Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sleep apnea, which affects 10% of men in the mean age group, is a common illness, and arterial hypertension one of its early symptoms. For the large group of, mainly young, patients with mild to moderate sleep apnea and arterial hypertension it is important to have a drug treatment available which will effectively control blood pressure without exacerbating symptoms of sleep apnea. We studied the effects of antihypertensive agents on blood pressure, sleep and sleep apnea in a randomized double-blind study of 24 patients with a sleep apnea activity of more than 10 apnea phases per hour of sleep and arterial hypertension with diastolic blood pressure values in the sitting position greater than or equal to 95 mm Hg. Mean age was 51 (range: 33-69) years, mean body mass index 31.4 (24.9-40.6) kg/m2. The study protocol envisaged two baseline measurements in the sleep laboratory, after which the medication was administered for 8 days. On the last 2 days of the treatment, polysomnographic leads were once again recorded in the sleep laboratory. The patients received either the beta-blocker metoprolol (1 x 100 mg/day) or the angiotensin-converting enzyme inhibitor cilazapril (1 x 2.5 mg/day). Systolic and diastolic blood pressure were decreased by both substances as expected. Total sleep time was 358 (233-425) min vs. 332 (255-383) min in the metoprolol group and 368 (295-424) min vs. 341 (265-434) min in the cilazapril group which is statistically not different between the two groups nor between the proportions of non-REM and REM sleep.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of antihypertensive drug therapy on sleep pattern and sleep apnea activity. 182 81

A review of the literature shows that more than 50% of examined patients suffering from coronary heart disease were also suffering from sleep-related apnea. We were able to diagnose a pathological sleep apnea in 9 out of 25 patients (36%) suffering from an angiographically confirmed coronary 2-vessel and 3-vessel disorder. Patients with this combination--this is the hypothesis derived from our study--are at risk due to nocturnal apnea-induced myocardial ischaemia and rhythmic disorders. In 15 patients with sleep apnea and coronary heart disease or small vessel disease, nocturnal polysomnography was conducted, in parallel a 6-channel ECG was recorded. The apnea index (second night) was on the average 33 phases/h, the maximal duration of an apnea phases being 120 seconds. The minimal blood gas saturation recorded during sleep was between 46 and 89% (median 76.0%). In 4 of the 15 patients it was possible to confirm myocardial ischaemia (correlated via REM and also via NREM) with a maximum duration of 60 seconds, mainly during the phases of maximal apnea activity and blood gas desaturation. On comparing the ventricular arrhythmias waking/sleep, the Lown class did not change in 12 patients; there was deterioration in 2 patients and in one patient a qualitative improvement during the sleep phase. Patients suffering from sleep-related respiratory disorders and coronary heart disease are at cardiac risk, the more so since long-lasting apneas can lead to conditions of hypoxia at the heart in pre-existing changes in the coronary arteries, restricted coronary reserves and reduced tolerance to hypoxia. Such hypoxia can in turn induce enhanced electrical instability and a disturbance of the contractile function.
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PMID:[Sleep-related respiratory disorders and coronary heart disease]. 186 2

Fifty-seven patients with obstructive sleep apnoea (OSA) were treated for at least six months with nasal continuous positive airway pressure (CPAP). At follow-up, sleep studies were performed in which CPAP was not used for the first half of the night. We compared the severity of OSA at follow-up without CPAP to the severity of OSA during the patient's initial diagnostic study. Apnoea and hypopnoea index (AHI) fell from 41.4 +/- 7.5 (mean +/- 95% CI) to 34.8 +/- 7.9 (p = 0.06 by Wilcoxon test) and minimum oxygen saturation rose from 71.6 +/- 3.2 to 78.5 +/- 2.6 (p less than 0.001). Some of this change may have been due to reduced REM sleep in the follow-up study (10.5 +/- 2.1% Total Sleep Time vs 7.4 +/- 2.4% TST, p less than 0.05). Long-term nasal CPAP was not associated with any reduction of obesity (BMI before CPAP 31.9 +/- 1.0, after CPAP 31.7 +/- 1.0 (p = 0.39). Systolic arterial pressure fell (before CPAP 143.0 +/- 4.5 mmHg, after CPAP 136.3 +/- 4.6, p less than 0.05) but diastolic pressure did not (before CPAP 88.5 +/- 3.0 mmHg, after CPAP 85.6 +/- 2.9 mmHg, p = 0.11). We concluded that the effect of CPAP treatment for six or more months was a small fall in AHI and a small rise in minimum SaO2, but that this would be of marginal clinical significance, and may be artefactual.
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PMID:Long-term nasal CPAP does not ameliorate obstructive sleep apnoea. 187 51

