Clinical trial NCT01165515: Endostatin Serum Levels During Bicycle Stress Test
Official title: Endostatin Serum Levels During Bicycle Stress Test in Different Samples
Study type: OBSERVATIONAL
Overall status: COMPLETED
Conditions: Smoking
Cardiac Diseases
Lead sponsor: Medical University of Vienna
Sponsor class: OTHER
First posted: 2010-07-20
Enrollment: 240
Sex: ALL
Minimum age (years): 18
Maximum age (years): 75
Standard ages: ADULT
OLDER_ADULT
Accepts healthy volunteers: yes
Time perspective: PROSPECTIVE
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,...)

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.


Eligibility criteria: 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

Primary outcomes:
measure: Endostatin
timeFrame: baseline/maximum
Secondary outcomes:
measure: catecholamine
timeFrame: baseline
measure: hemodynamic parameters
timeFrame: baseline
measure: catecholamine
timeFrame: day 1
Other outcomes:
Locations:
city: Vienna
country: Austria
facility: Medical University of Vienna
Study officials:
affiliation: MUV, Department of Internal Medicine II, Division of Cardiology
name: Jeanette Strametz-Juranek, MD
role: PRINCIPAL_INVESTIGATOR
References:
citation: 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.