scholarly journals Prevalence and risk factors of silent obstructive sleep apnea in patients with dentofacial deformities

2021 ◽  
Author(s):  
Rei Jokaji ◽  
Kazuhiro Ooi ◽  
Sayuri Takamichi ◽  
Yusuke Nakade ◽  
Shuichi Kawashiri ◽  
...  
Keyword(s):  
Risk Factors ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Rem Sleep ◽  
Orthognathic Surgery ◽  
Sleep Phase ◽  
Deep Bite ◽  
Mandibular Asymmetry ◽  
Dentofacial Deformities ◽  
Obstructive Sleep

Abstract Objective Prevalence of silent obstructive sleep apnea (OSA) in patients with dentofacial deformities is unknown, although OSA is severe risk of airway obstruction in perioperative orthognathic surgery or complication after surgery. The aim of this study was to investigate prevalence and risk factors of silent OSA in patients with dentofacial deformities. Methods We analyzed 72 patients (24 male, 48 female) with dentofacial deformities without previous OSA symptoms. Polysomnography was performed before orthognathic surgery. Prevalence and risk factors of silent OSA were statistically analyzed as related to Apnea hypopnea index (AHI). Results Mean AHI was 1.6 (range: 0-12.1) /h. Three patients of 72 patients (4.1%) were diagnosed silent OSA. AHI during REM sleep phase 3.7 (0-32.3) was higher than AHI during NREM sleep phase 1.0 (0-9.7). AHI of male patients was higher than that of female. AHI was increased according to high BMI. AHI was higher in deep bite than open bite, edge to edge bite and nomal bite. AHI of mandibular asymmetry cases were higher than that of symmetry cases. Conclusions The prevalence of silent OSA was 4.1%. Obesity, male, deep bite, mandibular asymmetry and REM sleep phase were risk factors of silent OSA.

Arterial blood pressure responses to graded transient arousal from sleep in normal humans

1993 ◽  
Vol 74 (3) ◽  
pp. 1123-1130 ◽  
Author(s):  
R. J. Davies ◽  
P. J. Belt ◽  
S. J. Roberts ◽  
N. J. Ali ◽  
J. R. Stradling
Keyword(s):  
Blood Pressure ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Confidence Interval ◽  
Rem Sleep ◽  
High Frequency ◽  
Pressure Rise ◽  
Nrem Sleep ◽  
Blood Pressure Rise ◽  
Obstructive Sleep

During obstructive sleep apnea, transient arousal at the resumption of breathing is coincident with a substantial rise in blood pressure. To assess the hemodynamic effect of arousal alone, 149 transient stimuli were administered to five normal subjects. Two electroencephalograms (EEG), an electrooculogram, a submental electromyogram (EMG), and beat-to-beat blood pressure (Finapres, Ohmeda) were recorded in all subjects. Stimulus length was varied to produce a range of cortical EEG arousals that were graded as follows: 0, no increase in high-frequency EEG or EMG; 1, increased high-frequency EEG and/or EMG for < 10 s; 2, increased high-frequency EEG and/or EMG for > 10 s. Overall, compared with control values, average systolic pressure rose [nonrapid-eye-movement (NREM) sleep 10.0 +/- 7.69 (SD) mmHg; rapid-eye-movement (REM) sleep 6.0 +/- 6.73 mmHg] and average diastolic pressure rose (NREM sleep 6.1 +/- 4.43 mmHg; REM sleep 3.7 +/- 3.02 mmHg) over the 10 s following the stimulus (NREM sleep, P < 0.0001; REM sleep, P < 0.002). During NREM sleep, there was a trend toward larger blood pressure rises at larger grades of arousal (systolic: r = 0.22, 95% confidence interval 0.02–0.40; diastolic: r = 0.48, 95% confidence interval 0.31–0.62). The average blood pressure rise in response to the grade 2 arousals was approximately 75% of that during obstructive sleep apnea. Arousal stimuli that did not cause EEG arousal still produced a blood pressure rise (mean systolic rise 8.6 +/- 7.0 mmHg, P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Obstructive Sleep Apnea: Epidemiology, Causes, and Consequences

2020 ◽  
Author(s):  
Diane C Lim ◽  
Richard J Schwab
Keyword(s):  
Risk Factors ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Cushing Syndrome ◽  
Upper Airway ◽  
Fat Distribution ◽  
Epidemiologic Studies ◽  
Obstructive Sleep ◽  
Upper Airway Muscles ◽  
Underlying Diseases

