本文選題：血小板內(nèi)皮聚集受體1 + 血小板反應(yīng)性��； 參考：《北京協(xié)和醫(yī)學(xué)院》2017年博士論文

【摘要】：背景:阿司匹林聯(lián)合氯吡格雷雙聯(lián)抗血小板治療是急性冠脈綜合征患者或行經(jīng)皮冠狀動(dòng)脈介入術(shù)患者的治療基石。然而,臨床實(shí)踐發(fā)現(xiàn),在抗血小板治療中血小板反應(yīng)性存在個(gè)體差異。一部分患者在接受阿司匹林或氯吡格雷治療后血小板不能獲得充分抑制,易導(dǎo)致血小板高反應(yīng)性。研究表明遺傳因素即基因多態(tài)性在抗血小板療效個(gè)體差異中起到了至關(guān)重要的作用。血小板內(nèi)皮聚集受體1(Platelet Endothelial Aggregation Receptor 1,PEAR1)是一種表達(dá)在血小板膜表面的跨膜蛋白,在血小板聚集中起著重要作用。本研究的目的是探討分析編碼PEAR1蛋白的PEAR1基因多態(tài)性對(duì)服用阿司匹林和氯吡格雷雙聯(lián)抗血小板治療的中國冠心病患者冠脈介入術(shù)后血小板反應(yīng)性的影響。方法:本研究納入2011年11月至2013年3月于我院行經(jīng)皮冠狀動(dòng)脈介入術(shù)的冠心病患者,所有患者均服用阿司匹林和氯吡格雷雙聯(lián)抗血小板治療。利用血栓彈力圖法檢測(cè)二磷酸腺苷(adenosine diphosphate,ADP)刺激下的血小板反應(yīng)性,結(jié)果記錄為血小板聚集抑制率(inhibition of platelet aggregation,IPA)。IPA 小于 30%定義為治療下血小板高反應(yīng)性(high on-treatment platelet reactivity,HTPR);IPA大于70%定義為治療下血小板低反應(yīng)性(low on-treatment platelet reactivity,LTPR)。依據(jù)血小板反應(yīng)性將患者分為HTPR組和LTPR組,采用病例對(duì)照研究模式分析基因多態(tài)性對(duì)血小板反應(yīng)性的影響。依據(jù)已發(fā)表文獻(xiàn)報(bào)道和人類基因組單倍體型網(wǎng)站(HAPMAP,http://hapmap.ncbi.nlm.nih.gov/),利用Haploview 4.2軟件篩選出本研究待分析的PEAR1基因單核苷酸多態(tài)性位點(diǎn)(single nucleotide polymorphism,SNP)。利用改良的多重鏈接酶檢測(cè)反應(yīng)測(cè)定PEAR1基因SNPs的分型,比較SNPs次要等位基因在HTPR和LTPR兩組間攜帶頻率的差異。結(jié)果:204名患者存在血小板高反應(yīng)性,201名患者存在血小板低反應(yīng)性�；谖墨I(xiàn)報(bào)道和HAPMAP分析結(jié)果,共16個(gè)PEAR1 SNPs納入本研究進(jìn)行基因分型。16個(gè)SNPs中發(fā)現(xiàn)有5個(gè)SNP與ADP刺激下的血小板聚集顯著相關(guān)。單因素分析發(fā)現(xiàn)在顯性模型中rs11264580的C次要等位基因(p=0.033),rs2644592的G次要等位基因(p=0.048),rs3737224的T次要等位基因(p=0.033)、rs41273215的T次要等位基因(p=0.025)以及單倍體型分析中C-G-T-T-C(p=0.034)在HTPR組攜帶率顯著高于LTPR組,表明與血小板高反應(yīng)性顯著相關(guān);在隱性模型中rs57731889 TT純合子基因型(p=0.009)以及單體型分析中T-A-C-C-T(p=0.009)在LTPR組攜帶率顯著高于HTPR組,表明與血小板低反應(yīng)性顯著相關(guān)。使用logistic多因素回歸模型校正混雜因素進(jìn)一步分析后顯示rs41273215的T次要等位基因(p=0.038)是血小板高反應(yīng)性的一個(gè)獨(dú)立預(yù)測(cè)因子,而rs57731889的TT純合子(p=0.003)則是血小板低反應(yīng)性的獨(dú)立預(yù)測(cè)因子。結(jié)論:(1)PEAR1基因多態(tài)性與中國冠心病患者ADP刺激下的血小板反應(yīng)性密切相關(guān);(2)PEAR1基因多態(tài)性的不同位點(diǎn)對(duì)血小板功能的影響明顯不同;(3)rs41273215導(dǎo)致血小板高反應(yīng)性,rs57731889導(dǎo)致血小板低反應(yīng)性。背景:血栓形成是引發(fā)急性冠狀動(dòng)脈綜合征的核心原因。血小板是血栓的最主要組成成分,其黏附、活化、聚集在血栓形成中起著至關(guān)重要的作用,因此抗血小板治療已成為防治血栓形成、減少臨床不良事件發(fā)生的的重要基石。臨床實(shí)踐發(fā)現(xiàn),抗血小板療效在患者中存在個(gè)體差異,部分患者對(duì)阿司匹林或氯吡格雷存在抵抗現(xiàn)象,易導(dǎo)致療效不佳、發(fā)生臨床不良缺血性事件。血小板內(nèi)皮聚集受體l(Platelet Endothelial Aggregation Receptor 1,PEAR1)是一種表達(dá)在血小板膜表面的跨膜蛋白,在血小板聚集中起著重要作用。本研究的目的是探討分析編碼PEAR1蛋白的PEAR1基因多態(tài)性對(duì)中國急性心機(jī)梗死患者冠狀動(dòng)脈介入術(shù)后1年的臨床預(yù)后影響。方法:本研究納入2011年11月至2013年3月于我院行冠狀動(dòng)脈介入術(shù)的急性心肌梗死患者,所有患者均服用阿司匹林和氯吡格雷雙聯(lián)抗血小板治療。本課題組前期工作中發(fā)現(xiàn)的與血小板高反應(yīng)性相關(guān)的PEAR1基因單核苷酸多態(tài)性位點(diǎn)(single nucleotide polymorphism,SNP)被納入本研究中,以探討它們對(duì)臨床預(yù)后的影響,由于本研究為探索性研究,故SNP的P值只要小于0.1即被納入。利用改良的多重鏈接酶檢測(cè)反應(yīng)測(cè)定PEAR1基因SNPs的分型。術(shù)后通過再入院記錄、門診及電話進(jìn)行12個(gè)月的臨床隨訪,隨訪事件包括全因死亡,心原性死亡,心肌梗死,非計(jì)劃血運(yùn)重建和支架內(nèi)血栓。復(fù)合缺血事件定義為包括心原性死亡、心肌梗死、非計(jì)劃血運(yùn)重建和支架內(nèi)血栓的復(fù)合臨床終點(diǎn)。