Insomnia and hypertension: A systematic review

Jarrin, Denise C.; Alvaro, Pasquale K.; Bouchard, Marc–André; Jarrin, Stephanie; Drake, Christopher L.; Morin, Charles M.

doi:10.1016/j.smrv.2018.02.003

Cited by 157 publications

(112 citation statements)

References 103 publications

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“…Interestingly, sleep efficiency had no impact at all in our model of the HP analysis. There is some evidence that both short sleep duration and insomnia might decrease cardiovascular health especially due to AHT (Anttalainen et al, 2018;Jarrin et al, 2018). However, our protocol only analyzed the percentage of wakefulness in the first 20 min of sleep.…”

Section: Discussionmentioning

confidence: 99%

The Importance of Sleep Fragmentation on the Hemodynamic Dipping in Obstructive Sleep Apnea Patients

et al. 2020

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Introduction: Obstructive sleep apnea (OSA) has been associated with non-dipping blood pressure (BP). The precise mechanism is still under investigation, but repetitive oxygen desaturation and arousal induced sleep fragmentation are considered the main contributors. Methods:We analyzed beat-to-beat measurements of hemodynamic parameters (HPs) during a 25-min period of wake-sleep transition. Differences in the mean HP values for heart rate (HR), systolic BP (SBP), and stroke volume (SV) during wake and sleep and their standard deviations (SDs) were compared between 34 controls (C) and 22 OSA patients. The Student's t-test for independent samples and the effect size by Cohen's d (d) were calculated. HP evolution was investigated by plotting the measured HP values against each consecutive pulse wave. After a simple regression analysis, the calculated coefficient beta (SCB) was used to indicate the HP evolution. We furthermore explored by a hierarchical block regression which variables increased the prediction for the SCB: model 1 BMI and age, model 2 + apnea/hypopnea index (AHI), and model 3 + arousal index (AI).Results: Between the two groups, the SBP increased in OSA and decreased in C resulting in a significant difference (p = 0.001; d = 0.92). The SV demonstrated a similar development (p = 0.047; d = 0.56). The wake/sleep variation of the HP measured by the SD was higher in the OSA group-HR: p < 0.001; d = 1.2; SBP: p = 0.001; d = 0.94; and SV: p = 0.005; d = 0.82. The hierarchical regression analysis of the SCB demonstrated in SBP that the addition of AI to AHI resulted in R 2 : +0.163 and F + 13.257 (p = 0.001) and for SV R 2 : +0.07 and F 4.83 (p = 0.003). The AI but not the AHI remained statistically significant in the regression analysis model 3-SBP: β = 0.717, p = 0.001; SV: β = 0.469, p = 0.033. Frontiers in Physiology | www.frontiersin.org 1 March 2020 | Volume 11 | Article 104 Staats et al. Sleep Fragmentation and Hemodynamic DippingConclusion: In this study, we demonstrated that in OSA, the physiological dipping in SBP and SV decreased, and the variation of all investigated parameters increased. Hierarchical regression analysis indicates that the addition of the AI to BMI, age, and AHI increases the prediction of the HP evolution following sleep onset for both SBP and SV and may be the most important variable.

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Section: Discussionmentioning

confidence: 99%

The Importance of Sleep Fragmentation on the Hemodynamic Dipping in Obstructive Sleep Apnea Patients

et al. 2020

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“…At the same time, the guidelines mention, that low predictive value on population level might be related to the lack of standardization in IMT assessment, its high variability and low reproducibility [21]. However, there is a correlation between carotid atherosclerosis and atherosclerotic involvement of other arterial territories, and carotid atherosclerosis remains one of the common tools for the evaluation of arterial disease [22]. Therefore, the use of ultrasound carotid atherosclerosis is reasonable for the assessment of atherosclerosis.…”

Section: Yesmentioning

confidence: 99%

Is self-reported insomnia a risk factor for subclinical carotid atherosclerosis?

