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Coronary Collateral Circulation in Sleep Apnea: A Cardioprotective Mechanism?

Lena Lavie, PhD; Peretz Lavie, PhD
Author and Funding Information

From the Unit of Anatomy and Cell Biology, The Ruth and Bruce Rappaport Faculty of Medicine, Technion Institute of Technology.

Correspondence to: Lena Lavie, Unit of Anatomy and Cell Biology, The Ruth and Bruce Rappaport Faculty of Medicine, Technion Institute of Technology, POB 9649, 31096, Haifa, Israel; e-mail: lenal@tx.technion.ac.il


Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Dr L. Lavie has no potential conflicts of interest with any companies/organizations whose products or services may be discussed in this article. Dr P. Lavie was a director at Itamar Medical Ltd. through September 31, 2009, and currently holds shares in the company.

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


© 2010 American College of Chest Physicians


Chest. 2010;137(3):511-512. doi:10.1378/chest.09-2657
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Cross-sectional, prospective, and interventional studies have demonstrated that obstructive sleep apnea (OSA) is an independent risk factor for cardiovascular morbidity and mortality. Intermittent hypoxia (IH)—the hallmark of OSA—which initiates a cascade of events involving oxidative stress and inflammatory processes leading to atherogenesis, pro­vides at least one pathway through which OSA affects the cardiovascular system.1 Interestingly, although mortality in OSA increases with syndrome severity, it was repeatedly shown to decline with aging.2 Moreover, unexpectedly, elderly patients with moderate OSA showed survival advantage in comparison with an age-, gender-, and ethnicity-matched cohort of the general population.3 The age decline trend in mortality of patients with OSA has led us to hypothesize that at least some patients with OSA develop an adaptive mechanism in the form of ischemic preconditioning in which repeated sublethal ischemia confers profound protection from infarction and further ischemic insults. In OSA, this could result from the nocturnal cycles of repeated hypoxia-reoxygenation events.4 Our hypothesis relied on two additional key findings. First, vascular endothelial growth factor (VEGF), which plays a major role in angiogenesis, showed OSA severity-dependent increases during sleep.5 Second, major individual differences were noted in fold VEGF mRNA increase in response to an identical hypoxic stimulus.6 Therefore, we proposed that in OSA: “Upregulation of VEGF may trigger the development of coronary collaterals that may protect the myocardium during periods of severe ischemia.”4 Although this could result from the specific hypoxic events characteristic of OSA, genetic variations in the response to hypoxia or obesity, which is highly prevalent in OSA but also triggers VEGF production, could largely affect VEGF levels and consequently blood vessel collateral formation.

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