• Sleep Medicine and Psychophysiology
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• v.2 no.1
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• pp.55-64
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• 1995

During sleep, relatively major respiratory physiological changes occur in healthy subjects. The contributions and interactions of voluntary and metabolic breathing control systems during waking and sleep are quite different Alterations of ventilatory control occur in chemosensitivity, response to mechanical loads, and stability of ventilation. The activities of intercostal muscles and muscles involved in regulating upper airway size are decreased during sleep. These respiratory physiological changes during sleep compromise the nocturnal ventilatory function, and sleep is an important physiological cause of the nocturnal alveolar hypoventilation. There are several causes of chronic alveolar hypoventilation including cardiopulmonary, neuromuscular diseases. Obstructive sleep apnea syndrome (OSAS) is an important cause of nocturnal hypoventilation and hypoxia. Coexistent cardiopulmonary or neuromuscular disease in patients with OSAS contributes to the development of diurnal alveolar hypoventilation, diurnal hypoxia and hypercapnia. The existing data indicates that nocturnal recurrent hypoxia and fragmentation of sleep in patients with OSAS contributes to the development of systemic hypertension and cardiac bradytachyarrhythmia, and diurnal pulmonary hypertension and cor pulmonale in patients with OSAS is usually present in patients with coexisting cardiac or pulmonary disease. Recent studies reported that untreated patients with OSAS had high long-term mortality rates, cardiovascular complications of OSAS had a major effect on mortality, and effective management of OSAS significantly decreased mortality.

• Sleep Medicine and Psychophysiology
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• v.7 no.1
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• pp.27-33
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• 2000

Objectives: The sensitivity and accuracy of thermistor airflow signal has been debated. The purposes of this study were to compare apnea-hypopnea index(AHI) detected from a conventional thermistor signal and a nasal pressure transducer of airflow(NPT), to evaluate the value of NPT for the diagnosis of upper airway resistance syndrome(UARS), and to measure airway pressure fluctuations which produced respiratory arousals in UARS by naso-oro-esophageal manometer catheter. The subjects were 30 patients with obstructive sleep apnea syndrome [mild(540), 10), and 6 UARS patients. Airway resistance arousal in this study was defined as arousals which were not associated with apnea or hypopnea of thermistor signal, but showed significant decrease of nasal airflow pressure just before arousal and a prompt recovery of nasal airflow pressure after arousal. The airway pressure fluctuations were measured during 260 airway resistance arousals observed in 10 patients with OSAS, 2 with UARS. Results: Mean AHIs of patients with OSAS were 33.4 by thermistor and 48.4 by NPT. The AHIs of mild, moderate and severe OSAS groups were 10.2, 32.1, 65.4 respectively by thermistor and 23.1, 45.9, 76.4 by NPT. The mean AHI of patients with UARS was 3.2 by thermistor and 10.8 by NPT. The mean AHI of patients with nonspecific arousals was 2.7 by thermistor and 4.4 by NPT. The mean airway pressure changes during respiratory arousals of different groups were $8.7\;cmH_2O$ in mild OSAS, $11.4\;cmH_2O$ in moderate OSAS, $24.7\;cmH_2O$ in severe OSAS and $6.6\;cmH_2O$ in UARS. Conclusion: The nasal pressure transducer of airflow was more sensitive and accurate for assessing respiratory disturbances of patients with OSAS and was extremely helpful for the diagnosis of UARS without esophageal pressure monitoring. From the results, we would like to propose carefully the NPT diagnostic criteria for sleep disordered breathing as follows: NPT-AHI 5-15 $\rightarrow$ UARS, 15-35 $\rightarrow$ mild OSAS, 35-55 $\rightarrow$ moderate OSAS and >55 $\rightarrow$ severe OSAS.

• 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.

