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Endothelial Damage and Atherosclerosis in Obstructive Sleep Apnea

The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.
 
ClinicalTrials.gov Identifier: NCT00942643
Recruitment Status : Terminated (Poor patient recruitment)
First Posted : July 21, 2009
Last Update Posted : July 4, 2012
Sponsor:
Information provided by (Responsible Party):
Lam Jamie Chung Mei, The University of Hong Kong

Tracking Information
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
 (submitted: July 20, 2009)
AGEs levels [ Time Frame: 4 weeks and 12 weeks ]
Original Primary Outcome Measures  ICMJE Same as current
Change History
Current Secondary Outcome Measures  ICMJE
 (submitted: July 20, 2009)
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:

  1. To explore the relationship between insulin resistance and AGEs in OSA
  2. To study the relationship between AGE and vascular endothelial dysfunction in OSA
  3. To study the relationship between AGE and early atherosclerosis in OSA
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.

Study Type  ICMJE Interventional
Study Phase  ICMJE Not Applicable
Study Design  ICMJE Allocation: Randomized
Intervention Model: Parallel Assignment
Masking: Single (Investigator)
Primary Purpose: Treatment
Condition  ICMJE
  • Obstructive Sleep Apnea
  • Insulin Resistance
  • Endothelial Function
  • Oxidative Stress
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
Study Arms  ICMJE
  • No Intervention: no treatment
    being observed at 4 weeks and 12 weeks
  • Active Comparator: CPAP treatment
    a machine delivers positive airway pressure into the upper airway via nasal mask
    Intervention: Device: CPAP machine
Publications * Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Recruitment Information
Recruitment Status  ICMJE Terminated
Actual Enrollment  ICMJE
 (submitted: July 3, 2012)
10
Original Estimated Enrollment  ICMJE
 (submitted: July 20, 2009)
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:

  • age 18-65 years old
  • AHI >= 15
  • BMI < 35

Exclusion Criteria:

  • Known cardiovascular disease, including hypertension
  • Diabetes
  • Acute or unstable chronic disease
  • Renal failure
  • Major organ system failure, including liver, renal, cardiac and respiratory failure
  • Taking long-term medications
Sex/Gender  ICMJE
Sexes Eligible for Study: All
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
Principal Investigator: Mary SM Ip, MD Queen Mary Hospital, The University of Hong Kong
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