No description available.

No description available.

STOP-Bang is a tool for predicting the likelihood for sleep-disordered breathing (SDB). In the conventional score, all variables are dichotomous. Our aim was to identify whether modifying the STOP-Bang scoring tool by weighting the variables could improve test characteristics.

The impact of sleep on quality of life (QoL) has been well documented; however, there is a great need for reliable QoL measures for persons with obstructive sleep apnea (OSA). We compared the QoL scores between the 36-Item Short Form of the Medical Outcomes Survey (SF-36), Calgary Sleep Apnea Quality of Life Index (SAQLI), and Functional Outcomes Sleep Questionnaire (FOSQ) in persons with OSA.

Purpose: Exercise testing modalities to assess the effects of a given intervention should prove to be reliable and reproducible. This study reports on test-retest reproducibility of the 3-min shuttle walking and step testing exercise protocols to assess exertional dyspnea and exercise physiology in COPD patients. / Methods: Stable COPD patients (N=43; 65 +/- 6.5 years; FEV1 = 49 +/- 16% pred.) equipped with a portable Jaeger Oxycon MobileRTM metabolic system repeated the walking or stepping tests on two occasions separated by 7 to 14 days. At each visit, participants performed, in a randomized order, four externally paced 3-min bouts of shuttle walking at speeds of 1.5, 2.5, 4.0 and 6.0 km·h-1 or of stepping at a constant rate of 18, 22, 26 and 32 steps·min-1, respectively. Each exercise bout was separated by a 10-min rest period. Ventilation, heart rate, gas exchange parameters and Borg dyspnea score were obtained for each bout during the last 30-seconds of exercise. / Results: The majority of patients completed stepping or walking at the slowest cadence but only 33% completed walking at 6.0 km·h -1 and 40% completed stepping at 32 steps·min-1. Test-retest Pearson correlation coefficients for ventilation, heart rate, gas exchange parameters and dyspnea scores over the four exercise bouts, all exceeded 0.80 with the highest coefficient found for ventilation (r≥.95). Intra-class correlation coefficients were similar to Pearson. Bland & Altman representation showed that a similar proportion of dyspnea data points (92 vs. 96%) lied within 2 SD of the mean difference between test-retest values for dyspnea Borg scores during walking and stepping. / Conclusion: Results show very good reproducibility for both 3-min shuttle walking and stepping exercise protocols in patients with COPD. / This study was supported by an unrestricted grant from Boehringer-Ingelheim/Pfizer.

Background: Obstructive sleep apnea (OSA) has been associated with atrial enlargement in response to high arterial and pulmonary pressures and increased sympathetic tone. Continuous positive airway pressure (CPAP) is the gold standard treatment for OSA; its impact on atrial electrical remodeling has not been investigated however. Signal-averaged p-wave (SAPW) is a non-invasive quantitative method to determine p-wave duration, an accepted marker for atrial electrical remodeling. The objective was to determine whether CPAP induces reverse atrial electrical remodeling in patients with severe OSA. Methods: Prospective study in consecutive patients attending the Sleep Clinic at Kingston General Hospital. All patients underwent full polysomnography. OSA-negative and severe OSA were defined as apnea-hypopnea index (AHI) < 5 events/hour and AHI ≥ 30 events/hour, respectively. In severe OSA patients, SAPW was determined pre- and post-intervention with CPAP for 4 - 6 weeks. In OSA-negative controls, SAPW was recorded at baseline and 4 - 6 weeks thereafter without any intervention. Results: A total of 19 severe OSA patients and 10 controls were included in the analysis. Mean AHI and minimum O2 saturation were 41.4 ± 10.1 events/hour and 80.5 ± 6.5% in severe OSA patients and 2.8 ± 1.2 events/hour and 91.4 ± 2.1% in controls. Baseline BMI was different between severe OSA patients and controls (34.3 ± 5.4 vs 26.6 ± 4.6 kg/m2; p < 0.001). At baseline, severe OSA patients had a greater SAPW duration than controls (131.9 ± 10.4 vs 122.8 ± 10.5 ms; p = 0.02). After CPAP intervention, there was a significant reduction of SAPW duration in severe OSA (131.9 ± 10.4 to 126.2 ± 8.8 ms; p < 0.001). In controls, SAPW duration did not change within 4 - 6 weeks. Conclusion: CPAP induced reverse atrial electrical remodeling in patients with severe OSA as represented by a significant reduction in SAPW duration. / Thesis (Master, Physiology) -- Queen's University, 2011-07-29 12:53:09.134

