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1.
Lancet Respir Med ; 2021 Nov 02.
Artículo en Inglés | MEDLINE | ID: mdl-34739861

RESUMEN

BACKGROUND: Preserved ratio impaired spirometry (PRISm) is defined as a FEV1 of less than 80% predicted and a FEV1/forced vital capacity (FVC) ratio of 0·70 or higher. Previous research has indicated that PRISm is associated with respiratory symptoms and is a precursor of chronic obstructive pulmonary disease (COPD). However, these findings are based on relatively small selective cohorts with short follow-up. We aimed to determine the prevalence, risk factors, clinical implications, and mortality of PRISm in a large adult general population. METHODS: For this cohort analysis, we used data from the UKBiobank to assess PRISm prevalence, risk factors and associated symptoms, and associated comorbidities in a large adult population. Participants with spirometry deemed acceptable by an investigator (best measure FEV1 and FVC values) at baseline were included. Participants were excluded if they did not have acceptable spirometry or were missing data on body-mass index or smoking status. Control spirometry was defined as a FEV1 of 80% or more predicted and a FEV1/FVC ratio of 0·70 or higher. Airflow obstruction was defined as a FEV1/FVC ratio of less than 0·70. We used multivariable regression to determine risk factors for PRISm and associated comorbidities. Individuals who lived within close proximity to an assessment centre were invited for follow-up, with repeat spirometry. Only participants who had been included at baseline were examined in follow-up. This allowed for a longitudinal analysis of PRISm over time and risk factors for transition to airflow obstruction. We also did the survival analysis for a 12-year period. FINDINGS: Participants were recruited by UK Biobank between Dec 19, 2006, and Oct 10, 2010. We included 351 874 UK Biobank participants (189 247 women and 162 627 men) in our study, with a median follow-up of 9·0 years (IQR 8·0-10·0). 38 639 (11·0%) of 351 874 participants had PRISm at baseline. After adjustment, PRISm was strongly associated with obesity (odds ratio [OR] 2·40 [2·26-2·55], p<0·0001), current smoking (1·48 [1·36-1·62], p<0·0001), and patient reported doctor-diagnosed asthma (1·76 [1·66-1·88], p<0·0001). Other risk factors identified included female sex, being overweight, trunk fat mass, and trunk fat percentage. PRISm was strongly associated with symptoms and comorbidity including increased risk of breathlessness (adjusted OR 2·0 [95% CI 1·91-2·14], p<0·0001) and cardiovascular disease (adjusted OR 1·71 [1·64-1·83], p<0·0001 for heart attack). Longitudinal analysis showed that 241 (12·2%) of 1973 participants who had PRISm at baseline had transitioned to airflow obstruction consistent with COPD. PRISm was associated with increased all-cause mortality (adjusted hazard ratio 1·61 [95% CI 1·53-1·69], p<0·0001) versus control participants. INTERPRETATION: PRISm was associated with breathlessness, multimorbidity, and increased risk of death, which does not seem to be explained by smoking, obesity, or existing lung disease. Although for many patients PRISm is transient, it is important to understand which individuals are at risk of progressive lung function abnormalities. Further research into the genetic, structural and functional pathophysiology of PRISm is warranted. FUNDING: UK Medical Research Council and University of Bristol.

