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

The purpose of this study was to survey patients with heart failure (HF) for sleep symptoms using a standardized questionnaire and correlate symptoms with conventional markers of clinical status. A self-report paper questionnaire was offered to patients presenting to a tertiary care HF clinic. Symptoms were grouped according to "risk" categories and correlated with routine clinical information. One hundred six (52.7% of 201 with all data) respondents had a high pretest probability for sleep apnea syndrome. Sixty three (31.3%) reported symptoms suggesting the presence of chronic insomnia; seven (3.5%) and eight (4%) reported symptoms of narcolepsy and restless legs syndrome, respectively. High-risk respondents for sleep apnea had a higher body mass index (p<0.001), were younger (p<0.05), and had a higher ejection fraction (p<0.05). The odds ratio (confidence interval) for paroxysmal nocturnal dyspnea (PND) to a complaint of sleepiness was 1.99 (1.1-3.6) and to a complaint of insomnia was 3.5 (1.8-6.5). In men, complaints of sleepiness in patients with PND were correlated, 4.47 (1.9-10.3), as was a correlation to high pretest probability for sleep apnea, 2.47 (1.1-5.5). There were no correlation of New York Heart Association status classification to high risk for sleep apnea, but a complaint of insomnia tended to occur with worsening functional status (p<0.05). There was only modest correlation of self-reported symptoms as elicited by a questionnaire and risk for sleep disorders with common clinical assessments for HF. Such collection of symptoms might be useful in establishing guidelines for routine sleep testing or as an adjunct to clinical trials.
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PMID:Sleep symptoms and clinical markers of illness in patients with heart failure. 1608 63

This article provides information and a commentary on landmark trials presented at the American College of Cardiology meeting held in March 2005, relevant to the pathophysiology, prevention and treatment of heart failure. All reports should be considered as preliminary data, as analyses may change in the final publication. CARE-HF showed that Cardiac Re-synchronisation Therapy, administered in addition to expert pharmacological management, reduced all cause mortality and CV hospitalisation in patients with moderate or severe heart failure and cardiac dyssynchrony. The Women's Health Study showed no benefit of vitamin E supplementation or aspirin in the primary prevention of CV disease. The TNT study showed that reducing LDL cholesterol to levels lower than currently recommended, produced a 22% reduction in the incidence of major cardiovascular events. In COMPASS, an implantable device that continuously monitors intra-cardiac pressures was shown to be safe and to improve care in patients with chronic heart failure. Tezosentan failed to show benefit in patients with acute heart failure in the VERITAS study. The CANPAP study failed to show a benefit of continuous positive airway pressure on mortality and heart transplantation in heart failure patients with central sleep apnoea. EECP therapy improved exercise capacity but had no effect on peak VO2 in heart failure patients in the PEECH study. In the PREMIER study the matrix metalloproteinase inhibitor PG-116800 failed to prevent LV remodelling following myocardial infarction.
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PMID:Clinical trials update from the American College of Cardiology meeting: CARE-HF and the remission of heart failure, Women's Health Study, TNT, COMPASS-HF, VERITAS, CANPAP, PEECH and PREMIER. 1608 44

Cor pulmonale frequently develops in patients with restrictive lung disease and neuromuscular disorders. Sleep disordered breathing, including nocturnal hypoventilation and obstructive apnea, has been associated with the development of cor pulmonale and may affect morbidity. The mechanisms responsible for sleep disordered breathing include defects in the control of breathing, respiratory muscle dysfunction, and abnormalities in chest wall and lung compliance. Symptoms of disturbed sleep may allow patients with sleep disordered breathing to be appropriately diagnosed and treated, often with nocturnal ventilation, before the development of right-sided heart failure.
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PMID:Cor pulmonale and sleep-disordered breathing in patients with restrictive lung disease and neuromuscular disorders. 1608 50

