[Symptoms associated with sleep apnea].
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Biomedical subjects
Publications and source records attributed to T Akashiba.
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To investigate pulmonary hemodynamics in patients with chronic respiratory failure, we performed right heart catheterization and also examined the effects of oxygen inhalation. Thirty-three patients were studied. Their mean age was 65 +/- 10 years, and FEV1.0% and PaO2 on room air were 47 +/- 16% and 63 +/- 14 mmHg, respectively. mPAP was 27 +/- 10 mmHg, and 26 (78%) had pulmonary hypertension. Although PVR was abnormally high, CI and PCWP were within normal limits. PaO2 was significant Significantly correlated with mPAP and PVR. Although oxygen inhalation (28%) for 30 minutes significantly changed PaO2, PaCO2, and PvO2, it did not significantly affect mPAP, PVR, CI, or PCWP. These results suggest that short-term oxygen inhalation does not affect pulmonary hemodynamics in patients with chronic respiratory failure. Radionuclid ventriculography was also done to evaluate cardiac function in 16 patients before and after home oxygen therapy (HOT). Both right ventricular ejection fraction (RVEP) and left ventricular ejection fraction (LVEF) were significantly increased by HOT, and the significant correlation between RVEF and LVEF that had been observed before HOT disappeared. These results suggest cardiac function improved and that the interdependence between the right and left ventricle was eliminated by HOT.
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To investigate the possible influence of genetics in subjects with obstructive sleep apnea syndrome (OSAS), HLA-A, B, C, and DR antigens were studied in 32 Japanese subjects with OSAS. The frequency of HLA-A2 antigen was markedly increased in the patients with OSAS compared with normal controls (81.3% vs 40.6%) and compared with the Japanese population (40.7%), Pc < 0.035 and Pc < 0.007, respectively. HLA-B39 was found more frequently in OSAS patients than in the Japanese population (Pc < 0.018), but not in the controls. No significant deviation was observed in the frequencies of HLA-C and DR antigens between the OSAS patients and the controls. We conclude that genetics is important in the development of OSAS.
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A 42-year-old male patient with obstructive sleep apnea syndrome (OSAS) suffering from biventricular heart failure is reported. He had been treated for OSAS with conventional therapy. However, he complained of severe dyspnea in association with extreme weight gain and general edema. Therefore, he was admitted to our department. He weighed 168 kg on admission, and marked edema was observed. Chest film revealed significant dilatation of the cardiac silhouette and pleural effusion. PaO2 was 37 mmHg and PaCO2 was 66 mmHg. Polysomnography showed an apnea index of 58.3 and severe oxygen desaturation during sleep. Right heart catheterization showed elevation of mean pulmonary artery pressure mPAP: 55 mmHg) and pulmonary capillary wedge pressure (Pcwp: 33 mmHg) suggesting biventricular heart failure. Digitalization and diuretic therapy were immediately initiated. In addition, nasal CPAP was applied to this patient during sleep, and sleep apnea and oxygen desaturation were almost completely reversed. Significant diuresis was observed, and blood gas data and sleep disturbance were improved. Fifty-nine days after admission, his weight had decreased to 96 kg, and mPAP and Pcwp decreased to 32 and 23 mmHg, respectively. This case demonstrates that nasal CPA is an effective tool for the treatment severe OSAS patients.
We studied the traffic accident rates and daytime sleepiness in obstructive sleep apnea syndrome (OSAS) patient, and evaluated the effectiveness of long-term nasal CPAP treatment. Traffic accidents were observed in 42% of 14 male OSAS patients (46 +/- 7 years old) and near-miss accidents were also observed in 64% during the past three years. Stanford Sleepiness Scale showed 4.7 +/- 1.0, suggesting marked excessive daytime sleepiness (EDS). During NCPAP treatment for 11 +/- 9 months, no traffic and near-miss accidents were reported. After NCPAP treatment, SSS decreased to 2.0 +/- 0.8, and the score of Uchida-Kraeplin test for the evaluation of working ability increased significantly. These results suggest the improvement of EDS and working ability following NCPAP treatment. We conclude that OSAS patients have the tendency of daytime sleepiness and high traffic accidents rates, and NCPAP treatment is effective to improve such problems.
