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Introduction In chronic obstructive pulmonary disease (COPD), endothelial dysfunction and stiffness of systemic arteries may contribute to increased cardiovascular risk. Pulmonary vascular disease (PVD) is frequent in COPD. The association between PVD and systemic vascular dysfunction has not been thoroughly evaluated in COPD. Methods A total of 108 subjects were allocated into four groups (non-smoking controls, smoking controls, COPD without PVD and COPD with PVD). In systemic arteries, endothelial dysfunction was assessed by flow-mediated dilation (FMD) and arterial stiffness by pulse wave analysis (PWA) and pulse wave velocity (PWV). PVD was defined by a mean pulmonary artery pressure (PAP) ≥25 mmHg at right heart catheterization or by a tricuspid regurgitation velocity >2.8 m/s at doppler echocardiography. Biomarkers of inflammation and endothelial damage were assessed in peripheral blood. Results FMD was lower in COPD patients, with or without PVD, compared to non-smoking controls; and in patients with COPD and PVD compared to smoking controls. PWV was higher in COPD with PVD patients compared to both non-smoking and smoking controls in a model adjusted by age and the Framingham score; PWV was also higher in patients with COPD and PVD compared to COPD without PVD patients in the non-adjusted analysis. FMD and PWV correlated significantly with forced expiratory volume in the first second (FEV1), diffusing capacity for carbon monoxide (DLCO) and systolic PAP. FMD and PWV were correlated in all subjects. Discussion We conclude that endothelial dysfunction of systemic arteries is common in COPD, irrespective if they have PVD or not. COPD patients with PVD show increased stiffness and greater impairment of endothelial function in systemic arteries. These findings suggest the association of vascular impairment in both pulmonary and systemic territories in a subset of COPD patients.

AIM We hypothesize that training-induced changes in muscle oxygen saturation (StO2 ) assessed by near-infrared spectroscopy (NIRS) during constant work rate cycling exercise (CWRE) may be a useful marker of the effects of training at 'vastus medialis' of the quadriceps in patients with chronic obstructive pulmonary disease (COPD). METHODS Incremental exercise [peak oxygen uptake (VO2 )] and CWRE at 70% pretraining peak VO2 , before and after 8-w training, were done in 10 healthy age-matched subjects (H) [80% men, 65(11) years, FEV1 105(14)%] and 16 COPD patients [94% men, 70(5) years, FEV1 46(11) %] encompassing the entire spectrum of disease severity, recruited in the outpatient clinics. NIRS was used to assess StO2 in the 'vastus medialis' of the left quadriceps. RESULTS Pretraining CWRE decreased StO2 (P

Chronic obstructive pulmonary disease (COPD) is an entity with a heterogeneous presentation. For this reason, attempts have been made to characterize different phenotypes and endotypes to enable a more individualized approach. The aim of the Biomarkers in COPD (BIOMEPOC) project is to identify useful biomarkers in blood to improve the characterization of patients. Clinical data and blood samples from a group of patients and healthy controls will be analyzed. The project will consist of an exploration phase and a validation phase. Analytical parameters in blood will be determined using standard techniques and certain 'omics' (transcriptomics, proteomics, and metabolomics). The former will be hypothesis-driven, whereas the latter will be exploratory. Finally, a multilevel analysis will be conducted. Currently, 269 patients and 83 controls have been recruited, and sample processing is beginning. Our hope is to use the results to identify new biomarkers that, alone or combined, will allow a better characterization of patients.

The phenotypic characteristics of chronic obstructive pulmonary disease (COPD) in individuals younger than 50 years of age (early COPD) are not well defined. This prospective, multi-centre, case-control study sought to describe these characteristics and compare them with those of smokers (>= 10 pack-years) of similar age with normal spirometry (controls). We studied 92 cases (post-bronchodilator forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC), In part, by CIBERES, SEPAR, FIS (CP16/00039, PI17/00369, PI18/01008) and an unrestricted grant from Boehringer-Ingelheim. Funding information for this article has been deposited with the Crossref Funder Registry.

