European Journal of Cardiovascular Medicine

Sleep, an essential physiological function, plays a pivotal role in maintaining overall health and well-being, particularly in regulating cardiovascular, metabolic, and immune systems. A growing body of evidence highlights the detrimental effects of poor sleep quality, duration, or architecture on cardiovascular health, placing sleep disorders at the forefront of public health challenges. Conditions such as obstructive sleep apnea (OSA), insomnia, restless leg syndrome (RLS), and circadian rhythm disturbances affect a significant proportion of the global population, often coexisting with and exacerbating cardiovascular diseases (CVDs), which are the leading cause of mortality worldwide (1). Despite their prevalence and clinical importance, sleep disorders are frequently underdiagnosed and undertreated, leaving a critical gap in preventive and therapeutic strategies (2, 3).

The mechanisms underlying the link between sleep disorders and cardiovascular risk are multifaceted and interconnected. OSA, for instance, is characterized by recurrent episodes of partial or complete upper airway obstruction during sleep, leading to intermittent hypoxia, arousals, and fragmented sleep. These events activate the sympathetic nervous system, induce systemic inflammation, and promote oxidative stress, all of which contribute to endothelial dysfunction, arterial stiffness, and the progression of atherosclerosis (4, 5). Similarly, chronic insomnia disrupts the hypothalamic-pituitary-adrenal (HPA) axis, resulting in elevated cortisol levels, increased sympathetic tone, and impaired glucose metabolism, which collectively heighten the risk of hypertension, coronary artery disease, and heart failure (6). RLS, a neurological disorder marked by an uncontrollable urge to move the legs during rest, disrupts sleep patterns and triggers nocturnal sympathetic overactivation, impairing vascular regulation (7). Circadian rhythm disturbances, often seen in shift workers or individuals with irregular sleep schedules, disrupt hormonal and metabolic homeostasis, further amplifying cardiovascular risk (8).

Despite compelling evidence linking sleep disorders to cardiovascular outcomes, several challenges hinder the effective integration of sleep health into routine cardiovascular care. Diagnostic barriers include the underreporting of sleep disturbances by patients and the limited availability of specialized diagnostic tools like polysomnography in many regions. Even when sleep disorders are identified, adherence to treatment regimens remains a significant obstacle. For example, while continuous positive airway pressure (CPAP) therapy for OSA has been shown to reduce blood pressure and improve cardiac function, poor compliance rates limit its efficacy in real-world settings (9). Behavioral interventions, such as cognitive-behavioral therapy for insomnia (CBT-I), are effective but remain underutilized due to insufficient access to trained providers and limited patient awareness (10).

How Sleep Disorders Hurt Heart Health

Sleep disorders harm heart health through several interconnected mechanisms. These include heightened sympathetic nervous system activity, systemic inflammation, and oxidative stress, which impair endothelial function and promote arterial stiffness and atherosclerosis. For instance, chronic sleep deprivation or fragmented sleep exacerbates metabolic dysregulation, increasing the risk of hypertension, obesity, and diabetes, which are major contributors to cardiovascular disease. Moreover, disruptions in the sleep-wake cycle disturb circadian rhythms, affecting blood pressure regulation and heart rate variability, further exacerbating cardiovascular stress.

This review aims to provide a comprehensive analysis of the relationship between sleep disorders and cardiovascular risk. By synthesizing evidence from recent studies, it explores the underlying pathophysiological mechanisms, evaluates the effectiveness of current therapeutic approaches, and identifies key gaps and future directions in research and clinical practice.

Literature Search

A systematic literature search was conducted using PubMed, MEDLINE, Scopus, and Web of Science databases for studies published between January 2000 and October 2023. The search strategy included combinations of keywords such as “sleep disorders,” “cardiovascular risk,” “obstructive sleep apnea,” “insomnia,” “hypertension,” “arrhythmias,” “atherosclerosis,” and “systemic inflammation.” Boolean operators (AND, OR) were employed to refine search results, and additional articles were identified by manually screening reference lists of selected primary studies and systematic reviews (11). The review adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines to ensure methodological rigor.

Inclusion and Exclusion Criteria

Inclusion Criteria:

1. Studies investigating the association between sleep disorders and cardiovascular outcomes.
2. Research focusing on pathophysiological mechanisms linking sleep disturbances to cardiovascular risk.
3. Peer-reviewed randomized controlled trials, cohort studies, systematic reviews, and meta-analyses.

