Mechanism of Endothelial Dysfunction in Obstructive Sleep Apnea (OSA)
Status: | Active, not recruiting |
---|---|
Conditions: | Insomnia Sleep Studies, Pulmonary |
Therapuetic Areas: | Psychiatry / Psychology, Pulmonary / Respiratory Diseases |
Healthy: | No |
Age Range: | 18 - 80 |
Updated: | 3/23/2019 |
Start Date: | November 2009 |
End Date: | December 2019 |
Mechanism of Endothelial Dysfunction in Obstructive Sleep Apnea
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.
of any cardiovascular disease will have early microcirculatory changes that are unique to
OSA, and therefore would resolve with treatment of OSA.
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.
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.
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.
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