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A combination of airway clearance techniques are applied for people with bronchiectasis, together with recommendations for exercise and suggestions for management of common comorbidities https://bit.ly/2U3c99H.

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STUDY OBJECTIVES: Obstructive Sleep Apnea (OSA) is associated with a poor prognosis in patients with coronary artery disease. We hypothesized that abnormalities of coronary blood flow (CBF) associated with obstructive apneas may predispose patients to ischemia. We aimed to determine CBF during respiratory events in patients with OSA. SETTING: University Hospital. PATIENTS: Ten subjects undergoing elective percutaneous coronary intervention DESIGN: We measured CBF and myocardial work (rate-pressure product [RPP]) in a non-culprit coronary artery in patients sleeping in the cardiac catheterization laboratory. Hemodynamic responses were matched to spontaneously occurring respiratory events. MEASUREMENTS AND RESULTS: Events comprised a mixture of obstructive apneas, central apneas and hypopneas. RPP increased at the termination of each type of respiratory event. Following the rise in RPP, there was a delay, identified with breakpoint analysis, before CBF began to increase (P<0.001) that differed in duration with event type: 8 sec for obstructive apnea, 5 sec for central apnea, and 4 sec for hypopnea. The delay in CBF with obstructive apnea was associated with an increase in coronary vascular resistance of 16% +/- 4% (P < 0.05). Stepwise multilinear regression analysis showed the increase in CBF was predicted by the rise in RPP (R=0.52, P<0.001) and presence of arousal from sleep (R=0.30, P<0.05), but not the degree of O2 desaturation. CONCLUSION: Following obstructive apneas there is a transient uncoupling of CBF from myocardial work and an increase in CVR. This disturbed flow-metabolic coupling may lead to nocturnal myocardial ischemia in patients with both OSA and coronary artery disease.

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STUDY OBJECTIVES: Patients with obstructive sleep apnea (OSA) and coronary artery disease have a poor long-term prognosis. It is unknown whether the coronary blood flow (CBF) response to OSA is appropriate for myocardial metabolic requirements. Therefore, CBF was assessed during OSA, before and after the development of coronary artery endothelial dysfunction. SETTING: University Hospital Animal Laboratory. PATIENTS OR PARTICIPANTS: Newborn lambs. INTERVENTIONS: Lambs were surgically instrumented for invasive hemodynamic monitoring and sleep-wake EEG recordings. A tracheostomy was inserted to control the upper airway and model OSA during sleep. Coronary artery endothelial dysfunction was created using infusions of lipopolysaccharide (LPS). The CBF response during OSA was assessed and compared to changes in myocardial work (rate-pressure product [RPP]), O2 saturation, and cortical arousal, before and after the LPS infusions. MEASUREMENTS AND RESULTS: During OSA, CBF increased by 8.6% +/- 2.4% above baseline in the pre-LPS condition and 8.8% +/- 1.9% post-LPS, peaking following termination of the respiratory event. Pre-LPS, change in CBF post-apnea was independently correlated with change in RPP (R2 = 0.50), minimum SpO2 (R2 = 0.11) and the presence of cortical arousal (R2 = 0.04) (P < 0.01, forward stepwise regression analysis). Following LPS, the only predictor of CBF was degree of O2 desaturation (R2 = 0.14, P < 0.05). CONCLUSION: Under baseline conditions, CBF correlates well with myocardial work following the termination of apnea in lambs. After the creation of coronary artery endothelial dysfunction with LPS, there is uncoupling of the normal CBF-myocardial work relationship.

