data indicate that glutamatergic transmission is altered in the cNTS of CIH rats and may contribute to the sympathetic and respiratory changes observed in this experimental model.

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The metabolic disorders that predispose patients to NASH (non-alcoholic steatohepatitis) include insulin resistance and obesity. Repeated hypoxic events, such as occur in obstructive sleep apnoea syndrome, have been designated as a risk factor in the progression of liver disease in such patients, but the mechanism is unclear, in particular the role of hypoxia. Therefore we studied the influence of hypoxia on the development and progression of steatohepatitis in an experimental mouse model. Mice with a hepatocellular-specific deficiency in the Pten (phosphatase and tensin homologue deleted on chromosome 10) gene, a tumour suppressor, were exposed to a 10% O2 (hypoxic) or 21% O2 (control) atmosphere for 7 days. Haematocrit, AST (aspartate aminotransferase), glucose, triacylglycerols (triglycerides) and insulin tolerance were measured in blood. Histological lesions were quantified. Expression of genes involved in lipogenesis and mitochondrial beta-oxidation, as well as FOXO1 (forkhead box O1), hepcidin and CYP2E1 (cytochrome P450 2E1), were analysed by quantitative PCR. In the animals exposed to hypoxia, the haematocrit increased (60+/-3% compared with 50+/-2% in controls; P<0.01) and the ratio of liver weight/body weight increased (5.4+/-0.2% compared with 4.7+/-0.3% in the controls; P<0.01). Furthermore, in animals exposed to hypoxia, steatosis was more pronounced (P<0.01), and the NAS [NAFLD (non-alcoholic fatty liver disease) activity score] (8.3+/-2.4 compared with 2.3+/-10.7 in controls; P<0.01), serum AST, triacylglycerols and glucose were higher. Insulin sensitivity decreased in mice exposed to hypoxia relative to controls. The expression of the lipogenic genes SREBP-1c (sterol-regulatory-element-binding protein-1c), PPAR-gamma (peroxisome-proliferator-activated receptor-gamma), ACC1 (acetyl-CoA carboxylase 1) and ACC2 (acetyl-CoA carboxylase 2) increased significantly in mice exposed to hypoxia, whereas mitochondria beta-oxidation genes [PPAR-alpha (peroxisome-proliferator-activated receptor-alpha) and CPT-1 (carnitine palmitoyltransferase-1)] decreased significantly. In conclusion, the findings of the present study demonstrate that hypoxia alone aggravates and accelerates the progression of NASH by up-regulating the expression of lipogenic genes, by down-regulating genes involved in lipid metabolism and by decreasing insulin sensitivity.

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High altitude periodic breathing (PB) shares some common pathophysiologic aspects with sleep apnea, Cheyne-Stokes respiration and PB in heart failure patients. Methods that allow quantifying instabilities of respiratory control provide valuable insights in physiologic mechanisms and help to identify therapeutic targets. Under the hypothesis that high altitude PB appears even during physical activity and can be identified in comparison to visual analysis in conditions of low SNR, this study aims to identify PB by characterizing the respiratory pattern through the respiratory volume signal. A number of spectral parameters are extracted from the power spectral density (PSD) of the volume signal, derived from respiratory inductive plethysmography and evaluated through a linear discriminant analysis. A dataset of 34 healthy mountaineers ascending to Mt. Muztagh Ata, China (7,546 m) visually labeled as PB and non periodic breathing (nPB) is analyzed. All climbing periods within all the ascents are considered (total climbing periods: 371 nPB and 40 PB). The best crossvalidated result classifying PB and nPB is obtained with Pm (power of the modulation frequency band) and R (ratio between modulation and respiration power) with an accuracy of 80.3% and area under the receiver operating characteristic curve of 84.5%. Comparing the subjects from 1(st) and 2(nd) ascents (at the same altitudes but the latter more acclimatized) the effect of acclimatization is evaluated. SaO(2) and periodic breathing cycles significantly increased with acclimatization (p-value < 0.05). Higher Pm and higher respiratory frequencies are observed at lower SaO(2), through a significant negative correlation (p-value < 0.01). Higher Pm is observed at climbing periods visually labeled as PB with > 5 periodic breathing cycles through a significant positive correlation (p-value < 0.01). Our data demonstrate that quantification of the respiratory volume signal using spectral analysis is suitable to identify effects of hypobaric hypoxia on control of breathing.

