Influence of platelet reactivity and response to clopidogrel on myocardial damage following percutaneous coronary intervention in patients with non-st-segment elevation acute coronary syndrome☆

Abstract 

Introduction

A wide variability in the response to clopidogrel and magnitude of post-treatment platelet reactivity has been described. However, this has been demonstrated by light transmittance aggregometry, a method too laborious for daily practice. Point-of-care devices may overcome this limitation, but little is known on the predictive value of such measurements. Our objective was to determine the relationship between platelet reactivity and the incidence of myocardial damage following percutaneous coronary intervention (PCI) in patients with Non-ST-segment Elevation Acute Coronary Syndrome (NSTEACS).

Materials and Methods

This prospective study included 93 patients with NSTEACS and PCI. All patients received a loading dose of 300 mg of clopidogrel and 250 mg of aspirin. Myocardial damage was defined as any elevation above upper limit of normal or previous levels of troponin T, assessed every 6 h for at least 24 h following PCI. Platelet reactivity not related to clopidogrel (BASE reactivity), related to P2Y12 inhibition (P2Y12 reactivity) and inhibition of platelet aggregation (IPA) were assessed immediately pre-PCI with the VerifyNow® device.

Results

Myocardial damage was detected in 60 patients (64.5%). Higher BASE reactivity was associated with myocardial damage (287.8±62.6 vs. 260±55.9 units, p=0.043) while a trend was found for P2Y12 reactivity (173.4±70.3 vs. 149.2±58.4 units, p=0.109). No relationship was detected for IPA. Multivariate logistic regression analysis confirmed that BASE reactivity (p=0.04) and P2Y12 reactivity (p=0.03) were independent predictors of myocardial damage.

Conclusions

Platelet reactivity before PCI appears to be better predictor of myocardial damage than does response to clopidogrel.

Abbreviations: ADP, Adenosine diphosphate, CK-MB, Creatine kinase MB fraction, GP IIb/IIIa, Glycoprotein IIb/IIIa, IPA, Inhibition of Platelet Aggregation, NSTEACS, Non-ST-segment Elevation Acute Coronary Syndrome, PCI, Percutaneous Coronary Intervention, PGE1, Prostaglandin E1, PRU, Platelet Reaction Units, TnT, Troponin T, ULN, Upper limit of normal

Keywords: Platelet Reactivity, Myonecrosis, Percutaneous Coronary Intervention, Acute Coronary Syndrome