結(jié)果:依據(jù)納入排除標(biāo)準(zhǔn),共647名急性心肌梗死患者被納入本研究。依據(jù)課題組前期研究結(jié)果,6個(gè)與血小板高反應(yīng)性相關(guān)的PEAR1 SNPs:rs11264580、rs2644592、rs3737224、rs41273215、rs56260937、rs822442 被納入本研究。在 1 年隨訪中,共66人(10.2%)發(fā)生不良臨床事件:全因死亡8例(1.2%)、心原性死亡4例(0.6%),心肌梗死6例(0.9%),因缺血驅(qū)動(dòng)的血運(yùn)重建61例(9.4%),未隨訪到發(fā)生支架內(nèi)血栓事件。在隱性模型分析中,相較主要等位基因攜帶者,rs56260937次要等位基因TT純合子攜帶者發(fā)生因缺血驅(qū)動(dòng)的血運(yùn)重建發(fā)生率顯著增高(16.7%vs 8.6%,P=0.034)。進(jìn)一步使用多因素Cox回歸分析校正混雜因素后,結(jié)果表明rs56260937是血運(yùn)重建的獨(dú)立危險(xiǎn)因素(HR=2.09,95%CI 1.07-4.06,p=0.031)。結(jié)論:(1)PEAR1基因多態(tài)性與中國急性心肌梗死患者介入術(shù)后1年的臨床預(yù)后顯著相關(guān);(2)rs56260937次要等位基因TT純合子基因型顯著增加血運(yùn)重建事件發(fā)生率;(3)進(jìn)行PEAR1基因檢測(cè),未來有可能用于指導(dǎo)臨床個(gè)體化抗血小板治療,以期改善患者臨床預(yù)后。背景:抗血小板治療是急性冠狀動(dòng)脈綜合征的治療基石。然而臨床實(shí)踐發(fā)現(xiàn),部分患者對(duì)抗血小板藥物存在抵抗現(xiàn)象,易導(dǎo)致治療下血小板高反應(yīng)性((high on-treatment platelet reactivity,HTPR)。目前,國內(nèi)外已有諸多研究表明臨床因素對(duì)患者服用藥物的反應(yīng)性有顯著影響,基于此,我們的研究旨在利用臨床常用指標(biāo),篩選出與血小板高反應(yīng)性相關(guān)的臨床危險(xiǎn)因素,并構(gòu)建血小板高反應(yīng)性臨床風(fēng)險(xiǎn)評(píng)分。該評(píng)分的構(gòu)建將有助于臨床醫(yī)師對(duì)患者血小板反應(yīng)性做出快速全面評(píng)估,從而給予針對(duì)性的個(gè)體化抗血小板治療。方法:本研究納入2013年1月至2013年12月在中國醫(yī)學(xué)科學(xué)院阜外醫(yī)院接受經(jīng)皮冠狀動(dòng)脈介入術(shù)且服用阿司匹林和氯吡格雷雙聯(lián)抗血小板治療的急性冠狀動(dòng)脈綜合征患者。利用血栓彈力圖檢測(cè)二磷酸腺苷(adenosine diphosphate,ADP)刺激下的血小板反應(yīng)性。血小板高反應(yīng)性定義為ADP刺激下的血小板-纖維蛋白凝塊強(qiáng)度(MAADP)大于47毫米。納入臨床常用指標(biāo),采用單因素和多因素logistic回歸分析,篩選出與血小板高反應(yīng)性獨(dú)立相關(guān)的危險(xiǎn)因素。對(duì)于連續(xù)性臨床變量,在分析前,依據(jù)臨床常用界值將其轉(zhuǎn)換為二分類變量。篩選出的與血小板高反應(yīng)性獨(dú)立相關(guān)(P0.05)的臨床危險(xiǎn)因素被納入風(fēng)險(xiǎn)評(píng)分模型,并依據(jù)比值比(OR)大小對(duì)臨床因素進(jìn)行賦分,由此構(gòu)建風(fēng)險(xiǎn)評(píng)分。對(duì)納入本研究的患者追蹤隨訪介入術(shù)后2年不良心腦血管事件包括全因死亡,心原性死亡,心肌梗死,非計(jì)劃血運(yùn)重建、支架內(nèi)血栓和腦卒中。結(jié)果:依據(jù)納入排除標(biāo)準(zhǔn),共2511例行經(jīng)皮冠狀動(dòng)脈介入治療的急性冠狀動(dòng)脈綜合征患者納入本研究。共有781名(31.10%)患者存在血小板高反應(yīng)性。單因素和多因素logistic回歸分析顯示共有五個(gè)臨床因素與血小板高反應(yīng)性獨(dú)立相關(guān),并依據(jù)OR值大小進(jìn)行相應(yīng)賦分:腎功能減低(Scr133umol/L,OR=3.06,95%CI 1.28-7.32)賦 3 分;女性(OR=2.84,95%CI 2.24-3.59)賦 2 分;糖尿病(OR=1.61,95%CI 1.33-1.95)賦1;血小板增多(30×109,OR=1.55,95%CI1 1.07-2.25)賦1分;使用質(zhì)子泵抑制劑(OR=1.25.95%CI 1.02-1.53)賦1分;由此構(gòu)建了 0-8分的血小板高反應(yīng)性臨床風(fēng)險(xiǎn)評(píng)分。依據(jù)患者得分,將患者分為低危組0-2分、中危組3-5分和高危組6-8分。三組血小板反應(yīng)性(TEG-MAADP)分別為 33.88± 17.75mm,45.69± 17.05mm和 50.90± 17.80mm;分別有 587(26.95%),192(58.18%)和 2(66.67%)例患者存在血小板高反應(yīng)性,三組間存在顯著差異(P0.001)。但研究結(jié)果顯示無論是單一事件還是復(fù)合臨床終點(diǎn)主要不良心腦血管事件的發(fā)生率在三組間均無顯著差異。結(jié)論:(1)臨床因素是導(dǎo)致血小板高反應(yīng)性的重要原因之一,臨床風(fēng)險(xiǎn)評(píng)分越高的患者越有可能表現(xiàn)出血小板高反應(yīng)性;(2)臨床風(fēng)險(xiǎn)評(píng)分有助于快速識(shí)別可能存在血小板高反應(yīng)性患者,從而指導(dǎo)個(gè)體化抗血小板治療,且無需額外檢測(cè)、花費(fèi);(3)本研究構(gòu)建的臨床風(fēng)險(xiǎn)因素評(píng)分僅能夠有效地預(yù)測(cè)血小板高反應(yīng)性,對(duì)介入術(shù)后2年的臨床不良事件不能進(jìn)行有效預(yù)測(cè)。