2.
Chron Respir Dis ; 18: 14799731211043530, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-34565203

RESUMEN

BackgroundThe sensitivity of patient-reported outcomes (PROs) to detect the effects of treatment change depends on the match between the change in items of the PRO and the change that takes place in a sample of people. The aim of this study is to compare the sensitivity of different PROs in detecting changes following the initiation of biologic treatment in asthma. Methods: Patients starting a biologic treatment as part of clinical care completed the Asthma Control Questionnaire (ACQ-6), the Severe Asthma Questionnaire (SAQ and SAQ-global scores) and the EQ5D (EQ-5D-5L and EQ5D-VAS) at baseline. They completed the ACQ-6, SAQ, SAQ-global and a retrospective global rating of change (GRoC) scale at weeks 4, 8 and 16 and completed the EQ-5D-5L and EQ5D-VAS at week 16. The SAQ-global and EQ5D-VAS differ but both are single item 100-point questions. Sensitivity was measured by Cohen's D effect size at each of the three time points. Results: 110 patients were recruited. Depending on the time of assessment, effect size varied between 0.45 and 0.64 for the SAQ, between 0.50 and 0.77 for the SAQ-global; between 0.45 and 0.69 for ACQ-6; between 0.91 and 1.22 for GRoC; 0.32 for EQ-5D-5L and 0.49 for EQ5D-VAS. Conclusion: The sensitivity to change of a questionnaire varies with the time of measurement. The three asthma-specific prospective measures (SAQ, SAQ-global and ACQ-6) have similar sensitivity to change. The single-item EQ5D-VAS was less sensitive than the asthma specific measures and less sensitive than the single-item SAQ-global. The EQ-5D-5L was least sensitive.


Asunto(s)
Asma , Productos Biológicos , Asma/tratamiento farmacológico , Productos Biológicos/uso terapéutico , Humanos , Medición de Resultados Informados por el Paciente , Estudios Prospectivos , Psicometría , Calidad de Vida , Estudios Retrospectivos , Encuestas y Cuestionarios
3.
BMC Pulm Med ; 21(1): 246, 2021 Jul 22.
Artículo en Inglés | MEDLINE | ID: mdl-34294062

RESUMEN

BACKGROUND: Observational studies show an association between reduced lung function and impaired cognition. Cognitive dysfunction influences important health outcomes and is a precursor to dementia, but treatments options are currently very limited. Attention has therefore focused on identifying modifiable risk factors to prevent cognitive decline and preserve cognition. Our objective was to determine if lung function or risk of COPD causes reduced cognitive function using Mendelian randomization (MR). METHODS: Single nucleotide polymorphisms from genome wide association studies of lung function and COPD were used as exposures. We examined their effect on general cognitive function in a sample of 132,452 individuals. We then performed multivariable MR (MVMR), examining the effect of lung function before and after conditioning for covariates. RESULTS: We found only weak evidence that reduced lung function (Beta - 0.002 (SE 0.02), p-value 0.86) or increased liability to COPD (- 0.008 (0.008), p-value 0.35) causes lower cognitive function. MVMR found both reduced FEV1 and FVC do cause lower cognitive function, but that after conditioning for height (- 0.03 (0.03), p-value 0.29 and - 0.01 (0.03) p-value 0.62, for FEV1 and FVC respectively) and educational attainment (- 0.03 (0.03) p-value 0.33 and - 0.01 (0.02), p-value 0.35) the evidence became weak. CONCLUSION: We did not find evidence that reduced lung function or COPD causes reduced cognitive function. Previous observational studies are probably affected by residual confounding. Research efforts should focus on shared risk factors for reduced lung function and cognition, rather than lung function alone as a modifiable risk factor.

7.
ERJ Open Res ; 7(1)2021 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-33564672

RESUMEN

Asthma therapy, including monoclonal antibodies, was not associated with #COVID19 infection or hospitalisation in a UK severe asthma population. Shielding led to a reported worsening of mental health in nearly half of patients contacted (47%). https://bit.ly/3jImUsG.

