miRNA―1和急性心肌梗死后心肌缺血程度的相關(guān)性研究

1、mirna-1和急性心肌梗死后心肌缺血程度的相關(guān)性研究摘要目的 研究循環(huán)mirna-1和急性心肌梗 死后心肌缺血程度的相關(guān)性。方法 入選經(jīng)冠狀動(dòng)脈造 影確診為非急性心肌梗死的冠狀動(dòng)脈粥樣硬化性心臟 病患者為對(duì)照組;符合2012年全球統(tǒng)一心肌梗死定義 的急性st段抬高心肌梗死患者為實(shí)驗(yàn)組；對(duì)兩組病例 采集血液標(biāo)本，采用qpcr技術(shù)檢測(cè)mirna-1表達(dá)水 平；同時(shí)對(duì)實(shí)驗(yàn)組進(jìn)行acc/aha冠脈造影評(píng)分，比較 兩組間mirna-1表達(dá)水平差異，并進(jìn)一步分析實(shí)驗(yàn)組 mirna-1表達(dá)水平和acc/aha冠脈造影評(píng)分的相關(guān)性。 結(jié)果入選42例病例，對(duì)照組21例，實(shí)驗(yàn)組21例。兩 組病例的micrna-

2、1相對(duì)表達(dá)量差異有統(tǒng)計(jì)學(xué)意義(p關(guān)鍵詞mirna-1；急性心肌梗死；心肌缺血中圖分類號(hào)r542.22 文獻(xiàn)標(biāo)識(shí)碼a 文章編號(hào) 1674-0742 (2015) 06 (c) -0003-03abstract objective to study the correlation between mirna-1 and the degree of myocardial ischemia after acute myocardial in fa ret i on (ami) methods the cor on ary atherosclerotic heart disease patients d

3、iagnosed with non-acute myocardial infarction by percuta neous translumi nal cor on ary angioplasty(ptc a) were selected as the control group, and cor on ary atherosclerotic heart disease patie nts with ami and acute st segment elevation met the criteria of the 2012 third universal definition of myo

4、cardial infarction were selected as the experimental group blood samples were obtained the expression level of mirna-1 was detected by real-time quantitative polymerase chain reaction (qpcr) detecting system. acc/aha score was evaluated in the experimental group the expression of mirna-1 was compare

5、d between the two groups and the correlation between the expression of mirna-1 and acc/aha score in the experimental group was further analyzed results 42 patients were selected and divided into the control group and the experimental group with 21 cases in each there was statistically significant di

6、fferenee in the relative expression of mirna(p=0.00021資料與方法1.1 一般資料1.1.1入選標(biāo)準(zhǔn)2013年12月一2014年3月入選 符合2012年全球統(tǒng)一心肌梗死定義的經(jīng)冠狀動(dòng)脈造 影確診為急性心肌梗死患者為實(shí)驗(yàn)組；非急性心肌梗 死的冠狀動(dòng)脈粥樣硬化性心臟病患者為對(duì)照組。急性心肌梗死診斷標(biāo)準(zhǔn)：根據(jù)2012年第三次心 肌梗死全球統(tǒng)一定義推薦的診斷標(biāo)準(zhǔn)制定。檢測(cè)到 心肌壞死標(biāo)志物（主要是肌鈣蛋白ctn）水平上升和/ 或下降，至少有1次超過(guò)參考值上限的第99%百分位 值，并至少伴有下列一項(xiàng)缺血的癥狀。 心肌缺血的癥狀； 新發(fā)生的缺血性ecg改

7、變（新發(fā)的st-t改變或 新出現(xiàn)左束支傳導(dǎo)阻滯（lbbb）； 心電圖出現(xiàn)病理性q波； 影像學(xué)證據(jù)顯示有新的心肌活性喪失或新發(fā)的 局部室壁運(yùn)動(dòng)異常；（5）冠狀動(dòng)脈造影或尸檢發(fā)現(xiàn)冠狀動(dòng)脈內(nèi)存在新 鮮血栓。1.1.2排除標(biāo)準(zhǔn) 先天性心臟病、慢性阻塞性肺病、 心功能衰竭、呼吸衰竭、腫瘤、近期感染、貧血等患 者排外。1.2研究方法1.2.1 一般情況記錄患者性別、年齡，危險(xiǎn)因素 包括高血壓、糖尿病、高脂血癥及吸煙病史。1.2.2血漿mirna-1檢測(cè) 在發(fā)病68 h采集血液 標(biāo)本，采用 qpcr （real-time quantitative pcr detectingsystem)技術(shù)檢測(cè)mirna-

