Bone mineral density and risk of cardiovascular disease in men and women: the HUNT study.

The association between bone mineral density (BMD) and cardiovascular disease (CVD) is not fully understood. We evaluated BMD as a risk factor for cardiovascular disease and specifically atrial fibrillation (AF), acute myocardial infarction (AMI), ischemic (IS) and hemorrhagic stroke (HS) and heart failure (HF) in men and women. This prospective population cohort utilized data on 22 857 adults from the second and third surveys of the HUNT Study in Norway free from CVD at baseline. BMD was measured using single and dual-energy X-ray absorptiometry in the non-dominant distal forearm and T-score was calculated. Hazard ratios (HR) and 95% confidence intervals (CI) were calculated from adjusted cox proportional hazards models. The analyses were sex-stratified, and models were adjusted for age, age-squared, BMI, physical activity, smoking status, alcohol use, and education level. Additionally, in women, we adjusted for estrogen use and postmenopause. During a mean follow-up of 13.6 ± 5.7 years, 2 928 individuals (12.8%) developed fatal or non-fatal CVD, 1 020 AF (4.5%), 1 172 AMI (5.1%), 1 389 IS (6.1%), 264 HS (1.1%), and 464 HF (2.0%). For every 1 unit decrease in BMD T-score the HR for any CVD was 1.01 (95% CI 0.98 to 1.04) in women and 0.99 (95% CI 0.94 to 1.03) in men. Point estimates for the four cardiovascular outcomes ranged from slightly protective (HR 0.95 for AF in men) to slightly deleterious (HR 1.12 for HS in men). We found no evidence of association of lower distal forearm BMD with CVD, AF, AMI, IS, HS, and HF.

Weight and weight change and risk of atrial fibrillation: the HUNT study.

AIMS: Although obesity has been associated with risk of atrial fibrillation (AF), the associations of long-term obesity, recent obesity, and weight change with AF risk throughout adulthood are uncertain. METHODS AND RESULTS: An ambispective cohort study was conducted which included 15 214 individuals. The cohort was created from 2006 to 2008 (the baseline) and was followed for incident AF until 2015. Weight and height were directly measured at baseline. Data on previous weight and height were retrieved retrospectively from measurements conducted 10, 20, and 40 years prior to baseline. Average body mass index (BMI) over time and weight change was calculated. During follow-up, 1149 participants developed AF. The multivariable-adjusted hazard ratios were 1.2 (95% confidence interval 1.0-1.4) for average BMI 25.0-29.9 kg/m2 and 1.6 (1.2-2.0) for average BMI ≥30 kg/m2 when compared with normal weight. The association of average BMI with AF risk was only slightly attenuated after adjustment for most recent BMI. In contrast, current BMI was not strongly associated with the risk of AF after adjustment for average BMI earlier in life. Compared with stable BMI, both loss and gain in BMI were associated with increased AF risk. After adjustment for most recent BMI, the association of BMI gain with AF risk was largely unchanged, while the association of BMI loss with AF risk was weakened. CONCLUSION: Long-term obesity and BMI change are associated with AF risk. Obesity earlier in life and weight gain over time exert cumulative effects on AF development even after accounting for most recent BMI.

Asthma, asthma control and risk of acute myocardial infarction: HUNT study.

Asthma, a chronic inflammatory airway disease, shares several common pathophysiological mechanisms with acute myocardial infarction (AMI). Our aim was to assess the prospective associations between asthma, levels of asthma control and risk of AMI. We followed 57,104 adults without previous history of AMI at baseline from Nord-Trøndelag health study (HUNT) in Norway. Self-reported asthma was categorised as active asthma (i.e., using asthma medication) and non-active asthma (i.e., not using asthma medication). Levels of asthma control were defined as controlled, partly controlled, and uncontrolled based on the Global Initiative for Asthma guidelines. AMI was ascertained by linking HUNT data with hospital records. A total of 2868 AMI events (5.0%) occurred during a mean (SD) follow-up of 17.2 (5.4) years. Adults with active asthma had an estimated 29% higher risk of developing AMI [adjusted hazard ratio (HR) 1.29, 95% CI 1.08-1.54] compared with adults without asthma. There was a significant dose-response association between asthma control and AMI risk, with highest risk in adults with uncontrolled asthma (adjusted HR 1.73, 95% CI 1.13-2.66) compared to adults with controlled asthma (p for trend < 0.05). The associations were not explained by smoking status, physical activity and C-reactive protein levels. Our study suggests that active asthma and poor asthma control are associated with moderately increased risk of AMI. Further studies are needed to evaluate causal relationship and the underlying mechanisms and to clarify the role of asthma medications in the risk of AMI.