Introduction: The impact of pulmonary hypertension (PH) on exercise tolerance in chronic obstructive pulmonary disease (COPD) has not been fully elucidated. It is necessary to characterize pulmonary hemodynamics in patients with moderate to severe COPD in order to improve their management. The aim of the study was to determine whether in COPD the presence of PH is associated with reduced exercise tolerance in a cohort of stable COPD patients. Methods: Cross-sectional analysis of 174 COPD patients clinically stable: 109 without PH and 65 with PH (COPD-PH). We assessed socio-demographic data, lung function, quality of life, dyspnea, cardiopulmonary exercise testing (CPET), constant workload endurance time (CWET), and six-minute walk test (6MWT). We elaborated a logistic regression model to explore the impact of PH on exercise capacity in COPD patients. Results: COPD-PH patients showed lower exercise capacity both at maximal (CPET) (43(20) versus 68(27) Watts and 50(19)% versus 71(18)% predicted peak oxygen consumption (VO2peak), COPD-PH and COPD, respectively), and at submaximal tests (6MWT) (382(94) versus 486(95) m). In addition, the COPD-PH group had lower endurance time than the non-PH COPD group (265(113) s and 295(164) s, respectively). Conclusions: The presence of PH is an independent factor that impairs exercise capacity in COPD. SPANISH Introducción: El impacto de la hipertensión pulmonar (HTP) en la tolerancia al ejercicio en la enfermedad pulmonar obstructiva crónica (EPOC) no se ha dilucidado en su totalidad. Es necesario caracterizar la hemodinámica pulmonar de los pacientes con EPOC moderada a grave para poder mejorar su manejo. El objetivo de este estudio fue determinar si la presencia de HTP en la EPOC se asociaba con una disminución en la tolerancia al ejercicio en una cohorte de pacientes con EPOC estable. Métodos: Estudio transversal de 174 pacientes con EPOC clínicamente estables: 109 de ellos no mostraban HTP y 65 de ellos sí (EPOC-HTP). Valoramos la información sociodemográfica, la función pulmonar, la calidad de vida, la disnea, realizamos una prueba de ejercicio cardiopulmonar (PECP), medimos el tiempo de tolerancia de ejercicio constante y realizamos de marcha de seis minutos (6MWT, por sus siglas en inglés). Elaboramos un modelo de regresión logística para explorar el impacto de la HTP en la capacidad de ejercicio de los pacientes con EPOC. Resultados: Los pacientes con EPOC-HTP mostraron una menor capacidad de ejercicio, tanto en las pruebas máximas (PECP) (43 (20) W frente a 68 (27) W y 50 (19)% frente a 71 (18)% de consumo de oxígeno máximo predicho (VO2 max), para pacientes con EPOC-HTP y pacientes con EPOC, respectivamente) como en las pruebas submáximas (6MWT) (382 (94) m frente a 486 (95) m). Además, el grupo de EPOC-HTP presentó un menor tiempo de resistencia que el grupo de EPOC sin HTP (265 (113) s y 295 (164) s, respectivamente). Conclusiones: La presencia de HTP es un factor independiente que afecta a la capacidad de ejercicio en la EPOC.

Background Pulmonary vascular abnormalities are a characteristic feature of chronic obstructive pulmonary disease (COPD). Cigarette smoking is the most important risk factor for COPD. It is believed that its constant exposure triggers endothelial cell damage and vascular remodelling. Under pathological conditions, progenitor cells (PCs) are mobilized from the bone marrow and recruited to sites of vascular injury. The aim of the study was to investigate whether in COPD the number of circulating PCs is related to the presence of bone marrow-derived cells in pulmonary arteries and the association of these phenomena to both systemic and pulmonary endothelial dysfunction. Methods Thirty-nine subjects, 25 with COPD, undergoing pulmonary resection because of a localized carcinoma, were included. The number of circulating PCs was assessed by flow cytometry using a triple combination of antibodies against CD45, CD133 and CD34. Infiltrating CD45+ cells were identified by immunohistochemistry in pulmonary arteries. Endothelial function in systemic and pulmonary arteries was measured by flow-mediated dilation and adenosine diphosphate-induced vasodilation, respectively. Results COPD patients had reduced numbers of circulating PCs (p

