Endostatin Serum Levels During Bicycle Stress Test

NCT01165515 | Completed DMC

• 1 other identifier: 220/2007
• Study Type: observational
• Target: 240
• Locations: 1 country
• Sites: 1

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.

Conditions

Smoking; Cardiac Diseases

Outcome Measures

Primary Outcomes (1)

• 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

Secondary Outcomes (3)

• catecholamine

  baseline

• hemodynamic parameters

  baseline

• catecholamine

  day 1

Study Arms (13)

Healthy young females

20 healthy females, aged between 18 and 35 years

Healthy young males

20 healthy males, aged between 18 and 35 years

Healthy elderly smokers

20 healthy smokers, aged between 45 and 75 years

Healthy elderly non-smokers

20 healthy non-smokers, aged between 45 and 75 years

Healthy young female smokers

20 healthy female smokers, aged between 18 and 35 years

Healthy young male smokers

20 healthy male smokers, aged between 18 and 35 years

Healthy postmenopausal women

20 healthy postmenopausal women

Female CMP Patients

20 female patients suffering from cardiomyopathy (ischemic or dilating)

Male CMP Patients

20 male patients suffering from cardiomyopathy (ischemic or dilating)

Female CHD patients

30 female patients suffering from cardiac heart disease, before aorto-coronary bypass surgery (and after)

Male CHD Patients

30 male patients suffering from cardiac heart disease, before aorto-coronary bypass surgery (and after)

male athlets

20 male athlets

female athlets

20 female athlets

Eligibility Criteria

• Age: 18 Years - 75 Years
• Sex: all
• Healthy Volunteers: Yes
• Age Groups: Adult (18-64), Older Adult (65+)
• Sampling Method: Probability Sample

Study Population

200 patients, divided into sub-groups, always both genders will be tested for different conditions (smoking, age, CMP, CHD,...)

You may qualify if:

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

You may not qualify if:

• Suffering from grave diseases

Sponsors & Collaborators

• Medical University of Vienna: lead

Study Sites (1)

Medical University of Vienna

Vienna, Vienna, 1090, Austria

Location

Related 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.

  PMID: 24393402 RESULT

MeSH Terms

Conditions

Smoking; Heart Diseases

Condition Hierarchy (Ancestors)

Behavior; Cardiovascular Diseases

Study Officials

• Jeanette Strametz-Juranek, MD

  MUV, Department of Internal Medicine II, Division of Cardiology

  PRINCIPAL INVESTIGATOR

Study Design

• Study Type: observational
• Time Perspective: PROSPECTIVE
• Sponsor Type: OTHER
• Responsible Party: PRINCIPAL INVESTIGATOR
• PI Title: Ao.Univ.Prof.Dr

Study Record Dates

• First Submitted: July 13, 2010
• First Posted: July 20, 2010
• Study Start: January 1, 2008
• Primary Completion: December 1, 2012
• Study Completion: April 1, 2013
• Last Updated: May 20, 2014

Record last verified: 2014-05

Locations

AU (1)