Endostatin Serum Levels During Bicycle Stress Test

Smoking Clinical Trial

Official title:

Endostatin Serum Levels During Bicycle Stress Test in Different Samples

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT01165515
• Other study ID #: 220/2007
• Status: Completed
• Phase: N/A
• First received: July 13, 2010
• Last updated: May 18, 2014
• Start date: January 2008
• Est. completion date: April 2013

Study information

• Verified date: May 2014
• Source: Medical University of Vienna
• Contact: n/a
• Is FDA regulated: No
• Health authority: Austria: Ethikkommission
• Study type: Observational

Clinical Trial 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.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 240
• Est. completion date: April 2013
• Est. primary completion date: December 2012
• Accepts healthy volunteers: Accepts Healthy Volunteers
• Gender: Both
• Age group: 18 Years to 75 Years

Eligibility

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

Time Perspective: Prospective

Related Conditions & MeSH terms

• Cardiac Diseases
• Heart Diseases
• Smoking

Locations

Country	Name	City	State
Austria	Medical University of Vienna	Vienna

Sponsors (1)

Lead Sponsor	Collaborator
Medical University of Vienna

Country where clinical trial is conducted

Austria, 

References & Publications (1)

Sponder M, Dangl D, Kampf S, Fritzer-Szekeres M, Strametz-Juranek J. Exercise increases serum endostatin levels in female and male patients with diabetes and controls. Cardiovasc Diabetol. 2014 Jan 6;13:6. doi: 10.1186/1475-2840-13-6. — View Citation

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Endostatin	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)	baseline/maximum	No
Secondary	catecholamine	baseline sample will be drawn at rest	baseline	No
Secondary	hemodynamic parameters	heart rate and blood pressure behavior will be monitored throughout the entire bicycle stress test	baseline	No
Secondary	catecholamine	a second sample will be drawn 5 minutes after each individual reaches its peak workload (average time 10 minutes)	day 1	No