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

Holter recordings of subjects apparently free from cardiovascular disease have demonstrated a moderate sinusal and nodal depression during sleep. This depression does not seem to be sufficient to create overt cardiovascular disorders in apparently healthy subjects, but it may aggravate or even reveal an underlying disorder of rhythm or conduction in elderly people or in patients taking drugs that potentiate its effects. In sleep apnea syndrome prolonged episodes of apnea may produce a paroxysmal, then permanent increase in pulmonary arterial pressure, which may lead to right heart failure. These episodes also increase the pre- and after-load and decrease myocardial contractility, thus facilitating the occurrence of left ventricular failure, potentiated by systemic arterial hypertension, overweight or even coronary disease, all conditions that are often present in these subjects. Arterial hypertension is so frequent in sleep apnea syndrome that some authors advocate a systematic search for the syndrome by Holter recordings before the hypertension is pronounced "essential". All studies confirm the existence of rhythm and conduction disorders directly related to apneic episodes. These disorders decrease or regress after a well-conducted treatment of the sleep apnea syndrome. They are mainly of the "hypokinetic" type, created by depression of sinus activity and conduction pathways. Their frequency, their severity and, in particular, the risk of sudden death they carry seem to have been overestimated, especially since no evidence has ever been produced of a potentially lethal rhythm disorder occurring during sleep apnea. Nevertheless, there is no certainty that these patients are not at risk of sudden death related to their sleep apnea syndrome.
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PMID:[Cardiovascular disorders during sleep]. 214 78

The most common causes of hypoxic cor pulmonale are chronic bronchitis and emphysema. Although the clinical situation in some patients is characterized early by hypoxemia, oedema is rare in patients with an arterial pO2 above 60 mm Hg. The presence of oedema can be regarded as an unfavorable prognostic indicator. For many years, peripheral oedema had been considered an expression of congestive cardiac failure; it may be assumed, however, that neither right nor left ventricular failure is prerequisite to the development of oedema. Oedema formation can be attributed to excessive retention of salt and water or a redistribution of body water into the extracellular compartment. Hypercapnia and acidosis affect direct stimulation of renal hydrogen ion secretion. The resulting electrochemical imbalance is compensated by reabsorption of sodium. Hypercapnia and, in acute phases possibly, hypoxia lead to a fall in renal blood flow mediated by alpha-adrenergic stimulation through activation of the renin-angiotensin-aldosterone system. An increase in plasma ADH may also contribute to development of oedema. The development of cor pulmonale or respiratory insufficiency can be enhanced by nocturnal hypoventilation and hypoxia during sleep as well as by sleep apnoea. Nocturnal hypoxia, smoking and reduced oxygen tension in the relevant kidney cells responsible for erythropoietin release promote the occurrence of secondary polycythaemia. For treatment of acute exacerbations in cor pulmonale associated with infections bronchitis antibiotics such as amoxycillin and cotrimoxacol are drugs of first choice. While the use of digoxin is of doubtful value, the cautious administration of diuretics may bring symptomatic relief. In addition to physiotherapy, beta-2-selective bronchodilators and nebulized bronchodilator therapy can be useful; theophyllines dilate airways and increase cardiac output but they can cause arrhythmias and a deterioration of arterial blood gases in hypoxic patients. If the patient has been treated chronically with corticosteroids, the dosage will have to be incremented; if asthma is suspected, corticosteroid treatment is essential. Controlled oxygen therapy is the most important single therapy aimed at relief of severe arterial hypoxaemia. Oxygen should be titrated initially (for the first one or two days) to achieve an arterial tension of at least 48 mm Hg. Thereafter, the oxygen flow should be increased to yield an arterial tension in excess of 60 mm Hg during continued treatment for two to three weeks.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypoxic cor pulmonale: a review. 294 54