Associations of Insomnia Symptoms With Blood Pressure and Resting Heart Rate: The HUNT Study in Norway.

OBJECTIVE: Although elevated heart rate and blood pressure might represent biologically plausible links for the association of insomnia symptoms with increased risk of cardiovascular disease (CVD), few large studies have investigated the associations of insomnia symptoms with these factors. Our aim was to investigate the associations of self-reported insomnia symptoms with systolic and diastolic blood pressure and resting heart rate in a large population-based study. PARTICIPANTS: Self-reported information on insomnia symptoms, including sleep initiation problems, frequent awakening and early awakenings during night, and measurements of resting heart rate and blood pressure were collected from a total of 50,806 men and women who participated in the third wave of the Nord-Trøndelag Health Study (HUNT-3) in 2006-2008. METHODS: In multivariable analyses, we adjusted for sociodemographic factors, lifestyle factors, established CVD risk factors, and snoring or breathing pauses. RESULTS: Compared to participants reporting none of the insomnia symptoms, those having all three insomnia symptoms several times a week had lower diastolic blood pressure (-0.80 [95% CI: -1.47 to -0.14] mmHg, p = 0.02), lower systolic blood (-1.69 [95% CI: -2.76 to -0.63) mmHg, p < 0.001), and higher resting heart rate (0.83 [95% CI: 0.11 to 1.55] beats/minute, p = 0.02). CONCLUSIONS: We found a modest positive association of insomnia symptoms with resting heart rate, and a modest inverse association of insomnia with blood pressure. However, the actual differences were small, and likely of less clinical importance. Prospective studies are needed to establish whether the potential link between insomnia and CVD is mediated through changes in heart rate and/or blood pressure.

Insomnia and left ventricular function - an echocardiography study.

OBJECTIVES: Recently, studies have reported an association of insomnia with incident heart failure but its causal relation is still uncertain. In patients with heart failure, the left ventricular function is impaired and the deterioration may start long before the patient experiences any symptoms. As the first study, we examined the association of insomnia with left ventricular function using state-of-the art echocardiography methods. DESIGN: In the echocardiography study, several indices of left ventricular function were examined in participants free from cardiovascular diseases, hypertension and diabetes. In total 788 participants with information on all relevant covariates were included. We calculated the least square mean of indices of left ventricular function associated with increasing number of insomnia symptoms (i.e. difficulties falling asleep, frequent awakenings and early awakenings), including systolic mitral annular excursion, peak velocities of systolic and diastolic motion of the mitral annulus and systolic deformation of the left ventricle. RESULTS: We found no clear evidence that increasing number of insomnia symptoms is associated with any of the left ventricular function indices. CONCLUSIONS: The methods that were used are sensitive to detect preclinical HF, and therefore, our findings do not support a causal relation between insomnia symptoms and HF.

Insomnia and the risk of incident heart failure: a population study.

AIMS: Insomnia is highly prevalent among heart failure patients, but only a few small studies have investigated insomnia symptoms and risk of heart failure. We aimed to assess the prospective association between self-reported insomnia symptoms and the risk of incident heart failure in a large Norwegian cohort. METHODS AND RESULTS: Baseline data on insomnia symptoms, including difficulty initiating sleep, difficulty maintaining sleep and having non-restorative sleep, socio-demographic variables, and health status, including established cardiovascular risk factors, were collected from 54 279 men and women 20-89 years of age who participated in the Nord-Trøndelag Health study (HUNT) between 1995 and 1997 and were free from known heart failure at baseline. The cohort was followed for incident heart failure from baseline through 2008. We used Cox proportional hazard models to assess the association of baseline insomnia symptoms with the risk of heart failure. A total of 1412 cases of heart failure occurred during a mean follow-up of 11.3 years (SD = 2.9 years), either identified at hospitals or by the National Cause of Death Registry. There was a dose-dependent association between the number of insomnia symptoms and risk of heart failure. The multi-adjusted hazard ratios were 0.96 (0.57-1.61), 1.35 (0.72-2.50), and 4.53 (1.99-10.31) for people with one, two, and three insomnia symptoms, compared with people with none of the symptoms (P for trend 0.021). CONCLUSIONS: Insomnia is associated with an increased risk of incident heart failure. If our results are confirmed by others and causation is proved, evaluation of insomnia symptoms might have consequences for cardiovascular prevention.

