ABSTRACT
BACKGROUND: The treatment of choice for sleep apnoea-hypopnoea syndrome (SAHS) is continuous positive airway pressure (CPAP). However, CPAP effectiveness strongly depends on patient adherence to treatment. The aim of this study was to determine the effectiveness of a low-cost, basic intervention on improving CPAP adherence. METHODS: A controlled parallel-group trial. Participants were SAHS patients for whom CPAP treatment was indicated. Those in the intervention group were shown the results of their sleep test and were told the importance of treatment adherence; the control group received neither. Outcomes for both groups were compared at 6 months. The primary outcome assessed was CPAP usage. RESULTS: One hundred fifty-four patients were included in the intervention group and 167 in the control group. At 6 months, the intervention group had 10% more participants with CPAP usage ≥4 h, significantly higher adherence as compared to controls (5 ± 1.8 h vs 4.3 ± 1.7, p = 0.031), mean: 0.7 h/day and fewer discontinuations of CPAP. A multiple linear regression model showed that intervention group and daytime sleepiness were variables independently associated with treatment adherence. CONCLUSIONS: An inexpensive basic intervention involving communication of sleep test results and the importance of CPAP adherence improves adherence to CPAP therapy. In addition, greater daytime sleepiness is associated with higher CPAP adherence.
Subject(s)
Continuous Positive Airway Pressure/psychology , Patient Compliance/psychology , Sleep Apnea, Obstructive/psychology , Sleep Apnea, Obstructive/therapy , Adult , Aged , Disorders of Excessive Somnolence/psychology , Disorders of Excessive Somnolence/therapy , Female , Humans , Male , Middle Aged , Patient Education as Topic , Polysomnography , Prospective Studies , Regression AnalysisABSTRACT
Introducción: El síndrome de apneas-hipopneas del sueño (SAHS) es un factor de riesgo cardiovascular y puede producir estrés miocárdico. Objetivos: Evaluar si un SAHS grave produce estrés miocárdico valorado este mediante marcadores séricos. Pacientes y métodos: Estudio prospectivo, observacional longitudinal realizado en pacientes con sospecha de padecer trastornos del sueño a los que se les solicitó una poligrafía cardiorrespiratoria. Fueron excluidos aquellos sujetos con patología pulmonar o extrapulmonar grave. Según el índice de apneas-hipopneas (IAH) los sujetos se asignaron al grupo con SAHS grave (IAH > 30) o al grupo sin SAHS (IAH < 5). Se compararon las cifras séricas de troponina I y mioglobina en ambos grupos. Resultados: Fueron incluidos 48 sujetos, 29 con SAHS grave y 19 sin SAHS, ambos grupos presentaron datos similares en edad, género e índice de masa corporal. Los enfermos con SAHS mostraron un número mayor de factores de riesgo vascular que fue estadísticamente significativo en la hipertensión arterial (p = 0,041). Respecto al grupo sin SAHS, los pacientes mostraron cifras de troponina I y mioglobina similares (p > 0,5). En el SAHS grave tampoco hubo correlación significativa entre los valores séricos de troponina I y mioglobina, y las variables de saturación periférica de oxígeno nocturna. Conclusiones: Respecto a los pacientes sin SAHS, en aquellos con un SAHS grave no se observaron cambios significativos en los marcadores séricos relacionados con estrés miocárdico. Los valores que determinan el grado de hipoxemia nocturna no mostraron correlación con las cifras séricas de troponina I ni mioglobina (AU)
Introduction: The apnea-hypopnea syndrome (SAHS) is a cardiovascular risk factor and can lead to myocardial stress. Objectives: Assess whether a myocardial stress produces severe SAHS rated this by serum markers. Patients and methods: this is a prospective, observational study of patients with suspected sleep disorders who were asked a polygraphy. We excluded those patients with severe pulmonary or extrapulmonary disease. According to the apnea-hypopnea index (AHI), subjects were assigned to the group with severe SAHS (AHI > 30) or the group without SAHS (AHI <5). We compared the serum levels of troponin I and myoglobin in both groups. Results: we included 48 subjects, 29 with severe SAHS and 19 without SAHS, both groups reported similar in age, gender and body mass index. Patients with SAHS showed an increased number of vascular risk factors, that was statistically significant for hypertension (p = 0.041). For the group without SAHS, patients showed troponin I and myoglobin similar (p > 0.5). In the severe SAHS also was no significant correlation between serum levels of troponin I and myoglobin and the variables of peripheral oxygen saturation at night. Conclusions: Compared to patients without SAHS, those with severe SAHS showed no significant changes in serum markers associated with myocardial stress. The values that determine the degree of nocturnal hypoxemia did not correlate with serum levels of troponin I and myoglobin (AU)