本文選題：調(diào)脾護(hù)心方 + 急性心肌梗死　； 參考：《安徽中醫(yī)藥大學(xué)》2016年碩士論文

【摘要】：目的:觀察調(diào)脾護(hù)心方對(duì)急性ST段抬高型心肌梗死(STEMI)的臨床療效,心肌酶肌鈣蛋白I(c Tn I)、肌酸激酶同工酶(CK-MB)、肌紅蛋白(MYO)的變化程度及藥物不良反應(yīng),以及實(shí)驗(yàn)觀察對(duì)急性心肌梗死大鼠的肌鈣蛋白T(c Tn T)、乳酸脫氫酶(LDH)、CK-MB,腦鈉肽(BNP),Ca2+-Mg2+ATP酶、Na1+-K1+ATP酶的比較及光鏡下心肌細(xì)胞的病理學(xué)觀察,闡述調(diào)脾護(hù)心方對(duì)STEMI的臨床療效及改善心肌能量代謝作用環(huán)節(jié)及機(jī)制,為調(diào)脾護(hù)心方治療臨床冠心病提供理論和實(shí)驗(yàn)依據(jù)。方法:1.臨床觀察:選擇40例入選患者,中醫(yī)辨證符合入選標(biāo)準(zhǔn)的冠心病STEMI患者,采用隨機(jī)的分組方法,把上述40例患者,分為治療組和對(duì)照組。兩組均給予符合臨床冠心病STEMI治療方案的方法治療。治療組在原有西藥治療的基礎(chǔ)上,同時(shí)加服調(diào)脾護(hù)心方(顆粒劑)。兩組療程均為2周。于治療2周后觀察中醫(yī)證候積分值,并檢測(cè)血清c Tn I、CK-MB、MYO,BNP、LVEF(左室射血分?jǐn)?shù),單位%)水平變化及藥物不良反應(yīng)情況。2.動(dòng)物實(shí)驗(yàn):(1)將64只實(shí)驗(yàn)大鼠編號(hào)后隨機(jī)分為4組,即調(diào)脾護(hù)心方高、低劑量治療組、鹽酸曲美他嗪對(duì)照組、模型手術(shù)組,每組均16只,同時(shí)選取16只相同類型大鼠作為正常對(duì)照組。(2)實(shí)驗(yàn)后采取HE染色制作各組大鼠的心肌標(biāo)本,光鏡下觀察AMI心肌細(xì)胞的病理變化;(3)采用增強(qiáng)化學(xué)發(fā)光法測(cè)定實(shí)驗(yàn)后各組大鼠的血清c Tn T、CK-MB、LDH、BNP水平;(4)采用免疫組織化學(xué)法,檢測(cè)實(shí)驗(yàn)藥物干預(yù)后各組大鼠心肌組織中的Ca2+-Mg2+ATP酶、Na1+-K1+ATP酶含量;(5)所有實(shí)驗(yàn)結(jié)果數(shù)據(jù)均依照SPSS 18.0軟件輸入數(shù)據(jù),再進(jìn)行統(tǒng)計(jì)學(xué)處理。結(jié)果:臨床觀察:1、通過(guò)SPSS軟件分析治療組和對(duì)照組的中醫(yī)證候積分,發(fā)現(xiàn)兩組之間的中醫(yī)證候積分無(wú)顯著性差異(p0.05),兩組分別給予試驗(yàn)設(shè)定治療方案治療后,發(fā)現(xiàn)兩組的中醫(yī)證候積分有如下變化,治療組的中醫(yī)證候積分較對(duì)照組下降明顯(p0.01)。2、治療前兩組c Tn I、CK-MB、MYO、BNP、LVEF水平無(wú)顯著性差異(p0.05),治療后發(fā)現(xiàn),治療組的c Tn I、CK-MB、MYO水平較對(duì)照組顯著降低(p0.01)。3、治療前統(tǒng)計(jì)學(xué)分析得出治療組與對(duì)照組BNP、LVEF指標(biāo)無(wú)顯著性差異(p0.05)。治療后,治療組較對(duì)照組的BNP的下降更明顯(p0.01),治療組的LVEF較對(duì)照組明顯增高(p0.01)。4、臨床觀察期間未發(fā)現(xiàn)調(diào)脾護(hù)心方明顯的藥物不良反應(yīng)。動(dòng)物實(shí)驗(yàn):1.本實(shí)驗(yàn)結(jié)束后對(duì)各組大鼠的心肌酶的變化觀察整理分析,發(fā)現(xiàn)模型對(duì)照組、曲美他嗪組、調(diào)脾護(hù)心方高、低劑量組與正常對(duì)照組比較均有明顯的升高(P0.01);但曲美他嗪組、調(diào)脾護(hù)心方高劑量中藥組、調(diào)脾護(hù)心方低劑量組與模型對(duì)照組比較,這三組的心肌酶均下降明顯(P0.01);而調(diào)脾護(hù)心方高劑量組、調(diào)脾護(hù)心方低劑量組與曲美他嗪組比較發(fā)現(xiàn),調(diào)脾護(hù)心方高劑量組心肌酶與曲美他嗪組較為接近(P0.05),而調(diào)脾護(hù)心方低劑量組與曲美他嗪組比較,心肌酶有較大差異(P0.05)。2.本實(shí)驗(yàn)中發(fā)現(xiàn)實(shí)驗(yàn)后各組大鼠的BNP水平與正常對(duì)照組比較均有明顯升高(P0.01),其中模型對(duì)照組BNP的水平最高。而調(diào)脾護(hù)心方高劑量組、調(diào)脾護(hù)心方低劑量組、曲美他嗪組的BNP水平較模型對(duì)照組有明顯的差異(P0.01),其中調(diào)脾護(hù)心方高劑量組與曲美他嗪組BNP較為接近(P0.05),調(diào)脾護(hù)心方低劑量組的BNP水平與調(diào)脾護(hù)心方低劑量組、曲美他嗪組比較有差異(P0.05)。3.實(shí)驗(yàn)結(jié)束后發(fā)現(xiàn)模型對(duì)照組大鼠心肌細(xì)胞呈空泡樣改變,壞死心肌細(xì)胞核不明顯,鏡下可見大量心肌纖維化表現(xiàn),邊緣散在存活心肌,排列不規(guī)則。調(diào)脾護(hù)心方高劑量組與曲美他嗪組中心肌細(xì)胞均有不同程度的壞死,但整體情況明顯優(yōu)于模型對(duì)照組而低于正常對(duì)照組。調(diào)脾護(hù)心方低劑量組則可見視野區(qū)偏暗,心肌細(xì)胞存活數(shù)、心肌排列緊密度、胞核完整度均較調(diào)脾護(hù)心方高劑量組、曲美他嗪組低。4.實(shí)驗(yàn)后經(jīng)過(guò)對(duì)各組大鼠的Ca2+-Mg2+ATP酶、Na1+-K1+ATP酶的比較發(fā)現(xiàn),其余四組Ca2+-Mg2+ATP酶、Na1+-K1+ATP酶的活力高于模型對(duì)照組(P0.01)。曲美他嗪組、調(diào)脾護(hù)心方高劑量中藥組、調(diào)脾護(hù)心方低劑量中藥組與模型對(duì)照組Ca2+-Mg2+ATP酶、Na1+-K1+ATP酶的比較,發(fā)現(xiàn)有差異(P0.01)。調(diào)脾護(hù)心方高劑量中藥組、調(diào)脾護(hù)心方低劑量中藥組之間的Ca2+-Mg2+ATP酶、Na1+-K1+ATP酶比較也有統(tǒng)計(jì)學(xué)差異性(P0.05)。