SAA、Tanis及CYP2C19基因与冠心病的发病风险、临床预后及个体化治疗
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摘要
目的：1）探讨参与炎症反应及脂质代谢SAA及其受体Tanis基因多态性与新疆不同民族冠心病及其危险因素的关系；2）探讨细胞色素P4502C19功能缺失等位基因和冠心病PCI术后患者预后的关系；3）探讨根据CYP2C19基因型进行个体化抗血小板治疗的近期疗效及其推广价值。方法：1）采用病例-对照研究的方法，选择经冠脉造影检查确诊的冠心病患者2004例和性别、年龄、民族均匹配的正常健康对照人群1902例，采用限制性片段长度多态性方法及实时荧光定量PCR方法对参与炎症反应、脂质代谢及糖代谢的SAA及其受体Tanis进行基因分型。分析SAA基因及Tanis基因标签SNP和冠心病及其危险因素（包括HDL、尿酸以及血糖水平）之间的关系；2）采用队列研究的方法，入选经皮冠状动脉内支架植入（PCI）术后患者1068例，采用限制性片段长度多态性方法对其进行CYP2C19、SAA及Tanis基因型检测，对其进行为期1年的随访，观察三组人群术后支架内血栓、非致死性心肌梗死、总死亡以及出血事件的发生率之间的差异；3）采用随机、对照设计入选301例冠心病行PCI术后患者，随机分为个体化治疗组151例和常规治疗组150例，个体化治疗组采用CYP2C19基因型快速检测试剂盒对其进行分型，按照不同的基因型采用个体化的抗血小板治疗方案，即EMs给予氯吡格雷50mg qd+拜阿司匹灵100mg qd；IMs给予氯吡格雷每天75mg qd+拜阿司匹灵100mg qd；PMs给予氯吡格雷每天75mg qd+拜阿司匹灵100mg qd，并同时给予西洛他唑100mg每天两次口服。常规治疗组不进行CYP2C19基因型检测，按照常规方法给予双联抗血小板治疗。观察两组患者术后30天及180天支架内血栓及不良事件的发生率之间的差异。结果：1）SAA基因rs12218及Tanis基因rs1384656和新疆维汉民族冠心病的发生具有关联。Rs12218CC基因型及rs1384656CC基因型显著增加冠心病的风险，在调整了其它因素的干扰后，rs12218及rs1384656基因多态性仍是维汉民族冠心病独立的危险因素；rs12218基因多态性明显影响健康人群血糖、HDL-C及SAA水平，rs1384656显著影响健康人群血糖和甘油三酯水平；2）在中国冠心病人群中，CYP2C19功能缺失型等位基因携带者的频率高达57.5%；CYP2C19基因慢代谢者发生心血管不良事件的风险显著增加，COX多因素回归分析显示，在调整了其它因素的影响后，CYP2C19慢代谢表型是冠心病患者PCI术后心血管不良事件发生的独立危险因素；SAA及其受体Tanis基因多态性和冠心病PCI术后不良预后没有相关性；3）基于CYP2C19基因型的个体化治疗组与常规治疗组比较，随访30天，支架内血栓、心肌梗死、总MACE事件、出血事件的发生率没有明显差别（均P＞0.05），死亡发生率明显降低（P=0.043）；随访180天，支架内血栓、心肌梗死的发生率没有明显差异（均P＞0.05），但总MACE事件、出血事件以及死亡的发生率差异具有统计学意义（均P＜0.05）。结论：1）SAA及其受体Tanis基因多态性和新疆维汉民族冠心病的发生存在关联，可能和SAA与Tanis基因突变导致的血糖、血脂及炎症因子的变化有关；2）SAA及其受体Tanis基因多态性和行PCI治疗的冠心病患者的预后没有明显的相关性；3）携带CYP2C19功能缺失型等位基因的冠心病患者PCI术后支架内血栓、死亡、心肌梗死的发生风险显著增高；4）基于CYP2C19基因型的个体化抗血小板治疗可以显著改善PCI术后患者的临床预后。
Objective:1) To explore the associations of genetic polymorphisms of SAA and itsreceptor Tanis which both involved in inflammation and lipid metabolism with coronaryheart disease and its risk factors in different ethnic groups in Xinjiang;2) to investigatethe relationship between cytochrome P4502C19loss-of-function alleles and prognosis ofcoronary artery disease after PCI;3) to explore the personalized antiplatelet therapyaccording to CYP2C19genotype in patients with coronary artery disease and itspromotional value. Methods:1) A case-control study including2004cases with coronaryheart disease confirmed by coronary angiography and1902gender-, age-, andethnic-matched normal healthy controls was desighed for the present study. Usingrestriction fragment length polymorphism and real-time PCR methods, we genotyped8SNPs in the SAA and Tanis genes and analyzed the relationship between these SNPs andcoronary artery disease and its risk factors (including HDL, uric acid and blood glucoselevels);2) A cohort study was designed to observe the relationship between geneticpolymorphisms of SAA, Tanis, and CYP2C19and prognosis of1068patients withcoronary artery disease after percutaneous coronary stent implantation (PCI), thegenotypes were detected by RFLP methods. All these1068patients were fellow-up forone year, we observed the differces in stent thrombosis, nonfatal myocardial infarction,total mortality and bleeding events among three genetypes in SAA, Tanis and CYP2C19gene, respectively;3) A single-center randomized-controlled including301patients withcoronary heart disease after PCI was designed to assess the safety and effective ofindividual theray according