Hovens Marcel M C, Snoep Jaapjan D, Eikenboom Jeroen C J, van der Bom Johanna G, Mertens Bart J A, Huisman Menno V
Department of General Internal Medicine and Endocrinology, Leiden University Medical Center, Leiden, The Netherlands.
Am Heart J. 2007 Feb;153(2):175-81. doi: 10.1016/j.ahj.2006.10.040.
The absolute risk of recurrences among patients using aspirin for prevention of cardiovascular events remains high. Persistent platelet reactivity despite aspirin therapy might explain this in part. Reported prevalences of this so-called aspirin resistance vary widely, between 0% and 57%.
The aim of the study was to systematically review all available evidence on prevalence of aspirin resistance and to study determinants of reported prevalence.
Using a predefined search strategy, we searched electronic databases MEDLINE, EMBASE, CENTRAL, and Web of Science. To be included in our analysis, articles had to contain a laboratory definition of aspirin resistance, use aspirin as secondary prevention, and report associated prevalence.
We included 34 full-text articles and 8 meeting abstracts. The mean prevalence of aspirin resistance was 24% (95% CI 20%-28%). After adjustment for differences in definition, used dosage, and population, a statistically significant higher prevalence was found in studies with aspirin dosage < or =100 mg compared with > or =300 mg (36% [95% CI 28%-43%] vs 19% [95% CI 11%-26%], P < .0001). Studies measuring platelet aggregation using light aggregometry with arachidonic acid as an agonist had a pooled unadjusted prevalence of 6% (95% CI 0%-12%). In studies using point-of-care platelet function-analyzing devices, the unadjusted prevalence was significantly higher, at 26% (95% CI 21%-31%).
Prevalences widely differ between studies reporting on aspirin resistance. Both aspirin dosage and the method of defining aspirin resistance strongly influence estimated prevalence, which explains found heterogeneity among studies. On average, it appears that about 1 in 4 individuals may express biochemically defined aspirin resistance.
使用阿司匹林预防心血管事件的患者复发的绝对风险仍然很高。阿司匹林治疗后血小板反应性持续存在可能部分解释了这一现象。报道的这种所谓阿司匹林抵抗的患病率差异很大，在0%至57%之间。
本研究的目的是系统评价关于阿司匹林抵抗患病率的所有现有证据，并研究报道患病率的决定因素。
使用预先定义的检索策略，我们检索了电子数据库MEDLINE、EMBASE、CENTRAL和科学网。要纳入我们的分析，文章必须包含阿司匹林抵抗的实验室定义，将阿司匹林用作二级预防，并报告相关患病率。
我们纳入了34篇全文文章和8篇会议摘要。阿司匹林抵抗的平均患病率为24%（95%可信区间20%-28%）。在对定义、使用剂量和人群差异进行调整后，与阿司匹林剂量≥300mg的研究相比，阿司匹林剂量≤100mg的研究中发现患病率在统计学上显著更高（36%[95%可信区间28%-43%]对19%[95%可信区间11%-26%]，P<.0001）。使用花生四烯酸作为激动剂的光聚集法测量血小板聚集的研究汇总未调整患病率为6%（95%可信区间0%-12%）。在使用即时血小板功能分析设备的研究中，未调整患病率显著更高，为26%（95%可信区间21%-31%）。
报道阿司匹林抵抗的研究之间患病率差异很大。阿司匹林剂量和定义阿司匹林抵抗的方法都强烈影响估计的患病率，这解释了研究中发现的异质性。平均而言，似乎约四分之一的个体可能表现出生化定义的阿司匹林抵抗。
