Response to Letter Regarding Article, “Cardiovascular Death and Nonfatal Myocardial Infarction in Acute Coronary Syndrome Patients Receiving Coronary Stenting Are Predicted by Residual Platelet Reactivity to ADP Detected by a Point-of-Care Assay: A 12-Month Follow-Up”
We thank de Miguel Castro et al for their interest in and thoughtful comments about our study.1 In response to their question on residual platelet reactivity values according to different clinical presentation, patients with ST-elevation myocardial infarction (STEMI) (n=191) had P2Y12 reaction unit (PRU) mean values higher than patients with unstable angina/non-STEMI (n=492) [197±84 versus 183±93], but this difference does not reach statistical significance (P=0.04). Sixty-three of 191 patients with STEMI (33%) and 156 of 492 patients with unstable angina/non-STEMI (31.7%) had PRU values >240. These data underscore the concept that patients with acute coronary syndrome have platelet activation even if it has been documentated as a spectrum that moves from lower levels in patients with unstable angina/non-STEMI patients to higher levels in patients with STEMI.
With regard to the second question, we did not detect a statistically significant difference between patients with or without GpIIb/IIIa inhibitors (PRU values: 187±95 versus 196±83, P=0.19). Seventy-two of 205 patients with Gp IIb/IIIa inhibitors (35.1%) and 147 of 478 patients without GpIIb/IIIa inhibitors (30.7%) had PRU values >240. These results show that the choice of timing of blood samples (6 days after the use of GpIIb/IIIa inhibitors) allows us to include patients with STEMI, who are at higher risk of recurrences, in the evaluation of platelet reactivity by VerifyNow P2Y12. Furthermore, the same protocol of timing of blood samples was used and reported in the Low Responsiveness to Clopidogrel and Sirolimus- or Paclitaxel-Eluting Stent Thrombosis (RECLOSE) trial,2 in which we demonstrated the correlation of high posttreatment platelet reactivity with stent thrombosis and cardiovascular death.
We believe that the timing of blood samples is linked to that of durability of high on-treatment platelet reactivity, which remains to be solved by ad hoc studies. Nevertheless, our results underline the concept that an aggressive platelet characterizes patients at higher risk of clinical recurrences even if this laboratory finding might not be stable over time.
We agree with de Miguel Castro et al that different clinical settings might be associated with different cutoff values for the diagnosis of high on-treatment platelet reactivity. Further studies enrolling patients with stable coronary artery disease are needed to explore the role of platelet hyperreactivity on antiplatelets in a chronic and stable clinical condition.
Marcucci R, Gori AM, Paniccia R, Giusti B, Valente S, Giglioli C, Buonamici PG, Antoniucci D, Abbate R, Gensini GF. Cardiovascular death and nonfatal myocardial infarction in acute coronary syndrome patients receiving coronary stenting are predicted by residual platelet reactivity to ADP detected by a point-of-care assay. Circulation. 2009; 119: 237–242.
Buonamici PG, Marcucci R, Migliorini A, Gensini GF, Santini A, Paniccia R, Moschi G, Gori AM, Abbate R, Antoniucci D. Impact of platelet reactivity after clopidogrel administration on drug-eluting stent thrombosis. J Am Coll Cardiol. 2007; 24: 2312–2317.