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

The prevalence of obstructive sleep apnea syndrome in patients up to the age of 60 is known to be two times higher in men then in women. Hormonal changes during menopause might underlie changes in this relationship in the elderly. This study was designed to detect differences in the type and frequency of sleep-disordered breathing between women and men over the age of 65 years, having the same body mass index. The study was conducted using a matched-pair approach consisting of a sample population of 40 pairs of patients over the age of 65. All patients met the following exclusion criteria: age below 65, heart failure, chronic obstructive lung disease. Polygraphy was conducted by means of a portable recorder. All measured indices were higher in men than in women. The apnea index was 2.8 +/-4.1 in men and 0.6 +/-1.4 in women. The apnea/hypopnea index was 10.2 +/-11.4 and 4.8 +/-3.9, respectively. These differences were significant (P<0.05). Significant differences also were observed when central (men 8.1 +/-13.1, women 3.1 +/-8.2), mixed (men 5.1 +/-11.4, women 0.4 +/-1.3), and obstructive (women men 8.6 +/-20.1, 1.0 +/-4.3) apnea indices were compared. In conclusion, the study demonstrates that elderly patients showed gender-dependent differences in the type and frequency of sleep-related breathing disorders. Men suffered from all kinds of apnea more frequently than women.
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PMID:Sleep disordered breathing in the elderly: comparison of women and men. 1620 80

In obstructive sleep apnea syndrome (OSAS), repetitive episodes of apnea cause increased sympathetic nerve activity, increased surges in arterial blood pressure, swings in intrathoracic pressure, oxidative stres, hypoxia and hypercapnia. The association of OSAS with some diseases, having endothelial dysfunction in their physiopathology, such as hypertension, diabetes mellitus, obesity, coronary artery diseases, stroke and heart failure is common. Increased sympathetic nerve activity and also endothelial dysfunction which are the results of hypoxia, have important roles in vascular complications of OSAS. When compared with healthy population, an important endothelial dysfunction in OSAS patients and relationship between OSAS severity and endothelial dysfunction have been shown. In this review, the relationship between OSAS and endothelial dysfunction was overviewed.
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PMID:[Obstructive sleep apnea syndrome, endothelial dysfunction and coronary atherosclerosis]. 1625 93

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

Obesity is becoming a global epidemic in both children and adults. It is associated with numerous comorbidities such as cardiovascular diseases (CVD), type 2 diabetes, hypertension, certain cancers, and sleep apnea/sleep-disordered breathing. In fact, obesity is an independent risk factor for CVD, and CVD risks have also been documented in obese children. Obesity is associated with an increased risk of morbidity and mortality as well as reduced life expectancy. Health service use and medical costs associated with obesity and related diseases have risen dramatically and are expected to continue to rise. Besides an altered metabolic profile, a variety of adaptations/alterations in cardiac structure and function occur in the individual as adipose tissue accumulates in excess amounts, even in the absence of comorbidities. Hence, obesity may affect the heart through its influence on known risk factors such as dyslipidemia, hypertension, glucose intolerance, inflammatory markers, obstructive sleep apnea/hypoventilation, and the prothrombotic state, in addition to as-yet-unrecognized mechanisms. On the whole, overweight and obesity predispose to or are associated with numerous cardiac complications such as coronary heart disease, heart failure, and sudden death because of their impact on the cardiovascular system. The pathophysiology of these entities that are linked to obesity will be discussed. However, the cardiovascular clinical evaluation of obese patients may be limited because of the morphology of the individual. In this statement, we review the available evidence of the impact of obesity on CVD with emphasis on the evaluation of cardiac structure and function in obese patients and the effect of weight loss on the cardiovascular system.
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PMID:Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss: an update of the 1997 American Heart Association Scientific Statement on Obesity and Heart Disease from the Obesity Committee of the Council on Nutrition, Physical Activity, and Metabolism. 1638 May 42

Obstructive sleep apnea (OSA) is a common medical condition that occurs in a considerable percentage of the population. 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. It is established that OSA may be implicated in stroke and transient ischemic attacks. OSA is associated with coronary heart disease, heart failure, and cardiac arrhythmias. Pulmonary hypertension may be associated with OSA, especially in patients with pre-existing 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 as important in the development of atherosclerosis. OSA 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, plasminogen activator inhibitor, and reduced fibrinolytic activity. OSA 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:Inflammatory aspects of sleep apnea and their cardiovascular consequences. 1646 39

