血小板糖蛋白 IIIa PlA1/PlA2 多态性可调节非糖尿病患者的心肌梗死风险

IF 1.6 Q2 MEDICINE, GENERAL & INTERNAL Journal of clinical medicine research Pub Date : 2024-03-01 DOI:10.14740/jocmr5094
Mohanad Altayeb Mohamed Ahmed, Elshazali Widaa Ali, Gamal Mahmoud Alimairi
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Results: The distribution of GPIIIa PlA1/PlA2 polymorphic genotypes among the study groups was significantly different (P value = 0.00). The PlA1/PlA2 and PlA2/PlA2 genotypes were more frequent in the patients with myocardial infarction while the genotype PlA1/ PlA1 was more prevalent in the control group. There was a statistically significant association between the PlA1/PlA1 genotype and reduced risk of both ST-segment elevation myocardial infarction (odds ratio (OR) = 0.19; 95% confidence interval (CI): 0.09 - 0.34, P value = 0.00) and non-ST-segment elevation myocardial infarction (OR = 0.21; 95% CI: 0.09 - 0.45, P value = 0.00). The genotype PlA1/PlA2 was found to be associated with an increased risk of both types of myocardial infarction (OR = 6.0; 95% CI: 2.61 - 13.8, P value = 0.00 for ST-segment elevation myocardial infarction and OR = 6.65; 95% CI: 2.69 - 16.45, P value = 0.00 for non-ST-segment elevation myocardial infarction. 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引用次数: 0

摘要

背景:血小板糖蛋白Ⅲa(GPⅢa基因)的基因多态性在多种血栓性疾病中已得到深入研究,但其在心血管疾病中的作用仍存在争议。本研究旨在探讨血小板糖蛋白 IIIa PlA1/PlA2 多态性与非糖尿病患者心肌梗死易感性之间的关系。研究方法共招募 200 人参与研究,其中 100 人为非糖尿病心肌梗死患者,100 人为表面健康的志愿者作为对照组。通过聚合酶链式反应-限制性片段长度多态性分析 GPIIIa PlA1/PlA2 的多态性。结果显示研究组中 GPIIIa PlA1/PlA2 多态性基因型的分布有显著差异(P 值 = 0.00)。PlA1/PlA2和PlA2/PlA2基因型在心肌梗死患者中更为常见,而基因型PlA1/ PlA1在对照组中更为普遍。在统计学上,PlA1/PlA1 基因型与 ST 段抬高型心肌梗死(几率比(OR)= 0.19;95% 置信区间(CI):0.09 - 0.34,P 值 = 0.00)和非 ST 段抬高型心肌梗死(OR = 0.21;95% CI:0.09 - 0.45,P 值 = 0.00)的风险降低有显著关联。研究发现,PlA1/PlA2 基因型与两种类型的心肌梗死风险增加有关(ST 段抬高型心肌梗死的 OR = 6.0;95% CI:2.61 - 13.8,P 值 = 0.00;非 ST 段抬高型心肌梗死的 OR = 6.65;95% CI:2.69 - 16.45,P 值 = 0.00)。在携带 PlA1/PlA2 基因型的患者中,如果有家族史,ST 段抬高型心肌梗死的风险会增加约 14 倍(OR:13.57;95% CI:1.42 - 130.03,P值=0.02),携带PlA2/PlA2基因型的吸烟者发生非ST段抬高型心肌梗死的风险增加了约18倍(OR:17.63,95% CI:0.96 - 324.70,P值=0.05)。结论GPIII PlA1/PlA1 基因型与 ST 段抬高型和非 ST 段抬高型心肌梗死风险的降低有关,而 PlA1/PlA2 基因型与这两种类型心肌梗死风险的增加有关。
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Platelet Glycoprotein IIIa PlA1/PlA2 Polymorphism Modulates the Risk of Myocardial Infarction in Non-Diabetics
Background: Genetic polymorphisms of platelet glycoprotein IIIa ( GPIIIa gene) have been investigated intensively in several thrombotic diseases, but their role in cardiovascular diseases remains controversial. This study aimed to investigate the association between platelet glycoprotein IIIa PlA1/PlA2 polymorphism and susceptibility to myocardial infarction in non-diabetics. Methods: A total of 200 participants were recruited for the study, 100 non-diabetic patients with myocardial infarction and 100 apparently healthy volunteers as a control group. GPIIIa PlA1/PlA2 polymorphism was analyzed by polymerase chain reaction-restriction fragment length polymorphism. Results: The distribution of GPIIIa PlA1/PlA2 polymorphic genotypes among the study groups was significantly different (P value = 0.00). The PlA1/PlA2 and PlA2/PlA2 genotypes were more frequent in the patients with myocardial infarction while the genotype PlA1/ PlA1 was more prevalent in the control group. There was a statistically significant association between the PlA1/PlA1 genotype and reduced risk of both ST-segment elevation myocardial infarction (odds ratio (OR) = 0.19; 95% confidence interval (CI): 0.09 - 0.34, P value = 0.00) and non-ST-segment elevation myocardial infarction (OR = 0.21; 95% CI: 0.09 - 0.45, P value = 0.00). The genotype PlA1/PlA2 was found to be associated with an increased risk of both types of myocardial infarction (OR = 6.0; 95% CI: 2.61 - 13.8, P value = 0.00 for ST-segment elevation myocardial infarction and OR = 6.65; 95% CI: 2.69 - 16.45, P value = 0.00 for non-ST-segment elevation myocardial infarction. In the patients carrying the PlA1/PlA2 genotype, the risk of ST-segment elevation myocardial infarction was increased to about 14 folds in the presence of family history (OR: 13.57, 95% CI: 1.42 - 130.03, P value = 0.02), and the risk of non-ST-segment elevation myocardial infarction increased to about 18 folds in the smokers carrying the genotype PlA2/PlA2 (OR: 17.63, 95% CI: 0.96 - 324.70, P value = 0.05). Conclusions: The GPIII PlA1/PlA1 genotype is associated with a reduced risk of ST-segment elevation and non-ST-segment elevation myocardial infarction, while PlA1/PlA2 is associated with an increased risk of both types of myocardial infarction.
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