[Abstract]:Background: aspirin combined with clopidogrel is the cornerstone of the treatment of patients with acute coronary syndrome or percutaneous coronary intervention. However, clinical practice has found that there are individual differences in platelet reactivity in antiplatelet therapy. Some patients receive small blood levels after the treatment of aspirin or clopidogrel. The study showed that genetic polymorphisms played a vital role in the individual difference in antiplatelet efficacy. The platelet endothelial aggregation receptor 1 (Platelet Endothelial Aggregation Receptor 1, PEAR1) is a transmembrane protein expressed on the surface of the platelet membrane, The purpose of this study was to investigate the effect of the PEAR1 gene polymorphism of the encoded PEAR1 protein on platelet reactivity after coronary intervention in Chinese coronary heart disease patients with aspirin and clopidogrel antiplatelet therapy. Methods: This study was included in my study from November 2011 to March 2013. All patients were treated with aspirin and clopidogrel antiplatelet therapy in patients who underwent percutaneous coronary intervention. Platelet reactivity under adenosine diphosphate (adenosine diphosphate, ADP) was detected by thrombus mapping. The results were recorded as platelet aggregation inhibition rate (inhibition of platelet aggregat). Ion, IPA).IPA less than 30% is defined as treatment of platelet hyperresponsiveness (high on-treatment platelet reactivity, HTPR); IPA greater than 70% is defined as thrombocytopenia under treatment (low on-treatment platelet). The effect of polymorphism on platelet reactivity. Based on published literature and human genome HAPMAP (http://hapmap.ncbi.nlm.nih.gov/), the PEAR1 single nucleotide polymorphic loci (single nucleotide polymorphism, SNP) in this study were screened using Haploview 4.2 software. The improved multiplicity was used. The genotyping of the PEAR1 gene SNPs was measured by the linked enzyme detection reaction. The differences in the frequency of the SNPs secondary alleles between the HTPR and LTPR two groups were compared. Results: 204 patients had platelet hyperresponsiveness and 201 patients had thrombocytopenia. Based on literature and HAPMAP analysis, a total of 16 PEAR1 SNPs were included in this study to carry out genes. In the.16 SNPs, 5 SNP were found to be significantly associated with platelet aggregation stimulated by ADP. Single factor analysis found that the C secondary allele (p=0.033), rs2644592's G secondary allele (p=0.048), rs3737224 T secondary alleles (0.033), minor alleles, and haploid genes were found in the dominant model. In somatotype analysis, the carrying rate of C-G-T-T-C (p=0.034) in group HTPR was significantly higher than that in group LTPR, indicating a significant correlation with platelet hyperresponsiveness. In the recessive model, the rs57731889 TT homozygote genotypes (p=0.009) and the T-A-C-C-T (p=0.009) in the haplotype analysis were significantly higher in the