:
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.
gamma-Aminobutyric acid-A (GABAA) agonists down-regulate GABAA/benzodiazepine receptor polypeptides from the surface of chick cortical neurons.
