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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The increased mortality among patients with obstructive sleep apnoea syndrome has been explained in part by the increased incidence of pulmonary hypertension and coronary artery disease (CAD). A decreased heart rate variability has been shown to be associated with an increased mortality as well. We therefore screened 53 patients for sleep-related breathing disorders (SRBD) and heart rate variability (HRV) during the sleeping period. Standard time domain parameters were compared in a univariate multifactorial model for patients with an oxygen desaturation index (ODI) of more or less than 5 including the factors CAD, diabetes and beta-blocker use. The percentage of differences between RR-intervals that differ more than 50 ms (pNN > 50: 9.0 +/- 11.1% vs 19.2 +/- 22.2%; p < 0.05) as well as the root mean square of these differences (rMSSD: 38.0 +/- 29.0 msec vs 59.2 +/- 51.5 msec; p < 0.05) were significantly decreased in patients with SRBD. These results favour HRV for inclusion in future risk stratification models in patients with sleep-related breathing disorders.
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PMID:[Heart rate variability in patients with sleep associated breathing disorders]. 934 Jun 28

Sleep apnea is a surprisingly common disorder in end-stage renal disease (ESRD) and chronic renal failure. The symptoms of sleep apnea frequently go unreported or may be misdiagnosed as uremia, depression, chronic illness, or insomnia. A review of the literature was performed to define the prevalence, morbidity, and treatment of sleep apnea syndrome in the ESRD patient. Sleep apnea occurs in at least 60% of ESRD patients. The known complications of sleep apnea include arrhythmias, pulmonary hypertension, and systemic hypertension. In addition, sleep apnea has been implicated in coronary artery disease and strokes. The contribution of sleep apnea to the high mortality from cardiac disease and stroke in peritoneal dialysis and hemodialysis patients is unknown. The causes of the increased prevalence of sleep apnea in ESRD patients are unknown and likely differ from the general population, but the treatment is similar. The literature suggests that modality of renal replacement therapy does not matter; however, large nocturnal volume peritoneal dialysis may worsen sleep apnea. Renal transplantation may be curative. In conclusion, sleep apnea may be an under-diagnosed disease in patients on dialysis. There are significant reasons to suspect that sleep apnea may worsen the morbidity and mortality of ESRD, and there are potential successful therapies.
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PMID:Sleep apnea in renal failure. 936 Jun 57

There have been very few studies assessing the long-term physiological effects of nasal continuous positive airway pressure (CPAP) for the obstructive sleep apnoea syndrome. We therefore investigated prospectively the evolution of lung function, arterial blood gases and pulmonary haemodynamics in patients with this syndrome treated with CPAP. Sixty five patients were included. The mean duration of home treatment with nasal CPAP was 64+/-6 months. Most of the patients (77%) were smokers at the baseline assessment. We observed a small, but significant, decrease in forced expiratory volume in one second (FEV1) from 80+/-21% at baseline (t0) to 76+/-21% of the predicted value at the follow-up evaluation (t5) (p<0.01). Arterial oxygen tension (P[a,O2]) for the group as a whole remained stable (9.4+/-1.5 kPa (71+/-11 mmHg) versus 9.4+/-1.2 kPa (71+/-9 mmHg)). However, P(a,O2) increased in the subgroup of patients with hypoxaemia at t0 (n=23), from 7.8+/-0.7 kPa (59+/-5 mmHg) to 8.9+/-1.2 kPa (67+/-9 mmHg). Arterial carbon dioxide tension (P[a,CO2]) for the group as a whole increased slightly, but significantly, from 5.2+/-0.7 kPa (39+/-5 mmHg) to 5.4+/-0.5 kPa (41+/-4 mmHg) (p<0.05). Mean pulmonary artery pressure (Ppa) at rest did not change (16+/-5 mmHg versus 17+/-5 mmHg; NS) nor did exercising Ppa. In the 11 patients with pulmonary hypertension at t0, Ppa was 24+/-5 mmHg at t0 versus 20+/-7 mmHg at t5 (NS). We conclude that the significant decrease of forced expiratory volume in one second after 5 yr follow-up was related to a high percentage of smokers and exsmokers in the study population. Daytime arterial oxygen tension and pulmonary artery pressure remained stable in an unselected series of 65 obstructive sleep apnoea syndrome patients treated for 5 yrs with nasal continuous positive airway pressure, unlike arterial carbon dioxide tension, which increased by a small, but significant, amount.
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PMID:Five-year effects of nasal continuous positive airway pressure in obstructive sleep apnoea syndrome. 942 98

