View clinical trials related to COPD Patients.
Filter by:Vascular comorbidities constitute a major burden in COPD patients. The atherosclerosis process is preceded by the onset of an endothelial dysfunction (assessed by the flow-mediated dilatation (FMD)), which is a risk factor for later ischemic vascular complications and death. In COPD, this endothelial dysfunction could be explained by intrinsic endothelial cell properties, or the effect of a pathogenic endothelial cell microenvironment (inflammation and/or oxidative stress). Exercise training constitue a powerful stimulus for the endothelial function, and could be mediated by the mobiliaztion and function of endothelial progenitors. While exercise training is an efficient intervention in COPD patients, its vascular effect appear blunted. The endothelial function response to training has appeared heterogeneous in COPD patients, and possibly linked to the endothelial cel lesion. Thus, endothelial function (assessed by the FMD) response to exercise training would be lower in COPD patients with a baseline impairment of the their FMD. In addition, of biological and functional factors could explained the magnitude of the FMD response in COPD patients.The aim of the study are thus : To compare the FMD change in COPD patients with FMD above (FMD+) and under the median FMD (FMD-) after 4 weeks of exercise training in the whole study population. To compare between COPD patients FMD+, COPD patients FMD- and healthy "control" subjects, the endothelial inflammation and senescence at baseline and the endothelial progenitor mobilization and function change induced by exercise (maximal exercise test and training). To compare between COPD patients FMD+, COPD patients FMD- and healthy "control" subjects the effect of the endothelial microenvironment on the cellular pathways regulating the endothelial function in vitro at baseline and changes after exercise training. To test in COPD patients the association between the magnitude of the FMD changes after training and biological, functional and clinical factors (inflammation oxidative stress markers, endothelial biomarkers, pulmonary impairment and phenotype, cardiovascular risks factors, vascular function, metabolic markers, physical activity level, …)
Background: The extent of increase in systolic pulmonary arterial pressure (PAPs) during exercise in patients with COPD is unpredictable from lung function data. The non-invasive assessment of pulmonary hemodynamics during exercise and flow-mediated vasodilatation measurement may give useful data in the rehabilitation of COPD patients. Methods: Patients with stable, severe COPD and healthy, age-matched subjects (H) perform semi supine echocardiography with PAPs measurement. COPD patients perform ramp protocol with gas exchange detection. Serum hsCRP level is also determined in COPD patients. Endothel dysfunction is detected by flow mediated vasodilation measurement after arm strangulation with Doppler ultrasonography. Primary endpoint: The degree of pulmonary artery systolic pressure change during exercise? Secondary endpoint: 1. The degree of right ventricular function change during exercise? 2. Is endothel dysfunction manifested with pulmonary artery pressure rise? 3. What is the correlation between the systemic inflammatory marker hsCRP and the degree of pulmonary artery pressure rise?