As part one of the three chapters on sleep-disordered breathing, this chapter reviews obstructive sleep apnea (OSA) epidemiology, causes, and consequences. When comparing OSA prevalence between 1988 to 1994 and 2007 to 2010, we observe that OSA is rapidly on the rise, paralleling increasing rates in obesity. Global epidemiologic studies indicate that there are differences specific to ethnicity with Asians presenting with OSA at a lower body mass index than Caucasians. We have learned that structural and physiologic factors increase the risk of OSA and both can be influenced by genetics. Structural risk factors include craniofacial bony restriction, changes in fat distribution, and the size of the upper airway muscles. Physiologic risk factors include airway collapsibility, loop gain, pharyngeal muscle responsiveness, and arousal threshold. The consequences of OSA include daytime sleepiness and exacerbation of many underlying diseases. OSA has been associated with cardiovascular diseases including hypertension, coronary heart disease, stroke, atrial fibrillation, and other cardiac arrhythmias; pulmonary hypertension; metabolic disorders such as type 2 diabetes, hypothyroidism, acromegaly, Cushing syndrome, and polycystic ovarian syndrome; mild cognitive impairment or dementia; and cancer. This review contains 4 figures, 1 table and 48 references. Key Words: cardiac consequences, craniofacial bony restriction, epidemiology, fat distribution, metabolic disease, neurodegeneration, obesity, obstructive sleep apnea

Abstract P195: Lack of Association between Sleep Duration and ECG Arrhythmia Risk Measures: Chicago Area Sleep Study

Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Jason Ng ◽  
Phyllis C Zee ◽  
Jeffrey J Goldberger ◽  
Kristen L Knutson ◽  
Kiang Liu ◽  
...  
Keyword(s):  
Risk Factors ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Sleep Duration ◽  
Low Risk ◽  
Qtc Interval ◽  
Sleep Study ◽  
Chicago Area ◽  
Obstructive Sleep ◽  
Pr Interval

Introduction Sleep duration is significantly associated with cardiovascular disease risk factors such as hypertension, diabetes, and obesity in adults at low risk for obstructive sleep apnea. Although it is known that apnea increases the risk for sudden cardiac death, it is not known whether adults with short sleep duration independent of apnea have a higher risk for cardiac arrhythmias Hypothesis We tested the hypothesis that sleep duration in adults at low risk for obstructive sleep apnea would be associated with ECG measures that are known risk factors for ventricular arrhythmias. Methods The Chicago Area Sleep Study recruited 610 participants via commercially available telephone listings. Participants were screened using in-home apnea detection equipment (ApneaLinkTM) for one night to exclude subjects with apnea/hypopnea index ≥ 15. Participants wore wrist actigraphs for 7 days to objectively determine sleep duration. A 10-minute 12-lead ECG was recorded for each subject. Standard measures of heart rate, PR interval, and QTc interval were obtained along with markers of ventricular repolarization, Tpeak to Tend interval (Tpe) and spatial QRS-T angle. Signal-averaged ECG analysis was performed to measure filtered QRS duration (fQRSd), RMS voltage of terminal 40 ms (RMS), and duration of terminal QRS signals <40μV (LAS). Participants with atrial fibrillation, >20% ectopic beats and those using antihypertensive and sleep medications were excluded from analysis. The effect of sleep duration on the ECG parameters was estimated using a multiple linear regression model adjusting for demographics (sex, age, and race) and cardiovascular risk factors (BMI, hypertension, coronary heart disease, and diabetes). Results ECGs from a total of 504 participants (200 male, 48±8 years old) were analyzed. Mean sleep duration was 7±1 hrs, heart rate was 64±9 bpm, PR interval was 165±18 ms, and QTc interval was 424±23 ms. Mean Tpe interval was 83±14 ms and spatial QRS-T angle was 29±26 deg. The signal-averaged ECG measures of fQRSd, RMS, and LAS had mean values of 78±12 ms, 58±34 μV, and 24±9 ms, respectively. In an unadjusted model, there was a borderline association between sleep duration and QTc (β=0.004 ms/hr, SE=0.0023, p=0.08). However, that association was no longer significant following adjustment with demographics and cardiovascular risk factors. No other ECG measures were associated with sleep duration. Conclusions In a population at low risk of obstructive sleep apnea, ECG-based measures of cardiovascular risks were not associated with sleep duration. Previously reported associations between short sleep and cardiovascular events may not be arrhythmic in origin.

scholarly journals Upper Airway Collapsibility During REM Sleep in Children with the Obstructive Sleep Apnea Syndrome

SLEEP ◽  
2009 ◽  
Vol 32 (9) ◽  
pp. 1173-1181 ◽  
Author(s):  
Jingtao Huang ◽  
Laurie R. Karamessinis ◽  
Michelle E. Pepe ◽  
Stephen M. Glinka ◽  
John M. Samuel ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Obstructive Sleep Apnea Syndrome ◽  
Rem Sleep ◽  
Sleep Apnea Syndrome ◽  
Upper Airway ◽  
Obstructive Sleep ◽  
Airway Collapsibility ◽  
Apnea Syndrome ◽  
Upper Airway Collapsibility
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