Why the study?
Obstructive sleep apnea is common, frequently overlooked, misdiagnosed, and untreated, yet intermittent hypoxia is linked to endothelial dysfunction, atherogenesis, and cerebrovascular incidents.
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Design
Review article
This review summarizes the pathophysiological mechanisms linking obstructive sleep apnea to cerebrovascular disease, emphasizing the roles of intermittent hypoxia, microparticles, and cyclooxygenase enzymes in promoting endothelial dysfunction and atherogenesis.
Obstructive Sleep Apnea (OSA) is a sleep disorder caused by breathing problems that occur during sleep due to airway obstruction. Obstructive Sleep Apnea is quite common, but is often overlooked and misdiagnosed and untreated. Many studies have proven the relationship between OSA and pathological diseases such as cardiovascular disease and stroke. Intermittent Hypoxia (IH) that occurs in OSA patients can cause endothelial dysfunction and play a role in the atherogenesis of peripheral and central blood vessels of the brain. Hypoxic conditions cause the release of microparticles, inflammatory mediators and increase the expression of the enzyme Cyclooxygenase (COX) in the vascular endothelium. This causes an increase in inflammation-related prostanoid production which in turn causes endothelial damage and increases the risk of atherosclerotic plaque formation. This review article will discuss the role of inflammatory mediators, especially COX enzymes in OSA-related cerebrovascular incidents.
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Togatorop et al. (2023) studied this question.
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