Continuous positive airway pressure improves vascular function in obstructive sleep apnoea/hypopnoea syndrome: A randomised controlled trial

M. D. Cross, N. L. Mills, M. Al-Abri, R. Riha, M. Vennelle, T. W. Mackay, D. E. Newby, N. J. Douglas

Research output: Contribution to journalArticle

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Abstract

Background: The obstructive sleep apnoea/hypopnoea syndrome (OSAHS) is associated with hypertension and increased cardiovascular risk, particularly when accompanied by marked nocturnal hypoxaemia. The mechanisms of these associations are unclear. We hypothesised that OSAHS combined with severe nocturnal hypoxaemia causes impaired vascular function that can be reversed by continuous positive airways pressure (CPAP) therapy. Methods: We compared vascular function in two groups of patients with OSAHS: 27 with more than 20 4% desaturations/h (desaturator group) and 19 with no 4% and less than five 3% desaturations/h (non-desaturator group). In a randomised, double blind, placebo controlled, crossover trial, the effect of 6 weeks of CPAP therapy on vascular function was determined in the desaturator group. In all studies, vascular function was assessed invasively by forearm venous occlusion plethysmography during intraarterial infusion of endothelium dependent (acetylcholine 5-20 μg/min and substance P 2-8 pmol/min) and independent (sodium nitroprusside 2-8 μg/min) vasodilators. Results: Compared with the non-desaturator group, patients with OSAHS and desaturations had reduced vasodilatation to all agonists (p = 0.007 for all). The apnoea/hypopnoea index and desaturation frequency were inversely related to peak vasodilatation with acetylcholine (r = -0.44, p = 0.002 and r = -0.43, p = 0.003) and sodium nitroprusside (r = -0.42, p = 0.009 and r = -0.37, p = 0.02). In comparison with placebo, CPAP therapy improved forearm blood flow to all vasodilators (p = 0.01). Conclusions: Patients with OSAHS and frequent nocturnal desaturations have impaired endothelial dependent and endothelial independent vasodilatation that is proportional to hypoxaemia and is improved by CPAP therapy. Impaired vascular function establishes an underlying mechanism for the adverse cardiovascular consequences of OSAHS.

Original languageEnglish
Pages (from-to)578-583
Number of pages6
JournalThorax
Volume63
Issue number7
DOIs
Publication statusPublished - Jul 2008

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Continuous Positive Airway Pressure
Obstructive Sleep Apnea
Blood Vessels
Randomized Controlled Trials
Vasodilation
Nitroprusside
Vasodilator Agents
Forearm
Acetylcholine
Placebos
Intra Arterial Infusions
Plethysmography
Apnea
Therapeutics
Substance P
Cross-Over Studies
Endothelium

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

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Continuous positive airway pressure improves vascular function in obstructive sleep apnoea/hypopnoea syndrome : A randomised controlled trial. / Cross, M. D.; Mills, N. L.; Al-Abri, M.; Riha, R.; Vennelle, M.; Mackay, T. W.; Newby, D. E.; Douglas, N. J.

In: Thorax, Vol. 63, No. 7, 07.2008, p. 578-583.

Research output: Contribution to journalArticle

Cross, M. D. ; Mills, N. L. ; Al-Abri, M. ; Riha, R. ; Vennelle, M. ; Mackay, T. W. ; Newby, D. E. ; Douglas, N. J. / Continuous positive airway pressure improves vascular function in obstructive sleep apnoea/hypopnoea syndrome : A randomised controlled trial. In: Thorax. 2008 ; Vol. 63, No. 7. pp. 578-583.
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abstract = "Background: The obstructive sleep apnoea/hypopnoea syndrome (OSAHS) is associated with hypertension and increased cardiovascular risk, particularly when accompanied by marked nocturnal hypoxaemia. The mechanisms of these associations are unclear. We hypothesised that OSAHS combined with severe nocturnal hypoxaemia causes impaired vascular function that can be reversed by continuous positive airways pressure (CPAP) therapy. Methods: We compared vascular function in two groups of patients with OSAHS: 27 with more than 20 4{\%} desaturations/h (desaturator group) and 19 with no 4{\%} and less than five 3{\%} desaturations/h (non-desaturator group). In a randomised, double blind, placebo controlled, crossover trial, the effect of 6 weeks of CPAP therapy on vascular function was determined in the desaturator group. In all studies, vascular function was assessed invasively by forearm venous occlusion plethysmography during intraarterial infusion of endothelium dependent (acetylcholine 5-20 μg/min and substance P 2-8 pmol/min) and independent (sodium nitroprusside 2-8 μg/min) vasodilators. Results: Compared with the non-desaturator group, patients with OSAHS and desaturations had reduced vasodilatation to all agonists (p = 0.007 for all). The apnoea/hypopnoea index and desaturation frequency were inversely related to peak vasodilatation with acetylcholine (r = -0.44, p = 0.002 and r = -0.43, p = 0.003) and sodium nitroprusside (r = -0.42, p = 0.009 and r = -0.37, p = 0.02). In comparison with placebo, CPAP therapy improved forearm blood flow to all vasodilators (p = 0.01). Conclusions: Patients with OSAHS and frequent nocturnal desaturations have impaired endothelial dependent and endothelial independent vasodilatation that is proportional to hypoxaemia and is improved by CPAP therapy. Impaired vascular function establishes an underlying mechanism for the adverse cardiovascular consequences of OSAHS.",
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T1 - Continuous positive airway pressure improves vascular function in obstructive sleep apnoea/hypopnoea syndrome

