COPDPhase 4NCT03611699
Static Lung Hyperinflation and Sympathetic Nerve Activity-Associated Large Artery Stiffness in COPD Patients
A Phase 4 study testing Umeclidinium / Vilanterol Dry Powder Inhaler in people with COPD, run by Gary L. Pierce at 1 site in United States.
Trial summary
The goal of this study is to evaluate the acute effects of a long-acting bronchodilator on pulmonary function, vascular function and muscle sympathetic nerve activity in individuals with COPD. Individuals will be recruited from previous pulmonary research cohorts at The University of Iowa hospitals and clinics. Read more about this study
- Who is it for?
- Ages 30 to 80 years
- Conditions the study is for
- COPD
- What is being tested?
- Umeclidinium / Vilanterol Dry Powder Inhaler
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 15 participants
- Where
- 1 siteUnited States
- Study dates
- 24 Jan 2019to 1 Apr 2020
- Phase
- Phase 4
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 30 to 80 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- Age 30-80
- Ability to comfortably lie flat for 2 hours
- Normal/corrected hearing and vision
- English speaking
- Airway predominate phenotype of COPD
Who cannot join
- Other concomitant respiratory disorder (including asthma)
- Use of antibiotics or steroids for a COPD exacerbation within the past month
- Use of 24-hour oxygen
- Pregnancy or suspected pregnancy
- Uncontrolled cancer within the last 5 years
- Radiation therapy to the chest
Show all 23Show fewer
- Lung surgery (LVRS, transplant, lobectomy)
- Lung cancer known or suspected
- Insulin-dependent diabetes
- Inability to use an inhaler bronchodilator
- Eye surgery in the last 5 weeks
- Chest or abdominal surgery in the past 3 months
- Heart attack in the last 3 months
- Hospitalization for any heart problem in the past month
- Renal failure
- Heart failure
- Substance use disorder
- Cystic fibrosis
- Glaucoma
- Prostate disorder
- Allergy to milk or milk products
- Cardiac arrhythmia
- Currently using a LAMA/LABA combination bronchodilator
Trial locations and contacts
1 site in 1 country.
United States1 site
The University of Iowa Hospital and Clinics
Iowa City, Iowa, 52242
About this study
The goal of this study is to evaluate the acute effects of a long-acting bronchodilator on pulmonary function, vascular function and muscle sympathetic nerve activity in individuals with COPD. Individuals will be recruited from previous pulmonary research cohorts at The University of Iowa hospitals and clinics. Individuals that are interested in the study and are deemed eligible to participate will have a total of 3 visits to the laboratory, which includes the screening and consent (visit 1) that will last approximately 1 hour. Visits 2 and 3 are experimental visits and will be more extensive (~4 hours). Participants will be randomized to receive either a long-acting bronchodilator or a placebo inhaler at the first experimental visit, followed by either the placebo inhaler or the long-acting bronchodilator at the second experimental visit. Assessments of pulmonary function, vascular function (via non-invasive, well-established techniques), and muscle sympathetic nerve activity will be performed at both experimental visits.