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BACKGROUND AND PURPOSE: Much remains unknown about the regulation of coronary artery blood flow (CBF), particularly during sleep and sleep-related disease states such as obstructive sleep apnoea (OSA). Mediators produced by the endothelium are known to be crucial in the regulation of CBF, particularly vasodilator substances such as nitric oxide. Endothelial dysfunction with altered vascular reactivity has been identified in disease states such as atherosclerosis, OSA and sepsis, but as yet its potential effects on CBF during sleep or OSA is unknown. We aimed to produce a novel animal model of coronary artery endothelial dysfunction, subsequently to be used to study the role of the endothelium in regulating CBF during OSA. METHODS: Lambs (n=6) were instrumented under general anaesthesia (2% Halothane, 50% O2, balance N2O) for recording CBF (Transonic flow probe around circumflex coronary artery), central arterial blood pressure (Pca), central venous pressure (Pjv) and sleep monitoring (bio-electrodes). Coronary vascular resistance (CVR) was calculated as (Pca-Pjv)/CBF. Following>or=72 h of recovery, endothelial damage was induced by infusing lipopolysaccharide (LPS, 2 microg/kg over 30 min) on 3 successive days. The day before and the day after the period of LPS infusion, sleep studies were performed and coronary artery endothelial function was assessed by comparing CBF and CVR responses to left atrial injection of endothelial-dependent (Acetylcholine [Ach]) and independent (sodium nitroprusside [SNP]) vasodilators. RESULTS: Prior to LPS, arterial blood pressure was lower in tonic active sleep (AS) and higher in phasic AS than wakefulness. CBF and arterial blood pressure were slightly higher in phasic AS compared to tonic AS, and were the same in quiet sleep compared to quiet wakefulness. CVR did not differ across sleep states. After LPS, systolic blood pressure was reduced compared to before LPS in all sleep states, while other parameters were unchanged. Prior to LPS treatment, increasing doses of Ach (0.0001-1.0 microg/kg) and SNP (0.45-4.5 microg/kg) led to progressive reductions in CVR and increases in CBF. After LPS treatment, the fall in CVR and increase in CBF in response to Ach was attenuated (two-way repeated measures analysis of variance (ANOVA), P<0.05), whereas it was unchanged in response to SNP. CONCLUSION: LPS leads to impaired coronary artery vasodilation in response to endothelial-dependent, but not endothelial-independent vasodilators. This novel model of coronary artery endothelial dysfunction in the sleeping lamb will provide the opportunity to study the regulation of CBF during OSA.

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STUDY OBJECTIVE: Central sleep apnea (CSA) associated with Cheyne-Stokes respiration in patients with congestive heart failure (CHF) is thought to be an acquired pattern of respiratory control instability related, at least in part, to elevated sympathetic nervous system activity. The effect of restoring heart function to normal with heart transplantation in patients with CHF and CSA has only been reported within weeks of the transplant and with varying results. The purpose of the study was to evaluate the impact of successful heart transplant on sympathetic nervous system activity and CSA severity in patients with CHF. DESIGN: Controlled prospective trial. SETTING: University hospital. PATIENTS: Twenty-two patients with CHF (13 patients with CSA, and 9 patients with no sleep-disordered breathing [SDB]). INTERVENTIONS AND MEASUREMENTS: Polysomnography, left ventricular ejection fraction (LVEF), and overnight urinary norepinephrine excretion (UNE) were measured before and > 6 months after successful heart transplantation. RESULTS: In the CSA group, there was a fall in apnea-hypopnea index (AHI) [mean +/- SD, 28 +/- 15 to 7 +/- 6/h; p < 0.001] and UNE (48.1 +/- 30.9 to 6.1 +/- 4.8 nmol/mmol creatinine, p < 0.001) associated with normalization of LVEF (19.2 +/- 9.3% to 53.7 +/- 6.1%, p < 0.001) at 13.2 +/- 8.3 months following heart transplantation. Of the CSA group following transplantation, seven patients had no SDB (AHI < 5/h), three patients had persistent CSA (AHI, 12.3 +/- 0.9/h) and four patients acquired obstructive sleep apnea (OSA) [AHI, 11.2 +/- 7.4/h]. In comparison, none of the control group acquired CSA or OSA after transplantation. CONCLUSIONS: We conclude that CSA may persist despite normalization of heart function and sympathetic nerve activity.

