Friday, November 8, 2024

Sex Differences Self-Reporting of Snoring and Cardiovasc | NSS

Must read

Introduction

Cardiovascular disease (CVD) is the leading cause of death, accounting for one-third of all mortality causes.1 CVD remains the leading cause of death in the United States population, and over the past 18 years, CVD has claimed the lives of more than 10 million individuals.1 CVD pose a significant health burden globally, accounting for a substantial number of deaths and disabilities.2 Identifying and understanding the risk factors and management of these conditions.3 The relationship between sleep apnea and cardiovascular disease is well established.4 However, studies on the relationship between snoring and cardiovascular disease are relatively scarce. Among patients with sleep apnea, 94% experience snoring, while approximately 43% of snorers are at risk for sleep apnea.4–6 A substantial proportion of the general population (10% to 60%) are habitual snorers, but most do not have sleep apnea.7 Compared to sleep apnea, snoring is easier to diagnose and more readily accepted by the public.5 Therefore, exploring the relationship between snoring and cardiovascular disease may be more meaningful. Hence, our study is conducted among snorers. Previous studies have confirmed that snoring can increase the risk of endothelial dysfunction and diabetes, as well as elevate sympathetic nervous system excitability.8–10 This may be a significant reason why snoring raises the risk of cardiovascular diseases. Moreover, even among the existing studies that have examined the association between snoring and CVD risk, the findings are contradictory.11,12 Therefore, it is essential to explore the relationship between snoring and CVD.

Disparities between men and women persist in the diagnosis, treatment, and prognosis of CVD.13 The in-hospital mortality rate for female patients with acute coronary syndrome is significantly higher than that of male patients.14 Research has indicated that women are more likely to experience complications, including bleeding, associated with coronary revascularization procedures.15 During midlife, around the time of peri- and post-menopause, sleep quality deteriorates, while CVD risk significantly increases in women compared to earlier decades.16 One of the most notable biological differences is the influence of sex hormones. Estrogen, which is more prevalent in premenopausal women, has been shown to have protective effects against CVD.17 It helps to maintain healthy lipid profiles, reduces inflammation, and improves endothelial function.17 Males tend to accumulate visceral fat, which is associated with a higher risk of metabolic syndrome and cardiovascular complications.18 The findings of these studies underscore the significant role of sex in CVD. Moreover, socioeconomic status and lifestyle have an impact on cardiovascular disease.19 Lower socioeconomic status is associated with higher rates of smoking, obesity, and limited access to healthcare services, all of which contribute to increased CVD risk.19 Men are more likely to engage in behaviors that increase CVD risk, such as heavy drinking and unhealthy eating patterns.20 Therefore, exploring gender differences in the association between snoring and cardiovascular disease risk can inform the development of health policies and guidelines, thereby improving overall cardiovascular disease outcomes.21 However, there is a lack of research examining sex differences in the connection between snoring and CVD risk. Therefore, it is particularly important to investigate these sex differences.

The present study aimed to investigate the sex differences in the association between snoring and CVD risk using data from the National Health and Nutrition Examination Survey (NHANES), a nationally representative sample in the United States.

Method

Study Population

The NHANES is an ongoing research program that provides population estimates related to the nutrition and health of adults and children in the United States. The survey utilizes a stratified, multistage probability design to recruit a representative sample of the U.S population. Data for the survey are obtained through personal structured interviews conducted at participants’ homes, health examinations conducted at a mobile examination center, and laboratory analysis of specimens.22 All data can be found on the NHANES website (http://www.cdc.gov/nchs/nhanes.htm). The study protocols were approved by the Institutional Review Board (IRB) of the National Center for Health Statistics, and written informed consent was obtained from each participant. Due to the combination of data from 2017–2018 with that of 2019–2020, the 2017–2018 data has been excluded. Our study included all participants in the NHANES from 2015 through 2020 who were 18 years of age or older and had available sleep data that included information on snoring. We were excluded participants under the age of 18 and those with incomplete key data.

Grouping Methods

In this study, we employed two grouping methods. The first method involved dividing participants into two groups based on the presence or absence of snoring. The second method involved classifying participants into five groups based on the severity of snoring: non-snoring group, mild snoring group, moderate snoring group, severe snoring group, and unclear snoring group. Within the population of individuals who reported snoring, we divided them into two groups based on their gender: male snorers and female snorers.

Medication Usage and Disease Definition

Participants were queried about their recent use of prescription medications within a 30-day period. Respondents who acknowledged taking such medications were asked to furnish the interviewers with the respective containers. If the containers were not accessible, participants were requested to disclose the names of the medications to the researchers. In this study, the presence of atrial fibrillation was determined if the investigator reported taking atrial fibrillation medication and provided evidence. For diabetes, the diagnosis was based on medication usage, blood glucose and HbA1c values, and past medical history. Hypertension was considered present if the blood pressure was consistently equal to or greater than 140/90 mmHg on three times or if the patient was currently taking hypertension medication or had a documented history of hypertension.

