Arteriosclerosis (AS) represents an early manifestation of the aging process within the vascular system, characterized by a deterioration in the arterial ability to contract and relax. This condition diminishes the elasticity of the arteries and results in an increase in pulse pressure, which subsequently inflicts direct damage on the cardiovascular system. In the progression of arterial lesions, the deterioration of contraction and relaxation functions typically precedes the onset of structural abnormalities. This deterioration gradually escalates into a series of serious cardiovascular events, including ischemia, infarction, and the potential for arterial rupture. Pulse Wave Velocity (PWV) measurement technology is a straightforward and non-invasive approach for assessing the stiffness of arteries. This methodology effectively evaluates arterial rigidity, providing valuable insights into cardiovascular health. A study has found [24] that 30 children who snore but do not demonstrate apnea or hypoventilation on polysomnography are considered to have primary snoring diagnosed with PS demonstrated significantly elevated blood pressure readings across several parameters compared to the control group. Specifically, the systolic blood pressure was measured at 112 ± 10 mmHg in the PS group, in contrast to 105 ± 8 mmHg in the control group (P = 0.001). The diastolic blood pressure was recorded at 60 ± 7 mmHg for the PS group, compared to 53 ± 9 mmHg for the control group (P = 0.004). Furthermore, the mean blood pressure in the PS group was 81 ± 7 mmHg, while 71 ± 8 mmHg in the control group (P < 0.001). Additionally, the PWV was notably higher in the PS group, registering at 9.7 ± 1.6 m/s as opposed to 7.9 ± 2.0 m/s in the control group (P = 0.001). Children with PS show significant daytime systemic blood pressure elevation and reduced arterial compliance. After adjusting for multiple regression analysis, PS was independently confirmed as the only key factor affecting reduced arterial compliance unaffected by body weight. This indicates that PS impacts atherosclerosis in early life, and this impact is not influenced by body weight. However, whether it ultimately progresses to adult hypertension and leads to cardiovascular events remains challenging to assess.

A cross-sectional study conducted in Taiwan Region reveals that compared to children who are not obese and do not have PS, those who are both obese and suffer from moderate to severe OSA have a significantly increased risk of poor blood pressure conditions by three times [25] . This study enrolled 1689 children, which is a sufficiently large size. While PS may not directly elevate the risk of severe adverse blood pressure, the combination of obesity and more significant sleep-disordered breathing does heighten the likelihood of developing such issues. Furthermore, higher blood pressure can exacerbate sleep apnea problems in patients with PS. A retrospective study conducted in Sichuan revealed that higher baseline diastolic blood pressure independently influenced the development of an increased AHI during subsequent follow-ups with PS patients, regardless of the duration of sleep apnea [26] . In a study conducted in Australia utilizing home monitoring technology to assess snoring and sleep conditions, objective snoring time data were collected from 12,287 participants over several nights. The findings revealed that a higher proportion of snoring time (specifically, 12% at the 75th percentile versus 0.04% at the 5th percentile) was associated with approximately a 1.9-fold increase in the risk of uncontrolled hypertension (OR [95%CI]: 1.87 [1.63, 2.15]). Notably, this association was independent of sleep apnea [6] . Even when the effects of sleep apnea are excluded, frequent snoring still increases the risk of poor blood pressure control. This may be more closely related to the chronic obstruction of breathing itself rather than to the impacts of hypoxia or sleep disorders. However, participants were also predominantly male, which limits generalization and raises the need for caution when interpreting sex difference comparisons. Participants were also self-selected based on their decision to purchase and regularly use the under-the-mattress sleep sensor and blood pressure monitor devices from which these data were derived. Consumer choices could reflect concerns about sleep and blood pressure, potentially contributing to a bias toward overestimating snoring prevalence. Additionally, a clinical trial hypothesized that patients with normal blood pressure exhibit a reduced sensitivity to the baroreflex during wakefulness and non-rapid eye movement (NREM) sleep. In contrast, this decrease in sensitivity is deemed absent in other cases. The intervention utilized nasal continuous positive airway pressure (nCPAP). During the application of nCPAP, baroreflex sensitivity was assessed in both the experimental and control groups. Non-apneic snorers exhibited a reduction in baroreflex sensitivity during sleep, but nCPAP treatment effectively mitigated this decline, restoring sensitivity levels to near those observed during wakefulness. In contrast, the control group showed no significant change in baroreflex sensitivity while asleep, and nCPAP treatment did not have a meaningful impact on their measurements [27] . Although adherence to nCPAP was self-reported by the participants, the measurements observed between the groups during the trial were similar. This suggests that PS may change baroreflex sensitivity at night, potentially occurring before noticeable alterations in other cardiovascular variables. Slow-wave sleep (SWS) is a vital component of the sleep cycle, characterized by high-amplitude, low-frequency synchronized slow waves (δ waves). These waves are crucial in body growth, physical recovery, alleviating fatigue, and maintaining endocrine balance. Research indicates a significant interaction between moderate to severe OSA and the duration of SWS with hypertension (P = 0.002). A reduction in SWS is linked to a higher incidence of hypertension in OSA patients, a trend not observed in those with primary sleep disorder [28] . This may relate to OSA affecting hypoxia, activating the sympathetic nervous system, and reducing slow-wave sleep (SWS), all of which affect blood pressure regulation. Therefore, a thorough and individualized assessment of PSG is critical. An objective evaluation of the underlying causes is crucial for effective airway management during sleep. This study used a large sample, improving generalizability. Nonetheless, it is essential to consider that office BP may not be representative of the 24-hour BP profile, And the white-coat phenomenon. Participants underwent only a single nocturnal polysomnography, so nocturnal variability and first-night effects cannot be ruled out. Additionally, research on the relationship between PS and uncontrolled hypertension is limited. Given the unequal distribution of medical resources, this area warrants greater attention in future medical practice.

