Endostatin Serum Levels During Bicycle Stress Test

Completed

• Conditions: Smoking; Cardiac Diseases

• Registration Number: NCT01165515
• Lead Sponsor: Medical University of Vienna

Brief Summary

Endostatin, a 20-kDa cleavage product of collagen XVIII, is a component of the extracellular matrix expressed in the basement membrane. As a potent inhibitor of angiogenesis, endostatin induces endothelial cell apoptosis and diminishes cell migration, adhesion and proliferation.

Endostatin may stop the progression of atherosclerosis. Atherosclerotic heart disease involves unwanted tissue growth. By cutting off the blood supply from a plaque the likelihood of plaque rupture may eventually be reduced. Recent data indicates that the loss of collagen XVIII/endostatin is related to the enhancement of neo-vascularization and vascular permeability in atherosclerosis. Plaque neo-vascularization strongly correlates with the regional content of inflammatory cells. Furthermore, increased vascular permeability enhances lipid accumulation in the vessel walls, hence increasing foam cells.

Therapeutic angiogenesis is a most promising strategy for the treatment of myocardial infarction. However, it remains unknown if and how endogenous angiogenesis inhibitors, such as endostatin, regulate angiogenesis in myocardial infarction. Rat models showed that after myocardial infarction endostatin neutralization displayed adverse left ventricular remodeling and severe heart failure compared with controls. Although angiogenesis was increased, tissue remodeling and interstitial fibrosis were further exaggerated in post-myocardial infarction hearts by endostatin neutralization.

However, several studies suggest that endostatin may locally modulate coronary collateral formation by inhibiting collateral vessel formation in patients with ischemic heart disease.

During treadmill exercise tests in healthy volunteers a significant increase in circulating endostatin levels can be observed. Exercise induces angiogenesis in cardiac and skeletal muscles by decreasing endostatin in the muscle tissues to increase blood flow to these metabolically active tissues. Thereby endostatin is released into the general circulation.

In summary, endostatin might be a new weapon to fight against atherosclerotic progression by inhibiting neo-vascularization of atherosclerotic plaques.

Detailed Description

Not available

Study Timeline

• Study Start: 2008-01
• Study First Submitted: 2010-07-13
• Study First Submitted QC: 2010-07-19
• Study First Posted: 2010-07-20
• Primary Completion: 2012-12
• Study Completion: 2013-04
• Status Verified: 2014-05
• Last Update Submitted: 2014-05-18
• Last Update Posted: 2014-05-20

Recruitment & Eligibility

• Status: COMPLETED
• Sex: All
• Target Recruitment: 240

Inclusion Criteria

• Smoking/Non smoking
• Healthy/non healthy (if for CMP, CHD study)
• Age (depending on the group affiliation)

Exclusion Criteria

• Suffering from grave diseases

Study & Design

• Study Type: OBSERVATIONAL
• Study Design: Not specified

Primary Outcome Measures

Name	Time	Method
Endostatin	baseline/maximum	baseline sample will be drawn at rest; a second sample will be drawn 5 minutes after each individual reaches its peak workload (average time 10 minutes)

Secondary Outcome Measures

Name	Time	Method
catecholamine	day 1	a second sample will be drawn 5 minutes after each individual reaches its peak workload (average time 10 minutes)
hemodynamic parameters	baseline	heart rate and blood pressure behavior will be monitored throughout the entire bicycle stress test

Trial Locations

Locations (1)

Medical University of Vienna; 🇦🇹 Vienna, Austria