Sociodemographic Characteristics and Snore Status

The study collected data on various sociodemographic characteristics and weight status of the participants. These included:1.Age: Participants reported their age. 2. Sex: Participants identified themselves as male or female. 3. Race and Ethnic Group: Participants identified their racial and ethnic background, including options such as Mexican American, Other Hispanic, non-Hispanic White, non-Hispanic Black, Non-Hispanic Asian, or other.4. Education: Participants reported their educational attainment, categorized as less than 11th grade, high school, some college, college graduate, or other.5. Family Income: Participants provided information about their family income, categorized as less than 1.3 of the federal poverty level, 1.3 to 3.49 of the federal poverty level, or equal to or greater than 3.5 of the federal poverty level.6.Drinking Status: Participants reported their smoking status as nondrinker, low-to-moderate drinker (2 drinks/day in men and >1 drinks/day in women).7.Smoking Status: Participants reported their smoking status as current smoker, former smoker, or never smoked. Individuals who reported smoking more than 100 cigarettes in their lifetime were classified as current smokers, while those who reported smoking more than 100 cigarettes but had quit smoking were classified as former smokers. 8. Snore Status: Participants were queried about the frequency of their snoring over the past 12 months during sleep. In cases where participants were unable to provide an answer, inquiries were made to other household members, including bed partners, regarding the snoring behavior. Participants reported their snore status as never, rarely snore, occasionally snore, frequently snore, or do not know snore. Individuals who reported snoring 1–2 nights a week were classified as rarely snore, while those who reported snoring 3–4 nights a week were classified as occasionally snore. Those who reported snoring 5 or more nights a week were classified as frequently snore, and those who reported not knowing whether they snore were classified as do not know snore. In addition to sociodemographic characteristics, weight status was assessed using body mass index (BMI), calculated as the weight in kilograms divided by the square of the height in meters. Participants were then classified into three weight-status groups: normal weight (BMI

Outcome Events

This study defined CVD events as including coronary heart disease, angina, atrial fibrillation, heart failure, stroke, heart attack, and hypertension.

Statistical Analysis

Percentages, means, and 95% confidence interval of key variables were calculated to describe the sample at each level of snoring. Logistic regression model was employed to examine the association between snoring and the outcome variables, while accounting for potential confounding variables. This logistic regression aimed to address any imbalances in potential confounding variables between the groups, thereby reducing their influence on the outcome measures.

The data analysis was conducted using V.15.1 (Stata Corp LP), incorporating survey analysis procedures to account for the complex sampling design. The survey examination weights were applied as appropriate to ensure the obtained estimates were nationally representative. In instances where data was absent for the primary variable, snoring, cases were excluded. For missing data pertaining to covariates, categorical variables with missing data were consolidated into a single category, while multiple imputation was employed for continuous variables. The utilization of multiple imputation was intended to enhance the comprehensiveness and precision of the analysis, while mitigating potential biases stemming from missing data. All statistical tests conducted were two-sided, and a significance level of P

Results

Study Population

Out of the 12,681 participants, a total of 3113 individuals who reported no snoring were included in the study based on the questionnaire survey regarding the presence of snoring in Table 1. Among the participants, there were 3009 individuals categorized as mild snorers, 2245 individuals categorized as moderate snorers, 3404 individuals categorized as severe snorers, and 910 individuals categorized as unclear snorers. The baseline data divided into two groups based on the presence or absence of snoring is presented in Table S1. A total of 4023 individuals were classified as the non-snoring group, while 8658 individuals were classified as the snoring group. In the snoring group, individuals were further categorized by gender: 4527 males and 4131 females (Table S2).

Table 1 Baseline Characteristics of Study Participants in NHANES 2015–2020 Grouped According to Snoring Severity

Relationship of Snoring to Cardiovascular Risks

In the unadjusted logistic regression model1, the odds ratios (OR) for moderate snoring (OR 1.569, 95% CI 1.335 to 1.843, P Table 2. In the adjusted logistic regression Model 2, which controlled for variables such as sex, race, age, education, and marital status, the odds ratios (OR) for mild snoring, moderate snoring, and severe snoring were 1.096 (95% CI 0.934 to 1.286, P = 0.262), 1.382 (95% CI 1.161 to 1.644, P Table 2 – Model 2). In the multivariable logistic regression Model 3, adjusted for variables including sex, race, age, education, marital status, creatinine (Cr), triglyceride (TG), uric acid (UA), total cholesterol (TC), high-density lipoprotein cholesterol (HDL), and low-density lipoprotein cholesterol (LDL), individuals in the moderate snoring group had an odds ratio (OR) of 1.418 (95% CI: 1.083 to 1.857, p = 0.011) compared to the non-snoring group. Similarly, individuals in the severe snoring group had an odds ratio (OR) of 1.882 (95% CI: 1.468 to 2.409, p Table 2-Model 3). Individuals who snored had a higher odds ratio compared to non-snorers (Table S3).

