[Effects of intensive antiplatelet therapy for patients with high on-treatment platelet reactivity after coronary stent implantation].

OBJECTIVE: To explore the effects of intensive antiplatelet therapy for patients with high on-treatment platelet reactivity (HPR) after coronary stent implantation.

METHODS: Between March 2009 and February 2011, a total of 3316 consecutive acute coronary syndrome patients undergoing drug-eluting stent implanting from 3 hospitals were enrolled. Among them, 840 patients (25.3%) were identified as HPR (defined as 20 µmol/L adenosine diphosphate induced platelet aggregation of ≥ 55% at 24 hours after administration of 300 mg clopidogrel loading dose and 300 mg aspirin). The HPR patients were randomly assigned to receive standard (aspirin 300 mg/d and clopidogrel 75 mg/d, n = 280) or intensified (n = 560) antiplatelet therapy by the ratio of 1:2. Patients in the intensive group were initially treated with a double maintenance dose of clopidogrel (150 mg/d) and aspirin (300 mg/d). After 3 days, patients with unsolved HPR received additional cilostazol treatment (50 - 100 mg, bid). The reversion rate of HPR and clinical events were observed.

RESULTS: In the intensive group, HPR reversed in 304 out of 560 patients (54.3%) at 3 days post therapy and the remaining 256 patients with HPR were treated with additional cilostazol regimen for another 3 days and the total reversion rate of HPR was 81.1% (454/560). The reversion rate of HPR at 30 days in the intensified group was significantly higher than that of the standard group (69.9% vs. 55.7%, P = 0.000). At 30 days after percutaneous coronary intervention, 1 patient suffered from subacute stent thrombosis (0.2%) in intensified group and no stent thrombosis was observed in standard group (P = 1.000). There were no death, major or minor bleeding in both two groups. Minimal bleeding was also similar in the two groups (intensive: 4.28% vs. standard: 2.14%, P = 0.166).

CONCLUSIONS: The intensified antiplatelet therapy regimens could significantly increase the reversion rate of HPR in acute coronary syndrome patients undergoing coronary stenting without increasing the risk of bleeding. The clinic impact of this strategy needs to be elucidated by long term follow-up outcome studies.