曲美他嗪組與調(diào)脾護(hù)心方高劑量中藥組的Ca2+-Mg2+ATP酶、Na1+-K1+ATP酶比較無(wú)明顯差異性(P0.05)。結(jié)論:1.調(diào)脾護(hù)心方可降低STEMI患者的心肌損傷標(biāo)志物c Tn I、CK-MB、MYO的水平,可改善心肌缺血,減輕患者臨床癥狀。2.調(diào)脾護(hù)心方可提升STEMI患者的LVEF水平,降低BNP水平,改善心肌梗死后患者的心功能狀況。3.調(diào)脾護(hù)心方可能通過(guò)調(diào)節(jié)AMI模型大鼠心肌細(xì)胞內(nèi)Ca2+-Mg2+ATP酶、Na1+-K1+ATP酶的活性,從而能改善心肌梗死細(xì)胞的能量代謝,達(dá)到治療AMI的目的。4.調(diào)脾護(hù)心方動(dòng)物實(shí)驗(yàn)發(fā)現(xiàn)調(diào)脾護(hù)心方有降低大鼠心肌酶及BNP的效果。5.調(diào)脾護(hù)心方治療AMI可能存在藥物劑量濃度的關(guān)系,在一定范圍內(nèi)加大調(diào)脾護(hù)心方劑量,可達(dá)到治療AMI的最佳效果。6.臨床試驗(yàn)及動(dòng)物實(shí)驗(yàn)均未發(fā)現(xiàn)調(diào)脾護(hù)心方有明顯的藥物不良作用。
[Abstract]:Objective: To observe the clinical efficacy of Tiao PI Hu Xin Fang on acute ST segment elevation myocardial infarction (STEMI), myocardial enzyme troponin I (C Tn I), creatine kinase isoenzyme (CK-MB), myoglobin (MYO) and drug adverse reactions, as well as experimental observation of cardiac troponin T (C Tn T), lactate dehydrogenase (LDH) in acute myocardial infarction rats. The comparison of brain natriuretic peptide (BNP), Ca2+-Mg2+ATP enzyme, Na1+-K1+ATP enzyme and the pathological observation of cardiac myocytes under light microscope, the clinical effect and the improvement of myocardial energy metabolism in the treatment of STEMI by regulating spleen and heart, and providing theoretical and experimental basis for the treatment of coronary heart disease by regulating spleen and heart prescription. Methods: 1. clinical observation: select 40 patients. Patients with coronary heart disease (STEMI) were divided into the treatment group and the control group. The two groups were divided into the treatment group and the control group. The two groups were all accorded with the clinical coronary heart disease (CAD) treatment scheme. On the basis of the original western medicine treatment, the treatment group was added to the spleen and heart prescription (granule). Two groups of treatment courses were taken. 2 weeks. After 2 weeks of treatment, the TCM syndrome scores were observed and serum C Tn I, CK-MB, MYO, BNP, LVEF (left ventricular ejection fraction, unit%) level and drug adverse reactions were observed in animal experiments: (1) 64 experimental rats were randomly divided into 4 groups, namely, the high, low dose treatment group, and the Trimetazine hydrochloride control group. In the operation group, 16 rats in each group were 16, and 16 rats of the same type were selected as the normal control group. (2) after the experiment, the myocardium specimens of the rats were made by HE staining and the pathological changes of the AMI myocardial cells were observed under light microscope. (3) the serum C Tn T, CK-MB, LDH, BNP level of the rats after the experiment were measured by enhanced chemiluminescence; (4) immunization was adopted. Histochemical method was used to detect the Ca2+-Mg2+ATP enzyme and Na1+-K1+ATP enzyme content in the myocardium of each group after the intervention of the experimental drug; (5) all the experimental data were entered into the data according