Endostatin Serum Levels During Bicycle Stress Test
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Purpose
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.
| Condition |
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Smoking Cardiac Diseases |
| Study Type: | Observational |
| Study Design: | Time Perspective: Prospective |
| Official Title: | Endostatin Serum Levels During Bicycle Stress Test in Different Samples |
- Endostatin [ Time Frame: baseline/maximum ] [ Designated as safety issue: No ]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)
- catecholamine [ Time Frame: baseline ] [ Designated as safety issue: No ]baseline sample will be drawn at rest
- hemodynamic parameters [ Time Frame: baseline ] [ Designated as safety issue: No ]heart rate and blood pressure behavior will be monitored throughout the entire bicycle stress test
- catecholamine [ Time Frame: day 1 ] [ Designated as safety issue: No ]a second sample will be drawn 5 minutes after each individual reaches its peak workload (average time 10 minutes)
| Estimated Enrollment: | 240 |
| Study Start Date: | January 2008 |
| Estimated Study Completion Date: | December 2013 |
| Estimated Primary Completion Date: | December 2012 (Final data collection date for primary outcome measure) |
| Groups/Cohorts |
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Healthy young females
20 healthy females, aged between 18 and 35 years
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Healthy young males
20 healthy males, aged between 18 and 35 years
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Healthy elderly smokers
20 healthy smokers, aged between 45 and 75 years
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Healthy elderly non-smokers
20 healthy non-smokers, aged between 45 and 75 years
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Healthy young female smokers
20 healthy female smokers, aged between 18 and 35 years
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Healthy young male smokers
20 healthy male smokers, aged between 18 and 35 years
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Healthy postmenopausal women
20 healthy postmenopausal women
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Female CMP Patients
20 female patients suffering from cardiomyopathy (ischemic or dilating)
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Male CMP Patients
20 male patients suffering from cardiomyopathy (ischemic or dilating)
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Female CHD patients
30 female patients suffering from cardiac heart disease, before aorto-coronary bypass surgery (and after)
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Male CHD Patients
30 male patients suffering from cardiac heart disease, before aorto-coronary bypass surgery (and after)
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Female AMI patients
20 female patients who survived an acute myocardial infarction
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Male AMI patients
20 male patients who survived an acute myocardial infarction
|
Eligibility| Ages Eligible for Study: | 18 Years to 75 Years |
| Genders Eligible for Study: | Both |
| Accepts Healthy Volunteers: | Yes |
| Sampling Method: | Probability Sample |
200 patients, divided into sub-groups, always both genders will be tested for different conditions (smoking, age, CMP, CHD,...)
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
Contacts and Locations| Contact: Jeanette Strametz-Juranek, MD | 0140400 ext 4816 | jeanette.strametz-juranek@meduniwien.ac.at |
| Contact: Michael Sponder, MD | 0140400 ext 6147 | michael.sponder@meduniwien.ac.at |
| Austria | |
| Medical University of Vienna | Recruiting |
| Vienna, Austria, 1090 | |
| Contact: Jeanette Strametz-Juranek, MD 0043140400 ext 4618 jeanette.strametz-juranek@meduniwien.ac.at | |
| Contact: Alia Sabri, MD 0140400 ext 6147 alia.sabri@meduniwien.ac.at | |
| Principal Investigator: | Jeanette Strametz-Juranek, MD | MUV, Department of Internal Medicine II, Division of Cardiology |
More Information
No publications provided
| Responsible Party: | Jeanette Strametz-Juranek, Ao.Univ.Prof.Dr, Medical University of Vienna |
| ClinicalTrials.gov Identifier: | NCT01165515 History of Changes |
| Other Study ID Numbers: | 220/2007 |
| Study First Received: | July 13, 2010 |
| Last Updated: | December 5, 2012 |
| Health Authority: | Austria: Ethikkommission |
Additional relevant MeSH terms:
|
Heart Diseases Smoking Cardiovascular Diseases Habits Endostatins Antineoplastic Agents Therapeutic Uses |
Pharmacologic Actions Angiogenesis Inhibitors Angiogenesis Modulating Agents Growth Substances Physiological Effects of Drugs Growth Inhibitors |
ClinicalTrials.gov processed this record on May 23, 2013