scholarly journals Considering Psychosocial Factors When Investigating Blood Pressure in Patients with Short Sleep Duration: A Propensity Score Matched Analysis

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Ningjing Qian ◽  
Dandan Yang ◽  
Huajun Li ◽  
Siyin Ding ◽  
Xia Yu ◽  
...  

Few studies have considered psychosocial characteristics when investigating the associations between sleep duration and blood pressure (BP). In this study, we took propensity score matching (PSM) to adjust for psychosocial characteristics when comparing BP between individuals with short sleep duration and those with normal sleep duration. A total of 429 participants were included. 72 participants with sleep duration ≤6 h and 65 participants with sleep duration >6 h were matched after PSM. We compared office BP, 24-hour BP, and prevalence of hypertension in the populations before and after PSM, respectively. In the unmatched population, participants with sleep duration ≤6 h were observed with higher office diastolic BP (DBP) and 24-h systolic BP (SBP)/DBP (all P < 0.05 ). In the matched populations, the differences between the two groups (sleep duration ≤6 h vs. sleep duration >6 h) in office DBP (88.4 ± 10.9 vs. 82.5 ± 11.1 mm Hg; P = 0.002 ), 24-h SBP (134.7 ± 12.0 vs. 129.3 ± 11.6 mm Hg; P = 0.009 ), and 24-h DBP (83.4 ± 9.9 vs. 78.1 ± 10.1 mm Hg; P = 0.002 ) become more significant. Participants with sleep duration ≤6 h only show higher prevalence of hypertension based on 24-h BP data, while analysis after PSM further revealed that these with sleep duration ≤6 h presented about 20% higher prevalence of elevated BP up to office diagnosed hypertension threshold. Therefore, psychosocial characteristics accompanied with short sleep duration should be fully valued in individuals at risks for elevated BP. This trial is registered with NCT03866226.

Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Kelly A Stockelman ◽  
Anthony R Bain ◽  
Dana M Withrow ◽  
Tracey A Larson ◽  
Elizabeth M Boland ◽  
...  

Elevated blood pressure (BP ≥130/80 mmHg) is associated with increased risk for myocardial infarction, heart failure, stroke and vascular disease. Insufficient nightly sleep (<7 h/night) has been linked not only to the etiology of elevated blood pressure but is a prevalent, often ignored, comorbidity. Indeed, short sleep duration is now considered to be a plausible risk factor for elevated blood pressure and a harbinger of increased cardiovascular risk. A high prevalence of insufficient nightly sleep has been reported in adults with elevated blood pressure. The influence of insufficient sleep on endothelial vasodilator function in adults with elevated blood pressure is unknown. We tested the hypotheses that chronic insufficient sleep is associated with diminished nitric oxide (NO)-mediated endothelium-dependent vasodilation in adults with elevated blood pressure. Moreover, the insufficient sleep-related reduction in endothelial vasodilator function is due, at least in part to increased oxidative stress. Thirty-five middle-aged and older adults with elevated blood pressure were studied: 15 with normal nightly sleep duration (11M/4F; age: 58±2 yr; BP: 136/82±1/2 mmHg; sleep: 7.6±0.2 h/night) and 20 with short nightly sleep duration (14M/6F; 58±1 yr; BP: 138/84±1/1 mmHg; sleep: 6.0±0.1 h/night). Forearm blood flow (FBF) responses to intra-arterial infusion of acetylcholine (ACh), in the absence and presence of the endothelial NO synthase inhibitor N G -monomethyl-L-arginine (L-NMMA) and the antioxidant vitamin C were determined by venous occlusion plethysmography. The FBF response to ACh was significantly lower (~20%) in the short sleep (from 3.8±0.2 to 11.0±0.6 ml/100 ml tissue/min) compared with the normal sleep duration group (from 4.2±0.2 to 13.6±0.6 ml/100 ml tissue/min). L-NMMA significantly reduced (~25%) the FBF response to ACh in the normal sleep but not the short sleep group. Vitamin C markedly increased (~35%; P<0.05) the vasodilator response to ACh in short sleepers only. In summary, habitual short sleep duration worsens NO-mediated endothelium-dependent vasodilation in adults with elevated blood pressure. Furthermore, the sleep-related diminishment in endothelial vasodilator function is due, in part, to increased oxidative stress.