Exclusion Criteria:

1. Articles unrelated to sleep or cardiovascular health.
2. Case reports, opinion pieces, or editorials lacking empirical data.
3. Studies with insufficient data on cardiovascular outcomes or sleep diagnostics.

Data Extraction and Quality Assessment

Data extraction was performed using a standardized template designed to capture key information from each study, including study design, population characteristics, diagnostic criteria for sleep disorders, cardiovascular outcomes, and intervention efficacy. This process ensured a consistent and systematic approach to analyzing the included studies. For randomized controlled trials, data on randomization methods, blinding, and allocation concealment were recorded. For observational studies, parameters such as participant recruitment methods, sample size, and follow-up duration were noted. Additionally, information regarding potential confounders and adjustments made in the statistical analysis was collected.

The quality of the included studies was assessed using the Cochrane Risk of Bias Tool for randomized trials and the Newcastle-Ottawa Scale for observational studies. The Cochrane tool evaluated domains such as selection bias, performance bias, detection bias, and attrition bias. For observational studies, the Newcastle-Ottawa Scale assessed the quality of participant selection, comparability between groups, and the adequacy of outcome assessments. Studies scoring high in quality were prioritized for quantitative synthesis, while studies with significant methodological limitations were used only for qualitative insights. Discrepancies in the assessment process were resolved through consensus among the reviewers to ensure reliability and accuracy in the evaluation of study quality (12).

PRISMA Flow Diagram

Obstructive Sleep Apnea (OSA)

OSA is one of the most extensively studied sleep disorders in relation to cardiovascular outcomes. The repeated episodes of intermittent hypoxia and sleep fragmentation characteristic of OSA trigger a cascade of physiological changes, including sympathetic nervous system activation, systemic inflammation, and oxidative stress. These processes result in endothelial dysfunction, arterial stiffness, and accelerated atherosclerosis (13, 14). Untreated OSA is strongly associated with an increased risk of hypertension, stroke, and arrhythmias, such as atrial fibrillation. CPAP therapy has demonstrated significant benefits in reducing nocturnal blood pressure and improving left ventricular function, though adherence remains a key challenge in clinical practice (15).

Insomnia and Cardiovascular Health

Insomnia, one of the most prevalent sleep disorders, is characterized by difficulty falling or staying asleep. It disrupts restorative sleep processes, leading to elevated cortisol levels, increased sympathetic activity, and systemic inflammation. Studies have shown that individuals with chronic insomnia are at a significantly higher risk of hypertension, coronary artery disease, and heart failure. Behavioral interventions such as cognitive-behavioral therapy for insomnia (CBT-I) have proven effective in improving sleep quality and reducing cardiovascular risk markers, though their availability remains limited in many settings (16, 17).

Restless Leg Syndrome (RLS)

RLS is characterized by involuntary leg movements during periods of rest, often accompanied by significant sleep disruption. This condition has been linked to increased nocturnal blood pressure variability and impaired vascular regulation, contributing to higher rates of hypertension and ischemic heart disease (18). Although dopaminergic therapies are effective in managing RLS symptoms, their impact on long-term cardiovascular outcomes remains unclear (19).

Narcolepsy

Narcolepsy, a chronic neurological disorder affecting the brain's ability to regulate sleep-wake cycles, has also been linked to cardiovascular risk. Individuals with narcolepsy often experience excessive daytime sleepiness, cataplexy, and fragmented nighttime sleep, which contribute to systemic inflammation and metabolic dysregulation. These factors elevate the risk of developing hypertension and ischemic heart disease, highlighting the need for tailored cardiovascular risk management in patients with narcolepsy.

Circadian Rhythm Disturbances

Circadian misalignments, commonly seen in shift workers, disrupt hormonal regulation and glucose metabolism, significantly increasing the risk of myocardial infarction, diabetes, and metabolic syndrome (20). Emerging therapies targeting circadian alignment, such as timed light exposure and melatonin supplementation, show promise but require further clinical validation (21).