Read the detailed description
COPD is a global health concern affecting more than 65 million people worldwide. In the U.S. alone, the estimated medical costs attributed to COPD surpassed $30 billion in 2010. A high percentage of this healthcare cost is attributed to the management of comorbidities associated with COPD, such as CVD. Although primarily a disease of the lungs, CVD accounts for up to 50% of all deaths among individuals with COPD. One likely mechanism contributing to the increased CVD risk observed in individuals with COPD is large central artery (i.e. carotid and aorta) stiffness. Elevated large artery stiffness is a robust predictor of CVD events and mortality in adults. Specifically, carotid-femoral pulse wave velocity (CFPWV), the reference standard measurement of aortic stiffness, is a robust, independent predictor of coronary heart events, and carotid artery stiffness, expressed as β-stiffness index, is strongly associated with incident stroke. Both CFPWV and carotid β-stiffness are markedly greater in individuals with COPD compared with age-matched controls suggesting that these mechanisms may contribute, at least in part, to the high CVD risk in this group. However, there is currently a gap in knowledge concerning the mechanisms that lead to increased large artery stiffness in individuals with COPD in part because assessing large artery stiffness among individuals with COPD has been limited to comparing aortic and carotid artery stiffness in all COPD patients with non-COPD controls, without differentiating between distinctive phenotypes of COPD. As a result of this overly simplistic approach, it has proven challenging to identify the mechanism(s) responsible for the accelerated large artery stiffness among COPD patients because different mechanisms may contribute to large artery stiffness in the various phenotypes of COPD. The two main computed tomography (CT)-quantifiable phenotypes that individuals with COPD can be subdivided into are emphysema-and airway-predominant phenotypes. COPD patients with an airway-predominant phenotype display characteristic signs of small airway disease including increased airway wall thickness, heightened airway inflammation and a greater concentration of mucus exudates in the small conducting airways. This structural remodeling leads to a greater amount of air to become trapped in the airways at residual volume and increases the resting volume of the lungs producing static lung hyperinflation. COPD patients with an airway-predominant phenotype have little or no emphysema and account for up to 60% of all mild-to-moderate COPD patients (i.e. Global Initiative for COPD; GOLD stage 1-2) and up to 25% of all severe-very severe COPD patients (GOLD 3-4). Although airway predominant patients are typically in the earlier stages of COPD progression, they are at greater CVD risk than emphysema-predominant COPD patients who make up the majority of severe-very severe (GOLD 3-4) COPD patients. However, the mechanisms responsible for the heighted CVD risk demonstrated in airway-predominant patients remain unclear. Our preliminary data demonstrate that static lung hyperinflation is strongly associated with carotid artery and aortic stiffness. These data suggest that static lung hyperinflation may be a mechanism contributing to the higher CVD risk in airway-predominant phenotypes of COPD in part from its effects on large artery stiffness. Bronchodilator therapy reduces static lung hyperinflation and improves respiratory symptoms in individuals with COPD, however the effects of bronchodilator therapy on CVD risk remain unclear. Combination long-acting muscarinic antagonist and long-acting beta2-agonist bronchodilator (LAMA/LABA) therapy reduces air-trapping and static lung hyperinflation to a greater extent than either monotherapy alone. This evidence suggests that a LAMA/LABA combination bronchodilator will elicit the greatest changes in large artery stiffness because of its superior effects on lung deflation compared with either medication alone.
Sympathetic nerve activity (SNA) is elevated in COPD patients compared with controls and is an independent predictor of morbidity and mortality in this group. However, the mechanisms underlying the hyperactivation of SNA in COPD remain incompletely understood. In healthy individuals, acute static lung hyperinflation, induced by Valsalva maneuver, is associated with a sustained increase in intrathoracic pressure and a subsequent decrease in central venous volume. This decrease in central venous volume in turn unloads the cardiopulmonary baroreceptors and results in sustained sympathetic activation. Importantly, in individuals with COPD, the positive pressure within hyperinflated lungs at the end of expiration from lung air-trapping raises intrathoracic pressure, reduces venous return and decreases ventricular filling theoretically unloading the cardiopulmonary baroreceptors. However, the effects of static lung hyperinflation on SNA and large artery stiffness in COPD patients remain unknown. Therefore, this novel study will provide important information regarding the underlying mechanisms that potentially contribute to the heightened CVD risk demonstrated in individuals with COPD.
- Conditions
- COPD
- Being tested
- Umeclidinium / Vilanterol Dry Powder Inhaler, Placebo
- Medical subject headings
- Pulmonary Disease, Chronic Obstructive
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Umeclidinium / Vilanterol Dry Powder InhalerDrug
Also called Anora Ellipta
umeclidinium/vilanterol dry powder inhaler
PlaceboDrug
Placebo inhaler
| Study group | Role | What they receive |
|---|---|---|
| Umeclidinium bromide/vilanterol | Active comparator | Umeclidinium bromide/vilanterol (umeclidinium bromide 62.5 mcg; vilanterol 25mcg inhalation powder; trade name Anoro Ellipta) is a combination long-acting bronchodilator that acts to reduce the amount of air trapped in the lungs at the end of of expiration. Receives: Drug: Umeclidinium / Vilanterol Dry Powder Inhaler |
| Placebo | Placebo comparator | A placebo inhaler will be administered to serve as a control comparator to the umeclidinium bromide/vilanterol inhaler. Receives: Drug: Placebo |
What is being measured
The primary outcome is the main question the study is designed to answer.
