Study objectives: Obstructive sleep apnea (OSA) is defined by pauses in breathing during sleep, but daytime breathing dysregulation may also be present. Sleep may unmask breathing instability in OSA that is usually masked by behavioral influences during wakefulness. A breath-hold (BH) challenge has been used earlier to demonstrate breathing instability. One measure of breathing stability is breathing rate variability (BRV). We aimed to assess BRV during rest and in response to BH in OSA.Methods. We studied 62 participants (31 untreated OSA: Respiratory Event Index (REI) [mean±s.d.] 20±15 events/hour, 12 females, age 51±14years, BMI 32±8kg/m 2 ; 31 control: 17 females, age 47±13; BMI 26±4). Breathing movements were collected using a chest belt for 5 minutes rest and during a BH protocol (60 s baseline, 30 s BH, 90 s recovery, 3 repeats). From the breathing movements, we calculated median breathing rate (BR) and interquartile BRV at rest. We calculated change in BRV during BH recovery from baseline. Group comparisons of OSA vs. control were conducted using analysis of covariance (ANCOVA) with age, sex and BMI as covariates.Results. We found 10% higher BRV in OSA vs. control (p<0.05) during rest. In response to BH, BRV increased 7% in OSA vs. 1% in controls (p<0.001). Resting BR was not significantly different in OSA and control, and sex and age did not have any significant interaction effects. BMI was associated with BR at rest (p<0.05) and change in BRV with BH (p<0.001), but no significant BMI-by-group interaction effect was observed. Conclusions.The findings suggest breathing instability as reflected by BRV is high in OSA during wakefulness, both at rest and in response to a stimulus. Breathing instability together with high blood pressure variability in OSA may reflect a compromised cardiorespiratory consequence in OSA during wakefulness.
Study Objectives: Cardiovascular comorbidities in obstructive sleep apnea (OSA) are difficult to treat, perhaps due to autonomic dysfunction. We assessed beat-to-beat blood pressure (BP) variability (BPV) in OSA while considering other markers derived from electrocardiogram and continuous BP signals.Methods: We studied 66 participants (33 participants with OSA: respiratory event index [mean ± SEM]: 21.1 ± 2.7 events/h; 12 females, aged 51.5 ± 2.4 years; body mass index: 32.8 ± 1.4 kg/m 2 ; 33 healthy controls: 20 females; aged 45.3 ± 2.4 years; body mass index: 26.3 ± 0.7 kg/m 2 ). We collected 5-minute resting noninvasive beat-to-beat BP and electrocardiogram values. From BP, we derived systolic, diastolic, and mean BP values, and calculated variability as standard deviations (systolic BPV, diastolic BPV, BPV). We also calculated diastole-to-systole time (time to peak). From the electrocardiogram, we derived QRS markers and calculated heart rate and heart rate variability. We performed a multivariate analysis of variance based on sex and group (OSA vs control), with Bonferronicorrected post hoc comparisons (P ≤ .05) between groups. We calculated correlations of BPV with biological variables. Results: Multivariate analysis of variance showed effects of diastolic BPV and BPV in OSA; post hoc comparisons revealed high diastolic BPV and BPV only in female participants with OSA vs controls. QRS duration was higher in OSA, with post hoc comparisons showing the effect only in males. BPV correlated positively with heart rate variability in controls but not in participants with OSA. BPV correlated positively with time to peak in females with OSA and OSA combined, whereas there was no BPV-time-to-peak correlation in healthy participants. Conclusions: The findings show sex-specific autonomic dysfunction reflected in beat-to-beat BP in OSA. The higher BPV may reflect poor baroreflex control or vascular damage in OSA, which are potential precursors to cardiovascular complications.
Introduction Cardiovascular co-morbidities in obstructive sleep apnea (OSA) are hard to treat, perhaps due to autonomic nervous system (ANS) dysfunction. In OSA, intermittent hypoxia and poor tissue oxygen perfusion damage endothelial and nervous tissue, potentially underlying the dysfunction. Moreover, OSA is strongly associated with anxiety, which is independently associated with ANS dysfunction. We assessed sex-specific relationships between anxiety and cardiovascular markers of ANS dysfunction in OSA. Methods We studied people diagnosed with OSA and healthy controls. We collected 5 minutes of wakeful resting ECG, continuous non-invasive blood pressure, and respiration data. We calculated heart rate (HR), heart rate variability (HRV; sympathetic-vagal balance related to brainstem ANS output), mean arterial blood pressure (MAP), beat-to-beat MAP variability (BPV; related to peripheral autonomic function) and breathing rate (BR). We analyzed these measures with a multivariate regression model of anxiety symptoms (generalized anxiety disorder; GAD-7 scores), sex, and group (OSA vs. control), age/BMI/AHI covariates, and Bonferroni-corrected post-hoc comparisons (p≤0.05). Results We analyzed 64 subjects (32 OSA: AHI [mean±SEM] 24±4events/hour, 12 female, age 52±21years, BMI 33±2kg/m2; 32 control: 19 female, age 46±2; BMI 26±1). We observed significant main effects of anxiety, BMI, AHI, sex on HRV, but only group on BPV; post-hoc comparisons revealed high BPV only in OSA females. Secondary analyses included classifying by anxiety symptoms (GAD-7≥5), showing only OSA females with anxiety had higher BPV. Males showed higher HRV. AHI and anxiety were positively correlated with HRV in OSA males. AHI was negatively correlated with BR in OSA females. Conclusion We observed higher anxiety associated with higher BPV in OSA, especially in females. Unexpectedly, BR was lower in OSA females; longer breaths may have led to the greater BPV. Higher HRV in males complicated by OSA severity and anxiety could be related to higher sympathetic tone. The slightly older control group may have influenced the findings. Overall, our findings suggest anxiety in OSA is associated with peripheral and centrally-mediated autonomic dysfunction, but in a sex-specific manner. Support National Institutes of Health R56-NR-017435 and RO1-HL-135562.
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