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

Obstructive sleep apnea (OSA) and obesity have been linked to systolic and diastolic dysfunction of the left ventricle. Right ventricular function is poorly understood in the 2 clinical conditions. Data from this study show that otherwise healthy obese patients with OSA had increased an left atrial volume index compared with similarly obese patients without OSA (16.3 +/- 1.2 ml/m in obese patients without OSA vs 20.2 +/- 1.0 ml/m in those with OSA, p = 0.02) and altered diastolic function reflected by changes in mitral annular late diastolic velocity (-5.7 +/- 0.7 cm/s in obese patients without OSA vs -7.3 +/- 0.7 cm/s in those with OSA, p = 0.007), mitral annular early diastolic velocity (-7.9 +/- 0.6 cm/s in obese patients without OSA vs -6.4 +/- 0.3 cm/s in those with OSA, p = 0.05), and early to late diastolic annular ratio >1 (82% of obese patients without OSA vs 26% of those with OSA, p = 0.001), which may be signs of early subclinical impairment of cardiac function. Importantly, healthy obese subjects had similarly increased left ventricular mass compared with obese patients with OSA but normal diastolic function and left atrial size. There was a trend toward abnormal right ventricular filling in patients with OSA, measured by altered superior vena cava diastolic velocity during expiration (-15 +/- 2 cm/s in obese patients without OSA vs -10 +/- 3 cm/s in those with OSA, p = 0.2) and a tendency toward diastolic dysfunction reflected by decreased lateral tricuspid annular early diastolic velocity (-7.2 +/- 0.5 cm/s in obese patients without OSA vs -6.1 +/- 0.5 cm/s in those with OSA, p = 0.1) beyond that seen in obesity alone. In conclusion, OSA independent of obesity may induce cardiac changes that could predispose to atrial fibrillation and heart failure.
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PMID:Comparison of cardiac structural and functional changes in obese otherwise healthy adults with versus without obstructive sleep apnea. 1747 61

Sleep related breathing disorders are common and their potential to disrupt sleep leading to daytime fatigue and hypersomnolence is widely acknowledged. In the future, obstructive sleep apnoea (OSA) may become even more important because obesity as a main risk factor is increasingly prevalent. Apart from disturbing sleep, OSA has also been recognised as a risk factor for hypertension, acute cardiovascular events and metabolic disturbance such as insulin resistance. Several randomised controlled trials demonstrated a positive effect of nasal continuous positive airway pressure (CPAP) treatment on arterial blood pressure, leading the "Joint National Council on High Blood Pressure" to list obstructive sleep apnoea as the first identifiable cause of arterial hypertension. Recently, a growing body of evidence demonstrated also a risk reduction of fatal and non-fatal cardiovascular events by treatment of obstructive sleep apnoea. A beneficial effect of treatment of OSA was also shown for patients with heart failure, or heart rhythm disturbance. Obstructive sleep apnoea may no longer be seen as a cause for daytime sleepiness and impaired quality of life only, but also as an independent risk factor, at least for the occurrence of hypertension but probably for any cardiovascular and cerebrovascular disease. While prospective controlled trials to document a reduction of cardiovascular morbidity and mortality are awaited, therapeutic nihilism seems no longer appropriate. With effective treatment available, subgroups that may profit best remain to be identified.
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PMID:Obstructive sleep apnea and cardiovascular disease - time to act! 1752 76

This paper presents data evidence supporting the value of diagnosing and treating obstructive sleep apnea (OSA) in reducing morbidity and mortality, improving comorbid disease processes, and improving patient quality of life. These data are derived from a PubMed-based meta-analysis of recent cost effectiveness, standards of practice, and epidemiological studies of OSA, which are ranked using a hierarchical strength of recommendation taxonomy. Cost and health care utilization data have been calculated for OSA and hypersomnolence as well as for diagnostic testing. Strong evidence (which is indicated by a strength of recommendation rating of "A") exists for the association of adult OSA with obesity, daytime sleepiness, hypertension, and motor vehicular accidents. Strong evidence also exists for requiring full-night or split-night attended polysomnography (PSG) for the diagnosis and treatment of adult OSA and for patients with systolic or diastolic heart failure not responding to optimal medical management. Good evidence (B) exists for the association of adult OSA with congestive heart failure, coronary artery disease, cerebral vascular accidents, metabolic syndrome, and increased mortality. Good evidence also exists to indicate that the nonattended PSG can be used to diagnose sleep breathing disorders, that autotitration systems can be used to titrate continuous positive airway pressure (CPAP) therapy, and that the multiple sleep latency test can be used in the assessment of daytime sleepiness.
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PMID:Obstructive sleep apnea (OSA) in primary care: evidence-based practice. 1761 20

Obesity is becoming a worldwide phenomenon. Myocardial changes associated with the obese state are increasingly recognized, independent of hypertension, obstructive sleep apnea and coronary artery disease. The existence of a cardiomyopathy of obesity is supported by a range of evidence: epidemiologic study findings, which have shown an association between obesity and heart failure; clinical studies that have confirmed the association of adiposity with left ventricular dysfunction, independent of hypertension, coronary artery disease and other heart disease; and experimental evidence of structural and functional changes in the myocardium in response to increased adiposity. The most important mechanisms in the development of obesity cardiomyopathy are metabolic disturbances (insulin resistance, increased free fatty acid levels, and also increased levels of adipokines), activation of the renin-angiotensin-aldosterone and sympathetic nervous systems, myocardial remodeling, and small-vessel disease (both microangiopathy and endothelial dysfunction). In the first part of this two-part Review, we seek to evaluate the emerging evidence for the existence of a cardiomyopathy of obesity and clarify the responsible mechanisms.
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PMID:Obesity cardiomyopathy: pathogenesis and pathophysiology. 1765 16