Carotid artery stiffness
Carotid artery stiffness as determined by carotid sonography
Measured: 2 hours
Aortic stiffness
Aortic stiffness as determined by the carotid-femoral pulse wave velocity technique
Measured: 2 hours
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted2 Aug 2018
- Study start24 Jan 2019
- Primary completion1 Apr 2020
- Study completion1 Apr 2020
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (21)Papers the sponsor has linked to this study.
- Other trials for COPDStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase 4
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Double blind
- Who is masked
- Participant, Investigator
- Enrolment
- 15 participants (actual)
Sponsor and investigators
- Lead sponsor
- Gary L. Pierce
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor-investigator, Gary L. Pierce, University of Iowa
- Investigators
- Gary L Pierce, PhD, Principal investigator, University of Iowa
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT03611699
- Sponsor's protocol ID
- 201805782
- Status last verified
- Jul 2020
- First submitted
- 26 Jul 2018
- Last updated
- 14 Jul 2020
- Results posted
- No
- Data monitoring committee
- Yes
- FDA-regulated drug
- Yes
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Ford ES, Murphy LB, Khavjou O, Giles WH, Holt JB, Croft JB. Total and state-specific medical and absenteeism costs of COPD among adults aged >/= 18 years in the United States for 2010 and projections through 2020. Chest. 2015 Jan;147(1):31-45. doi: 10.1378/chest.14-0972.
PubMed 25058738Sin DD, Anthonisen NR, Soriano JB, Agusti AG. Mortality in COPD: Role of comorbidities. Eur Respir J. 2006 Dec;28(6):1245-57. doi: 10.1183/09031936.00133805.
PubMed 17138679Mitchell GF, Hwang SJ, Vasan RS, Larson MG, Pencina MJ, Hamburg NM, Vita JA, Levy D, Benjamin EJ. Arterial stiffness and cardiovascular events: the Framingham Heart Study. Circulation. 2010 Feb 2;121(4):505-11. doi: 10.1161/CIRCULATIONAHA.109.886655. Epub 2010 Jan 18.
PubMed 20083680van Sloten TT, Schram MT, van den Hurk K, Dekker JM, Nijpels G, Henry RM, Stehouwer CD. Local stiffness of the carotid and femoral artery is associated with incident cardiovascular events and all-cause mortality: the Hoorn study. J Am Coll Cardiol. 2014 May 6;63(17):1739-47. doi: 10.1016/j.jacc.2013.12.041. Epub 2014 Feb 26.
PubMed 24583306Mills NL, Miller JJ, Anand A, Robinson SD, Frazer GA, Anderson D, Breen L, Wilkinson IB, McEniery CM, Donaldson K, Newby DE, Macnee W. Increased arterial stiffness in patients with chronic obstructive pulmonary disease: a mechanism for increased cardiovascular risk. Thorax. 2008 Apr;63(4):306-11. doi: 10.1136/thx.2007.083493. Epub 2007 Nov 16.
PubMed 18024535Albu A, Fodor D, Bondor C, Suciu O. Carotid arterial stiffness in patients with chronic obstructive pulmonary disease. Acta Physiol Hung. 2011 Jun;98(2):117-27. doi: 10.1556/APhysiol.98.2011.2.3.
PubMed 21616770Lynch DA, Austin JH, Hogg JC, Grenier PA, Kauczor HU, Bankier AA, Barr RG, Colby TV, Galvin JR, Gevenois PA, Coxson HO, Hoffman EA, Newell JD Jr, Pistolesi M, Silverman EK, Crapo JD. CT-Definable Subtypes of Chronic Obstructive Pulmonary Disease: A Statement of the Fleischner Society. Radiology. 2015 Oct;277(1):192-205. doi: 10.1148/radiol.2015141579. Epub 2015 May 11.