8.
Eur Respir J ; 58(3)2021 09.
Artículo en Inglés | MEDLINE | ID: mdl-33574079

RESUMEN

BACKGROUND: Observational studies suggest an association between reduced lung function and risk of coronary artery disease and ischaemic stroke, independent of shared cardiovascular risk factors such as cigarette smoking. We use the latest genetic epidemiological methods to determine whether impaired lung function is causally associated with an increased risk of cardiovascular disease. METHODS AND FINDINGS: Mendelian randomisation uses genetic variants as instrumental variables to investigate causation. Preliminary analysis used two-sample Mendelian randomisation with lung function single nucleotide polymorphisms. To avoid collider bias, the main analysis used single nucleotide polymorphisms for lung function identified from UKBiobank in a multivariable Mendelian randomisation model conditioning for height, body mass index and smoking.Multivariable Mendelian randomisation shows strong evidence that reduced forced vital capacity (FVC) causes increased risk of coronary artery disease (OR 1.32, 95% CI 1.19-1.46 per standard deviation). Reduced forced expiratory volume in 1 s (FEV1) is unlikely to cause increased risk of coronary artery disease, as evidence of its effect becomes weak after conditioning for height (OR 1.08, 95% CI 0.89-1.30). There is weak evidence that reduced lung function increases risk of ischaemic stroke. CONCLUSION: There is strong evidence that reduced FVC is independently and causally associated with coronary artery disease. Although the mechanism remains unclear, FVC could be taken into consideration when assessing cardiovascular risk and considered a potential target for reducing cardiovascular events. FEV1 and airflow obstruction do not appear to cause increased cardiovascular events; confounding and collider bias may explain previous findings of a causal association.


Asunto(s)
Isquemia Encefálica , Enfermedades Cardiovasculares , Accidente Cerebrovascular , Enfermedades Cardiovasculares/epidemiología , Enfermedades Cardiovasculares/genética , Humanos , Pulmón , Análisis de la Aleatorización Mendeliana , Polimorfismo de Nucleótido Simple , Factores de Riesgo , Accidente Cerebrovascular/epidemiología , Accidente Cerebrovascular/genética
9.
Expert Rev Respir Med ; 15(1): 9-11, 2021 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-32811226
10.
J Health Serv Res Policy ; : 1355819620974054, 2020 Nov 23.
Artículo en Inglés | MEDLINE | ID: mdl-33225763

RESUMEN

OBJECTIVES: To investigate the effects of an admission avoidance pathway within a new integrated respiratory service on the number of Chronic Obstructive Pulmonary Disease (COPD)-related hospital admissions in England. METHODS: We used interrupted time series analysis to estimate the effects of the admission avoidance pathway on COPD hospital admissions, length of stay, and 30-day readmissions. We included all unplanned admissions with COPD as primary diagnosis using Hospital Episode Statistics, comparing the intervention region with a demographically similar control region in the two years before and one year after the implementation of the new service. RESULTS: Unplanned hospital admissions for COPD exacerbations followed a clear seasonal pattern, peaking in early winter. We found no evidence that the admission avoidance pathway influenced the rate of hospital admissions or 30-day readmissions. We found weak evidence of a trend change in length of stay following the launch of the admission avoidance pathway. CONCLUSIONS: Our study adds to the growing body of evidence that suggests that additional admission avoidance capacity alone does not lead to a measurable reduction in admissions or length of stay. Further investigation is required to understand the reasons why. A longer follow-up may be required to see some of the potential benefits.

11.
Health Qual Life Outcomes ; 18(1): 336, 2020 Oct 09.
Artículo en Inglés | MEDLINE | ID: mdl-33036615

RESUMEN

BACKGROUND: The Severe Asthma Questionnaire (SAQ) is a health related quality of life (HRQoL) questionnaire validated for use in severe asthma. It is scored using the mean value of 16 items (SAQ score) in addition to a single item global rating of HRQoL (SAQ-global). The aim was to validate clinically relevant subscales using exploratory factor analysis (EFA). METHODS: The SAQ was completed, along with measures of asthma control and EQ5D-5L by patients attending six UK severe asthma centres. Clinical data were included in the analysis. EFA using principal axis factoring and oblimin rotation was used to achieve simple structure of data. RESULTS: 460 patients with severe asthma participated, 65% women, mean age 51 (16-83) years. A three factor solution achieved best fit and showed that the SAQ items formed three distinct but inter-correlated groups of items where items were grouped in a way that was consistent with item content. The three subscales were differentially associated with clinically relevant variables (lung function and mood). Males and females interpreted the question of night disturbance in different ways. CONCLUSIONS: This paper provides a template for best practice in the use of EFA when validating HRQoL subscales. The SAQ can be scored as three subscales with content reflecting three different constructs people with severe asthma use when making judgements about their lives. The subscale 'My Life' assesses the impact of severe asthma on different life activities, 'My Mind' assesses the perceived emotional impact and 'My Body' the impact of extra-pulmonary symptoms and side effects.


