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

Completed

• Conditions: Inflammatory Disease; Chronic Obstructive Pulmonary Disease (COPD); Endothelial Dysfunction

• Registration Number: NCT01460082
• Lead Sponsor: LudwLudwig Boltzmann Institute for COPD and Respiratory Epidemiology

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.

Study Timeline

• Study Start: 2008-08
• Primary Completion: 2010-09
• Study Completion: 2010-09
• Study First Submitted: 2011-10-25
• Study First Submitted QC: 2011-10-25
• Study First Posted: 2011-10-26
• Status Verified: 2014-03
• Last Update Submitted: 2014-03-10
• Last Update Posted: 2014-03-12

Recruitment & Eligibility

• Status: COMPLETED
• Sex: All
• Target Recruitment: 29

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

• Study Type: OBSERVATIONAL
• Study Design: Not specified

Primary Outcome Measures

Name	Time	Method
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

Secondary Outcome Measures

Name	Time	Method
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

Trial Locations

Locations (1)

1.Department of Respiratory and Critical Care Medicine and Ludwig Boltzmann Institute for COPD, Otto-Wagner Hospital; 🇦🇹 Vienna, Austria