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A modified uvulopalatopharyngoplasty (UPPP) was carried out between January 1992 and December 2003 at the ENT Department of the Inselspital in Bern in 146 patients with habitual or complicated rhonchopathy. The operation consisted of a classical tonsillectomy or residual tonsil resection and additional shortening of the uvula. The natural mucosal fold between the uvula and the upper pole of the tonsils was carefully preserved. A wide opening to the rhinopharynx was created by asymmetric suturing of the glossopalantine and pharyngopalatine arches. A retrospective questionnaire with regard to rhonchopathy, phases of apnea, daytime drowsiness, obstruction of nasal breathing, long-term complications and patient satisfaction was used to evaluate the short-term and long-term effectiveness of the modified UPPP as well as the incidence of adverse side effects. Complete postoperative courses were evaluated in 116 patients. Surgical complications were restricted to one case with postoperative hemorrhage. A velum insufficiency or postoperative rhinopharyngeal stenosis did not occur. Eighty-three patients (72%) confirmed a persistent suppression or substantial improvement of the rhonchopathy. Disappearance or decrease of sleep apnea was confirmed in 12 (63%) out of 19 postoperative polysomnographic follow-up investigations. Long-term complications occurred in a total of 27 (23%) of 116 patients. They were confined to minor problems such as dryness of the mouth (n = 12), slight difficulty in swallowing (n = 7), discrete speech disturbances (n = 1), and slight pharyngeal dysesthesias (n = 7) with feeling of a lump in the throat and compulsive clearing of the throat. Eighty-five patients (73%) reported that they were satisfied with the postoperative result even several years after the operation. Looking back, 31 patients (27%) would no longer have the operation performed. The inadequate result of the rhonchopathy was specified as the reason by 21 patients. Ten patients had unpleasant memories of the operation because of intensive postoperative pain. Snoring and apneic phases are suppressed or improved by non-traumatic UPPP in the majority of patients. This effect persisted even years after the operation.

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We present a novel approach using both sustained vowels and connected speech, to detect obstructive sleep apnea (OSA) cases within a homogeneous group of speakers. The proposed scheme is based on state-of-the-art GMM-based classifiers, and acknowledges specifically the way in which acoustic models are trained on standard databases, as well as the complexity of the resulting models and their adaptation to specific data. Our experimental database contains a suitable number of utterances and sustained speech from healthy (i.e control) and OSA Spanish speakers. Finally, a 25.1% relative reduction in classification error is achieved when fusing continuous and sustained speech classifiers. Index Terms: obstructive sleep apnea (OSA), gaussian mixture models (GMMs), background model (BM), classifier fusion.

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Introdução: A obesidade é uma afecção com alta prevalência no Brasil e no mundo. É fator de risco para comorbidades como Diabetes tipo 2 (DM2), Hipertensão Arterial Sistêmica (HAS), Dislipidemia, Apneia Obstrutiva do Sono (AOS), entre outras. Seu tratamento é complexo e a cirurgia bariátrica, executada por diferentes técnicas, tem sido uma das opções. Objetivo: Analisar os resultados publicados na literatura em relação às técnicas cirúrgicas de Banda Gástrica Ajustável (BGA), Gastrectomia Vertical (GV), Gastroplastia com derivação em Y de Roux (GDYR) e Derivação Biliopancreática (DBP) - técnica de \"Scopinaro\" e de \"Duodenal Switch\" quanto às complicações operatórias, à mortalidade, à perda do excesso de peso (PEP) e ao reganho, e a resolução das comorbidades após a operação. Método: Foram analisados 116 estudos selecionados na base de dados MEDLINE por meio da PubMed publicados na Língua Inglesa entre 2003 e 2014. Para comparar as diferentes técnicas cirúrgicas (BGA, GV, GDYR e DBP), realizou-se estudo estatístico por meio da análise de variância (ANOVA) aplicando os testes de Duncan e de Kruskal Wallis avaliando: complicações pós-operatórias (fístula, sangramento e óbito); perda e reganho do excesso de peso, e resolução das comorbidades. Resultados: A ocorrência de sangramento foi de 0,6% na média entre todos os estudos, sendo 0,44% na BGA; 1,29% na GV; 0,81% na GDYR e 2,09% na DBP. Já a ocorrência de fístulas foi de 1,3% na média entre todos os estudos, 0,68% para BGA; 1,93% para GV; 2,18% para GDYR e 5,23% para DBP. A mortalidade nos primeiros 30 dias pós-operatórios foi de 0,9% na média entre todos os estudos, 0,05% na BGA; 0,16% na GV; 0,60% na GDYR e 2,52% na DBP. A PEP após cinco anos na média entre todos os estudos foi de 63,86%, especificamente na BGA, foi de 48,35%; 52,7% na GV; 71,04% na GDYR e 77,90% na DBP. A taxa de DM2 resolvida foi de 76,9% na média entre todos os estudos, sendo 46,80% na BGA; 79,38% na GV; 79,86% na GDYR e 90,78% na DBP. A taxa de Dislipidemia resolvida após a operação foi de 74,0% na média de todo o estudo, sendo 51,28% na BGA; 58,00% na GV; 73,28% na GDYR e 90,75% na DBP. A taxa de HAS resolvida após a operação foi de 61,80% na média de todo o estudo, sendo 54,50% na BGA; 52,27% na GV; 68,11% na GDYR e 82,12% na DBP. A taxa de AOS resolvida após a operação foi de 75,0% na média de todo o estudo, sendo 56,85% na BGA; 51,43% na GV; 80,31% na GDYR e 92,50% na DBP. Conclusão: quando analisadas e comparada as quatro técnicas observa-se que nos primeiros 30 dias pós-operatório a taxa de sangramento é superior nos pacientes submetidos à DBP e taxa de fístula inferior nos pacientes da BGA. Quanto à mortalidade observou-se taxa mais pronunciada nos pacientes submetidos à DBP e menos nos submetidos à BGA. Quanto à PEP observou-se uma uniformidade entre os pacientes submetidos à GV, GDYR E DBP até o terceiro ano. Após esse período observa-se reganho de peso nos submetidos à GV até o quinto ano de seguimento. Já nos pacientes submetidos à BGA observou-se taxas de PEP menos pronunciadas em relação às demais desde o início do seguimento. Quanto à resolução das comorbidades observou-se taxas de resolução de DM2 inferiores nos pacientes submetidos à BGA, e não houve diferença entre nenhuma técnica quanto à resolução das demais comorbidades: HAS, AOS e dislipidemia

