Platelet reactivity and coronary microvascular impairment after percutaneous revascularization in stable patients receiving clopidogrel or prasugrel.

BACKGROUND AND AIMS

Increased platelet reactivity (PR) associated with variable degree of coronary microvascular impairment has been reported in patients on clopidogrel after elective percutaneous coronary intervention (PCI). Prasugrel provides more potent platelet inhibition than clopidogrel, though it is unknown whether it might also prevent PCI-related platelet activation. In stable patients undergoing elective PCI, we compared: (1) the effects of prasugrel vs. clopidogrel on peri-procedural variations of PR and (2) the correlation of platelet inhibition potency with PCI-induced coronary microvascular impairment.

METHODS

Forty thienopyridine-naive patients were randomly assigned to a loading dose of either prasugrel 60 mg (n = 20) or clopidogrel 600 mg (n = 20) at least 12 h before PCI. At the time of PCI, we assessed adenosine diphosphate (ADP)-induced PR with the Multiplate Analyzer, and the pressure-derived index of microvascular resistance (IMR) in the treated coronary, both at baseline and post-procedure.

RESULTS

ADP-induced PR was significantly lower in the prasugrel compared with clopidogrel group both at baseline (16.0 ± 8.7 vs. 33.9 ± 18.0 aggregation units [AU], p < 0.001) and post-procedure (16.2 ± 9.0 vs. 39.0 ± 18.6 AU, p < 0.001). A significant peri-procedural increase in PR was observed in the clopidogrel group (p = 0.008), but not in the prasugrel group (p = 0.822). A significant correlation was found between IMR and PR both at baseline (r = 0.458, p = 0.003) and post-PCI (r = 0.487, p = 0.001).

CONCLUSIONS

A loading dose of prasugrel compared with clopidogrel is able to attenuate PCI-related increase in PR in patients with stable CAD undergoing PCI, which might contribute to the beneficial effect of this drug on peri-procedural coronary microvascular function.