to the SPSS 18 software, and then the statistical treatment was carried out. Results: clinical observation: 1, the TCM syndrome scores of the treatment group and the control group were analyzed by SPSS software, and two groups were found. There was no significant difference in TCM syndrome score (P0.05). After the treatment of the two groups, the TCM syndrome scores of the two groups were found to have the following changes. The TCM syndrome score of the treatment group was significantly lower than the control group (P0.01).2. There was no significant difference (P0.05) between the two groups of C Tn I before treatment, CK-MB, MYO, BNP and LVEF (P0.05). It was found that the level of C Tn I, CK-MB and MYO in the treatment group was significantly lower than that of the control group (P0.01).3. There was no significant difference in LVEF index between the treatment group and the control group before the treatment (P0.05). After treatment, the treatment group was more obvious than the control group (P0.01), and the treatment group was significantly higher than the control group. No obvious adverse drug reaction was found in the prescription of regulating spleen and heart. 1. after the experiment, the changes of myocardial enzymes in the rats were observed and analyzed. The results showed that the model control group, the Trimetazine group, the spleen and the heart of the heart were high, the low dose group was significantly higher than the normal control group (P0.01); but the Trimetazine group, the spleen and the heart of the heart was high. Compared with the model control group, the myocardial enzymes in the three groups were significantly lower than those in the model control group (P0.01), while the high dose group, the low dose group and the trimetazidine group found that the myocardial enzymes in the high dose group were close to that of the trimetazidine group (P0.05), while the low dose of the spleen and the heart was low. Compared with the group of trimetazidine, there was a significant difference in myocardial enzyme between the group and the trimetazidine group (P0.05).2. in this experiment, it was found that the BNP level of the rats in each group was significantly higher than that in the normal control group (P0.01), and the level of BNP in the model control group was the highest. The high dose group, the low dose of the spleen and the nurse heart prescription, the BNP level of the trimetazidine group were more than the model. There was significant difference between the control group and the control group (P0.01), in which the BNP of the high dose and the trimetazidine group was close (P0.05), the BNP level in the low dose group of the spleen and the heart of the spleen and the low dose group was compared with the low dose group of the regulating spleen and the heart, and the group of the Trimetazine group had a difference (P0.05) after the conclusion of the.3. experiment, the myocardial cells in the model control group