Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nocturnal secretion profile of the newly identified natriuretic peptide (NP), brain natriuretic peptide (BNP), was studied in 14 patients with obstructive sleep apnoea syndrome (OSAS) (apnoea hypopnoea index: 60.5 +/- 3.4, mean +/- SE) during two separate nights before and during nasal continuous positive airway pressure (NCPAP) therapy. Plasma levels of NPs (atrial natriuretic peptides; ANP and BNP) were measured at 2-h intervals during sleep. Simultaneously, blood pressure was measured by a non-invasive method (Finapres, Ohmeda, Englewood, CO, USA) and urine was collected for determining volume and catecholamine levels. Urinary and serum sodium concentration were determined before and after the study. Eight non-snoring subjects were also studied for the investigation of normal nocturnal profiles of BNP levels. To understand the discrete secretion profiles of the two NPs during sleep, blood was sampled from an additional seven patients every 5 min over a 30-min period around 00.00 and 04.00 hours before NCPAP. In patients with OSAS, plasma BNP levels increased from the beginning of sleep (22:00 h) to the morning (06:00 h) before NCPAP therapy (P < 0.01, ANOVA). Baseline BNP levels were not significantly correlated with patient's clinical and polysomnographic parameters. However, in the latter half of the sleep period (02:00-06:00 h), increases in BNP levels during the night before NCPAP therapy were significantly correlated with blood pressure elevations (systolic: r = 0.784 P < 0.01, diastolic: r = 0.587 P < 0.01) and with apnoea duration (r = 0.582 P < 0.01). In normal subjects BP and BNP levels were not changed significantly during sleep. Plasma BNP levels were well correlated with concomitant ANP levels (P < 0.001). NCPAP therapy reduced ANP and BNP levels during sleep and in the morning (P < 0.01). Plasma levels of BNP at 5 min intervals before NCPAP therapy revealed few variations. On the other hand, ANP levels fluctuated over the 30-min period. Changes in BNP levels during sleep in the patients with OSAS may be related to blood pressure variations, but may be too small to play a significant physiological role in regulating diuresis in OSAS. Further work is required to determine the precise role of dual natriuretic system in cardiovascular load and natriuresis in OSAS.
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PMID:The nocturnal secretion of cardiac natriuretic peptides during obstructive sleep apnoea and its response to therapy with nasal continuous positive airway pressure. 978 75

A 57-year-old man was admitted with dyspnea. Clinical evaluation revealed atrial fibrillation and congestive heart failure (CHF). Standard medical therapy of CHF failed to completely improve the dyspnea and polysomnography revealed Cheyne-Stokes respiration with central sleep apnea (CSR-CSA). He was equipped with noninvasive positive pressure ventilation (NPPV) with bilevel positive airway pressure (BiPAP). The combined therapy of medical treatment of the CHF and administration of NPPV with BiPAP reduced the CSR-CSA. This regimen resulted in marked improvement of cardiac function, evaluated by echocardiography, and reduction of plasma concentration of brain natriuretic peptide. After the patient recovered from CHF and was discharged from hospital, he continued to use NPPV with BiPAP at home. In patients with CHF, it is important to be aware of sleep-related breathing disorders because treatment will not only improve the hypoxemia, but also the cardiac dysfunction.
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PMID:Improvement of cheyne-stokes respiration, central sleep apnea and congestive heart failure by noninvasive bilevel positive pressure and medical treatment. 1532 13