LTPR group than that in the HTPR group, indicating a significant correlation with the platelet hyper reactivity. Logistic multifactor regression model was used to correct confounding factors and further analysis showed that the T secondary allele (p=0.038) was an independent predictor of platelet hyperresponsiveness, and rs57731889 TT homozygote (p=0.003) was an independent pretest factor for platelet hypo reactivity. Conclusion: (1) the polymorphism of PEAR1 gene and the Chinese crown. Platelet reactivity is closely related to ADP stimulation in patients with heart disease; (2) the effect of different loci of PEAR1 gene polymorphism on platelet function is distinct; (3) rs41273215 leads to platelet hyperresponsiveness, and rs57731889 leads to thrombocytopenia. Background: thrombosis is the core cause of acute coronary syndromes. Platelets are The most important component of thrombus, its adhesion, activation and aggregation plays a vital role in the formation of thrombus, so antiplatelet therapy has become an important cornerstone for preventing thrombosis and reducing the occurrence of adverse events. Clinical practice has found that there are individual differences in antiplatelet efficacy in patients, and some patients with aspirin or Clopidogrel has a resistance phenomenon, which leads to poor efficacy and adverse clinical ischemic events. Platelet endothelial aggregation receptor L (Platelet Endothelial Aggregation Receptor 1, PEAR1) is a transmembrane protein expressed on the surface of platelets and plays an important role in platelet aggregation. The purpose of this study is to explore the analysis of coded PE. The effect of the PEAR1 gene polymorphism of AR1 protein on the clinical prognosis of 1 years after coronary intervention in patients with acute myocardial infarction in China. Methods: This study was included in patients with acute myocardial infarction in our hospital from November 2011 to March 2013. All patients were treated with aspirin and clopidogrel. The PEAR1 gene polymorphic loci (single nucleotide polymorphism, SNP) associated with platelet hyperresponsiveness (SNP), which was associated with platelet hyperresponsiveness, was included in this study to explore their effects on the clinical prognosis. Because this study is an exploratory study, the P value of SNP is incorporated as long as less than 0.1 of the P value is included. The relinked enzyme detection reaction was used to determine the type of PEAR1 gene SNPs. After readmission, the clinic and telephone were followed up for 12 months, including all causes of death, cardiac death, myocardial infarction, unplanned revascularization, and stent thrombosis. Complex ischemic events were defined as cardiogenic death, myocardial infarction, and unplanned. Results: a total of 647 patients with acute myocardial infarction were included in this study according to the exclusion criteria. According