• Tuberculosis and Respiratory Diseases
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• v.45 no.1
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• pp.153-168
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• 1998

Background: The existing data indicate that obstructive sleep apnea syndrome contributes to the development of cardiovascular dysfunction such as systemic hypertension and cardiac arrhythmias, and the cardiovascular dysfunction has a major effect on high long-term mortality rate in obstructive sleep apnea syndrome patients. To a large extent the various studies have helped to clarify the pathophysiology of obstructive sleep apnea, but many basic questions still remain unanswered. Methods: In this study, the influence of obstructive sleep apnea on systemic blood pressure, cardiac rhythm and urinary catecholamines concentration was evaluated. Over-night polysomnography, 24-hour ambulatory blood pressure and ECG monitoring, and measurement of urinary catecholamines, norepinephrine (UNE) and epinephrine (UEP), during waking and sleep were undertaken in obstructive sleep apnea syndrome patients group (OSAS, n=29) and control group (Control, n=25). Results: 1) In OSAS and Control, UNE and UEP concentrations during sleep were significantly lower than during waking (P<0.01). In UNE concentrations during sleep, OSAS showed higher levels compare to Control (P<0.05). 2) In OSAS, there was a increasing tendency of the number of non-dipper of nocturnal blood pressure compare to Control (P=0.089). 3) In both group (n=54), mean systolic blood pressure during waking and sleep showed significant correlation with polysomnographic data including apnea index (AI), apnea-hypopnea index (AHI), arterial oxygen saturation nadir ($SaO_2$ nadir) and degree of oxygen desaturation (DOD). And UNE concentrations during sleep were correlated with AI, AHI, $SaO_2$ nadir, DOD and mean diastolic blood pressure during sleep. 4) In OSAS with AI>20 (n==14), there was a significant difference of heart rates before, during and after apneic events (P<0.01), and these changes of heart rates were correlated with the duration of apnea (P<0.01). The difference of heart rates between apneic and postapneic period (${\Delta}HR$) was significantly correlated with the difference of arterial oxygen saturation between before and after apneic event (${\Delta}SaO_2$) (r=0.223, P<0.001). 5) There was no significant difference in the incidence of cardiac arrhythmias between OSAS and Control In Control, the incidence of ventricular ectopy during sleep was significantly lower than during waking. But in OSAS, there was no difference between during waking and sleep. Conclusion : These results suggested that recurrent hypoxia and arousals from sleep in patients with obstructive sleep apnea syndrome may increase sympathetic nervous system activity, and recurrent hypoxia and increased sympathetic nervous system activity could contribute to the development of cardiovascular dysfunction including the changes of systemic blood pressure and cardiac function.

• Sleep Medicine and Psychophysiology
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• v.9 no.1
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• pp.24-33
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• 2002

Objectives: Nasal continuous positive airway pressure (CPAP) corrected elevated blood pressure (BP) in some studies of obstructive sleep apnea syndrome (OSAS) but not in others. Such inconsistent results in previous studies might be due to differences in factors influencing the effects of CPAP on BP. The factors referred to include BP monitoring techniques, the characteristics of subjects, and method of CPAP application. Therefore, we evaluated the effects of one night CPAP application on BP and heart rate (HR) reactivity using non-invasive beat-to-beat BP measurement in normotensive and hypertensive subjects with OSAS. Methods: Finger arterial BP and oxygen saturation monitoring with nocturnal polysomnography were performed on 10 OSAS patients (mean age $52.2{\pm}12.4\;years$; 9 males, 1 female; respiratory disturbance index (RDI)>5) for one baseline night and another CPAP night. Beat-to-beat measurement of BP and HR was done with finger arterial BP monitor ($Finapres^{(R)}$) and mean arterial oxygen saturation ($SaO_2$) was also measured at 2-second intervals for both nights. We compared the mean values of cardiovascular and respiratory variables between baseline and CPAP nights using Wilcoxon signed ranks test. Delta ($\Delta$) BP, defined as the subtracted value of CPAP night BP from baseline night BP, was correlated with age, body mass index (BMI), baseline night values of BP, BP variability, HR, HR variability, mean $SaO_2$ and respiratory disturbance index (RDI), and CPAP night values of TWT% (total wake time%) and CPAP pressure, using Spearman's correlation. Results: 1) Although increase of mean $SaO_2$ (p<.01) and decrease of RDI (p<.01) were observed on the CPAP night, there were no significant differences in other variables between two nights. 2) However, delta BP tended to increase or decease depending on BP values of the baseline night and age. Delta systolic BP and baseline systolic BP showed a significant positive correlation (p<.01), but delta diastolic BP and baseline diastolic BP did not show a significant correlation except for a positive correlation in wake stage (p<.01). Delta diastolic BP and age showed a significant negative correlation (p<.05) during all stages except for REM stage, but delta systolic BP and age did not. 3) Delta systolic and diastolic BPs did not significantly correlate with other factors, such as BMI, baseline night values of BP variability, HR, HR variability, mean SaO2 and RDI, and CPAP night values of TWT% and CPAP pressure, except for a positive correlation of delta diastolic pressure and TWT% of CPAP night (p<.01). Conclusions: We observed that systolic BP and diastolic BP tended to decrease, increase or remain still in accordance with the systolic BP level of baseline night and aging. We suggest that BP reactivity by CPAP be dealt with as a complex phenomenon rather than a simple undifferentiated BP decrease.