Snoring, which arises from oscillating pressure waves in the upper airway, can propagate through the surrounding tissues to the wall of the carotid artery. Considering the short distance between the carotid bifurcation and the lateral wall of the pharynx, it is likely that these vibrations influence the carotid artery. In a prospective paired cohort study with a median follow-up period of five years, the findings indicated that childhood primary snoring exposure was significantly correlated with adverse cardiovascular outcomes. Specifically, there was a noted deterioration in endothelial function, an increase in carotid intima-media thickness (IMT), and elevated 24-hour ambulatory blood pressure measurements at the five-year mark. regardless of obstructive sleep apnea severity [29] , similar results were found in adult PS [30] . PS presents a significant risk to cardiovascular health during the early stages of growth and development. Further, longitudinal studies must be conducted to investigate the long-term implications of PS. PS may expedite subclinical alterations in adjacent arterial structures, potentially mediated by mechanisms such as mechanical vibration of the mucosal surface or other pathophysiological processes [31] . The duration of PS significantly impacts vascular sclerosis. A generalized propensity score analysis was conducted to examine the carotid IMT among 180 participants who snored and a control group of non-snoring individuals following PSG. The findings revealed an independent association with subclinical alterations in IMT was present solely in female participants who snored for at least 25% of their sleep duration. Specifically, the average carotid IMT demonstrated a progressive increase correlated with snoring duration: non-snoring individuals exhibited an IMT of 0.707 mm, and mild snorers had an IMT of 0.718 mm. In comparison, moderate to severe snorers showed an IMT of 0.774 mm [32] . Morphological differences between men and women, such as fat distribution in neck and soft tissue volumes in the upper airway, could cause gender differences due to snoring. Although IMT itself is not a direct causal factor in the elevation of blood pressure, the progressive thickening of IMT can lead to a gradual narrowing of the carotid artery lumen. This narrowing results in increased resistance to blood flow. Consequently, the heart must augment its output to sustain adequate cerebral perfusion, contributing to increased blood pressure.