This article reviews controversies in cardiac pacing in four areas: methods to prevent unnecessary right ventricular pacing and optimal ventricular pacing sites in the bradycardia population, pacing for prevention of atrial fibrillation (AF), a novel pacing technique for the treatment of heart failure, and pacing for the treatment of sleep apnea. Frequent right ventricular pacing has been reported to increase the incidence of AF and congestive heart failure. However, many patients with pacemakers for bradycardia have intrinsic atrioventricular conduction most of the time. Optimal programming of pacemakers and new algorithms designed to reduce unnecessary ventricular pacing are discussed. Pacing algorithms for prevention of AF have generally been shown to be ineffective. Atrial antitachycardia pacing has been shown to reduce the burden of atrial tachyarrhythmias in selected patients. Cardiac contractility modulation has recently been reported to be a promising new approach to the treatment of heart failure. Some pacing techniques may be effective in the treatment of sleep apnea but larger, long-term clinical trials are required to demonstrate a significant clinical benefit.
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PMID:Controversies in pacing: indications and programming. 1610 88

Sleep-disordered breathing is very common and is associated with an increased risk of cardiovascular disease, cardiac arrhythmia and stroke. There are two types of sleep apnea: obstructive and central. The objective of this review is to provide a broad perspective of the pathophysiological and clinical aspects of the two types of apnea and to discuss their cardiovascular adverse effects. The diagnosis of sleep apnea syndrome is based on polysomnography, and severity is measured with an apnea-hypopnea index that counts the total number of apneas per hour of sleep. Recent large epidemiologic studies have shown that sleep apnea affects about 16% of men and 5% of women between 30 and 65 years of age. Obstructive sleep apnea is characterized by abnormal collapse of the pharyngeal airway during sleep, snoring, vigorous inspiratory efforts causing frequent arousal, and excessive daytime drowsiness. Central sleep apnea with Cheyne-Stokes respiration is a form of periodic breathing with frequent periods of hyperventilation, and carries a poor prognosis in patients with heart failure. Obstructive apnea can also have substantial health consequences. Although the exact mechanism linking sleep apnea with cardiovascular disease is unknown, there is evidence that obstructive apnea is associated with a group of proinflammatory and prothrombic factors that are also important in the development of atherosclerosis. Nocturnal and daytime sympathetic activity is elevated after sleep apnea. Autonomic abnormalities include an increased resting heart rate, decreased cardiac rhythm activity, and increased blood pressure variability. Obstructive apnea is associated with endothelial dysfunction, increased C-reactive protein and cytokine expression, elevated fibrinogen levels and decreased fibrinolytic activity. Enhanced platelet activity and aggregation, leukocyte adhesion and accumulation of endothelial cells are common in both obstructive apnea and atherosclerosis. Surges in sympathetic activity, blood pressure, ventricular wall tension and afterload adversely affect ventricular function. Many studies have shown that patients with obstructive apnea have an increased incidence of daytime hypertension, and this syndrome is recognized as an independent risk factor for hypertension. Obstructive apnea is associated with myocardial ischemia (silent or symptomatic), acute coronary events, stroke and transient ischemic attacks, cardiac arrhythmia, pulmonary hypertension and heart failure. Central sleep apnea is frequent in severe heart failure. Most heart failure patients with pulmonary congestion chronically hyperventilate because of stimulation of vagal irritant receptors and central and peripheral chemosensitivity. When PaCO2 falls below the threshold required to stimulate breathing, the central drive to respiratory muscles and air inflow ceases and central apnea ensues. Apnea, hypoxia, CO2 retention and arousals provoke elevated sympathetic activity, increased afterload and elevated left ventricular transmural pressure, and promote the progression of heart failure. Tentative relationships have been identified between central apnea and markers of inflammation, oxidative stress and endothelial dysfunction. Recent mid-terms trials showed that nocturnal use of positive airway pressure in patients with the two types of apnea alleviates symptoms, reduces sympathetic activity, improves ventricular function and quality of life, and reduces daytime drowsiness. More studies are needed to understand the mechanisms underlying the relationship between sleep apnea and cardiovascular disease, but clinicians should be aware of this link and should attempt to identify patients with these syndromes.
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PMID:[Sleep apnea syndromes and cardiovascular disease]. 1614 10

