Malý J, Pecka M, Gregor J, Dulícek P, Blazek M, Malý R, Pudil R, Bláha M
Katedra internich oborů LF UK a FN, Hradec Králové.
Cas Lek Cesk. 2005;144 Suppl 3:23-9.
The interest in aspirin resistance has been increasing during the last few years, with researchers earnestly pursuing alternative anti-platelet therapies and devices for measuring platelet aggregation. The recent studies suggest that 5-45% of patients taking aspirin do not experience adequate anti-platelet effects.
There is scant evidence proving that aspirin resistance has some clinical consequences. To assess the prevalence of aspirin resistance in patients with ischemic heart disease (IHD) two independent methods were used: platelet aggregation in platelet rich plasma (PRP) after induction by propylgallate (CPG), and assessment of platelet function by PFA 100 method. The study population consisted of 424 patients treated for IHD on the 2nd Dept. of Medicine, Teaching Hospital, Hradec Kralove. The age, gender, diagnosis and effect of therapy were characterized in this group of the patients. Daily ASA dose was 100 mg. We used two methods to monitor ASA treatment efficacy: a) thrombocyte aggregation after induction by CPG, b) the assessment of platelet function by PFA 100 method. a) Of the patients studied by CPG platelet aggregation, 51 (12.1%) pts were resistant to ASA dose 100 mg/day, and 32 (7.6%) pts remained resistant even after increasig the dose to 200 mg/day. In 80 (20%) pts, the daily ASA dose of less than 100 mg was sufficient to inhibit platelet function. b) Although the PFA-100 system is not able to detect the difference between low and high ASA dose, we found 53 (15.2%) patients aspirin resistant using this method.
In the patients with IHD treated with 100 mg of ASA per day, our study has shown that the prevalence of aspirin resistance was 12.1% using CPG method, and 15.2% using PFA-100 method. Aspirin resistance was dose dependent. Prevalence of ASA resistance in patients treated with 200 mg of ASA per day was only 7.6% using the CPG method.
在过去几年中，对阿司匹林抵抗的关注不断增加，研究人员积极寻求替代的抗血小板疗法以及测量血小板聚集的设备。最近的研究表明，服用阿司匹林的患者中有5% - 45%未获得足够的抗血小板效果。
几乎没有证据证明阿司匹林抵抗会产生某些临床后果。为评估缺血性心脏病（IHD）患者中阿司匹林抵抗的发生率，使用了两种独立的方法：用棓丙酯（CPG）诱导后富血小板血浆（PRP）中的血小板聚集，以及通过PFA 100方法评估血小板功能。研究人群包括在赫拉德茨克拉洛韦教学医院第二内科接受IHD治疗的424例患者。对该组患者的年龄、性别、诊断和治疗效果进行了描述。每日阿司匹林剂量为100毫克。我们使用两种方法监测阿司匹林治疗效果：a）CPG诱导后的血小板聚集，b）通过PFA 100方法评估血小板功能。a）在通过CPG血小板聚集研究的患者中，51例（12.1%）患者对每日100毫克的阿司匹林剂量有抵抗，甚至在将剂量增加到200毫克/天后，仍有32例（7.6%）患者有抵抗。在80例（20%）患者中，每日阿司匹林剂量低于100毫克就足以抑制血小板功能。b）尽管PFA - 100系统无法检测低剂量和高剂量阿司匹林之间的差异，但使用该方法我们发现53例（15.2%）患者存在阿司匹林抵抗。
在每天服用100毫克阿司匹林治疗的IHD患者中，我们的研究表明，使用CPG方法时阿司匹林抵抗的发生率为12.1%，使用PFA - 100方法时为15.2%。阿司匹林抵抗与剂量有关。使用CPG方法时，每天服用200毫克阿司匹林治疗的患者中阿司匹林抵抗的发生率仅为7.6%。