Hypertension can harm the vascular endothelium, encourage lipid deposition, and expedite the development of atherosclerosis. This condition, in turn, decreases vascular elasticity and subsequently raises blood pressure further. However, the influence of snoring on atherosclerosis can differ across various body regions. In a study involving 110 participants without obstructive sleep apnea, severe snoring was found to have a significant association with carotid atherosclerosis, demonstrating an (OR = 10.5; 95%CI: 2.1 - 51.8; P = 0.004). In contrast, this association was not found concerning femoral atherosclerosis. [33] . In addition, the study group consisted of patients with relatively mild degrees of nocturnal hypoxia. due to the bias towards the selection of snoring subjects over OSA patients. The study was not designed or powered to test for nocturnal hypoxia as a risk factor for atherosclerosis。Therefore, the lack of association should not be interpreted as excluding hypoxia as a risk factor for atherosclerosis in other study populations. The vibrations and mechanical stresses caused by snoring can be transmitted to the tissues and blood vessels in the neck, potentially resulting in endothelial dysfunction and worsening atherosclerosis, as well as increasing the risk of carotid plaque rupture. Furthermore, the vibrations associated with snoring may elevate local inflammatory responses in the upper airway tissues, further contributing to atherosclerosis in the neck’s blood vessels.

Metabolic Syndrome (MetS) is a complex pathological condition defined by the presence of abdominal obesity, dyslipidemia, hypertension, hyperglycemia, and insulin resistance, among other interrelated factors that interact synergistically. These elements are interrelated and function synergistically, notably increasing the risk of cardiovascular and cerebrovascular diseases, as well as diabetes. A cross-sectional study [34] conducted in China revealed that patients with obstructive sleep apnea exhibited more pronounced metabolic disorders and a higher prevalence of metabolic syndrome compared to individuals without snoring. PS was significantly associated with an increased risk of MetS in all participants (OR = 2.328, 95%CI: 1.340 - 4.045) and female participants (OR = 2.382, 95%CI: 1.136 - 4.994). About the components of MetS, PS was significantly associated with an increased likelihood of hypertension (OR = 1.730, 95%CI: 1.130 - 2.650); in terms of the Mets component, PS was significantly associated with an increased chance of hypertension (OR = 1.730, 95%CI: 1.130 - 2.650). Moreover, most cross-sectional studies have investigated the correlation between habitual snoring and MetS and its subclinical-related indicators, suggesting that snoring may precede the occurrence of MetS. It has been suggested that sleep-disordered breathing caused by snoring may affect the hyperactivity of the sympathetic nervous system [35] . Thus, by increasing glycogenolysis and gluconeogenesis, it damages glucose homeostasis and induces insulin resistance [36] . Moreover, hypoxia promotes the release of pro-inflammatory cytokines, including tumor necrosis factor-alpha and interleukin-6, leading to impaired glucose tolerance. However, the assessment of snoring in these studies was mainly based on self-reported snoring frequency, and patients with sleep apnea were not excluded. Large-scale prospective studies are still needed to determine the causal relationship between PS and metabolic abnormalities.

In the exploration of cardiovascular and cerebrovascular events, akin to investigations of metabolic syndrome, most association studies generally assess the link between snoring and cardiovascular or cerebrovascular diseases by considering factors such as the frequency and intensity of snoring, and the duration of snoring episodes. A significant number of these studies concentrate on middle-aged men, likely due to the higher incidence of both snoring and cardiovascular diseases within this demographic. Presently, there exists a limited number of studies that objectively assess the relationship between snoring and the prevalence of cardiovascular and cerebrovascular diseases. Notably, one community cohort study that quantitatively measured snoring indicated that both in an unadjusted Cox regression model and in a model that accounted for OSA and other confounding risk factors, snoring—whether considered as a categorical or continuous variable—did not demonstrate a statistically significant association with mortality, cardiovascular disease, or stroke [37] . Despite the potential implications of the findings, this cohort is characterized by a limited sample size, necessitating further investigation through a larger cohort study to achieve validation.