The effect of obstructive sleep apnoea on hypoxic and inflammatory markers during CPAP withdrawal: Further evidence from three randomised control trials
<p>Background and objective: Obstructive sleep apnoea (OSA) is associated with cardiovascular disease. Intermittent hypoxia, endothelial dysfunction and adipose tissue mediated inflammation have all been linked to cardiovascular disease in OSA. We have therefore explored the effect of OSA on r...
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Format: | Journal article |
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Wiley
2016
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author | Turnbull, C Rossi, V Santer, P Schwarz, E Stradling, J Petousi, N Kohler, M |
author_facet | Turnbull, C Rossi, V Santer, P Schwarz, E Stradling, J Petousi, N Kohler, M |
author_sort | Turnbull, C |
collection | OXFORD |
description | <p>Background and objective: Obstructive sleep apnoea (OSA) is associated with cardiovascular disease. Intermittent hypoxia, endothelial dysfunction and adipose tissue mediated inflammation have all been linked to cardiovascular disease in OSA. We have therefore explored the effect of OSA on relevant associated blood markers; adrenomedullin, endocan, endothelin-1, resistin and vascular endothelial growth factor.</p> <p>Methods: Patients with OSA, established on and compliant with continuous positive airways pressure (CPAP) therapy for > 1 year were included from three randomised controlled trials, conducted at two centres. Patients were randomised to either continued therapeutic CPAP or sham CPAP (CPAP withdrawal) for two weeks. Blood markers were measured at baseline and at 14 days, and the treatment effect between sham CPAP and therapeutic CPAP was analysed.</p> <p>Results: 109 patients were studied (therapeutic CPAP n=54, sham CPAP n=55). Sham CPAP was associated with a return of OSA (between-group difference in ODI +36.0/h, 95%CI +29.9 to +42.2, p<0.001). Sham CPAP was associated with a reduction in adrenomedullin levels at 14 days (-26.0 pg/ml, 95%CI 47.8 to -4.3, p=0.02), compared to therapeutic CPAP. Return of OSA was not associated with changes in endocan, endothelin-1, resistin or vascular endothelial growth factor.</p> <p>Conclusions: Whilst CPAP withdrawal was associated with return of OSA, it was associated with an unexpected significant reduction in the vasodilator adrenomedullin and not with expected increases in hypoxia-induced markers, markers of endothelial function, or resistin. We propose that the vascular effects occurring in OSA may be brought about by other mechanisms, perhaps partly through a reduction in adrenomedullin.</p> |
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format | Journal article |
id | oxford-uuid:4726a9a5-e9e3-46be-85b1-ea889726dad1 |
institution | University of Oxford |
last_indexed | 2024-03-06T21:38:43Z |
publishDate | 2016 |
publisher | Wiley |
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spelling | oxford-uuid:4726a9a5-e9e3-46be-85b1-ea889726dad12022-03-26T15:18:27ZThe effect of obstructive sleep apnoea on hypoxic and inflammatory markers during CPAP withdrawal: Further evidence from three randomised control trialsJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:4726a9a5-e9e3-46be-85b1-ea889726dad1Symplectic Elements at OxfordWiley2016Turnbull, CRossi, VSanter, PSchwarz, EStradling, JPetousi, NKohler, M<p>Background and objective: Obstructive sleep apnoea (OSA) is associated with cardiovascular disease. Intermittent hypoxia, endothelial dysfunction and adipose tissue mediated inflammation have all been linked to cardiovascular disease in OSA. We have therefore explored the effect of OSA on relevant associated blood markers; adrenomedullin, endocan, endothelin-1, resistin and vascular endothelial growth factor.</p> <p>Methods: Patients with OSA, established on and compliant with continuous positive airways pressure (CPAP) therapy for > 1 year were included from three randomised controlled trials, conducted at two centres. Patients were randomised to either continued therapeutic CPAP or sham CPAP (CPAP withdrawal) for two weeks. Blood markers were measured at baseline and at 14 days, and the treatment effect between sham CPAP and therapeutic CPAP was analysed.</p> <p>Results: 109 patients were studied (therapeutic CPAP n=54, sham CPAP n=55). Sham CPAP was associated with a return of OSA (between-group difference in ODI +36.0/h, 95%CI +29.9 to +42.2, p<0.001). Sham CPAP was associated with a reduction in adrenomedullin levels at 14 days (-26.0 pg/ml, 95%CI 47.8 to -4.3, p=0.02), compared to therapeutic CPAP. Return of OSA was not associated with changes in endocan, endothelin-1, resistin or vascular endothelial growth factor.</p> <p>Conclusions: Whilst CPAP withdrawal was associated with return of OSA, it was associated with an unexpected significant reduction in the vasodilator adrenomedullin and not with expected increases in hypoxia-induced markers, markers of endothelial function, or resistin. We propose that the vascular effects occurring in OSA may be brought about by other mechanisms, perhaps partly through a reduction in adrenomedullin.</p> |
spellingShingle | Turnbull, C Rossi, V Santer, P Schwarz, E Stradling, J Petousi, N Kohler, M The effect of obstructive sleep apnoea on hypoxic and inflammatory markers during CPAP withdrawal: Further evidence from three randomised control trials |
title | The effect of obstructive sleep apnoea on hypoxic and inflammatory markers during CPAP withdrawal: Further evidence from three randomised control trials |
title_full | The effect of obstructive sleep apnoea on hypoxic and inflammatory markers during CPAP withdrawal: Further evidence from three randomised control trials |
title_fullStr | The effect of obstructive sleep apnoea on hypoxic and inflammatory markers during CPAP withdrawal: Further evidence from three randomised control trials |
title_full_unstemmed | The effect of obstructive sleep apnoea on hypoxic and inflammatory markers during CPAP withdrawal: Further evidence from three randomised control trials |
title_short | The effect of obstructive sleep apnoea on hypoxic and inflammatory markers during CPAP withdrawal: Further evidence from three randomised control trials |
title_sort | effect of obstructive sleep apnoea on hypoxic and inflammatory markers during cpap withdrawal further evidence from three randomised control trials |
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