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Updated: Aug 20, 2026

Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function
Published on: March 15, 2022
Effect of tirofiban on percutaneous coronary intervention-induced endothelial dysfunction in patients with stable
Ascan Warnholtz1, Mir Abolfazl Ostad, Thomas Heitzer
1Division of Cardiology, The University Hospital Eppendorf, Hamburg, Germany. warnholtz@2-med.klinik.uni-mainz.de <warnholtz@2-med.klinik.uni-mainz.de>
Insights
Percutaneous coronary intervention (PCI) impairs arterial function. Tirofiban, a glycoprotein IIb/IIIa receptor antagonist, significantly improved endothelial function in conductance vessels after PCI, reversing this impairment.
Area of Science:
- Cardiovascular Medicine
- Pharmacology
Background:
- Glycoprotein (GP) IIb/IIIa receptor antagonists improve endothelial dysfunction in resistance vessels.
- The effect of these antagonists on conductance vessels after percutaneous coronary intervention (PCI) is not well understood.
Purpose of the Study:
- To evaluate the acute effect of tirofiban on endothelial function of arterial conductance vessels in patients undergoing PCI.
Main Methods:
- Sixty-six patients undergoing PCI were divided into tirofiban and control groups.
- Endothelial function was assessed using brachial artery flow-mediated dilation (FMD) before and after PCI.
- Nitroglycerin-induced vasodilation was also measured.
Main Results:
- Tirofiban significantly improved FMD post-PCI (6.0% to 7.8%), while FMD deteriorated in the control group (6.1% to 4.7%).
- Nitroglycerin-induced dilation remained unchanged, indicating specific effects on endothelium-dependent function.
- Coronary angiography alone did not affect FMD in a separate patient group.
Conclusions:
- PCI induces endothelial dysfunction in forearm conductance vessels.
- Tirofiban effectively reverses PCI-induced endothelial dysfunction in these vessels.
Abstract:
Recent studies demonstrated that glycoprotein (GP) IIb/IIIa receptor antagonists improve endothelial dysfunction of forearm resistance vessels in patients with stable coronary artery disease. However, it remains unclear whether these findings can be extended to the conductance vessel level. In this study, we aimed to evaluate the acute effect of tirofiban on endothelial function of arterial conductance vessels in patients undergoing percutaneous coronary intervention (PCI). Endothelial function was examined by ultrasonographic measurement of flow-mediated vasodilation (FMD) of the brachial artery. Endothelium-independent vasodilation was determined in response to nitroglycerin. Sixty-six patients who underwent PCI were included in the study. Thirty-three patients received a bolus of 10 microg/kg body weight of tirofiban, whereas 33 patients who did not receive tirofiban served as the control group. FMD was measured in all patients before and 30 minutes after PCI. Tirofiban significantly improved FMD (6.0 +/- 0.4% before vs 7.8 +/- 0.5% after PCI, p <0.0001), whereas FMD deteriorated in patients in the control group (6.1 +/- 0.6% before vs 4.7 +/- 0.7% after PCI, p = 0.006). Nitroglycerin-induced dilation remained unaltered in response to PCI. In another group of 11 patients with coronary artery disease, FMD did not change after coronary angiography without coronary intervention. In conclusion, PCI induces endothelial dysfunction in forearm conductance vessels that can be reversed with tirofiban.
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