Abstract
Obstructive sleep apnea (OSA) is often accompanied by sleep bruxism (SB). A low respiratory arousal threshold (AT) may contribute to the induction or exacerbation of SB. The aim of this study was to assess the impact of the AT on the intensity of bruxism in individuals with OSA and SB. The prospective observational study was undertaken in 117 subjects with suspected sleep disorder (47% females, average age 44.83 years) who undergone video-polysomnography. Among the study participants, 77 (64.1%) were found to have a low AT, while 42 (35.9%) had a high AT. Participants with low AT’s had significantly higher bruxism episode index (BEI) and phasic BEI values than patients with a high AT (6.06 ± 4.46 vs. 4.54 ± 3.18; p = 0.04 and 3.18 ± 3.49 vs. 1.84 ± 1.74; p = 0.03, respectively). The positive correlation between BEI and a low AT and a higher percentage of hypopneas were found (R = 0.190, p = 0.040; R = 0.278, p = 0.002, respectively). Summarizing, there is a higher intensity of SB observed in patients with a low AT, than in those with a high one. This effect is more pronounced in men. SB accompanying low AT may be a protective factor in OSA patients, by terminating respiratory events. Thus patients with a low AT and SB could be better protected from OSA complications.
Subject terms: Sleep disorders, Dental diseases
Introduction
Obstructive sleep apnea (OSA) is a prevalent sleep disorder characterized by the recurrent collapse of the upper airway, resulting in cessation of airflow and arterial oxygen desaturation1. These obstructive apneas and hypopneas may lead to significant changes in intrathoracic pressure, intermittent hypoxemia, and sleep arousals2. While these arousals generally do not fully awaken the patient, they contribute to sleep fragmentation, which is the primary cause of excessive sleepiness in individuals with OSA3,4. Arousals from sleep are triggered when the respiratory arousal threshold (AT) is reached, which is defined as the level of ventilatory drive required to terminate a respiratory event5,6. A low AT has been pointed out in the pathogenesis of OSA and may affect up to one-third of patients with moderate to severe OSA7,8. Untreated OSA, due to its heterogenous pathophysiology, has multiple consequences for the cardiovascular9, metabolic10, neurocognitive11, and social12 functions. A crucial approach is to understand the various pathophysiological causes of OSA, as this may contribute to the unveiling of new therapeutic targets and create opportunities to develop targeted treatments13.
Moreover, among sleep disorders, OSA is often accompanied by sleep bruxism (SB) due to its common pathophysiology14,15. It was previously shown that the increase of sympathetic drive, which is a well-recognized phenomenon in OSA, occurs before a bruxism event (RMMA). It may be noticed in polysomnography records as an increase in heart rate, blood pressure, and respiration rate before bruxism events16. Snoring, which is a symptom of airway obstruction, was related to SB in a polysomnographic study17. Another polysomnographic study demonstrated that SB activity is likely to increase motor activity in non-REM 1 sleep18. In summary, the mechanisms of OSA and SB may overlap but are certainly not simple and sufficiently clarified. The definition and classification of SB has evolved over the years19. Currently, SB is classified as a sleep-related movement disorder in the International Classification of Sleep Disorders—Third Edition (ICSD-3)20, whereas it was previously categorized as a parasomnia by the American Academy of Sleep Medicine (AASM)21. According to the ICSD-3, the clinical criteria for SB include: (1) the presence of regular or frequent tooth grinding sounds occurring during sleep, and (2) one or more of the following clinical signs: abnormal tooth wear consistent with reports of tooth grinding, transient morning jaw muscle pain or fatigue, temporal headaches, and/or jaw locking upon awakening. The etiology of SB is thought to involve both the central and autonomic nervous systems, which could share common pathophysiological mechanisms with OSA22.
A low respiratory AT may contribute to the induction or exacerbation of SB. Individuals with a lower AT are more susceptible to frequent arousals in response to minor respiratory disturbances during sleep. This heightened arousability could activate physiological responses associated with bruxism, potentially leading to increased episodes of jaw muscle activity and teeth grinding during sleep. Understanding the relationship between low AT and SB may provide insight into new therapeutic approaches for managing both conditions.
The aim of this study was to assess the impact of the AT on the intensity of bruxism in individuals with OSA and SB.