Patients with chronic obstructive pulmonary disease (COPD) become hypoxemic during sleep, particularly during rapid eye movement (REM) sleep. Those who are most hypoxemic when awake experience the most severe hypoxemia during sleep. The major cause of REM hypoxemia is hypoventilation, with additional contributions from alteration in ventilation/perfusion matching and functional residual capacity (FRC) reduction. REM hypoxemia probably contributes to the development of pulmonary hypertension and polycythemia and may predispose to cardiac arrhythmias in some patients. The most effective form of therapy is nocturnal oxygen therapy, but the indications for the use of nocturnal oxygen therapy are entirely based on daytime oxygenation levels. Routine polysomnography is not indicated in patients with COPD but should be performed in patients who have symptoms suggestive of coexisting sleep apnea/ hypopnea syndrome.
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PMID:Sleep in patients with chronic obstructive pulmonary disease. 955 22

Obstructive sleep apnoea (OSA) is described by some authors as a potentially lethal disease and by others as an almost harmless condition. Excessive daytime sleepiness, neuropsychological dysfunction, altered quality of life, cardiovascular disease (systemic and pulmonary hypertension, cardiac arrhythmias, stroke and ischaemic heart disease) and increased mortality have been described as OSA complications. There is little argument that OSA may determine sleepiness, alter cognitive functions, and worsen quality of life, although with great interindividual variability: this should induce OSA to be considered an important illness per se, since sleepiness in OSA was shown to lead to important consequences, like road traffic accidents. Besides, OSA may interact with coexisting cardiac and respiratory disease and favour the appearance of heart and respiratory failure. Therefore, OSA is certainly also worth careful consideration as an important aggravating factor of other diseases. The evidence that obstructive sleep apnoea is an independent risk factor for cardiovascular complications other than owing to the recurrent transient blood pressure surges associated with apnoeas during sleep, and for an increased mortality is more conflicting. More studies are necessary to identify which characteristics of obstructive sleep apnoea may be considered important markers of its severity and as risk factors for different possible complications.
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PMID:What is the evidence that obstructive sleep apnoea is an important illness? 1006 35

The prevalence of sleep apnea syndrome (SAS) is approximately 7.5% in Japanese adults aged 18-68 years old. SAS is characterized by repeated episodes of apnea, especially obstructive apnea, during sleep. Severe SAS has life-threatening complications such as pulmonary hypertension, arrhythmias, right heart failure or brain damage, which could be caused by hypoxemia and/or hypercapnia. Upper airway relaxation is responsible for the obstruction during apnea, and an increase in the activities of the upper airway muscles dilates and stiffens the upper airway wall. Maintaining the activities of the upper airway muscles may contribute to keeping the airway patent. Submental electrical stimulation of the upper airway muscles would be a novel treatment method for obstructive apnea.
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PMID:New strategies of screening and treatment for sleep apnea syndrome. 1032 56

