Cardiac Diseases, Smoking
Conditions
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.
Interventions
None listed
Sponsors
Medical University of Vienna
Study design
Time perspective
PROSPECTIVE
Eligibility
Sex/Gender
ALL
Age
18 Years to 75 Years
Healthy volunteers
Yes
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
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| 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
| Measure | Time frame | Description |
|---|---|---|
| catecholamine | baseline | baseline sample will be drawn at rest |
| hemodynamic parameters | baseline | heart rate and blood pressure behavior will be monitored throughout the entire bicycle stress test |
Countries
Austria
Outcome results
None listed