were vacuolated. The nucleus of the dead heart muscle was not obvious, and a large number of myocardial fibrosis were found under the microscope, the edge scattered in the surviving myocardium and irregular arrangement. There were different degrees of necrosis in the high dose group and the central muscle cells of the group of Trimetazine, but the overall situation was obviously superior to the model control group. The area of the visual field was dark, the number of cardiac myocytes, the tightness of the myocardium and the integrity of the nucleus were all higher than the high dose group of the spleen and heart control. After the low.4. experiment in the group of trimetazidine, the comparison of the Ca2+-Mg2+ATP enzyme and Na1+-K1+ATP enzyme showed that the other four groups of Ca2+-Mg2+ATP enzymes and Na1+-K1+ATP enzyme activity were higher than those of the model control group (P0.01). In the group of zetazine, the high dose Chinese medicine group of regulating spleen and heart prescription, the comparison of the Ca2+-Mg2+ATP enzyme and Na1+-K1+ATP enzyme in the low dose Chinese medicine group with the model control group and the model control group, found the difference (P0.01). The high dose Chinese medicine group with the spleen and heart prescription, the Ca2+ -Mg2+ATP enzyme between the low dose Chinese medicine group and the low dose of the spleen and the heart of the spleen, and the Na1+-K1+ATP enzyme were also statistically different (P0.0 5). There is no significant difference between the Ca2+-Mg2+ATP enzyme and Na1+-K1+ATP enzyme in the high dose group of the trimetazidine group and the high dose of the spleen and heart prescription (P0.05). Conclusion: 1. the spleen protecting heart can reduce the myocardial damage markers of STEMI patients C Tn I, CK-MB, MYO level, can improve the myocardial ischemia, and reduce the clinical symptoms of the patients with the spleen and heart can improve STEMI patients. The level of LVEF, reduce the level of BNP, improve the cardiac function of patients with myocardial infarction,.3. regulating spleen and protecting heart may improve the activity of Ca2+-Mg2+ATP enzyme and Na1+-K1+ATP enzyme in the myocardial cells of AMI model rats, thus can improve the energy metabolism of myocardial infarction cells, and achieve the purpose of treating AMI by regulating spleen and protecting the heart by regulating spleen and protecting spleen. The effect of Xin Fang on reducing myocardial enzyme and BNP in rats.5. may have the relationship of drug dose concentration in the treatment of AMI by regulating spleen and heart prescription, and adding the dosage of spleen protecting heart in a certain range, the best effect of treating AMI can be achieved,.6. clinical trial and animal experiment have not found obvious adverse drug effects in the prescription of regulating spleen and protecting the heart.
【學(xué)位授予單位】：安徽中醫(yī)藥大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2016
【分類號(hào)】：R259

