Verdoia M, et al. - This research was initiated in order to gauge the upshot of platelet reactivity and pre-procedural dual antiplatelet therapy (DAPT) on periprocedural myocardial infarction (PMI) in patients undergoing percutaneous coronary interventions, (PCI) with adjunctive tirofiban. No link was determined between preprocedural DAPT and baseline platelet reactivity with the risk of periprocedural myocardial infarction or myonecrosis in subjects undergoing PCI with adjunctive glycoprotein (GP) IIb-IIIa inhibitors. Experts supported the role of periprocedural Gp IIb-IIIa inhibitors for overcoming any suboptimal inhibition of platelet aggregation at the time of the procedure as a result of drug-resistance or delayed (downstream) administration of ADP antagonists, particularly for complex high-risk procedures.

Methods

• The eligible candidates included patients undergoing PCI with tirofiban (intracoronary/intravenous ± prolonged infusion).
• Among these subjects, periprocedural myonecrosis was defined as troponin I increase by 3 times the ULN or by 50% of an elevated baseline value, whereas PMI as CKMB increase by 3 times the ULN or 50% of baseline.
• An analysis was performed of the platelet function through impedance aggregometry.

Results

• This study included 168 patients, 77 (45.8%) of whom were on DAPT at the time of PCI.
• Findings disclosed that subjects on DAPT had more often a history of previous PCI (p=0.03), higher ACS at admission (p < 0.001) and creatinine levels (p=0.03).
• Patients without DAPT presented more frequently with coronary calcifications and type C lesions (p=0.02 and p=0.03, respectively), as much as TIMI flow < 3 (p=0.03).
• The procedural characteristics were found to be comparable.
• A substantial reduction was reported in the baseline platelet reactivity in DAPT treated patients (p < 0.001 for ASPI, COL and ADP tests).
• No variation was discovered in the rate of periprocedural myonecrosis according to pre-procedural DAPT (68.4%vs 67%, p=0.87; adjusted OR[95%CI] = 1.34[0.71-2.53], p=0.36) and neither the occurrence of PMI (13.3% vs 12.6%, p=0.99; adjusted OR[95%CI] = 1.24[0.51-3.1], p=0.64).
• Data also demonstrated similar baseline platelet reactivity in patients with and without PMI/myonecrosis, with no link between platelet function and troponin I peak.