Dissertation > Medicine, health > Internal Medicine > Heart, blood vessels ( circulatory ) disease > Heart disease > Coronary arteries ( atherosclerosis ),heart disease (CHD)

Effects of Intensive Antiplatelet Therapy for Patients with High On-treatment Platelet Reactivity After Coronary Stent Implantation

Author GuanShaoYi
Tutor HanYaLing
School Dalian Medical University
Course Cardiovascular within science
Keywords acute coronary syndrome drug-eluting stents post-treatent platelet reactivity cilostazol
CLC R541.4
Type Master's thesis
Year 2011
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Objectives: The purpose of this study was to observe the feasibility, efficacy and safety of antiplatelet therapy in acute coronary syndrome (ACS) patients with high on-treatment platelet reactivity (HPR) undergoing coronary stent implantation.Methods: This study was a prospective, randomized multicentre study. Between March 2009 and February 2011, a total of 3316 ACS patients who were undergoing at least one DES implantation in the General Hospital of Shenyang Military Region, the First Hospital of China Medical University and 463 Hospital of PLA were enrolled. At 24 h after clopidogrel loading (300mg), post-treatment platelet reactivity (PPR) was evaluated by platelet aggregation rate which was induced by 20μmol/L adenosine diphosphate (ADP) and measured with light transmittance aggregometry (LTA). According to the results of preliminary studies, HPR was defined as a post-treatment platelet aggregation of≥55%. Between the enrolled patients, 840 (25.3%) were identified as HPR. All HPR patients were randomly assigned to two groups by the ratio of 1:2. Standard group (n=280): Patients received routine 75 mg/d clopidogrel maintenance dose for 1 year. Intensive group (n=560): Patients received a high clopidogrel loading dose of 150 mg/d for 3 days. If the PPR were less than 55% at 3 days, the same dose of clopidogrel was continued for another 27 days. If the PPR were still higher than 55% at 3 days, the remained HPR patients were randomly divided into two subgroups by the ratio of 1:1 once again, that is, group of cilostazol 50 mg and group of cilostazol 100mg. For the patients in the subgroup of cilostazol 50 mg, the antiplatelet regime was clopidogrel 150mg/d for 27 days and cilostazol 50 mg/bid for 6 months; for the patients in the subgroup of cilostazol 100 mg, clopidogrel is 75 mg/d and cilostazol 100mg/bid for 6 months; After 30 days, all patients of intensive group received a maintenance dose of 75 mg/d clopidogrel for another 11months. All patients receive aspirin 300mg/d for 30 days followed with 75mg/d indefinitely.The primary end point was the remission rate of the HPR at 30 days’. The secondary end points were the incidences of cardiac death, nonfatal myocardial infarction, stroke, urgent target vessel revascularization, or stent thrombosis, and the incidences of major or minor bleeding.Results: In the intensive group, 304 out of 560 patients (54.3%) had their HPR reversed at 3 days. Other 256 patients with HPR who were treated with different cilostazol regimens for 3 days had similar remission rate of HPR (cilostazol 50mg/bid:59.4%, cilostazol 100mg/bid:57.8%, p=0.80).The overall remission rate of HPR was 81.1% after 6 days’intensified antiplatelet therapy. The remission rate of the HPR at 30 days in the intensive group was significantly higher than that of the standard group (69.9% vs 55.7%, p<0.001). The remission rate of HPR at 30 days was similar between patients received different cilostazol regimens (cilostazol 50mg/bid: 68.8%, cilostazol 100mg/bid: 68.2%, p=0.98). At 30 days, only 1 patient suffered from subacute stent thrombosis (0.18%) in intensified group and no stent thrombosis was occurred in standard group, of which the difference was still no statistics (p=1.0). There were no death, major or minor bleeding in either two groups happened. The tendency of minimal bleeding was higher in standard group compared with intensive group, but the difference was not statistically significant (4.28% vs 2.14%; p=0.166).Conclusions: The intensified antiplatelet therapy regimes could attenuate the HPR in ACS patients undergoing coronary stenting significantly and not increase the risk of bleeding, but the clinic benefits of this strategy should be elucidated by the study with larger sample size and long follow-up outcomes.

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