The therapeutic efficacy and the incidence of significant side effects of nasal continuous positive airway pressure (nCPAP) treatment was investigated in 1140 patients with sleep-related apnoea (1089 men, 51 women; mean age 53.2 +/- 9.2 [16-84] years). All had been treated for the condition with nCPAP at the Marburg University Medical Polyclinic between 1986 and 1992. The mean number of attacks of apnoea and/or hypopnoea per hour of sleep ("respiratory disturbance index", RDI) was 45.8 +/- 25.6 before treatment and 3.5 +/- 4.8 under nCPAP. 21.1% of patients had an apnoea index of no more than 10/h. 11.6% an RDI of no more than 15/h. The average airway pressure was 8.7 (3-18) cm H2O. The treatment was successful in 1023 patients and these decided to continue the treatment long-term. The RDI could not be lowered under 10/h in 63 patients, while 4 patients declined ambulant treatment despite the demonstrated efficacy of nCPAP. Three patients developed acute left ventricular failure in the initial phase of the treatment, while in another 16 patients long-persisting central hypoventilation was shown to occur. These data show that treatment with nCPAP can be employed for all degrees of severity of obstructive sleep apnoea. However, because of the potentially life-threatening side effects, the introduction of the treatment must be undertaken in the sleep laboratory under continuous monitoring.
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PMID:[Nasal continuous positive airway pressure (nCPAP) therapy in obstructive sleep breathing disorders]. 778 9

We reviewed clinical data, autopsy reports, and microscopic slides on 10 patients with sleep apnea/obesity hypoventilation syndrome (SA/OHS) to define the cardiopulmonary pathological features and establish clinicopathologic correlations. Ten obese (>136 kg) patients without SA/OHS were studied as controls. Patients with SA/OHS exhibited biventricular cardiac failure and pulmonary hypertension with a higher prevalence of moderate/severe pulmonary hemosiderosis (8 v 0 patients), alveolar hemorrhage (7 v 4 patients), capillary proliferation (4 v 0 patients), iron encrustation of elastica (1 v 0 patients) and medial hypertrophy of muscular pulmonary arteries (11.9 +/- 2.4 v 9.7 +/- 1.6%) (P < .05). In two patients capillary proliferation resembled capillary hemangiomatosis. Mean right ventricular thickness was higher in the SA/OHS group (0.71 +/- 0.17 v 0.42 +/- 0.1 cm) (P < .01). Four patients with SA/OHS and three controls had moderate/severe myocardial fibrosis. Biventricular cardiac failure caused death in seven patients with SA/OHS. Hypoxia is probably the most important cause of pulmonary hypertension, arterial muscularization, and right ventricular hypertrophy in SA/ OHS. Left ventricular failure in some SA/OHS patients may be the result of hypertensive cardiac disease. In others, the etiology of left ventricular failure was not determined morphologically, suggesting functional abnormalities related to obesity and/or apneic episodes.
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PMID:Cardiopulmonary pathology in patients with sleep apnea/obesity hypoventilation syndrome. 938 47

The effect of inhaled long-acting beta 2-agonists on obstructive sleep apnoea syndrome (OSAS) is unknown, though from the pharmacological point of view both therapeutic and adverse effects might be discussed. The purpose of this study was to obtain data on the efficacy and safety of Salmeterol in patients with OSAS. In a randomised, double-blind, placebo-controlled, crossover study effects of Salmeterol were investigated in 20 patients with OSAS: 4 female, 16 male; age 53.0 +/- 7.8 years, body mass index (BMI) 28.0 +/- 3.0 kg.m-2; apnoea hypopnoea index (AHI) 35.6 +/- 17.8 h-1. Patients with asthma, chronic obstructive pulmonary disease (COPD), and left heart failure were excluded. Placebo or verum (50 micrograms Salmeterol) were administered at 7 p.m. by metered dose inhaler and spacer device. All patients underwent full polysomnography during baseline, placebo, and verum night. Statistical analysis was performed by Student's t-test (p < 0.05). Between placebo and verum there were no differences in total sleep time, sleep stages, apnoea index (AI), AHI, and nadir SaO2. There was, however, a significant deterioration of mean SaO2 (placebo 93.1 +/- 2.0 vs Salmeterol 92.5 +/- 2.2%) and of relative time spent with SaO2 < or = 90% (placebo 13.1 +/- 14.5 vs Salmeterol 19.5 +/- 20.8%), as well as a significant increase in heart rate (placebo 63.1 +/- 9.2 vs Salmeterol 65.6 +/- 9.3 h-1). Thus, in patients with OSAS Salmeterol had no adverse effect on quality of sleep, AI or AHI. The slight increase in heart rate and the deterioration of oxygen saturation are clinically irrelevant. The latter might be due to ventilation-perfusion-mismatch. This study demonstrates that Salmeterol has no influence on obstructive sleep apnoea and hypopnoea, but on the other hand provides an acceptable safety profile in OSAS. This might be of special importance in patients suffering from both OSAS and obstructive airway disease.
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PMID:[Effect of salmeterol in obstructive sleep apnea syndrome]. 954 Mar 64

