Trials / Completed
CompletedNCT01210157
Galectin-3 Binding Protein in Cardiovascular Disease and Chronic Heart Failure
GALectin-3 Binding Protein for Risk Assessment in Coronary arTery dIsease and Chronic Heart Failure
- Status
- Completed
- Phase
- —
- Study type
- Observational
- Enrollment
- 373 (actual)
- Sponsor
- Heidelberg University · Academic / Other
- Sex
- All
- Age
- —
- Healthy volunteers
- Not accepted
Summary
The purpose of this study is to determine whether galectin-3 binding protein plasma levels can predict adverse cardiovascular events in patients with coronary artery disease and/or heart failure.
Detailed description
Chronic heart failure represents an important cause of disease burden in Western countries. Heart failure can be either caused by vascular disease (i.e. cardiomypathy (CMP) due to coronary artery disease ("ischemic/ICMP")) or by myocardial conditions (i.e. dilated cardiomyopathies (DCMP) resulting from other causes like familial disposition, drug toxicity, etc.). Gold standard for the diagnosis of CMPs is the coronary angiography in conjunction with left ventricular angiography and myocardial biopsy, non-invasive markers include C-reactive protein (CRP) for ICMP and brain natriuretic protein (BNP) for DCMP. We have previously identified G3BP to be overexpressed in foam cells and plasma-derived microparticles, both potentially important in formation of atherosclerotic plaque. Galectin-3 binding protein (G3BP) is a secreted protein that is involved in cell adhesion and immune activation. The purpose of the current study is to test, whether G3BP plasma levels (a) are able to non-invasively differentiate causes of CMP and (b) are a suitable means for future risk assessment in CMP patients.
Conditions
Timeline
- Start date
- 2008-06-01
- Primary completion
- 2008-09-01
- Completion
- 2010-08-01
- First posted
- 2010-09-28
- Last updated
- 2010-09-28
Locations
1 site across 1 country: Germany
Source: ClinicalTrials.gov record NCT01210157. Inclusion in this directory is not an endorsement.