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Trabalho Final do Curso de Mestrado Integrado em Medicina, Faculdade de Medicina, Universidade de Lisboa, 2014

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Objective: Respiratory health of Indigenous and minority ethnic groups in affluent countries is poorer than their non-minority counterparts and sleep disorders are no exception. In children, obstructive sleep apnoea has the potential to result in serious long-term consequences. In 1999, we studied 1650 children and adolescents living in the Torres Strait and the Northern Peninsula Area, Australia. Here we report prevalence of snoring in these communities and relate its association with asthma symptoms. Methods: A population-based cross-sectional study was conducted in the Torres Strait region. Five indigenous communities were randomly selected and information was collected using a structured face-to-face interview based on a standardized questionnaire. There was a 98% response rate, and 1650 children, 0-17 years of age, were included in the study. Results: Overall, the prevalence of snoring was 14.2% (95% CI 12.5-15.9); 3.6% (95% CI 2.7-4.6) reported snorting, and 6% (95% CI 4.9-7.2) reported restless sleep. The prevalence of snoring was significantly higher among males (17.1% for males and 10.8 for females, P = 0.005). Children were five times more likely to have experienced snoring and snorting if they reported wheezing in the last 12 months. Conclusion: We conclude that the prevalence of symptoms suggestive of obstructive sleep problems is relatively high in children of this region. This highlights the need for awareness among the community patients and physicians about the problem of obstructive sleep-disordered breathing, especially in children with asthma, and for the need for further studies to measure prevalence of sleep breathing disorders among Indigenous Australians.

