View clinical trials related to Chronic Obstructive Pulmonary Disease.
Filter by:The functional, social, and economic burden of chronic obstructive lung disease (COPD) on the healthcare system is extraordinary. COPD is the fourth leading cause of death in the United States, and some estimates attribute up to $33.2 billion in health care costs to COPD-associated morbidity and mortality annually. The burden of COPD to the VA Healthcare system parallels these findings. According to the VA HSR&D Health Economics Resource Center, COPD ranks 5th among the 40 most common chronic clinical conditions in the U.S. Veteran patient population, is responsible for >14,000 VA hospital admission annually, and increases by $1,051/patient the total annual health care cost burden on the VA Healthcare system. Importantly, COPD is associated with frequent emergency room visitation and/or hospitalization patients. Pulmonary hypertension is a common co-morbid condition that worsen morbidity and mortality in patients with COPD. This study will examine the potential for tadalafil, a phosphodiesterase type-5 (PDE-5) inhibitor to improve functional status by decreasing pulmonary hypertension. Results from this study are expected to define the potential use of PDE-5 inhibitors in COPD-induced pulmonary hypertension. If successful, this treatment option may improve quality of life and outcomes for the large number of Veterans afflicted with PH due to COPD.
As part of the long-term goal of successfully implementing tissue regeneration strategies in an individualized manner for patients with thoracic diseases including, but not limited to: cystic fibrosis, pulmonary fibrosis and pulmonary hypertension, the investigators will assess the feasibility of collecting skin biopsies from patients undergoing surgery for thoracic disease, culturing skin fibroblasts from the biopsy, and reprogramming these skin fibroblasts into induced pluripotent cells.
This is a prospective, open-label, multicenter Phase 3 study evaluating the performance of the Albuterol Spiromax dose counter in patients with a diagnosis of asthma and/or COPD. The purpose of this study is to evaluate the functionality, reliability, and accuracy of the Albuterol Spiromax inhaler integrated dose counter in a clinical setting.
The purpose of this preliminary study is to examine the effects of a program that includes two-months of structured lab-based training. The proposed study will examine the effects of a lifestyle physical activity intervention designed to increase PA in people with moderate and severe COPD. The intervention includes a combination of (a) structured laboratory-based exercises with a behavioral intervention, (b) structured home-based exercises and (c) lifestyle physical activities performed at home. The subjects will be followed for a total of 18 weeks.
The purpose of this study is to evaluate the safety, tolerability, and clinical activity of ASM-024 administered as a dry powder for inhalation formulation to patients with GOLD 2 or GOLD 3 COPD.
The primary purpose of this study is to determine the effectiveness of a hospital-based intervention, using motivational interviewing and interactive voice response (IVR), to reduce hospital readmissions within 90 days of enrollment compared to usual care, for patients with heart failure and chronic obstructive pulmonary disease.
This is a multicenter, randomized, double-blind, parallel group, chronic-dosing (24 weeks), placebo-controlled study to assess the efficacy and safety of Glycopyrrolate (GP and Formoterol Fumarate (FF) combination metered-dose inhaler (MDI) (GFF; PT003), GP MDI (PT001), and FF MDI (PT005) compared with Placebo MDI in subjects with moderate to very severe COPD.
The overall objective of this study is to assess the efficacy and safety of treatment with PT003 (GFF MDI), PT005 (FF MDI), PT001 (GP MDI), and open-label tiotropium bromide inhalation powder compared with each other and Placebo MDI over 24 weeks in subjects with moderate to very severe COPD.
In previous studies we demonstrated that endogenous opioids (inhibitory neuropeptides) modulate the perception of breathing difficulty in patients with chronic obstructive pulmonary disease (COPD). Recently, we found that antagonism of substance P (an excitatory neuropeptide) with aprepitant did not affect the perception of breathing difficulty. However, after administration of aprepitant, blood levels of both substance P(+ 54 ± 39%) and beta-endorphin (+ 27 ± 17%) increased significantly. As these blood levels reflect cellular/tissue activity, we postulated that the concomitant release of excitatory (substance P) and inhibitory (beta-endorphin) neuropeptides had opposing effects (counterbalanced each other) on the perception of breathing difficulty. The objective of the present study is to further examine the possible role of substance P on the perception of breathlessness. We propose to administer oral aprepitant and oral placebo in a randomized clinical trial in patients with COPD. However, four hours after patients take these medications, intravenous naloxone will be administered in order to block the effects of endogenous opioids (beta-endorphin) on opioid receptors. Five minutes later, patients will breathe thru a tube with fine wire mesh to provoke breathing difficulty, and then provide ratings of the intensity and unpleasantness of breathlessness every minute. The two competing hypothesis of the study are: 1. if breathlessness ratings with aprepitant/naloxone = placebo/naloxone, then substance P has no effect on perception of breathing difficulty; 2. if breathlessness ratings with aprepitant/naloxone ≠ placebo/naloxone, then substance P has an effect on perception of breathing difficulty.
- Among many other causes, Bronchial obstruction in Chronic Obstructive Pulmonary Disease (COPD) is also caused by inflammation of peripheral airways walls. - Neutrophils and other inflammatory mediators like Interleukin-6 (IL6), Interleukin-8 (IL8), Interleukin-1 alpha (IL-1 alpha),Interleukin-1beta (IL-1 beta), Tumor Necrosis Factor alfa (TNF-alfa), Reactive Oxygen Species (ROS), Leukotriene B4 (LTB4), Nitric Oxyde (NO) are implicated in the inflammation. - NO is produced in response to physical and chemical stress on bronchial epithelium and plays a critical role in small airways remodelling - Exhaled NO concentration is usually used to monitor bronchial inflammation - The relationship between stretch and strain of small airways and bronchial inflammation is not well understood. - The investigators hypothesis is that cyclic opening and closure of peripheral obstructed airways through the consequent stretching and strain acting on them can provoke an inflammatory response which can be monitored by exhaled NO. - The pharmacological effects of bronchodilators may play a role on bronchial inflammation by reducing the stretching stress on bronchiolar walls thus reducing the production of NO in exhalate - Data about these physiopathological aspects is missing in literature.