Materials and methods
The prospective observational study was undertaken in the Sleep Laboratory at the Department and Clinic of Diabetology, Hypertension and Internal Medicine, at Wroclaw Medical University in Poland. 117 patients, consisting of 52 females and 66 males, were recruited for the study by experienced researchers working at the department of Sleep Laboratory in years 2021–2023. Participants were recruited into the study through a continuous sampling process. Participants were referred for PSG by their family doctors due to complaints of sleep disorders. They were then admitted to the Sleep Laboratory, where PSG was performed. Then if any of the exclusion criteria was recorded, the participant was excluded.
The study was conducted according to the principles set out in the Declaration of Helsinki. In conforming with the declaration, written informed consent was obtained from the participants. The Ethics Committee at Wroclaw Medical University approved the study (no. KB-523/2021). Furthermore, the study was registered at clinicaltrials.gov. The reference number to the examination is NCT049370361.
Study participants
PSG examination with video recording was conducted on patients that had been admitted to the Department and Clinic of Diabetology, Hypertension and Internal Medicine at Wroclaw Medical University in Poland. Three inclusion criteria had to be met by patients for them to be admitted to the study: participants had to be at least 18 years of age, possess a strong suspicion of having a sleep disorder and had to have provided informed written consent to taking part in the study. A number of exclusion criteria were also defined. These included the presence of certain illnesses:current malignancy or inflammation, decompensated heart failure, decompensated respiratory insufficiency, severe asthma, chronic obstructive pulmonary disease (COPD), hypothyroidism, chronic kidney disease. Pregnancy was another exclusion criteria, as was the inability to undergo PSG examination and less than 4 h of recorded sleep during examination. These criteria were used by medical doctors to subdivide patients into the previously discussed study groups. A comprehensive overview of the patient recruitment process for this study is shown in Fig. 1.
Fig. 1.
Flowchart illustrating the qualification process of patients for the study.
Polysomnographic examination
The criteria enforced by the American Academy of Sleep Medicine (AASM) were utilised in conducting the polysomnographic examination in the study participants and International Consensus on the Assessment of Bruxism was used23. The NOX-A1 polysomnographic system was used in carrying out the study (Nox Medical, Reykjavik, Iceland). Multiple features were assessed during the PSG examination. The bioelectrical activity of the brain was examined using electroencephalography (EEG), eye movements were recorded using electrooculography, a nasal pressure sensor recorded airflow, movements in the chest and abdomen were recorded using inductive plethysmography and an electromyogram with tibial electrodes demonstrated muscular tension. Lateral masseter electromyography was performed, and the patient’s body position was also recorded. To measure oxygen saturation, a NONIN WristOx2 3150 pulse oximeter (Nonin Medical, Plymouth, MN, USA) was employed. The data obtained from each PSG examination was manually analyzed by author HM, one of the qualified physicians at the Sleep Laboratory situated at Wroclaw Medical University in Poland. The AASM guidelines were utilised in defining the sleep disorders24.
SB was diagnosed using bilateral masseter muscle electromyography (together with an additional electrode in the chin region), which was used to record rhythmic masseter muscle activity (RMMA). The skin had to be adequately prepared prior to pasting the electrodes, to provide for optimum contact with the skin and ultimately contribute to favourable bioelectrical results. The preparation included the inspection of the skin for wounds, cleanliness and dryness. Next, water, along with an abrasive skin prepping-gel, was used to clean the skin. In case of excessive skin oiliness, alcohol wipes were additionally utilised to clean it. Pauses of less than 3 s between EMG bursts, indicated a single SB episode. These bursts were required to have an electromyographic amplitude that was double that of the background EMG activity. The AASM guidelines were used to classify these bruxism episodes into one of three groups: mixed, tonic and phasic forms. Furthermore, the number of bruxism episodes occurring each hour, was used to calculate the bruxism episode index (BEI). This helped to classify the intensity of the SB. A BEI score of < 2 defined SB as being insignificant, a score of 2–4 classified it as being mild or moderate while severe SB was found to occur in participants with a BEI of > 4.
The feature taking precedence in this study was the AT. Only invasive examination utilising either an oesophageal or epiglottic pressure catheter is able to precisely quantify the AT, and has been considered the gold standard for determining the AT. However Edwards et al. has provided a solution for estimating AT non-invasively6. This solution was utilized by the researchers conducting the study. Three criteria were taken into account in the estimation of the AT. A point was assigned to each criterion that was fulfilled. These criteria include: an apnea/hypopnea index (AHI) of < 30 events per hour, a minimum SpO2 of 82.5%, and a hypopnea fraction of > 58.3%. Participants with OSA, that had met at least two of these criteria, were determined as being likely to have a low AT.
