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Insomnia and Cardiovascular Disease: Untangling a Complex Relationship

失眠症 孟德尔随机化 医学 人口 疾病 社会心理的 睡眠呼吸暂停 致死性家族性失眠 血压 队列 痴呆 临床试验 阻塞性睡眠呼吸暂停 风险因素 不利影响 队列研究 精神科 随机对照试验 临床心理学 前瞻性队列研究 内科学 重症监护医学
作者
Martino F. Pengo,Sogol Javaheri,Giuseppe Maiolino,Susan Redline,Carolina Lombardi
出处
期刊:Journal of Sleep Research [Wiley]
卷期号:: e70299-e70299
标识
DOI:10.1111/jsr.70299
摘要

Insomnia is the most prevalent sleep disorder, affecting up to one third of the adult population and is increasingly recognised as a potential contributor to cardiovascular disease (CVD), a leading cause of global morbidity and mortality. This narrative review examines the complex relationship between insomnia and CVD, integrating epidemiological, genetic and mechanistic evidence to assess whether insomnia represents a causal cardiovascular risk factor. Large prospective cohort studies and meta-analyses consistently show that insomnia symptoms and clinically diagnosed insomnia are associated with increased risks of hypertension, myocardial infarction, stroke, heart failure and cardiovascular mortality, with stronger associations observed in individuals with short sleep duration or persistent insomnia. Mendelian randomization studies involving millions of participants further support a likely causal link, suggesting that genetic liability to insomnia increases the risk of multiple cardiometabolic outcomes. Biological plausibility is supported by evidence of autonomic imbalance, hypothalamic-pituitary-adrenal axis activation, inflammation and adverse blood pressure profiles in individuals with insomnia. However, insomnia is a heterogeneous condition, frequently coexisting with other sleep disorders and influenced by psychosocial and circadian factors, which complicates causal inference. Importantly, evidence that treatment of insomnia reduces cardiovascular risk remains limited. While cognitive behavioural therapy for insomnia improves sleep outcomes and some cardiometabolic biomarkers, randomised trials have not demonstrated clear benefits on blood pressure or other cardiovascular endpoints and some pharmacological treatments may even be associated with harm. Overall, current evidence suggests that insomnia is a plausible and potentially causal risk factor for CVD, but definitive proof of reversibility through treatment is lacking. Well-powered, rigorously designed trials targeting patients with clinically defined insomnia are needed to determine whether effective insomnia treatment can meaningfully reduce cardiovascular risk and inform future prevention strategies.
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