BACKGROUND: The minimum controlling dose of treatment must be established in patients with asthma, but the outcome of step-down is unpredictable. OBJECTIVE: To identify factors associated with risk of control loss when stepping down asthma treatment and to develop a score to predict this risk. METHODS: A prospective, multicenter study including adults with well-controlled asthma was performed. Treatment was stepped up or stepped down over a 12-month period to maintain asthma control. We determined associations between clinical and functional variables and step-down failure. Finally, we derived a score to predict loss of control in 1 cohort and validated it in an independent cohort. RESULTS: The derivation cohort consisted of 228 patients; 218 completed at least 1 step-down episode and a total of 495 step-down episodes were evaluated. A medical-record documented postbronchodilator spirometry result of = 1 severe exacerbation in the previous 12 months (OR = 2.43; 95% CI: 1.48-4.01), and Asthma Control Test score < 25 (OR = 2.30; 95% CI: 1.35-3.92) were independently associated with failure. The score showed an area under the curve of 0.690 (95% CI: 0.633-0.747; P < .05) in the derivation cohort and 0.76 (95% CI: 0.643-0.882; P < .001) in a validation cohort of 114 patients. A score 8 implies a high risk (>40%). CONCLUSION: This score can facilitate the prediction of step-down failure before medication taper in patients with well-controlled asthma. (C) 2018 American Academy of Allergy, Asthma & Immunology

Background and objective Non-anaemic iron deficiency (NAID) might alter the oxygen pathway in health and disease. The current study aims at assessing the impact of NAID on aerobic capacity in patients with chronic obstructive pulmonary disease (COPD). Methods A prospective sample of 70 non-anaemic COPD patients candidate to participate in an 8-week pulmonary rehabilitation (PR) programme was studied. Incremental cycling exercise to peak oxygen uptake (V'O2peak) and constant work-rate exercise at 80% V'O2peak to exhaustion were assessed pre- and post-PR. Training-induced increase of endurance time (ET) ≥33%, which represented the minimal clinically important difference, classified patients as responders to exercise training. Results The prevalence of NAID was 48% (n = 34) showing no relationship with the Global Initiative for Chronic Obstructive Lung Disease stages (P = 0.209). Patients with NAID showed lower pre-training ET (P = 0.033) and V'O2peak (P = 0.007) than normal iron status (NIS) patients after adjustment for potential covariates. Significant training-induced physiological changes were seen in the NIS group (ΔV'O2peak 68(132) mL/min; P = 0.009), but not in the NAID group (ΔV'O2peak 26 (126) mL/min; P = 0.269). The NAID group showed lower percentage of responders to training (56%) than the NIS group (78%) (P = 0.041). Conclusions COPD patients with NAID showed lower pre-training aerobic capacity and reduced training-induced response than NIS patients after adjusting for potential confounding variables.

Background The relationship between airway hyperresponsiveness (AHR) and obesity, a low-grade systemic inflammatory condition, remains largely unknown. It is established that AHR to indirect stimuli is associated with active airway inflammation. The objectives were to investigate the rate of AHR to mannitol in obese subjects and its changes 1 year after bariatric surgery (BS). Methods We enrolled 58 candidates to BS severely obese (33 nonsmokers and 25 smokers) without history of asthma and 20 healthy, nonobese participants and related AHR to functional findings and serum and exhaled biomarkers. Results Before surgery, AHR was observed in 16 (28 %) obese with the provocation doses of mannitol to induce a 15 % fall in FEV1 (PD15) of (geometric mean [95 % CI]) 83 (24–145) mg. Compared to control participants, obese participants had lower spirometric values and higher serum and exhaled biomarkers (p

Background and Aim Both interval (IT) and continuous (CT) exercise training results in an improvement of aerobic capacity in patients with chronic obstructive pulmonary disease (COPD); however, their effects on cardiac autonomic function remains unclear. The aim of our study was to evaluate the effect of a supervised CT vs IT on autonomic cardiac function in COPD patients. Methods COPD patients were divided into two different groups according to training modality (IT or CT). Autonomic cardiac dysfunction (ACD) was defined as a heart rate recovery lower than 12 bpm heart rate after the first minute of maximal exercise (HRR1) and an abnormal chronotropic response (CR) to exercise (

Portillo K, Torralba Y, Blanco I, et al. International Journal of Chronic Obstructive Pulmonary Disease. 2015;10:1313–1320. On page 1319, Acknowledgments section, missing acknowledgment, need to add: This work was performed as part of the doctoral program in Internal Medicine at the Universitat Autónoma de Barcelona.Read the original article