Statistical analysis of the results
The dataset, comprising data from 117 individuals, was analyzed using Statistica 13.3 (Statsoft, Poland). Descriptive statistics are expressed as the mean and standard deviation. The selection of analytical methods was guided by the satisfaction of relevant statistical assumptions. Initially, the dataset was assessed through an analysis of its distribution and homogeneity of variance. To evaluate these properties, the Shapiro–Wilk test was employed to assess normality, while Levene’s test was used to examine variance equality. For variables meeting parametric criteria, classical parametric tests, specifically the independent samples T-test, were used to compare differences between two groups. When the data failed to meet the assumptions required for parametric tests, non-parametric alternatives, such as the Mann–Whitney U test, were applied. Spearman’s rank correlation coefficient was utilized to assess relationships between variables. Statistical significance was recognized for a p-value < 0.05.
Results
A total of 117 participants were qualified for the study, of which 55 (47%) were women and 53% were men. The average age of the subjects was 44.83 ± 14.84 years. All participants underwent polysomnographic examination, and those with an AHI < 30, SpO2 > 82.5%, and a hypopnea fraction > 58.3% constituted 74.36%, 63.25%, and 39.32% of the entire group, respectively. Among the study participants, 77 (64.1%) were found to have a low AT while 42 (35.9%) patients had a high AT. A detailed characterization of the study group is presented in Table 1.
Table 1.
The characteristics of studied group.
| Parameter | Total | Men | Women | Parameter | Total | Men | Women |
|---|---|---|---|---|---|---|---|
| Age (years) | 44.83 ± 14.84 | 46.56 ± 14.47 | 42.87 ± 15.14 | AT = 1 | 32 (27.35%) | 21 (33.87%) | 11 (20.00%) |
| AHI < 30 | 87 (74.36%) | 42 (67.74%) | 45 (81.82%) | AT = 2 | 49 (41.88%) | 20 (32.26%) | 29 (52.73%) |
| SpO2 > 82.5% | 74 (63.25%) | 33 (53.23%) | 41 (74.55%) | AT = 3 | 26 (22.22%) | 14 (22.58%) | 12 (21.82%) |
| Hypopneas > 58.3% | 46 (39.32%) | 28 (45.16%) | 18 (32.73%) | AT low (2/3pkt) | 75 (64.10%) | 34 (54.84%) | 41 (74.55%) |
| Arousal threshold = 0 | 10 (8.55%) | 7 (11.29%) | 3 (5.45%) | AT high (0/1pkt) | 42 (35.90%) | 28 (45.16%) | 14 (25.45%) |
SpO2 mean oxygen saturation, AHI apnea/hypopnea index, AT arousal threshold.
The diagnosis of SB was made on the basis of the conducted polysomnographic examinations. The degree of disease severity was established on the grounds of the BEI values. There were 15 participants without bruxism (12.82%), 32 with mild bruxism (27.35%), and 70 with severe bruxism (59.83%). In the subgroup of patients with mild bruxism, 16 participants were identified as having a low AT, and a further 16 were determined to have high ATs. In the severe bruxism subgroup, 51 patients (72.86%) had a low AT, while 19 participants (27.14%) had a high AT. Detailed data is included in Table 2.
Table 2.
Severity of bruxism in relation to gender and arousal threshold.
| BEI < 2 (n, %) | BEI 2–4 (n, %) | BEI > 4 (n, %) | |
|---|---|---|---|
| Total (n = 117) | 15, 12.82% | 32, 27.35% | 70, 59.83% |
| Women (n = 55) | 8, 14.55% | 19, 34.55% | 28, 50.91% |
| Men (n = 62) | 7, 11.29% | 13, 20.97% | 42, 67.74% |
| AT low (n = 75) | 8, 53.33% | 16, 50.00% | 51, 72.86% |
| AT high (n = 42) | 7, 46.67% | 16, 50.00% | 19, 27.14% |
AT arousal threshold, BEI bruxism episode index.