Table 2 Snoring and Indicators of Cardiovascular Disease Risk Grouped According to the Severity of Snoring

Gender Differences in the Association Between Snoring and Cardiovascular Risk

Males with snoring demonstrated a higher incidence rate of CVD (OR 1.414, 95% CI 1.099–1.819, p=0.007) in comparison to females (Table 3). The odds ratios (OR) for male patients with snoring were higher than those for females in various CVDs, including atrial fibrillation (OR 3.441, 95% CI 1.513 to 7.827, p = 0.003), coronary heart disease (OR 2.019, 95% CI 1.409 to 2.892, p Figure 1). However, for stroke patients, the odds ratio (OR) for males was lower than that for females (OR 0.850, 95% CI 0.609 to 1.186, p = 0.339) (Figure 1).

Table 3 Logistic Regression Analysis of the Association Between Snoring and Various Cardiovascular Diseases Stratified by Sex

Figure 1 Unadjusted Logistic Regression Analysis of the Association Between Snoring and Various Cardiovascular Diseases Stratified by Sex.

After adjusting for variables such as race, age, education, and marital status, male patients exhibited a higher odds ratio (OR 1.444, 95% CI 1.260 to 1.654, p Table 3). The odds ratios (OR) for male patients with snoring were higher than those for females in various CVD, including atrial fibrillation (OR 3.213, 95% CI 1.474 to 7.006, p = 0.003), coronary heart disease (OR 2.639, 95% CI 1.759 to 3.957, p Figure 2). However, for stroke patients, the odds ratio (OR) for males was lower than that for females (OR 0.987, 95% CI 0.689 to 1.415, p = 0.945) (Figure 2).

Figure 2 Adjusting for Race, Age, Education, and Marital Status: Association Between Snoring and Various Cardiovascular Diseases Stratified by Sex.

After adjusting for race, age, education, marital status, Cr, TG, UA, TC, HDL, and LDL, male patients exhibited a higher odds ratio (OR 1.414, 95% CI 1.099–1.819, p = 0.007) for CVD compared to females (Table 3). After adjusting for race, age, education, marital status, Cr, TG, UA, TC, HDL, and LDL, male patients showed a higher odds ratio for hypertension (HTN) (1.358, 95% CI 1.051 to 1.755, p = 0.021) compared to females (Figure 3). After adjusting for race, age, income, marital status, diabetes, education, heart failure (HF), angina, BMI, coronary heart disease (CHD), heart attack (HA), HTN, Cr, TG, UA, TC, HDL, and LDL, male patients exhibited a higher odds ratio for atrial fibrillation (4.945, 95% CI 1.187 to 20.598, p = 0.028) compared to females (Figure 3). After adjusting for race, age, income, marital, diabetes, education, angina, marital, HTN, BMI, HA, Cr, TG, UA, TC, HDL, and LDL, Male patients exhibited a lower odds ratio for heart failure (0.812, 95% CI 0.399 to 1.651, p = 0.566) compared to females (Figure 3). Adjusted for race, age, income, marital status, diabetes, education, angina, BMI, heart attack, Cr, TG, UA, TC, HDL, and LDL, male patients exhibited a higher odds ratio for coronary heart disease (2.002, 95% CI 1.152 to 3.479, p = 0.014) compared to females (Figure 3).After adjusting for variables including race, age, income, marital, education, diabetes, HTN, BMI, Cr, TG, UA, TC, HDL, and LDL, male patients showed a decreased odds ratio for stroke (0.866, 95% CI 0.504 to 1.487, p = 0.601) in comparison to females (Figure 3). Adjusted for race, age, income, marital, education, diabetes, HTN, BMI, TG, UA, TC, HDL, and LDL, male patients exhibited a lower odds ratio for angina (1.625, 95% CI 0.697 to 3.779, p = 0.261) compared to females (Figure 3). Adjusted for race, age, income, marital, diabetes, education, angina, HTN, HF, BMI, CHD, Cr, TG, UA, TC, HDL, and LDL, male patients exhibited a lower odds ratio for heart attack (1.723, 95% CI 1.054 to 2.817, p = 0.261) compared to females (Figure 3).

Figure 3 Adjusting for Potentially Relevant Variables: Association Between Snoring and Various Cardiovascular Diseases Stratified by Sex.

