Mechanisms of Endothelial Cell Dysfunction in Sleep Apnea

NCT ID: NCT00859950

Last Updated: 2019-02-04

Basic Information

• Recruitment Status: COMPLETED
• Clinical Phase: NA
• Total Enrollment: 70 participants
• Study Classification: INTERVENTIONAL
• Study Start Date: 2009-04-30
• Study Completion Date: 2015-08-31

Brief Summary

Sleep apnea is a common sleep disorder characterized by temporary stops in breathing during sleep and has been associated with the development of cardiovascular disease. This research will investigate one potential mechanism leading to the development of cardiovascular disorder, specifically, the blockage of blood vessels called "vascular occlusion", in subjects with sleep apnea. A group of healthy controls will be used for comparison. All subjects will undergo clinical evaluation followed by an overnight sleep study and a morning blood draw. Subjects with sleep apnea will be treated according to standard clinical management and followed under the research protocol for one month. At the end of one month, a repeat blood draw will be performed on the sleep apnea subjects for comparative analysis. If a control subject is found to have any abnormality during this research study, he or she will be referred for further clinical evaluation.

Detailed Description

The importance of this project is to investigate mechanisms of vascular disease in sleep apnea and determine pathways for intervention, aiming to prevent the development of cardiovascular disease in these individuals.

This proposed research aims to evaluate both NTPDase activity in lymphocytes and levels of circulating endothelial cells (CECs) in patients with intermittent hypoxemia (IH) due to obstructive sleep apnea (OSA) and healthy controls. This is an original approach to define mechanisms which underlie the high incidence of occlusive vascular events in patients with OSA. The evaluation of such pathophysiological mechanisms will lead to a better understanding of the pathways involved and the development of therapeutic strategies targeting the reduction or avoidance of endothelial injury with the ultimate goal of reducing morbidity and mortality associated with these pathologic events in sleep apnea. The standard of care will be used in this protocol, which involves the use of CPAP (continuous positive airway pressure) for treating sleep apnea.

Conditions

Obstructive Sleep Apnea; Hypoxemia

Study Design

• Allocation Method: NON_RANDOMIZED
• Intervention Model: PARALLEL
• Primary Study Purpose: BASIC_SCIENCE
• Blinding Strategy: NONE

Study Groups

Sleep Apnea

Subjects found to have Obstructive Sleep Apnea (OSA) with Intermittent Hypoxemia (IH). This arm will undergo a pre-treatment blood draw, one month of Continuous Positive Airway Pressure (CPAP) to treat OSA, and a post-treatment blood draw.

Group Type: ACTIVE_COMPARATOR

Continuous Positive Airway Pressure (CPAP)

Intervention Type: DEVICE

Continuous positive airway pressure (CPAP) is a method of respiratory ventilation which is accepted as the gold standard to treat Obstructive Sleep Apnea (OSA). Subjects found to have OSA after the Nocturnal Polysomnography (NPSG) will be trained in the use of CPAP and will be instructed to use CPAP every night for 30 nights. These subjects will then return for a post-treatment blood draw.

Normal Control

Subject found to have no evidence of Obstructive Sleep Apnea (OSA) after Nocturnal Polysomnography (NPSG). These subjects will only undergo a blood draw and will not have the Continuous Positive Airway Pressure (CPAP) treatment.

Group Type: NO_INTERVENTION

No interventions assigned to this group

Interventions

Continuous Positive Airway Pressure (CPAP)

Continuous positive airway pressure (CPAP) is a method of respiratory ventilation which is accepted as the gold standard to treat Obstructive Sleep Apnea (OSA). Subjects found to have OSA after the Nocturnal Polysomnography (NPSG) will be trained in the use of CPAP and will be instructed to use CPAP every night for 30 nights. These subjects will then return for a post-treatment blood draw.

Intervention Type: DEVICE

Eligibility Criteria

Inclusion Criteria

• 21 years or older
• Presence of intermittent hypoxemia (IH) and obstructive sleep apnea (OSA)
• No diagnosis of hypertension, coronary artery disease, diabetes, stroke, or evidence of underlying vascular disease

• 21 years or older
• No diagnosis of intermittent hypoxemia (IH) or obstructive sleep apnea (OSA)
• No diagnosis of hypertension, coronary artery disease, diabetes, stroke, or evidence of underlying vascular disease

Exclusion Criteria

• Smoking
• Pregnancy
• Known cardiovascular disease, stroke, or diabetes
• Current or previous treatment for sleep apnea
• Central or Cheyne-Stokes sleep apnea
• Use of supplemental oxygen at night
• Alcohol abuse
• Regular use of sedatives
• Regular use of aspirin or cholesterol lowering agents

Study Group 2: Normal Controls

• Smoking
• Pregnancy
• Known cardiovascular disease, stroke, or diabetes
• Use of supplemental oxygen at night
• Alcohol abuse
• Regular use of sedatives
• Regular use of aspirin or cholesterol lowering agents

• Minimum Eligible Age: 21 Years
• Eligible Sex: ALL
• Accepts Healthy Volunteers: Yes

Sponsors

Weill Medical College of Cornell University

OTHER

Sponsor Role: lead

National Institutes of Health (NIH)

NIH

Sponsor Role: collaborator

National Heart, Lung, and Blood Institute (NHLBI)

NIH

Sponsor Role: collaborator

Responsible Party

Ana C. Krieger

Dr. Ana Krieger, MD. MPH

Responsibility Role: PRINCIPAL_INVESTIGATOR

Principal Investigators

Ana C Krieger, MD, MPH

Role: PRINCIPAL_INVESTIGATOR

Weill Medical College of Cornell University

Locations

Weill Cornell Medical College - Weill Cornell Pulmonary Associates

New York, New York, United States

Countries

United States

References

Krieger AC, Anand R, Hernandez-Rosa E, Maidman A, Milrad S, DeGrazia MQ, Choi AJ, Oromendia C, Marcus AJ, Drosopoulos JHF. Increased platelet activation in sleep apnea subjects with intermittent hypoxemia. Sleep Breath. 2020 Dec;24(4):1537-1547. doi: 10.1007/s11325-020-02021-4. Epub 2020 Feb 8.

Reference Type: DERIVED

PMID: 32036486 (View on PubMed)

Other Identifiers

1K23HL094358-01A2

Identifier Type: NIH

Identifier Source: secondary_id

View Link

0811010102

Identifier Type: -

Identifier Source: org_study_id