to CYP2C29genoty. These301patients were randomlydivided into the personalized treatment group (n=151) and conventional therapy group(n=150). In the personalized group, the CYP2C19genotype was detected by use of rapidtest kit before treatment with antiplatelet angent. The patients with extensive metabolizer(EMs) were given clopidogrel50mg·qd plus aspirin100mg·qd; the patients withintermediate metabolizer (IMs) were given clopidogrel75mg·qd plus aspirin100mg·qd; the patients with poor metabolizer (PMs) treated with clopidogrel75mg·qd and aspirin100mg·qd plus Cilostazol100mg twice daily. The conventional treatment group were notdetected the CYP2C19genotype and were given dual antiplatelet therapy (clopidogrel75mg·qd and aspirin100mg·qd). The differences in stent thrombosis, nonfatal myocardialinfarction, total mortality and bleeding events between these two groups were observed30days and180days after PCI. Results:1) rs12218in the SAA gene and rs1384656inthe Tanis gene was associated with coronary artery disease in both Han ethnic and Uygurethnic in Xinjiang. Rs12218CC genotypes and rs1384656CC genotype significantlyincreased the risk of coronary heart disease, after adjustment for other factors, rs12218and rs1384656gene polymorphism was still independent risk factors for coronary heartdisease; rs12218gene polymorphism significantly affected plasma GLU, HDL-C, andSAA levels, and rs1384656significantly affect plasma GLU and triglyceride levels inhealthy people;2) the frequencie of CYP2C19loss-of-function allele was high up to57.5%in Chinese coronary heart disease population; CYP2C19poor metabolizerssignificantly increased risk of cardiovascular adverse events. By COX multivariateregression analysis showed that after adjusting for other factors CYP2C19poormetabolizer phenotype is an independent risk factor of cardiovascular adverse events incoronary heart disease patients after PCI; no association of SAA and its receptor Tanisgene polymorphism with adverse prognosis of coronary heart disease after PCI;3) After30-day follow-up, the CYP2C19genotype-based personalized group have lower totalmortality (P=0.043) compare to that in the conventional group. There were significantdifference in incidence of stent thrombosis, myocardial infarction, and bleeding eventsbetween these two groups (all P＞0.05); after180-days follow-up, there were notsignificant difference in incidence of stent thrombosis, myocardial infarction betweenthese two groups (all P＞0.05), but the incidence of overall MACE events, bleedingevents and death in the personalized group was lower than those in conventional group (P＜0.05). Conclusion:1) genetic polymorphisms of SAA and Tanis were associated withcoronary heart disease in both Uygur and Han ethnic, which maybe result from alterationof plasma GLU, triglyceride and SAA levels with genetic mutation in SAA and Tanis;2)There were no associations between genetic polymorphisms of SAA and Tanis and adversprognosis of coronary artery disease after PCI;3) The carriers with CYP2C19loss-of-function alleles have higher risk of stent thrombosis, death, and myocardialinfarction;4) CYP2C19genotype-based individualization of antiplatelet therapy cansignificantly improve the clinical outcome after PCI in patients with coronary artery disease.