• Tuberculosis and Respiratory Diseases
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• v.49 no.6
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• pp.715-723
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• 2000

Background : Obstructive sleep apnea syndrome (OSAS) affects systemic blood pressure and cardiac function. The development of cardiovascular dysfunction including the changes of systemic blood pressure and cardiac rhythm, suggests that recurrent hypoxia and arousals from sleep may increase a sympathetic nervous system activity. Continuous positive airway pressure (CPAP) therapy has been found to be an effective treatment of OSAS. However, only a few studies have investigated the cardiovascular and sympathetic effects of CPAP therapy. We evaluated influences of nasal CPAP therapy on the cardiovascular system and the sympathetic activity in patients with OSAS. Methods : Thirteen patients with OSAS underwent CPAP therapy and were monitored using polysomnography, blood pressure, heart rate, presence of arrhythmia and the concentration of plasma catecholamines, before and with CPAP therapy. Results: The apnea-hypopnea index (AHI) was significant1y decreased (p<0.01) and the lowest arterial oxygen saturation level was elevated significantly after applying CPAP (p<0.01). Systolic blood pressure tended to decrease after CPAP but without statistical significance. Heart rates during sleep were not significantly different after CPAP. However, the frequency and number of types of arrhythmia decreased and sinus bradytachyarrhythmia disappeared after CPAP. Although there was no significant difference in the level of plasma epinephrine concentration, plasma norepinephrine concentration significantly decreased after CPAP (p<0.05). Conclusion : CPAP therapy decreased the apnea-hypopnea index, hypoxic episodes and plasma norepinephrine concentration. In addition, it decreased the incidence of arrhythmia and tended to decrease the systemic blood pressure. These results indicate that CPAP may play an important role in the prevention of cardiovascular complications in patients with OSAS.

• Sleep Medicine and Psychophysiology
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• v.15 no.2
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• pp.67-70
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• 2008

Overlap syndrome can be defined as a coexistence of chronic obstructive pulmonary disease (COPD) and sleep apnea-hypopnea syndrome (SAHS). The association of COPD and SAHS has been suspected because of the frequency of both diseases. Prevalence of COPD and SAHS is respectively 10 and 5% of the adult population over 40 years of age. However, a recent study has shown that the prevalence of SAHS is not higher in COPD than in the general population. The coexistence of the two diseases is only due to chance. SAHS does not affect the pathophysiology of COPD and vice versa. Prevalence of overlap syndrome is expected to occur in about 0.5% of the adult population over 40 years of age. Patients with overlap syndrome have a more profound hypoxemia, hypercapnia, and pulmonary hypertension when compared with patients with SAHS alone or usual COPD patients without SAHS. To treat the overlap syndrome, nocturnal noninvasive ventilation (NIV) or nasal continuous positive airway pressure (nCPAP) can be applied with or without nocturnal oxygen supplement.

• Sleep Medicine and Psychophysiology
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• v.4 no.2
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• pp.129-139
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• 1997

The data collected to date indicate that sleep-related breathing disorders, including sleep-disordered breathing(sleep apnea) and underlying respiratory system diseases, are one of the important risk factors for cardiovascular dysfunction. Sleep-disordered breathing(sleep apnea) is now recognized as one of the leading causes of systemic hypertension, cardiac arrhythmias, coronary heart disease, pulmonary hypertension, right heart failure, and stroke. Sleep may exert a profound effect on breathing in patients with underlying respiratory system disease including bronchopumonary diseases, chest wall abnormalities, central alveolar hypoventilation syndromes or respiratory neuromuscular disorders. Chronic hypoxia and hypercapnia in these patients may accelerate the development of long term cardiovascular complications such as cardiac arrhythmias, pulmonary hypertension, and right heart failure(cor pulmonale). Several recent studies reported that sleep-related breathing disorders are associated with long-term cardiovascular morbidity and mortality. Careful assessment of respiratory and cardiovascular function in these patients is critical. Aggressive and highly effective treatment of sleep-related breathing disorders using tracheostomy, mechanical ventilation, nasal continuous positive airway pressure therapy(nCPAP), intercurrent oxygen therapy or other interventions can reduce the prevalence of cardiovascular dysfunction and the long-term mortality.