In patients with congestive heart failure (CHF), sleep disordered breathing (SDB)--including obstructive and central sleep apnoea as well as periodic breathing--is a common condition and is believed to increase the risk of mortality. Treatment of SDB is considered important in the management of CHF. Improvements in SDB have a positive effect on cardiac output, measured with left ventricular ejection fraction (LVEF); on neurohormonal activity, measured as brain natriuretic peptide (BNP); and on the quality of life. Continuous positive airway pressure has been the traditional method used to treat SDB in patients with CHF, but compliance and tolerability are poor. A mandibular advancement device (MAD) is a dental device recommended for the treatment of sleep apnoea, but the method has never been evaluated in patients with CHF. The aims of the present studies were to evaluate the practical use of the MAD for the treatment of SDB in patients with CHF and to test the hypothesis that this intervention increases the dimensions of the pharyngeal airway (PAW), reduces SDB and BNP, and improves LVEF and the quality of life. Patients with mild to moderate CHF and SDB were evaluated using a portable polysomnographic device, lateral radiographs, cardiological and odontological examinations, and quality of life measures prior to and following intervention with an custom-made MAD. At the short-term follow-up 4-6 weeks after habituation with the MAD, the severity of SDB according to the apnoea-hypopnoea index had decreased from 25.1 +/- 9.4 (mean +/- SD) to 14.7 +/- 9.7 (p = 0.003). An increase in the inferior region of the PAW (7 +/- 5 mm) was observed on radiographs (p = 0.0001). However, no correlation between the effect of the MAD on the dimensions of the PAW and its effect on SDB was found. At the 6-month follow-up, the sleep apnoea-related symptoms had decreased by 31% (p = 0.003). Quality of life remained stable. BNP were reduced from 195.8 +/- 180.5 pg/ml to 148.1 +/- 139.9 pg/ml (p = 0.035). LVEF, however, remained unchanged. At the 12-month follow-up, 64 % of the patients were still using the MAD. Three patients withdrew from the study because of discomfort with the MAD. In most patients, MAD treatment had no severe side effect on the signs or symptoms of temporomandibular disorders. However, dental complications were observed. In conclusion, in patients with stable CHF who are experiencing problems with SDB, MAD intervention appears to reduce the severity of SDB, sleep apnoea-related symptoms, and neurohormonal activity. A lower tendency for PAW collapse may explain the effect observed on SDB. The reduction in plasma BNP may indicate decreased cardiac strain as a result of treatment of SDB. The 5-year survival rate, measured from the start of MAD intervention, was higher in the group that used a MAD than in the group that did not use a MAD (p = 0.036). No severe side effects on the stomatognathic system were observed during the intervention, and most patients--edentulous included--tolerated the treatment well. Impaired oral health, including reduced dentition and edentulousness, seemed to limit the use of the MAD in this group of elderly patients, both because of technical difficulties and because of the increased risk of dental complications. However, because the treatment of SDB is important in the management of CHF, the MAD intervention seems to be a valuable method in the treatment arsenal of SDB.
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PMID:Sleep apnoea in patients with stable congestive heart failure an intervention study with a mandibular advancement device. 1563 33

A 74-year-old man with ischemic cardiomyopathy was repeatedly admitted for congestive heart failure. His left ventricular ejection fraction was 21% and diastolic left ventricular dimension was 73.5mm by echocardiography. He was treated with biventricular pacing and heart failure improved from New York Heart Association class III to II. Before the treatment, brain natriuretic peptide was 600.5 pg/ml. Apnea hypopnea index was 23.8 and all events were central type. After biventricular pacing, apnea hypopnea index was improved to 21.9 after 11 days, 14.0 after 33 days, and 4.8 after 48 days. His left ventricular ejection fraction was 36%, diastolic left ventricular dimension was 71.4mm, and brain natriuretic peptide was 383.8 pg/ml. In this patient, central sleep disordered breathing was improved by biventricular pacing therapy after only 48 days.
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PMID:[Improvement of central sleep disordered breathing with severe congestive heart failure by biventricular pacing therapy: a case report]. 1647 70