【相似文獻(xiàn)】

相關(guān)期刊論文 前10條

1 李貴才,潘景會(huì),孟憲剛,楊金旗;原發(fā)性血小板增多癥并急性心肌梗死1例報(bào)告[J];新醫(yī)學(xué);2000年02期

2 ;全國(guó)急性心肌梗死學(xué)術(shù)研討會(huì)征文通知[J];中華心血管病雜志;2000年06期

3 李柏英,胡亞軒,馬淑娟;應(yīng)警惕特殊表現(xiàn)的急性心肌梗死[J];邯鄲醫(yī)學(xué)高等專科學(xué)校學(xué)報(bào);2000年04期

4 許文成;以腹脹為首發(fā)癥狀的急性心肌梗死1例[J];邯鄲醫(yī)學(xué)高等�？茖W(xué)校學(xué)報(bào);2000年04期

5 蔡昕,牛淑華,郭玉花,唐宏梅;急性心肌梗死的護(hù)理體會(huì)[J];黑龍江醫(yī)學(xué);2000年05期

6 孫雪蓮,劉鳳奎;急性一氧化碳中毒合并急性心肌梗死3例分析[J];急診醫(yī)學(xué);2000年03期

7 ;急性心肌梗死經(jīng)皮冠狀動(dòng)脈成形術(shù)治療的遠(yuǎn)近期療效[J];嶺南心血管病雜志;2000年04期

8 ;直接經(jīng)皮冠狀動(dòng)脈腔內(nèi)成形術(shù)治療青年人急性心肌梗死療效分析[J];嶺南心血管病雜志;2000年04期

9 洪紹彩,趙麗霞,吳旭輝;急性心肌梗死并發(fā)急性呼吸窘迫綜合征尸檢1例[J];內(nèi)科急危重癥雜志;2000年03期

10 劉荷生,朱曉萍;以呃逆為突出表現(xiàn)的急性心肌梗死1例[J];中國(guó)全科醫(yī)學(xué);2000年06期

相關(guān)會(huì)議論文 前10條

1 顧彬;朱莉;;經(jīng)綠色通道 搶救45例急性心肌梗死分析[A];中華醫(yī)學(xué)會(huì)急診醫(yī)學(xué)分會(huì)第十三次全國(guó)急診醫(yī)學(xué)學(xué)術(shù)年會(huì)大會(huì)論文集[C];2010年

2 龍曉鳳;張維疆;呂振芳;;梗死部位、治療方法對(duì)急性心肌梗死成本-效果的影響[A];第十一次全國(guó)急診醫(yī)學(xué)學(xué)術(shù)會(huì)議暨中華醫(yī)學(xué)會(huì)急診醫(yī)學(xué)分會(huì)成立二十周年慶典論文匯編[C];2006年

3 張梅;;發(fā)病24小時(shí)內(nèi)急性心肌梗死三種治療的療效分析[A];中華醫(yī)學(xué)會(huì)心血管病學(xué)分會(huì)第十次全國(guó)心血管病學(xué)術(shù)會(huì)議匯編[C];2008年