• Tuberculosis and Respiratory Diseases
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• v.42 no.2
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• pp.206-217
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• 1995

Background: In patients with obstructive sleep apnea syndrome(OSAS), there are several factors increasing upper airway resistance and there is a predisposition to compromised respiratory function during waking and sleep related to constitutional factors including a tendency to obesity. Several recent studies have suggested a possible relationship between sleep apnea(SA) and systemic hypertension. But the possible pathophysiologic link between SA and hypertension is still unclear. In this study, we have examined the relationship among age, body mass index(BMI), pulmonary function parameters and polysomnographic data in patients with OSAS. And also we tried to know the difference among these parameters between hypertensive OSAS and normotensive OSAS patients. Methods: Patients underwent a full night of polysomnography and measured pulmonary function during waking. OSAS was diagnosed if patients had more than 5 apneas per hour(apnea index, AI). A careful history of previously known or present hypertension was obtained from each patient, and patients with systolic blood pressure $\geq$ 160mmHg and/or diastolic blood pressure $\geq$ 95mmHg were classified as hypertensives. Results: The noctural nadir of arterial oxygen saturation($SaO_2$ nadir) was negatively related to AI and respiratory disturbance index(RDI), and the degree of noctural oxygen desaturation(DOD) was positively related to AI and RDI. BMI contributed to AI, RDI, $SaO_2$ nadir and DOD values. And also BMI contributed to $FEV_1,\;FEV_1/FVC$ and DLco values. There was a correlation between airway resistance(Raw) and AI, and there was a inverse correlation between DLco and DOD. But there was no difference among these parameters between hypertensive OSAS and normotensive OSAS patients. Conclusion: The obesity contributed to the compromised respiratory function and the severity of OSAS. AI and RDI were important factors in the severity of hypoxia during sleep. The measurement of pulmonary function parameters including Raw and DLco may be helpful in the prediction and assessment of OSAS patients. But we could not find clear difference between hypertensive and normotensive OSAS patients.

• Tuberculosis and Respiratory Diseases
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• v.45 no.2
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• pp.404-415
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• 1998

Background: Sleep apnea syndrome, which occurs in 1~4 % of the adult population, frequently has different cardiovascular complications such as hypertension, ischemic heart disease, cardiac arrythmia as well as sleep-wake disorder such as excessive daytime hypersomnolence or insomnia. Mortality and vascular morbidity are reported to be significantly higher in sleep apnea syndrome patients than in normal population. According to the recent studies, autonomic dysfunction as well as hypoxemia, hypercapneic acidosis, and increased respiratory effort, may playa role in the high prevalence of cardiovascular complications in patients with sleep apnea syndrome. However the cause and mechanism of autonomic neuropathy in patients with sleep apnea syndrome are not well understood. We studied the existence of autonomic neuropathy in patients with sleep apnea syndrome and factors which influence the pathogenesis of autonomic neuropathy. Method: We used the cardiovascular autonomic neuropathy(CAN) test as a method for evaluation of autonomic neuropathy. The subjects of this study were 20 patients who diagnosed sleep apnea syndrome by polysomnography and 15 persons who were normal by polysomnography. Results: Body mass index and resting systolic blood pressure were higher in sleep apnea group than control group. Apnea index(Al), respiratory disturbance index(RDI) and snoring time percentage were significantly higher in sleep apnea group compared with control group. But there were no significant differences in saturation of oxygen and sleep efficiency in two groups. In the cardiac autonomic neuropathy test, the valsalva ratio was significantly low in sleep apnea group compared with control group but other tests had no differences between two groups. The CAN scores and corrected QT(QTc) interval were calculated significantly higher in sleep apnea group, but there were no significant correlations between CAN scores and QTc interval. There were no significant data of polysomnography to correlate to the CAN score. It meant that the autonomic neuropathy in patients with sleep apnea was affected by other multiple factors. Conclusion: The cardiovascular autonomic neuropathy test was a useful method for the evaluation of autonomic neuropathy in patients with sleep apnea syndrome and abnormalities of cardiovascular autonomic neuropathy were observed in patients with sleep apnea syndrome. However, we failed to define the factors that influence the pathogenesis of autonomic neuropathy of sleep apnea syndrome. This study warrants futher investigations in order to define the pathogenesis of autonomic neuropathy in patients with sleep apnea syndrome.

