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Endothelial Damage and Atherosclerosis in Obstructive Sleep Apnea

This study has been terminated.
(Poor patient recruitment)
Information provided by (Responsible Party):
Lam Jamie Chung Mei, The University of Hong Kong Identifier:
First received: July 20, 2009
Last updated: July 3, 2012
Last verified: July 2012

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

Condition Intervention
Obstructive Sleep Apnea
Insulin Resistance
Endothelial Function
Oxidative Stress
Device: CPAP machine

Study Type: Interventional
Study Design: Allocation: Randomized
Intervention Model: Parallel Assignment
Masking: Single Blind (Investigator)
Primary Purpose: Treatment
Official Title: Endothelial Damage and Atherosclerosis in Obstructive Sleep Apnea: the Role of Advanced Glycation End-products

Resource links provided by NLM:

Further study details as provided by The University of Hong Kong:

Primary Outcome Measures:
  • AGEs levels [ Time Frame: 4 weeks and 12 weeks ]

Secondary Outcome Measures:
  • endothelial function as assessed by reactive hyperemia-induced peripheral arterial tone response [ Time Frame: 4 weeks and 12 weeks ]

Enrollment: 10
Study Start Date: May 2008
Study Completion Date: March 2010
Primary Completion Date: March 2010 (Final data collection date for primary outcome measure)
Arms Assigned Interventions
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
Device: CPAP machine
a machine delivers positive airway pressure into the upper airway via a nasal mask
Other Name: Continuous Positive Airway Pressure

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.


Ages Eligible for Study:   18 Years to 65 Years   (Adult)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   Yes

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
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Please refer to this study by its identifier: NCT00942643

Hong Kong
Queen Mary Hospital
Pokfulam, Hong Kong
Sponsors and Collaborators
The University of Hong Kong
Principal Investigator: Mary SM Ip, MD Queen Mary Hospital, The University of Hong Kong
  More Information

Responsible Party: Lam Jamie Chung Mei, Honorary clinical assistant professor, The University of Hong Kong Identifier: NCT00942643     History of Changes
Other Study ID Numbers: HKCTR-772
Study First Received: July 20, 2009
Last Updated: July 3, 2012

Additional relevant MeSH terms:
Sleep Apnea Syndromes
Sleep Apnea, Obstructive
Insulin Resistance
Respiration Disorders
Respiratory Tract Diseases
Signs and Symptoms, Respiratory
Signs and Symptoms
Sleep Disorders, Intrinsic
Sleep Wake Disorders
Nervous System Diseases
Glucose Metabolism Disorders
Metabolic Diseases
Arterial Occlusive Diseases
Vascular Diseases
Cardiovascular Diseases processed this record on April 27, 2017