الفهرس 
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Abstract
Introduction: OSA is associated with repetitive nocturnal arterial O2 desaturation and intrathoracic negative pressure swings and acute increase in pulmonary artery pressure and also intermittent hypoxaemia for several hours per day to mimic OSA developed pulmonary vascular remodeling and sustained pulmonary hypertension.
Aim of work: The aims of this study were to investigate whether OSA by it self without any other cardiac or lung disease can lead to pulmonary hypertension , and to asses the effect of CPAP therapy on pulmonary artery pressure.
Patients and methods: This study was done on 54 patients of OSA i.e. AHI > 5 and no other concomitant heart or lung diseases that may affect pulmonary haemodynamics. All patients were subjected to: 1-Full history taking. 2-Physical examinations. 3-Laboratory tests. 4-Plain chest X- ray. 5-C.T chest (spiral C.T and HRCT). 6-spirometric Pulmonary function tests. 7-Calculation of Body mass index. 8- Echocardiography. 9-full night attended Polysomnography. 10-CPAP theraby.
Results: There were significant higher (BMI, neck circumference, Epworth sleepiness scale, Berlin quitionnaire and AHI ) in severe OSA patients VS non severe OSA patients (p = < .001). However, there were no significant difference between two groups in according to age and sex. There were no significant difference in spirometric pulmonary function tests between severe OSA patients and non severe OSA patients. both (paO2 and saO2) were significantly lower in severe OSA patients VS non severe OSA patients (p=< .001), however there were no significant difference in paCO2 between two groups. There were significant lower (Basal SPO2, Minimum SPO2) in severe OSA patients VS non severe OSA patients (p= < .001), and there were significant higher ODI in severe OSA patients VS non severe OSA patients (p= < .001). There were significant higher PASP and mPAP in severe OSA patients VS non severe OSA patients (p= < .001) for each. There were significant positive correlation between AHI and (BMI, ODI, PASP and mPAP) (p < 0.001 for each), and there were significant negative correlation between AHI and (PaO2, Basal SPO2 and Minimum SPO2) (P < 0.001 for each), however there were no significant correlation between AHI and PaCO2 (P = 0.053).
Conclusions: OSA is associated with high prevalence of pulmonary hypertension which increased with its severity. Nocturnal O2 desaturation parameters and increased BMI are important risk factors in pathogenesis of pulmonary hypertension in OSA patients. Improvement of pulmonary hypertension through controlling OSA by CPAP therapy signify that OSA may play a crucial role in pathogenesis of pulmonary hypertension.