The relationship between sleep disorders and cardiovascular diseases (CVDs) is complex and multifaceted, with mounting evidence supporting the mechanistic pathways through which disrupted sleep contributes to adverse cardiovascular outcomes. Obstructive sleep apnea (OSA), for example, highlights the interplay between intermittent hypoxia, sympathetic nervous system activation, systemic inflammation, and oxidative stress. These processes exacerbate endothelial dysfunction, atherosclerosis, and hypertension, creating a vicious cycle that perpetuates cardiovascular risk. Insomnia, while less visibly connected to cardiovascular pathology, drives its risk through dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis. Elevated cortisol levels, increased sympathetic tone, and systemic inflammation form the foundation for metabolic syndrome, insulin resistance, and subsequent cardiovascular complications such as coronary artery disease and heart failure (15, 16). Restless leg syndrome (RLS) and circadian rhythm disturbances, though less studied compared to OSA and insomnia, similarly disrupt vascular regulation and hormonal balance, contributing to the development and progression of CVDs.

Despite these well-documented associations, significant gaps persist in translating this knowledge into effective prevention and treatment strategies. For instance, continuous positive airway pressure (CPAP) therapy for OSA has shown substantial benefits in reducing nocturnal blood pressure and improving cardiac function, yet patient adherence remains a major limitation, reducing its real-world impact. Similarly, while cognitive-behavioral therapy for insomnia (CBT-I) has demonstrated efficacy in improving sleep quality and reducing inflammatory markers, access to trained providers and patient awareness of these interventions are often insufficient. RLS therapies, such as dopaminergic agents, focus on symptom relief rather than addressing the cardiovascular consequences of the disorder, leaving room for further research into comprehensive management approaches. Circadian rhythm misalignments, particularly among shift workers, are another area requiring targeted interventions such as personalized light therapy or pharmacological modulation of the circadian clock to reduce cardiovascular risk.

Emerging technologies, including wearable devices and digital health platforms, offer promising solutions for improving the diagnosis, monitoring, and management of sleep disorders. These tools can facilitate early detection of sleep disturbances, track treatment adherence, and provide real-time data on sleep metrics, enabling more personalized and effective care. However, integrating these technologies into clinical practice will require overcoming barriers such as cost, patient engagement, and clinician training. Furthermore, population-level interventions, including public awareness campaigns and workplace policies that prioritize sleep health, are critical for addressing the broader societal factors contributing to sleep disorders (22).

Looking ahead, multidisciplinary collaboration between sleep specialists, cardiologists, psychologists, and public health professionals will be essential to advance the field. Research should focus on identifying biomarkers of sleep disorders that can predict cardiovascular risk, refining existing treatment protocols to enhance adherence, and developing novel therapies that address both sleep quality and cardiovascular outcomes. By integrating sleep health into cardiovascular care frameworks, clinicians can better address the interconnected nature of these conditions, ultimately reducing the global burden of CVDs and improving patient outcomes.

Sleep disorders are increasingly recognized as significant contributors to cardiovascular disease (CVD) risk, mediated through mechanisms such as systemic inflammation, oxidative stress, sympathetic overactivation, and metabolic dysregulation. Conditions like obstructive sleep apnea (OSA), insomnia, restless leg syndrome (RLS), and circadian rhythm disturbances not only exacerbate existing cardiovascular conditions but also act as independent risk factors for the development of hypertension, coronary artery disease, arrhythmias, and heart failure. Despite the growing body of evidence linking sleep disorders to cardiovascular outcomes, significant challenges remain in translating this knowledge into clinical practice.

Effective management of sleep disorders is crucial for mitigating cardiovascular risk, but adherence to existing treatments like continuous positive airway pressure (CPAP) for OSA and cognitive-behavioral therapy for insomnia (CBT-I) remains a significant barrier. Furthermore, the underdiagnosis of sleep disorders due to limited access to diagnostic tools and the underreporting of symptoms by patients highlights the need for standardized screening protocols and increased clinician awareness. Population-level strategies, such as promoting sleep education and addressing societal factors like shift work, are equally important in reducing the prevalence of sleep disorders and their cardiovascular consequences.

Future research should focus on developing innovative, accessible, and cost-effective solutions that integrate sleep health into cardiovascular care frameworks. This includes leveraging wearable technology, exploring pharmacological interventions targeting circadian alignment, and advancing precision medicine approaches to tailor treatments based on individual risk profiles. Multidisciplinary collaboration among healthcare providers, researchers, and policymakers will be essential to address the intertwined challenges of sleep disorders and cardiovascular risk comprehensively. By prioritizing sleep health in both clinical and public health domains, it is possible to reduce the burden of cardiovascular diseases significantly and enhance overall population health.

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