PubMed 25961632McDonough JE, Yuan R, Suzuki M, Seyednejad N, Elliott WM, Sanchez PG, Wright AC, Gefter WB, Litzky L, Coxson HO, Pare PD, Sin DD, Pierce RA, Woods JC, McWilliams AM, Mayo JR, Lam SC, Cooper JD, Hogg JC. Small-airway obstruction and emphysema in chronic obstructive pulmonary disease. N Engl J Med. 2011 Oct 27;365(17):1567-75. doi: 10.1056/NEJMoa1106955.
PubMed 22029978Hogg JC, Chu F, Utokaparch S, Woods R, Elliott WM, Buzatu L, Cherniack RM, Rogers RM, Sciurba FC, Coxson HO, Pare PD. The nature of small-airway obstruction in chronic obstructive pulmonary disease. N Engl J Med. 2004 Jun 24;350(26):2645-53. doi: 10.1056/NEJMoa032158.
PubMed 15215480Deesomchok A, Webb KA, Forkert L, Lam YM, Ofir D, Jensen D, O'Donnell DE. Lung hyperinflation and its reversibility in patients with airway obstruction of varying severity. COPD. 2010 Dec;7(6):428-37. doi: 10.3109/15412555.2010.528087.
PubMed 21166631Camiciottoli G, Bigazzi F, Magni C, Bonti V, Diciotti S, Bartolucci M, Mascalchi M, Pistolesi M. Prevalence of comorbidities according to predominant phenotype and severity of chronic obstructive pulmonary disease. Int J Chron Obstruct Pulmon Dis. 2016 Sep 14;11:2229-2236. doi: 10.2147/COPD.S111724. eCollection 2016.
PubMed 27695310O'Donnell DE, Casaburi R, Frith P, Kirsten A, De Sousa D, Hamilton A, Xue W, Maltais F. Effects of combined tiotropium/olodaterol on inspiratory capacity and exercise endurance in COPD. Eur Respir J. 2017 Apr 19;49(4):1601348. doi: 10.1183/13993003.01348-2016. Print 2017 Apr.
PubMed 28424359Andreas S, Haarmann H, Klarner S, Hasenfuss G, Raupach T. Increased sympathetic nerve activity in COPD is associated with morbidity and mortality. Lung. 2014 Apr;192(2):235-41. doi: 10.1007/s00408-013-9544-7. Epub 2013 Dec 22.
PubMed 24362752Macefield VG. Sustained activation of muscle sympathetic outflow during static lung inflation depends on a high intrathoracic pressure. J Auton Nerv Syst. 1998 Feb 5;68(3):135-9. doi: 10.1016/s0165-1838(97)00129-x.
PubMed 9626939Stone IS, Barnes NC, James WY, Midwinter D, Boubertakh R, Follows R, John L, Petersen SE. Lung Deflation and Cardiovascular Structure and Function in Chronic Obstructive Pulmonary Disease. A Randomized Controlled Trial. Am J Respir Crit Care Med. 2016 Apr 1;193(7):717-26. doi: 10.1164/rccm.201508-1647OC.
PubMed 26550687
Study at a glance
From the registry record, last updated by the sponsor on 14 Jul 2020. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Static Lung Hyperinflation and Sympathetic Nerve Activity-Associated Large Artery Stiffness in COPD Patients
- ClinicalTrials.gov ID
- NCT03611699
- Acronym / sponsor ID
- 201805782
- Conditions
- COPD
- Phase
- Phase 4
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 15 participants (actual)
- Lead sponsor
- Gary L. PierceUniversity, hospital or other
- Study start
- 24 Jan 2019 (actual)
- Primary completion
- 1 Apr 2020 (actual)
- Study completion
- 1 Apr 2020 (actual)
- First posted
- 2 Aug 2018 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
The goal of this study is to evaluate the acute effects of a long-acting bronchodilator on pulmonary function, vascular function and muscle sympathetic nerve activity in individuals with COPD. Individuals will be recruited from previous pulmonary research cohorts at The University of Iowa hospitals and clinics. Individuals that are interested in the study and are deemed eligible to participate will have a total of 3 visits to the laboratory, which includes the screening and consent (visit 1) that will last approximately 1 hour. Visits 2 and 3 are experimental visits and will be more extensive (~4 hours). Participants will be randomized to receive either a long-acting bronchodilator or a placebo inhaler at the first experimental visit, followed by either the placebo inhaler or the long-acting bronchodilator at the second experimental visit. Assessments of pulmonary function, vascular function (via non-invasive, well-established techniques), and muscle sympathetic nerve activity will be performed at both experimental visits.
