Christ Günter, Siller-Matula Jolanta M, Francesconi Marcel, Dechant Cornelia, Grohs Katharina, Podczeck-Schweighofer Andrea
5th Medical Department with Cardiology, Kaiser Franz Josef Hospital, Vienna, Austria.
Department of Cardiology, Medical University of Vienna, Vienna, Austria.
BMJ Open. 2014 Oct 31;4(10):e005781. doi: 10.1136/bmjopen-2014-005781.
To evaluate the clinical utility of individualising dual antiplatelet therapy (DAPT) after percutaneous coronary intervention (PCI) in an all-comers population, including ST-elevation myocardial infarction (STEMI) patients.
Tertiary care single centre registry.
1008 consecutive PCI patients with stent implantation, without exclusion criteria.
Peri-interventional individualisation of DAPT, guided by multiple electrode aggregometry (MEA), to overcome high on-treatment platelet reactivity (HPR) to ADP-induced (≥50 U) and arachidonic acid (AA)-induced aggregation (>35 U).
The primary efficacy end point was definite stent thrombosis (ST) at 30 days. The primary safety end point was thrombolysis in myocardial infarction (TIMI) major and minor bleeding. Secondary end points were probable ST, myocardial infarction, cardiovascular death and the combined end point: major cardiac adverse event (MACE).
53% of patients presented with acute coronary syndrome (9% STEMI, 44% non-ST-elevation). HPR to ADP after 600 mg clopidogrel loading occurred in 30% of patients (73±19 U vs 28±11 U; p<0.001) and was treated by prasugrel or ticagrelor (73%), or clopidogrel (27%) reloading (22±12 U; p<0.001). HPR to ADP after prasugrel loading occurred in 2% of patients (82±26 U vs 19±10 U; p<0.001) and was treated with ticagrelor (34±15 U; p=0.02). HPR to AA occurred in 9% of patients with a significant higher proportion in patients with HPR to ADP (22% vs 4%, p<0.001) and was treated with aspirin reloading. Definite ST occurred in 0.09% of patients (n=1); probable ST, myocardial infarction, cardiovascular death and MACE occurred in 0.19% (n=2), 0.09% (n=1) and 1.8% (n=18) of patients. TIMI major and minor bleeding did not differ between patients without HPR and individualised patients (2.6% for both).
Individualisation of DAPT with MEA minimises early thrombotic events in an all-comers PCI population to an unreported degree without increasing bleeding. A randomised multicentre trial utilising MEA seems warranted.
http://www.clinicaltrials.gov; NCT01515345.
评估在包括ST段抬高型心肌梗死（STEMI）患者在内的所有患者群体中，经皮冠状动脉介入治疗（PCI）后个体化双联抗血小板治疗（DAPT）的临床实用性。
三级医疗单中心注册研究。
1008例连续接受支架植入且无排除标准的PCI患者。
在介入治疗期间，以多电极凝集试验（MEA）为指导，对DAPT进行个体化，以克服对ADP诱导（≥50 U）和花生四烯酸（AA）诱导的聚集（>35 U）的高治疗期血小板反应性（HPR）。
主要疗效终点为30天时明确的支架内血栓形成（ST）。主要安全性终点为心肌梗死溶栓（TIMI）大出血和小出血。次要终点为可能的ST、心肌梗死、心血管死亡以及联合终点：主要心脏不良事件（MACE）。
53%的患者表现为急性冠状动脉综合征（9%为STEMI，44%为非ST段抬高型）。600 mg氯吡格雷负荷剂量后出现ADP诱导的HPR的患者占30%（73±19 U对28±11 U；p<0.001），并接受普拉格雷或替格瑞洛治疗（73%），或氯吡格雷再负荷治疗（27%）（22±12 U；p<0.001）。普拉格雷负荷剂量后出现ADP诱导的HPR的患者占2%（82±26 U对19±10 U；p<0.001），并接受替格瑞洛治疗（34±15 U；p=0.02）。9%的患者出现AA诱导的HPR，其中ADP诱导的HPR患者比例显著更高（22%对4%，p<0.001），并接受阿司匹林再负荷治疗。0.09%的患者（n=1）出现明确的ST；0.19%（n=2）、0.09%（n=1）和1.8%（n=18）的患者出现可能的ST、心肌梗死、心血管死亡和MACE。无HPR患者与个体化治疗患者之间的TIMI大出血和小出血情况无差异（均为2.6%）。
采用MEA对DAPT进行个体化可将所有接受PCI治疗患者群体中的早期血栓形成事件降至未报道的程度，且不增加出血风险。开展一项使用MEA的随机多中心试验似乎是必要的。
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