Maternal exposure to ambient temperature and the risks of preterm birth and stillbirth in Brisbane, Australia.

Almost 10% of all births are preterm, and 2.2% are stillbirths. Recent research has suggested that environmental factors may be a contributory cause of these adverse birth outcomes. The authors examined the relation between ambient temperature and preterm birth and stillbirth in Brisbane, Australia, between 2005 and 2009 (n = 101,870). They used a Cox proportional hazards model with livebirth and stillbirth as competing risks. They also examined whether there were periods in pregnancy where exposure to high temperatures had a greater effect. Higher ambient temperatures in the last 4 weeks of the pregnancy increased the risk of stillbirth. The hazard ratio for stillbirth was 0.3 at 12°C relative to the reference temperature of 21°C. The temperature effect was greatest at less than 36 weeks of gestation. There was an association between higher temperature and shorter gestation, as the hazard ratio for livebirth was 0.96 at 15°C and 1.02 at 25°C. This effect was greatest at later gestational ages. These results provide strong evidence of an association between increased temperature and increased risk of stillbirth and shorter gestation.

The influence of season and ambient temperature on birth outcomes: a review of the epidemiological literature.

Seasonal patterns of birth outcomes, such as low birth weight, preterm birth and stillbirth, have been found around the world. As a result, there has been an increasing interest in evaluating short-term exposure to ambient temperature as a determinant of adverse birth outcomes. This paper reviews the epidemiological evidence on seasonality of birth outcomes and the impact of prenatal exposure to ambient temperature on birth outcomes. We identified 20 studies that investigated seasonality of birth outcomes, and reported statistically significant seasonal patterns. Most of the studies found peaks of preterm birth, stillbirth and low birth weight in winter, summer or both, which indicates the extremes of temperature may be an important determinant of poor birth outcomes. We identified 13 studies that investigated the influence of exposure to ambient temperature on birth weight and preterm birth (none examined stillbirth). The evidence for an adverse effect of high temperatures was stronger for birth weight than for preterm birth. More research is needed to clarify whether high temperatures have a causal effect on fetal health.

Vulnerability of eco-environmental health to climate change: the views of government stakeholders and other specialists in Queensland, Australia.

BACKGROUND: There is overwhelming scientific evidence that human activities have changed and will continue to change the climate of the Earth. Eco-environmental health, which refers to the interdependencies between ecological systems and population health and well-being, is likely to be significantly influenced by climate change. The aim of this study was to examine perceptions from government stakeholders and other relevant specialists about the threat of climate change, their capacity to deal with it, and how to develop and implement a framework for assessing vulnerability of eco-environmental health to climate change. METHODS: Two focus groups were conducted in Brisbane, Australia with representatives from relevant government agencies, non-governmental organisations, and the industry sector (n = 15) involved in the discussions. The participants were specialists on climate change and public health from governmental agencies, industry, and non-governmental organisations in South-East Queensland. RESULTS: The specialists perceived climate change to be a threat to eco-environmental health and had substantial knowledge about possible implications and impacts. A range of different methods for assessing vulnerability were suggested by the participants and the complexity of assessment when dealing with multiple hazards was acknowledged. Identified factors influencing vulnerability were perceived to be of a social, physical and/or economic nature. They included population growth, the ageing population with associated declines in general health and changes in the vulnerability of particular geographical areas due to for example, increased coastal development, and financial stress. Education, inter-sectoral collaboration, emergency management (e.g. development of early warning systems), and social networks were all emphasised as a basis for adapting to climate change. To develop a framework, different approaches were discussed for assessing eco-environmental health vulnerability, including literature reviews to examine the components of vulnerability such as natural hazard risk and exposure and to investigate already existing frameworks for assessing vulnerability. CONCLUSION: The study has addressed some important questions in regard to government stakeholders and other specialists' views on the threat of climate change and its potential impacts on eco-environmental health. These findings may have implications in climate change and public health decision-making.