Detailed description
COPD is a global health concern affecting more than 65 million people worldwide. In the U.S. alone, the estimated medical costs attributed to COPD surpassed $30 billion in 2010. A high percentage of this healthcare cost is attributed to the management of comorbidities associated with COPD, such as CVD. Although primarily a disease of the lungs, CVD accounts for up to 50% of all deaths among individuals with COPD. One likely mechanism contributing to the increased CVD risk observed in individuals with COPD is large central artery (i.e. carotid and aorta) stiffness. Elevated large artery stiffness is a robust predictor of CVD events and mortality in adults. Specifically, carotid-femoral pulse wave velocity (CFPWV), the reference standard measurement of aortic stiffness, is a robust, independent predictor of coronary heart events, and carotid artery stiffness, expressed as β-stiffness index, is strongly associated with incident stroke. Both CFPWV and carotid β-stiffness are markedly greater in individuals with COPD compared with age-matched controls suggesting that these mechanisms may contribute, at least in part, to the high CVD risk in this group. However, there is currently a gap in knowledge concerning the mechanisms that lead to increased large artery stiffness in individuals with COPD in part because assessing large artery stiffness among individuals with COPD has been limited to comparing aortic and carotid artery stiffness in all COPD patients with non-COPD controls, without differentiating between distinctive phenotypes of COPD. As a result of this overly simplistic approach, it has proven challenging to identify the mechanism(s) responsible for the accelerated large artery stiffness among COPD patients because different mechanisms may contribute to large artery stiffness in the various phenotypes of COPD. The two main computed tomography (CT)-quantifiable phenotypes that individuals with COPD can be subdivided into are emphysema-and airway-predominant phenotypes. COPD patients with an airway-predominant phenotype display characteristic signs of small airway disease including increased airway wall thickness, heightened airway inflammation and a greater concentration of mucus exudates in the small conducting airways. This structural remodeling leads to a greater amount of air to become trapped in the airways at residual volume and increases the resting volume of the lungs producing static lung hyperinflation. COPD patients with an airway-predominant phenotype have little or no emphysema and account for up to 60% of all mild-to-moderate COPD patients (i.e. Global Initiative for COPD; GOLD stage 1-2) and up to 25% of all severe-very severe COPD patients (GOLD 3-4). Although airway predominant patients are typically in the earlier stages of COPD progression, they are at greater CVD risk than emphysema-predominant COPD patients who make up the majority of severe-very severe (GOLD 3-4) COPD patients. However, the mechanisms responsible for the heighted CVD risk demonstrated in airway-predominant patients remain unclear. Our preliminary data demonstrate that static lung hyperinflation is strongly associated with carotid artery and aortic stiffness. These data suggest that static lung hyperinflation may be a mechanism contributing to the higher CVD risk in airway-predominant phenotypes of COPD in part from its effects on large artery stiffness. Bronchodilator therapy reduces static lung hyperinflation and improves respiratory symptoms in individuals with COPD, however the effects of bronchodilator therapy on CVD risk remain unclear. Combination long-acting muscarinic antagonist and long-acting beta2-agonist bronchodilator (LAMA/LABA) therapy reduces air-trapping and static lung hyperinflation to a greater extent than either monotherapy alone. This evidence suggests that a LAMA/LABA combination bronchodilator will elicit the greatest changes in large artery stiffness because of its superior effects on lung deflation compared with either medication alone.