Previous investigators have demonstrated in patients with obstructive sleep apnea that weight reduction results in a decrease in apnea severity. Although the mechanism for this decrease is not clear, we hypothesize that decreases in upper airway collapsibility account for decreases in apnea severity with weight loss. To determine whether weight loss causes decreases in collapsibility, we measured the upper airway critical pressure (Pcrit) before and after a 17.4 +/- 3.4% (mean +/- SD) reduction in body mass index in 13 patients with obstructive sleep apnea. Thirteen weight-stable control subjects matched for age, body mass index, gender (all men), and non-REM disordered breathing rate (DBR) also were studied before and after usual care intervention. During non-REM sleep, maximal inspiratory airflow was measured by varying the level of nasal pressure and Pcrit was determined by the level of nasal pressure below which maximal inspiratory airflow ceased. In the weight loss group, a significant decrease in DBR from 83.3 +/- 31.0 to 32.5 +/- 35.9 episodes/h and in Pcrit from 3.1 +/- 4.2 to -2.4 +/- 4.4 cm H2O (p less than 0.00001) was demonstrated. Moreover, decreases in Pcrit were associated with nearly complete elimination of apnea in each patient whose Pcrit fell below -4 cm H2O. In contrast, no significant change in DBR and a minimal reduction in Pcrit from 5.2 +/- 2.3 to 4.2 +/- 1.8 cm H2O (p = 0.031) was observed in the "usual care" group. We conclude that (1) weight loss is associated with decreases in upper airway collapsibility in obstructive sleep apnea, and that (2) the resolution of sleep apnea depends on the absolute level to which Pcrit falls.
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PMID:Effect of weight loss on upper airway collapsibility in obstructive sleep apnea. 189 85

Nasal CPAP has been shown to improve nocturnal asthma in those patients with associated sleep apnea. We studied seven nonapneic, nonsnoring asthmatics to determine the effect of CPAP in this patient population. On the CPAP night vs the baseline night, there was a significant worsening of sleep architecture. This included increased awake time and decreased REM sleep. For the group, the overnight decrement in FEV1 was not improved. Of interest, two patients did have a marked improvement in FEV1 associated with improved oxygen saturation on the CPAP night. These individuals were restudied only on supplemental oxygen. This intervention also improved the overnight FEV1 and allowed the patients to have better sleep compared to the CPAP night. We concluded that CPAP is associated with disrupted sleep architecture in nonapneic asthmatics and nocturnal oxygen desaturation may play a role in the development of nocturnal asthma.
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PMID:Nasal CPAP in nonapneic nocturnal asthma. 191 51

To study the effect of apnea and hypoventilation-induced hypoxemia on the heart, we carried out polysomnographic recordings over 4 nights with electrocardiographic tracings in 30 patients with and without coronary heart disease. Evaluations of the data were based on the 2nd and 4th nights. In six subjects, five with coronary heart disease, we found 85 episodes of nocturnal ischemia, mainly during REM sleep (83.5%), high apnea activity, and sustained and progressive hypoxemia. Complex ventricular ectopy was observed in 14/13 patients (nights 2/4) and repetitive ventricular ectopy in 5/3. There was no significant difference in the quality and quantity of ventricular ectopy during wake and sleep states between the CHD group and the control group. In one patient ventricular bigeminy was observed only at a threshold of SaO2 below 60%. Bradyarrhythmia was made evident in four subjects from the CHD group and correlated mainly with apnea activity. We suppose that patients with sleep apnea and CHD are at cardiac risk because coronary heart disease can be aggravated by insufficient arterial oxygen supply due to cumulative phase of apnea and hypoventilation. The reduced hypoxic tolerance of the heart may lead to myocardial ischemia and increased electrical instability.
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PMID:Nocturnal myocardial ischemia and cardiac arrhythmia in patients with sleep apnea with and without coronary heart disease. 192 Dec 30