Asunto(s)
Asma/psicología , Calidad de Vida , Encuestas y Cuestionarios/normas , Asma/fisiopatología , Análisis Factorial , Femenino , Humanos , Masculino , Persona de Mediana Edad , Reproducibilidad de los Resultados
12.
Int J Chron Obstruct Pulmon Dis ; 14: 1855-1866, 2019.
Artículo en Inglés | MEDLINE | ID: mdl-31686798

RESUMEN

Background: Brain damage and cardiovascular disease are extra-pulmonary manifestations of chronic obstructive pulmonary disease (COPD). Cardiovascular risk factors and smoking are contributors to neurodegeneration. This study investigates whether there is a specific, COPD-related deterioration in brain structure and function independent of cardiovascular risk factors and smoking. Materials and methods: Neuroimaging and clinical markers of brain structure (micro- and macro-) and function (cognitive function and mood) were compared between 27 stable COPD patients (age: 63.0±9.1 years, 59.3% male, forced expiratory volume in 1 second [FEV1]: 58.1±18.0% pred.) and 23 non-COPD controls with >10 pack years smoking (age: 66.6±7.5 years, 52.2% male, FEV1: 100.6±19.1% pred.). Clinical relationships and group interactions with brain structure were also tested. All statistical analyses included correction for cardiovascular risk factors, smoking, and aortic stiffness. Results: COPD patients had significantly worse cognitive function (p=0.011), lower mood (p=0.046), and greater gray matter atrophy (p=0.020). In COPD patients, lower mood was associated with markers of white matter (WM) microstructural damage (p<0.001), and lower lung function (FEV1/forced vital capacity and FEV1) with markers of both WM macro (p=0.047) and microstructural damage (p=0.028). Conclusion: COPD is associated with both structural (gray matter atrophy) and functional (worse cognitive function and mood) brain changes that cannot be explained by measures of cardiovascular risk, aortic stiffness, or smoking history alone. These results have important implications to guide the development of new interventions to prevent or delay progression of neuropsychiatric comorbidities in COPD. Relationships found between mood and microstructural abnormalities suggest that in COPD, anxiety, and depression may occur secondary to WM damage. This could be used to better understand disabling symptoms such as breathlessness, improve health status, and reduce hospital admissions.


Asunto(s)
Encefalopatías/etiología , Encéfalo , Enfermedades Cardiovasculares/etiología , Enfermedad Pulmonar Obstructiva Crónica/etiología , Fumar/efectos adversos , Afecto , Anciano , Encéfalo/diagnóstico por imagen , Encéfalo/fisiopatología , Encefalopatías/diagnóstico por imagen , Encefalopatías/fisiopatología , Encefalopatías/psicología , Enfermedades Cardiovasculares/diagnóstico , Enfermedades Cardiovasculares/fisiopatología , Estudios de Casos y Controles , Cognición , Femenino , Volumen Espiratorio Forzado , Humanos , Pulmón/fisiopatología , Masculino , Persona de Mediana Edad , Degeneración Nerviosa , Neuroimagen/métodos , Valor Predictivo de las Pruebas , Pronóstico , Enfermedad Pulmonar Obstructiva Crónica/diagnóstico , Enfermedad Pulmonar Obstructiva Crónica/fisiopatología , Factores de Riesgo , Rigidez Vascular , Capacidad Vital
13.
PLoS One ; 14(10): e0223297, 2019.
Artículo en Inglés | MEDLINE | ID: mdl-31581226