Notes: a: cardiovascular diseases model 3 adjusted for sex, race, age, education, marital, body mass index (BMI), creatinine (Cr), triglyceride (TG), uric acid (UA), total cholesterol (TC), high-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL). b: hypertension adjusted for race, age, education, marital, BMI, Cr, TG, UA, TC, LDL, LDL. c: atrial fibrillation model 3 adjusted for race, age, income, marital, diabetes, education, hypertension (HTN), heart failure (HF), angina, marital, BMI, coronary heart disease (CHD), heart attack (HA), Cr, TG, UA, TC, HDL, LDL. d: heart failure model 3 adjusted for race, age, income, marital, diabetes, education, angina, marital, HTN, BMI, HA, Cr, TG, UA, TC, HDL, LDL. e: coronary heart disease model 3 adjusted for race, age, income, marital, diabetes, education, angina, marital, HF, BMI, HA, Cr, TG, UA, TC, HDL, LDL. f: stork model 3 adjusted for race, age, income, marital, education, diabetes, HTN, BMI, Cr, TG, UA, TC, HDL, LDL. g: angina model 3 adjusted for race, age, income, marital, education, diabetes, HTN, BMI, TG, UA, TC, HDL, LDL. h: heart attack model 3 adjusted for race, age, income, marital, diabetes, education, angina, marital, HTN, HF, BMI, CHD, Cr, TG, UA, TC, HDL, LDL.

Discussion

Notably, our study revealed that male patients who snore have a notably higher prevalence of CVD, including hypertension, atrial fibrillation, coronary heart disease, and heart disease, in comparison to their female counterparts. Specifically, the risk of atrial fibrillation in male snorers is almost five times greater than in female snorers. The risk of coronary heart disease is twice as high in male snorers compared to females. Additionally, male snorers have a higher risk of developing hypertension and heart disease compared to their female counterparts. These findings emphasize the importance of considering sex-specific factors in assessing CVD risk associated with snoring. This novel contribution expands our understanding of the complex relationship between snoring and CVD risk and highlights the need for further research to explore the underlying mechanisms driving these gender-specific differences.

Our study’s findings are consistent with previous research, which underscores the potential role of snoring as a risk factor for CVD events.23–25 Snoring, a common sleep disorder, is characterized by loud and intermittent sounds produced during sleep.26 It has been linked to various health implications, including CVD such as HTN, CHD, and stroke.27,28 Our study contributes to the existing literature by providing further evidence of the association between snoring and CVD risk. Snoring may predispose individuals to AF, which is the most common cardiac arrhythmia.29,30 This can occur through various mechanisms, such as hypoxemia, hypercapnia, and subsequent increases in blood pressure and heart rate.29,30 Snoring can lead to intermittent hypoxia, resulting in oxidative stress and inflammatory responses in the body.31 Snoring may consequently result in endothelial dysfunction and organ dysfunction.32 Snoring can impact lipid and protein metabolism at the genetic level, potentially leading to an elevated CVD risk.33 However, these results have paid little attention to the difference sex.

Sex differences in the association between snoring and CVD risk were also evident in our study. Male participants demonstrated a higher risk of CVD events compared to females. This finding highlights the importance of considering gender-specific factors when assessing the relationship between snoring and CVD health. The overactivation of the sympathetic nervous system is not only crucial in the early stages of hypertension development, but is also associated with several comorbidities commonly linked to hypertension.34 Males have higher sympathetic nervous system activity than females, which may explain the higher risk of hypertension in male patients with similar snoring conditions.35 This is consistent with our research findings. Hormonal differences, anatomical variations, and sleep patterns may contribute to the observed gender disparities.36 Indeed, estrogen has been found to have the ability to modulate the excitability of the sympathetic nervous system and regulate endothelial function.37,38 Sex hormones have been suggested to influence the reabsorption of renal sodium and vascular resistance, which could potentially explain the differences in hypertension observed between men and women.39 This might partially explain the gender difference in hypertension among patients with snoring.