2020 ◽  
Vol 7 ◽  
pp. 100062
Author(s):  
Marwah Abdalla ◽  
Joseph E. Schwartz ◽  
Talea Cornelius ◽  
Bernard P. Chang ◽  
Carmela Alcántara ◽  
...  

2017 ◽  
Vol 41 (S1) ◽  
pp. s853-s853
Author(s):  
J. Isaac ◽  
C. Santos ◽  
A. Matos Pires

BackgroundInsomnia is a highly prevalent complaint, largely associated with mental disease. Clinical evidence classifies insomnia in 2 subtypes: with sleep misperception (WSM) and without sleep misperception (wSM). That presents distinctive pathophysiologic pathways and different public health implications.ObjectivesDescribe the main differences between primary insomnia WSM and wSM regarding:– clinical features;– diagnosis;– management;– implications.MethodsWe conducted a systematic review. PubMed, Embase and PsycInfo were searched from 2000–2016. The reference lists of systematic reviews, narrative synthesis and some important articles were included. Following the inclusion criteria, we selected 25 studies from 59 articles.ResultsThe prevalence of sleep-state misperception in primary insomniacs (total sleep time > 6.5 h and sleep efficiency > 85%) is around 26%. Insomniacs with normal sleep duration showed a profile of high depression and anxiety and low ego strength, whereas insomniacs with short sleep duration showed a profile of a medical disorder.Cortical hyperarousal is higher in insomniacs and could be related to an alteration in sleep protection mechanisms. The sleep architecture was relatively normal for the WSM comparing with the group wSM. Risk of cardiometabolic, neurocognitive morbidity and mortality, and responses to treatment are different between these two insomnia phenotypes. Patients with short sleep duration may respond better to biological treatments, whereas insomnia with normal sleep duration may respond primarily to psychological therapies.ConclusionsThe clinical characteristics of patients with sleep-state misperception differed from those without this condition. Available research related to these conditions is expanding rapidly, but many questions remain unanswered.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Lili Huang ◽  
Jiajun Lyu ◽  
Zichong Long ◽  
Yuanqing Xia ◽  
Yiting Chen ◽  
...  

Purpose. We conducted this study to add the evidence regarding the gender-specific association between sleep duration and blood pressure (BP) in children. Methods. A secondary analysis was performed among 1000 children aged 7–13 years, who had at least two rounds of survey records in China Health and Nutrition Survey through 2004–2015. Generalized estimating equation was used to explore the gender-specific association of sleep duration with BP. The subgroup analysis was applied in those participants with normal weight. Results. The time trend of decreasing sleep duration, along with increasing BP level, was observed in each age group during the survey period. Short sleepers (<9 hours per day) have higher level of both systolic BP (SBP) and diastolic BP (DBP) than long sleepers in girls (all p < 0.05). By contrast, only SBP was higher in short sleepers among boys (p < 0.05). There was gender difference in the association between sleep duration and DBP (p for interaction <0.05). The stratification analysis showed that short sleep duration could consistently predict a higher level of diastolic BP (DBP) in both crude (β = 2.968, 95% CI: 1.629, 4.306) and adjusted models (β = 1.844, 95% CI: 0.273, 3.416) only in girls. Sleep duration was also analyzed as continuous variable, and the very similar associations were observed. Moreover, the established associations can be verified among children with normal weight. Conclusions. There was a time trend of decreasing sleep duration alongside increasing BP among children from 2004 to 2015. Short sleep duration was independently associated with increased DBP; however, only girls were susceptible to the association.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Kazuo Eguchi ◽  
Thomas G Pickering ◽  
Joseph E Schwartz ◽  
Satoshi Hoshide ◽  
Joji Ishikawa ◽  
...  