The aim of this study was to determine the prevalence of sleep-related breathing disorders (SDB) in a UK general heart failure (HF) population, and assess its impact on neurohumoral markers and symptoms of sleepiness and quality of life. Eighty-four ambulatory patients (72 male, mean (SD) age 68.6 (10) yrs) attending UK HF clinics underwent an overnight recording of respiratory impedance, SaO2 and heart rate using a portable monitor (Nexan). Brain natriuretic peptide (BNP) and urinary catecholamines were measured. Subjective sleepiness and the impairment in quality of life were assessed (Epworth Sleepiness Scale (ESS), SF-36 Health Performance Score). SDB was classified using the Apnoea/Hypopnoea Index (AHI). The prevalence of SDB (AHI > 15 events h(-1)) was 24%, increasing from 15% in mild-to-moderate HF to 39% in severe HF. Patients with SDB had significantly higher levels of BNP and noradrenaline than those without SDB (mean (SD) BNP: 187 (119) versus 73 (98) pg mL(-1), P = 0.02; noradrenaline: 309 (183) versus 225 (148) nmol/24 h, P = 0.05). There was no significant difference in reported sleepiness or in any domain of SF-36, between groups with and without SDB (ESS: 7.8 (4.7) versus 7.5 (3.6), P = 0.87). In summary, in a general HF clinic population, the prevalence of SDB increased with the severity of HF. Patients with SDB had higher activation of a neurohumoral marker and more severe HF. Unlike obstructive sleep apnoea, SDB in HF had little discernible effect on sleepiness or quality of life as measured by standard subjective scales.
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PMID:Sleep-disordered breathing in a general heart failure population: relationships to neurohumoral activation and subjective symptoms. 1649 6

The aim of the present study was to investigate the effect of a mandibular advancement device (MAD) for the treatment of sleep apnea (SA) on plasma brain natriuretic peptide (BNP), left ventricular ejection fraction (LVEF), and health-related qualify of life (HRQL) in patients with mild to moderate stable congestive heart failure (CHF). Seventeen male patients aged 68.4+/-5.5 with an apnea-hypopnea index (AHI) >or=10 were equipped with an individually fitted MAD. SA was evaluated using a portable respiratory multirecording system before and after the initiation of treatment. Eleven patients completed follow-up and were evaluated after 6 months of treatment. The AHI reduced from 25.4+/-10.3 to 16.5+/-10.0 (p=0.033) compared to baseline and mean plasma BNP levels decreased from 195.8+/-180.5 pg/ml to 148.1+/-139.9pg/ml (p=0.035). SA-related symptoms, e.g., excessive daytime sleepiness, were also reduced (p=0.003). LVEF and HRQL were unchanged. We conclude that SA treatment with a MAD on patients with mild to moderate stable CHF appears to result in the reduction of plasma BNP levels. Further studies to investigate if the observed reduction in BNP concentrations also result in improved prognosis are warranted.
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PMID:Treatment of sleep apnea in congestive heart failure with a dental device: the effect on brain natriuretic peptide and quality of life. 1653 92

It has recently been recognized that many patients with congestive heart failure (CHF) are anemic. The anemia is very often associated with chronic kidney disease (CKD). The more severe the anemia the more severe the CHF, with higher mortality, morbidity, and hospitalization rate. The only way to prove that the anemia is itself a causative factor in the progression of both the CKD and the CHF is to correct it. In this paper we review the results of published papers and some preliminary reports about correction of this anemia in CHF. These studies frequently showed that erythropoietic stimulating agents (ESA) with oral or IV iron often resulted in improvement in left ventricular systolic and diastolic function, dilation, and hypertrophy, stabilization or improvement in renal function, reduced hospitalizations, diuretic dose, mitral regurgitation, pulmonary artery pressure, plasma volume, heart rate, serum brain natriuretic peptide levels, and the inflammatory markers C reactive protein and Interleukin 6, and an improvement in New York Heart Association class, exercise capacity, oxygen utilization during exercise, sleep apnea, caloric intake, depression, and quality of life. The activity of endothelial progenitor cells was also increased. Iron deficiency may also play an important role in the anemia, because significant improvement of cardiac, renal, and functional status in these anemic CKD-CHF has been seen after treatment with IV iron alone. Clearly more work is needed to clarify the relationship between anemia, CKD and CHF.
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PMID:The correction of anemia in patients with the combination of chronic kidney disease and congestive heart failure may prevent progression of both conditions. 1867 Jul 32