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OBJECTIVES: To compare and establish the relevance of the relative degree of sympathetic nervous system activity (SNSA) in groups of patients with congestive heart failure (CHF) and obstructive sleep apnea (OSA), and in a control group. BACKGROUND: Elevated SNSA is a characteristic feature of CHF, as well as of OSA and nonhypercapnic central sleep apnea (CSA). OSA and CSA commonly occur with CHF; however, the relative contribution of apnea-related hypoxemia and sleep fragmentation to the SNSA of patients with CHF is not known. METHODS: This was a prospective, controlled, observational trial in which the overnight urinary norepinephrine (UNE) level, which is a measure of integrated overnight SNSA while asleep, was measured in 15 healthy male volunteers, 15 male OSA patients who did not have CHF, and 90 CHF patients (77 men). CHF patients also had right heart pressure measurements and then were grouped by the presence of sleep apnea. RESULTS: Compared with healthy individuals, the mean (+/- SD) UNE level was significantly elevated in the OSA group and was even further elevated in the CHF group (13.4 +/- 5.6 vs 19.7 +/- 12.3 vs 32.2 +/- 20.2 nmol/mmol creatinine, respectively; p < 0.001 [by analysis of variance]). Within the CHF group, the mean UNE levels were greatest in the CHF-CSA group compared with the CHF-OSA group and the CHF nonapnea group (43.9 +/- 24.1 vs 24.0 +/- 10.8 vs 22.4 +/- 8.9 nmol/mmol creatinine, respectively; p < 0.001). Using a multivariate regression model, the variance of the UNE level in the CHF group was predicted, in descending order, by pulmonary capillary wedge pressure (14% variance), rapid eye movement sleep (8%), and the mean sleep pulse oximetry level (7%). CONCLUSIONS: Overnight SNSA is significantly greater in CHF patients than in OSA patients. Moreover, the hemodynamic severity of CHF contributes to the elevation of SNSA in CHF patients to a greater degree than apnea-related hypoxemia.

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BACKGROUND: Congestive heart failure (CHF) patients with central sleep apnea (CHF-CSA) have elevated plasma norepinephrine (NE) compared with CHF patients without apnea (CHF-N). Patients with CHF-CSA also demonstrate higher mean pulmonary artery pressure (PAP), which is suggestive of worse cardiac function. Whether CSA contributes to chronic elevation of sympathetic nerve activity or is associated with more severe CHF remains unknown. We measured awake total body and cardiac NE spillover and related these to measurements of cardiac hemodynamics and apnea severity in CHF patients with CSA, with normal breathing, and with obstructive sleep apnea (CHF-OSA). METHODS AND RESULTS: A total of 55 CHF patients underwent right heart catheterization and measurements of total body and cardiac NE spillover using NE radioisotope dilution methodology. After polysomnography, patients were grouped by apnea type: 19 were CHF-N, 15 were CHF-OSA, and 21 were CHF-CSA. Compared with the CHF-N and CHF-OSA groups, the CHF-CSA group had significantly higher total body NE spillover (4.62+/-0.56 versus 4.47+/-0.54 versus 6.95+/-0.89 nmol/min, respectively; P=0.03), cardiac NE spillover (0.25+/-0.05 versus 0.21+/-0.05 versus 0.42+/-0.06 nmol/min, respectively; P=0.02) and mean PAP (23.5+/-2.4 versus 21.2+/-0.8 versus 30.4+/-0.2 mm Hg, respectively; P<0.02). However, controlling for severity of CHF resulted in no significant differences in NE kinetics among the 3 groups. In a stepwise regression, only mean PAP independently correlated with total body (r=0.33, P=0.03) and cardiac NE spillover (r=0.44, P=0.002). Sleep apnea severity bore no relationship to markers of sympathetic nerve activity. CONCLUSION: Total body and cardiac sympathetic nerve activity are elevated in CHF-CSA compared with CHF-OSA and CHF-N patients and are related to heart failure not apnea severity.

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