Sleep is an essential life process for organisms to survive, and the quality of sleep directly affects the physiological functions of the cardiovascular system, immune and endocrine systems, and is essential for the maintenance of internal environmental homeostasis. In recent years, with the accelerated pace of life and increased social pressure, the incidence of sleep disorders is increasing, and the number of physical diseases caused by sleep problems, especially cardiovascular diseases, is subsequently increasing, which seriously affects public health. Therefore, an in-depth understanding of the relationship between sleep and cardiovascular disease can help us to adopt intervention strategies to reduce the incidence of cardiovascular disease and optimize clinical treatment strategies. I. Epidemiological survey Insomnia disorder is the most prominent sleep problem today, and the prevalence of insomnia disorder in the population is estimated to be as high as 20%]. Many studies have shown the close relationship between insomnia and cardiovascular disease. The incidence of cardiovascular disease is significantly increased after chronic insomnia and most patients with cardiovascular disease have concomitant sleep problems. a 2014 meta-analysis that combined 17 cohort studies containing 310,000 subjects showed that insomnia increases the risk of cardiovascular disease and increases cardiovascular mortality, with a 1.5-3.9-fold increased risk of cardiovascular disease after insomnia, which is comparable to smoking, diabetes and obesity. The clinical manifestations of insomnia disorder are mainly difficulty in falling asleep, difficulty in maintaining sleep, early awakening and decreased sleep quality, etc. Studies suggest that the clinical manifestations of insomnia disorder are symptom-dependently associated with the occurrence of cardiovascular diseases such as acute myocardial infarction and heart failure, i.e., the more manifestations of insomnia symptoms, the greater the risk of cardiovascular diseases such as heart infarction and heart failure. In addition, insomnia patients have an increased susceptibility to cardiovascular disease risk factors such as hypertension, hyperlipidemia, and metabolic syndrome. Therefore, it has been suggested that insomnia can be seen as a manifestation of the prodromal phase of cardiovascular disease and that the development of cardiovascular disease should be alerted after the onset of insomnia symptoms. There is also a close association between objective sleep duration and the development of cardiovascular disease when not accompanied by subjective sleep problems. With social development, people’s habits have gradually changed, and the average sleep duration has shortened by 1.5-2 hours in the past 50 years, with about 30% of people sleeping less than 6 hours a day, and short sleep duration predicts an increased risk of cardiovascular diseases such as coronary heart disease and hypertension. In addition, studies also suggest that long sleep duration, daytime sleepiness and even naps longer than one hour are also risk factors that contribute to the development of cardiovascular disease or lead to adverse outcomes. However, it has also been suggested that insomnia or sleep duration by itself is not sufficient to cause cardiovascular disease, but only when insomnia is accompanied by shortened objective sleep duration, it promotes the occurrence of cardiovascular disease and death, and the presence of both alone does not increase the risk of cardiovascular disease. In summary, it is suggested that insomnia with shortened objective sleep duration is the most severe phenotype of insomnia disorder and has the greatest impact on the cardiovascular system. The biological mechanism of the interaction between sleep and cardiovascular disease is not fully understood, and the existing studies mainly explore the relationship between the two in terms of physiological hyperarousal, molecular genetics, epigenetics, and inflammatory immunity. The biological basis of physiological hyperarousal, such as increased activity of the sympathetic nervous system and increased secretion of stress-related hormones such as adrenocorticotropic hormone and cortisol, is also responsible for the pathogenesis of cardiovascular disease, and thus increases the risk of cardiovascular disease in patients with insomnia. A recent study comparing circadian heart rate variability in patients with chronic insomnia and normal controls found significant differences in heart rate variability between patients and normal controls during pre-sleep and stage 2 sleep, but not during slow-wave sleep, rapid eye movement sleep, or post-sleep wakefulness. Sleep, as a physiological process influenced by both genetic and environmental factors, may share a common genetic basis with cardiovascular disease. Genome-wide association analysis showed that the length of sleep latency was associated with polymorphic sites on the third intron of the CACNA1C gene, which mainly encodes the L-type calcium channel subunit, and the L-type calcium channel plays an important role in regulating the excitability of cardiomyocytes, while the copy number variation of the CACNA1C gene was significantly associated with the QT interval prolongation syndrome, suggesting that Rhythm genes such as CLOCK not only regulate the biological rhythm of the body, but also affect energy intake, and a healthy diet can help improve endothelial cell function, suppress inflammatory responses in the body, and reduce the incidence of cardiovascular disease. The study found that the polymorphic loci rs12649507 and rs6858749 of the CLOCK gene have a relationship between sleep duration and energy intake, and those carrying the rs12649507 allele G will consume more polyunsaturated fatty acids per hour of sleep, while