In the first stage of the statistical analysis, participants who were diagnosed with SB, were further subdivided into two groups: (1) patients with a low AT, and (2) patients with a high AT. The mean BMI in the whole group was 28.1 ± 3.39. Patients with high AT had slightly, although not significantly, higher mean BMI than patients with low AT (28.95 ± 4.50 vs. 27.63 ± 3.08, p = 0.067, respectively). Participants with low ATs were found to have significantly higher BEI and phasic BEI values than patients with a high AT (6.06 ± 4.46 vs. 4.54 ± 3.18; p = 0.04 and 3.18 ± 3.49 vs. 1.84 ± 1.74; p = 0.03, respectively). This was deemed to be statistically significant. Furthermore, patients with a low AT exhibited a significantly higher tonic maximum value than the rest of the group (2.35 ± 0.82 vs. 2.05 ± 0.80; p = 0.01). Other sleep parameters were also analyzed in the low and high AT groups. Detailed results are presented in Table 3.
Table 3.
Sleep and bruxism parameters in patients with low and high arousal threshold.
| Parameter | AT Low (n = 75) | AT high (n = 42) | p | Parameter | AT low (n = 75) | AT high (n = 42) | p |
|---|---|---|---|---|---|---|---|
| BEI (n/h) | 6.06 ± 4.46 | 4.54 ± 3.18 | 0.0413 | Snore (% of TSF) | 13.83 ± 15.96 | 29.06 ± 22.85 | 0.0004 |
| Phasic BEI (n/h) | 3.18 ± 3.49 | 1.84 ± 1.74 | 0.0270 | Apnea index (n/h) | 2.01 ± 3.38 | 18.61 ± 23.58 | 0.00001 |
| Tonic BEI (n/h) | 1.87 ± 1.66 | 1.86 ± 1.82 | 0.9253 | OA (n/h) | 1.30 ± 2.94 | 15.86 ± 22.57 | 0.00001 |
| Mixed BEI (n/h) | 1.05 ± 0.95 | 0.91 ± 1.03 | 0.1128 | MA (n/h) | 0.08 ± 0.26 | 1.12 ± 2.56 | 0.00001 |
| TST (min) | 430.22 ± 54.55 | 436.38 ± 49.59 | 0.5044 | CA (n/h) | 0.50 ± 1.04 | 1.43 ± 3.24 | 0.0593 |
| SE (%) | 87.08 ± 7.87 | 83.92 ± 11.88 | 0.2393 | HI (n/h) | 6.79 ± 7.19 | 12.39 ± 11.16 | 0.0069 |
| WASO (min) | 40.82 ± 35.61 | 54.79 ± 42.91 | 0.0730 | Mean SpO2 (%) | 93.96 ± 1.83 | 91.53 ± 4.33 | 0.0001 |
| SL (min) | 19.61 ± 16.84 | 15.22 ± 14.27 | 0.1396 | Min SpO2, (%) | 86.40 ± 6.51 | 75.54 ± 10.95 | 0.00001 |
| N1 (% of TST) | 4.50 ± 4.00 | 8.62 ± 7.70 | 0.0011 | SpO2, < 90% | 4.36 ± 11.41 | 17.61 ± 24.67 | 0.00001 |
| N2 (% of TST) | 48.61 ± 10.04 | 50.49 ± 10.33 | 0.5776 | Average desat drop (% of TST) | 3.61 ± 0.81 | 5.73 ± 3.52 | 0.00001 |
| N3 (% of TST) | 23.97 ± 8.22 | 21.32 ± 8.61 | 0.1321 | Arousals (n/h) | 4.95 ± 4.26 | 8.56 ± 14.06 | 0.0712 |
| REM (% of TST) | 22.92 ± 7.14 | 19.49 ± 7.55 | 0.0255 | Pulse aver. (n/min) | 61.30 ± 6.86 | 64.34 ± 7.99 | 0.0540 |
| AHI (n/h) | 11.77 ± 8.77 | 41.00 ± 24.86 | 0.00001 | Pulse max. (n/min) | 99.12 ± 21.56 | 102.22 ± 21.74 | 0.3395 |
| ODI (n/h) | 8.86 ± 9.05 | 31.24 ± 28.04 | 0.00001 | Pulse min. (n/min) | 47.65 ± 9.01 | 51.63 ± 29.08 | 0.8379 |
Values presented as mean ± SD. Statistically significant differences (p < 0.05) marked as bold.
AHI apnea–hypopnea index, ODI oxygen desaturation index, TST total sleep time (min), SL sleep latency, REML REM latency, WASO wake after sleep onset, SE sleep efficiency, N1 sleep stage 1, N2 sleep stage 2, N3 sleep stage 3, REM rapid eye movement sleep stage, mean SpO2 mean oxygen saturation, minimal SpO2 minimal oxygen saturation, BEI bruxism episode index, Max maximum, Min minimum, SpO2 < 90% time with oxygen saturation < 90% (% of TST), AT arousal thresholds, OA obstructive apneas, MA mixed apneas, CA central apneas, SD standard deviation.
