Endostatin Serum Levels During Bicycle Stress Test

Medical University of Vienna

Status: Completed

Conditions: Cardiac Diseases; Smoking

Study type: Observational

Funder types: Other

Identifiers

NCT01165515

220/2007

Details and patient eligibility

About

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.

Enrollment: 240 patients

Sex: All

Ages: 18 to 75 years old

Volunteers: Accepts Healthy Volunteers

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

Trial design

240 participants in 13 patient groups

Healthy young females

Description:

20 healthy females, aged between 18 and 35 years

Healthy young males

Description:

20 healthy males, aged between 18 and 35 years

Healthy elderly smokers

Description:

20 healthy smokers, aged between 45 and 75 years

Healthy elderly non-smokers

Description:

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

Healthy young female smokers

Description:

20 healthy female smokers, aged between 18 and 35 years

Healthy young male smokers

Description:

20 healthy male smokers, aged between 18 and 35 years

Healthy postmenopausal women

Description:

20 healthy postmenopausal women

Female CMP Patients

Description:

20 female patients suffering from cardiomyopathy (ischemic or dilating)

Male CMP Patients

Description:

20 male patients suffering from cardiomyopathy (ischemic or dilating)

Female CHD patients

Description:

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

Male CHD Patients

Description:

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

male athlets

Description:

20 male athlets

female athlets

Description:

20 female athlets