T2 - A randomised controlled trial

AU - Cross, M. D.

AU - Mills, N. L.

AU - Al-Abri, M.

AU - Riha, R.

AU - Vennelle, M.

AU - Mackay, T. W.

AU - Newby, D. E.

AU - Douglas, N. J.

PY - 2008/7

Y1 - 2008/7

N2 - Background: The obstructive sleep apnoea/hypopnoea syndrome (OSAHS) is associated with hypertension and increased cardiovascular risk, particularly when accompanied by marked nocturnal hypoxaemia. The mechanisms of these associations are unclear. We hypothesised that OSAHS combined with severe nocturnal hypoxaemia causes impaired vascular function that can be reversed by continuous positive airways pressure (CPAP) therapy. Methods: We compared vascular function in two groups of patients with OSAHS: 27 with more than 20 4% desaturations/h (desaturator group) and 19 with no 4% and less than five 3% desaturations/h (non-desaturator group). In a randomised, double blind, placebo controlled, crossover trial, the effect of 6 weeks of CPAP therapy on vascular function was determined in the desaturator group. In all studies, vascular function was assessed invasively by forearm venous occlusion plethysmography during intraarterial infusion of endothelium dependent (acetylcholine 5-20 μg/min and substance P 2-8 pmol/min) and independent (sodium nitroprusside 2-8 μg/min) vasodilators. Results: Compared with the non-desaturator group, patients with OSAHS and desaturations had reduced vasodilatation to all agonists (p = 0.007 for all). The apnoea/hypopnoea index and desaturation frequency were inversely related to peak vasodilatation with acetylcholine (r = -0.44, p = 0.002 and r = -0.43, p = 0.003) and sodium nitroprusside (r = -0.42, p = 0.009 and r = -0.37, p = 0.02). In comparison with placebo, CPAP therapy improved forearm blood flow to all vasodilators (p = 0.01). Conclusions: Patients with OSAHS and frequent nocturnal desaturations have impaired endothelial dependent and endothelial independent vasodilatation that is proportional to hypoxaemia and is improved by CPAP therapy. Impaired vascular function establishes an underlying mechanism for the adverse cardiovascular consequences of OSAHS.

AB - Background: The obstructive sleep apnoea/hypopnoea syndrome (OSAHS) is associated with hypertension and increased cardiovascular risk, particularly when accompanied by marked nocturnal hypoxaemia. The mechanisms of these associations are unclear. We hypothesised that OSAHS combined with severe nocturnal hypoxaemia causes impaired vascular function that can be reversed by continuous positive airways pressure (CPAP) therapy. Methods: We compared vascular function in two groups of patients with OSAHS: 27 with more than 20 4% desaturations/h (desaturator group) and 19 with no 4% and less than five 3% desaturations/h (non-desaturator group). In a randomised, double blind, placebo controlled, crossover trial, the effect of 6 weeks of CPAP therapy on vascular function was determined in the desaturator group. In all studies, vascular function was assessed invasively by forearm venous occlusion plethysmography during intraarterial infusion of endothelium dependent (acetylcholine 5-20 μg/min and substance P 2-8 pmol/min) and independent (sodium nitroprusside 2-8 μg/min) vasodilators. Results: Compared with the non-desaturator group, patients with OSAHS and desaturations had reduced vasodilatation to all agonists (p = 0.007 for all). The apnoea/hypopnoea index and desaturation frequency were inversely related to peak vasodilatation with acetylcholine (r = -0.44, p = 0.002 and r = -0.43, p = 0.003) and sodium nitroprusside (r = -0.42, p = 0.009 and r = -0.37, p = 0.02). In comparison with placebo, CPAP therapy improved forearm blood flow to all vasodilators (p = 0.01). Conclusions: Patients with OSAHS and frequent nocturnal desaturations have impaired endothelial dependent and endothelial independent vasodilatation that is proportional to hypoxaemia and is improved by CPAP therapy. Impaired vascular function establishes an underlying mechanism for the adverse cardiovascular consequences of OSAHS.

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