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Study objectives: Currently, esophageal pressure monitoring is the "gold standard" measure for inspiratory efforts, hut its invasive nature necessitates a better tolerated and noninvasive method to be used on children. Pulse transit time (PTT) has demonstrated its potential as a noninvasive surrogate marker for inspiratory efforts. The principle velocity determinant of PTT is the change in stiffness of the arterial wall and is inversely correlated to BP. Moreover, PTT has been shown to identify changes in inspiratory effort via the BP fluctuations induced by negative pleural pressure swings. In this study, the capability of PTT to classify respiratory, events during sleep as either central or obstructive in nature was investigated. Setting and participants: PTT measure was used in adjunct to routine overnight polysomnographic studies performed on 33 children (26 boys and 7 girls; mean +/- SD age, 6.7 +/- 3.9 years). The accuracy of PTT measurements was then evaluated against scored corresponding respiratory events in the polysomnography recordings. Results: Three hundred thirty-four valid respiratory events occurred and were analyzed. One hundred twelve obstructive events (OEs) showed a decrease in mean PTT over a 10-sample window that had a probability of being correctly ranked below the baseline PTT during tidal breathing of 0.92 (p < 0.005); 222 central events (CEs) showed a decrease in the variance of PTT over a 10-sample window that had a probability of being ranked below the baseline PTT of 0.94 (p < 0.005). This indicates that, at a sensitivity of 0.90, OEs can be detected with a specificity of 0.82 and CEs can be detected with a specificity of 0.80. Conclusions: PTT is able to categorize CEs and OEs accordingly in the absence of motion artifacts, including hypopneas. Hence, PTT shows promise to differentiate respiratory, events accordingly and can be an important diagnostic tool in pediatric respiratory sleep studies.< 0.005); 222 central events (CEs) showed a decrease in the variance of PTT over a 10-sample window that had a probability of being ranked below the baseline PTT of 0.94 (p < 0.005). This indicates that, at a sensitivity of 0.90, OEs can be detected with a specificity of 0.82 and CEs can be detected with a specificity of 0.80. Conclusions: PTT is able to categorize CEs and OEs accordingly in the absence of motion artifacts, including hypopneas. Hence, PTT shows promise to differentiate respiratory, events accordingly and can be an important diagnostic tool in pediatric respiratory sleep studies.');"

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OBJECTIVES The purpose of this research was to identify the determinants of right ventricular (RV) dysfunction in overweight and obese subjects. BACKGROUND Right ventricular dysfunction in obese subjects is usually ascribed to comorbid diseases, especially obstructive sleep apnea. We used tissue Doppler imaging to identify the determinants of RV dysfunction in overweight and obese subjects. METHODS Standard and tissue Doppler echocardiography was performed in 112 overweight (body mass index [BMI] 25 to 29.9 kg/m(2)) or obese (BMI >30 kg/m(1)) subjects and 36 referents (BMI 35 kg/m(2) had reduced RV function compared with referent subjects, evidenced by reduced s(m) (6.5 +/- 2.4 cm/s vs. 10.2 +/- 1.5 cm/s, p < 0.001), peak strain (-21 +/- 4% vs. -28 +/- 4%, p < 0.001), peak strain rate (-1.4 +/- 0.4 s(-1) vs. -2.0 +/- 0.5 s(-1), p < 0.001), and e(m) (6.8 +/- 2.4 cm/s vs. -10.3 +/- 2.5 cm/s, p < 0.001), irrespective of the presence of sleep apnea. Similar but lesser degrees of reduced systolic function (p < 0.05) were present in overweight (BMI 25 to 29.9 kg/m(2)) and mildly obese (BMI 30 to 35 kg/m(2)) groups. Differences in RV e(m), s(m), and strain indexes were demonstrated between the severely versus overweight and mildly obese groups (p < 0.05). Body mass index remained independently related to RV changes after adjusting for age, log insulin, and mean arterial pressures. In obese patients, these changes were associated with reduced exercise capacity but not the duration of obesity and presence of sleep apnea or its severity. CONCLUSIONS Increasing BMI is associated with increasing severity of RV dysfunction in overweight and obese subjects without overt heart disease, independent of sleep apnea.

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In disorders such as sleep apnea, sleep is fragmented with frequent EEG-arousal (EEGA) as determined via changes in the sleep-electroencephalogram. EEGA is a poorly understood, complicated phenomenon which is critically important in studying the mysteries of sleep. In this paper we study the information flow between the left and right hemispheres of the brain during the EEGA as manifested through inter-hemispheric asynchrony (IHA) of the surface EEG. EEG data (using electrodes A1/C4 and A2/C3 of international 10-20 system) was collected from 5 subjects undergoing routine polysomnography (PSG). Spectral correlation coefficient (R) was computed between EEG data from two hemispheres for delta-delta(0.5-4 Hz), theta-thetas(4.1-8 Hz), alpha-alpha(8.1-12 Hz) & beta-beta(12.1-25 Hz) frequency bands, during EEGA events. EEGA were graded in 3 levels as (i) micro arousals (3-6 s), (ii) short arousals (6.1-10 s), & (iii) long arousals (10.1-15 s). Our results revealed that in beta band, IHA increases above the baseline after the onset of EEGA and returns to the baseline after the conclusion of event. Results indicated that the duration of EEGA events has a direct influence on the onset of IHA. The latency (L) between the onset of arousals and IHA were found to be L=2plusmn0.5 s (for micro arousals), 4plusmn2.2 s (short arousals) and 6.5plusmn3.6 s (long arousals)