• Sleep Medicine and Psychophysiology
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• v.22 no.1
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• pp.11-19
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• 2015

Objectives: Whether daytime sleepiness is proportional to the severity of sleep apnea in obstructive sleep apnea syndrome (OSAS) is controversial. In this study we investigated how insomnia severity affects the association between daytime sleepiness and sleep apnea severity in OSAS. Methods: The present study included 235 male subjects who were diagnosed with OSAS based on clinical history and nocturnal polysomnography. Pearson's correlation analysis was conducted among sleep and mood-related self-reported data, polysomnographic data and demographic data of all subjects. Based on Pittsburgh Sleep Quality Index (PSQI), the subjects were divided into 2 groups; group A (n = 75; $PSQI{\leq}5$) and group B (n = 160; PSQI > 5). Partial correlation analysis was performed between the Epworth Sleepiness Scale (ESS) and other data in both groups. Multiple linear regression analysis was conducted to investigate the factors which affected the ESS in group A. Results: Pearson's correlation analysis showed weak or non-existent correlations between ESS and apnea severity data such as apnea-hypopnea index (AHI) (r = 0.148, p = 0.023), apnea index (AI) (r = 0.137, p = 0.036), hypopnea index (HI) (r = 0.058, p = 0.377), oxygen desaturation index (ODI) (r = 0.149, p = 0.022) and arousal total index (ATI) (r = 0.129, p = 0.048). Positive correlations between ESS and apnea severity data such as AHI ($r_p=0.313$, p = 0.008), AI ($r_p=0.339$, p = 0.004), ODI ($r_p=0.289$, p = 0.015) and ATI ($r_p=0.256$, p = 0.031) were observed only in group A. Multiple regression analysis showed that AI (t = 2.996, p = 0.004) and BAI (t = 2.721, p = 0.008) were associated with ESS in group A. Conclusion: The correlation between daytime sleepiness and sleep apnea severity was shown only in group A. This result suggests that associations between daytime sleepiness in OSAS and sleep apnea severity will become prominent when controlling for insomnia-related variables.

• Tuberculosis and Respiratory Diseases
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• v.56 no.4
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• pp.364-373
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• 2004

Background : Obstructive sleep apnea is a contributory factor of hypertension, arrhythmia, ischemic heart disease and other cardiovascular diseases. However, the pathophysiology underlying this relationship is unclear. Recent reports have shown that the soluble intercellular adhesion molecule-1(sICAM-1) and vascular endothelial growth factor(VEGF) are involved in the initiation and progression of atherosclerosis, and some reports state that increased levels of these cytokines are found in patients with obstructive sleep apnea. In this study, the levels of sICAM-1 and VEGF were measured in patients with obstructive sleep apnea in order to determine if obstructive sleep apnea is involved in the pathophysiology of cardiovascular diseases. Methods : Thirty-seven patients were chosen amongst a population who visited the Sleep Disorders Clinic of St. Paul's Hospital in Seoul, Korea for a diagnosis of obstructive sleep apnea and who had subsequently undergone an overnight polysomnography at the clinic. The sera from these patients were retrieved after an overnight polysomnography session and the samples were kept at $-70^{\circ}C$. The cytokine levels were determined with ELISA and the relationships between the serum levels of sICAM-1 and VEGF along with polysomnography parameters were analyzed. Results : No statistically significant correlation was observed between the sICAM-1 levels and the apnea-hypopnea index(r=0.27, P>0.05). Positive correlations were found between the apnea-hypopnea index and serum VEGF levels (r=0.50, P<0.01), the apnea index and the serum sICAM-1 levels (r=0.31, P<0.01), and the apnea index and the serum VEGF levels (r=0.45, P<0.01). Conclusions : Obstructive apnea or hypopnea leads to an increase in the sICAM-1 and VEGF levels. Such an increase in the cytokine levels most likely leads to the higher incidence of cardiovascular diseases observed in patients with obstructive sleep apnea.