Arterial blood pressure patterns in 12 men with sleep apnea and arterial hypertension were studied at baseline and after 6 months' therapy with nasal continuous positive airway pressure (nCPAP). Preexisting antihypertensive medication was discontinued 1 week before baseline measurements. Weight did not change during the study period; body mass index was 29.3 (range, 25.4-38.5) vs. 29.3 (25.0-38.5). During therapy the apnea index decreased from 58 (range 30-73) to 2 (range 0-7) apneic episodes per hour (p less than 0.01). Intra-arterial systolic (BP sys.) and diastolic (BP dias.) blood pressure and heart rate decreased during therapy (p less than 0.001). Mean values +/- 95% confidence intervals were as follows: BP sys., 147.1 (+/- 1.6) mm Hg vs. 126.4 (+/- 1.5) mm Hg; BP dias., 81.6 (+/- 0.8) mm Hg vs. 69.4 (+/- 0.6) mm Hg; heart rate, 68.8 (+/- 0.7) beats/min vs. 65.4 (+/- 0.7) beats/min. Furthermore, the variability of these parameters decreased during therapy: variability BP sys., 53.8 (+/- 1.1) mm Hg vs. 25.6 (+/- 1.1) mm Hg; variability BP dias., 35.6 (+/- 0.7) mm Hg vs. 17.9 (+/- 0.7) mm Hg; variability of heart rate, 28.1 (+/- 0.7) beats/min vs. 14.9 (+/- 0.7) beats/min (p less than 0.001). During treatment we found that blood pressure scores already dropped during the awake phase, with a further decrease during non-REM and REM sleep (p less than 0.001). Our results, which demonstrate the reversibility of high blood pressure upon treatment of sleep apnea, indicate that sleep apnea can be an etiological factor in hypertension. Sleep apnea should therefore be considered in the differential diagnosis of arterial hypertension.
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PMID:Blood pressure and sleep apnea: results of long-term nasal continuous positive airway pressure therapy. 193 70

Polysomnographic studies were performed in 6 patients with obstructive sleep apnoea syndrome (OSA). The sleep study consisted of: electroencephalography, electromyography, electrooculography, electrocardiography, pulse oximetry and observation of respiration. During day multiple sleep latency tests were performed. In all patients fragmentation of sleep with prevalent stages 1. and 2. of NREM and occasionally deep sleep and REM phase were observed. Concomitantly with the appearance of electrophysiologic sleep stages the muscle tone decreased and episodes of obstructive apnoea occurred. The periods of sleep and apnoea alternated with wakefulness and breathing. In MSLF the mean latency was 3 +/- 2 min. In OSA syndrome episodes of obstructive sleep apnoea cause sleep fragmentation and prevalence of light sleep stages. Excessive daytime somnolence observed in this syndrome is caused by sleep disturbances. MSLT demonstrated pathologic hypersomnolence in OSA syndrome.
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PMID:[Electrophysiological recording of nocturnal sleep and the multiple sleep latency test in obstructive sleep apnea syndrome]. 196 75

Two polysomnographic studies were performed in 35 subjects who had a clinical suspicion of sleep apnea syndrome: one study was done at night (N) (from 10:00 p.m. to 8:00 a.m.) and the other during the day (D) starting after lunch (from noon to 5:00 p.m.). N and D sleep studies were performed in random order at a minimal interval of 36 h. No treatment (drug, CPAP) was initiated between the two studies. Both studies included the recording of sleep stages (EEG, EOG, EMG), nasal and mouth flows, thoracoabdominal movements, electrocardiogram, and SaO2 (ear oximetry). D sleep was present in all but one subject. As expected, the total sleep time (TST) was significantly shorter during the D than during the N study (2.6 +/- 0.2 and 6.2 +/- 0.2 h, respectively, mean +/- SEM, p less than 0.001, Wilcoxon's signed-rank test). Stages III-IV and REM were significantly less represented during the D (13.1 +/- 2.4 and 7.7 +/- 1.3%, respectively) than during the N study (18.5 +/- 1.7 and 15.3 +/- 0.8%, p less than or equal to 0.005). From the results of the N study, the diagnosis of sleep apnea syndrome (apnea index greater than 5 and/or apnea + hypopnea index greater than 10) was made in 25 patients, and it was confirmed by the same criteria in 22 by the D sleep recording. There was a significant correlation between the N and D values for these indices (r greater than or equal to 0.9, p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Validity of diurnal sleep recording in the diagnosis of sleep apnea syndrome. 202 48

Daytime somnolence and fatigue are frequently ignored symptoms in acromegaly. To examine whether sleep apnea or other abnormalities in the sleep structure is the underlying cause, 9 young patients with active untreated acromegaly for 2-7 years were studied with all night polysomnography. It revealed a decrease in REM sleep time in all the acromegalics compared to age- and sex-matched normal subjects (p less than 0.001) and also a reduction in delta sleep (p less than 0.05). None had obstructive sleep apnea. At reexamination 12-15 months posttreatment the daytime sleepiness had disappeared in all patients. REM sleep time increased in all patients (p less than 0.001) to normal level; delta sleep time increased moderately (p less than 0.05). Thus sleepiness in patients with high fasting level of growth hormone (GH) is not related to sleep apnea but more likely to a reduced amount of REM sleep time. By normalizing the GH concentration, REM sleep time became normal and the daytime sleepiness disappeared in all patients.
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PMID:Sleep in acromegaly before and after treatment with adenomectomy. 204 66


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