Inducers of post-apneic blood pressure fluctuation monitored by pulse transfer time measurement in obstructive sleep apnea varied with syndrome severity

2019 ◽  
Vol 23 (3) ◽  
pp. 769-776 ◽  
Author(s):  
Jing Xu ◽  
Ning Ding ◽  
Liang Chen ◽  
Yi Zhang ◽  
Mao Huang ◽  
...  
Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Takeshi Takamura ◽  
Kaoru Dohi ◽  
Katsuya Onishi ◽  
Emiyo Ogawa ◽  
Hiroshi Nakajima ◽  
...  

Background: Sleep apnea-hypopneas induce transient increases in arterial blood pressure (BP). We test the hypothesis that periodic nocturnal apneic events augment those hemodynamic responses in patients both with central and obstructive sleep apnea syndrome (SAS). Methods: Eleven patients with central SAS (CSAS: mean age 70 ± 10 years), 11 patients with obstructive SAS (OSAS: mean age 64 ± 12 years), and 8 normal controls (Control) were studied. Polysomnography was performed and BP was measured on a beat-by-beat basis by finger plethysmography all through the sleep. Severity of SAS was assessed by apnea-hypopnea index (AHI). The degree of BP fluctuation associated with periodic nocturnal apnea-hypopnea was assessed by spectral analysis of mean BP variability. Spectral plots of mean BP were calculated in 2-min segments using a maximum entropy method. Power spectrum of mean BP variability was quantified by measuring the area in the very-low-frequency band which coincides with frequency of apnea-hypopneas (sleep apnea band: 0.01– 0.03 Hz), and was normalized by dividing by the total power in the spectrum up to 0.4 Hz. Results: AHI was similar in CSAS and OSAS (38.3 ± 9.5* and 39.8 ± 11.3*, *p<0.05 vs. Control: 2.5±1.6*). Repetitive fluctuations in BP coincided with periodic apnea-hypopneas were clearly observed in patients with SAS, and were more prominent in CSAS (Normalized spectral power of mean BP in sleep apnea band: 0.72 ± 0.10*† in CSAS, 0.62 ±0.13* in OSAS, and 0.46±0.07 in Control, * p<0.05 vs. Control, and †p<0.05 vs. OSAS). Conclusion: Periodic nocturnal apneic events augment blood pressure fluctuation in patients both with central and obstructive SAS.smoking.


2021 ◽  
Vol 10 (7) ◽  
pp. 1387
Author(s):  
Raphael Boneberg ◽  
Anita Pardun ◽  
Lena Hannemann ◽  
Olaf Hildebrandt ◽  
Ulrich Koehler ◽  
...  

Obstructive sleep apnea (OSA) independent of obesity (OBS) imposes severe cardiovascular risk. To what extent plasma cystine concentration (CySS), a novel pro-oxidative vascular risk factor, is increased in OSA with or without OBS is presently unknown. We therefore studied CySS together with the redox state and precursor amino acids of glutathione (GSH) in peripheral blood mononuclear cells (PBMC) in untreated male patients with OSA (apnea-hypopnea-index (AHI) > 15 h−1, n = 28) compared to healthy male controls (n = 25) stratifying for BMI ≥ or < 30 kg m−2. Fifteen OSA patients were reassessed after 3–5-months CPAP. CySS correlated with cumulative time at an O2-saturation <90% (Tu90%) (r = 0.34, p < 0.05) beside BMI (r = 0.58, p < 0.001) and was higher in subjects with “hypoxic stress” (59.4 ± 2.0 vs. 50.1 ± 2.7 µM, p < 0.01) defined as Tu90% ≥ 15.2 min (corresponding to AHI ≥ 15 h−1). Moreover, CySS significantly correlated with systolic (r = 0.32, p < 0.05) and diastolic (r = 0.31, p < 0.05) blood pressure. CPAP significantly lowered CySS along with blood pressure at unchanged BMI. Unexpectedly, GSH antioxidant capacity in PBMC was increased with OSA and reversed with CPAP. Plasma CySS levels are increased with OSA-related hypoxic stress and associated with higher blood pressure. CPAP decreases both CySS and blood pressure. The role of CySS in OSA-related vascular endpoints and their prevention by CPAP warrants further studies.


Respiration ◽  
2021 ◽  
pp. 1-10
Author(s):  
Wei-Hsiu Chang ◽  
Hsien-Chang Wu ◽  
Chou-Chin Lan ◽  
Yao-Kuang Wu ◽  
Mei-Chen Yang

<b><i>Background:</i></b> Most patients with mild obstructive sleep apnea (OSA) are positional dependent. Although mild OSA worsens over time, no study has assessed the natural course of positional mild OSA. <b><i>Objectives:</i></b> The aim of this study was to evaluate the natural course of positional mild OSA, its most valuable progression predictor, and its impact on blood pressure (BP) and the autonomic nervous system (ANS). <b><i>Methods:</i></b> This retrospective observational cohort study enrolled 86 patients with positional mild OSA and 26 patients with nonpositional mild OSA, with a follow-up duration of 32.0 ± 27.6 months and 37.6 ± 27.8 months, respectively. Polysomnographic variables, BP, and ANS functions were compared between groups at baseline and after follow-up. <b><i>Results:</i></b> In patients with positional mild OSA after follow-up, the apnea/hypopnea index (AHI) increased (9.1 ± 3.3/h vs. 22.0 ± 13.2/h, <i>p</i> = 0.000), as did the morning systolic BP (126.4 ± 13.3 mm Hg vs. 130.4 ± 15.9 mm Hg, <i>p</i> = 0.011), and the sympathetic activity (49.4 ± 12.3% vs. 55.3 ± 13.1%, <i>p</i> = 0.000), while the parasympathetic activity decreased (50.6 ± 12.3% vs. 44.7 ± 13.1%, <i>p</i> = 0.000). The body mass index changes were the most important factor associated with AHI changes among patients with positional mild OSA (Beta = 0.259, adjust <i>R</i><sup>2</sup> = 0.056, <i>p</i> = 0.016, 95% confidence interval 0.425 and 3.990). The positional dependency disappeared over time in 66.3% of patients with positional mild OSA while 69.2% of patients with nonpositional mild OSA retained nonpositional. <b><i>Conclusions:</i></b> In patients with positional mild OSA, disease severity, BP, and ANS regulation worse over time. Increased weight was the best predictor for its progression and the loss of positional dependency. Better treatments addressing weight control and consistent follow-up are needed for positional mild OSA.


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