Abstract P183: Influence of Insufficient Sleep on Endothelial Fibrinolytic Capacity in Adults With Elevated Blood Pressure

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.


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.


Author(s):  
Kelly A. Stockelman ◽  
Anthony R. Bain ◽  
Caitlin A. Dow ◽  
Kyle J. Diehl ◽  
Jared J. Greiner ◽  
...  

Insufficient sleep is associated with endothelial vasomotor dysfunction and increased cardiovascular risk. Regular aerobic exercise is an effective lifestyle strategy for improving endothelial function and, in turn, reducing cardiovascular risk. 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 <7 h/night. Thirty-six healthy, middle-aged adults were studied: 16 with normal sleep duration (age: 57±2 yr; sleep duration: 7.4±0.1 h/night) and 20 with short sleep duration (56±1 yr; 6.2±0.1 h/night). The 20 short sleepers completed a 3-month aerobic exercise training intervention. Forearm blood flow was determined (via plethysmography) in response to intra-arterial acetylcholine (ACh), BQ-123 (ETAreceptor antagonist), ACh+BQ-123 and sodium nitroprusside. Forearm blood flow 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. In response to BQ-123, the short sleep group had a significantly greater increase in resting forearm blood flow than the normal sleep group (~25% vs ~8%). ACh+BQ-123 resulted in a significant (~25%) increase in the ACh-vasodilation in the short sleep group only. After exercise training, although nightly sleep duration was unchanged (6.4±0.1 h/night), ACh-mediated vasodilation was significantly higher (~20%), ET-1-mediated vasoconstriction was significantly lower (~80%) and the vasodilator response to ACh was not increased with ETAreceptor blockade. Regular aerobic exercise, independent of changes in nightly sleep duration, can counteract insufficient sleep-related endothelial vasomotor dysfunction.


2013 ◽  
Vol 110 (5) ◽  
pp. 949-959 ◽  
Author(s):  
Sarah Bel ◽  
Nathalie Michels ◽  
Tineke De Vriendt ◽  
Emma Patterson ◽  
Magdalena Cuenca-García ◽  
...  

Evidence has grown supporting the role for short sleep duration as an independent risk factor for weight gain and obesity. The purpose of the present study was to examine the relationship between sleep duration and dietary quality in European adolescents. The sample consisted of 1522 adolescents (aged 12·5–17·5 years) participating in the European multi-centre cross-sectional ‘Healthy Lifestyle in Europe by Nutrition in Adolescence’ study. Sleep duration was estimated by a self-reported questionnaire. Dietary intake was assessed by two 24 h recalls. The Diet Quality Index for Adolescents with Meal index (DQI-AM) was used to calculate overall dietary quality, considering the components dietary equilibrium, dietary diversity, dietary quality and a meal index. An average sleep duration of ≥ 9 h was classified as optimal, between 8 and 9 h as borderline insufficient and < 8 h as insufficient. Sleep duration and the DQI-AM score were positively associated (β = 0·027, r 0·130, P< 0·001). Adolescents with insufficient (62·05 (sd 14·18)) and borderline insufficient sleep (64·25 (sd 12·87)) scored lower on the DQI-AM than adolescents with an optimal sleep duration (64·57 (sd 12·39)) (P< 0·001; P= 0·018). The present study demonstrated in European adolescents that short sleep duration was associated with a lower dietary quality. This supports the hypothesis that the health consequences of insufficient sleep may be mediated by the relationship of insufficient sleep to poor dietary quality.


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.


SLEEP ◽  
2021 ◽  
Author(s):  
Adam D Cooper ◽  
Claire A Kolaja ◽  
Rachel R Markwald ◽  
Isabel G Jacobson ◽  
Evan D Chinoy

Abstract Study Objectives Sleep loss is common in the military, which can negatively affect health and readiness; however, it is largely unknown how sleep varies over a military career. This study sought to examine the relationships between military-related factors and the new onset and reoccurrence of short sleep duration and insomnia symptoms. Methods Millennium Cohort Study data were used to track U.S. military service members over time to examine longitudinal changes in sleep. Outcomes were self-reported average sleep duration (categorized as ≤5 hours, 6 hours, or 7–9 hours [recommended]) and/or insomnia symptoms (having trouble falling or staying asleep). Associations between military-related factors and the new onset and reoccurrence of these sleep characteristics were determined, after controlling for multiple health and behavioral factors. Results Military-related factors consistently associated with an increased risk for new onset and/or reoccurrence of short sleep duration and insomnia symptoms included active duty component, Army or Marine Corps service, combat deployment, and longer than average deployment lengths. Military officers and noncombat deployers had decreased risk for either sleep characteristic. Time-in-service and separation from the military were complex factors; they lowered risk for ≤5 hours sleep but increased risk for insomnia symptoms. Conclusions Various military-related factors contribute to risk of short sleep duration and/or insomnia symptoms over time, although some factors affect these sleep characteristics differently. Also, even when these sleep characteristics remit, some military personnel have an increased risk of reoccurrence. Efforts to improve sleep prioritization and implement interventions targeting at-risk military populations, behaviors, and other significant factors are warranted.