to the results of the previous study group, 6 PEAR1 SNPs:rs11264580, rs2644592, rs3737224, rs41273215, rs56260937, and rs822442 related to platelet hyperresponsiveness were included in this study. During the 1 year follow-up, 66 people (10.2%) had adverse clinical events: 8 cases of total death (1.2%), 4 cardiac death (0.6%), 6 myocardial infarction (0.9%), 61 cases (9.4%) due to ischemia driven blood transport and 61 cases (9.4%) without follow-up. In the recessive model analysis, the secondary allele of rs56260937 was compared with the main allele carriers. The incidence of blood transport reconstruction driven by TT homozygous carriers increased significantly (16.7%vs 8.6%, P=0.034). Further using multiple factor Cox regression analysis to correct confounding factors, the results showed that rs56260937 was an independent risk factor for revascularization (HR=2.09,95%CI 1.07-4.06, p=0.031). Conclusion: (1) the polymorphism of PEAR1 gene and the urgency of China The clinical prognosis of 1 years after interventional therapy in patients with myocardial infarction is significantly related; (2) the rs56260937 secondary allele TT homozygous genotype significantly increases the incidence of revascularization events; (3) PEAR1 gene detection, and the future may be used to guide clinical individualized antiplatelet therapy in order to improve the patient's clinical prognosis. Background: antiplatelet therapy Therapy is the cornerstone of the treatment of acute coronary syndrome. However, clinical practice has found that some patients have resistance to platelets, which may lead to high on-treatment platelet reactivity (HTPR). At present, many studies have shown that the clinical factors are responsive to the drug response to patients. Significantly, based on this, our study aims to use clinical indicators to screen out clinical risk factors associated with platelet hyperresponsiveness and to construct a clinical risk score for platelet hyperresponsiveness. The construction of this score will help clinicians to make a rapid and comprehensive assessment of the patient's platelet reactivity, thus giving specific targets. Individualized antiplatelet therapy. Methods: This study was included in patients with acute coronary syndromes from January 2013 to December 2013 at the Fuwai Hospital of the Chinese Academy of Medical Sciences, who received percutaneous coronary intervention and taken aspirin and clopidogrel antiplatelet therapy. The blood thrombus elasto map was used to detect adenosine two (adenosine DIPH). Osphate, ADP) stimulated platelet reactivity. The platelet hyperresponsiveness is defined as the platelet fibrin clot intensity (MAADP) greater than 47 mm under the stimulation of ADP. Inclusion of clinical indicators, using single factor and multifactor logistic regression analysis, screening risk factors independent of platelet hyperresponsiveness. For