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Review
. 2024 Sep 24;84(13):1208-1223.
doi: 10.1016/j.jacc.2024.02.059.

Interactions of Obstructive Sleep Apnea With the Pathophysiology of Cardiovascular Disease, Part 1: JACC State-of-the-Art Review

Affiliations
Review

Interactions of Obstructive Sleep Apnea With the Pathophysiology of Cardiovascular Disease, Part 1: JACC State-of-the-Art Review

Shahrokh Javaheri et al. J Am Coll Cardiol. .

Abstract

The American Heart Association considers sleep health an essential component of cardiovascular health, and sleep is generally a time of cardiovascular quiescence, such that any deviation from normal sleep may be associated with adverse cardiovascular consequences. Many studies have shown that both impaired quantity and quality of sleep, particularly with obstructive sleep apnea (OSA) and comorbid sleep disorders, are associated with incident cardiometabolic consequences. OSA is associated with repetitive episodes of altered blood gases, arousals, large negative swings in intrathoracic pressures, and increased sympathetic activity. Recent studies show that OSA is also associated with altered gut microbiota, which could contribute to increased risk of cardiovascular disease. OSA has been associated with hypertension, atrial fibrillation, heart failure, coronary artery disease, stroke, and excess cardiovascular mortality. Association of OSA with chronic obstructive lung disease (overlap syndrome) and morbid obesity (obesity hypoventilation syndrome) increases the odds of mortality.

Keywords: atrial fibrillation; cardiovascular disease; cardiovascular mortality; coronary heart disease; hypertension; obstructive sleep apnea.

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Conflict of interest statement

Funding Support and Author Disclosures No funding was received for this study. Dr Shahrokh Javaheri is funded by the National Institutes of Health (NIH) for an oxygen trial; has received income related to medical education from Jazz and Idorsia Pharmaceutical; and has served as a consultant to ZOLL Respicardia. Dr Sogol Javaheri has received grant funding from Zoll, the Massachusetts Technology Collaborative, and an internal health equity grant from Harvard Medical School. Dr Somers is funded by the National Heart, Lung, and Blood Institute (HL65176 and HL160619); has served as a consultant for Bayer, Jazz Pharmaceuticals, Huxley, Apnimed, ResMed, Lilly, Wesper, and ZOLL; and is on the Sleep Number Scientific Advisory Board. Dr Gozal is funded by the NIH for research on sleep apnea, mineralocorticoid receptors, and Alzheimer disease, University of Missouri grants, and the Leda J. Sears Foundation. Dr Mehra is supported by American Academy of Sleep Medicine and American Heart Association grants; has received honorarium from the American Academy of Sleep Medicine for speaking; and has received royalties from UpToDate. Dr Zee is funded by the NIH; has served as a consultant to Eisai, Idorsia, Jazz, Harmony, and Sanofi; and reports grants to Northwestern University from Vanda. Dr Cistulli has an appointment to an endowed academic Chair at the University of Sydney that was established from ResMed funding; has received research support from ResMed and SomnoMed; is a consultant to ResMed, SomnoMed, Signifier Medical Technologies, Bayer, and Sunrise Medical; and has a pecuniary interest in SomnoMed related to a role in research and development (2004). Dr Malhotra is funded by the NIH; has received income related to medical education from Jazz, LivaNova, Eli Lilly, and Zoll; and ResMed provided a philanthropic donation to UC San Diego. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Figures

FIGURE 1
FIGURE 1. 30-Second Epoch of Obstructive Sleep Apnea
These tracings show that during an obstructive apnea, airflow is absent while breathing effort continues. Breathing resumes with the onset of arousal. The first tracing is a chin electromyogram, the second and third tracings are an electroencephalogram, fourth is electrocardiogram, fifth and sixth are airflow measured by thermocouple (fifth) and carbon dioxide (CO2) (sixth), seventh and eighth are rib cage (seventh) and abdominal (eighth), ninth is oxyhemoglobin saturation measured by pulse oximetry, and tenth is esophageal pressure. Reproduced with permission from Javaheri et al. PCO2 = partial pressure of carbon dioxide; PO2 = partial pressure of oxygen.
FIGURE 2
FIGURE 2. Prevalence of Sleep Disordered Breathing Types
The bar graph details the prevalence of specific types of sleep disordered breathing among patients with a range of left ventricular dysfunction to overt heart failure. Adapted from Javaheri et al. ACPE = acute cardiogenic pulmonary edema; ADHF = acute diastolic heart failure; AHI = apnea hypopnea index; CSA = central sleep apnea; HFpEF = heart failure with preserved ejection fraction; HFrEF = heart failure with reduced ejection fraction; LVDD = left ventricular diastolic dysfunction; LVSD = left ventricular systolic dysfunction; OSA = obstructive sleep apnea.
FIGURE 3
FIGURE 3. Patterns of Oxygen Desaturation During Sleep
Depiction of oxygen desaturation patterns during sleep in individual patients with chronic obstructive pulmonary disease (COPD) alone, overlap syndrome of COPD and obstructive sleep apnea (OSA), and OSA alone. The COPD example shows stable desaturation during nonrapid eye movement sleep that is more pronounced during rapid eye movement. The OSA example shows intermittent desaturations during apnea with resaturation to normal levels in between events. The overlap example shows more pronounced baseline desaturation with superimposed intermittent further desaturations during apnea.
CENTRAL ILLUSTRATION
CENTRAL ILLUSTRATION. Pathophysiological Consequences of Sleep Apnea and Hypopnea
Pleural pressure (Ppl) is a surrogate of the pressure surrounding the heart and other vascular structures. Reproduced from Javaheri et al.

References

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