Pilot study of the effects of bariatric surgery and continuous positive airway pressure treatment on vascular function in obese subjects with obstructive sleep apnoea
Background The mechanisms by which obesity and obstructive sleep apnoea (OSA) may contribute to endothelial dysfunction are unclear. Aims We sought to follow up a sample of obese subjects undergoing either bariatric surgery or continuous positive airway pressure (CPAP) therapy to treat OSA. We hypot...
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Published in | Internal medicine journal Vol. 43; no. 9; pp. 993 - 998 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Australia
Blackwell Publishing Ltd
01.09.2013
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Subjects | |
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Abstract | Background
The mechanisms by which obesity and obstructive sleep apnoea (OSA) may contribute to endothelial dysfunction are unclear.
Aims
We sought to follow up a sample of obese subjects undergoing either bariatric surgery or continuous positive airway pressure (CPAP) therapy to treat OSA. We hypothesised improved vascular function with both therapeutic approaches, consistent with a reversible OSA effect on the circulation.
Methods
Twenty‐seven obese (BMI ≥30 kg/m2) subjects with OSA underwent either bariatric surgery without CPAP (n = 12, median BMI 43.7 kg/m2 IQR 9.4) or CPAP (n = 15, median BMI 33.8 kg/m2 IQR 6.6). Polysomnography and vascular testing (flow‐mediated dilation of the brachial artery measured with high‐resolution ultrasound, endothelium‐dependent change in skin blood flow measured with laser Doppler flowmetry, and arterial stiffness measured with applanation tonometry) took place at baseline and after 6 months.
Results
Both groups showed significant improvements in the apnoea–hypopnea index and overnight oxygen saturation. Endothelium‐dependent microvascular reactivity was 45.6% (IQR 37.5) at baseline in the CPAP group, which increased to 69.1% (IQR 62.3) post‐treatment (P < 0.05). No significant changes were observed in the surgery group, despite significant weight loss (post‐surgery BMI 32.7 kg/m2 IQR 8.6 (P < 0.01); no change in BMI was observed in the CPAP group. There were no significant changes in brachial artery flow‐mediated dilation in either group.
Conclusions
This pilot study demonstrates that 6 months of CPAP may be sufficient to improve endothelium‐dependent microvascular reactivity, while substantial surgically induced weight loss did not result in improvements. Further research should be directed towards comparative effectiveness trials using these novel surrogate outcomes, as well as hard cardiovascular outcomes. |
---|---|
AbstractList | Abstract
Background
The mechanisms by which obesity and obstructive sleep apnoea (
OSA
) may contribute to endothelial dysfunction are unclear.
Aims
We sought to follow up a sample of obese subjects undergoing either bariatric surgery or continuous positive airway pressure (
CPAP
) therapy to treat
OSA
. We hypothesised improved vascular function with both therapeutic approaches, consistent with a reversible
OSA
effect on the circulation.
Methods
Twenty‐seven obese (
BMI
≥30 kg/m
2
) subjects with
OSA
underwent either bariatric surgery without
CPAP
(
n
= 12, median
BMI
43.7 kg/m
2
IQR
9.4) or
CPAP
(
n
= 15, median
BMI
33.8 kg/m
2
IQR
6.6). Polysomnography and vascular testing (flow‐mediated dilation of the brachial artery measured with high‐resolution ultrasound, endothelium‐dependent change in skin blood flow measured with laser
D
oppler flowmetry, and arterial stiffness measured with applanation tonometry) took place at baseline and after 6 months.
Results
Both groups showed significant improvements in the apnoea–hypopnea index and overnight oxygen saturation. Endothelium‐dependent microvascular reactivity was 45.6% (
IQR
37.5) at baseline in the
CPAP
group, which increased to 69.1% (
IQR
62.3) post‐treatment (
P
< 0.05). No significant changes were observed in the surgery group, despite significant weight loss (post‐surgery
BMI
32.7 kg/m2
IQR
8.6 (
P
< 0.01); no change in
BMI
was observed in the
CPAP
group. There were no significant changes in brachial artery flow‐mediated dilation in either group.