Korostovtseva

Alieva

Rotar

et al. 2019

Arterial Hypertension

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Background. Insomnia is considered an additional cardiovascular (CV) risk factor (RF). However, the data on its association with vascular damage is controversial. We analyzed the relation between self-reported insomnia and carotid atherosclerosis in the population-based sample. Material and methods. We selected 985 (males -38%; mean age 45.2 ± 11.6 years) participants of the St Petersburg population-based sample (the ESSE-RF study) who did not have previously known CV events. All subjects underwent a structured interview (lifestyle, medical history). Insomnia was diagnosed when complaints occurred ≥ 3 times/week (the questions: "How often did you have difficulties in falling asleep for > 30 min after going to bed in the last month?", "How often did you have difficulties in falling asleep after midnight awakening in the last month?"). Subclinical atherosclerosis was assessed by carotid intima-media thickness (IMT): normal ≤ 0.9 mm, increased IMT 0.9-13 mm, IMT > 13 mm indicated an atherosclerotic plaque. Results. In total, 209 subjects reported at least one insomnia complaint; 79 participants (8%) reported both sleeponset and sleep-maintenance problems. IMT thickening was found in 142 subjects (14.4%). IMT values were higher in those with frequent nocturnal awakenings vs. non-insomniacs (0.75 ± 0.18 vs. 0.71 ± 0.17 mm, p = 0.006). They also showed greater prevalence of thickened IMT (c 2 = 4.6, p = 0.026). Mean IMT weakly correlated with insomnia complaints (r = 0.10, p = 0.002), but the association was no longer significant after adjustment for age, BP and total cholesterol level. Conclusion. We demonstrated an association between insomnia complaints and subclinical carotid atherosclerosis, although we assume it to be weak compared to the common CV RF.

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“…IOSSD is the most biologically severe phenotype of insomnia. Studies have demonstrated the association of IOSSD with physiological arousal and several chronic diseases including diabetes, 5 hypertension, 6 cardiovascular disease, 7 neurocognitive impairment, 8 and depression. 9 Inflammation caused by sleep disturbance is regarded as one of main underlying mechanisms of this association.…”

Section: Introductionmentioning

confidence: 99%

<p>Objective Short Sleep Duration is Related to the Peripheral Inflammasome Dysregulation in Patients with Chronic Insomnia</p>

Wang¹,

Wu²,

Liang³

et al. 2020

NSS

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Objective: Insomnia with objective short sleep duration (IOSSD) is associated with an increased risk of cardiovascular morbidity, diabetes, neurocognitive impairment, and mortality. Inflammation is believed to be one of the main links between IOSSD and these diseases. The role of nucleotide-binding domain and leucine-rich repeat protein-3 (NLRP3) inflammasome in inducing activation of inflammatory signaling in IOSSD is not clear. In this study, we investigated the expression of NLRP3 inflammasome in patients with IOSSD to clarify this issue. Methods: Thirty-six patients with insomnia and 20 age-and sex-matched healthy controls were sequentially recruited. Subjects were categorized into three groups: IOSSD (sleep duration < 6h, n=20), insomnia with objective normal sleep duration (IONSD, sleep duration ≥ 6h, n=16) and healthy controls (n=20). Objective sleep parameters were measured by overnight polysomnography. Peripheral NLRP3 inflammasome protein levels [NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), caspase l] and cytokines [interleukin (IL)-1β and IL-18] were assessed by Western blotting and ELISA, respectively. Results: IOSSD group showed significantly increased protein expressions of ASC and caspase-1 compared to IONSD and healthy controls and significantly increased IL-18 levels compared to healthy controls. On correlation analysis, total sleep time showed an inverse correlation with NLRP3, ASC, IL-18, and IL-1β levels. Wake after sleep onset (WASO) showed a positive correlation with NLRP3, ASC, caspase-1, and IL-1β levels. N3 sleep ratio showed a significant negative correlation with NLRP3, ASC, and IL-18 levels. Conclusion: The current study demonstrated upregulation of NLRP3 inflammasome in IOSSD. Short sleep duration, decreased slow wave sleep, and sleep fragmentation may contribute to dysregulation of NLRP3 inflammasome.

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Insomnia and hypertension: A systematic review

Cited by 157 publications

References 103 publications

The Importance of Sleep Fragmentation on the Hemodynamic Dipping in Obstructive Sleep Apnea Patients

The Importance of Sleep Fragmentation on the Hemodynamic Dipping in Obstructive Sleep Apnea Patients

Is self-reported insomnia a risk factor for subclinical carotid atherosclerosis?

<p>Objective Short Sleep Duration is Related to the Peripheral Inflammasome Dysregulation in Patients with Chronic Insomnia</p>

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