The possibility that natriuretic peptides' effects are important in hypoxia responses of vertebrates is reviewed. Both the transcription and release of natriuretic peptides are affected by oxygen tension. Furthermore, many of the effects observed in hypoxia, such as diuresis and a reduction of plasma volume, are also caused by treatment of the animal with natriuretic peptides. Also, several clinical observations about changes in natriuretic peptide levels in, e.g., sleep apnea and cyanotic congenital heart disease, are consistent with the idea that hypoxia is involved in the etiology of conditions, in which natriuretic peptide levels increase. Virtually all published information on the relationship between oxygen and natriuretic peptides is based on human studies. Because hypoxic conditions are more common in aquatic than terrestrial environments, future studies about the possible role of natriuretic peptides in hypoxia, as well as the role of hypoxia in the evolution of natriuretic peptides, including the different subtypes, should increasingly involve also aquatic organisms.
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PMID:Natriuretic peptides in hormonal regulation of hypoxia responses. 1900 14

Background Carvedilol may reduce the severity of central sleep apnea (CSA) in patients with chronic heart failure (CHF). Methods and Results This study prospectively examined the effect of carvedilol on the severity of CSA in patients with CHF. Polysomnographic findings, left ventricular (LV) function, and plasma brain natriuretic peptide (BNP) level were evaluated before and 6 months after induction of carvedilol in 16 patients with CHF (New York Heart Association functional class II or III and LV ejection fraction <50%) who had CSA (central apnea index [CAI] >5 with dominant central apneic events). All patients tolerated carvedilol. The 6-month treatment with carvedilol increased the LV ejection fraction (32+/-7.4% to 45+/-9.8%, P<0.001) and decreased the BNP level (159 [69-458] pg/ml to 38 [16-193] pg/ml, P=0.017). The polysomnographic findings showed that the treatment decreased the apnea-hypopnea index (34+/-13 to 14+/-13, P=0.003) and CAI (13+/-11 to 1.9+/-4.3, P<0.001), whereas it increased the obstructive apnea index (1.1+/-1.5 to 3.1+/-3.4, P=0.04). Conclusion This preliminary study shows that treatment with carvedilol reduces the severity of CSA in patients with CHF, but that episodes of obstructive sleep apnea sometimes increase after the treatment.
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PMID:Carvedilol reduces the severity of central sleep apnea in chronic heart failure. 1912 6

Sleep-disordered breathing (SDB) and cardiovascular disease (CVD) are closely related; however, the effect of SDB on the long-term prognosis of patients with CVD is unknown. Our aim in this study was to assess the association between SDB and fatal cardiovascular events in patients with CVD. We performed a long-term follow-up study of 135 patients with CVD. The average observation period was 610 +/- 268 days. The patients were classified into 2 groups based on their apnea index: patients with apnea index >or=5/h (Group H) were diagnosed with SDB (n = 43), and those with apnea index <5/h (Group L) were diagnosed without SDB (n = 92). In Group H, obstructive sleep apnea (OSA) was diagnosed if obstructive apnea index was >or=5/h, and central sleep apnea was diagnosed if central apnea index was >or=5/h. Group H had a significantly lower survival rate than Group L (p <0.005), particularly those with OSA in Group H (p <0.0005). In a Cox proportional hazards model with presence of OSA, age, brain natriuretic peptide, left ventricular ejection fraction, and cardiovascular risk factors, the odds ratio of fatal cardiovascular events was 2.45 (95% confidence interval 1.26 to 5.08) for OSA (p <0.01), which was associated with an increased risk of mortality. In conclusion, our results suggest that SDB is associated with a poorer long-term prognosis and that the presence of OSA is a strong predictor of fatal cardiovascular events in patients with CVD.
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PMID:Influence of untreated sleep-disordered breathing on the long-term prognosis of patients with cardiovascular disease. 1923 43


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