4 扎西多杰;王翔飛;王齊兵;樊冰;葛雷;周京敏;錢菊英;葛均波;;急性心肌梗死患者新發(fā)房顫預(yù)測(cè)因素的前瞻性臨床研究[A];中華醫(yī)學(xué)會(huì)第十五次全國(guó)心血管病學(xué)大會(huì)論文匯編[C];2013年

5 孫海濤;閆志暉;趙子彥;;急性心肌梗死發(fā)病時(shí)間生物學(xué)研究[A];2009全國(guó)時(shí)間生物醫(yī)學(xué)學(xué)術(shù)會(huì)議論文集[C];2009年

6 張抒揚(yáng);;急性心肌梗死的治療原則[A];中華護(hù)理學(xué)會(huì)全國(guó)精神科護(hù)理學(xué)術(shù)交流暨專題講座會(huì)議論文匯編[C];2009年

7 池菊芳;郭航遠(yuǎn);彭放;楊彪;周妍;徐超;;非ST段抬高急性心肌梗死患者的臨床特點(diǎn)及住院事件發(fā)生率[A];中華醫(yī)學(xué)會(huì)第11次心血管病學(xué)術(shù)會(huì)議論文摘要集[C];2009年

8 張抒揚(yáng);;急性心肌梗死的治療原則[A];中華護(hù)理學(xué)會(huì)全國(guó)第7屆糖尿病護(hù)理學(xué)術(shù)交流暨專題講座會(huì)議論文匯編[C];2009年

9 張抒揚(yáng);;急性心肌梗死的治療原則[A];中華護(hù)理學(xué)會(huì)全國(guó)第7屆血液凈化護(hù)理學(xué)術(shù)交流暨專題講座會(huì)議論文匯編[C];2009年

10 張抒揚(yáng);;急性心肌梗死的治療原則[A];中華護(hù)理學(xué)會(huì)全國(guó)內(nèi)科護(hù)理學(xué)術(shù)交流暨專題講座會(huì)議論文匯編[C];2009年

