Endothelin-Receptor Blockade in Coronary Heart Disease
Drug: BQ-123 and BQ-788
|Study Design:||Allocation: Randomized
Intervention Model: Parallel Assignment
Primary Purpose: Diagnostic
|Official Title:||Selective and Non-Selective Endothelin-Receptor Blockade in Coronary Artey Disease|
- minimal lumen diameter measured directly after infusion of the ET-antagonist(s)
- fractional flow reserve, coronary flow reserve, intramyocardial resistance measured directly after infusion of the ET-antagonist(s)
|Study Start Date:||May 2003|
|Estimated Study Completion Date:||August 2006|
Endothelin (ET) is the most potent vasoconstrictor known and plays a major role in the development of coronary artery disease as well as in acute vasoconstriction. This effect is mainly mediated by the vascular ET-A receptor, whereas the ET-B receptor mediates vasodilation and cleavage of ET. Currently, there are both selective ET-A antagonists and non-selective ET-A and ET-B antagonists under investigation. The aim of the study is to test the effect of ET-receptor blockade on the vasoreagibility of epicardial and intramyocardial coronary arteries in patients undergoing cardiac catheterization. We randomly use the selective ET-A receptor BQ-123 (Group A) and the combination of BQ-123 and the ET-B receptor antagonist BQ-788 (Group B). The tested infusion will be applied selectively into the assessed coronary artery by a special infusion catheter. To evaluate the morphometric changes we use quantitative coronary angiography to measure the diameter of the coronary artery before and after intracoronary infusion of the tested substances. Furthermore we will use Pressure Wire to measure the hemodynamic conditions before and after infusion, thus evaluating the epicardial and the intramyocardial blood perfusion.
Comparison: Coronary artery diameter as measured by quantitative angiography (minimal lumen diameter) and parameters indicative of epicardial and intramyocardial blood flow as determined by Pressure Wire (fractional flow reserver, coronary flow reserve, intramyocardial resistance) before and after ET-antagonist infusion will be compared.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00427232
|Dept. of Internal Medicine II, Medical University of Vienna|
|Vienna, Austria, A-1090|
|Principal Investigator:||Thomas Neunteufl, MD||Dept. of Internal Medicine II, Medical University of Vienna|