Symptoms of anxiety and depression and risk of atrial fibrillation-The HUNT study.

BACKGROUND: Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia. Anxiety and depression may activate the autonomic nervous system which is likely to play an important role in the etiology of AF. However, little is known about the association between symptoms of anxiety and depression and risk of AF. OBJECTIVE: This study aimed to assess the association between symptoms of anxiety and depression and risk of AF. METHODS: In a population-based study, 37,402 adult residents were followed for incident AF from 2006 to 2008 until 2015. Participants were classified according to data on anxiety and depression symptoms. Cox proportional regression models were used to adjust for common AF risk factors. RESULTS: During a median follow-up of 8.1 years, 1433 (3.8%) participants developed AF. In comparisons with no anxiety symptoms, the multivariable-adjusted hazard ratios (HRs) were 1.1 (95% CI: 0.9-1.5) for mild to moderate anxiety symptoms and 1.0 (95% CI: 0.8-1.4) for severe anxiety symptoms. In comparisons with no depression symptoms, the multivariable-adjusted HRs were 1.5 (95% CI: 1.2-1.8) for mild to moderate depression symptoms and 0.9 (95% CI: 0.6-1.3) for severe depression symptoms. Recurrent anxiety/depression symptoms were not associated with increased AF risk. CONCLUSIONS: In this large, population-based study, we found no evidence of an association between symptoms of anxiety or severe depression and AF risk, even for recurrent anxiety or depression symptoms. An unexpected association of symptoms of mild to moderate depression with increased AF risk requires confirmation in other studies. Our findings add to the sparse literature on symptoms of anxiety and depression and risk of AF.

Metabolically Healthy Obesity and Risk for Atrial Fibrillation: The HUNT Study.

OBJECTIVE: Atrial fibrillation (AF) is the most common arrhythmia and has been described as a global epidemic. Although AF is associated with both obesity and its metabolic consequences, little is known about the association between metabolically healthy obesity and AF. METHODS: In a population-based study, 47,870 adults were followed for incident AF from 2006 to 2008 until 2015. Participants were classified according to BMI and metabolic status (using waist circumference, triglycerides, high-density lipoprotein cholesterol, blood pressure, and glucose) at baseline. RESULTS: During a median follow-up of 8.1 years, 1,758 participants developed AF. Compared with metabolically healthy individuals with BMI < 25 kg/m2 , the multivariable-adjusted hazard ratios for metabolically healthy and unhealthy obesity were 1.6 (95% CI: 1.2 to 2.1) and 1.6 (95% CI: 1.3 to 1.9), respectively. AF risk increased according to the severity of obesity. CONCLUSIONS: Metabolically healthy and unhealthy obesity increased AF risk to a similar extent. Severity of obesity was positively associated with AF risk regardless of metabolic status.

Genome-wide association analysis of self-reported daytime sleepiness identifies 42 loci that suggest biological subtypes.

Excessive daytime sleepiness (EDS) affects 10-20% of the population and is associated with substantial functional deficits. Here, we identify 42 loci for self-reported daytime sleepiness in GWAS of 452,071 individuals from the UK Biobank, with enrichment for genes expressed in brain tissues and in neuronal transmission pathways. We confirm the aggregate effect of a genetic risk score of 42 SNPs on daytime sleepiness in independent Scandinavian cohorts and on other sleep disorders (restless legs syndrome, insomnia) and sleep traits (duration, chronotype, accelerometer-derived sleep efficiency and daytime naps or inactivity). However, individual daytime sleepiness signals vary in their associations with objective short vs long sleep, and with markers of sleep continuity. The 42 sleepiness variants primarily cluster into two predominant composite biological subtypes - sleep propensity and sleep fragmentation. Shared genetic links are also seen with obesity, coronary heart disease, psychiatric diseases, cognitive traits and reproductive ageing.

Biological and clinical insights from genetics of insomnia symptoms.