相關(guān)重要報(bào)紙文章 前10條

1 周虹;急性心肌梗死后該怎樣鍛煉？[N];大眾衛(wèi)生報(bào);2007年

2 楊步月;防急性心肌梗死,專家提醒警惕“魔鬼時(shí)間”[N];新華每日電訊;2007年

3 本報(bào)記者 曹玉祥;炎夏尤須防急性心肌梗死[N];醫(yī)藥養(yǎng)生保健報(bào);2008年

4 關(guān)愛;防急性心肌梗死注意魔鬼時(shí)間[N];農(nóng)村醫(yī)藥報(bào)（漢）;2009年

5 本報(bào)記者 王霞;急性心肌梗死治療須“救急”[N];醫(yī)藥經(jīng)濟(jì)報(bào);2012年

6 周穎;北京5所中醫(yī)院聯(lián)合攻研急性心肌梗死[N];中國(guó)中醫(yī)藥報(bào);2004年

7 程守勤　蔣廷玉;“晨練不當(dāng)”頻頻引發(fā)急性心肌梗死[N];新華日?qǐng)?bào);2006年

8 記者 張淑會(huì);石市成立急性心肌梗死救治中心[N];河北日?qǐng)?bào);2009年

9 記者 田雁;我市急性心肌梗死患者呈低齡化趨勢(shì)[N];大同日?qǐng)?bào);2011年

10 記者王淑軍;中醫(yī)藥治療急性心肌梗死作用顯著[N];人民日?qǐng)?bào);2003年

相關(guān)博士學(xué)位論文 前10條

1 李廷武;慢病毒介導(dǎo)的miR-210對(duì)豬急性心肌梗死血管新生影響及機(jī)制的研究[D];鄭州大學(xué);2014年

2 廉慧;極端溫度對(duì)北京地區(qū)居民心血管病發(fā)生的時(shí)間序列分析[D];北京協(xié)和醫(yī)學(xué)院;2016年

3 孫麗敏;丁酰膽堿酯酶對(duì)急性心肌梗死患者預(yù)后作用及其機(jī)制的研究[D];天津醫(yī)科大學(xué);2016年

4 范廣慈;血清松馳素在急性心肌梗死的發(fā)病和預(yù)后中的診斷價(jià)值[D];山東大學(xué);2014年

5 扎西多杰;急性心肌梗死患者并發(fā)新發(fā)房顫的相關(guān)臨床研究[D];復(fù)旦大學(xué);2013年

6 齊曉云;丹參聯(lián)合骨髓間充質(zhì)干細(xì)胞移植對(duì)兔急性心肌梗死后膠原重構(gòu)及心功能的影響[D];遼寧中醫(yī)藥大學(xué);2009年

7 欒云;機(jī)械打孔復(fù)合緩釋支架聯(lián)合干細(xì)胞移植對(duì)急性心肌梗死的作用研究[D];中國(guó)協(xié)和醫(yī)科大學(xué);2010年

8 倪玉霞;冠心Ⅱ號(hào)聯(lián)合骨髓間充質(zhì)干細(xì)胞移植治療急性心肌梗死的實(shí)驗(yàn)研究[D];廣西醫(yī)科大學(xué);2008年

9 農(nóng)一兵;中西醫(yī)結(jié)合治療對(duì)急性心肌梗死遠(yuǎn)期預(yù)后影響的臨床研究[D];北京中醫(yī)藥大學(xué);2005年

10 楊茗;粒細(xì)胞集落刺激因子動(dòng)員自體骨髓干細(xì)胞治療急性心肌梗死的研究[D];復(fù)旦大學(xué);2011年

相關(guān)碩士學(xué)位論文 前10條

1 賴衛(wèi)強(qiáng);表面增強(qiáng)拉曼光譜技術(shù)診斷急性心肌梗死的實(shí)驗(yàn)研究[D];福建醫(yī)科大學(xué);2015年

2 王新潔;急性心肌梗死患者氯吡格雷代謝基因多態(tài)性及其與院內(nèi)不良事件的關(guān)系[D];北京協(xié)和醫(yī)學(xué)院;2015年

3 孔雪;經(jīng)橈動(dòng)脈行急診PCI的急性心�；颊叩脑缙诳祻�(fù)[D];石河子大學(xué);2015年

4 王園園;院前急救中應(yīng)用抗血小板治療對(duì)ST段抬高急性心肌梗死患者近期心血管事件的影響[D];河北醫(yī)科大學(xué);2015年

5 程龍;不同年齡急性心肌梗死發(fā)病及冠脈病變特點(diǎn)分析[D];河北醫(yī)科大學(xué);2015年

6 羅東雷;生長(zhǎng)分化因子-15血清水平及基因多態(tài)位點(diǎn)+2438C/G:rs1058587與急性心肌梗死的相關(guān)性[D];河北醫(yī)科大學(xué);2015年

7 梁樹霞;血清YKL-40水平與急性心肌梗死患者心室重構(gòu)的相關(guān)性研究[D];河北醫(yī)科大學(xué);2015年

8 王剛;碎裂QRS波對(duì)急性心肌梗死長(zhǎng)期預(yù)后的預(yù)測(cè)價(jià)值[D];河北醫(yī)科大學(xué);2015年

9 宋歌;三維與二維斑點(diǎn)追蹤技術(shù)評(píng)價(jià)急性心肌梗死犬左心室局部收縮功能的實(shí)驗(yàn)研究[D];鄭州大學(xué);2015年

10 姜佳慧;大鼠急性心肌梗死后c-kit~+心臟干細(xì)胞增殖分化的時(shí)序觀察[D];復(fù)旦大學(xué);2014年

，

本文編號(hào)：2096943