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

Endothelial Dysfunction and Systemic Inflammation in Patients With Acute Exacerbations of Chronic Obstructive Pulmonary Disease

Status
Completed
Phases
Unknown
Study type
Observational
Source
ClinicalTrials.gov
Registry ID
NCT01460082
Acronym
EDAECOPD
Enrollment
29
Registered
2011-10-26
Start date
2008-08-31
Completion date
2010-09-30
Last updated
2014-03-12

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

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

Keywords

chronic obstructive pulmonary disease, acute exacerbation, endothelial dysfunction, flow mediated dilation, systemic inflammation

Brief 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.

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.

Interventions

None listed

Sponsors

LudwLudwig Boltzmann Institute for COPD and Respiratory Epidemiology
Lead SponsorNETWORK

Study design

Observational model
CASE_ONLY
Time perspective
CROSS_SECTIONAL

Eligibility

Sex/Gender
ALL
Age
40 Years to No maximum
Healthy volunteers
No

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

* 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

Design outcomes

Primary

MeasureTime frame
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 COPDBaseline, Week 6-8

Secondary

MeasureTime frame
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) levelsbaseline, week 6-8

Countries

Austria

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026