RESUMEN

BACKGROUND: Mild cognitive impairment is a common systemic manifestation of chronic obstructive pulmonary disease (COPD). However, its pathophysiological origins are not understood. Since, cognitive function relies on efficient communication between distributed cortical and subcortical regions, we investigated whether people with COPD have disruption in white matter connectivity. METHODS: Structural networks were constructed for 30 COPD patients (aged 54-84 years, 57% male, FEV1 52.5% pred.) and 23 controls (aged 51-81 years, 48% Male). Networks comprised 90 grey matter regions (nodes) interconnected by white mater fibre tracts traced using deterministic tractography (edges). Edges were weighted by the number of streamlines adjusted for a) streamline length and b) end-node volume. White matter connectivity was quantified using global and nodal graph metrics which characterised the networks connection density, connection strength, segregation, integration, nodal influence and small-worldness. Between-group differences in white matter connectivity and within-group associations with cognitive function and disease severity were tested. RESULTS: COPD patients' brain networks had significantly lower global connection strength (p = 0.03) and connection density (p = 0.04). There was a trend towards COPD patients having a reduction in nodal connection density and connection strength across the majority of network nodes but this only reached significance for connection density in the right superior temporal gyrus (p = 0.02) and did not survive correction for end-node volume. There were no other significant global or nodal network differences or within-group associations with disease severity or cognitive function. CONCLUSION: COPD brain networks show evidence of damage compared to controls with a reduced number and strength of connections. This loss of connectivity was not sufficient to disrupt the overall efficiency of network organisation, suggesting that it has redundant capacity that makes it resilient to damage, which may explain why cognitive dysfunction is not severe. This might also explain why no direct relationships could be found with cognitive measures. Smoking and hypertension are known to have deleterious effects on the brain. These confounding effects could not be excluded.


Asunto(s)
Disfunción Cognitiva/etiología , Disfunción Cognitiva/fisiopatología , Conectoma , Enfermedad Pulmonar Obstructiva Crónica/complicaciones , Sustancia Blanca/fisiología , Anciano , Anciano de 80 o más Años , Cognición , Disfunción Cognitiva/psicología , Imagen de Difusión Tensora , Femenino , Humanos , Procesamiento de Imagen Asistido por Computador , Masculino , Persona de Mediana Edad , Enfermedad Pulmonar Obstructiva Crónica/diagnóstico , Pruebas de Función Respiratoria , Índice de Severidad de la Enfermedad , Sustancia Blanca/diagnóstico por imagen
14.
Clin Interv Aging ; 14: 1-8, 2019.
Artículo en Inglés | MEDLINE | ID: mdl-30587948

RESUMEN

Purpose: People with COPD have cognitive dysfunction, which is greater in those hospitalized for exacerbations than in stable outpatients. We tested the hypothesis that cognitive dysfunction at exacerbation is a disease-specific feature of COPD, rather than a nonspecific feature of hospitalization for acute illness, by comparing cognition between patients hospitalized for acute COPD exacerbations and those with worsening heart failure (HF). Patients and methods: A total of 40 hospital inpatients were recruited, 20 patients with COPD exacerbations and 20 patients with congestive or left-sided HF. Exclusion criteria included previous stroke, known neurological disease, and marked alcohol excess. Participants completed the Montreal cognitive assessment (MoCA) and Hospital Anxiety and Depression Scale (HADS) and underwent spirometry and review of clinical records. Results: Age (mean±SD, COPD 73±10; HF 76±11 years), acute illness severity (Acute Physiology and Chronic Health Evaluation [APACHE]-II, COPD 15.4±3.5; HF 15.9±3.0), comorbidities (Charlson index, COPD 1.3±1.9; HF 1.6±1.5), and educational background were similar between COPD and HF groups. MoCA total was significantly lower in COPD than in HF (COPD 20.6±5.6; HF 24.8±3.5, P=0.007); however, significance was lost after correction for age, sex, and pack year smoking history. When compared with HF patients, the COPD cohort performed worse on the following domains of the MoCA: visuospatial function (median [IQR], COPD 0 [1]; HF 2 [1], P=0.003), executive function (COPD 2 [1]; HF 3 [1], P=0.035), and attention (COPD 4 [3]; HF 6 [2], P=0.020). Age (P=0.012) and random glucose concentration (P=0.041) were associated with cognitive function in whole group analysis, with pack year smoking history reaching borderline significance (P=0.050). Conclusion: Total MoCA score for COPD and HF indicated that both groups had mild cognitive impairment, although this was greater in people with COPD. Mechanisms underlying the observed cognitive dysfunction in COPD remain unclear but appear related to blood glucose concentrations and greater lifetime smoking load.


