TY - JOUR
T1 - Excessive daytime sleepiness
T2 - an emerging marker of cardiovascular risk
AU - Bock, Joshua
AU - Covassin, Naima
AU - Somers, Virend
N1 - Funding Information:
JB is funded by the National Institutes of Health grant T32-HL007111. NC is supported by the National Institutes of Health grants HL134885 and HL134808, Mayo Clinic Marie Ingalls Research Career Development Award and a grant from Sleep Number Corporation to Mayo Clinic. VS is funded by the National Institutes of Health grants HL134885 and HL065176 as well as a grant from Sleep Number Corporation to Mayo Clinic for studies of the cardiovascular implications of sleepiness.
Publisher Copyright:
© Author(s) (or their employer(s)) 2022.No commercial re-use.See rights and permissions.Published by BMJ.
PY - 2022/10/28
Y1 - 2022/10/28
N2 - Excessive daytime sleepiness (EDS) is classically viewed as a consequence of insufficient sleep or a symptom of sleep disorders.Epidemiological and clinical evidence have shown that patients reporting EDS in tandem with sleep disorders (e.g., obstructive sleep apnoea) are at greater cardiovascular risk than non-sleepy patients.While this may simply be attributable to EDS being present in patients with a more severe condition, treatment of sleep disorders does not consistently alleviate EDS, indicating potential aetiological differences.Moreover, not all patients with sleep disorders report EDS, and daytime sleepiness may be present even in the absence of any identifiable sleep disorder; thus, EDS could represent an independent pathophysiology.The purpose of this review is twofold: first, to highlight evidence that EDS increases cardiovascular risk in the presence of sleep disorders such as obstructive sleep apnoea, narcolepsy and idiopathic hypersomnia and second, to propose the notion that EDS may also increase cardiovascular risk in the absence of known sleep disorders, as supported by some epidemiological and observational data.We further highlight preliminary evidence suggesting systemic inflammation, which could be attributable to dysfunction of the gut microbiome and adipose tissue, as well as deleterious epigenetic changes, may promote EDS while also increasing cardiovascular risk; however, these pathways may be reciprocal and/or circumstantial.Additionally, gaps within the literature are noted followed by directions for future research.
AB - Excessive daytime sleepiness (EDS) is classically viewed as a consequence of insufficient sleep or a symptom of sleep disorders.Epidemiological and clinical evidence have shown that patients reporting EDS in tandem with sleep disorders (e.g., obstructive sleep apnoea) are at greater cardiovascular risk than non-sleepy patients.While this may simply be attributable to EDS being present in patients with a more severe condition, treatment of sleep disorders does not consistently alleviate EDS, indicating potential aetiological differences.Moreover, not all patients with sleep disorders report EDS, and daytime sleepiness may be present even in the absence of any identifiable sleep disorder; thus, EDS could represent an independent pathophysiology.The purpose of this review is twofold: first, to highlight evidence that EDS increases cardiovascular risk in the presence of sleep disorders such as obstructive sleep apnoea, narcolepsy and idiopathic hypersomnia and second, to propose the notion that EDS may also increase cardiovascular risk in the absence of known sleep disorders, as supported by some epidemiological and observational data.We further highlight preliminary evidence suggesting systemic inflammation, which could be attributable to dysfunction of the gut microbiome and adipose tissue, as well as deleterious epigenetic changes, may promote EDS while also increasing cardiovascular risk; however, these pathways may be reciprocal and/or circumstantial.Additionally, gaps within the literature are noted followed by directions for future research.
KW - hypertension
KW - inflammation
KW - obesity
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U2 - 10.1136/heartjnl-2021-319596
DO - 10.1136/heartjnl-2021-319596
M3 - Review article
C2 - 35102000
AN - SCOPUS:85134273042
SN - 1355-6037
JO - Heart
JF - Heart
M1 - 319596
ER -