Sleep Apnea and Cardiovascular Disease: An Enigmatic Risk Factor
Abstract
Synchronization of molecular, metabolic, and cardiovascular circadian oscillations is fundamental to human health. Sleep-disordered breathing, which disrupts such temporal congruence, elicits hemodynamic, autonomic, chemical, and inflammatory disturbances with acute and long-term consequences for heart, brain, and circulatory and metabolic function. Sleep apnea afflicts a substantial proportion of adult men and women but is more prevalent in those with established cardiovascular diseases and especially fluid-retaining states. Despite the experimental, epidemiological, observational, and interventional evidence assembled in support of these concepts, this substantial body of work has had relatively modest pragmatic impact, thus far, on the discipline of cardiology. Contemporary estimates of cardiovascular risk still are derived typically from data acquired during wakefulness. The impact of sleep-related breathing disorders rarely is entered into such calculations or integrated into diagnostic disease-specific algorithms or therapeutic recommendations. Reasons for this include absence of apnea-related symptoms in most with cardiovascular disease, impediments to efficient diagnosis at the population level, debate as to target, suboptimal therapies, difficulties mounting large randomized trials of sleep-specific interventions, and the challenging results of those few prospective cardiovascular outcome trials that have been completed and reported. The objectives of this review are to delineate the bidirectional interrelationship between sleep-disordered breathing and cardiovascular disease, consider the findings and implications of observational and randomized trials of treatment, frame the current state of clinical equipoise, identify principal current controversies and potential paths to their resolution, and anticipate future directions.
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Carotid body chemoreceptors are believed to have a pivotal role in sympathetic dysregulation in obstructive sleep apnoea.
“Carotid body chemoreceptors are believed to have a pivotal role in sympathetic dysregulation in OSA, although other mechanisms may also contribute183,184.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [184]
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Obesity, kidney dysfunction and hypertension: mechanistic links
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- Authors
- Floras, J. S.
- Affiliations
- University Health Network (CA)
- Corresponding author
- Floras, John S.
- ORCID
- Floras, John S.
- Venue
- Circulation Research
- Published
- 2018-06-08
- Volume
- 122
- Issue
- 12
- Pages
- 1741-1764
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2805115566
- Cited by
- 209
- References
- 276
- Citations by year
- 2026: 20 · 2025: 16 · 2024: 23 · 2023: 21 · 2022: 26 · 2021: 41 · 2020: 33 · 2019: 21 · 2018: 7
- FWCI
- 3.36
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canadian Institutes of Health Research
- Topics
- Health Sciences › Medicine › Physiology › Obstructive Sleep Apnea Research
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and related disorders
- Health Sciences › Medicine › Pharmacology › Apelin-related biomedical research
- Keywords
- sleep apnea, sleep-disordered breathing, cardiovascular disease, circadian rhythm, autonomic dysfunction, inflammation, fluid retention, cardiovascular risk assessment, sleep apnea treatment, cardiovascular outcome trials, bidirectional relationship
- MeSH terms
- Cardiovascular Diseases, Female, Humans, Male, Risk Factors, Sleep Apnea Syndromes, Prevalence, Randomized Controlled Trials as Topic, Observational Studies as Topic
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