8、1表達(dá)水平。1.2.3冠脈造影和冠脈造影評(píng)分目前主要用于冠 狀動(dòng)脈造影評(píng)估血管病變的評(píng)分方法有l(wèi)eaman評(píng)分 法、gensini評(píng)分法、美國(guó)心臟病學(xué)會(huì)/美國(guó)心臟學(xué)會(huì)(acc/aha)評(píng)分法和syntax評(píng)分法。acc/aha評(píng)分 法是冠狀動(dòng)脈造影指南推薦的冠狀動(dòng)脈病變?cè)u(píng)分法， 冠狀動(dòng)脈樹劃分簡(jiǎn)單易行，計(jì)算方便，也能較好的反 映冠狀動(dòng)脈病變的嚴(yán)重程度4。該研究采用acc/aha 評(píng)分法對(duì)入選病例進(jìn)行冠脈造影評(píng)分，評(píng)估冠狀動(dòng)脈 病變的嚴(yán)重程度。常規(guī)經(jīng)橈動(dòng)脈途徑或股動(dòng)脈入路， 按美國(guó)心臟病學(xué)會(huì)和美國(guó)心臟協(xié)會(huì)(acc/aha)的冠 狀動(dòng)脈造影指南，采用judkins法取7個(gè)體位造影。分 別選擇左主干

9、、左前降支近段、前降支中段、第丨對(duì) 角支、左回旋支近段、左回旋支中段、右冠脈近段、 右冠脈中段8支主要血管段根據(jù)acc/aha評(píng)分法進(jìn)行 評(píng)分。若間隔支、第2對(duì)角支、鈍緣支及前降支遠(yuǎn)段 中任一血管的直徑超過(guò)上述8支中的任一血管，即用 該血管取代直徑較小的血管。所選血管按其狹窄最嚴(yán) 重處評(píng)分，狹窄小于10%為0分,狹窄10%49%為1 分，狹窄50%74%為2分，狹窄75%89%為3分. 狹窄90%100%為4分。每支血管的權(quán)重系數(shù)均為1。 每支血管的冠脈評(píng)分二每支血管的權(quán)重系數(shù)x狹窄程度權(quán)重系數(shù)。最后總分為8支血管評(píng)分的總和。1.3統(tǒng)計(jì)方法采用spss 16.0統(tǒng)計(jì)軟件進(jìn)行數(shù)據(jù)分析，計(jì)量資料

10、以均數(shù)士標(biāo)準(zhǔn)差(x±s)表示，行t檢驗(yàn)，計(jì)數(shù)資料 以頻數(shù)表示，并進(jìn)行相關(guān)性分析，p0.05)(表1)。2.2兩組間mirna-1相對(duì)表達(dá)水平的比較急性心肌梗死組mirna-1相對(duì)表達(dá)量2-delta ct 為(4.268±0.9562),非心肌梗死組mirna-1相對(duì)表 達(dá)量 2-delta ct 為(0.3597±0.07215)；對(duì)兩組 mirna-1 相對(duì)表達(dá)量2-delta ct進(jìn)行t檢驗(yàn)發(fā)現(xiàn)急性心肌梗死組 mirna-1表達(dá)水平明顯增高，差異有統(tǒng)計(jì)學(xué)意義(p 參考文獻(xiàn)1 chen j f, mandel e m, thomson j m, et al.t

11、he role of microrna-1 and microrna-133 in skeletal muscle proliferation and differentiationj. nat genet, 2006,38 (2)： 228-233.2 van rooij e, sutherland l b, qi x， et al.control of stressdependent cardiac growth and gene expression by a micrornaj. scienee, 2007,316(5824)：575-579 3 yunhui cheng, ning

12、tan, jian yang, et al.atranslational study of circulating cell-free microrna-1 inacute myocardial in fa ret i on卩.clin sei (lon d), 2010, 119 (2)：87-954 馬梅，尹滸嘩，賈文軍，等.不同冠狀動(dòng)脈評(píng) 分方法評(píng)價(jià)冠心病嚴(yán)重程度的關(guān)系研究j.中國(guó)循環(huán) 雜志，2007 (22)： 340-342.5 guangwen long，feng wang, quanlu duan, et al. human circulating microrna-1 and

13、microrna-126 as potential novel indicators for acute myocardialin fa ret i onj in ter nation al jour nal biological scie nces, 2012, 8(6) : 811-818.6 han zx, lin qx, deng cy, et al.mir-l/mir-206 regulate hsp60 sexpression contributing to glucose-mediated apoptosis in cardiomyocytesj. febs letters, 2

14、010 (584)： 3592-3600.7 xu cq, lu yj, pan zw, et al.the muscle-spec hie micror nas mir-1 and mir-133 produce opposing effects on apoptosis by targeting hsp60, hsp70 and caspase-9 in cardiomyocytesj. journal of cell science, 2007 (120)： 3045-30528 tang yh，zheng jy，sun y，et al. microrna-1 regulates car

15、diomyocyte apoptosis by targeting bd-2j. international heart journal, 2009 (50)： 377-387.9 terentyev d, belevych ae, terentyeva r, et al.mir-1 overexpression enhances ca2+ release and promotes cardiac arrhythmogenesis by targeting pp2a regulatory sub unit b56 alph and causi ng camkii-dependent hyper

16、phosphorylation of ryr2j.circulation research, 2009, 104 (4)： 514-521.10 yang bf, lin hx，xiaojn, et al.the muscle-specific microrna mir-1 regulates cardiac arrhythmogenic potential by targeting gjal and kcnj2j. nature medicine, 2007 (13)： 486-491.11 care a, catalucci d, felicetti f, et al.microrna-133 controls cardiac hypertrophyj. nat med, 2007,13 (5)：613-61812 sayed d, hong c, chen iy, et al. micrornasplay an embryessential role in th