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Clopidogrel pretreatment abolishes increase of PAI-1 after coronary stent implantation
Katharina M Katsaros1, Stefan P Kastl, Kurt Huber
1Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.
Insights
Intensive platelet inhibition with clopidogrel pretreatment prevents the post-PCI rise in plasminogen activator inhibitor-1 (PAI-1). This suggests platelet activation significantly contributes to PAI-1 elevation and potential thrombus risk after coronary stenting.
Area of Science:
- Cardiology
- Vascular Biology
- Pharmacology
Background:
- Plasminogen activator inhibitor-1 (PAI-1) increases post-percutaneous coronary intervention (PCI).
- The source of PAI-1 increase (platelets, vascular cells, or acute phase response) remains unclear.
- Investigated role of platelet inhibition and C-reactive protein (CRP) in PAI-1 elevation.
Purpose of the Study:
- To determine if intensive platelet inhibition modulates PAI-1 levels after PCI.
- To assess the association between PAI-1 increase and CRP levels post-PCI.
Main Methods:
- 51 stable angina patients undergoing elective PCI with stent implantation were studied.
- Compared 17 patients without clopidogrel pretreatment to 34 patients pretreated 12-24 hours before PCI.
- Measured PAI-1, t-PA, and CRP levels before and 24 hours after PCI.
Main Results:
- PCI significantly increased PAI-1 in non-pretreated patients; no increase observed with clopidogrel pretreatment.
- PAI-1 levels were significantly lower 24 hours post-PCI in the clopidogrel pretreated group.
- No association found between CRP and pre- or post-procedural PAI-1 levels.
Conclusions:
- Clopidogrel pretreatment effectively prevents PAI-1 increase after coronary stent implantation.
- Peri-procedural platelet activation appears critical for post-PCI PAI-1 elevation.
- Reduced fibrinolytic system due to PAI-1 increase may heighten acute/subacute thrombus risk.
Background:
Plasminogen activator inhibitor-1 (PAI-1) has been shown to increase after percutaneous coronary intervention (PCI). Whether activated platelets, local trauma with activation of resident vascular cells or the acute phase response is the source of this PAI-1 increase is not well defined. Therefore we examined whether intensive platelet inhibition may modulate PAI-1 levels or whether the PAI-1 increase is associated with the acute phase protein C-reactive protein (CRP).
Methods:
We included 51 patients with stable angina who underwent elective PCI with stent implantation. At the time of study, routine pretreatment with clopidogrel before PCI was not standard of care, but left to the discretion of the referring cardiologist. We matched 17 patients with stable angina that were not pretreated with clopidogrel but received a loading dose of 300 mg immediately after stent implantation according age, sex and smoking with 34 patients that received clopidogrel at least 12 to 24 hours before PCI. Blood samples for measurement of PAI-1, t-PA and CRP were taken directly before and 24 hours after the procedure.
Results:
PAI-1 and t-PA active antigen plasma levels before PCI were not different in patients with and without clopidogrel pretreatment. Whereas PCI induced a significant increase of PAI-1 levels in patients without pretreatment (p<0.05), the procedure had no effect on PAI-1 active antigen in patients pretreated with clopidogrel. This resulted in significant lower PAI-1 plasma levels 24 hours after PCI in patients with pretreatment (p<0.05). CRP was not associated with pre- or postprocedural PAI-1 levels.
Conclusion:
Clopidogrel pretreatment completely abolishes the increase of PAI-1 active antigen after coronary stent implantation. This suggests that peri-procedural platelet activation might play a major role for the increase of PAI-1 after PCI thus increasing the risk of acute and subacute thrombus formation based on a reduced endogenous fibrinolytic system.
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