New and emerging research is helping clinicians better understand the role of untreated obstructive sleep apnea in the development or worsening of comorbidities.
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“The reason we treat sleep apnea is, number one, to improve quality of life and, number two, to improve cardiovascular health, although arguably there are other health benefits,” says Reena Mehra, MD, MS, Director of Sleep Disorders Research in Cleveland Clinic’s Sleep Disorders Center.
Dr. Mehra explains the link between sleep apnea and cardiovascular, neurological and metabolic comorbidities in the newest episode of Cleveland Clinic’s Neuro Pathways podcast. She also discusses:
Click the podcast player above to listen to the episode now, or read on for a short edited excerpt. Check out more Neuro Pathways episodes at clevelandclinic.org/neuropodcast or wherever you get your podcasts.
Dr. Mehra: Obstructive sleep apnea is characterized by upper airway collapse, which leads to cessation of breathing. When there’s cessation of breathing, oxygen levels decline. With the apneas and also partial upper airway closure (the hypopneas), there is sympathetic nervous system activation — alterations in the autonomic nervous system. During the event there’s enhanced parasympathetic tone, and then subsequent to the event there is sympathetic surge. So, there’s this juxtaposition of parasympathetic and sympathetic activation that occurs, and there are rises in carbon dioxide. Times of hypoxia and then resaturation are times of vulnerability to oxidative stress and increased systemic inflammation.
Taken together, these pathophysiologic consequences of obstructive sleep apnea confer risk not only immediately during sleep but also during the daytime. There are data to show that in those with severe sleep apnea over time, vascular remodeling occurs. This sets the stage for increased cardiovascular consequences because of alterations in the autonomic nervous system that can be increased in the setting of sleep apnea — hypoxia, hypercapnia, increased systemic inflammation, oxidative stress, a prothrombotic state. The vascular remodeling sets the stage for metabolic consequences as well, with insulin resistance. All of these taken together can increase the risk for cardiovascular events, meaning myocardial infarction, stroke, heart failure and, something our group has been very interested in, cardiac arrhythmia. Arrhythmogenesis likely increases partly due to remodeling the heart structurally and also electrically.
In terms of the neurologic aspects in addition to stroke, there are relationships between not only sleep apnea but also sleep disruption and sleep deprivation with neurodegeneration, in particular Alzheimer’s dementia. Some really compelling data has emerged over the last several years, showing that in experimental models curtailment of sleep impairs beta-synuclein clearance and causes buildup of this pathology and, therefore, can contribute to neurodegeneration. In addition, there are data to suggest that the progression of neurodegeneration over time may be related to the nocturnal hypoxia associated with sleep apnea.