الفهرس 
TitleOnly 14 pages are availabe for public view
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Abstract
OSA is a common global breathing disorder related to sleep. Its great clinical significance is growing in patients with recurrent symptoms and signs related to the cessation of breathing during sleep, with a large sector of patients is still undiagnosed.
OSA pathophysiology is a multifaceted process that could be resulted from diminished pharyngeal dimensions, such as maxillofacial anatomical disproportions or obesity with increased susceptibility of the upper airways to collapse due to diminished reflexes keeping them patent and deterioration of the neuromuscular integrity during sleep.
The mechanistic link between OSA and CVDs is incompletely understood, due to the heterogeneous criteria of OSA and its close association with obesity. Also, it is not clear whether inflammatory and metabolic changes are caused by OSA or associated with OSA due to obesity.
Treatment of OSA with CPAP therapy has been suggested to improve microvascular endothelial dysfunction. It has an ameliorating impact upon airway inflammation with a major effect on some systemic inflammation parameters in moderate to severe OSA.
60 subjects were included in this study, 50 adult subjects with evidence of untreated OSA (AHI ≥ 5 events/hour of sleep) diagnosed by PSG and 10 control subjects with no evidence of OSA.
The following investigations were carried out:
1) Overnight PSG.
2) Anthropometric measurements including age, weight, height, BMI, NC, neck-height ratio, waist circumference, hip circumference, and waist-hip ratio.
3) Endothelial function testing, including flow-mediated vasodilatation and carotid intima-media thickness by doppler imaging.
4) Tissue doppler imaging by Echocardiography.
5) Physiological assessment of the sympathetic nervous system functions by cold pressor test, HR and BP response to the orthostatic test, and Valsalva maneuver response.
6) Assessment of early renal dysfunction through measurement of microalbuminuria level by urinary albumin excretion.
7) Determination of the level of TNF-α in the serum by ELISA technique.
8) Data were calculated and analyzed using (SPSS ver.20 Chicago, IL, USA).
Summary, Conclusions & Recommendations
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The following results were obtained:
• Significant difference considering NC, neck-height ratio, waist circumference, and waist-hip ratio between OSA patients and controls, with a significant difference in NC between OSA groups were observed.
• AHI showed significant correlation with each of TNF-α, desaturation index, minimal SpO2, baseline SpO2, SVB (minimal, average, maximal), average SBP during sleep, and index of increase in BP during sleep.
• TNF-𝛼 blood level showed significant difference between OSA patients and controls, with a significant correlation between TNF-α and each of AHI, especially in the severe group, pre-test DBP, index of increase in BP during sleep, and microalbuminuria.
• Significant correlation between average SBP during sleep and post-test HR was observed.
• Significant correlation between SBP difference (80% of pre-test SBP during wakefulness - average SBP during sleep) and microalbuminuria was observed.
• Using the stepwise multiple linear regression models, CIMT was more significantly correlated with post-test SBP rather than other parameters, E/e’ was in more significant negative correlation with post-test PR interval rather than other parameters, and microalbuminuria was more significantly correlated with post-test SBP and post-test DBP rather than other parameters.
6.2. Conclusions
• The autonomic sympathetic dysregulation was more predominant contributing mechanism than other mechanisms in the pathophysiology of CVDs in OSA.
• TNF-α showed significant weak positive correlation with AHI. This correlation may play a role as a contributing mechanism of CVDs in OSA. • Hypertension can explain the link between OSA and atherosclerosis, and the coexistence of OSA with hypertension was found to have more synergistic effects on early markers of atherosclerosis. • The association of OSA with microalbuminuria could provide more explanation for the OSA related risk in hypertension.
• The mechanistic link between inflammation and sympathetic dysregulation was evident and can be explained by repetitive episodes of apnea, hypopnea, and resultant hypoxemia triggered the chance of disturbed sympathetic tone and initiated the inflammatory cascade in OSA.
Summary, Conclusions & Recommendations
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6.3. Recommendations
▪ Further studies should be conducted to shed more light on the possible role of autonomic sympathetic dysregulation as a predominant causative link between OSA, CVDs, and MetS.
▪ It is advisable to study the effects of leptin, insulin resistance, and other inflammatory cytokines in the development of OSA and to strengthen the association between OSA and MetS.