Asunto(s)
Disfunción Cognitiva/etiología , Insuficiencia Cardíaca/psicología , Enfermedad Pulmonar Obstructiva Crónica/psicología , Factores de Edad , Anciano , Anciano de 80 o más Años , Atención , Glucemia/metabolismo , Estudios de Casos y Controles , Cognición , Disfunción Cognitiva/sangre , Progresión de la Enfermedad , Función Ejecutiva , Femenino , Insuficiencia Cardíaca/fisiopatología , Hospitalización , Humanos , Masculino , Pruebas de Estado Mental y Demencia , Persona de Mediana Edad , Estudios Prospectivos , Fumar/efectos adversos
15.
BMJ Open Respir Res ; 5(1): e000310, 2018.
Artículo en Inglés | MEDLINE | ID: mdl-30555707

RESUMEN

Introduction: Widespread white matter damage and cognitive impairment have been demonstrated in chronic obstructive pulmonary disease (COPD). However, it remains unclear if brain atrophy is a global phenomenon or if specific subregions are differentially affected. The aims of this study are, first, to test a simple, validated visual analogue grading technique. Second, we hypothesised that frontal regions of the brains of patients with COPD will show greater signs of atrophy compared with control subjects. Third, any localised regions of atrophy would correlate with components of cognitive performance. Finally, the severity of cerebral atrophy would be associated with measures of respiratory disease severity. Methods: We used a simple, validated visual analogue grading technique to assess the degree of regional atrophy in multiple brain regions from cerebral MR images in patients with stable non-hypoxaemic COPD (n=25) and age-matched control subjects (n=25). We also explored correlations between regional brain atrophy with demographics, cognitive performance measures and disease severity. Measures of cognitive performance focused on executive function, working memory, verbal memory, overall memory and processing speed. Measures of disease severity include lung function, gas exchange, health status and breathlessness questionnaires. Results: The visual grading scale found that patients with COPD had significantly greater frontal atrophy than control subjects (p=0.02), independent of smoking history, comorbid depression or anxiety. Cognitive function was significantly worse in the COPD group for executive function (p<0.001), working memory (p=0.02), verbal memory (p=0.03) and processing speed (p=0.001). Group differences in atrophy did not appear to account for differences in cognitive function. We were unable to identify meaningful correlations between regional atrophy and disease severity or cognitive function. Conclusion: Further work is needed to identify causative mechanisms behind unexplained structural brain changes in COPD.

16.
BMJ Open Respir Res ; 5(1): e000309, 2018.
Artículo en Inglés | MEDLINE | ID: mdl-29955365

RESUMEN

Introduction: Dyspnoea has been defined as a 'subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity'. However, the majority of available dyspnoea measures treat it as a single entity and rely on quantitative methodology. We propose that qualitative research can enhance our understanding of dyspnoea, in particular, how perception varies so much among patients with similar disease states. In this paper, we focus on how a specific type of inner attention-mindfulness-may alter perceptions of dyspnoea. The aim is to characterise mindfulness attention, which impacts on perceptions of dyspnoea and relate these to the multidimensional model of dyspnoea. We explore how an individual can change their perception and therefore relationship to similar disease states. Method: 22 patients with asthma or chronic obstructive pulmonary disease were recruited from primary and secondary care to an 8-week course in mindfulness-based cognitive therapy (MBCT). 12 patients took part in an in-depth qualitative interview 2 months after completing the MBCT course. Data were recorded, transcribed and then analysed using a framework approach, drawing on components of the multidimensional model of dyspnoea (multidimensional dyspnoea profile, MDP). Results: We found that MBCT training involves developing three types of mindful attention (broad attention, informative attention and re-directive attention), which impact on perceptions of the sensory dimension of dyspnoea. MBCT appears to target affective and sensory perceptions articulated in the MDP model. Conclusion: More research is needed into how mindfulness-based interventions may mediate the relationship between affective experience and the sensory perception of dyspnoea symptoms.

