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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relationship between obstructive sleep apnea syndrome (OSAS), cardiac arrhythmias, and conduction disturbances in adults remains controversial. Early studies showed a higher prevalence than more recent and designed epidemiological studies. To clarify the actual prevalence of cardiac arrhythmias and conduction disturbances in patients referred for assessment of OSAS, a prospective cohort study was conducted: 147 consecutive patients (103 men; mean age of 54.5 +/- 10.7 years) underwent time-synchronized polysomnography and ECG Holter monitoring. OSAS was diagnosed in 66 (44.9%) of them based on an apnea hypopnea index (AHI) > or = 10. Prevalence of heart failure, of prior myocardial infarction, of hypertension, and of ventricular arrhythmias were similar in patients with or without OSAS. Nocturnal paroxysmal asystole was significantly more prevalent in OSAS patients (10.6 vs 1.2%; P < 0.02) and the number of episodes of bradycardia and pauses increased with the severity of the syndrome. Almost all bradycardic events occurred in patients with severe OSAS (AHI > 30), prolonged periods of arterial oxyhemoglobin desaturation, and low diurnal awake PaO2. Moreover, using heart rate variability analysis, nocturnal sinusal dysfunction contrasted with a blunted diurnal parasympathetic modulation of the sinus node. Frequent nocturnal nonsustained supraventricular tachycardias were predominantly found in patients with severe sleep related breathing disorders; however, an increased risk of ventricular arrhythmias was not found. Under continuous positive airway pressure treatment, the 1-year follow-up of OSAS patients with nocturnal pauses did not reveal any arrhythmic event justifying a specific intervention.
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PMID:Relationship among the severity of sleep apnea syndrome, cardiac arrhythmias, and autonomic imbalance. 1269 66

Sleep apnea is associated with several cardiovascular disease conditions. A causal relationship between sleep apnea and each of these diseases is likely, but remains to be proven. The clearest evidence implicating OSA in the development of new cardiovascular disease involves data that show an increased prevalence of new hypertension in patients with OSA followed over 4 years [3]. Circumstantial evidence and data from small study samples suggest that OSA, in the setting of existing cardiovascular disease, may exacerbate symptoms and accelerate disease progression. The diagnosis of OSA always should be considered in patients with refractory heart failure, resistant hypertension, nocturnal cardiac ischemia, and nocturnal arrhythmias, especially in individuals with risk factors for sleep apnea (e.g., central obesity, age, and male gender). Treating sleep apnea may help to achieve better clinical control in these diseases and may improve long-term cardiovascular prognosis.
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PMID:Cardiovascular consequences of obstructive sleep apnea. 1280 Jul 78

Sleep-disordered breathing, namely obstructive sleep apnea (OSA) and central sleep apnea (CSA), are both often encountered in the setting of heart failure (HF), and have distinct differences in terms of prevalence, pathophysiology and consequences. OSA is independently associated with an increased risk for cardiovascular disease and for congestive HF in the general population. It is conceivable that this breathing disorder may have particularly deleterious effects in patients with coexisting heart disease, especially in those with a failing heart. There are considerable data addressing the interaction between OSA and the cardiovascular system, which underscore the importance of an early detection of this breathing disorder, especially in patients with HF. CSA is generally considered a consequence rather than a cause of HF, and is correlated with the severity of hemodynamic impairment. However, when present, it is associated with increased arrhythmic risk and higher cardiac mortality. Potential mechanisms implicated in the genesis of this breathing pattern and the possible therapeutic options, which have been proven to be effective in the clinical setting, are discussed.
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PMID:Sleep-disordered breathing in heart failure: characteristics and implications. 1285 7

This mini-review summarizes the present knowledge regarding central oxygen-chemosensitive sites with special emphasis on their function in regulating changes in cardiovascular and respiratory responses. These oxygen-chemosensitive sites are distributed throughout the brain stem from the thalamus to the medulla and may form an oxygen-chemosensitive network. The ultimate effect on respiratory or sympathetic activity presumably depends on the specific neural projections from each of these brain stem oxygen-sensitive regions as well as on the developmental age of the animal. Little is known regarding the cellular mechanisms involved in the chemotransduction process of the central oxygen sensors. The limited information available suggests some conservation of mechanisms used by other oxygen-sensing systems, e.g., carotid body glomus cells and pulmonary vascular smooth muscle cells. However, major gaps exist in our understanding of the specific ion channels and oxygen sensors required for transducing central hypoxia by these central oxygen-sensitive neurons. Adaptation of these central oxygen-sensitive neurons during chronic or intermittent hypoxia likely contributes to responses in both physiological conditions (ascent to high altitude, hypoxic conditioning) and clinical conditions (heart failure, chronic obstructive pulmonary disease, obstructive sleep apnea syndrome, hypoventilation syndromes). This review underscores the lack of knowledge about central oxygen chemosensors and highlights real opportunities for future research.
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PMID:Oxygen-sensing neurons in the central nervous system. 1466 Apr 98