Sympathetic nerve activity (SNA) is elevated in COPD patients compared with controls and is an independent predictor of morbidity and mortality in this group. However, the mechanisms underlying the hyperactivation of SNA in COPD remain incompletely understood. In healthy individuals, acute static lung hyperinflation, induced by Valsalva maneuver, is associated with a sustained increase in intrathoracic pressure and a subsequent decrease in central venous volume. This decrease in central venous volume in turn unloads the cardiopulmonary baroreceptors and results in sustained sympathetic activation. Importantly, in individuals with COPD, the positive pressure within hyperinflated lungs at the end of expiration from lung air-trapping raises intrathoracic pressure, reduces venous return and decreases ventricular filling theoretically unloading the cardiopulmonary baroreceptors. However, the effects of static lung hyperinflation on SNA and large artery stiffness in COPD patients remain unknown. Therefore, this novel study will provide important information regarding the underlying mechanisms that potentially contribute to the heightened CVD risk demonstrated in individuals with COPD.
Study design
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Double blind (participant, investigator)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Umeclidinium bromide/vilanterol | Active comparator | Drug: Umeclidinium / Vilanterol Dry Powder InhalerUmeclidinium bromide/vilanterol (umeclidinium bromide 62.5 mcg; vilanterol 25mcg inhalation powder; trade name Anoro Ellipta) is a combination long-acting bronchodilator that acts to reduce the amount of air trapped in the lungs at the end of of expiration. |
| Placebo | Placebo comparator | Drug: PlaceboA placebo inhaler will be administered to serve as a control comparator to the umeclidinium bromide/vilanterol inhaler. |
Who may qualify
- Ages
- 30 to 80 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (5 listed)
- Age 30-80
- Ability to comfortably lie flat for 2 hours
- Normal/corrected hearing and vision
- English speaking
- Airway predominate phenotype of COPD
Key exclusion criteria (23 listed)
- Other concomitant respiratory disorder (including asthma)
- Use of antibiotics or steroids for a COPD exacerbation within the past month
- Use of 24-hour oxygen
- Pregnancy or suspected pregnancy
- Uncontrolled cancer within the last 5 years
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Umeclidinium / Vilanterol Dry Powder InhalerAlso: Anora Elliptaumeclidinium/vilanterol dry powder inhaler | Drug | Umeclidinium bromide/vilanterol |
| PlaceboPlacebo inhaler | Drug | Placebo |
Primary outcome
Carotid artery stiffness
Time frame: 2 hours
Carotid artery stiffness as determined by carotid sonography
Aortic stiffness
Time frame: 2 hours
Aortic stiffness as determined by the carotid-femoral pulse wave velocity technique
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 14 Jul 2020.
- Background: PubMed 25058738Ford ES, Murphy LB, Khavjou O, Giles WH, Holt JB, Croft JB. Total and state-specific medical and absenteeism costs of COPD among adults aged >/= 18 years in the United States for 2010 and projections through 2020. Chest. 2015 Jan;147(1):31-45. doi: 10.1378/chest.14-0972.
- Background: PubMed 17138679Sin DD, Anthonisen NR, Soriano JB, Agusti AG. Mortality in COPD: Role of comorbidities. Eur Respir J. 2006 Dec;28(6):1245-57. doi: 10.1183/09031936.00133805.
- Background: PubMed 20083680Mitchell GF, Hwang SJ, Vasan RS, Larson MG, Pencina MJ, Hamburg NM, Vita JA, Levy D, Benjamin EJ. Arterial stiffness and cardiovascular events: the Framingham Heart Study. Circulation. 2010 Feb 2;121(4):505-11. doi: 10.1161/CIRCULATIONAHA.109.886655. Epub 2010 Jan 18.
- Background: PubMed 24583306van Sloten TT, Schram MT, van den Hurk K, Dekker JM, Nijpels G, Henry RM, Stehouwer CD. Local stiffness of the carotid and femoral artery is associated with incident cardiovascular events and all-cause mortality: the Hoorn study. J Am Coll Cardiol. 2014 May 6;63(17):1739-47. doi: 10.1016/j.jacc.2013.12.041. Epub 2014 Feb 26.