Our study has identified a correlation between snoring and an elevated risk of atrial fibrillation (AF). Previous studies have also established a link between sleep apnea and an increased risk of AF.40 The co-occurrence of snoring and sleep apnea in some of our patients suggests a potential explanation for the heightened risk observed in our study. We found that the risk of AF in male snoring patients is nearly five times that of females. Although previous studies have confirmed the association between snoring and AF,41 there have been no studies that have examined whether this association differs by sex. Differences in atrial anatomy or tissue fibrosis may be involved in sex-specific responses to snoring in the development of AF.42,43 Females exhibit a greater anti-inflammatory profile as a compensatory mechanism, mediated by the angiotensin type 2 receptor.44 Postmenopausal women face an elevated risk of AF.45 Cardiac fibrosis is crucial for the development of AF.46 The more pronounced fibrosis in women may be associated with the upregulation of the TGFβ/Smad3 pathway and older age.46 In our study, female patients had an average age of approximately 47 years, which may, in part, account for the gender disparities in the link between snoring and AF. Male cardiomyocytes exhibited greater late sodium current, calcium transients, and sarcoplasmic reticulum calcium content in the left atrial posterior wall than female cardiomyocytes, potentially contributing to increased ectopic activity.47 Male mice had faster spontaneous beating rates in the pulmonary veins, greater burst firing, and longer periods of delayed afterdepolarizations compared to female mice.48 Sympathetic stimulation can also contribute to the promotion of AF through various mechanisms.49 This includes increasing the release of calcium ions (Ca2+), which can influence the conduction properties and refractoriness of cardiac tissue.49 Additionally, sympathetic stimulation can lead to the formation of afterdepolarizations, which are abnormal electrical events in cardiac cells, and these afterdepolarizations can trigger or sustain AF.49 Males have higher sympathetic nervous system activity than females.35 This may potentially explain the elevated risk of AF in male patients with snoring. It has been confirmed that female snoring patients have a higher risk of CVDs compared to males in this study. Currently, there appears to be a tendency to focus more on the CVD health of male snoring patients, which includes healthcare professionals, while potentially overlooking the significance of snoring in female patients.50 Similarly, male snoring patients have a significantly higher rate of referrals to higher-level hospitals compared to female snoring patients, enabling them to receive better treatment.51 However, women with AF were more frequently symptomatic than men, and they experienced more severe symptoms.52 In previous studies, women with AF exhibited notably higher rates of life-threatening adverse events, such as the development of acquired long QT syndrome when treated with class Ia or III antiarrhythmic drugs.53,54 Compared to male patients, female atrial fibrillation patients have a higher rate of surgical complications, and the surgical outcomes are also less favorable.55,56 Therefore, it’s crucial to also pay attention to female snorers.

Our study underscores the distinct gender disparities in the connection between snoring and CVDs, notably atrial fibrillation. Nonetheless, the underlying mechanisms and clinical characteristics are intricate. Further research into gender variations in the correlation between snoring and CVDs is imperative. Additional cohort studies or interventional studies are required to investigate the potential causal association between snoring and CVDs. Nevertheless, these discoveries carry substantial implications for the implementation of clinical practices for preventing CVDs. There is a need for increased clinical awareness and focused screening for snoring and cardiovascular risk factors in male. Moreover, it is imperative to advocate for the implementation of routine screening for snoring in primary care settings, with a particular focus on male individuals who snore. Simultaneously, public health initiatives should focus on increasing awareness and providing community-based screening programs to facilitate early detection and management of CVDs in this male. Developing targeted clinical guidelines and health policies specifically for men may be more effective in reducing the cardiovascular disease risks associated with snoring.

Limitations

Limitations to the present study deserve attention. Firstly, despite adjusting for numerous potential confounders in the statistical models, the outcomes of the current study, being observational in nature, may have been influenced by unaccounted-for cardiovascular disease and snoring risk factors. Secondly, the reliance on self-reported data, particularly regarding snoring frequency and CVD risk factors, may introduce recall bias and misclassification. Finally, our findings can only demonstrate the existence of an association between snoring and CVD, rather than a causal relationship between the two. Further longitudinal studies are needed to investigate whether duration of increased snoring has cumulative effects on CVD.

Conclusion

Our study has revealed a significant correlation between snoring and CVD, with notable differences observed between sexes. Among snoring patients, males demonstrated a higher CVD risk compared to females. Male snorers have approximately five times the risk of developing AF and roughly double the risk of CAD compared to female patients. Increased clinical awareness and targeted screening for snoring in men can help reduce cardiovascular disease risks. Developing specific guidelines and policies for men may be more effective in addressing this issue.

Ethics Approval

The NHANES study received approval from the Institutional Review Board of the National Center for Health Statistics (No. Continuation of Protocol #2011-17 and Protocol #2018-01). More information can be found at https://www.cdc.gov/nchs/nhanes/irba98.htm. Due to the NHANES data being publicly available, this study is exempted by our institutional ethics committee.

Consent to Participate

All participants provided written informed consent.

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Funding

This study was supported by Sichuan Provincial Cadre Health Research Project, China (Sichuan Ganyan ZH2024-101) and by 135 project for disciplines of excellence–Clinical Research Incubation Project, West China Hospital, Sichuan University (Grant number: 2021HXFH061, Sichuan, China).

Disclosure

The authors report no conflicts of interest in this work.