Breathing-related sleep disorders, particularly obstructive sleep apnea, have been largely undiagnosed in people with cardiovascular disease, probably due to limited health care provider awareness of the association between the two conditions. Solid evidence is emerging that the apneic events that occur during sleep lead to acute and chronic hemodynamic changes during wake time, including elevated sympathetic tone, decreased stroke volume and cardiac output, increased heart rate, and changes in circulating hormones that regulate blood pressure, fluid volume, vasoconstriction, and vasodilation. Obstructive sleep apnea is associated with known cardiovascular risk factors such as obesity and hyperlipidemia, and is considered by many sleep clinicians to be an independent risk factor for hypertension. Additionally, sleep apnea has been implicated in the pathogenesis of heart failure and stroke. Treatment with positive airway pressure during sleep eliminates the apneic events and the ensuing acute hemodynamic changes. Improvements in daytime blood pressure and left ventricular function also have been noted in persons with hypertension and heart failure. Because effective treatment is available for sleep apnea, this condition needs to be diagnosed and treated in persons with cardiovascular disease.
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PMID:Sleep-disordered breathing and the association with cardiovascular risk. 1501 52

Obstructive sleep apnoea (OSA) is a common entity in children, most present with sleep disturbances such as snoring, choking during sleep, enuresis, restless sleep, or apnoeic spells. Other symptoms include poor school performance, hyperactivity, failure to thrive, heart failure and cor pulmonale. Most authors would concur that the polysomnogram (PSG) is the gold standard for the diagnosis of OSA, and that adenotonsillectomy is the surgical procedure of choice, with high curative rates and relatively low morbidity. Close post-operative monitoring of all children with OSA cannot be over-emphasized. The focus has been, traditionally, to anticipate post-operative airway and respiratory complications in this group of children. We present 73 children with clinical OSA and 36 children with proven OSA on PSG, with only one child having respiratory complications (mixed apnoea), and all with uneventful recovery. In view of our low complication rates, low post-operative morbidity, cost and facility factor, the need for a mandatory overnight PSG pre-operatively is questioned, and clinical criteria for performing a PSG preoperatively are suggested.
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PMID:Paediatric obstructive sleep apnoea: is a polysomnogram always necessary? 1511 65

Previous small-scale studies of the effect of sleep-disordered breathing (SDB) on prognosis in congestive heart failure (CHF) are either lacking or conflicting. The aim of this study was to assess the impact of the presence and type of SDB on mortality in a patient group with severe CHF referred to a specialised heart failure centre. Out of 78 patients ((mean +/- SD) 53 +/- 9 yrs, left ventricular ejection fraction 19.9 +/- 7.2% and pulmonary capillary wedge pressure 16.5 +/- 8.3 mmHg) followed-up over a median period of 52 months, 29% had no apnoea (CHF-N), 28% had obstructive sleep apnoea (CHF-OSA) and 42% had central sleep apnoea (CHF-CSA). At 52 months, their overall mortality was 40%, and combined mortality and transplantation was 72%. Mortality rates were similar between the three apnoea groups. Survivors had a similar prevalence of SDB (71%) as the nonsurvivors (70%). Although a significant increase in mortality was evident at 500 days in those patients with either CHF-SDB or CHF-CSA as compared with CHF-N, this was not significant at final follow-up (52 months) using Kaplan Meier analysis. Multivariate analysis identified transplantation but not SDB type or severity as a significant predictor of survival. In conclusion, sleep-disordered breathing impacts upon early (500 day), but not long-term (52 month), mortality in a specialised heart failure centre.
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PMID:Increased long-term mortality in heart failure due to sleep apnoea is not yet proven. 1517 74

