Zeng Weiwei, Chu Tanya Tw, Chow Elaine Yk, Hu Miao, Fok Benny Sp, Chan Juliana Cn, Yan Bryan Py, Tomlinson Brian
Shenzhen Longgang Second People's Hospital, 518112, China.
Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Shatin, Hong Kong SAR, China.
Heliyon. 2024 Jul 14;10(14):e34552. doi: 10.1016/j.heliyon.2024.e34552. eCollection 2024 Jul 30.
Associations between single nucleotide polymorphisms (SNPs) and aspirin resistance (AR) have been studied with variable results. The associations of genetic variants with AR may be helpful to explain why some individuals demonstrate aspirin insensitivity with this anti-platelet therapy. The purpose of this research was to investigate the effect of different genotypes in candidate genes on aspirin response in patients taking long-term aspirin therapy by measuring the serum thromboxane B2 (TXB2) and platelet function using the Multiplate® analyser.
A total of 266 patients with stable coronary heart disease (CHD) taking low-dose aspirin for long periods of time and without any other anti-platelet drugs medications were enrolled into the study. They were required to take 80 mg of aspirin every morning for a week including the day before blood tests. Blood samples were collected 24 h after the last dose. The 80 mg dose of aspirin was taken orally and blood samples were collected again 1 h later. The serum TXB2 levels were measured in samples at 24 h post-dose and 1 h post-dose using the EIA kit and platelet activity was determined using the Multiplate® Impedance Platelet Aggregometry (ASPI) assay. Genotyping assays were performed by the TaqMan SNP genotyping technique.
Of the 266 patients, only 251 patients were enrolled in the present study. The -1676 A G (rs1330344) and the -765 G C (rs20417) SNPs showed significant associations with the ASPI measurements in samples taken at 24 h post-dose, but not with the values at 1 h post-dose or with the TXB2 levels ( < 0.05).
Our results suggest that polymorphisms in the and the genes may be associated with reduced anti-aggregatory effects and increased the risk of AR, but future larger-scale cohort studies are necessary for further validation.
对单核苷酸多态性（SNP）与阿司匹林抵抗（AR）之间的关联进行了研究，结果各异。基因变异与AR之间的关联可能有助于解释为何一些个体在接受这种抗血小板治疗时表现出阿司匹林不敏感。本研究的目的是通过使用Multiplate®分析仪测量血清血栓素B2（TXB2）和血小板功能，来研究候选基因中不同基因型对长期服用阿司匹林治疗的患者阿司匹林反应的影响。
共有266例长期服用低剂量阿司匹林且未服用任何其他抗血小板药物的稳定型冠心病（CHD）患者纳入本研究。要求他们每天早晨服用80毫克阿司匹林，持续一周，包括血液检测前一天。在最后一剂药物服用24小时后采集血样。口服80毫克剂量的阿司匹林，1小时后再次采集血样。使用酶免疫分析试剂盒在给药后24小时和给药后1小时的样本中测量血清TXB2水平，并使用Multiplate®阻抗血小板聚集测定法（ASPI）测定血小板活性。通过TaqMan SNP基因分型技术进行基因分型检测。
266例患者中，本研究仅纳入251例患者。-1676 A>G（rs1330344）和-765 G>C（rs20417）单核苷酸多态性与给药后24小时采集样本中的ASPI测量值显著相关，但与给药后1小时的值或TXB2水平无关（P<0.05）。
我们的结果表明，[此处原文可能缺失具体基因名称]基因中的多态性可能与抗聚集作用降低和AR风险增加有关，但未来需要更大规模的队列研究进行进一步验证。
