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Mechanism of Endothelial Dysfunction in Obstructive Sleep Apnea (OSA)

Mechanism of Endothelial Dysfunction in Obstructive Sleep Apnea

Status
Terminated
Phases
Unknown
Study type
Observational
Source
ClinicalTrials.gov
Registry ID
NCT01027078
Enrollment
90
Registered
2009-12-07
Start date
2009-11-30
Completion date
2022-02-04
Last updated
2022-06-28

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Obstructive Sleep Apnea

Brief summary

The investigators hypothesized that patients with Obstructive Sleep Apnea (OSA) who are free of any cardiovascular disease will have early microcirculatory changes that are unique to OSA, and therefore would resolve with treatment of OSA.

Detailed description

Impaired vascular regulation of the microcirculation is a consequence of Obstructive Sleep Apnea (OSA). Nitric Oxide (NO) related endothelial dysfunction occurs in OSA as the earliest vascular abnormality prior to the manifestation of vascular disease and it results in impaired vasodilatory response to hypoxia. These abnormalities have already been described in OSA patients. The role of oxidative stress in endothelial dysfunction is present in vascular disorders. The presence of oxidative stress in OSA patients is also well established. The effect of increased superoxide on endothelial function has also been described in the literature. The mechanism of this effect is unknown and is the focus of this research. We hypothesized that patients with Obstructive Sleep Apnea (OSA) who are free of any cardiovascular disease will have early microcirculatory changes that are unique to OSA, and therefore would resolve with treatment of OSA.

Interventions

None listed

Sponsors

Ohio State University
Lead SponsorOTHER

Study design

Observational model
COHORT
Time perspective
PROSPECTIVE

Eligibility

Sex/Gender
ALL
Age
18 Years to 80 Years
Healthy volunteers
Yes

Inclusion criteria

1\. Apnea-Hypopnea Index (AHI) \> 15 events per hours.

Exclusion criteria

1. Hypertension defined by existing treatment with antihypertensives or any measurement of systolic pressure above 130 mmHg, or diastolic pressure above 85 mmHg; 2. Dyslipidemia defined by fasting cholesterol above 200; or fasting LDL over 150 mg/dl; 3. Diabetes defined as existing diagnosis, hemoglobin A1C \>7 or fasting glucose \>110 on two separate measurements (standard fasting glucose or HbA1C criteria); 4. CAD defined by history of angina, coronary event or abnormal stress test; 5. Peripheral Vascular Disease (PVD) defined by history of stroke, claudication or abnormal Ankle brachial index; 6. Concurrent smoking; 7. Pregnancy; 8. Use of erectile dysfunction drugs, or any medications for chronic conditions; 9)Chronic liver or renal disease. Fasting blood test for glucose, cholesterol, on all participants who have not had these tests in the 6 month prior to enrollment, will be obtained at the time of screening. The remaining criteria will be evaluated by reviewing the medical records and history taking on the day of first visit.

Design outcomes

Primary

MeasureTime frameDescription
eNOS ExpressionMeasured at basline and 3-months post-treatment (CPAP) initiationAll measurements will be obtained upon diagnosis of OSA and 12 weeks after effective treatment with continuous positive airway pressure (CPAP). Controls will receive all measurements at baseline.

Secondary

MeasureTime frameDescription
Peroxynitrite FormationMeasured at basline and 3-months post-treatment (CPAP) initiationAll measurements will be obtained upon diagnosis of OSA and 12 weeks after effective treatment with continuous positive airway pressure (CPAP). Controls will receive all measurements at baseline.

Other

MeasureTime frameDescription
Superoxide ProductionMeasured at basline and 3-months post-treatment (CPAP) initiationAll measurements will be obtained upon diagnosis of OSA and 12 weeks after effective treatment with continuous positive airway pressure (CPAP). Controls will receive all measurements at baseline.
Plasma BH2 and BH4 LevelsMeasured at basline and 3-months post-treatment (CPAP) initiationAll measurements will be obtained upon diagnosis of OSA and 12 weeks after effective treatment with continuous positive airway pressure (CPAP). Controls will receive all measurements at baseline. The BH2/BH4 ratio will be measured using high pressure liquid chromatography (HPLC).
Plasma ADMA LevelsMeasured at basline and 3-months post-treatment (CPAP) initiationAll measurements will be obtained upon diagnosis of OSA and 12 weeks after effective treatment with continuous positive airway pressure (CPAP). Controls will receive all measurements at baseline. Plasma ADMA levels will be measured using high pressure liquid chromatography (HPLC).

Countries

United States

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026