To analyze the function of cardiac autonomic regulation in patients with obstructive sleep apnea syndrome (OSAS), we enrolled 36 patients with OSAS and divided them according to the apnea hypopnea index (AHI) into 2 groups: Group I (n=19) had mild OSAS (AHI < 20) and Group II (n=17) had severe OSAS (AHI > or = 20). The findings were compared with those of 24 healthy control subjects who were matched for age, sex, blood pressure, and body mass index. All participants underwent 24-hour Holter monitoring, with continuous time-dependent and spectral analysis of heart rate variability. In addition, we performed arrhythmia analysis. Frequent or repetitive ventricular arrhythmias (> or = 30 premature ventricular beats/hour) were detected in 15 (42%) patients with OSAS and in 6 (25%) members of the control group. In both mild and severe OSAS, SDNN was significantly lower than in controls, and SDANN findings were similar. In mild OSAS, RMSSD values were not significantly lower than in controls, but in severe OSAS they were. The ULF, VLF, LF and LF/HF values of both groups of OSAS patients were significantly higher than those of controls, but their HF values were lower. The mean LF/HF ratio during the same period was significantly higher in Group II than in Group I and the control group. Our results suggest that cardiac autonomic activity may be altered in patients with OSAS throughout a 24-hour period, that this alteration occurs even in the absence of hypertension, heart failure, or other disease states, and that it is linked to the severity of OSAS.
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PMID:Cardiac autonomic activity in obstructive sleep apnea: time-dependent and spectral analysis of heart rate variability using 24-hour Holter electrocardiograms. 1521 22

Obstructive sleep apnea (OSA) is a common medical condition that occurs in approximately 5% to 15% of the population. The pathophysiology of OSA is characterized by repetitive occlusions of the posterior pharynx during sleep that obstruct the airway, followed by oxyhemoglobin desaturation, persistent inspiratory efforts against the occluded airway, and termination by arousal from sleep. Obstructive sleep apnea is associated with daytime sleepiness and fatigue, likely due to fragmented sleep from recurrent arousals. Substantial evidence shows that patients with OSA have an increased incidence of hypertension compared with individuals without OSA and that OSA is a risk factor for the development of hypertension. Recent studies show that OSA may be implicated in stroke and transient ischemic attacks. Obstructive sleep apnea appears to be associated with coronary heart disease, heart failure, and cardiac arrhythmias. Pulmonary hypertension may be associated with OSA, especially in patients with preexisting pulmonary disease. Although the exact cause that links OSA with cardiovascular disease is unknown, there is evidence that OSA is associated with a group of proinflammatory and prothrombotic factors that have been identified to be important in the development of atherosclerosis. Obstructive sleep apnea is associated with increased daytime and nocturnal sympathetic activity. Autonomic abnormalities seen in patients with OSA include increased resting heart rate, decreased R-R interval variability, and increased blood pressure variability. Both atherosclerosis and OSA are associated with endothelial dysfunction, increased C-reactive protein, interleukin 6, fibrinogen, and plasminogen activator inhibitor, and reduced fibrinolytic activity. Obstructive sleep apnea has been associated with enhanced platelet activity and aggregation. Leukocyte adhesion and accumulation on endothelial cells are common in both OSA and atherosclerosis. Clinicians should be aware that OSA may be a risk factor for the development of cardiovascular disease.
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PMID:Obstructive sleep apnea and cardiovascular disease. 1530 32

Sleep apnea syndrome (SAS) in patients with chronic heart failure (CHF) increases the risk of death. SAS was divided into 4 types: obstructive sleep apnea-hypopnea syndrome (OSAHS), upper airways resistance syndrome (UARS), central sleep apnea syndrome (CSAS), and sleep hypoventilation syndrome (SHVS). CSAS is caused by temporary cessation of central drive to respiratory muscles, OSAHS results from partial or complete collapse of the pharynx, UARS have typical symptoms of OSAHS and no changes on polysomnography, whereas SHVS results from pathological PCO2 increase with subsequent hypoxemia. Increase in sympathetic activity, renin-angiotensin-aldosterone activation, impaired baroreflex and tonic vagal heart rate control are markers of increased risk of sudden death. CSAS is frequent in patients with CHF. Decreased cardiac output causes delayed transmission of changes in arterial blood gas tensions from the lungs to the chemoreceptors. Increase chemoreceptor sensitivity results from hypoxia and pulmonary congestion. Both types of apneas (OSAHS and CSAS) may occur in the same patient. Periodic cessation in central drive to respiratory muscles (CSAS) causes obstructive apneas/hypopneas by decreased tone of pharyngeal muscles and their collapse. Obstructive apneas (OSAHS) may lead to central apneas by frequent arousals, decreased left ventricular function and prolongation of circulation. Treatment of SAS is based on improvement of cardiovascular function, nocturnal supplementation of O2 and various forms of noninvasive positive airway pressure (i.e. CPAP).
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PMID:[Sleep apnea syndrome in patients with chronic heart failure]. 1530 26


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