2021 ◽  
pp. oemed-2021-107643
Author(s):  
Aron Peter Sherry ◽  
Stacy A Clemes ◽  
Yu-Ling Chen ◽  
Charlotte Edwardson ◽  
Laura J Gray ◽  
...  

ObjectivesTo profile sleep duration and sleep efficiency in UK long-distance heavy goods vehicle (HGV) drivers and explore demographic, occupational and lifestyle predictors of sleep.MethodsCross-sectional analyses were carried out on 329 HGV drivers (98.5% men) recruited across an international logistics company within the midland’s region, UK. Sleep duration and efficiency were assessed via wrist-worn accelerometry (GENEActiv) over 8 days. Proportions of drivers with short sleep duration (<6 hour/24 hours and <7 hour/24 hours) and inadequate sleep efficiency (<85%) were calculated. Demographic, occupational and lifestyle data were collected via questionnaires and device-based measures. Logistic regression assessed predictors of short sleep duration and inadequate sleep efficiency.Results58% of drivers had a mean sleep duration of <6 hour/24 hours, 91% demonstrated <7-hour sleep/24 hours and 72% achieved <85% sleep efficiency. Sleeping <6 hour/24 hours was less likely in morning (OR 0.45, 95% CI 0.21 to 0.94) and afternoon (OR 0.24, CI 0.10 to 0.60) shift workers (vs night) and if never smoked (vs current smokers) (OR 0.45, CI –0.22 to 0.92). The likelihood of sleeping <7 hour/24 hours reduced with age (OR 0.92, CI 0.87 to 0.98). The likelihood of presenting inadequate sleep efficiency reduced with age (OR 0.96, CI 0.93 to 0.99) and overweight body mass index category (vs obese) (OR 0.47, CI 0.27 to 0.82).ConclusionsThe high prevalence of short sleep duration and insufficient sleep quality (efficiency) rate suggest that many HGV drivers have increased risk of excessive daytime sleepiness, road traffic accidents and chronic disease. Future sleep research in UK HGV cohorts is warranted given the road safety and public health implications.


Circulation ◽  
2016 ◽  
Vol 133 (suppl_1) ◽  
Author(s):  
Julio Fernandez-Mendoza ◽  
Fan He ◽  
Alexandros N Vgontzas ◽  
Duanping Liao ◽  
Edward O Bixler

Introduction: Short sleep duration has been associated with increased risk of cardiovascular and cerebrovascular disease (CVD), cognitive impairment (CI) and mortality. However, the role of sleep duration in predicting mortality in the context of CVD and CI is still not well-understood. Hypothesis: Short sleep duration is a key effect modifier of the relationship between CI associated with CVD and all-cause mortality. Methods: We addressed this hypothesis in the Penn State Adult Cohort, a random, general population sample of 1,741 middle-aged adults who were studied in the sleep lab and followed-up for 15y. An in-lab, 8-hour polysomnography was performed to ascertain sleep duration. CI associated with CVD was defined by the presence of hypertension, diabetes, heart disease and/or stroke with impaired higher-order, executive cognitive functioning, including slow processing speed. We tested the interaction between sleep duration and CI associated with CVD on all-cause mortality with multiple logistic regression while adjusting for sex, age, race, obesity, smoking, cholesterol, depression, insomnia, dementia, and sleep apnea. Results: The odds of mortality associated with CI-alone, CVD-alone, and CI associated with CVD were 1.3 (95% CI: 0.7-2.4), 1.7 (95% CI: 1.1-2.8), and 4.6 (95% CI: 2.8-7.7), respectively. As shown in Figure 1, the interaction between CI associated with CVD and sleep duration was significant (p < .01), indicating that the probability of mortality increased significantly as a function of shorter sleep duration in individuals with CI associated with CVD. Conclusion: We found that objective sleep duration modifies the relationship between CI associated with CVD and all-cause mortality in a dose-response manner. Short sleep duration in individuals with probable vascular cognitive impairment (VCI) may serve as a biomarker of the severity of central autonomic dysfunction. Future studies should examine whether improving sleep reduces the odds of mortality in individuals with VCI.


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.


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