We assessed pulmonary function and exercise tolerance in 10 BMT patients. Their underlying disorders were as follows; chronic myeloid leukemia 5 cases, acute lymphoblastic leukemia 2 cases, aplastic anemia, acute myeloid leukemia and non-Hodgkin's lymphoma one case each. Their mean age was 26 +/- 9 years old. When the patients were healthy and free of serious complications and anemia, arterial blood gas examination, pulmonary function tests and incremental treadmill exercise test were examined repeatedly. Although %VC and FEV1.0% kept within normal range, PaO2 at rest, %DLCO, VO2max, VO2max/kg and O2-pulsemax remained low at one year after BMT. There were significant correlations between VO2max and O2-pulsemax [r = 0.955 (p < 0.001)], %VC [r = 0.758 (p < 0.02)], VE/VO2max [r = -0.749 (p < 0.02)] and delta SaO2/VO2/kg [r = -0.731 (p < 0.02)], suggesting that exercise intolerance in BMT patients may be based on both cardiac and gas exchange abnormalities. To evaluate cardiac dysfunction, we compared exercise parameters obtained at an exercise level of 75% predicted heart rate max in five age-matched normal subjects to those in six BMT patients who did not demonstrate desaturation during exercise. As a result, the mean values of VO2max/kg and O2-pulse/m2 in BMT patients were significantly lower than those in normal subjects, suggesting that cardiac dysfunction may be due to insufficiency of stroke volume during exercise. It is concluded that exercise intolerance in BMT patients may be mainly due to cardiac dysfunction.
We treated 23 patients with obstructive sleep apnea syndrome (OSAS) by nasal continuous positive airway pressure (NCPAP) at home, and examined the long-term compliance, clinical effects, and complications after NCPAP therapy. Nineteen patients continued and four patients discontinued the therapy during the mean observation period of 15 months, and the compliance was 83%. There was no significant difference in age, weight, and sleep data between the compliant group (C) and non-compliant group (NC). The causes of discontinuation of therapy were lack of adaptation to the apparatus (2 cases), improvement of clinical symptoms due to weight reduction (1 case), and induction of asthma attack (1 case). Disappearance of excessive daytime sleepiness, improvement of sleep quality, and disappearance of nocturia were observed in most cases, and disappearance of morning headache and improvement of sexual ability and emotional instability were also observed in several cases. Nine cases (39%) complained of discomfort due to the nasal mask and 6 cases (26%) complained of dryness of the mouth and nose, whereas 10 cases (43%) experienced no adverse effects. No serious complications were observed. These findings suggest that long-term home NCPAP is an effective and safe treatment for OSAS patients.
The prevalence and mechanisms of daytime pulmonary hypertension were examined in 24 cases of obstructive sleep apnea syndrome (OSAS). All patients were free from chronic lung disease. They underwent pulmonary function tests and blood gas analysis in the sitting and supine position, hypercapnic ventilatory response test, exercise test and right heart catheterization. Elevation of mean pulmonary arterial pressure (m-PAP) above 20 mmHg was observed in 5 out of 24 cases (20.8%). The group with pulmonary hypertension (PG+: m-PAP = 22.2 +/- 2.7 mmHg) showed marked obesity (p < 0.001), significant decrease of supine FRC/TLC (p < 0.05), increase of supine CC/FRC (p < 0.01), decrease of supine PaO2 (p < 0.02) and desaturation during exercise (p < 0.05) in comparison with the group without pulmonary hypertension (PH-: 13.9 +/- 3.1 mmHg). m-PAP was positively correlated with %IBW and desaturation during exercise (p < 0.01, p < 0.02) and negatively correlated with supine PaO2 (p < 0.01). Various changes in pulmonary function and pulmonary hemodynamics due to obesity seem to lead to daytime pulmonary hypertension of OSAS.
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We assessed ventricular performance during exercise in 16 COPD patients and 8 normal control subjects by means of radionuclide equilibrium angiography using technetium-99m as a tracer. Supine exercise on a bicycle ergometer was performed until symptom-limited exhaustion. Data were accumulated for 300 heart beats at rest and 150 heart beats during exercise. We used the standard voxel count method to calculate the ventricular volumes. Age, FEV1.0%, %VC, PaO2 and PaCO2 of the COPD patients were 63 +/- 8 yr, 46 +/- 11%, 69 +/- 18%, 68 +/- 11 Torr and 44 +/- 7 Torr (mean +/- SD), respectively. Systolic dysfunction of both the left and right ventricles was well confirmed in the present study. In 12 patients who also underwent hemodynamic studies, resting total pulmonary vascular resistance index (TPVRI) and mean pulmonary artery pressure (Ppa) significantly correlated with right ventricular end-systolic volume index (RVESVI) obtained by RI angiography; gamma = 0.769 (p less than 0.01) and gamma = 0.631 (p less than 0.05), respectively. A significant relationship was also observed between left ventricular dysfunction and the degree of hypercapnia. In response to exercise testing, 10 of 16 patients exhibited insufficient augmentation of stroke volume, and both left and right end-diastolic volumes decreased in half of 10 patients. It is suggested that cardiac function may be disturbed by mechanical factors such as pulmonary hyperinflation in COPD patients.
