From the Journals

Too much, too little sleep linked to atherosclerosis

 

Key clinical point: Even among healthy men and women, both too much and too little sleep are associated with atherosclerosis.

Major finding: Sleeping less than 6 hours a night was independently associated with a higher noncardiac atherosclerotic burden (OR ,1.27; 95% CI, 1.06-1.52; P = .008)

Study details: Spanish study of 3,974 bank employees.

Disclosures: The work was funded by CNIC and Banco Santander, among others. The study lead had no disclosures. Investigator Hector Bueno, MD, PhD, reported research funding and fees from a number of companies, including AstraZeneca and Novartis. The second author, Valentín Fuster, MD, PhD, is the editor of the Journal of the American College of Cardiology, which published the report.

Source: Domínguez F et al. J Am Coll Cardiol. 2019;73:134-44.

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It’s time for a prospective CV sleep study

This study extends the published reports on sleep duration and vascular disease to an early middle-aged cohort by using an objective measure of sleep duration and sensitive measures of atherosclerosis in multiple vascular territories.

Ultimately, studies of sleep extension are needed to determine whether modification of sleep behaviors will improve vascular health outcomes. The potentially enormous impact of sleep deprivation and disruption on population health, reinforced by the present study, is ample justification for such trials, which are needed to place sleep with confidence alongside diet and exercise as a key pillar of a healthy lifestyle.

However, both hypertension and diabetes were more common in the group sleeping fewer than 6 hours per night, but neither blood pressure nor glucose metabolism was assessed with sufficiently comprehensive measures to explore these factors as potential effect mediators.

More importantly, the causes of short sleep duration and sleep fragmentation in this cohort are unknown. It is unclear to what extent short sleep duration in this cohort reflects voluntary behaviors that limit time available for sleep versus insomnia. Insomnia is itself associated with increased risk of vascular disease.

Deepak Bhatt , MD, professor of cardiovascular medicine, and Daniel Gottlieb , MD, an associate professor of medicine at Harvard Medical School, Boston, made these comments in an accompanying editorial ( J Am Coll Cardiol. 2019 Jan 14;73[2]:145-7 ). Dr. Gottlieb is also the director of the Boston Veterans Affairs Sleep Disorders Center. Dr. Bhatt reported research funding and income from a number of companies, including Abbott, Boehringer Ingelheim, and Medtronic.


 

FROM THE JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY

Too little and too much sleep, along with fragmented sleep, were independently linked with increased subclinical, noncardiac atherosclerotic plaque in healthy middle-aged men and women in a Spanish investigation of bank employees.

A sad-looking woman trying to sleep Wavebreak Media/Thinkstockphotos

“Overall, our findings support the potential role of healthy sleeping in protecting against atherosclerosis. Thus, recommending a good sleep hygiene” – 7-8 hours a night – “should be part of the lifestyle modifications provided in our daily clinical practice,” said investigators led by Fernando Domínguez, MD, PhD, of Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid. The report is in the Journal of the American College of Cardiology.

Studies have linked sleep problems to increased cardiovascular risk before, but the investigations tended to focus on patients with obstructive sleep apnea (OSA) and other problems, and often relied on patient self-report. The investors wanted to see if the relationship held in healthy adults, using an objective measure.

The participants – all with no known cardiovascular disease – wore Acti Trainers accelerometers (Actigraph, Pensacola, Fla.) around their waists for 7 days to record sleep duration and quality. Subjects also had their plaque burdens assessed by 3-dimensional vascular ultrasound (VUS) at their carotid and femoral arteries bilaterally. Cardiac CT was used to assess coronary artery calcification as a surrogate for coronary artery atherosclerosis.

The 3,974 participants had a mean age of 46 years, and a third were women; they had a low prevalence of both hypertension and diabetes. OSA patients were excluded from the study. Overall, 27% had very short sleep duration (VSSD), less than 6 hours a night; 38% had short sleep duration (SSD), 31% slept from 7 to 8 hours per night, and served as the reference group for healthy sleep habits; and 4% had long sleep duration (LSD), greater than 8 hours.

After adjustment for a wide range of cardiovascular risk factors, including body mass index, hypertension, and smoking, VSSD was independently associated with a higher atherosclerotic burden, compared to the reference group (odds ratio, 1.27; 95% confidence interval, 1.06-1.52; P = 0.008). Participants in the highest quintile of sleep fragmentation were more likely to have plaques at multiple sites (OR, 1.34; 95% CI, 1.09-1.64; P = 0.006). The Framingham risk score at both 10 and 30 years was significantly higher in participants with VSSD or SSD, and in the highest quintiles of sleep fragmentation.

LSD was also associated with a higher plaque burden, which reached statistical significance in women. “Too-long sleep duration may not be healthy either ... Recommendations should be restricted to 7 to 8 hours,” the investigators said.

Sleep duration and quality were not associated with inflammation markers or coronary artery calcification. The investigators noted that CT for coronary artery calcification might not be as sensitive as VUS for picking up subclinical atherosclerosis.

Short sleepers tended to have higher intakes of alcohol and caffeine than did those in the 7- to 8-hour group.

The work was funded by CNIC and Banco Santander, among others. Dr. Domínguez had no disclosures. Investigator Hector Bueno, MD, PhD, reported research funding and fees from a number of companies, including AstraZeneca and Novartis. The second author, Valentín Fuster, MD, PhD, is the editor of the Journal of the American College of Cardiology, which published the report.

SOURCE: Domínguez F et al. J Am Coll Cardiol 2019;73:134-44.

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