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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 is an increasingly recognized medical problem. The recent attention to its frequency in the general population and its important role in metabolic, vascular, and behavioral aspects have sharply increased the number and nature of investigations, thereby revealing new aspects that open new approaches in research. Whereas obstructive sleep apnea is a well-known phenomenon accompanying obesity and diabetes, new findings strongly suggest that this close relationship may also operate in the opposite direction. Indeed obstructive sleep apnea may be a primary feature inducing or aggravating a series of vascular and metabolic disturbances closely resembling the metabolic syndrome. This review will discuss established and potential mechanisms responsible for these changes. Obstructive sleep apnea indeed appears to gather all the elements necessary to induce insulin resistance, hypertension, and possibly heart failure. After careful analysis of these modifications and considering how they are intertwined, we propose that microcirculation could represent the common denominator mediating the progression of this pathology, as it is eventually the case in the metabolic syndrome and diabetes domain. This plausible hypothesis is discussed in detail and should be verified by appropriate preclinical and clinical protocols, which are now achievable by using noninvasive techniques in humans.
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PMID:Obstructive sleep apnea and insulin resistance: a role for microcirculation? 1683 59

Heart failure (HF) affects approximately 5 million persons in the United States; more than 550,000 new cases of HF are reported each year. Prevalence of HF with a normal left ejection fraction increases with age and is higher in older women than older men. Both underlying and precipitating causes of HF should be treated when possible. Hypertension, especially isolated systolic hypertension, should be treated with diuretics, ACE inhibitors, and beta blockers. Myocardial ischemia should be treated with nitrates and beta blockers. Anemia should be treated, as should hyperthyroidism, hypothyroidism, and obstructive sleep apnea. Use of inappropriate drugs, such as nonsteroidal anti-inflammatory drugs, should be avoided. Coronary revascularization should be performed in selected individuals.
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PMID:Heart failure update: treatment of heart failure with a normal left ventricular ejection fraction in the elderly. 1690 Nov 93

In patients with heart failure, apnea type can shift overnight from mainly obstructive to mainly central in association with reductions in PCO(2) and increases in periodic breathing cycle length, indicative of a fall in cardiac output. We hypothesized that the predominant apnea type could also vary from one night to another in association with alterations in PCO(2) and cycle length. We studied 12 men with heart failure in whom the predominant apnea type changed from one night to the next over periods of at least 1 month, and two groups with either predominantly obstructive or central sleep apnea (OSA or CSA) in whom apnea type remained stable over time. In patients with unstable apnea type (n = 12, duration between sleep studies 9.0 +/- 4.4 months), PCO(2) was significantly lower (37.6 +/- 1.6 mmHg versus 41.7 +/- 1.9 mmHg, P < 0.01), and cycle length significantly longer (61.9 +/- 3.4 s versus 51.0 +/- 1.9 s, P < 0.001) during nights with predominantly central than nights with predominantly obstructive apnea. In contrast, in both the stable central (n = 8, duration between sleep studies 11.9 +/- 5.3 months) and the stable obstructive (n = 8, duration between studies 6.9 +/- 5.2 months) sleep apnea groups, neither PCO(2) nor cycle length changed significantly between the baseline and follow-up sleep studies. We conclude that in some patients with heart failure, OSA and CSA are part of a spectrum of periodic breathing that can shift over time in association with alterations in PCO(2), cycle length and probably cardiac function.
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PMID:Night-to-night alterations in sleep apnea type in patients with heart failure. 1691 Oct 35

One hundred twenty-six eligible consecutive Chinese heart failure (HF) patients classified by New York Heart Association (NYHA) Classes II-IV underwent historic data collection and a sleep study. Seventy-one percent of HF patients were diagnosed with sleep apnea (SA), of which 65% were central sleep apnea (CSA) and 35% were obstructive sleep apnea (OSA). Higher body mass index (BMI), metabolic syndrome, habitual snoring, and nocturia were independent risk factors for OSA; NYHA classes III and IV were independent risk factors for CSA in the HF patients. There was a high prevalence of SA in Chinese patients with HF. HF patients with obesity, metabolic syndrome, snoring, nocturia and NYHA classes III and IV were more susceptible to OSA and CSA.
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PMID:Prevalence and clinical characteristics of sleep apnea in Chinese patients with heart failure. 1691 41