The next step of the analysis compared specific features of SB within each gender. Considering the threshold of arousals, no statistically significant differences were observed between the parameters characterizing SB amongst women. However, in the male demographic, the subgroup with a low AT was found to have a significantly higher phasic BEI value than the subgroup of male patients with a high threshold of awakenings (3.08 ± 2.33 vs. 1.76 ± 1.82; p = 0.014). Patients with a low AT were characterized by a significantly higher minimum tonic value than the remaining participants (2.46 ± 1.14 vs. 1.93 ± 0.56; p = 0.03).
An analysis of correlations between BEI values was also conducted. It demonstrated a significant positive correlation between BEI and a low AT as well as a higher percentage of hypopneas (R = 0.196, p = 0.034; R = 0.278, p = 0.002, respectively). The analysis also identified a positive correlation between phasic BEI and a low AT, as well as between phasic BEI and AHI < 30 (R = 0.23, p = 0.012; R = 0.206, p = 0.026, respectively). In contrast, tonic and mixed BEI correlated positively only with a hypopnea fraction > 58.3% (R = 0.220, p = 0.017; R = 0.237, p = 0.010, respectively, Table 4).
Table 4.
The correlation analysis between BEI and arousal threshold.
| Parameter | BEI | Phasic BEI | Tonic BEI | Mixed BEI | ||||
|---|---|---|---|---|---|---|---|---|
| R | p | R | p | R | p | R | p | |
| AT | 0.196 | 0.034 | 0.231 | 0.012 | 0.014 | 0.879 | 0.171 | 0.065 |
| AHI < 30 | 0.100 | 0.282 | 0.206 | 0.026 | -0.143 | 0.123 | 0.044 | 0.637 |
| SpO2 > 82.5% | -0.004 | 0.966 | 0.118 | 0.207 | -0.094 | 0.315 | 0.051 | 0.587 |
| hypopneas > 58.3% | 0.278 | 0.002 | 0.139 | 0.136 | 0.220 | 0.017 | 0.237 | 0.010 |
AT arousal threshold, SpO2 oxygen saturation, AHI apnea–hypopnea index, BEI bruxism episode index.
Discussion
The most important result in our study is without a doubt the presence of an increased intensity of SB in patients with a low AT as opposed to a high AT (6.06 ± 4.46 vs 4.54 ± 3.18, p = 0.0413). Phasic bruxism was also increased in the low AT group (3.18 ± 3.49 vs 1.84 ± 1.74, p = 0.027). On the other hand, in the group characterised by severe SB (BEI > 4), a low AT occurred 2.6 times more frequently than a high AT (72.86% vs 27.14%), while in participants with mild or irrelevant SB (BEI ≤ 4), the proportion of patients with low vs. high AT patients was either equal, or very similar (50% vs 50% and 53.33% vs 46.67%, respectively).
The possible protective role of SB in the population of adult patients with OSA has previously been discussed in the literature25. The present study demonstrates that in patients with a low AT the intensity of SB is higher than in those with a high AT. The observation seems to be logical and in agreement with the existing research data, which has shown an increased intensity of SB in mild and moderate OSA compared to severe OSA15,26. The data also revealed an increased O2 saturation and lower AHI in participants with a low AT, as opposed to those with a high AT patients27.
It has recently been indicated that the majority of the SB episodes (85.7% of rhytmic masticatory muscle activity, RMMA), are time-related to arousals in adults with OSA28. It has additionally been reported that during the N1 and N2 stages of sleep, most SB episodes are observed in relation to arousals. These arousals are positively associated with SB onset in the moderate to high intensity SB subjects29. Our observation is in line with studies that highlight a low AT as the marker of arousability, in these same two SB intensity groups.
We also observed a positive correlation between SB (BEI) and a low AT, as well as between phasic bruxism and a low AHI < 30. However no significant connection was observed betweeen the AT and tonic bruxism. The observation may indicate different etiologies and significance of tonic and phasic bruxism.