the rs6858749 polymorphic locus regulates the relationship between sleep duration and protein intake, suggesting that This study suggests that genetic polymorphic loci associated with biological rhythms have a regulatory role in cardiovascular disease risk factors. In addition, epigenetic alterations also mediate the biological basis of the link between sleep and cardiovascular disease, as chronic sleep restriction can affect the transcription of genes related to sleep homeostasis (IL6, STAT3, KCNV2, CAMK2D), oxidative stress (PRDX2, PRDX5) and metabolism (SLC2A3, SLC2A5, GHRL, ABCA1), which in turn affect biological processes such as inflammation, immunity, stress and organismal metabolism, reflecting the pathological basis for the promotion of cardiovascular disease after short periods of sleep. The inflammatory response plays an important role in the development of cardiovascular diseases and is one of the current targets for the treatment of cardiovascular diseases. C-reactive protein is a biomarker of systemic inflammation, and studies by the National Health and Nutrition Examination Group (NHANES) have shown that C-reactive protein levels are significantly increased in those with non-restorative sleep, and in young women with poor sleep, and in people of different ethnic groups. A survey of different ethnic groups showed that long or short sleep also affected C-reactive protein levels, suggesting that sleep can affect the systemic inflammatory response in the body and lead to the development of cardiovascular disease. Nuclear factor κB (NF-Κb), a transcription factor that plays an important role in inflammatory signaling at the cellular level, significantly increases NF-Κb levels in peripheral blood mononuclear cells after a night of sleep restriction, suggesting that abnormal sleep may affect gene expression of leukocyte inflammatory factors and increase the risk of inflammation-related diseases. When healthy subjects underwent a 1-week sleep restriction, their endothelium-dependent vasodilatory function was abnormal, as evidenced by reduced vascular conductance maxima in vinblastine and heat-induced skin, and altered levels of pro-inflammatory cytokines such as monocyte chemotactic protein-1 (MCP-1) and tumor necrosis factor alpha (TNF-α), even after sleep compensation, the above changes These changes do not return to normal even after sleep compensation. Other pro-inflammatory cytokines such as interleukin-6 (IL-6) are also significantly elevated in patients with sleep disorders. The incidence of cardiovascular disease decreases with improved sleep. After 4 months of cognitive behavioral therapy or tai chi exercise, elderly patients with insomnia not only showed significant improvement in insomnia symptoms, but also significant reduction in biological indicators associated with cardiovascular disease, such as blood lipid levels and inflammatory factors, with effects maintained for up to 1 year. Both behavioral treatments work by inhibiting the expression of pro-inflammatory cytokines, with cognitive behavioral therapy mainly improving the systemic inflammatory response, as evidenced by a decrease in peripheral blood C-reactive protein levels; tai chi exercise reduces the cellular inflammatory response, as evidenced by a decrease in monocyte NF-Κb levels. Biofeedback is also a commonly used behavioral therapy to help patients regulate their physiology based on feedback system cues, which can effectively improve heart rate variability, reduce sympathetic nervous system activity and inhibit the inflammatory cascade response, playing a role in regulating sleep and improving cardiovascular disease. In addition, studies suggest that exercise may also improve cardiovascular and sleep problems in patients with cardiovascular disease. Melatonin is secreted by the pineal gland and has a role in regulating biological rhythms. Studies have shown that melatonin levels in the body predict the likelihood of developing heart failure in patients with hypertensive cardiomyopathy, and the lower the melatonin levels in the body, the greater the likelihood of developing heart failure in the future, suggesting the important role of rhythm regulation in the development of cardiovascular disease, and that exogenous melatonin supplementation may be an important means of slowing the progression of cardiovascular disease. beta-blockers are widely used in patients with cardiovascular disease, and it is estimated that Beta blockers are widely used in patients with cardiovascular disease, and it is estimated that at least 22 million people in the United States use them to treat cardiovascular disease while also suppressing endogenous melatonin production at night, which can cause sleep problems and diminish the therapeutic effect. Combined administration of beta-blockers and melatonin not only improves sleep problems, but also has cardioprotective effects. IV. Outlook In summary, it can be seen that sleep and cardiovascular disease are closely related, and studying the interaction between them and exploring the mechanism of insomnia disorder and high co-morbidity of cardiovascular disease has become a hot issue in current clinical research, and more evidence is urgently needed to support it. Although previous studies have provided some strong support, there are still some problems that limit the depth of research and the development of novel treatments. Firstly, most of the existing studies have not excluded the interference of depressive disorders and other factors in the relationship between sleep and cardiovascular disease; secondly, future studies should focus more on differentiating the differences between sleep problems as a factor of initiation and maintenance of cardiovascular disease, which will help to take more targeted preventive and therapeutic measures.