Insomnia is a common disorder linked with adverse long-term medical and psychiatric outcomes. The underlying pathophysiological processes and causal relationships of insomnia with disease are poorly understood. Here we identified 57 loci for self-reported insomnia symptoms in the UK Biobank (n = 453,379) and confirmed their effects on self-reported insomnia symptoms in the HUNT Study (n = 14,923 cases and 47,610 controls), physician-diagnosed insomnia in the Partners Biobank (n = 2,217 cases and 14,240 controls), and accelerometer-derived measures of sleep efficiency and sleep duration in the UK Biobank (n = 83,726). Our results suggest enrichment of genes involved in ubiquitin-mediated proteolysis and of genes expressed in multiple brain regions, skeletal muscle, and adrenal glands. Evidence of shared genetic factors was found between frequent insomnia symptoms and restless legs syndrome, aging, and cardiometabolic, behavioral, psychiatric, and reproductive traits. Evidence was found for a possible causal link between insomnia symptoms and coronary artery disease, depressive symptoms, and subjective well-being.

Associations of Asthma and Asthma Control With Atrial Fibrillation Risk: Results From the Nord-Trøndelag Health Study (HUNT).

Importance: Asthma, a chronic inflammatory airway disease, and atrial fibrillation (AF) share several common pathophysiological mechanisms. Research on the association between asthma and atrial fibrillation is lacking, and to our knowledge, no previous studies have assessed the dose-response association between levels of asthma control and AF. Objective: To assess the association between asthma, levels of asthma control, and AF. Design, Setting, and Participants: This prospective population cohort analyzed data on adults from a second and third iteration of the survey-based Nord-Trøndelag Health Study (HUNT) in Norway. All included participants were free from AF at baseline. Atrial fibrillation was ascertained by linking HUNT data with hospital records from the 2 hospitals in Nord-Trøndelag County. Data analysis was completed from May 2017 to November 2017. Exposures: Self-reported asthma was categorized into 3 groups: those who had ever had asthma, those who self-report being diagnosed with asthma, and those who had active asthma. Asthma control was defined according to Global Initiative for Asthma guidelines and was categorized into controlled, partly controlled, and uncontrolled cases. Main Outcomes and Measures: Atrial fibrillation. Results: A total of 54 567 adults were included (of whom 28 821 [52.8%] were women). Of these, 5961 participants (10.9%) reported ever having asthma, 3934 participants (7.2%) reported being diagnosed with asthma, and 2485 participants (4.6%) reported having active asthma. During a mean (SD) follow-up of 15.4 (5.8) years, 2071 participants (3.8%) developed AF. Participants with physician-diagnosed asthma had an estimated 38% higher risk of developing AF (adjusted hazard ratio, 1.38 [95% CI, 1.18-1.61]) compared with participants without asthma. There was a dose-response association between levels of asthma control and risk of AF with the highest risk for AF in participants with uncontrolled asthma (adjusted hazard ratio, 1.74 [95% CI, 1.26-2.42]; P for trend < .001). Conclusions and Relevance: Asthma and lack of asthma control were associated with moderately increased risks of AF in a dose-response manner. Further studies are needed to explore the underlying mechanisms and clarify causal pathways between asthma and AF.

Self-reported sleep duration and coronary heart disease mortality: A large cohort study of 400,000 Taiwanese adults.

BACKGROUND: Most previous studies on sleep duration and coronary heart disease (CHD) have been small and have inadequately controlled for cardiovascular risk factors and chronic diseases. Therefore, our aim was to prospectively examine the associations of sleep duration with CHD while accounting for these factors. METHODS: Prospective cohort study of 392 164 adults at age 20years or older who attended a health check-up program from 1994 to 2011 in Taiwan and who have information on sleep duration, sleep medications and potential confounders. Participants answered the question: "How long do you sleep for?"-there were four response categories: (a) 0-4h; (b) 4-6h; (c) 6-8h and (d) >8h. The participants were then followed for CHD mortality from the Taiwanese cause-of-death register. RESULTS: When compared to those who slept 6-8h per night, the risk of dying from CHD was increased by 34% (HR 1.34, 95% Confidence Interval [CI] 0.87-2.07) and 35% (HR 1.35, 95% CI 1.11-1.65) in those who slept less than 4h per night and more than 8h per night, respectively. When stratifying by sex and age, we found some evidence for a stronger U-shaped association in females than in males and in older adults than in younger adults (p for interaction=0.01 and 0.13, respectively). CONCLUSIONS: Adequate sleep duration should be considered an important component of a healthy lifestyle. Further studies are needed to better elucidate the underlying mechanisms.