Obstructive sleep apnea (OSA) remains a significant public health problem because of its neurocognitive sequelae. Additionally, with persistent obstruction, it has an impact on the cardiovascular system, leading to hypertension and cardiac failure as one of its causative or comorbid factors. For the surgeon managing OSA, there is a stepwise sequence of surgical procedures, from improving nasal airflow to facial skeletal maxillary-mandibular advancement, with the cumulative goal of volumetrically increasing the retropharyngeal airway space. Familiarity with conventional orthognathic principles is essential in achieving this goal.
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PMID:Facial skeletal surgery in the management of adult obstructive sleep apnea syndrome. 1769 12

Patients with heart failure or OSA (obstructive sleep apnoea) have reduced HF-HRV (high-frequency heart rate variability), indicating reduced cardiac vagal modulation, a marker of poor prognosis. CPAP (continuous positive airway pressure) abolishes OSA in patients with heart failure, but effects on daytime HF-HRV have not been determined. We hypothesized that, in patients with heart failure, treatment of coexisting OSA by CPAP would increase morning HF-HRV. In 19 patients with heart failure (left ventricular ejection fraction <45%) and OSA (>/=20 apnoeas and hypopnoeas/h of sleep), HF-HRV was quantified before and 1 month after randomization to a control or CPAP-treated group. In the control group (n=7), there were no changes in HF-HRV over the 1 month study during wakefulness in the morning. In the CPAP-treated group (n=12) HF-HRV increased significantly during wakefulness in the morning [from 2.43+/-0.55 to 2.82+/-0.50 log(ms(2)/Hz); P=0.002] due to an increase in transfer function between changes in lung volume and changes in HF-HRV (92.37+/-96.03 to 219.07+/-177.14 ms/l; P=0.01). In conclusion, treatment of coexisting OSA by nocturnal CPAP in patients with heart failure increases HF-HRV during morning wakefulness, indicating improved vagal modulation of heart rate. This may contribute to improved prognosis.
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PMID:Continuous positive airway pressure increases heart rate variability in heart failure patients with obstructive sleep apnoea. 1782 46

Increased longevity and population aging will increase the number of men with relative testosterone deficiency, as systemic levels of testosterone decrease by about 1% each year. Androgen deficiency should only be diagnosed in men with definite signs and symptoms, accompanied by low total testosterone levels measured in the morning by a reliable assay. Although clinical trials data are limited, current practice guidelines recommend testosterone replacement therapy for symptomatic men with low testosterone levels to improve bone mineral density, muscle mass and strength, sexual function, and quality of life. Testosterone replacement is not recommended for all older men with low testosterone levels, and should be avoided in patients with prostate or breast cancer, hyperviscosity, erythrocytosis, untreated obstructive sleep apnea, or severe heart failure. The goal of all available testosterone treatment modalities (intramuscular injections, nongenital patch or gel, bioadhesive buccal and oral testosterone, and pellets) is to achieve serum testosterone levels in the mid-normal range during treatment. Cost varies widely among these preparations and may limit their use. Patients receiving testosterone replacement therapy should be re-evaluated 3 months after testosterone initiation and at least annually thereafter.
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PMID:Considerations for the diagnosis and treatment of testosterone deficiency in elderly men. 1790 50

Over the last decade the pathophysiology of obstructive sleep apnea (OSA)-related cardiovascular disease has been further elucidated in animal models employing dogs and rats/mice. It was demonstrated that, under the conditions of chronic intermittent hypoxia (CIH), endothelial dysfunction, i. e., a reduction in endothelial-dependent vasorelaxation, occurs. Furthermore, animals were shown to develop arterial hypertension when subjected to CIH for some weeks. Other aspects of the cardiovascular morbidity linked to OSA such as pulmonary hypertension, heart failure and atherosclerosis were also found in these animal models. The common result of these studies is that, apart from sympathetic over-activity, an increased oxidative stress seems to play a key role in the development of OSA-associated cardiovascular disease. It is anticipated that animal studies will continue to enhance our understanding of the pathogenesis of these disorders.
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PMID:[Sleep apnea and cardiovascular disease--results from animal studies]. 1796 May 21

This research aims to develop a non-intrusive system to monitor obstructive sleep apnea (OSA) in heart failure patients. Heart sounds and ECG are used to develop a support vector machine (SVM) based classifier. The RMS energy in wavelet sub-bands are used as feature vectors. Feature reduction is performed to minimize complexity without loss of performance. Data from 17 patients is parsed into two minute epochs and randomly partitioned into training and test datasets. The training set is used for parameter optimization of the SVM algorithm and a test data set is used to estimate the generalization error of the algorithm. The proposed algorithm has a 85.5% sensitivity and 92.2% specificity for the detection of OSA epochs.
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PMID:Monitoring of obstructive sleep apnea in heart failure patients. 1800 39

Patients with obstructive sleep apnea (OSA) have an increased prevalence of systemic and pulmonary hypertension, left ventricular (LV) hypertrophy, LV systolic and diastolic dysfunction, and congestive heart failure, increased platelet aggregability, and increased susceptibility to thrombotic and embolic cardiac and cerebrovascular events. Patients with OSA have an increased prevalence of coronary artery disease, myocardial infarction, nocturnal angina, and myocardial ischemia, arrhythmias, and sudden cardiac death. Patients with OSA also have an increased prevalence of stroke. Treatment of OSA with continuous positive airway pressure improves cardiac efficiency in patients with heart failure, causes a reduction in the frequency of nocturnal ischemic ST-segment depression, relieves nocturnal angina, and causes a reduction in the occurrence of new cardiovascular events and an increase in the time to such events.
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PMID:Cardiovascular manifestations seen in obstructive sleep apnea. 1800 19


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