- Background: PubMed 18024535Mills NL, Miller JJ, Anand A, Robinson SD, Frazer GA, Anderson D, Breen L, Wilkinson IB, McEniery CM, Donaldson K, Newby DE, Macnee W. Increased arterial stiffness in patients with chronic obstructive pulmonary disease: a mechanism for increased cardiovascular risk. Thorax. 2008 Apr;63(4):306-11. doi: 10.1136/thx.2007.083493. Epub 2007 Nov 16.
- Background: PubMed 21616770Albu A, Fodor D, Bondor C, Suciu O. Carotid arterial stiffness in patients with chronic obstructive pulmonary disease. Acta Physiol Hung. 2011 Jun;98(2):117-27. doi: 10.1556/APhysiol.98.2011.2.3.
- Background: PubMed 25961632Lynch DA, Austin JH, Hogg JC, Grenier PA, Kauczor HU, Bankier AA, Barr RG, Colby TV, Galvin JR, Gevenois PA, Coxson HO, Hoffman EA, Newell JD Jr, Pistolesi M, Silverman EK, Crapo JD. CT-Definable Subtypes of Chronic Obstructive Pulmonary Disease: A Statement of the Fleischner Society. Radiology. 2015 Oct;277(1):192-205. doi: 10.1148/radiol.2015141579. Epub 2015 May 11.
- Background: PubMed 22029978McDonough JE, Yuan R, Suzuki M, Seyednejad N, Elliott WM, Sanchez PG, Wright AC, Gefter WB, Litzky L, Coxson HO, Pare PD, Sin DD, Pierce RA, Woods JC, McWilliams AM, Mayo JR, Lam SC, Cooper JD, Hogg JC. Small-airway obstruction and emphysema in chronic obstructive pulmonary disease. N Engl J Med. 2011 Oct 27;365(17):1567-75. doi: 10.1056/NEJMoa1106955.
- Background: PubMed 15215480Hogg JC, Chu F, Utokaparch S, Woods R, Elliott WM, Buzatu L, Cherniack RM, Rogers RM, Sciurba FC, Coxson HO, Pare PD. The nature of small-airway obstruction in chronic obstructive pulmonary disease. N Engl J Med. 2004 Jun 24;350(26):2645-53. doi: 10.1056/NEJMoa032158.
- Background: PubMed 21166631Deesomchok A, Webb KA, Forkert L, Lam YM, Ofir D, Jensen D, O'Donnell DE. Lung hyperinflation and its reversibility in patients with airway obstruction of varying severity. COPD. 2010 Dec;7(6):428-37. doi: 10.3109/15412555.2010.528087.
- Background: PubMed 27695310Camiciottoli G, Bigazzi F, Magni C, Bonti V, Diciotti S, Bartolucci M, Mascalchi M, Pistolesi M. Prevalence of comorbidities according to predominant phenotype and severity of chronic obstructive pulmonary disease. Int J Chron Obstruct Pulmon Dis. 2016 Sep 14;11:2229-2236. doi: 10.2147/COPD.S111724. eCollection 2016.
- Background: PubMed 28424359O'Donnell DE, Casaburi R, Frith P, Kirsten A, De Sousa D, Hamilton A, Xue W, Maltais F. Effects of combined tiotropium/olodaterol on inspiratory capacity and exercise endurance in COPD. Eur Respir J. 2017 Apr 19;49(4):1601348. doi: 10.1183/13993003.01348-2016. Print 2017 Apr.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Gary L Pierce, PhD principal investigator
University of Iowa
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A Phase 4 study testing Umeclidinium / Vilanterol Dry Powder Inhaler in people with COPD, run by Gary L. Pierce at 1 site in United States.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 5 inclusion and 23 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 14 Jul 2020. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United States. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. Some participants in this study may receive a placebo. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
What does this phase mean?
Phase 4 studies take place after a treatment is approved, to learn more about its long-term benefits and risks in everyday use.
Not every study follows the same path, and some studies (observational studies, device studies) have no phase.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Carotid artery stiffness (time frame: 2 hours). The study lists 2 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT03611699, which also lists 21 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 14 Jul 2020.