Different pathophysiological mechanisms underlie the morbid associations observed between sleep apnea syndrome (SAS) and cardiovascular disease. Cardiovascular responses to apnea can be divided into acute cardiovascular modifications following each nocturnal respiratory event and chronic adaptations of the cardiovascular system. The same stimuli always trigger acute cardiovascular response: hypoxemia, hypercapnea, changes in the intra-thoracic pressure, micro-arousals. Each obstructive or central respiratory event is associated with a peak in blood pressure, changes in the heart rate, generally bradycardia at onset of apnea and tachycardia when respiration is renewed. Oxygen desaturation is the strongest stimulus explaining the observed acute cardiovascular responses. When these stimuli are repeated every night, the cardiovascular system adapts with a higher sympathetic tone and lower parasympathetic tone during the diurnal period. Baroreceptors also become less sensitive in apneic patients. Finally, endothelial function is altered in SAS patients with a desensitization of the alpha and beta-2 adrengeric receptors, altered NO-dependent vasodilatation, and hypersensitivity to vasoconstriction induced, for example, by angiotensin 2. The cardiovascular morbidity associated with SAS is currently thought to concern the development of diurnal hypertension (dose-effect response), left ventricular failure, higher risk of coronary or cerebral events. Very recently, epidemiological studies suggested that continuous positive pressure ventilation in SAS patients can reduce the cardiovascular risk.
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PMID:[Pathophysiology of cardiovascular risk in sleep apnea syndrome (SAS)]. 1238 23

Nocturnal breathing disorders are rather frequently observed in patients with left ventricular failure. When an obstructive sleep apnoea is present, nCPAP therapy is the preferred treatment method; the treatment probably also positively affects the left ventricular failure itself. Central sleep apnoea and in particular, the special form Cheyne-Stokes respiration have an unfavourable prognosis with increased mortality in patients with left ventricular failure. The indication for either nCPAP therapy or adaptive servoventilation cannot yet be regarded as verified and is the subject of ongoing clinical studies.
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PMID:[Sleep apnoea and left ventricular failure]. 1798 42

Chronic congestive heart failure is a highly prevalent and progressive disorder associated with excess morbidity and mortality; it has huge economic impact. Left heart failure may be systolic or may occur as isolated diastolic dysfunction. The diastolic form predominates in older people. Sleep disorders are frequent in both types. Most systematic studies have been performed in patients with systolic heart failure. Prospective studies show the presence of obstructive and central sleep apnea, periodic limb movements, and significant alterations in sleep architecture, characterized by poor efficiency, excess stage 1 and arousals, and lack of deep sleep. Both obstructive sleep apnea and central sleep apnea occur in patients with heart failure and have been shown to be associated with excess mortality. Obstructive sleep apnea is best treated with continuous positive airway pressure (CPAP) devices. Central sleep apnea is also best treated with CPAP, but only about 50% of the patients are considered responders. Survival improves when heart failure patients are effectively treated with CPAP for both central and obstructive sleep apnea. A new positive airway pressure device, a pressure support servo-ventilator, is the next best choice for heart failure patients whose central sleep apnea does not respond to CPAP. Nocturnal oxygen should be used for patients whose central sleep apnea does not respond to positive pressure devices. Both periodic limb movements and insomnia could have adverse hemodynamic consequences for the failing heart. There are no guidelines or long-term studies regarding treatment of these conditions in heart failure. For restless legs syndrome with or without periodic limb movements, pramipexole and ropinirole have been approved. Treatment of insomnia comorbid with heart failure depends on the cause. In the absence of any known cause, a trial of ramelteon is the first choice.
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PMID:Sleep dysfunction in heart failure. 1878 5