The area of upper airway (from the nasopharynx to the hypopharynx) was measured by means of computed tomography (CT) scan in 15 confirmed cases of obstructive sleep apnea (OSA) and in 4 normal controls while they were awake. The minimum cross-sectional area (MA) of the upper airway was 14.7 +/- 20.0 mm2 in OSA patients and 80.0 +/- 33.1 mm2 in normal controls and the difference was statistically significant (p less than 0.01). In OSA patients, MA did not correlate with age, body weight, apnea index, desaturation index, mean nadir-SO2 and lowest SO2. MA was also measured with OSA patients while nasal continuous positive airway pressure (NCPAP) of 10 cmH2O was applied and it was found that MA was significantly widened when NCPAP therapy was performed. We conclude that upper airway narrowing is consistent finding in OSA patients but the degree of narrowing does not correlate with parameters of apnea and gas exchange during sleep, and NCPAP is effective to widen the area of upper airway in OSA patients.
Nocturnal renal function was examined in 8 patients with obstructive sleep apnea syndrome (OSAS) and the effects of nasal CPAP (NCPAP) on renal function were also studied. Nocturia was observed more than twice in all cases when no treatment was performed, but it disappeared after initiation of NCPAP. Fractional nocturnal urine volume and creatinine clearance decreased significantly from 1.36 +/- 0.15 ml/min to 0.75 +/- 0.20 ml/min (p less than 0.01) and from 116.8 +/- 46.5 ml/min to 101.1 +/- 33.0 ml/min (p less than 0.05), respectively, after initiation of NCPAP. Although the serum Na and creatinine did not change following NCPAP, the urine Na and creatinine changed significantly after NCPAP therapy. The serum renin, aldosterone, and ADH did not change after NCPAP therapy. The significant positive correlation (p less than 0.05) between the fractional nocturnal urine volume and DI, and also significant inverse correlation (p less than 0.05) between the fractional urine volume and %FRC were observed. These results suggest that the abnormal renal function seen in cases of OSAS is related to the hypoxemia during sleep. It was concluded that the nocturnal renal function in cases of OSAS was different from those in normal controls and NCPAP therapy induced the recovery of these abnormalities.
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Recent studies have shown that nasal CPAP is very effective in the treatment of patients with obstructive sleep apnea syndrome (OSA). To clarify the characteristics of pulmonary function testing and to evaluate the effect of short term nasal CPAP therapy in 13 cases of OSA patients, nasal CPAP was used for 10 to 14 days and polysonography was performed on two consecutive nights without nasal CPAP and at one night with nasal CPAP. Pulmonary function tests and the Uchida-Kraepelin test were performed before the initiation of nasal CPAP therapy and also 7 to 14 days after the nasal CPAP therapy. Apnea index reduced significantly in all cases from 5.10 +/- 19.6 episodes/hour without therapy to 3.1 +/- 3.5 with nasal CPAP (p less than 0.001). Nasal CPAP significantly reduced the frequency of obstructive (p less than 0.001) and mixed apnea (p less than 0.01), but the frequency of central apnea did not change with nasal CPAP. During the nasal CPAP, mean nadir SaO2 rose from 87.3 +/- 2.9% to 92.7 +/- 1.1% (p less than 0.001) and the lowest SaO2 rose from 73.3 +/- 6.4% to 92.0 +/- 2.1% (p less than 0.001). Before the nasal CPAP therapy, daytime PaO2 was 80.6 +/- 6.4 Torr and closing capacity (CC)/FRC ratio was higher when patients were in a supine than in a sitting position. After short term nasal CPAP therapy, daytime PaO2 increased significantly (p less than 0.001), and FRC/TLC in a supine position increased and CC/FRC in a supine position decreased in some patients.(ABSTRACT TRUNCATED AT 250 WORDS)