Introduction: Patients with pulmonary arterial hypertension (PAH) show endothelial dysfunction and increased stiffness in pulmonary arteries. Patients with PAH also show endothelial dysfunction in systemic arteries. It is unknown whether or not patients with PAH show increased stiffness in systemic arteries. Aims and Objectives: The aim of the study was to assess endothelial function and stiffness of systemic arteries in patients with PAH and evaluate their relationship with PAH severity. Metodhs: We studied 27 control subjects (48±14 years, 59% women) and 74 patients with PAH (51±14 years, 66% women). Endothelial function was assessed by flow mediated dilation (FMD) of the brachial artery. Arterial stiffness was assessed by means of the carotid-femoral pulse wave velocity (PWV). Results: Compared with control subjects, patients with PAH had reduced FMD (10.6±3.9 and 7.5±6.3, respectively; p Conclusions: Patients with PAH show altered vascular function in systemic arteries. Given the relationship between PWV and PAH severity, systemic arterial stiffness might serve as a marker of disease severity and response to treatment. *Supported by grants from ISCiii (FIS PI12/00510), SOCAP and FCHP.

Karina Portillo,1 Yolanda Torralba,1,2 Isabel Blanco,1,2 Felip Burgos,1,2 Roberto Rodriguez-Roisin,1,2 Jose Rios,3 Josep Roca,1,2 Joan A Barberà1,21Department of Pulmonary Medicine, Hospital Clínic-Institut d’Investigacions Biomèdiques August Pi iSunyer (IDIBAPS), University of Barcelona, Barcelona, Spain; 2Centro de Investigación Biomédica en Redde Enfermedades Respiratorias (CIBERES), Madrid, Spain; 3Biostatistics and Data Management Core Facility, Hospital Clínic-Institut d’Investigacions Biomèdiques AugustPi iSunyer (IDIBAPS), Biostatistics Unit, School of Medicine, Universitat Autònoma deBarcelona, Barcelona, SpainIntroduction: Few data are available in regards to the prevalence of pulmonary hypertension (PH) in the broad spectrum of COPD. This study was aimed at assessing the prevalence of PH in a cohort of COPD patients across the severity of airflow limitation, and reporting the hemodynamic characteristics at rest and during exercise.Methods: We performed a retrospective analysis on COPD patients who underwent right-heart catheterization in our center with measurements obtained at rest (n=139) and during exercise (n=85). PH was defined as mean pulmonary artery pressure (mPAP) ≥25 mmHg and pulmonary capillary wedge pressure 3.Results: PH was present in 25 patients (18%). According to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) classification, PH prevalence in GOLD 2 was 7% (3 patients); 25% (14 patients) in GOLD 3; and 22% (8 patients) in GOLD 4. Severe PH (mPAP ≥35 mmHg) was identified in four patients (2.8%). Arterial partial oxygen pressure was the outcome most strongly associated with PH (r=-0.29, P

Background: Women employed in domestic cleaning are at increased risk for symptoms of obstructive lung disease, but the agents responsible are unknown. Aims: To investigate common tasks and products in occupational domestic cleaning in relation to respiratory morbidity. Methods: Case-control study in domestic cleaning women nested within a large population based survey of women aged 30–65 years; 160 domestic cleaning women with asthma symptoms, chronic bronchitis symptoms, or both and 386 without a history of respiratory symptoms were identified. Detailed exposures were evaluated for 40 cases who reported still having symptoms at the recruitment interview, and 155 controls who reported not having symptoms. All tasks performed and products used when cleaning houses were determined in a face-to-face interview. Lung function, methacholine challenge, and serum IgE testing were performed. Personal exposure measurements of airborne chlorine and ammonia were performed in a subsample. Associations between asthma, chronic bronchitis, and cleaning exposures were evaluated using multiple logistic regression analysis. Results: Airborne chlorine (median level 0–0.4 ppm) and ammonia (0.6–6.4 ppm) were detectable during occupational domestic cleaning activities. Cases used bleach more frequently than controls; adjusted odds ratio (OR) for intermediate exposure was 3.3 (95% CI 0.9 to 11) and for high exposure 4.9 (1.5 to 15). Other independent associations included accidental inhalation of vapours and gases from cleaning agents and washing dishes. These associations were more pronounced for cases with asthma symptoms than for those with symptoms of chronic bronchitis, but were not related to sensitisation to common allergens. Conclusions: Asthma symptoms in domestic cleaning women are associated with exposure to bleach and possibly other irritant agents. The public health impact of the use of irritant cleaning products could be widespread since the use of these products is common both in the workplace and at home.

