Abnormal PFA-100 closure time is associated with increased platelet aggregation in patients presenting with chest pain.
Abnormal PFA-100 closure time is associated with increased platelet aggregation in patients presenting with chest pain.
复制标题
PFA-100 闭合时间异常与胸痛患者血小板聚集增加有关。
DOI：
10.1007/s11239-007-0045-5
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发表时间：
2008
影响因子：
4
通讯作者：
Williams,MarleneS
中科院分区：
文献类型：
--
作者：
Atiemo,AndrewD;Ng'Alla,LadinaS;Vaidya,Dhananjay;Williams,MarleneS
背景抗血小板治疗已被证明是有效的一级和二级预防心肌梗死，中风和心血管死亡。然而，接受阿司匹林治疗的患者中有很大比例发生缺血性事件。许多前瞻性研究表明，通过各种方法测量的抗血小板治疗反应性降低与临床事件的增加密切相关。我们的目的是表征血小板功能的胸痛患者使用即时检测，PFA-100®和相关的结果与传统的血小板聚集测定，以确定是否与阿司匹林无反应性的患者有增加的临床symptoms.MethodsPlatelet功能进行了评估，使用PFA-100®，流式细胞术，光学聚集测定94例胸痛急诊科。所有患者每天服用阿司匹林81-325 mg。记录了索引住院期间发生的临床事件。ResultsForty-seven例患者（50%）被PFA-100®定义为阿司匹林无应答者（胶原-肾上腺素闭合时间≤ 193）。与阿司匹林应答者相比，阿司匹林无应答者对二磷酸腺苷（ADP）（P= 0.004）和高剂量肾上腺素（P= 0.03）的平均血小板聚集水平更高。此外，与阿司匹林应答者相比，阿司匹林无应答者的PAC-1表达显著增加（分别为P= 0.003和P = 0.0006）。没有显着差异，在指数住院期间的临床事件之间的阿司匹林non-responses和阿司匹林responses.ConclusionPatients胸痛谁有异常PFA-100关闭时间增加血小板聚集和活化，但这种阿司匹林无反应性并不相关的指数住院增加的临床事件。
BackgroundAntiplatelet therapy has been proven to be effective for both primary and secondary prevention of myocardial infarction, stroke, and cardiovascular death. However, a significant proportion of patients treated with aspirin experience ischemic events. A number of prospective studies have demonstrated that decreased responsiveness to antiplatelet therapy as measured by various methods, is strongly associated with an increase in clinical events. Our objective was to characterize platelet function in patients presenting with chest pain using a point-of-care assay, PFA-100®and correlating results to traditional platelet aggregometry to determine if patients with aspirin non-responsiveness have increased clinical sequelae.MethodsPlatelet function was assessed using PFA-100®, flow cytometry, and optical aggregometry in 94 patients presenting to the emergency department with chest pain. All patients were on aspirin 81–325 mg daily. Clinical events occurring during the index hospitalization were documented.ResultsForty-seven patients (50%) were defined as aspirin non-responders by PFA-100®(collagen-epinephrine closure time ≤ 193). Compared to aspirin responders, aspirin non-responders had higher levels of mean platelet aggregation to adenosine diphosphate (ADP) (P= 0.004) and high dose epinephrine (P= 0.03). Furthermore, expression of PAC-1 was significantly increased in patients with aspirin nonresponse as compared to aspirin responders (P= 0.003 andP= 0.0006 respectively). No significant difference in clinical events during the index hospitalization was noted between aspirin non-responders and aspirin responders.ConclusionPatients presenting with chest pain who have abnormal PFA-100 closure times have increased platelet aggregation and activation however this aspirin non-responsiveness does not correlate with increased clinical events in the index hospitalization.