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

Snoring is a nuisance at least! The inspiratory vibrations of pharyngeal soft tissue may exceed 85 dB. For thousands of years snoring has led to social and marital disharmony in many cases. The treatment of the symptom snoring has been of interest for the medical profession for the same time. Today, we know that snoring is the most common presenting symptom of obstructive sleep apnea (OSA). The wider recognition of OSA and its impact on the development of systemic and pulmonary hypertension, cardiac arrhythmias, heart failure and daytime sleepiness has occurred in the last decade. The treatment of OSA has become a medical issue apart from its social aspects.
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PMID:UPPP or LAUP: Is This All Surgeons Should Talk About? 1189 7

Heart failure during the immediate period of an acute myocardial infarction constitutes a major insult to this pathology; since, once installed, it is associate to ventricular dysfunction and expansion of the left ventricle. It can appear either early or delayed. Subsequent to the acute insult, the myocardium is subjected to diverse changes in its anatomical conformation and to diastolic and systolic alterations, which will affect the hemodynamic constants of the patient. Changes in the parietal ventricular architecture as well as at the neurohumoral level will also occur. The clinical signs of heart failure are: dyspnea, pallor, tachycardia, diaphoresis, cold skin, oliguria, somnolence, and gallop, which can be observed at the very beginning of the coronary occlusion. Its clinical identification, through in-hospital studies supported by adequate hemodynamic monitoring, is of utter relevance since it will lead to appropriate and fast treatment. The groups of patients with acute myocardial infarction with high risk for the development of cardiac failure are: patients with extensive Q wave infarction, diabetic, patients over 65 years of age, and those with a history of previous myocardial infarction(s). The cornerstone of treatment must be focused on reducing the myocardial ischemia, which can be achieved through the use of modern therapeutics and, given the case, pharmacological agents, coronary intervention procedures, or cardiac surgery must be taken into account. At present it is known that angiotensin converting enzyme inhibitors, betablockers, inotropics, are useful to improve ventricular function in patients with acute myocardial infarction.
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PMID:[Heart failure in acute myocardial infarction]. 1200 71

Heart failure is associated with Cheyne-Stokes breathing, which fragments patients' sleep. Correction of respiratory disturbance may reduce sleep fragmentation and excessive daytime sleepiness. This randomized prospective parallel trial assesses whether nocturnal-assist servoventilation improves daytime sleepiness compared with the control. A total of 30 subjects (29 male) with Cheyne-Stokes breathing (mean apnea-hypopnea index 19.8 [SD 2.6] and stable symptomatic chronic heart failure (New York Heart Association Class II-IV) were treated with 1 month's therapeutic (n = 15) or subtherapeutic adaptive servoventilation. Daytime sleepiness (Osler test) was measured before and after the trial with change in measured sleepiness the primary endpoint. Secondary endpoints included brain natriuretic peptide levels and catecholamine excretion. Active treatment reduced excessive daytime sleepiness; the mean Osler change was +7.9 minutes (SEM 2.9), when compared with the control, the change was -1.0 minutes (SEM, 1.7), and the difference was 8.9 minutes (95% confidence interval, 1.9-15.9 minutes; p = 0.014, unpaired t test). Significant falls occurred in plasma brain natriuretic peptide and urinary metadrenaline excretion. We conclude that adaptive servoventilation produces an improvement in excessive daytime sleepiness in patients with Cheyne-Stokes breathing and chronic heart failure. This study suggests improvements in neurohormonal activation with this treatment.
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PMID:A randomized controlled trial of adaptive ventilation for Cheyne-Stokes breathing in heart failure. 1292 10

Sleep-related breathing disorders are common in heart failure patients and can have significant adverse impact on clinical outcomes. If sleep-disordered breathing or considerable daytime sleepiness exists, assessment and treatment recommendations include the following: 1) carefully assess and correct hemodynamic status; heart failure exacerbations can induce central sleep apneas; 2) if overweight, encourage patient weight loss; 3) elevate head of bed; 4) discourage sleeping on back; 5) order polysomnography, to assess type and extent of sleep-related breathing disorder; and 6) treat sleep-disordered breathing with nasal continuous positive airway pressure or bilevel positive airway pressure.
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PMID:Sleep-disordered Breathing in Heart Failure. 1457 23