Conclusions
This pilot study demonstrates that 6 months of
CPAP
may be sufficient to improve endothelium‐dependent microvascular reactivity, while substantial surgically induced weight loss did not result in improvements. Further research should be directed towards comparative effectiveness trials using these novel surrogate outcomes, as well as hard cardiovascular outcomes. BACKGROUNDThe mechanisms by which obesity and obstructive sleep apnoea (OSA) may contribute to endothelial dysfunction are unclear. AIMSWe sought to follow up a sample of obese subjects undergoing either bariatric surgery or continuous positive airway pressure (CPAP) therapy to treat OSA. We hypothesised improved vascular function with both therapeutic approaches, consistent with a reversible OSA effect on the circulation. METHODSTwenty-seven obese (BMI ≥30 kg/m(2)) subjects with OSA underwent either bariatric surgery without CPAP (n = 12, median BMI 43.7 kg/m(2) IQR 9.4) or CPAP (n = 15, median BMI 33.8 kg/m(2) IQR 6.6). Polysomnography and vascular testing (flow-mediated dilation of the brachial artery measured with high-resolution ultrasound, endothelium-dependent change in skin blood flow measured with laser Doppler flowmetry, and arterial stiffness measured with applanation tonometry) took place at baseline and after 6 months. RESULTSBoth groups showed significant improvements in the apnoea-hypopnea index and overnight oxygen saturation. Endothelium-dependent microvascular reactivity was 45.6% (IQR 37.5) at baseline in the CPAP group, which increased to 69.1% (IQR 62.3) post-treatment (P < 0.05). No significant changes were observed in the surgery group, despite significant weight loss (post-surgery BMI 32.7 kg/m2 IQR 8.6 (P < 0.01); no change in BMI was observed in the CPAP group. There were no significant changes in brachial artery flow-mediated dilation in either group. CONCLUSIONSThis pilot study demonstrates that 6 months of CPAP may be sufficient to improve endothelium-dependent microvascular reactivity, while substantial surgically induced weight loss did not result in improvements. Further research should be directed towards comparative effectiveness trials using these novel surrogate outcomes, as well as hard cardiovascular outcomes. The mechanisms by which obesity and obstructive sleep apnoea (OSA) may contribute to endothelial dysfunction are unclear. We sought to follow up a sample of obese subjects undergoing either bariatric surgery or continuous positive airway pressure (CPAP) therapy to treat OSA. We hypothesised improved vascular function with both therapeutic approaches, consistent with a reversible OSA effect on the circulation. Twenty-seven obese (BMI ≥30 kg/m(2)) subjects with OSA underwent either bariatric surgery without CPAP (n = 12, median BMI 43.7 kg/m(2) IQR 9.4) or CPAP (n = 15, median BMI 33.8 kg/m(2) IQR 6.6). Polysomnography and vascular testing (flow-mediated dilation of the brachial artery measured with high-resolution ultrasound, endothelium-dependent change in skin blood flow measured with laser Doppler flowmetry, and arterial stiffness measured with applanation tonometry) took place at baseline and after 6 months. Both groups showed significant improvements in the apnoea-hypopnea index and overnight oxygen saturation. Endothelium-dependent microvascular reactivity was 45.6% (IQR 37.5) at baseline in the CPAP group, which increased to 69.1% (IQR 62.3) post-treatment (P < 0.05). No significant changes were observed in the surgery group, despite significant weight loss (post-surgery BMI 32.7 kg/m2 IQR 8.6 (P < 0.01); no change in BMI was observed in the CPAP group. There were no significant changes in brachial artery flow-mediated dilation in either group. This pilot study demonstrates that 6 months of CPAP may be sufficient to improve endothelium-dependent microvascular reactivity, while substantial surgically induced weight loss did not result in improvements. Further research should be directed towards comparative effectiveness trials using these novel surrogate outcomes, as well as hard cardiovascular outcomes. Background The mechanisms by which obesity and obstructive sleep apnoea (OSA) may contribute to endothelial dysfunction are unclear. Aims We sought to follow up a sample of obese subjects undergoing either bariatric surgery or continuous positive airway pressure (CPAP) therapy to treat OSA. We hypothesised improved vascular function with both therapeutic approaches, consistent with a reversible OSA effect on the circulation. Methods Twenty‐seven obese (BMI ≥30 kg/m2) subjects with OSA underwent either bariatric surgery without CPAP (n = 12, median BMI 43.7 kg/m2 IQR 9.4) or CPAP (n = 15, median BMI 33.8 kg/m2 IQR 6.6). Polysomnography and vascular testing (flow‐mediated dilation of the brachial artery measured with high‐resolution ultrasound, endothelium‐dependent change in skin blood flow measured with laser Doppler flowmetry, and arterial stiffness measured with applanation tonometry) took place at baseline and after 6 months. Results Both groups showed significant improvements in the apnoea–hypopnea index and overnight oxygen saturation. Endothelium‐dependent microvascular reactivity was 45.6% (IQR 37.5) at baseline in the CPAP group, which increased to 69.1% (IQR 62.3) post‐treatment (P < 0.05). No significant changes were observed in the surgery group, despite significant weight loss (post‐surgery BMI 32.7 kg/m2 IQR 8.6 (P < 0.01); no change in BMI was observed in the CPAP group. There were no significant changes in brachial artery flow‐mediated dilation in either group. Conclusions This pilot study demonstrates that 6 months of CPAP may be sufficient to improve endothelium‐dependent microvascular reactivity, while substantial surgically induced weight loss did not result in improvements. Further research should be directed towards comparative effectiveness trials using these novel surrogate outcomes, as well as hard cardiovascular outcomes. |
Author | Bakker, J. P. Tecilazich, F. Balachandran, J. S. Veves, A. DeYoung, P. N. Smales, E. Malhotra, A. |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23800096$$D View this record in MEDLINE/PubMed |
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Snippet | Background
The mechanisms by which obesity and obstructive sleep apnoea (OSA) may contribute to endothelial dysfunction are unclear.
Aims
We sought to follow... The mechanisms by which obesity and obstructive sleep apnoea (OSA) may contribute to endothelial dysfunction are unclear. We sought to follow up a sample of... Abstract Background The mechanisms by which obesity and obstructive sleep apnoea ( OSA ) may contribute to endothelial dysfunction are unclear. Aims We sought... BACKGROUNDThe mechanisms by which obesity and obstructive sleep apnoea (OSA) may contribute to endothelial dysfunction are unclear. AIMSWe sought to follow up... |
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SubjectTerms | Adult Bariatric Surgery - methods Blood Flow Velocity - physiology cardiovascular Continuous Positive Airway Pressure - methods Cross-Sectional Studies endothelium Endothelium, Vascular - physiology Female Follow-Up Studies Humans Laser-Doppler Flowmetry - methods Male microvascular Middle Aged Obesity - epidemiology Obesity - physiopathology Obesity - therapy obstructive sleep apnoea Pilot Projects Polysomnography - methods Sleep Apnea, Obstructive - epidemiology Sleep Apnea, Obstructive - physiopathology Sleep Apnea, Obstructive - therapy Treatment Outcome |
Title | Pilot study of the effects of bariatric surgery and continuous positive airway pressure treatment on vascular function in obese subjects with obstructive sleep apnoea |
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