References

1. Benjamin EJ, Muntner P, Alonso A, et al. Heart disease and stroke statistics-2019 update: a report from the American heart association. Circulation. 2019;139(10):e56–e528. doi:10.1161/CIR.0000000000000659

2. Roth GA, Mensah GA, Johnson CO, et al. Global burden of cardiovascular diseases and risk factors, 1990-2019: update from the gbd 2019 study. J Am Coll Cardiol. 2020;76(25):2982–3021. doi:10.1016/j.jacc.2020.11.010

3. Lloyd-Jones DM, Huffman MD, Karmali KN, et al. Estimating longitudinal risks and benefits from cardiovascular preventive therapies among medicare patients: the million hearts longitudinal ASCVD risk assessment tool: a special report from the American heart association and American college of cardiology. Circulation. 2017;135(13):e793–e813. doi:10.1161/CIR.0000000000000467

4. Mokhlesi B, Varga AW. Obstructive sleep apnea and cardiovascular disease. rem sleep matters! Am J Respir Crit Care Med. 2018;197(5):554–556. doi:10.1164/rccm.201710-2147ED

5. Alshaer H, Hummel R, Mendelson M, Marshal T, Bradley TD. Objective relationship between sleep apnea and frequency of snoring assessed by machine learning. J Clin Sleep Med. 2019;15(3):463–470. doi:10.5664/jcsm.7676

6. Al Shaikh YG, Haytham Shieb MM, Koruturk S, Alghefari A, Hassan Z, Mussa BM. The symptoms and risk of sleep apnea among adults in the United Arab Emirates. Ann Thorac Med. 2018;13(3):168–174. doi:10.4103/atm.ATM_245_17

7. Teculescu D, Hannhart B, Cornette A, Montaut-Verient B, Virion JM, Michaely JP. Prevalence of habitual snoring in a sample of French males. role of ”minor” nose-throat abnormalities. Respiration; Intl Rev Thorac Dis. 2001;68(4):365–370. doi:10.1159/000050528

8. Michalek-Zrabkowska M, Martynowicz H, Wieckiewicz M, Smardz J, Poreba R, Mazur G. Cardiovascular implications of sleep bruxism-a systematic review with narrative summary and future perspectives. J Clin Med. 2021;10(11):2245. doi:10.3390/jcm10112245

9. Baguet JP, Courand PY, Lequeux B, et al. Snoring but not sleepiness is associated with increased aortic root diameter in hypertensive patients. The SLEEPART study. Int J Cardiol. 2016;202:131–132. doi:10.1016/j.ijcard.2015.03.319

10. Xiong X, Zhong A, Xu H, Wang C. Association between self-reported habitual snoring and diabetes mellitus: a systemic review and meta-analysis. J Diabetes Res. 2016;2016:1958981. doi:10.1155/2016/1958981

11. Ikehara S, Iso H, Date C, et al. JS: association of sleep duration with mortality from cardiovascular disease and other causes for Japanese men and women: the JACC study. Sleep. 2009;32(3):295–301. doi:10.1093/sleep/32.3.295

12. Marshall N, Wong K, Liu P, Cullen S, Knuiman M, Grunstein RJS. Sleep apnea as an independent risk factor for all-cause mortality: the Busselton health study. Sleep. 2008;31(8):1079–1085.

13. Holtzman JN, Kaur G, Hansen B, Bushana N, Gulati M. Sex differences in the management of atherosclerotic cardiovascular disease. Atherosclerosis. 2023;384:117268. doi:10.1016/j.atherosclerosis.2023.117268

14. Champney KP, Frederick PD, Bueno H, et al. The joint contribution of sex, age and type of myocardial infarction on hospital mortality following acute myocardial infarction. Heart. 2009;95(11):895–899. doi:10.1136/hrt.2008.155804

15. Ahmed B, Dauerman HL. Women, bleeding, and coronary intervention. Circulation. 2013;127(5):641–649. doi:10.1161/CIRCULATIONAHA.112.108290

16. Mong JA, Cusmano DM. Sex differences in sleep: impact of biological sex and sex steroids. Philos Trans R Soc London, Ser B. 2016;371(1688):20150110. doi:10.1098/rstb.2015.0110

17. Garcia M, Mulvagh SL, Merz CN, Buring JE, Manson JE. Cardiovascular disease in women: clinical perspectives. Circ Res. 2016;118(8):1273–1293. doi:10.1161/CIRCRESAHA.116.307547

18. Karastergiou K, Smith SR, Greenberg AS, Fried SK. Sex differences in human adipose tissues – the biology of pear shape. Biol Sex Differ. 2012;3(1):13. doi:10.1186/2042-6410-3-13

19. Kaplan GA, Keil JE. Socioeconomic factors and cardiovascular disease: a review of the literature. Circulation. 1993;88(4 Pt 1):1973–1998. doi:10.1161/01.CIR.88.4.1973

20. Emslie C, Hunt K, Macintyre S. How similar are the smoking and drinking habits of men and women in non-manual jobs? Eur J Public Health. 2002;12(1):22–28. doi:10.1093/eurpub/12.1.22

21. Everett BM, Brooks MM, Vlachos HEA, Chaitman BR, Frye RL, Bhatt DL. Sex differences in cardiac troponin and the risk of death or major cardiovascular events. J Am Coll Cardiol. 2016;68(9):978–980. doi:10.1016/j.jacc.2016.06.013

22. Akinbami L, Chen T, Davy O, et al. National Health and Nutrition Examination Survey, 2017-March 2020 Prepandemic File: Sample Design, Estimation, and Analytic Guidelines. Vital Health Stat. 2022(190):1–36.