Snoring is a very common source of complaints from partners and neighbours. Snorers themselves are less likely to be affected, unless they have associated daytime sleepiness caused by the sleep disruption from obstructive sleep apnoea. There is increasingly firm evidence that obstructive sleep apnoea is associated with hypertension, cardiovascular, cerebrovascular and metabolic problems such as insulin resistance, even at mild levels which may not cause much daytime somnolence. In addition, the central and obstructive apnoeas found in cardiac failure affect heart muscle function. Treatment of the apnoea improves blood pressure and cardiac function and is likely to have a beneficial effect on mortality. Since obstructive sleep apnoea is common it should be sought by appropriate questioning in these patient groups. The treatments for obstructive sleep apnoea are effective but cumbersome and this remains a challenge if patients do not achieve obvious early benefits such as reduction in sleepiness or breathlessness.
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PMID:Snoring, not just a social nuisance. 1468 70

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

Amongst the principal metabolic situations that can require emergency attention in the oncology patient we find: hypercalcaemia, hyponatraemia, tumoural lysis syndrome, lactic acidosis, hyperuricaemia, renal failure, hyperammonaemia, hypermpotasaemia, etc. Hypercalcaemia is the most frequent metabolic complication in oncology, appearing in 10-30% of these patients. It has two main mechanisms, tumoural lysis and humoural hypercalcaemia mediated by PTHrP (a protein related to parathormone). The principal factor for its diagnosis is suspicion, since some symptoms are non-specific and can be attributed to other causes such as somnolence, constipation, etc. Treatment will be based on intensity and is started with calciuretic measures with an intense hydration with physiological serum and on some occasions with furosemide. Anti-reabsorptive measures include calcitonin, bisphosphonates, mithramycin, gallium nitrate and on occasions corticoids. Bisphosphonates such as pamidronate and zoledronate seem to be highly useful in these cases. Hyponatraemia is classified depending on plasmatic osmorality; when this is low we find ourselves facing an authentic hyponatraemia that can develop with an extra-cellular volume that is high (cardiac insufficiency, cirrhosis, nephrotic syndrome and renal insufficiency), low (renal and extra-renal sodium losses) and normal (principally SIADH, related to a high elimination of sodium in the urine with high urinary osmolarity in spite of this being low in blood). Several types of tumour and different chemotherapy drugs can produce this SIADH. Treatment will vary according to the type and intensity, but in general this is based on hydric restriction and the replacement of the sodium deficit, either through physiological serum or through hypertonic saline serums depending on the case, and on occasions furosemide for the elimination of excess water.
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PMID:[Metabolic emergencies in the oncology patient]. 1572 5

Despite recent therapeutic advances, chronic cardiac failure is still associated with a significant morbidity and mortality. Sleep apnoea syndrome is common in this population, affecting almost half of these patients. However, it is rarely diagnosed and treated. There are two types of sleep apnoea syndrome, which can sometimes co-exist: the obstructive apnoea syndrome with collapse of the upper airways, and the central apnoea syndrome with cyclical Cheyne-Stokes respiration, linked with anomalies of central control. Apnoea leads to sympathetic stimulation and an increase in the left ventricular post-charge which can alter cardiac function and the prognosis. Diagnosis of sleep apnoea syndromes is now made with small ambulatory oxymeters which do not disturb sleep and which allow precise detection of episodes of desaturation. Treatment with positive pressure ventilation brings an improvement in daytime symptoms (fatigue, drowsiness) as well as an improvement in cardiac function. Screening for sleep apnoea is thus essential in patients with chronic heart failure, especially in those resistant to optimal drug treatment, in order to improve their management.
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PMID:[Sleep apnoea syndrome and cardiac failure]. 1581 21

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

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


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