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

Endothelial Dysfunction Clinical Trial

— EDAECOPD  

Official title:

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

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT01460082
• Other study ID #: EDAECOPD
• Status: Completed
• Phase: N/A
• First received: October 25, 2011
• Last updated: March 10, 2014
• Start date: August 2008
• Est. completion date: September 2010

Study information

• Verified date: March 2014
• Source: LudwLudwig Boltzmann Institute for COPD and Respiratory Epidemiology
• Contact: n/a
• Is FDA regulated: No
• Health authority: Austria: Institutional Review Board of the Vienna city council
• Study type: Observational

Clinical Trial 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.

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.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 29
• Est. completion date: September 2010
• Est. primary completion date: September 2010
• Accepts healthy volunteers: No
• Gender: Both
• Age group: 40 Years and older

Eligibility

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

Study Design

Observational Model: Case-Only, Time Perspective: Cross-Sectional

Related Conditions & MeSH terms

• Chronic Obstructive Pulmonary Disease (COPD)
• Endothelial Dysfunction
• Inflammatory Disease
• Lung Diseases
• Lung Diseases, Obstructive
• Pulmonary Disease, Chronic Obstructive

Locations

Country	Name	City	State
Austria	1.Department of Respiratory and Critical Care Medicine and Ludwig Boltzmann Institute for COPD, Otto-Wagner Hospital	Vienna

Sponsors (1)

Lead Sponsor	Collaborator
LudwLudwig Boltzmann Institute for COPD and Respiratory Epidemiology

Country where clinical trial is conducted

Austria, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	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		Baseline, Week 6-8	No
Secondary	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		baseline, week 6-8	No