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CompletedNCT01460082EDAECOPDUpdated Mar 12, 2014

Endothelial Dysfunction in Acute Exacerbations of Chronic Obstructive Pulmonary Disease (COPD)

An observational study in Chronic Obstructive Pulmonary Disease (COPD), Inflammatory Disease and Endothelial Dysfunction, sponsored by LudwLudwig Boltzmann Institute for COPD and Respiratory Epidemiology. Completed at 1 site in Austria. Open to participants aged 40 Years and older. Per ClinicalTrials.gov, last updated 2014-03-12.

Sponsored by LudwLudwig Boltzmann Institute for COPD and Respiratory Epidemiology · Observational

Study type
Observational
Model
Case-only
Time perspective
Cross-sectional
Enrollment
29
Ages
40 Years and older
Sex
All
01

Study summary

The purpose of the study is to determine a possible association between the clinical entity of exacerbation, markers of systemic inflammation and endothelial dysfunction in patients with COPD.

Read the detailed description

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease of the lungs; however, there is cumulating data suggesting that the inflammatory reaction associated with COPD is not restricted to the lungs but has systemic effects. Patients with COPD have increased cardiovascular morbidity and mortality. The suspected link between increased cardiovascular mortality and systemic inflammation is endothelial dysfunction, which in turn is caused by impaired activity of NO. Endothelial dysfunction has been demonstrated in patients with COPD. Furthermore there is a close correlation between endothelial dysfunction in coronary and peripheral vessels, which allows assessing flow-mediated dilation (FMD) in the brachial artery via high resolution ultrasound as an early predictor of atherosclerosis. Moreover, systemic inflammatory markers correlate with endothelial dysfunction in patients with stable COPD.

Exacerbations of COPD are episodes of worsening symptoms characterized by increased airway and systemic inflammation. If systemic inflammation is a cause of endothelial dysfunction in COPD, endothelial function would be suspected to be further impaired during exacerbation and recover thereafter. The purpose of this study is to determine a possible association between the clinical entity of exacerbation, markers of systemic inflammation and endothelial dysfunction in patients with COPD.

02

Conditions studied

  • Chronic Obstructive Pulmonary Disease (COPD)
  • Inflammatory Disease
  • Endothelial Dysfunction

Keywords

  • chronic obstructive pulmonary disease
  • acute exacerbation
  • endothelial dysfunction
  • flow mediated dilation
  • systemic inflammation
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In context

Lung Diseases

3,303 studies on the registry are indexed under Lung Diseases; 355 are open to participants now.

This study's enrollment of 29 is below the median of 157 across 929 observational studies indexed under Lung Diseases.

Browse Lung Diseases studies →

Lead sponsor

LudwLudwig Boltzmann Institute for COPD and Respiratory Epidemiology is the lead sponsor of 5 studies on the registry; none are open to participants now.

Counted across the registry records on this site, refreshed daily.

04

Who can participate

Ages eligible
40 Years and older
Sexes eligible
All
Accepts healthy volunteers
No
Sampling method
Non-probability sample

Study population

Patients with COPD diagnosed according to standard criteria in the state of acute exacerbation

Inclusion criteria

  • presence of COPD according to standard criteria
  • acute exacerbation of COPD according to recommended international criteria
  • over 40 years of age
  • history of at least 10 py

Exclusion criteria

Exclusion Criteria:

  • pneumonia
  • history or signs of congestive heart failure,
  • acute myocardial infarction
  • thoracotomy incl. resection of lungtissue
  • interstitial lung disease
  • acute or chronic renal failure
  • active malignancy
  • autoimmune disease
05

Study design

Observational model
Case-only
Time perspective
Cross-sectional
Enrollment
29 participants (actual)
Biospecimen retention
Samples without dna

Groups and cohorts

  • Exacerbation

    The study sample will consist of patients admitted to the hospital because of an acute exacerbation of COPD

06

What researchers measure

Primary outcomes

  1. change of endothelial dysfunction (impaired vasomotor reactivity due to shaer stress) confirmed by non-invasive measurement of flow mediated dilation (FMD) 6-8 weeks after acute exacerbation of COPD

    Time frame: Baseline, Week 6-8

Secondary outcomes

  1. change of systemic inflammation 6-8 weeks after COPD-exacerbation confirmed by inflammatory markers such as interleukin-6 (IL-6), fibrinogen levels, and C-reactive protein (CRP) levels

    Time frame: baseline, week 6-8

07

Study locations

1 site
  • 1.Department of Respiratory and Critical Care Medicine and Ludwig Boltzmann Institute for COPD, Otto-Wagner Hospital
    Vienna, 1140, Austria
08

Updates

Tracking since Sep 25, 2026
No changes since tracking began. The registry record was last updated on Mar 12, 2014, before this site started recording changes on Sep 25, 2026. Its history is on ClinicalTrials.gov ↗
09

Registry details

Key details

Study ID
NCT01460082
Lead sponsor
LudwLudwig Boltzmann Institute for COPD and Respiratory Epidemiology
Responsible party
Matthias Urban (M.D., Study coordinator, LudwLudwig Boltzmann Institute for COPD and Respiratory Epidemiology) — Principal investigator
First posted
Oct 26, 2011
Start date
Aug 2008
Primary completion
Sep 2010
Completion
Sep 2010
Last update
Mar 12, 2014

Study contacts

Georg C Funk, M.D.
principal investigator · 1. Department of Respiratory and Critical Care Medicine and Ludwig Boltzmann Institute for COPD, Otto-Wagner Hospital, Vienna, Austria

Oversight

Data monitoring committee
No
View the source record on ClinicalTrials.gov ↗

Not currently enrolling

This study is completed, as verified in Mar 2014. You cannot join it, but the record below documents what was studied.

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