Rationale. There is a need for the development of a field test to evaluate exertional dyspnea in the primary care setting. This study examined the applicability of a 3-minute constant rate step test in patients with COPD. / Methods. This test involved 4 stepping rates (18, 22, 26, 32 steps.min-1) equivalent to approximately 4.5, 5.3, 6.0, and 7.2 MET with the ultimate goal that in its final development, the assessment will be made a single stepping rate based on disease severity. Stable COPD patients (N = 43; 65 +/- 6.5 years; FEV1 = 49 +/- 16% pred.; SpO2 (%) rest: 95 +/- 2) were equipped with a portable Jaeger Oxycon MobileRTM metabolic system and followed an audio signal for stepping up and down a single 20 cm step for 3 minutes. Borg dyspnea scores were obtained at the end each stepping bout. A 10-min rest was given between each stepping bout. / Results. Of the 43 patients, 80% completed stages 1 and 2, 74 and 37% stages 3 and 4 while no patient of MRC class 4 or 5 (N = 8) completed stage 1. Breathing frequency (breaths.min-1) spanned from 26.5 +/- 4.1 to 39.0 +/- 6.4 but VT (L) remained unchanged (1.4 +/- 0.3 vs. 1.5 +/- 0.4) from stage 1 to 4 while Borg scores were 3 +/- 1, 4 +/- 1, 5 +/- 2, 6 +/- 3 respectively and SpO2 (%) were 92 +/- 5, 91 +/- 4, 91 +/- 4 and 90 +/- 4. / Conclusions. Preliminary findings indicate that a 3-minute constant rate step test may present a feasible alternative to laboratory testing to assess exertional dyspnea in moderately severe COPD. In this population, a stepping rate of 26 steps.min-1 could be sustained by the majority of patients while producing a level of dyspnea potentially amenable to therapy. / This study was supported by an unrestricted grant from Boehringer-Ingelheim/Pfizer.

Diss. (sammanfattning) Uppsala : Univ., 2003. / Härtill 4 uppsatser.

Ipratropium bromide is a short-acting, non-selective, muscarinic antagonist frequently prescribed for the treatment of Chronic Obstructive Pulmonary Disease (COPD) and as an emergency adjunct therapy for acute asthma. Within the past decade, there has been an accumulating wealth of clinical evidence which indicates that anti-muscarinic drugs, such as ipratropium, are responsible for an increased risk of stroke or, an adverse cardiovascular outcome (including increasing the risk and severity of myocardial infarction (MI)). MI remains the highest risk factor of death for COPD patients due to the systemic co-morbidities associated with COPD, which includes ischaemic heart disease (IHD). Despite the knowledge that approximately 22% of COPD patients also suffer from underlying IHD, the cardiovascular safety of muscarinic antagonists, such as ipratropium, has not been tested in a non-clinical setting of IHD or MI. In order to address this, the current project was designed to investigate, for the first time, the effects of ipratropium on the myocardium in a non-clinical setting. It was identified that under normoxic conditions, ipratropium did not have a significant effect on cardiac myocyte viability or infarction, from 3 month Sprague Dawley rats. In addition to this, following simulated ischaemia, ipratropium also did not appear to exacerbate myocardial injury. However, when ipratropium was administered in the context of simulated ischaemia followed by reperfusion, there was a significant exacerbation in myocardial injury which was characterised by increases in infarction, apoptosis, necrosis and a loss of resilience of oxidative stress. In order to characterise the mechanism by which ipratropium exerts the observed cardio-toxic effects, it was investigated whether acetylcholine (ACh) or cyclosporin A (CsA) were capable of attenuating the ipratropium induced cardiotoxicity. Both agents showed significant limitation of injury when co-administered with ipratropium indicating that ipratropium exerts its cardio-toxic effect through a mechanism which links muscarinic signalling to the mitochondrial permeability transition pore (mPTP). This supports previously published work where the protective signalling of ACh has been shown to promote the phosphorylation of pro-survival kinases, such as Akt and Erk1/2 and that this provides inhibition of the mPTP. Western blotting was employed to identify whether there was an involvement of the pro-survival kinases Akt and Erk1/2, as well as the stress induced kinase JNK. Ipratropium significantly increased levels of phospho-Akt and phospho-Erk1/2. However, JNK levels appeared to be insignificantly altered in comparison with the control groups. Both ACh and CsA were capable of limiting these increases. Further to this, an aged study was carried out, which showed that, within the aged myocardium, ipratropium is capable of eliciting further injury in comparison with the 3 month age groups. The effect of ipratropium on tolerance of oxidative stress was not significant, but, also, ACh and CsA were shown as unable to protect. Significant levels of JNK were also observed in the aged animals in comparison with the 3 month groups. In combination, the results presented here demonstrate, for the first time, that ipratropium is capable of exacerbating ischaemia/reperfusion injury in in vitro models of myocardial ischaemia/reperfusion. In addition, ACh and CsA are capable of limiting this injury, implying a role for pro-survival kinases and the mPTP in ipratropium induced myocardial injury. In the aged study, ipratropium still exacerbated injury, however, ACh and CsA appeared unable to protect, therefore promoting previous work that cellular signalling is altered in the senescent myocardium. In conclusion, further studies must be carried out in order to fully characterise the cardio-vascular safety profile of ipratropium.

No description available.