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Direct Characterization of the Vascular Endothelium in Sleep ApneaCharacterization of Endothelium in Sleep Apnea

Sanja Jelic, MD
Author and Funding Information

From the Division of Pulmonary, Allergy, and Critical Care Medicine, Columbia University College of Physicians and Surgeons.

Correspondence to: Sanja Jelic, MD, Columbia University College of Physicians and Surgeons, Division of Pulmonary, Allergy, and Critical Care Medicine, PH8 Center, Room 101, 630 W 168th St, New York, NY 10032; e-mail: sj366@columbia.edu

Financial/nonfinancial disclosures: The author has reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


Financial/nonfinancial disclosures: The author has reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Financial/nonfinancial disclosures: The author has reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


Chest. 2011;140(6):1400-1401. doi:10.1378/chest.11-1376
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Obstructive sleep apnea (OSA), a condition that affects one-quarter of American adults, triples the risk for hypertension, ischemic stroke, and coronary artery disease and increases all-cause mortality.1,2 OSA is characterized by repetitive cessations of breathing followed by arousals from sleep. The resulting episodes of hypoxia/reoxygenation promote platelet aggregation, leukocyte and monocyte adhesion, and macrophage activation leading to arterial and venous endothelial activation, a key step in the development and progression of cardiovascular diseases.1 Insights into OSA-related endothelial activation have been previously derived from indirect measurements of nitric oxide-mediated arterial and venous vascular tone and increased levels of soluble markers of inflammation and oxidative stress.1 However, the precise cellular pathways that are activated by repetitive hypoxia/reoxygenation have not been well characterized in the peripheral endothelium in OSA, in part owing to the limited availability of human endothelial cells. Recent development of a minimally invasive technique of endothelial harvesting from a forearm vein allows for safe collection and direct examination of endothelial cells without the artifact of culture conditions.3

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