23. Aljawadi MH, Khoja AT, BaHammam AS, Alyahya NM, Alkhalifah MK, AlGhmadi OK. Determining the prevalence of symptoms and risk of obstructive sleep apnoea among old Saudis. J Taibah Univ Sci. 2021;16(3):402–412. doi:10.1016/j.jtumed.2020.10.024

24. Xie D, Li W, Wang Y, et al. Sleep duration, snoring habits and risk of acute myocardial infarction in China population: results of the INTERHEART study. BMC Public Health. 2014;14(1):531. doi:10.1186/1471-2458-14-531

25. Nagayoshi M, Tanigawa T, Yamagishi K, et al. Self-reported snoring frequency and incidence of cardiovascular disease: the circulatory risk in communities study (CIRCS). J Epidemiol. 2012;22(4):295–301. doi:10.2188/jea.JE20110109

26. Palinkas M, Marrara J, Bataglion C, et al. Analysis of the sleep period and the amount of habitual snoring in individuals with sleep bruxism. Med Oral Patologia Oral y Cirugia Bucal. 2019;24(6):e782–e786. doi:10.4317/medoral.23136

27. Endeshaw Y, Rice TB, Schwartz AV, et al. Snoring, daytime sleepiness, and incident cardiovascular disease in the health, aging, and body composition study. Sleep. 2013;36(11):1737–1745. doi:10.5665/sleep.3140

28. Shivalkar B, Van de Heyning C, Kerremans M, et al. Obstructive sleep apnea syndrome: more insights on structural and functional cardiac alterations, and the effects of treatment with continuous positive airway pressure. J Am Coll Cardiol. 2006;47(7):1433–1439. doi:10.1016/j.jacc.2005.11.054

29. Titova O, Yuan S, Baron J, Lindberg E, Michaëlsson K, Larsson S. Self-reported symptoms of sleep-disordered breathing and risk of cardiovascular diseases: observational and Mendelian randomization findings. J Sleep Res. 2022;31(6):e13681. doi:10.1111/jsr.13681

30. Marulanda-Londoño E, Chaturvedi S. The interplay between obstructive sleep apnea and atrial fibrillation. Front Neurol. 2017;8:668. doi:10.3389/fneur.2017.00668

31. Lavie L. Intermittent hypoxia: the culprit of oxidative stress, vascular inflammation and dyslipidemia in obstructive sleep apnea. Expert Rev Respir Med. 2008;2(1):75–84. doi:10.1586/17476348.2.1.75

32. Loke YK, Brown JW, Kwok CS, Niruban A, Myint PK. Association of obstructive sleep apnea with risk of serious cardiovascular events: a systematic review and meta-analysis. Circ Cardiovasc Qual Outcomes. 2012;5(5):720–728. doi:10.1161/CIRCOUTCOMES.111.964783

33. Wain LV, Shrine N, Artigas MS, et al. Genome-wide association analyses for lung function and chronic obstructive pulmonary disease identify new loci and potential druggable targets. Nature Genet. 2017;49(3):416–425. doi:10.1038/ng.3787

34. DeLalio LJ, Sved AF, Stocker SD. Sympathetic nervous system contributions to hypertension: updates and therapeutic relevance. Can J Cardiol. 2020;36(5):712–720. doi:10.1016/j.cjca.2020.03.003

35. Du XJ, Dart AM, Riemersma RA. Sex differences in the parasympathetic nerve control of rat heart. Clin Exp Pharmacol Physiol. 1994;21(6):485–493. doi:10.1111/j.1440-1681.1994.tb02545.x

36. Raymond AR, Norton GR, Woodiwiss AJ, Brooksbank RL. Impact of gender and menopausal status on relationships between biological aging, as indexed by telomere length, and aortic stiffness. Am J Hypertens. 2015;28(5):623–630. doi:10.1093/ajh/hpu212

37. Mercuro G, Podda A, Pitzalis L, et al. Evidence of a role of endogenous estrogen in the modulation of autonomic nervous system. Am j Cardiol. 2000;85(6):787–789. doi:10.1016/S0002-9149(99)00865-6

38. Schulman IH, Aranda P, Raij L, Veronesi M, Aranda FJ, Martin R. Surgical menopause increases salt sensitivity of blood pressure. Hypertension. 2006;47(6):1168–1174. doi:10.1161/01.HYP.0000218857.67880.75