Heart failure and sleep apnoea are major health problems with an increasingly recognized association; evidence suggests that sleep apnoea may play a role in the progression of heart failure. However, confounding factors such as obesity, hypertension and coronary heart disease make this relationship uncertain and an independent correlation remains unproven. Diagnosis of sleep apnoea is suboptimal, as it is often asymptomatic and polysomnography is expensive and time-consuming. A simple and reliable screening protocol is required. All heart failure patients should be considered to be at high risk of sleep apnoea, as this association might be linked to adverse outcome. Continuous positive airway pressure has shown some beneficial effects, but long-term outcome and improvement in survival remains to be demonstrated. Despite recent advances in the understanding of the complex relationship between heart failure and sleep apnoea, there are a number of areas requiring further investigation, which may have important implications for the management and prognosis of a significant number of patients.
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PMID:Heart failure and sleep apnoea: to sleep perchance to dream. 1713 38

One of the factors that contribute to the progressively declining course of heart failure could be sleep apnea. Whether treating sleep apnea improves the clinical outcomes of patients with heart failure needs to be tested in randomized clinical trials.
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PMID:Sleep apnea is linked to heart failure, but does treatment improve outcome? 1654 44

Sympathetic activation and sleep apnea are present in most patients with symptomatic systolic heart failure (HF). Acutely, obstructive and central apneas increase muscle sympathetic activity (MSNA) during sleep by eliciting recurrent hypoxia, hypercapnia, and arousal. In obstructive sleep apnea patients with normal systolic function, this increase persists after waking. Whether coexisting sleep apnea augments daytime MSNA in HF is unknown. We tested the hypothesis that its presence exerts additive effects on MSNA during wakefulness. Overnight sleep studies and morning MSNA recordings were performed on 60 subjects with ejection fraction <45%. Of these, 43 had an apnea-hypopnea index > or =15 per hour. Subjects with and subjects without sleep apnea were similar for age, ejection fraction, HF etiology, body mass index, blood pressure, and heart rate. Daytime MSNA was significantly higher in those with sleep apnea (76+/-2 versus 63+/-4 bursts per 100 heartbeats [mean+/-SEM], P=0.005; 58+/-2 versus 50+/-3 bursts/min, P=0.037), irrespective of its etiology (the mean difference for central sleep apnea was 17 bursts per 100 heartbeats; n=14; P=0.006; and for obstructive sleep apnea, 11 bursts per 100 heartbeats; n=29; P=0.032). In a subgroup (n=8), treatment of obstructive sleep apnea lowered MSNA by 12 bursts per 100 heartbeats (P=0.003). Convergence of independent excitatory influences of HF and sleep apnea on central sympathetic neurons results in higher MSNA during wakefulness in HF patients with coexisting sleep apnea. This additional stimulus to central sympathetic outflow may accelerate the progression of HF; its attenuation by treatment of sleep apnea represents a novel nonpharmacological opportunity.
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PMID:Muscle sympathetic nerve activity during wakefulness in heart failure patients with and without sleep apnea. 1628 69

Heart failure is an increasingly common public health problem that is strongly linked to both central and obstructive sleep apnea, collectively referred to as sleep-disordered breathing. Much attention has been given to the deleterious effects of sleep-disordered breathing on the failing heart and potential mechanisms by which treatment of sleep-disordered breathing may result in improved cardiac performance and long-term outcomes. However, there is compelling evidence that cardiac dysfunction may contribute to sleep-disordered breathing. Although there is recognized overlap between pathophysiological mechanisms in central sleep apnea and obstructive sleep apnea, data supporting the role of cardiac function are certain forms of central sleep apnea are well established, whereas investigation into the relationship with obstructive sleep apnea is less mature but continues to evolve. This review will examine experimental and observational data that explore possible pathophysiological mechanisms and potential targets for therapy in heart failure and sleep-disordered breathing.
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PMID:Influence of cardiac function and failure on sleep-disordered breathing: evidence for a causative role. 1628 1

Mortality risk in heart failure relates to the degree of chronic sympathetic nervous system activation. Do acute increases in central sympathetic outflow, as occur nightly in patients with sleep apnea, augment this risk? This review explores 4 novel concepts: 1) sleep disordered breathing is common in heart failure, 2) the acute effects of sleep apnea and the chronic effects of heart failure on the sympathetic nervous system are additive when these conditions coexist, 3) such convergence has adverse clinical and prognostic implications, and 4) treating sleep apnea can attenuate sympathetic nervous system activation and improve ventricular systolic function.
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PMID:Sleep apnea in heart failure: implications of sympathetic nervous system activation for disease progression and treatment. 1633 15


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