We aimed this study to test the hypothesis that short duration of sleep is independently associated with incident cardiovascular diseases (CVD) in hypertensive patients. We performed ambulatory BP monitoring (ABPM) in 1255 subjects with hypertension (mean age: 70.4 ± 9.9 years) and they were followed for an average of 50 ± 23 months. Short sleep duration was defined as <7.5 hrs (20 th percentile). Multivariable Cox hazard models predicting CVD events were used to estimate the adjusted hazard ratio (HR) and 95% CI for short sleep duration. A riser pattern was defined when average nighttime SBP exceeded daytime SBP. The end point was cardiovascular events: stroke, fatal or non-fatal myocardial infarction (MI), and sudden cardiac death. In multivariable analyses, short duration of sleep (<7.5 hrs) was associated with incident CVD (HR=1.68; 1.06 –2.66, P=.03). A synergistic interaction was observed between short sleep duration and the riser pattern (P=.089). When subjects were categorized on the basis of their sleep time and riser/non-riser patterns, the shorter sleep+riser group had a highest incidence of CVD among the 4 groups ( Figure ), and substantially and significantly higher incidence of CVD than the predominant normal sleep+non-riser group (HR=4.43; 2.09 –9.39, P<0.001), independent of covariates. Short duration of sleep is associated with incident CVD risk, and the combination of riser pattern and short duration of sleep that is most strongly predictive of future CVD, independent of ambulatory BP levels. Physicians should inquire about sleep duration in the risk assessment of hypertensive patients.


Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Anthony R Bain ◽  
Caitlin A Dow ◽  
Kyle J Diehl ◽  
Tyler D Bammert ◽  
Jared J Greiner ◽  
...  

The capacity of the endothelium to release tissue-type plasminogen activator (t-PA) is impaired in adults with elevated BP, leading to an increased risk of thrombotic events. Insufficient sleep is independently associated with elevated BP and impaired t-PA release. However, the compounded influence of insufficient sleep on t-PA release in adults with elevated BP is unknown. We tested the hypothesis that impairments in the capacity of the endothelium to release t-PA in adults with elevated BP is worse in those who sleep <7 h/night (short sleep duration) compared with those who sleep 7 to 9 h/night (normal sleep duration). We studied 38 sedentary, middle-aged adults: 10 with normal BP and normal nightly sleep duration (6M/4F; age: 55±2 yr; BP: 114/94±2/3 mmHg, sleep duration: 7.4±0.2 h); 14 with elevated BP and normal nightly sleep duration (8M/6F; 60±2 yr; 141/87±2/2 mmHg; 7.8±0.1 h); and 14 with elevated BP and short nightly sleep duration (10M/4F; 57±2 yr; 139/85±2/2 mmHg; 6.1±0.2 h). All subjects were free of overt metabolic and coronary disease. Net endothelial release of t-PA was determined, in vivo, in response to intra-brachial infusions of bradykinin (BK: 125-500 ng/min) and sodium nitroprusside (SNP: 2.0-8.0 μg/min). In the normal sleep groups, as expected, endothelial t-PA release in response to BK was significantly blunted (~30%) in the adults with elevated BP (from -1.2±0.8 to 50.2±4.8 ng/100mL tissue/min) compared with normal BP (from 0.9±3.4 to 73.0±8.0 ng/100mL tissue/min); and total t-PA release (area under the BK curve) was ~25% lower (p<0.05) in the adults with elevated (307±33 ng/100mL tissue) vs. normal (396±27 ng/100mL tissue) BP. Importantly, net endothelial release rate (from -1.5±1.0 to 40.6±4.3 ng/100mL tissue/min) and total amount of t-PA released (222±28 ng/100mL tissue) in response to BK were markedly lower (~25% and 30%, respectively, P<0.05) in the elevated BP and short sleep duration group compared with the elevated BP and normal sleep duration group. In the elevated BP population, sleep duration was positively correlated with total t-PA release (r=0.46, P<0.05). There was no effect of SNP on t-PA release in any group. In summary, insufficient sleep is associated with exacerbated impairments in t-PA release in adults with elevated BP.


Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Kelly A Stockelman ◽  
Anthony R Bain ◽  
Caitlin A Dow ◽  
Jared J Greiner ◽  
Brian L Stauffer ◽  
...  