continuous clinical trials Variables, before analysis, were converted to two categorical variables according to the clinical common boundary value. The clinical risk factors that were screened for independent platelet hyperresponsiveness (P0.05) were included in the risk score model, and the clinical factors were assigned according to the ratio Ratio (OR) size, and the risk score was constructed. The follow-up follow-up of the patients included in this study was followed up. 2 years of adverse cardiac and cerebrovascular events after intervention included all causes of death, cardiac death, myocardial infarction, unplanned blood revascularization, stent thrombosis and stroke. Results: according to the inclusion criteria, 2511 patients with acute coronary syndromes with percutaneous coronary intervention were included in this study. A total of 781 (31.10%) patients were present. Platelet hyperresponsiveness. Single factor and multiple factor Logistic regression analysis showed a total of five clinical factors independent of platelet hyperresponsiveness, and according to the value of OR values: renal dysfunction (Scr133umol/L, OR=3.06,95%CI 1.28-7.32) 3; women (OR= 2.84,95%CI 2.24-3.59) 2; diabetes (OR=1.61,95%CI 1.). 33-1.95) Fu 1; thrombocytosis (30 x 109, OR=1.55,95%CI1 1.07-2.25) 1 points; 1 points using proton pump inhibitor (OR=1.25.95%CI 1.02-1.53); thus, a 0-8 point platelet hyperreactive clinical risk score was constructed. According to the patient's score, the patients were divided into low risk group 0-2, 3-5 in middle risk group and 6-8 in high-risk group. Three platelets reaction. TEG-MAADP was 33.88 + 17.75mm, 45.69 + 17.05mm and 50.90 + 17.80mm, respectively, there were 587 (26.95%), 192 (58.18%) and 2 (66.67%) patients with high reactivity of platelets. There were significant differences between the three groups (P0.001). But the results showed that the major adverse cardiac and cerebrovascular events occurred in either single or compound clinical endpoint. There is no significant difference in the rate between the three groups. Conclusion: (1) the clinical factors are one of the important causes of the hyperresponsiveness of platelets. The more patients with higher clinical risk score, the more likely to show the hyperreactivity of platelets; (2) the clinical risk score is helpful for the rapid identification of patients with high responsiveness to the platelets, thus guiding the individualized antiplatelet. Treatment, without additional detection, costs; (3) the clinical risk factor score constructed in this study can only effectively predict the hyperresponsiveness of the platelets and can not effectively predict the clinical adverse events of the 2 year after intervention.
【學(xué)位授予單位】：北京協(xié)和醫(yī)學(xué)院
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2017
【分類號(hào)】：R541.4

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