18.
J Am Med Dir Assoc ; 18(12): 1097.e11-1097.e24, 2017 Dec 01.
Artículo en Inglés | MEDLINE | ID: mdl-29169740

RESUMEN

BACKGROUND: Patients with chronic obstructive pulmonary disease (COPD) can be classified into groups A/C or B/D based on symptom intensity. Different threshold values for symptom questionnaires can result in misclassification and, in turn, different treatment recommendations. The primary aim was to find the best fitting cut-points for Global initiative for chronic Obstructive Lung Disease (GOLD) symptom measures, with an modified Medical Research Council dyspnea grade of 2 or higher as point of reference. METHODS: After a computerized search, data from 41 cohorts and whose authors agreed to provide data were pooled. COPD studies were eligible for analyses if they included, at least age, sex, postbronchodilator spirometry, modified Medical Research Council, and COPD Assessment Test (CAT) total scores. MAIN OUTCOMES: Receiver operating characteristic curves and the Youden index were used to determine the best calibration threshold for CAT, COPD Clinical Questionnaire, and St. Georges Respiratory Questionnaire total scores. Following, GOLD A/B/C/D frequencies were calculated based on current cut-points and the newly derived cut-points. FINDINGS: A total of 18,577 patients with COPD [72.0% male; mean age: 66.3 years (standard deviation 9.6)] were analyzed. Most patients had a moderate or severe degree of airflow limitation (GOLD spirometric grade 1, 10.9%; grade 2, 46.6%; grade 3, 32.4%; and grade 4, 10.3%). The best calibration threshold for CAT total score was 18 points, for COPD Clinical Questionnaire total score 1.9 points, and for St. Georges Respiratory Questionnaire total score 46.0 points. CONCLUSIONS: The application of these new cut-points would reclassify about one-third of the patients with COPD and, thus, would impact on individual disease management. Further validation in prospective studies of these new values are needed.


Asunto(s)
Progresión de la Enfermedad , Guías de Práctica Clínica como Asunto , Enfermedad Pulmonar Obstructiva Crónica/clasificación , Enfermedad Pulmonar Obstructiva Crónica/terapia , Evaluación de Síntomas/métodos , Factores de Edad , Anciano , Medicina Basada en la Evidencia , Femenino , Salud Global , Humanos , Masculino , Persona de Mediana Edad , Enfermedad Pulmonar Obstructiva Crónica/diagnóstico , Medición de Riesgo , Índice de Severidad de la Enfermedad , Factores Sexuales , Perfil de Impacto de Enfermedad
19.
BMC Pulm Med ; 17(1): 92, 2017 Jun 19.
Artículo en Inglés | MEDLINE | ID: mdl-28629404