Patients with obstructive sleep apnea syndrome (OSAS) have an elevated incidence of cardiovascular events that may be related to an increased ventricular load and hypoxemia caused by apneas and hypopneas. N-terminal pro-brain natriuretic peptide (NTproBNP) appears to be an excellent marker of myocardial stretch and could serve as an indicator of subclinical cardiac stress, thereby identifying a patient population at risk for cardiac effects from OSAS. Adult patients presenting with suspected OSAS and scheduled for nocturnal polysomnography were recruited. Patients with heart or renal failure or severe lung disease were excluded. NTproBNP was measured the evening before and the morning after sleep. Blood pressure (BP) was monitored intermittently throughout the night. Fifteen male and 15 female subjects with a mean +/- SD body mass index of 38.2 +/- 9.8 were studied. Mean Apnea-Hypopnea Index (AHI) was 38.4 +/- 26, with 17 subjects having severe OSAS (AHI > 30). No subject had a significant rise in BP. NTproBNP values overnight decreased in 19 patients and rose in 11 (mean change 3.8 +/- 33 pg mL(-1)), but only one patient had an abnormal morning value. Three patients had an abnormal NTproBNP value prior to sleep, but their levels decreased with sleep. No correlations were detected between the evening baseline or postsleep NTproBNP levels and OSAS. Monitoring pre- and postsleep NTproBNP levels revealed no association with the occurrence or degree of OSAS, making it unlikely that NTproBNP could serve as a marker of cardiac stress in OSAS patients with stable BP and without overt heart failure.
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PMID:N-terminal pro-brain natriuretic peptide for detection of cardiovascular stress in patients with obstructive sleep apnea syndrome. 1711 99

Obstructive sleep apnea (OSA) affects approximately 5% of women and 15% of men in the middle-aged adults, and associated with adverse health outcomes. Cardiovascular disturbances are the most serious complications of OSA. These complications include heart failure, left/right ventricular dysfunction, acute myocardial infarction, arrhythmias, stroke, systemic and pulmonary hypertension. All these cardiovascular complications increase morbidity and mortality of OSA. Several epidemiologic studies have demonstrated that sleep related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic activity, and altered baroreflex control during sleep. Arterial hypertension, obesity, diabetes mellitus and coronary artery disease (CAD) which are independent predictors of left ventricular dysfunction, often have co-existence with OSA. Especially severe OSA patients having diastolic dysfunction might have an increased risk of heart failure, since diastolic dysfunction might be combined with systolic dysfunction. Early recognition and appropriate therapy of ventricular dysfunction is advisable to prevent further progression to heart failure and death. Patients with acute myocardial infarction, especially if they had apneas and hypoxemia without evident heart failure should be evaluated for sleep disorders. So, patients with CAD should be evaluated for OSA and vice versa. Early recognition and treatment of OSA may improve cardiovascular functions. Continuous positive airway pressure (CPAP) applied by nasal mask, is still the gold standard method for treatment of the disease and prevention of complications.
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PMID:Cardiovascular diseases in obstructive sleep apnea. 1720 27

Evidence is mounting that obstructive sleep apnea causes or contributes to many chronic medical diseases, and that treatment with continuous positive airway pressure (CPAP) often improves concomitant diseases. The author reviews the association of obstructive sleep apnea with arterial hypertension, pulmonary hypertension, stroke, coronary artery disease, heart failure, sudden death, gastroesophageal reflux disease, and diabetes mellitus.
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PMID:The effect of obstructive sleep apnea on chronic medical disorders. 1737 50

