| Background and purpose: Aspirin is widely used in the treatment and prevention of ischemic stroke.However,individual sensitivity to aspirin may be variable.Among them,the platelet aggregation rate of some patients is still not effectively inhibited after taking aspirin,which eventually leads to the occurrence of ischemic events,this phenomenon is called aspirin resistance（AR）.In addition,some individuals who take aspirin for a long time may have some serious adverse reactions,such as gastrointestinal bleeding,asthma,rash,etc.,which may affect patient compliance and drug bioavailability.Aspirin resistance and intolerance ultimately affect the prognosis and quality of life of patients with ischemic stroke.In this regard,scholars have conducted a lot of research,trying to find the mechanism of individual platelet response differences from various aspects.At present,the most popular and controversial thing is ARrelated gene polymorphisms.So far,it has been found that there are gene polymorphisms in COX enzymes and various receptors on the platelet surface.Materials and methods: A total of 81 patients with ischemic stroke who were hospitalized in the Department of Neurology,First Hospital of Jilin University from August 2020 to October 2021 were enrolled.We recorded the general clinical data and comorbidities of the patients and detected routine laboratory biochemistry Indicators,platelet aggregation rate after taking aspirin,and their GP1 BA genotyping.According to the platelet aggregation rate（PLADP≥70%and/or PLAA≥20%）,they were divided into the aspirin-resistant group（AR）and aspirin-sensitive group（AS）.We used SPSS26.0statistical software to analyze the differences between AS group and AR group in general data,laboratory parameters,and GP1 BA genotype distribution.According to the results of GP1 BA gene detection,they were divided into the CC genotype group,CT genotype group,and TT genotype group.SPSS26.0 statistical software was used to analyze the correlation between the GP1 BA genotype and platelet aggregation rate.Results: 1.The prevalence of AR（36 cases）was 44.44% in our study population.2.The mutation rate of the GP1 BA gene was24.69%.There were 61 cases（75.31%）with CC genotype and 20cases（24.69%）with CT+TT genotype.In AS group,there were 30cases（37.04%）of CC genotype and 15 cases（18.52%）of CT+TT genotype;In the AR group,there were 31 cases（86.11%）of CC genotype and 5 cases（13.89%）of CT+TT genotype.3.Statistical analysis showed that gender（χ2=5.601,P=0.018）,diabetes（χ2=5.697,P=0.017）,smoking history（χ2=4.510,P=0.034）,degree of cerebral vascular stenosis（χ2=4.542,P=0.019）,red blood cell count（Z=-2.025,P=0.043）,glycosylated hemoglobin（Z=-2.347,P=0.019）and uric acid（t=-0.780,P=0.005）had statistically significant differences between the AR group and the AS group.4.Statistical analysis revealed that the proportion of AR in patients with CC genotype was significantly higher than that in patients with CT+TT genotype（χ2=4.067,P=0.044）;and the median platelet aggregation rate in patients with CC genotype was higher than that in patients with CT/TT genotype,the difference was statistically significant（Z=-6.820,P＜0.001）.5.Multivariate Logistic regression analysis found that male（OR=0.135,95%CI: 0.031～0.587,P=0.008）,smoking（OR=0.165,95%CI: 0.038～0.707,P=0.015）and cerebral vascular stenosis（OR=2.328,95%CI: 1.031～5.255,P=0.042）may be independent risk factors for AR.Conclusion: 1.Univariate analysis showed that AR was associated with gender,smoking,cerebral vascular stenosis,degree of cerebral vascular stenosis,red blood cell count,glycosylated hemoglobin,and uric acid.2.GP1 BA gene polymorphism was associated with AR,and the risk of AR was higher in CC genotype patients.3.Male,smoking,and glycosylated hemoglobin may be independent risk factors for AR. |
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