RESUMEN

BACKGROUND: Brain pathology is relatively unexplored in chronic obstructive pulmonary disease (COPD). This study is a comprehensive investigation of grey matter (GM) and white matter (WM) changes and how these relate to disease severity and cognitive function. METHODS: T1-weighted and fluid-attenuated inversion recovery images were acquired for 31 stable COPD patients (FEV1 52.1% pred., PaO2 10.1 kPa) and 24 age, gender-matched controls. T1-weighted images were segmented into GM, WM and cerebrospinal fluid (CSF) tissue classes using a semi-automated procedure optimised for use with this cohort. This procedure allows, cohort-specific anatomical features to be captured, white matter lesions (WMLs) to be identified and includes a tissue repair step to correct for misclassification caused by WMLs. Tissue volumes and cortical thickness were calculated from the resulting segmentations. Additionally, a fully-automated pipeline was used to calculate localised cortical surface and gyrification. WM and GM tissue volumes, the tissue volume ratio (indicator of atrophy), average cortical thickness, and the number, size, and volume of white matter lesions (WMLs) were analysed across the whole-brain and regionally - for each anatomical lobe and the deep-GM. The hippocampus was investigated as a region-of-interest. Localised (voxel-wise and vertex-wise) variations in cortical gyrification, GM density and cortical thickness, were also investigated. Statistical models controlling for age and gender were used to test for between-group differences and within-group correlations. Robust statistical approaches ensured the family-wise error rate was controlled in regional and local analyses. RESULTS: There were no significant differences in global, regional, or local measures of GM between patients and controls, however, patients had an increased volume (p = 0.02) and size (p = 0.04) of WMLs. In patients, greater normalised hippocampal volume positively correlated with exacerbation frequency (p = 0.04), and greater WML volume was associated with worse episodic memory (p = 0.05). A negative relationship between WML and FEV1 % pred. approached significance (p = 0.06). CONCLUSIONS: There was no evidence of cerebral atrophy within this cohort of stable COPD patients, with moderate airflow obstruction. However, there were indications of WM damage consistent with an ischaemic pathology. It cannot be concluded whether this represents a specific COPD, or smoking-related, effect.


Asunto(s)
Cerebro/patología , Cognición , Sustancia Gris/patología , Enfermedad Pulmonar Obstructiva Crónica/fisiopatología , Sustancia Blanca/patología , Anciano , Atrofia/diagnóstico por imagen , Cerebro/diagnóstico por imagen , Femenino , Volumen Espiratorio Forzado , Sustancia Gris/diagnóstico por imagen , Hipocampo/diagnóstico por imagen , Hipocampo/patología , Humanos , Imagen por Resonancia Magnética , Masculino , Memoria Episódica , Persona de Mediana Edad , Neuroimagen , Tamaño de los Órganos , Enfermedad Pulmonar Obstructiva Crónica/complicaciones , Índice de Severidad de la Enfermedad , Sustancia Blanca/diagnóstico por imagen
20.
Front Physiol ; 8: 65, 2017.
Artículo en Inglés | MEDLINE | ID: mdl-28223945

RESUMEN

Introduction: There is increasing interest in technologies that may enable remote monitoring of respiratory disease. Traditional methods for assessing respiratory function such as spirometry can be expensive and require specialist training to perform and interpret. Remote, non-contact tracking of chest wall movement has been explored in the past using structured light, accelerometers and impedance pneumography, but these have often been costly and clinical utility remains to be defined. We present data from a 3-Dimensional time-of-flight camera (found in gaming consoles) used to estimate chest volume during routine spirometry maneuvres. Methods: Patients were recruited from a general respiratory physiology laboratory. Spirometry was performed according to international standards using an unmodified spirometer. A Microsoft Kinect V2 time-of-flight depth sensor was used to reconstruct 3-dimensional models of the subject's thorax to estimate volume-time and flow-time curves following the introduction of a scaling factor to transform measurements to volume estimates. The Bland-Altman method was used to assess agreement of model estimation with simultaneous recordings from the spirometer. Patient characteristics were used to assess predictors of error using regression analysis and to further explore the scaling factors. Results: The chest volume change estimated by the Kinect camera during spirometry tracked respiratory rate accurately and estimated forced vital capacity (FVC) and vital capacity to within ± <1%. Forced expiratory volume estimation did not demonstrate acceptable limits of agreement, with 61.9% of readings showing >150 ml difference. Linear regression including age, gender, height, weight, and pack years of smoking explained 37.0% of the variance in the scaling factor for volume estimation. This technique had a positive predictive value of 0.833 to detect obstructive spirometry. Conclusion: These data illustrate the potential of 3D time-of-flight cameras to remotely monitor respiratory rate. This is not a replacement for conventional spirometry and needs further refinement. Further algorithms are being developed to allow its independence from spirometry. Benefits include simplicity of set-up, no specialist training, and cost. This technique warrants further refinement and validation in larger cohorts.

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