The effect of sleep stage change on pulmonary circulation has not been well documented in patients with obstructive sleep apnea syndrome (OSAS). We investigated whether or not stage-specific change can affect pulmonary artery pressure (Ppa) in patients with OSAS. Thirty-one patients with OSAS underwent right cardiac catheterization in the daytime and the following night, including 19 patients in whom Ppa could be measured throughout non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. Ten of the 19 patients had daytime pulmonary hypertension (PH) defined by a mean Ppa (Ppa) >/= 20 mm Hg. Then we analyzed Ppa response to hypoxia spontaneously occurring during the period of sleep apnea. The slopes of the regression lines between arterial oxygen saturation measured by pulse oximeter (SpO2) and Ppa curves were almost the same in both NREM and REM patient groups with or without daytime PH, whereas the response curve was significantly shifted upward in REM compared with NREM patients with daytime PH. Furthermore, Ppa was elevated more markedly in association with REM burst, phasic REM, compared with tonic REM. We conclude that vascular tone of pulmonary artery could be elevated in association with REM sleep which is independent of the degree of hypoxia, and that this state-specific change is manifested in patients with daytime PH.
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PMID:Manifestation of pulmonary hypertension during REM sleep in obstructive sleep apnea syndrome. 1035 16

Chronic continuous hypoxia increases haematocrit and causes right ventricular hypertrophy and pulmonary hypertension. In obstructive sleep apnoea, the exposure to hypoxia is intermittent rather than continuous but the effects of chronic intermittent hypoxia on haematocrit and right ventricular mass are unclear. Wistar rats were exposed to alternating periods of hypoxia and normoxia twice per min for 8 h per day for 5 weeks in order to mimic the intermittent hypoxia of obstructive sleep apnoea in humans. Haematocrit was significantly raised at day 7, 14, 21, 28 and 35 of the treatment period. At the end of the treatment, there was a significant increase in right ventricular mass. Therefore, chronic intermittent hypoxia increases haematocrit and right heart mass. These results suggest that the raised haematocrit and pulmonary arterial pressure observed in some cases of obstructive sleep apnoea in humans may be caused by intermittent nocturnal hypoxaemia.
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PMID:Chronic intermittent hypoxia increases haematocrit and causes right ventricular hypertrophy in the rat. 1050 79

There is a renewed interest in pulmonary hypertension (PH) complicating obstructive sleep apnoea (OSA). The prevalence of PH in populations of patients with less severe OSA was documented to be around 10%. The most recent data from both catheterization and echocardiographic studies indicate that as many as 40% of patients with OSA have PH. It has been shown that non-obese patients with normal respiratory function tests can develop pulmonary hypertension. One of the other possible mechanisms involved may be the presence of heightened pulmonary artery pressure response to hypoxia. There are now data available to indicate that treatment with nasal CPAP can decrease or even normalize pulmonary artery pressure in patients with sleep apnoea.
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PMID:Pulmonary artery pressure in sleep apnoea and snoring. 1060 98

Endothelin-1 (ET-1), a potent vasoconstrictor, is released mainly by vascular endothelial cells under the influence of hypoxia and other stimuli. ET-1 is related to endothelial dysfunction, as well as arterial and pulmonary hypertension, all of which are thought to be associated with obstructive sleep apnoea (OSA). This study evaluated venous plasma concentrations of ET-1 and noradrenaline and 24-h systemic blood pressure in 29 patients with OSA (age=56.9+/-1.6 yrs; body mass index=29.5+/-0.7 kg x m2 (mean+/-SEM)). Blood samples were taken in the morning, evening and during sleep. In the same way, the patients were assessed during a night of continuous positive airway pressure (CPAP) and after 13.9+/-1.4 months while still on CPAP. ET-1 levels were compared to those of control subjects, who were selected from in- and outpatients and were matched to patients for age, sex, presence of arterial hypertension and coronary artery disease. ET-1 plasma levels were not elevated in the patients compared to the controls (41.6+/-2.2 and 44.9+/-1.3 pg x mL(-1), respectively, p=0.20). The ET-1 concentration did not change significantly, neither during sleep nor in the first night on CPAP therapy, nor under long-term treatment with CPAP. ET-1 neither correlated to the severity of OSA nor to that of systemic hypertension. The results suggest that endothelin-1 does not play a crucial role in the pathophysiology of obstructive sleep apnoea.
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PMID:Endothelin-1 plasma levels are not elevated in patients with obstructive sleep apnoea. 1110 27


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