• Korean Journal of Clinical Laboratory Science
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• v.46 no.3
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• pp.106-110
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• 2014

Obstructive sleep apnea-hypopnea (OSAH) is known to be related to nocturnal blood pressure (BP) and hypertension. The aim of this study was to evaluate the prevalence of hypertension according to the apnea-hypopnea grading. A total of 2,210 adults with snoring and obstructive sleep apnea were referred to our sleep center from July 2009 to May 2013. Clinical blood pressure (BP) was measured before sleeping (bedtime BP) and immediately after waking up in the next morning (morning BP). Subjects were classified into four groups based on the apnea-hypopnea index (AHI) from PSG as follows: control group (n=470) simple snoring and with AHI<5; mild group (n=577) with $AHI{\geq}5$ and <15; moderate group (n=508) $AHI{\geq}15$ and <30; and severe group (n=655) with $AHI{\geq}30$. The differences and correlations between BP and PSG parameters according to the AHI groups were analyzed. Patient's were classified as nomentensive (blood pressure <120/90 mmHg, n=700), prehypertensive (blood pressure < $140-120{\leq}mmHg$, n=1297) hypertensive (blood pressure ${\geq}140/90mmHg$, n=214) according to the office blood pressure measurements. The comparison of sleep parameters showed that OSA groups had a significantly higher stage N1 (control group vs. moderate OSA, severe OSA; $66.4{\pm}30.7$ vs. $85.5{\pm}36.6$, $128.4{\pm}57.3$, p<0.001) and total arousal number (control vs. moderate OSA, severe OSA; $110.7{\pm}47.7$ vs. $150.8{\pm}56.6$, $236.6{\pm}95.8$, p<0.001) compared to control group. The comparison of sleep parameters showed that OSA groups had a significantly lower stage N2 (control group vs. moderate OSA, severe OSA; $172.6{\pm}47.2$ vs. $150.7{\pm}50.5$, $120.3{\pm}57.4$, p<0.001), stage N3 (control group vs. moderate OSA, severe OSA; $38.4{\pm}33.4$ vs. $27.4{\pm}26.0$, $56.1{\pm}27.5$, p<0.001), REM (control group vs. moderate OSA, severe OSA; $64.3{\pm}25.5$ vs. $56.1{\pm}27.5$, $47.3{\pm}25.9$, p<0.001) and mean SaO2% (control group vs. moderate OSA, severe OSA; $90.0{\pm}3.5$ vs. $82.5{\pm}5.5$, $70.0{\pm}8.8$, p<0.001) compared to control group. The Apnea-hypopnea index was significantly higher in OSA groups, increased systolic and diastolic blood pressure than in the nomentensive group (bed time systolic pressure vs. AHI; <120 vs. 120-139, 140-159, >159; $17.5{\pm}18.6$ vs. $24.9{\pm}21.0$, $31.0{\pm}25.7$, $42.3{\pm}31.7$, p<0.001), (bed time diastolic pressure vs. AHI; 60-79 vs. 80-89, 90-99, >99; $19.3{\pm}19.7$ vs. $22.4{\pm}20.3$, $29.8{\pm}23.3$, $38.8{\pm}28.5$, p<0.001). AHI was positively correlated with morning systolic pressure, diastolic pressure, bed time systolic pressure and diastolic pressure (r=0.314, 0.279, 0.233 and 0.200, respectively, p<0.001). We conclude that BMI, Age, neck circumference and AHI increase with the blood pressure.