RESUMO
PURPOSE: Obstructive sleep apnea (OSA) has been related to vascular inflammation and production of endothelial cell adhesion molecules (CAMs). We aimed to determine night-morning variation of CAMs in patients with OSA compared to controls and the effect of one-night continuous positive airway pressure (CPAP) treatment on them. METHODS: Nonsmoking men went through a full-attended polysomnography (PSG) study. Participants with moderate to severe OSA went through another PSG study while being treated with CPAP. Participants who did not have OSA composed the control group. Serum levels of intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), and E-selectin were measured before and after sleep on both nights. RESULTS: Of 30 men, 20 had moderate to severe OSA while 10 did not. Night and morning ICAM-1 levels of patients with OSA were significantly higher than controls (p = 0.002 and p < 0.0001 respectively), while both night and morning VCAM-1 and E-selectin levels were not. Morning ICAM-1 levels of controls were significantly lower than night levels (p = 0.031), while morning ICAM-1, VCAM-1, and E-selectin levels of patients with OSA and morning VCAM-1 and E-selectin levels of controls were not. After CPAP treatment, the morning ICAM-1 levels, but not VCAM-1 levels, of patients with OSA were significantly lower than night levels (p = 0.006) and E-selectin levels showed a tendency for reduction (p = 0.06). CONCLUSIONS: OSA is associated with elevated night and morning ICAM-1 levels in adult men with OSA. Even one night of CPAP treatment restores the normal night-morning variation of ICAM-1 levels and may have an effect on E-selectin levels, as well.
Assuntos
Moléculas de Adesão Celular/sangue , Ritmo Circadiano/fisiologia , Pressão Positiva Contínua nas Vias Aéreas , Apneia Obstrutiva do Sono/terapia , Adulto , Estudos de Casos e Controles , Selectina E/sangue , Humanos , Molécula 1 de Adesão Intercelular/sangue , Masculino , Pessoa de Meia-Idade , Polissonografia , Apneia Obstrutiva do Sono/sangue , Resultado do Tratamento , Molécula 1 de Adesão de Célula Vascular/sangueAssuntos
Insuficiência Cardíaca/terapia , Coração Auxiliar/psicologia , Suporte Ventilatório Interativo/psicologia , Qualidade de Vida/psicologia , Apneia Obstrutiva do Sono/terapia , Idoso , Respiração de Cheyne-Stokes/diagnóstico , Respiração de Cheyne-Stokes/psicologia , Respiração de Cheyne-Stokes/terapia , Distúrbios do Sono por Sonolência Excessiva/diagnóstico , Distúrbios do Sono por Sonolência Excessiva/psicologia , Distúrbios do Sono por Sonolência Excessiva/terapia , Insuficiência Cardíaca/diagnóstico , Insuficiência Cardíaca/psicologia , Humanos , Masculino , Satisfação do Paciente , Polissonografia , Apneia Obstrutiva do Sono/diagnóstico , Apneia Obstrutiva do Sono/psicologiaAssuntos
Bradicardia/diagnóstico , Parada Cardíaca/diagnóstico , Parada Cardíaca/fisiopatologia , Polissonografia , Parada Sinusal Cardíaca/diagnóstico , Apneia Obstrutiva do Sono/diagnóstico , Sistema Nervoso Autônomo/fisiopatologia , Pressão Sanguínea/fisiologia , Bradicardia/fisiopatologia , Bradicardia/terapia , Pressão Positiva Contínua nas Vias Aéreas , Morte Súbita Cardíaca/etiologia , Morte Súbita Cardíaca/prevenção & controle , Feminino , Coração/inervação , Parada Cardíaca/terapia , Frequência Cardíaca/fisiologia , Humanos , Pessoa de Meia-Idade , Processamento de Sinais Assistido por Computador , Parada Sinusal Cardíaca/fisiopatologia , Parada Sinusal Cardíaca/terapia , Apneia Obstrutiva do Sono/fisiopatologia , Apneia Obstrutiva do Sono/terapia , Complexos Ventriculares Prematuros/diagnóstico , Complexos Ventriculares Prematuros/fisiopatologia , Complexos Ventriculares Prematuros/terapiaRESUMO
INTRODUCTION: Sleep apnoea syndrome (OSAS) may induce albuminuria during sleep which could reflect one of the possible pathogenetic mechanisms regarding cardiovascular risk. MATERIALS AND METHODS: We studied 224 patients with newly diagnosed OSAS, free of any chronic disease, and any regular drug therapy. The levels of urine albumin/creatinine ratio (ACR) before (ACR-bsleep) and immediately after (ACR-asleep) a sleep study were determined. The same procedure was repeated during the first night on CPAP treatment (n = 121) and in 46 reevaluated patients, after 3 months, on CPAP therapy. Ambulatory blood pressure was monitored in 133 of the patients. RESULTS: ACR-asleep was significantly higher in patients (17.82 ± 31.10 mg/g) compared with controls (6.54 ± 6.53 mg/g, p < 0.001). The mean percent change in ACR levels between after and before sleep (%dACR) was increased by 8.82% ± 61.06 in OSAS patients and reduced by 26.87% ± 18.95 in controls (p < 0.001). During the first sleep study on CPAP, the %dACR was reduced by 21.40% ± 24.59, in contrast to the increase observed during the initial study (10.73% ± 69.93, p < 0.001). This beneficial effect of CPAP treatment was preserved in the reevaluated patients. The %dACR was +29.33% ± 57.67 in nondippers (44% of the patients) and -5.57% ± 40.81 in dippers (p < 0.001). It was negatively correlated to the percent change of systolic (rho = -0.284, p = 0.003) and diastolic (rho = -0.341, p < 0.001) blood pressure between wakefulness and sleep. Contrary to normal people, ACR is increased in OSAS patients during sleep, at least partially, related to the nondipping phenomenon observed in these patients. Following CPAP treatment, urinary albumin excretion is reduced.