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La prévalence de l’obésité sévère ne cesse d’augmenter. La problématique associée à l’obésité sévère est la présence possible de nombreuses comorbidités qui peuvent coexister et altérer le système cardiovasculaire, pulmonaire, endocrinien, articulaire et même favoriser le développement de certains cancers. L’excès de poids, plus particulièrement l’excès de tissu adipeux, sont tous deux liés au développement de ces comorbidités. Aucune donnée n’est disponible quant au rôle de la déposition ectopique du tissu adipeux. Considérant le caractère morbide de l’obésité sévère, la mortalité de toute cause augmentée et l’espérance de vie réduite, à ce jour le seul traitement dit efficace à long terme pour le traitement de l’obésité sévère est la chirurgie bariatrique. L’efficacité est définie par la perte de poids, le maintien à long terme de cette perte de poids ainsi que par l’amélioration ou la résolution des comorbidités. L’intérêt clinique et scientifique pour la chirurgie bariatrique est grandissant. Un nombre important d’études s’intéresse aux mécanismes sous-jacents de la résolution des comorbidités. Le diabète de type 2 est la comorbidité la plus étudiée et peu d’études se sont intéressées aux déterm meil.inants de la résolution de l’hypertension artérielle et de l’apnée obstructive du som Comme premier objectif, cette thèse visait à caractériser les différences de la composition corporelle et de la distribution du tissu adipeux de patients obèses sévères avec ou sans diagnostic de diabète de type 2, d’hypertension artérielle et d’apnée obstructive du sommeil. Le deuxième objectif de cette thèse visait à comparer l’évolution postopératoire suite à une chirurgie bariatrique sur les changements de la composition corporelle et de la distribution du tissu adipeux selon le statut de résolution du diabète de type 2, de l’hypertension artérielle et de l’apnée obstructive du sommeil. De plus, considérant le peu d’évidences dans la littérature au sujet des déterminants de la résolution de l’hypertension artérielle et de l’apnée obstructive du sommeil, l’évaluation du profil inflammatoire, des adipokines et de l’activité du système nerveux autonome ont aussi été caractérisés. Premièrement, nous avons documenté qu’en présence d’obésité sévère, la déposition ectopique du tissu adipeux était plus importante chez les patients avec un diabète de type 2, une hypertension artérielle et une apnée obstructive du sommeil comparativement à ceux n’ayant pas ces comorbidités. Nous avons par la suite montré que la résolution du diabète de type 2 et de l’hypertension artérielle était caractérisée par une réduction plus importante du tissu adipeux viscéral. Au contraire, la résolution de l’apnée obstructive du sommeil était plutôt caractérisée par une réduction plus importante du tissu adipeux sous-cutané à la mi-cuisse et par une tendance à une perte de poids plus élevée. De plus, nous avons observé que chez les patients qui n’avaient pas résolu leur diabète de type 2, leur hypertension artérielle et leur apnée obstructive du sommeil, la quantité de tissu adipeux viscéral, à 12 mois suivant la chirurgie bariatrique, était plus importante comparativement à celle mesurée chez les patients n’ayant pas résolu ces comorbidités. Spécifiquement à l’évaluation du profil inflammatoire et des adipokines, nous avons observé que chez les patients obèses sévères, la présence de l’hypertension artérielle et de l’apnée obstructive du sommeil n’était pas caractérisée par un profil altéré au niveau des marqueurs inflammatoires et des adipokines. Également, nous n’avons pas observé de changements majeurs qui pouvaient expliquer, en partie, la résolution de l’hypertension artérielle et de l’apnée obstructive du sommeil. Quant à l’activité du système nerveux autonome, nous avons observé une faible activité du système nerveux parasympathique chez les patients obèses sévères avec hypertension artérielle et apnée obstructive du sommeil. Nous avons également documenté que la résolution de l’hypertension artérielle et de l’apnée obstructive du sommeil était associée à une tendance à une augmentation plus importante de l’activité parasympathique du système nerveux autonome. Les résultats obtenus au cours de ce doctorat supportent l’importance de la déposition ectopique du tissu adipeux en situation d’obésité sévère, particulièrement le rôle du tissu adipeux viscéral, dans le développement du diabète de type 2, de l’hypertension artérielle et de l’apnée obstructive du sommeil ainsi que dans la résolution de ces comorbidités suivant une chirurgie bariatrique. D’autres recherches devront davantage s’intéresser à la mobilisation des dépôts ectopiques de tissu adipeux comme un déterminant important dans la résolution à plus long terme de ces comorbidités.