Abstract 13217: Aspirin Reload Before Percutaneous Coronary Intervention: Impact on Reperfusion Indexes
Background: Incomplete aspirin (ASA) platelet inhibition and interventional microvascular obstruction (MVO) have been suggested as putative mechanisms of adverse clinical outcome in patients undergoing elective percutaneous coronary intervention (PCI) despite optimal dual antiplatelet therapy. Thromboxane (TX) A2 might be involved as a key mediator of platelet activation and as a potent coronary vasoconstrictor.
Aim and Methods: Pre-procedural Aspirin reload for Native coronary disease Treated by Angioplasty: Reperfusion indexes Evaluation and Improvement of clinical outcome (PANTAREI) study is an interventional, multicenter, randomized study planned to evaluate the effect of ASA reload (325 mg orally at-least 1 hour before elective PCI) on: (i) serum TxB2 levels (stable metabolite of TxA2) changes after 60 and 120 min; (ii) changes of reperfusion indexes, evaluated by corrected TIMI Frame Count (cTFC) and myocardial blush grade (MBG); (iii) modifications of myocardial injury indexes expressed by serum cardiac Troponin I (TnI) tested at 6, 12 and 24 hours after PCI.
Results: We enrolled 91 patients (74 M and 17 F, 66 ± 10 yrs.), already on chronic low-dose ASA therapy, scheduled for elective PCI and randomly assigned to receive ASA reload (N=46) or no-reload (N=45) before the procedure. Compared to no-reload group, TxB2 significantly decreased after 120’ from PCI in ASA reload group. After procedure, both groups showed a statistically significant reduction in cTFC and in percentage of patients with MBG≤2 (Reload= 39%; No-Reload=69%). Moreover, at the end of procedure, both reperfusion indexes were lower in the ASA reload group compared with the no-reload group (p<0.01). Patients who achieved a normal microvascular perfusion showed a significantly lower TxB2 serum values (p=0.05).
Conclusions: The present study shows that 325-mg ASA loading dose, before elective PCI, would provide a significant clinical benefit. These findings suggest a possible physiopathological role of serum thromboxane complete inhibition in the prevention of “interventional MVO”.
- Coronary microcirculation
- Antiplatelet drugs
- Myocardial revascularization
- Percutaneous coronary intervention
- © 2013 by American Heart Association, Inc.