经皮冠状动脉介入治疗后血小板聚集率高的患者强化抗血小板治疗的研究

来源 :中华心血管病杂志 | 被引量 : 0次 | 上传用户:lubiaofs
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目的研究经皮冠状动脉介入治疗(PCI)后血小板聚集率仍然高的患者强化抗血小板治疗与主要心脏事件的关系。方法选择2004年1月至2006年6月我院住院进行择期 PCI 的冠心病患者1556例,服药前、术后24小时、28天检测二磷酸腺苷(ADP)诱导的血小板聚集率。其中有402例患者[男178例,女224例,平均年龄(57.34±6.47)岁]术后血小板聚集率仍然高,其24小时的血小板聚集度与基线(服药前)的绝对值<30%。把这部分患者随机分为两组,对照组(n=201)继续服用阿司匹林100 mg、氯吡格雷75 mg;治疗组(n=201)除继续服用阿司匹林100 mg、氯吡格雷75mg,每天加西洛他唑200 mg,分两次服用。连续应用6个月,观察两组患者6个月主要心脏不良事件(包括死亡、非致死性急性心肌梗死、急性或亚急性血栓、靶血管重建、脑卒中)以及出血等不良事件的发生率。结果28天血小板聚集的抑制<30%患者对照组有89.6%(180/201),治疗组有9.4%(19/201),两组相比,差异有统计学意义(P<0.05)。两组均无急性血栓发生;亚急性血栓对照组有3.0%(6/201),治疗组有0.5%(1/201),两组相比,差异无统计学意义(P>0.05);对照组有2例死亡,治疗组无死亡;两组均未发生脑卒中;非致死性急性心肌梗死对照组1.5%(3/201),治疗组0.5%(1/201);两组相比,差异无统计学意义(P>0.05);靶血管重建对照组有15.9%(32/201),治疗组6.5%(13/201),两组相比,差异有统计学意义(P<0.01);出血的发生率对照组4.0%(8/201),治疗组6.0%(12/201),两组相比,差异无统计学意义(P>0.05)。主要心脏事件的累计危险率治疗组低于对照组,差异有统计学意义(P<0.05)。结论 PCI 后应用抗血小板药物,血小板聚集率经治疗后仍然高(即血小板聚集抑制<30%)的患者,强化抗血小板治疗可以减少主要心脏事件的累计危险率,而没有增加出血并发症。 Objective To investigate the relationship between intensive antiplatelet therapy and major cardiac events in patients with high platelet aggregation after percutaneous coronary intervention (PCI). Methods From January 2004 to June 2006, 1556 CHD patients hospitalized for elective PCI in our hospital were collected. Pretreatment, 24 hours and 28 days after operation were used to detect the platelet aggregation rate induced by adenosine diphosphate (ADP). There were 402 patients (178 males and 224 females with an average age of 57.34 ± 6.47 years) with high platelet aggregation after 24 hours of platelet aggregation compared to baseline (pre-dose) of <30% . The patients were randomly divided into two groups. The control group (n = 201) continued aspirin 100 mg and clopidogrel 75 mg. The treatment group (n = 201) received aspirin 100 mg and clopidogrel 75 mg daily, Lorazole 200 mg, taken in two doses. The patients were followed up for 6 months. The incidences of major adverse cardiac events (including death, non-fatal acute myocardial infarction, acute or subacute thrombosis, target revascularization, stroke) and bleeding were observed at 6 months in both groups. Results The inhibition of platelet aggregation in 28 days was 89.6% (180/201) in the control group and 9.4% (19/201) in the control group. There was significant difference between the two groups (P <0.05). There was no acute thrombosis in both groups; 3.0% (6/201) in subacute thrombus control group and 0.5% (1/201) in treatment group, there was no significant difference between the two groups (P> 0.05) There were 2 deaths in the treatment group and no death in the treatment group; no stroke occurred in both groups; 1.5% (3/201) in the non-fatal acute myocardial infarction control group and 0.5% (1/201) in the treatment group; (P> 0.05). There were 15.9% (32/201) in the control group and 6.5% (13/201) in the control group. There was significant difference between the two groups (P <0.01) The incidence of hemorrhage was 4.0% (8/201) in the control group and 6.0% (12/201) in the treatment group. There was no significant difference between the two groups (P> 0.05). The cumulative risk of major cardiac events in the treatment group was lower than that in the control group, with a significant difference (P <0.05). Conclusions In patients treated with antiplatelet agents after PCI, those with high platelet aggregation after treatment (ie, platelet aggregation inhibition <30%) may be able to reduce the cumulative risk of major cardiac events without an increase in bleeding complications.
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