BackgroundObstructive sleep apnea (OSA) is associated with coronary artery disease (CAD). Intermittent hypoxia associated with OSA increases sympathetic activity and may cause systemic inflammation, which may contribute to CAD in patients with OSA. Treatment with continuous positive airway pressure (CPAP) has been shown to change levels of inflammatory markers. We analyzed data from published studies by a systematic meta-analysis.ObjectiveTo asses if treatment for sleep apnea by CPAP will affect levels of inflammatory markers.Data resourcesPubMed, Embase and Cochrane library.MethodsStudy eligibility criteria full text English studies of adult, human subjects, addressing values of at least one of the inflammatory markers before and after CPAP treatment. We used the definition of OSA as an apnea-hypopnea index (AHI) of ≥ 5/h, reported values in mean and standard deviation or median with range.ParticipantsAdult, human.InterventionsCPAP treatment for OSA.Study appraisal and synthesis methodA total of 3835 studies were reviewed for inclusion, while 23 studies pooled for analysis. A total of 14 studies with 771 patients were pooled for C-reactive protein (CRP); 9 studies with 209 patients were pooled for tumor necrosis factor-alpha (TNF-α); and 8 studies with 165 patients were pooled for interleukin-6 (IL-6).Endpoint definitionsThe following inflammatory markers were chosen: CRP, TNF-α, and IL-6.ResultsC-reactive protein: Study level means ranged from 0.18 to 0.85 mg/dl before CPAP treatment and 0.10 to 0.72 mg/dl after CPAP treatment. Mean differences, at a study level, ranged from −0.05 to 0.50. The pooled mean difference was 0.14 [95% confidence interval 0.08 to 0.20, p < 0.00001]. There was heterogeneity in this endpoint (df = 13, p < 0.00001, I2 = 95%).Tumor necrosis factor-α: Study level means ranged from 1.40 to 50.24 pg/ml before CPAP treatment and 1.80 to 28.63 pg/ml after CPAP treatment. Mean differences, at a study level, ranged from −1.23 to 21.61. The pooled mean difference was 1.14 [95% confidence interval 0.12 to 2.15, p = 0.03]. There was heterogeneity in this endpoint (df = 8, p < 0.00001, I2 = 89%).Interleukin-6: Study level means ranged from 1.2 to 131.66 pg/ml before CPAP treatment and 0.45 to 66.04 pg/ml after CPAP treatment. Mean differences, at a study level, ranged from −0.40 to 65.62. The pooled mean difference was 1.01 [95% confidence interval −0.00 to 2.03, p = 0.05]. There was heterogeneity in this endpoint (df = 7, p < 0.00001, I2 = 95%).LimitationsOnly published data. Studies pooled were mainly small, non-randomized trials.ConclusionSleep apnea treatment with CPAP improves levels of inflammatory markers.
CPAP treatment for OSA seems to improve dyslipidemia (decrease in total cholesterol and LDL, and increase in HDL). It does not appear to affect TG levels.
Background. Obstructive sleep apnea (OSA) is associated with coronary artery disease. Intermittent hypoxia associated with OSA increases sympathetic activity and may cause systemic inflammation, which may contribute to atherosclerosis leading to an increase in the size of carotid intima media thickness (CIMT). Methods. PubMed and Cochrane library were reviewed by utilizing different combinations of key words: sleep apnea, carotid disease, intima media thickness, and carotid atherosclerosis. Inclusion criteria were English articles; studies with adult population with OSA and without OSA; CIMT recorded by ultrasound in mean and standard deviation or median with 95% confidence interval; and OSA defined as apnea hypopnea index of ≥5/h. A total of 95 studies were reviewed for inclusion, with 16 studies being pooled for analysis. Results. Ninety-five studies were reviewed, while 16 studies were pooled for analysis; since some studies have more than one data set, there were 25 data sets with 1415 patients being pooled for meta-analysis. All studies used ultrasound to measure CIMT. CIMT standardized difference in means ranged from −0.883 to 8.01. The pooled standardized difference in means was 1.40 (lower limit 0.996 to upper limit 1.803, (P < 0.0001). Conclusion. Patients with OSA appear to have increased CIMT suggestive of an atherosclerotic process.
Based on coping theory, the current research examines how and why COVID-19 phobia affects frontline healthcare professionals’ mental health, as well as their burnout and work-related stress. We focused on the mediating role of burnout and work-related stress in this study. In the current study, we also examined the moderating influence of healthcare professionals’ handwashing behavior using the Hayes Process model. We employed a daily diary approach to collect data from respondents in Pakistan’s frontline healthcare professionals (n = 79, 79 × 10 = 790) who were directly treating COVID-19 patients during the omicron wave. According to the findings of the study, COVID-19 phobia significantly disturbs healthcare professionals’ mental health, as well as significantly strengthens burnout and work-related stress. The findings also demonstrated that burnout significantly negatively influences mental health. The mediation influence of burnout and work-related stress in the association between COVID-19 phobia and mental health has shown to be significant. The moderation analysis revealed that high handwashing behavior significantly buffers the negative impact of COVID-19 phobia, as well as the adverse effect of burnout on healthcare professionals’ mental health. Moreover, our findings have theoretical and managerial implications, as well as new research directions for scholars to understand the adverse impact of daily obstacles on professionals’ (nurses and doctors, etc.) mental health and work performance, as well as issues based on resource conversation philosophy.
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