The connection of SB with sympathetic nervous system activity has been widely observed and discussed16,29–32. Our observation highlights the relationship between a, low AT and hypothetically, the same autonomic cardiac activity mechanisms as in SB, across the sleep cycle in patients with OSA. It has previously been reported that an increase in sympathetic nervous system activity precedes the onset of SB (in patients with moderate to severe SB)29. RMMA episodes were secondary to increase of heart rate and respiration rate. This backs our present observation29,30. There is also data supporting the connection of the A3 phase of sleep (typically a phase with stronger arousal processes) with SB. In fact, it has previously been suggested that this phase of sleep appears to be a permissive window of RMMA/SB activity29,31. According to past research, subjects with SB had greater sleep instability than the participants in the control group, which is in line with our observation31. Additionally, according to demonstrative data the SB and arousal episodes in young healthy subjects diagnosed with SB were all associated with blood pressure fluctuations during sleep, with elevations in BP occurring most frequently. This underlines the connection of autonomic nervous activity with SB and arrousals16.
It is also worth noting that in our study, patients with a low AT, had an almost 4 times lower AHI (11.77 vs 41.00) and 9 times lower apnea index, as opposed to patients with high AT (2.01 vs 18.61). This clearly suggests that these participants had milder OSA and could be better protected from OSA complications. In our observation, low AT patients are also characterised by a visibly higher oxygen saturation, and the presence of more hypopneas (rather than apneas) in PSG screening. Our results are in agreement with fresh pilot observations. The data from these studies has demonstrated a high prevalence of low AT in patients with mild OSAS and a low, almost absent, prevalence of a low AT in patients with severe OSAS27. In the present study, we also noted a decreased AHI, ODI, snore and apnea index in low AT subjects, which is very much in agreement with existing data and pathophysiological deliberation. In some of the available research, it has beeen shown that SB episodes might be clearly related to the preceding slight desaturations appearing in the few seconds before the onset of RMMA32. Furthermore, it has been indicated that SatO2 becomes significantly higher in the several seconds after the onset of the recorded SB episode. Thes brief oxygen fluctuations preceding RMMA may reflect a physiological response that seems to have little influence on the genesis of SB32. It has been also reported that a low respiratory AT appeared more frequently in non-obese (rather than obese) OSA patients, suggesting a low AT as being one of the non-anatomical patophysiologic basis of OSA33. However, other research has reported a higher prevalence of low AT in obese OSA patients with coexisting asthma27.
Our results, together with the concomitant existing data, support the hypothesis that both SB and arousals may be protective elements in OSA for terminating apneic events, with neuromuscular and autonomic responses interrupting, or at least shortening, respiratory episodes and preventing prolonged oxygen deprivation during sleep. We postulate a possible protective role of a low AT in the population of adult patients with OSA and SB.
The study shows that SB accompanying low AT may be a protective factor in OSA patients. However, the next question is why do low AT and SB not become a protective factor in severe OSA. Its worth noting, that severe OSA is related to significant metabolic alternations and increased cardiovascular risk. Thus, the consequences of severe OSA are much more serious than the mild one. Therefore, the protective mechanisms may vary regarding the OSA severity. The hiperventilation between respiratory events may be one of the protective mechanisms, as well as increased movement activity18. Bruxism may not be very sufficient as a protecitve factor in more severe OSA, hence being replaced by more effective mechanisms.
There are a few limitations of the study, Firstly, there was no adaptive night prior to conducting the PSG examination, due to the organisation of the polish healthcare system. Secondly, our study focused only on the OSA type of SB.
Our findings may be crucial for future work related to establishing appropriate OSA therapeutic strategies, as the AT can be manipulated pharmacologically using sedative/hypnotic agents, which could potentialy be harmful in increasing the effort-related AT in response to hypercapnia34.
Conclusions
There is a higher intensity of SB observed in patients with a lowAT, than in those with a high one. This effect is more pronounced in men rather than in women.
SB accompanying low AT may be a protective factor in OSA patients, by terminating respiratory events. Thus patients with a low AT and SB could be better protected from OSA complications. However further studies on cardiovascular risk in SB are needed.
Author contributions
Conceptualization and study design: HM and MWP. Data interpretation and statistical analysis: DN. Writing and editing the manuscript, preparation of tables and figures: HM, JK, GL, AJ, PM, WF and KM. Critical review and revision of the manuscript: HM, MWP, KM. All authors have read and approved the manuscript.
Funding
Supported by Wroclaw Medical University SUBZ.A490.24.060.
Data availability
The datasets analysed during the study are available from the corresponding author on reasonable request.
Declarations
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The datasets analysed during the study are available from the corresponding author on reasonable request.