39. Ashraf MS, Vongpatanasin W. Estrogen and hypertension. Curr Hypertens Rep. 2006;8(5):368–376. doi:10.1007/s11906-006-0080-1

40. Mehra R, Benjamin EJ, Shahar E, et al. Association of nocturnal arrhythmias with sleep-disordered breathing: the sleep heart health study. Am J Respir Crit Care Med. 2006;173(8):910–916. doi:10.1164/rccm.200509-1442OC

41. Lin GM, Colangelo LA, Lloyd-Jones DM, et al. Association of sleep apnea and snoring with incident atrial fibrillation in the multi-ethnic study of atherosclerosis. J Am Coll Cardiol. 2015;182(1):49–57. doi:10.1093/aje/kwv004

42. Forleo GB, Tondo C, De Luca L, et al. Gender-related differences in catheter ablation of atrial fibrillation. EP Europace. 2007;9(8):613–620. doi:10.1093/europace/eum144

43. Cochet H, Mouries A, Nivet H, et al. Age, atrial fibrillation, and structural heart disease are the main determinants of left atrial fibrosis detected by delayed-enhanced magnetic resonance imaging in a general cardiology population. J Cardiovasc Electrophysiol. 2015;26(5):484–492. doi:10.1111/jce.12651

44. Gillis EE, Sullivan JC. Sex differences in hypertension: recent advances. Hypertension. 2016;68(6):1322–1327. doi:10.1161/HYPERTENSIONAHA.116.06602

45. Ko D, Rahman F, Martins MA, et al. Atrial fibrillation in women: treatment. Nat Rev Cardiol. 2017;14(2):113–124. doi:10.1038/nrcardio.2016.171

46. Pfannmüller B, Boldt A, Reutemann A, et al. Gender-specific remodeling in atrial fibrillation? J Thorac Cardiovasc Surg. 2013;61(1):66–73. doi:10.1055/s-0032-1332795

47. Tsai WC, Chen YC, Kao YH, Lu YY, Chen SA, Chen YJ. Distinctive sodium and calcium regulation associated with sex differences in atrial electrophysiology of rabbits. Int J Cardiol. 2013;168(5):4658–4666. doi:10.1016/j.ijcard.2013.07.183

48. Tsai WC, Chen YC, Lin YK, Chen SA, Chen YJ. Sex differences in the electrophysiological characteristics of pulmonary veins and left atrium and their clinical implication in atrial fibrillation. Circ Arrhythm Electrophysiol. 2011;4(4):550–559. doi:10.1161/CIRCEP.111.961995

49. Insulander P, Juhlin-Dannfelt A, Freyschuss U, Vallin H. Electrophysiologic effects of mental stress in healthy subjects: a comparison with epinephrine infusion. J Electrocardiol. 2003;36(4):301–309. doi:10.1016/S0022-0736(03)00078-5

50. Sawatari H, Chishaki A, Ando SI. The epidemiology of sleep disordered breathing and hypertension in various populations. Curr Hypertens Rev. 2016;12(1):12–17. doi:10.2174/1573402112666160114093307

51. Larsson L, Lindberg A, Franklin K, Lundbäck BJC. Gender differences in symptoms related to sleep apnea in a general population and in relation to referral to sleep clinic. Chest. 2003;124(1):204–211. doi:10.1378/chest.124.1.204

52. Linde C, Bongiorni MG, Birgersdotter-Green U, et al. Sex differences in cardiac arrhythmia: a consensus document of the European heart rhythm association, endorsed by the heart rhythm society and Asia Pacific heart rhythm society. Europace. 2018;20(10):1565–1565ao. doi:10.1093/europace/euy067

53. Rienstra M, Van Veldhuisen DJ, Hagens VE, et al. Gender-related differences in rhythm control treatment in persistent atrial fibrillation: data of the rate control versus electrical cardioversion (RACE) study. J Am Coll Cardiol. 2005;46(7):1298–1306. doi:10.1016/j.jacc.2005.05.078

54. Lehmann MH, Timothy KW, Frankovich D, et al. Age-gender influence on the rate-corrected QT interval and the QT-heart rate relation in families with genotypically characterized long QT syndrome. J Am Coll Cardiol. 1997;29(1):93–99. doi:10.1016/S0735-1097(96)00454-8

55. Patel N, Deshmukh A, Thakkar B, et al. Gender, race, and health insurance status in patients undergoing catheter ablation for atrial fibrillation. Am j Cardiol. 2016;117(7):1117–1126. doi:10.1016/j.amjcard.2016.01.040

56. Chang YT, Chen YL, Kang HY. Revealing the influences of sex hormones and sex differences in atrial fibrillation and vascular cognitive impairment. Int J Mol Sci. 2021;22(16):8776. doi:10.3390/ijms22168776

Latest article