Endothelial Damage and Atherosclerosis in Obstructive Sleep Apnea
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ClinicalTrials.gov Identifier: NCT00942643 |
Recruitment Status :
Terminated
(Poor patient recruitment)
First Posted : July 21, 2009
Last Update Posted : July 4, 2012
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Tracking Information | ||||
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First Submitted Date ICMJE | July 20, 2009 | |||
First Posted Date ICMJE | July 21, 2009 | |||
Last Update Posted Date | July 4, 2012 | |||
Study Start Date ICMJE | May 2008 | |||
Actual Primary Completion Date | March 2010 (Final data collection date for primary outcome measure) | |||
Current Primary Outcome Measures ICMJE |
AGEs levels [ Time Frame: 4 weeks and 12 weeks ] | |||
Original Primary Outcome Measures ICMJE | Same as current | |||
Change History | ||||
Current Secondary Outcome Measures ICMJE |
endothelial function as assessed by reactive hyperemia-induced peripheral arterial tone response [ Time Frame: 4 weeks and 12 weeks ] | |||
Original Secondary Outcome Measures ICMJE | Same as current | |||
Current Other Pre-specified Outcome Measures | Not Provided | |||
Original Other Pre-specified Outcome Measures | Not Provided | |||
Descriptive Information | ||||
Brief Title ICMJE | Endothelial Damage and Atherosclerosis in Obstructive Sleep Apnea | |||
Official Title ICMJE | Endothelial Damage and Atherosclerosis in Obstructive Sleep Apnea: the Role of Advanced Glycation End-products | |||
Brief Summary | The investigators hypothesize that obstructive sleep apnea (OSA) may lead to increased formation/accumulation of advanced glycation ends (AGEs), and that the increase in AGEs is contributed in part by increased insulin resistance. The investigators further hypothesize that AGEs contribute to vascular endothelial damage and ultimately atherosclerosis in OSA. The objectives of this study are:
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Detailed Description | There is growing evidence to suggest that pathophysiology of OSA may lead to atherosclerosis, independent of confounding variables which are often present in these subjects with OSA. Many mechanisms have been reported to contribute to vasculopathy in OSA, but whether increased AGEs formation contribute significantly to the pathogenesis of cardiovascular morbidity in OSA remains to be determined. Advanced glycation product is formed by non-enzymatic reaction of reducing sugars such as glucose with the amino groups of proteins, and subsequent glycoxidation. AGEs can form on long-lived extracellular proteins as well as short-lived molecules, cytoplasmic proteins and nuclear acids. AGEs cause a number of adverse cellular events and they have been demonstrated in fatty streaks and atherosclerotic plaques. The formation and tissue accumulation of AGE is shown to be enhanced by hyperglycemia and/or increased oxidative stress. There is increasing evidence to support this as an important mechanism of vascular and other end organ damage in diabetes and some other diseases. In OSA, there is evidence to support an increased insulin resistance and excessive oxidative stress, both of which may predispose to AGE formation. We have preliminary data to suggest increased levels of circulating AGE in non-diabetic OSA subjects. Since insulin resistance with elevated blood glucose levels, albeit not up to diabetic thresholds, may partially contribute to increase in AGE. Many potential mechanisms of atherosclerosis have been reported, but direct evidence for atherosclerosis is still lacking. Subjects with OSA also have comorbidities which may give rise to atherosclerosis. With the advancement of non-invasive techniques for detection of vascular endothelial damage and early atherosclerosis, it is possible to detect early vascular abnormalities in otherwise healthy OSA subjects. This hypothesis underlies our objectives to explore the relationship between AGE and the markers of endothelial dysfunction and early atherosclerosis. Some of these early changes, especially at endothelial level, may be reversible if the insult of OSA is removed. Thus a longitudinal comparison of OSA-treated and OSA-untreated subjects on such changes would further help to clarify the issue. |
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Study Type ICMJE | Interventional | |||
Study Phase ICMJE | Not Applicable | |||
Study Design ICMJE | Allocation: Randomized Intervention Model: Parallel Assignment Masking: Single (Investigator) Primary Purpose: Treatment |
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Condition ICMJE |
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Intervention ICMJE | Device: CPAP machine
a machine delivers positive airway pressure into the upper airway via a nasal mask
Other Name: Continuous Positive Airway Pressure
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Study Arms ICMJE |
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Publications * | Not Provided | |||
* Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline. |
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Recruitment Information | ||||
Recruitment Status ICMJE | Terminated | |||
Actual Enrollment ICMJE |
10 | |||
Original Estimated Enrollment ICMJE |
50 | |||
Actual Study Completion Date ICMJE | March 2010 | |||
Actual Primary Completion Date | March 2010 (Final data collection date for primary outcome measure) | |||
Eligibility Criteria ICMJE | Inclusion Criteria:
Exclusion Criteria:
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Sex/Gender ICMJE |
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Ages ICMJE | 18 Years to 65 Years (Adult, Older Adult) | |||
Accepts Healthy Volunteers ICMJE | Yes | |||
Contacts ICMJE | Contact information is only displayed when the study is recruiting subjects | |||
Listed Location Countries ICMJE | Hong Kong | |||
Removed Location Countries | ||||
Administrative Information | ||||
NCT Number ICMJE | NCT00942643 | |||
Other Study ID Numbers ICMJE | HKCTR-772 | |||
Has Data Monitoring Committee | Yes | |||
U.S. FDA-regulated Product | Not Provided | |||
IPD Sharing Statement ICMJE | Not Provided | |||
Responsible Party | Lam Jamie Chung Mei, The University of Hong Kong | |||
Study Sponsor ICMJE | The University of Hong Kong | |||
Collaborators ICMJE | Not Provided | |||
Investigators ICMJE |
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PRS Account | The University of Hong Kong | |||
Verification Date | July 2012 | |||
ICMJE Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP |