Abstract P167: Chronic Circadian Disruption Impairs Cardiovascular Rhythms In Mice

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Paramita Pati ◽  
Megan K Rhoads ◽  
Rachel Meek ◽  
Jackson Colson ◽  
David M Pollock ◽  
...  
Keyword(s):  
Heart Rate ◽  
Locomotor Activity ◽  
Diurnal Variation ◽  
Disease Risk ◽  
Time Of Day ◽  
Circadian Disruption ◽  
Dark Phase ◽  
Light Cycle ◽  
Dark Control ◽  
Increased Risk

Shift workers have an increased risk of developing hypertension and higher incidence of metabolic syndrome. Circadian rhythm disruption increases cardiometabolic disease risk in humans and animals. We hypothesized that chronic circadian disruption (CCD) disrupts blood pressure, heart rate, and locomotor activity rhythms. Male 8-week old C57BL/6J mice were under a standard light/dark cycle (12-h light, 12-h dark, control) or a CCD protocol (10-h light, 10-h dark, T20) with ad libitum food and water for 10 weeks. T20 mice gained significantly more body weight (n=6, p=0.04; time: p<0.001, light cycle: p<0.001). Mean arterial pressure (MAP), heart rate (HR), and locomotor activity were measured by telemetry after 10 weeks of CCD. Average MAP, HR, and activity were calculated during light and dark periods. MAP between the light and dark periods was significantly different in control mice (12:12 LD), while T20 mice (10:10 LD) did not show diurnal variation (Control 119±3 mm Hg vs.101±2 mm Hg, dark vs. light, respectively, p<0.001; T20 114±13 mm Hg vs.113±12 mm Hg, dark vs. light, respectively, p=0.86; n=3-4 in all groups). Control mice showed a diurnal variation in HR, whereas T20 mice did not show a light-dark difference (Control 584±11 bpm Hg vs. 511±4 bpm, dark vs. light, respectively, p=0.001; T20 537±14 bpm vs. 526±5 bpm, dark vs. light, respectively, p=0.48; n=3-4 in all groups). Dark phase HR was significantly decreased in T20 mice (p=0.01, control dark vs. T20 dark). Control mice showed a light-dark difference in activity, while T20 mice lacked diurnal variation in the activity rhythm (Control 9.6±1.3 counts/min Hg vs. 3.1±0.3 counts/min, dark vs. light, respectively, p<0.001; T20 6.9±0.3 counts/min vs. 6.0±0.8 counts/min, dark vs. light, respectively, p=0.92; n=3-4 in all groups). T20 mice also displayed significantly higher activity during the light phase (p=0.04, control light vs. T20 light). Time of day and the interaction between time of day and light cycle, respectively, were significant between control and T20 mice for MAP, HR, and activity (n=3-4, MAP: p=0.001 and p=0.002; HR: p=0.001 and p=0.004; Activity: p=0.001 and p=0.004). These results indicate that CCD impairs cardiovascular and behavioral rhythms, which may lead to cardiovascular disease.

α1-Adrenoreceptor activity does not explain lower morning endothelial-dependent, flow-mediated dilation in humans

2011 ◽  
Vol 300 (6) ◽  
pp. R1437-R1442 ◽  
Author(s):  
Helen Jones ◽  
Nia C. S. Lewis ◽  
Daniel J. Green ◽  
Philip N. Ainslie ◽  
Samuel J. E. Lucas ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Shear Rate ◽  
Diurnal Variation ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Time Of Day ◽  
Flow Mediated Dilation ◽  
Nerve Activity ◽  
Dependent Flow

Early morning reduction in endothelium-dependent, flow-mediated dilation (FMD) may contribute to the high incidence of sudden cardiac death at this time of day. The mechanisms underpinning diurnal variation in FMD are unclear, but potentially relate to a circadian rhythm in sympathetic nerve activity. We hypothesized that blockade of α1-mediated sympathetic nerve activity would act to attenuate the diurnal variation in FMD. In a randomized and placebo-controlled design, we measured brachial artery FMD in 12 participants (mean age = 26 yr, SD = 3) at 0600 and 1600 after ingestion of an α1-blocker (prazosin, 1 mg/20 kg body mass) or placebo. Arterial diameter and shear rate were assessed using edge-detection software. Heart rate and blood pressure were also measured. Data were analyzed using linear mixed modeling. Following placebo, FMD was 8 ± 2% in the morning compared with 10 ± 3% in the afternoon ( P = 0.04). Blockade with prazosin led to a slight but nonsignificant increase in morning FMD ( P = 0.24) and a significant ( P = 0.04) decrease in afternoon FMD, resulting in no diurnal variation ( P = 0.20). Shear rate did not differ in the morning or afternoon under either condition ( P > 0.23). Blood pressure was lower following prazosin compared with placebo ( P < 0.02), an effect that was similar at both times of day ( P > 0.34). Heart rate and norepinephrine levels were higher in the afternoon following prazosin. These data indicate that α1-adrenoreceptor activity does not explain lower morning endothelium-dependent FMD.

Effects of photoperiod reduction on rat circadian rhythms of BP, heart rate, and locomotor activity

2000 ◽  
Vol 279 (1) ◽  
pp. R169-R178 ◽  
Author(s):  
Bei-Li Zhang ◽  
Erika Zannou ◽  
Frédéric Sannajust
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Locomotor Activity ◽  
Circadian Rhythms ◽  
Wistar Rats ◽  
Dark Period ◽  
Dark Phase ◽  
Mean Values ◽  
Shift Response ◽  
H 20

The effects of a photoperiod reduction in the entrainment of circadian rhythms of systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), and spontaneous locomotor activity (SLA) were determined in conscious Wistar rats by using radiotelemetry. Two groups of seven rats were maintained in a 12:12-h light-dark (12L/12D) photoperiod for 11 wk and then placed in a reduced photoperiod of 8:16-h light-dark (8L/16D) by advancing a 4-h darkness or by advancing and delaying a 2-h darkness for 6 wk. Finally, they were resynchronized to 12L/12D. Advancing a 4-h dark phase induced a 1-h advance of acrophase for SBP, DBP, and HR, but not for SLA. The percent rhythm, amplitude, and the 12-h mean values of all parameters were significantly decreased by the photoperiod reduction. When symmetrically advancing and delaying a 2-h dark phase, a 1 h 20 min delay of acrophases and a decrease in percent rhythms and amplitudes of SBP, DBP, HR, and SLA were observed. Only the 12-h mean values of HR and SLA were decreased. Our findings show that the cardiovascular parameters differ from SLA in phase-shift response to photoperiod reduction and that the adjustment of circadian rhythms to change from 12L/12D to 8L/16D photoperiod depends on the direction of the extension of the dark period.

scholarly journals Diurnal Variation of Heart Rate, Locomotor Activity, and Body Temperature in Interleukin-1.ALPHA./.BETA. Doubly Deficient Mice.

2002 ◽  
Vol 51 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Masashi FURUZAWA ◽  
Masayoshi KUWAHARA ◽  
Keiji ISHII ◽  
Yoichiro IWAKURA ◽  
Hirokazu TSUBONE
Keyword(s):  
Heart Rate ◽  
Locomotor Activity ◽  
Body Temperature ◽  
Diurnal Variation ◽  
Interleukin 1 ◽  
Alpha Beta ◽  
Deficient Mice

Cardiovascular responses to caloric restriction and thermoneutrality in C57BL/6J mice

2002 ◽  
Vol 282 (5) ◽  
pp. R1459-R1467 ◽  
Author(s):  
T. D. Williams ◽  
J. B. Chambers ◽  
R. P. Henderson ◽  
M. E. Rashotte ◽  
J. M. Overton
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Locomotor Activity ◽  
Caloric Restriction ◽  
Food Restriction ◽  
Cardiovascular Function ◽  
Cardiovascular Responses ◽  
Negative Energy ◽  
Light Period ◽  
Dark Phase

We utilized variations in caloric availability and ambient temperature (Ta) to examine interrelationships between energy expenditure and cardiovascular function in mice. Male C57BL/6J mice ( n = 6) were implanted with telemetry devices and housed in metabolic chambers for measurement of mean arterial pressure (MAP), heart rate (HR), O2 consumption (V˙o 2), and locomotor activity. Fasting (Ta = 23°C), initiated at the onset of the dark phase, resulted in large and transient depressions in MAP, HR, V˙o 2, and locomotor activity that occurred during hours 6–17, which suggests torporlike episodes. Food restriction (14 days, 60% of baseline intake) at Ta = 23°C resulted in progressive reductions in MAP and HR across days that were coupled with an increasing occurrence of episodic torporlike reductions in HR (<300 beats/min) and V˙o 2 (<1.0 ml/min). Exposure to thermoneutrality (Ta = 30°C, n = 6) reduced baseline light-period MAP (−14 ± 2 mmHg) and HR (−184 ± 12 beats/min). Caloric restriction at thermoneutrality produced further reductions in MAP and HR, but indications of torporlike episodes were absent. The results reveal that mice exhibit robust cardiovascular responses to both acute and chronic negative energy balance. Furthermore, we conclude that Tais a very important consideration when assessing cardiovascular function in mice.

scholarly journals The genetic case for cardiorespiratory fitness as a clinical vital sign and the routine prescription of physical activity in healthcare

2020 ◽  
Author(s):  
Ken B. Hanscombe ◽  
Elodie Persyn ◽  
Matthew Traylor ◽  
Kylie P. Glanville ◽  
Mark Hamer ◽  
...  
Keyword(s):  
Physical Activity ◽  
Heart Rate ◽  
Cardiorespiratory Fitness ◽  
Vital Sign ◽  
Genome Wide Association Study ◽  
Cell Function ◽  
Disease Risk ◽  
Heart Association ◽  
Rate Of Increase ◽  
Increased Risk

AbstractBackgroundCardiorespiratory fitness (CRF) and physical activity (PA) are well-established predictors of morbidity and all-cause mortality. However, CRF is not routinely measured and PA not routinely prescribed as part of standard healthcare. The American Heart Association (AHA) recently presented a scientific case for the inclusion of CRF as a clinical vital sign based on epidemiological and clinical observation. Here, we leverage genetic data in the UK Biobank (UKB) to strengthen the case for CRF as a vital sign, and make a case for the prescription of PA.MethodsWe derived two CRF measures from the heart rate data collected during a submaximal cycle ramp test: CRF-vo2max, an estimate of the participants’ maximum volume of oxygen uptake, per kilogram of body weight, per minute; and CRF-slope, an estimate of the rate of increase of heart rate during exercise. Average PA over a 7-day period was derived from a wrist-worn activity tracker. After quality control, 38,160 participants had data on the two derived CRF measures, and 75,799 had PA data. We performed genome-wide association study (GWAS) analyses by sex, and post-GWAS techniques to understand genetic architecture of the traits and prioritize functional genes for follow-up.ResultsWe found strong evidence that genetic variants associated with CRF and PA influenced genetic expression in a relatively small set of genes in heart, artery, lung, skeletal muscle, and adipose tissue. These functionally relevant genes were enriched among genes known to be associated with coronary artery disease (CAD), type 2 diabetes (T2D), and Alzheimer’s disease (three of the top 10 causes of death in high-income countries) as well as Parkinson’s disease, pulmonary fibrosis, and blood pressure, heart rate, and respiratory phenotypes. Genetic variation associated with lower CRF and PA was also correlated with several disease risk factors (including greater body mass index, body fat and multiple obesity phenotypes); a typical T2D profile (including higher insulin resistance, higher fasting glucose, impaired beta-cell function, hyperglycaemia, hypertriglyceridemia); increased risk for CAD and T2D; and a shorter lifespan.ConclusionsGenetics supports three decades of evidence for the inclusion of CRF as a clinical vital sign. Given the genetic, clinical, and epidemiological evidence linking CRF and PA to increased morbidity and mortality, regular measurement of CRF as a marker of health and routine prescription of PA is a prudent strategy to support public health.

scholarly journals The genetic case for cardiorespiratory fitness as a clinical vital sign and the routine prescription of physical activity in healthcare

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Ken B. Hanscombe ◽  
Elodie Persyn ◽  
Matthew Traylor ◽  
Kylie P. Glanville ◽  
Mark Hamer ◽  
...  
Keyword(s):  
Physical Activity ◽  
Heart Rate ◽  
Cardiorespiratory Fitness ◽  
Vital Sign ◽  
Genome Wide Association Study ◽  
Cell Function ◽  
Disease Risk ◽  
Heart Association ◽  
Rate Of Increase ◽  
Increased Risk

Abstract Background Cardiorespiratory fitness (CRF) and physical activity (PA) are well-established predictors of morbidity and all-cause mortality. However, CRF is not routinely measured and PA not routinely prescribed as part of standard healthcare. The American Heart Association (AHA) recently presented a scientific case for the inclusion of CRF as a clinical vital sign based on epidemiological and clinical observation. Here, we leverage genetic data in the UK Biobank (UKB) to strengthen the case for CRF as a vital sign and make a case for the prescription of PA. Methods We derived two CRF measures from the heart rate data collected during a submaximal cycle ramp test: CRF-vo2max, an estimate of the participants' maximum volume of oxygen uptake, per kilogram of body weight, per minute; and CRF-slope, an estimate of the rate of increase of heart rate during exercise. Average PA over a 7-day period was derived from a wrist-worn activity tracker. After quality control, 70,783 participants had data on the two derived CRF measures, and 89,683 had PA data. We performed genome-wide association study (GWAS) analyses by sex, and post-GWAS techniques to understand genetic architecture of the traits and prioritise functional genes for follow-up. Results We found strong evidence that genetic variants associated with CRF and PA influenced genetic expression in a relatively small set of genes in the heart, artery, lung, skeletal muscle and adipose tissue. These functionally relevant genes were enriched among genes known to be associated with coronary artery disease (CAD), type 2 diabetes (T2D) and Alzheimer’s disease (three of the top 10 causes of death in high-income countries) as well as Parkinson’s disease, pulmonary fibrosis, and blood pressure, heart rate, and respiratory phenotypes. Genetic variation associated with lower CRF and PA was also correlated with several disease risk factors (including greater body mass index, body fat and multiple obesity phenotypes); a typical T2D profile (including higher insulin resistance, higher fasting glucose, impaired beta-cell function, hyperglycaemia, hypertriglyceridemia); increased risk for CAD and T2D; and a shorter lifespan. Conclusions Genetics supports three decades of evidence for the inclusion of CRF as a clinical vital sign. Given the genetic, clinical and epidemiological evidence linking CRF and PA to increased morbidity and mortality, regular measurement of CRF as a marker of health and routine prescription of PA could be a prudent strategy to support public health.

Family Environment and Its Correlation with Anxiety and Depression: A Study on Heart Patients

2016 ◽  
Vol 3 (2) ◽  
Author(s):  
Dr. Meena Jain ◽  
Saloni Chandalia
Keyword(s):  
Heart Disease ◽  
Family Environment ◽  
Heart Attack ◽  
Psychiatric Symptoms ◽  
Disease Risk ◽  
Positive Association ◽  
Anxiety And Depression ◽  
Depression And Anxiety ◽  
Increased Risk ◽  
Artery Disease

This research paper deals with the Family Environment and its Correlation with Anxiety and Depression level among persons with Heart Disease. There had been a number of researches that investigated that ischemic heart disease patients who suffer significant anxiety have close to a 5-fold increased risk of experiencing frequent angina and those with depression have more than a 3-fold increased risk for these episodes. This observed link between psychiatric symptoms and angina underlines the importance of treating anxiety and depression in cardiac patients, according to study co author Dr Mark D Sullivan (University of Washington School of Medicine, Seattle). To gather the needed data, Hamilton Anxiety Scale and Becks Depression Inventory were used. As stated from literatures, for people with heart dysfunction, depression and anxiety can increase the risk of an adverse cardiac event such as a heart attack or blood clots. For people who do not have heart disease, depression and anxiety can also increase the risk of a heart attack and development of coronary artery disease. Researchers have also emphasized on the role of family psychosocial environment and its positive association with the Coronary Heart Disease risk.

Cardiovascular Complications of Sleep Disorders: A Better Night’s Sleep for a Healthier Heart / From Bench to Bedside

2020 ◽  
Vol 19 (2) ◽  
pp. 210-232 ◽  
Author(s):  
Theodora A. Manolis ◽  
Antonis A. Manolis ◽  
Evdoxia J. Apostolopoulos ◽  
Helen Melita ◽  
Antonis S. Manolis
Keyword(s):  
Sleep Disorders ◽  
Disease Risk ◽  
Behavioral Therapy ◽  
Benzodiazepine Receptor ◽  
Cardiovascular Complications ◽  
Gamma Aminobutyric Acid ◽  
Acid Type ◽  
Increased Risk ◽  
Cv Disease ◽  
Meta Analyses

: Sleep is essential to and an integral part of life and when lacking or disrupted, a multitude of mental and physical pathologies ensue, including cardiovascular (CV) disease, which increases health care costs. Several prospective studies and meta-analyses show that insomnia, short (<7h) or long (>9h) sleep and other sleep disorders are associated with an increased risk of hypertension, metabolic syndrome, myocardial infarction, heart failure, arrhythmias, CV disease risk and/or mortality. The mechanisms by which insomnia and other sleep disorders lead to increased CV risk may encompass inflammatory, immunological, neuro-autonomic, endocrinological, genetic and microbiome perturbations. Guidelines are emerging that recommend a target of >7 h of sleep for all adults >18 years for optimal CV health. Treatment of sleep disorders includes cognitive-behavioral therapy considered the mainstay of non-pharmacologic management of chronic insomnia, and drug treatment with benzodiazepine receptor agonists binding to gamma aminobutyric acid type A (benzodiazepine and non-benzodiazepine agents) and some antidepressants. However, observational studies and meta-analyses indicate an increased mortality risk of anxiolytics and hypnotics, although bias may be involved due to confounding and high heterogeneity in these studies. Nevertheless, it seems that the risk incurred by the non-benzodiazepine hypnotic agents (Z drugs) may be relatively less than the risk of anxiolytics, with evidence indicating that at least one of these agents, zolpidem, may even confer a lower risk of mortality in adjusted models. All these issues are herein reviewed.

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