Insomnia symptoms and risk for unintentional fatal injuries--the HUNT Study.

STUDY OBJECTIVES: To assess the association between insomnia symptoms and risk of fatal unintentional injuries. DESIGN: Population-based prospective cohort study with a mean follow-up of 14 y, linking health survey data with information on insomnia symptoms to the National Cause of Death Registry. SETTING: Nord-Trøndelag County, Norway. PARTICIPANTS: A total of 54,399 men and women 20-89 y of age who participated in the Nord-Trøndelag Health Study between 1995 and 1997. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: There were 277 unintentional fatal injuries, including 57 fatal motor vehicle injuries during follow-up. There was a dose-dependent association between the number of insomnia symptoms and risk of unintentional fatal injuries (P for trend 0.001) and fatal motor vehicle injuries (P for trend 0.023), respectively. The proportion of unintentional fatal injuries cases that could have been prevented in the absence of difficulties initiating sleep, difficulties maintaining sleep, and having a feeling of nonrestorative sleep were 8%, 9%, and 8%, respectively. The corresponding estimates for motor vehicle injuries were 34%, 11%, and 10%. CONCLUSION: Insomnia is a major contributor to both unintentional fatal injuries in general as well as fatal motor vehicle injuries. Increasing public health awareness about insomnia and identifying persons with insomnia may be important in preventing unintentional fatal injuries.

Insomnia symptoms and cardiorespiratory fitness in healthy individuals: the Nord-Trøndelag Health Study (HUNT).

STUDY OBJECTIVES: Previous studies have found an inverse association between insomnia and self-reported physical activity, but it is not clear whether insomnia is associated with cardiorespiratory fitness. Our aim was to investigate different insomnia symptoms in relation to the gold standard measure of cardiorespiratory fitness, i.e., peak oxygen uptake (VO(2peak)). DESIGN: Cross-sectional population study. SETTING: Nord-Trøndelag County, Norway. PARTICIPANTS: The group comprised 3,489 men and women who were free from cardiovascular or pulmonary diseases, cancer, and sarcoidosis and who did not use antihypertensive medication. They were included in the fully adjusted model when assessing all insomnia symptoms simultaneously. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: For insomnia, the participants reported how often they had experienced sleep problems during the past 3 months, including difficulties falling asleep at night, repeated awakenings during the night, early awakenings without being able to go back to sleep, and daytime sleepiness. Response options were "never/almost never," "sometimes" or "several times a wk." To measure cardiorespiratory fitness, the participants were asked to walk or run on a treadmill with increasing speed and/or incline until exhaustion, and VO(2peak) was recorded. We found a modest inverse and graded association of the insomnia symptoms with VO(2peak). The association was independent of self-reported physical activity and was apparent for all insomnia symptoms except for early awakenings. We found a dose-response relation for a cumulative combination of insomnia symptoms and VO(2peak) for experiencing zero, one to two, or three to four symptoms (P for trend < 0.001). CONCLUSIONS: We found a modest inverse association of insomnia with VO(2peak) independent of the conventional cardiovascular risk factors and self-reported physical activity.

Insomnia and endothelial function - the HUNT 3 fitness study.

BACKGROUND: Insomnia is associated with increased risk of coronary heart disease (CHD), but the underlying mechanisms are not understood. To our knowledge, no previous studies have examined insomnia in relation to endothelial function, an indicator of preclinical atherosclerosis. Our aim was to assess the association of insomnia with endothelial function in a large population based study of healthy individuals. METHODS: A total of 4 739 participants free from known cardiovascular or pulmonary diseases, cancer, and sarcoidosis, and who were not using antihypertensive medication were included in the study. They reported how often they had experienced difficulties falling asleep at night, repeated awakenings during the night, early awakenings without being able to go back to sleep, and daytime sleepiness. Endothelial function was measured by flow mediated dilation (FMD) derived from the brachial artery. RESULTS: We found no consistent association between the insomnia symptoms and endothelial function in multiadjusted models, but individual insomnia symptoms may be related to endothelial function. Among women who reported early awakenings, endothelial function may be lower than in women without this symptom (p = 0.03). CONCLUSIONS: This study provided no evidence that endothelial function, an early indicator of atherosclerosis, is an important linking factor between insomnia and CHD. Further studies are needed to explore the complex interrelation between sleep and cardiovascular pathology.