Objective:1) To explore the associations of genetic polymorphisms of SAA and itsreceptor Tanis which both involved in inflammation and lipid metabolism with coronaryheart disease and its risk factors in different ethnic groups in Xinjiang;2) to investigatethe relationship between cytochrome P4502C19loss-of-function alleles and prognosis ofcoronary artery disease after PCI;3) to explore the personalized antiplatelet therapyaccording to CYP2C19genotype in patients with coronary artery disease and itspromotional value. Methods:1) A case-control study including2004cases with coronaryheart disease confirmed by coronary angiography and1902gender-, age-, andethnic-matched normal healthy controls was desighed for the present study. Usingrestriction fragment length polymorphism and real-time PCR methods, we genotyped8SNPs in the SAA and Tanis genes and analyzed the relationship between these SNPs andcoronary artery disease and its risk factors (including HDL, uric acid and blood glucoselevels);2) A cohort study was designed to observe the relationship between geneticpolymorphisms of SAA, Tanis, and CYP2C19and prognosis of1068patients withcoronary artery disease after percutaneous coronary stent implantation (PCI), thegenotypes were detected by RFLP methods. All these1068patients were fellow-up forone year, we observed the differces in stent thrombosis, nonfatal myocardial infarction,total mortality and bleeding events among three genetypes in SAA, Tanis and CYP2C19gene, respectively;3) A single-center randomized-controlled including301patients withcoronary heart disease after PCI was designed to assess the safety and effective ofindividual theray according to CYP2C29genoty. These301patients were randomlydivided into the personalized treatment group (n=151) and conventional therapy group(n=150). In the personalized group, the CYP2C19genotype was detected by use of rapidtest kit before treatment with antiplatelet angent. The patients with extensive metabolizer(EMs) were given clopidogrel50mg·qd plus aspirin100mg·qd; the patients withintermediate metabolizer (IMs) were given clopidogrel75mg·qd plus aspirin100mg·qd; the patients with poor metabolizer (PMs) treated with clopidogrel75mg·qd and aspirin100mg·qd plus Cilostazol100mg twice daily. The conventional treatment group were notdetected the CYP2C19genotype and were given dual antiplatelet therapy (clopidogrel75mg·qd and aspirin100mg·qd). The differences in stent thrombosis, nonfatal myocardialinfarction, total mortality and bleeding events between these two groups were observed30days and180days after PCI. Results:1) rs12218in the SAA gene and rs1384656inthe Tanis gene was associated with coronary artery disease in both Han ethnic and Uygurethnic in Xinjiang. Rs12218CC genotypes and rs1384656CC genotype significantlyincreased the risk of coronary heart disease, after adjustment for other factors, rs12218and rs1384656gene polymorphism was still independent risk factors for coronary heartdisease; rs12218gene polymorphism significantly affected plasma GLU, HDL-C, andSAA levels, and rs1384656significantly affect plasma GLU and triglyceride levels inhealthy people;2) the frequencie of CYP2C19loss-of-function allele was high up to57.5%in Chinese coronary heart disease population; CYP2C19poor metabolizerssignificantly increased risk of cardiovascular adverse events. By COX multivariateregression analysis showed that after adjusting for other factors CYP2C19poormetabolizer phenotype is an independent risk factor of cardiovascular adverse events incoronary heart disease patients after PCI; no association of SAA and its receptor Tanisgene polymorphism with adverse prognosis of coronary heart disease after PCI;3) After30-day follow-up, the CYP2C19genotype-based personalized group have lower totalmortality (P=0.043) compare to that in the conventional group. There were significantdifference in incidence of stent thrombosis, myocardial infarction, and bleeding eventsbetween these two groups (all P＞0.05); after180-days follow-up, there were notsignificant difference in incidence of stent thrombosis, myocardial infarction betweenthese two groups (all P＞0.05), but the incidence of overall MACE events, bleedingevents and death in the personalized group was lower than those in conventional group (P＜0.05). Conclusion:1) genetic polymorphisms of SAA and Tanis were associated withcoronary heart disease in both Uygur and Han ethnic, which maybe result from alterationof plasma GLU, triglyceride and SAA levels with genetic mutation in SAA and Tanis;2)There were no associations between genetic polymorphisms of SAA and Tanis and adversprognosis of coronary artery disease after PCI;3) The carriers with CYP2C19loss-of-function alleles have higher risk of stent thrombosis, death, and myocardialinfarction;4) CYP2C19genotype-based individualization of antiplatelet therapy cansignificantly improve the clinical outcome after PCI in patients with coronary artery disease.
引文
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