Background: In healthy subjects, Nordic walking (NW) generates higher oxygen uptake (V˙O2) than standard walking at an equal rate of perceived exertion (RPE). The feasibility and positive outcomes of NW in patients with chronic obstructive pulmonary disease (COPD) have been reported. Objectives: The aim of the current study is to assess the physiological responses and RPE during NW in COPD patients. Methods: In 15 COPD patients [mean (SD) age 67 (9) years] with a forced expiratory volume in the 1st s of 55% (15)], V˙O2, minute ventilation and heart rate were measured with a portable system during the 6-min walking test (6MWT), incremental shuttle walking test (SWT), 6-min NW on solid ground (6mNWground) and 6-min NW on soft dry beach sand (6mNWsand). The RPE using a modified Borg scale was assessed after each test. Results: 6mNWground and 6mNWsand showed a higher V˙O2 plateau compared with the 6MWT and peak V˙O2 measured during SWT [mean (SD) V˙O2 21 (3), 22 (4), 18 (4) and 19 (5) ml·kg-1·min-1, respectively; p < 0.05 each]. However, no differences in RPE were observed among 6mNWground, 6MWT and SWT [modified Borg scale score for dyspnea 4.2 (2.0), 4.1 (1.8) and 4.3 (1.7), respectively; nonsignificant]. However, RPE in 6mNWsand was significantly higher than in all the other exercise protocols [modified Borg scale score for dyspnea 5.2 (2.2); p < 0.05]. Conclusions: In COPD patients, the use of Nordic poles generates higher V˙O2 than standard walking with no differences in the dyspnea score. The results indicate the potential to enhance community-based training programs in these patients.

Background: Abnormalities of autonomic function have been reported in patients with chronic obstructive pulmonary disease. The effect of the exercise training in heart rate recovery (HRR) has not been established in patients with COPD. Objective: To assess the effects of 8-weeks’ endurance training program on parasympathetic nervous system response measured as heart rate recovery in a sample of moderateto-severe COPD patients. Methods: We recruited a consecutive sample of patients with COPD candidates to participate in a pulmonary rehabilitation program from respiratory outpatient clinics of a tertiary hospital. HRR was calculated, before and after training, as the difference in heart rate between end-exercise and one minute thereafter (HRR1) in a constant-work rate protocol. Results: A total of 73 COPD patients were included: mean (SD) age 66 (8) years, median (P25-P75) post-bronchodilator FEV1 39 (29–53)%. The prevalence of slow HRR1 (≤12 beats) at baseline was 63%, and was associated with spirometric severity (mean FEV1 35% in slow HRR1 vs 53 in normal HRR1, p < 0.001). After 8-weeks training, HRR1 improved from mean (SD) 10 (7) to 12 (7) beats (p = 0.0127). Multivariate linear regression models showed that the only variable related to post-training HRR1 was pre-training HRR1 (p < 0.001). Conclusions: These results suggest that training enhances HRR in patients with moderate-to-severe COPD. HRR is an easy tool to evaluate ANS such that it may be a useful clinical marker of parasympathetic nervous system response in patients with COPD.

Background In chronic obstructive pulmonary disease (COPD), decreased progenitor cells and impairment of systemic vascular function have been suggested to confer higher cardiovascular risk. The origin of these changes and their relationship with alterations in the pulmonary circulation are unknown. Objectives To investigate whether changes in the number of circulating hematopoietic progenitor cells are associated with pulmonary hypertension or changes in endothelial function. Methods 62 COPD patients and 35 controls (18 non-smokers and 17 smokers) without cardiovascular risk factors other than cigarette smoking were studied. The number of circulating progenitors was measured as CD45+CD34+CD133+ labeled cells by flow cytometry. Endothelial function was assessed by flow-mediated dilation. Markers of inflammation and angiogenesis were also measured in all subjects. Results Compared with controls, the number of circulating progenitor cells was reduced in COPD patients. Progenitor cells did not differ between control smokers and non-smokers. COPD patients with pulmonary hypertension showed greater number of progenitor cells than those without pulmonary hypertension. Systemic endothelial function was worse in both control smokers and COPD patients. Interleukin-6, fibrinogen, high sensitivity C-reactive protein, vascular endothelial growth factor and tumor necrosis factor were increased in COPD. In COPD patients, the number of circulating progenitor cells was inversely related to the flow-mediated dilation of systemic arteries. Conclusions Pulmonary and systemic vascular impairment in COPD is associated with cigarette smoking but not with the reduced number of circulating hematopoietic progenitors. The latter appears to be a consequence of the disease itself not related to smoking habit.