Patients with untreated obstructive sleep apnea hypopnea (OSAH) are predisposed to developing hypertension, and therapy with continuous positive airway pressure (CPAP) may reduce blood pressure (BP). The purpose of this study was to assess the impact of CPAP therapy on BP in patients with OSAH. We performed a comprehensive literature search up to July 2006 [Medline, PubMed, EMBASE, Cochrane Database of Systematic Reviews (CDSR), Cochrane controlled trials register (CCTR), and Database of Abstract and Reviews of Effect (DARE)] to identify clinical studies and systemic reviews that examined the impact of CPAP on BP. Studies were included if they (1) were randomized controlled trials with an appropriate control group, (2) included systolic and diastolic BP measurements before and after CPAP/control in patients with OSAH, and (3) contained adequate data to perform a meta-analysis. To calculate pooled results, studies were weighted by inverse variances, with either a fixed or a random effects model used depending on the presence of heterogeneity (assessed with Q test). Ten studies met our inclusion criteria (587 patients): three studies were crossover (149 patients) and seven were parallel in design. Seven studies (421 patients) used 24-h ambulatory BP and three used one-time measurements. Two studies were of patients with heart failure (41 patients). Overall, the effects of CPAP were modest and not statistically significant; CPAP (compared to control) reduced systolic BP (SBP) by 1.38 mmHg (95% CI: 3.6 to -0.88, p = 0.23) and diastolic BP (DBP) by 1.52 mmHg (CI: 3.1 to -0.07; p = 0.06). Six of the trials studied more severe OSAH (mean AHI > 30/h, 313 patients); in these six trials, CPAP reduced SBP by 3.03 mmHg (CI 6.7 to -0.61; p = 0.10) and DBP by 2.03 mmHg (CI: 4.1 to -0.002; p = 0.05). There was a trend for SBP reduction to be associated with CPAP compliance. In unselected patients with sleep apnea, CPAP has very modest effects on BP. However, we cannot exclude the possibility that certain subgroups of patients may have more robust responses-this may include patients with more severe OSAH or difficult-to-control hypertension. Future randomized controlled trials in this area should potentially concentrate on these subgroups of patients.
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PMID:Impact of continuous positive airway pressure therapy on blood pressure in patients with obstructive sleep apnea hypopnea: a meta-analysis of randomized controlled trials. 1739 40

Sleep-disordered breathing, broadly characterized by obstructive sleep apnea (OSA) and central sleep apnea (CSA), is an increasingly recognized public health burden. OSA, consisting of apneas or hypopneas associated with respiratory efforts in the face of upper airway narrowing or collapse, is a common disorder that can be effectively treated with continuous positive airway pressure (CPAP). OSA not only results in daytime sleepiness and impaired executive function, but also has been implicated as a possible cause of systemic disease, particularly of the cardiovascular system. CSA, which may coexist with OSA, has gained attention because of the association of Cheyne-Stokes respiration with an ever-increasing prevalence of heart failure in an aging population. This article reviews some of the extensive literature on pathophysiologic mechanisms as they may relate to the development of cardiac and vascular disease and examine the evidence suggesting OSA as a specific cause of certain cardiovascular conditions. Available evidence regarding the implications of CSA in the context of heart failure is discussed.
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PMID:Sleep-disordered breathing and cardiovascular risk. 1742 25

Sleep apnea syndrome (SAS), a common disorder, is characterized by repetitive episodes of cessation of breathing during sleep, resulting in hypoxemia and sleep disruption. The consequences of the abnormal breathing during sleep include daytime sleepiness, neurocognitive dysfunction, development of cardiovascular disorders, metabolic dysfunction, and impaired quality of life. There are two types of SAS: obstructive sleep apnea syndrome (OSAS) and central sleep apnea syndrome (CSAS). OSAS is a prevalent disorder in which there is snoring, repetitive apneic episodes, and daytime sleepiness. Anatomical conditions causing upper airway obstruction (obesity or craniofacial abnormalities such as retrognathia or micrognathia) can cause OSAS. CSAS, much less common than OSAS, is a disorder characterized by cessation of breathing which is caused by reduced respiratory drive from the central nervous system to the muscles of respiration. The latter condition is common in patients with heart failure and cerebral neurologic diseases. The diagnosis of SAS requires assessment of subjective symptoms and apneic episodes during sleep documented by polysomnography. Treatments of OSAS include continuous positive airway pressure (CPAP), oral appliances, and surgery; patients with CSAS are treated with oxygen, adaptive servo-ventilation, or CPAP. With assessment and treatment of the SAS, patients usually have resolution of their disabling symptoms, subsequently resulting in improved quality of life.
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PMID:Sleep apnea: clinical investigations in humans. 1747 21


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