Insufficient sleep, defined as chronic short sleep duration (<7 h/night), is an independent risk factor for cardiovascular disease (CVD). We have previously demonstrated that insufficient sleep is associated with reduced endothelium-dependent vasodilation and enhanced endothelin (ET)-1-mediated vasoconstrictor tone. Impaired endothelial vasomotor regulation is thought to contribute mechanistically to the increased risk of atherosclerotic vascular disease incurred with chronic insufficient sleep. Regular aerobic exercise is an effective lifestyle strategy for improving endothelial function and, in turn reducing cardiovascular risk. It is currently unknown if regular aerobic exercise can counteract the negative impact of insufficient sleep on endothelial vasomotor regulation. We tested the hypotheses that regular aerobic exercise would: 1) improve endothelial vasodilation; and 2) decrease ET-1-mediated vasoconstrictor tone in middle-aged adults who chronically sleep less than 7 h/night. We studied 36 healthy, middle-aged adults: 16 with normal sleep duration (10M/6F; age: 57±2 yr; sleep duration: 7.4±0.1 h/night) and 20 with short sleep duration (11M/9F; 56±1 yr; sleep duration: 6.2±0.1 h/night). The 20 short sleepers completed a 3-month aerobic exercise training intervention. Forearm blood flow (FBF; plethysmography) was determined in response to intra-arterial doses of acetylcholine (ACh), sodium nitroprusside (SNP), BQ-123 (ET A receptor antagonist) and ACh + BQ-123 in both groups and after the exercise intervention in the short sleepers. As expected, forearm vasodilator responses to ACh were lower (20%; P<0.05) in the short (from 4.2±0.2 to 10.5±0.6 mL/100 mL tissue/min) vs normal (4.2±0.2 to 12.7±0.6 mL/100 mL tissue/min) sleepers. FBF responses to SNP were comparable between the groups. In response to BQ-123, short sleep group had a greater increase in resting FBF than normal sleep group (~25% vs ~8%; P< 0.05). ACh+BQ-123 resulted in an ~25% increase in the ACh-vasodilation in the short sleep group only. After exercise training, although nightly sleep duration was not affected (6.4±0.1 h/night), ACh-mediated vasodilation was ~20% higher (P<0.05), ET-1-mediated vasoconstriction was ~90% lower (P<0.05) and vasodilator response to ACh was not significantly increased with ET A receptor blockade. These results indicate that regular aerobic exercise can reverse the negative influence of insufficient sleep on endothelial vasomotor function, independent of changes in nightly sleep duration.


2020 ◽  
Author(s):  
Heming Wang ◽  
Raymond Noordam ◽  
Brian E Cade ◽  
Karen Schwander ◽  
Thomas W Winkler ◽  
...  

AbstractLong and short sleep duration are associated with elevated blood pressure (BP), possibly through effects on molecular pathways that influence neuroendocrine and vascular systems. To gain new insights into the genetic basis of sleep-related BP variation, we performed genome-wide gene by short or long sleep duration interaction analyses on four BP traits (systolic BP, diastolic BP, mean arterial pressure, and pulse pressure) across five ancestry groups using 1 degree of freedom (1df) interaction and 2df joint tests. Primary multi-ancestry analyses in 62,969 individuals in stage 1 identified 3 novel loci that were replicated in an additional 59,296 individuals in stage 2, including rs7955964 (FIGNL2/ANKRD33) showing significant 1df interactions with long sleep duration and rs73493041 (SNORA26/C9orf170) and rs10406644 (KCTD15/LSM14A) showing significant 1df interactions with short sleep duration (Pint < 5×10−8). Secondary ancestry-specific two-stage analyses and combined stage 1 and 2 analyses additionally identified 23 novel loci that need external replication, including 3 and 5 loci showing significant 1df interactions with long and short sleep duration, respectively (Pint < 5×10−8). Multiple genes mapped to our 26 novel loci have known functions in sleep-wake regulation, nervous and cardiometabolic systems. We also identified new gene by long sleep interactions near five known BP loci (≤1Mb) including NME7, FAM208A, MKLN1, CEP164, and RGL3/ELAVL3 (Pint < 5×10−8). This study indicates that sleep and primary mechanisms regulating BP may interact to elevate BP level, suggesting novel insights into sleep-related BP regulation.


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