Obstructive sleep apnea is a common disorder characterized by repetitive collapse of the pharyngeal airway during sleep. The disorder results primarily from an anatomically small upper airway in conjunction with pharyngeal dilator muscles that can compensate for the anatomic deficiency awake, but not asleep. Ventilatory control instability and a low arousal threshold may contribute to the disorder as well. The consequences of sleep apnea fall into two domains: (1) neurocognitive dysfunction (sleepiness and decreased quality of life) resulting from sleep fragmentation and (2) cardiovascular disease (hypertension, stroke, myocardial infarction, and heart failure) likely resulting from the intermittent hypoxia. The disorder is generally diagnosed in the sleep laboratory over the course of a night, although alternative approaches in the home are also utilized. A number of treatment options are available. Continuous positive airway pressure remains the most consistently effective approach, although oral appliances (generally mandibular-advancing devices) and a number of surgical procedures have some demonstrated efficacy. Thus, therapy must be individualized to the patient's desires and the severity of the apnea.
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PMID:Sleep apnea. 1649 60

Obstructive and central sleep apnea are common in heart failure, and may participate in its progression by exposing the heart to intermittent hypoxia, increased preload and afterload, sympathetic activation, and vascular endothelial dysfunction. Treatment of sleep apnea in patients with heart failure may reverse these detrimental effects, in addition to alleviating symptoms of sleep apnea. In patients with heart failure and obstructive sleep apnea, short-term randomized trials have demonstrated that continuous positive airway pressure (CPAP) improves cardiac function, and lowers sympathetic activity and blood pressure. However, there are no data on whether treating obstructive sleep apnea in patients with heart failure improves morbidity and mortality. Various treatments have been tested in heart failure patients with central sleep apnea, particularly oxygen and CPAP. Both reduce the frequency of central respiratory events, and lower sympathetic activity. In addition, CPAP improves cardiac function. However, the largest randomized trial did not demonstrate any beneficial effect of CPAP on the rate of mortality and cardiac transplantation (32 vs. 32 events in the control and treatment groups, respectively; p=0.54), but ultimately lacked power to conclude with certainty whether CPAP has an effect on morbidity and mortality in such patients. Thus, although there are data to indicate that treating both obstructive and central sleep apnea in patients with heart failure improves cardiovascular function, larger randomized trials involving interventions such as oxygen, CPAP, or other forms of positive airway pressure will be required to determine whether treating these sleep-related breathing disorders reduces clinically important outcomes such as morbidity and mortality.
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PMID:Treatment of sleep apnea in heart failure. 1652 15

Congestive heart failure (CHF) is a common clinical disorder that results in pulmonary vascular congestion and reduced cardiac output. CHF should be considered in the differential diagnosis of any adult patient who presents with dyspnea and/or respiratory failure. The diagnosis of heart failure is often determined by a careful history and physical examination and characteristic chest-radiograph findings. The measurement of serum brain natriuretic peptide and echocardiography have substantially improved the accuracy of diagnosis. Therapy for CHF is directed at restoring normal cardiopulmonary physiology and reducing the hyperadrenergic state. The cornerstone of treatment is a combination of an angiotensin-converting-enzyme inhibitor and slow titration of a beta blocker. Patients with CHF are prone to pulmonary complications, including obstructive sleep apnea, pulmonary edema, and pleural effusions. Continuous positive airway pressure and noninvasive positive-pressure ventilation benefit patients in CHF exacerbations.
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PMID:Congestive heart failure: Diagnosis, pathophysiology, therapy, and implications for respiratory care. 1656 94

Nontuberculous mycobacteria are ubiquitous and infrequently cause disease in humans, most commonly in immunocompromised hosts. One type of nontuberculous mycobacteria is Mycobacterium abscessus. This rapidly growing mycobacterium is a soil or water saprophyte. It was previously classified as a subspecies of Mycobacterium chelonae; however, current taxonomy now designates it as a separate species. Rapidly growing mycobacteria are resistant to the usual antituberculous drugs. This emphasizes the need for tissue diagnosis and obtaining specimens for culture and drug susceptibility testing. M abscessus has been reported to cause infection in renal transplant patients, but is less well described in cardiac transplant recipients. We report the case of a 65-year-old man who presented 5 years after transplantation for heart failure, with a 2-day history of progressive right lower extremity swelling and redness. He recalled no antecedent trauma and denied any unusual epidemiologic exposure. Medical history included diabetes with peripheral neuropathy and renal insufficiency, hypertension, and right-sided heart failure felt to be due to obstructive sleep apnea. A punch biopsy of the area grew M abscessus sensitive only to clarithromycin (MIC not reported), amikacin (30 microg/mL), and kanamycin (30 microg/mL). On subsequent clinic visits, the patient had decreased leg swelling and resolution of the papular lesions. Ten weeks into antimycobacterial therapy, the patient had an increase in creatinine to 4.9 mg/dL from a baseline of 2.0 with fluid overload necessitating discontinuation of aminoglycoside therapy. He completed 6 months of treatment with oral clarithromycin. We describe these findings and review the literature in this report.
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PMID:Cutaneous infection with rapidly-growing mycobacterial infection following heart transplant: a case report and review of the literature. 1679 50


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