本文選題：虛擬組織學(xué)血管內(nèi)超聲 + 靜脈移植血管　； 參考：《天津醫(yī)科大學(xué)》2017年碩士論文

【摘要】：目的:連續(xù)入選于天津市胸科醫(yī)院就診并在血管內(nèi)超聲(Intravenous Ultrasound,IVUS)的指導(dǎo)下選擇于靜脈移植血管(Saphenous Vein Graft,SVG)行經(jīng)皮冠狀動脈介入治療(Percutaneous Coronary Intervention,PCI)的冠狀動脈旁路移植術(shù)(Coronary Artery Bypass Grafting,CABG)后再發(fā)心絞痛的患者,通過研究這些患者的臨床基線資料、實驗室化驗指標(biāo)、冠狀動脈造影(Coronary Arteriography,CAG)復(fù)查結(jié)果、既往CABG基本情況及虛擬組織學(xué)血管內(nèi)超聲(Virtual Histology Intravascular Ultrasound,VH-IVUS)的檢查結(jié)果,探討分析導(dǎo)致SVG介入治療出現(xiàn)慢復(fù)流或無復(fù)流現(xiàn)象的危險因素,以及VH-IVUS在該慢復(fù)流或無復(fù)流現(xiàn)象中的預(yù)測價值,同時根據(jù)隨訪結(jié)果,探索VH-IVUS在SVG介入治療的SVGD患者預(yù)后的預(yù)測價值。方法:于2015年4月—2016年9月在天津市胸科醫(yī)院就診的CABG術(shù)后再發(fā)心絞痛患者中,連續(xù)入選經(jīng)冠狀動脈和移植血管造影復(fù)查證實SVG病變狹窄大于或等于50%的需要PCI術(shù)治療的患者32例,收集研究對象的臨床基線資料、既往CABG基本情況、心臟彩超及左心室射血分?jǐn)?shù)(LVEF)及入院血常規(guī)、生化常規(guī)等實驗室檢驗結(jié)果,并在IVUS指導(dǎo)下SVG介入治療,所有患者在PCI前均進(jìn)行IVUS及VH-IVUS檢查,測量病變SVG狹窄最重處管腔橫截面積(Lumen Cross-sectional Area,Lumen CSA)、外彈力膜橫截面積(External Elastic Membrane Cross-sectional Area,EEM CSA)、斑塊負(fù)荷,利用VH軟件重建靶病變的組織圖像,測量病變SVG病變總體長度、總體斑塊體積、壞死核心組織總體積的絕對值及該組織成分占斑塊總體積的組織比例、致密鈣化組織總體積的絕對值及該組織成分占斑塊總體積的組織比例、纖維組織總體積的絕對值及該組織成分占斑塊總體積的組織比例、纖維脂質(zhì)組織總體積的絕對值及該組織成分占斑塊總體積的組織比例;測量病變SVG狹窄最重處壞死核心組織面積的絕對值及其占狹窄最重處斑塊面積的比值、致密鈣化組織面積絕對值及其占狹窄最重處斑塊面積的比值、纖維組織面積絕對值及其占狹窄最重處斑塊面積的比值、纖維脂質(zhì)組織面積絕對值及其占狹窄最重處斑塊面積的比值等數(shù)據(jù),根據(jù)PCI術(shù)后的評價性CAG的校正TIMI記幀(Corrected TIMI Frame Count,CTFC)測定結(jié)果,當(dāng)CTFC28時定義為正常血流,當(dāng)CTFC≥28時定義為慢血流,完全無前向血流定義為無復(fù)流,將患者分為慢復(fù)流或無復(fù)流組(n=6)及正常復(fù)流組(n=26),分析導(dǎo)致SVG介入治療出現(xiàn)慢復(fù)流或無復(fù)流現(xiàn)象的危險因素,以及VH-IVUS在該慢復(fù)流或無復(fù)流現(xiàn)象中的預(yù)測價值,同時根據(jù)隨訪結(jié)果,探索VH-IVUS在SVG介入治療的SVGD患者預(yù)后的預(yù)測價值。結(jié)果:共入選患者32例,包括慢復(fù)流或無復(fù)流組患者6例、正常復(fù)流組患者26例。對比兩組患者的臨床基線資料發(fā)現(xiàn),正常復(fù)流組患者和慢復(fù)流組或無復(fù)流組患者的收縮壓水平(SBP:136.92±19.75 vs.116.50±12.23)差異具有統(tǒng)計學(xué)意義(P0.05)。對比兩組患者的血常規(guī)化驗及生化常規(guī)化驗結(jié)果發(fā)現(xiàn),慢復(fù)流或無復(fù)流組患者和正常復(fù)流組患者紅細(xì)胞平均體積(94.25±9.20 vs.88.96±4.55)、總膽固醇水平(TC:4.79±0.89 vs.4.01±0.74)及高密度脂蛋白膽固醇(HDL-C:1.25±0.40 vs.0.98±0.23)差異均具有統(tǒng)計學(xué)意義(P0.05)。根據(jù)線性回歸結(jié)果,提示病變SVG狹窄最重處的斑塊負(fù)荷同纖維組織的比值呈負(fù)相關(guān)(R2=0.234,P=0.005)而同纖維脂質(zhì)組織的比值呈正相關(guān)(R2=0.123,P=0.049);病變SVG狹窄最重處的斑塊面積同纖維組織的比值呈負(fù)相關(guān)(R2=0.192,P=0.012)。對比兩組患者的病變SVG的VH-IVUS檢查結(jié)果發(fā)現(xiàn),慢復(fù)流或無復(fù)流組患者和正常復(fù)流組患者的病變長度(79.43±48.68 vs.47.28±29.14)、病變SVG壞死核心組織比例(23.12±10.09 vs.14.39±7.79)、病變SVG致密鈣化組織比例(7.33±4.66 vs.3.09±3.42)、病變SVG纖維組織比例(58.82±6.53 vs.66.32±5.55)、病變SVG狹窄最重處壞死核心組織面積(2.07±1.57 vs.0.75±0.78)、病變SVG狹窄最重處壞死核心組織比值(23.38±12.72 vs.12.52±10.86)、病變SVG狹窄最重處致密鈣化組織面積(0.30±0.17 vs.0.07±0.13)及病變SVG狹窄最重處致密鈣化組織比值(3.85±2.18 vs.1.30±2.44)的結(jié)果存在差異,且均具有統(tǒng)計學(xué)意義(P0.05)。單因素Logistic回歸分析結(jié)果表明,患者收縮壓水平[OR(95%CI):1.093(1.007~1.186),P=0.033]及病變SVG纖維組織比例[OR(95%CI):1.241(1.038~1.484),P=0.018]的增高是SVG介入治療的保護(hù)因素,而患者總膽固醇(TC)水平[OR(95%CI):0.311(0.096~1.000),P=0.050]、病變SVG壞死核心組織比例[OR(95%CI):0.887(0.790~0.996),P=0.043]、病變SVG致密鈣化組織比例[OR(95%CI):0.786(0.627~0.985),P=0.036]、病變SVG狹窄最重處壞死核心組織面積[OR(95%CI):0.328(0.118~0.915),P=0.033]以及病變SVG狹窄最重處致密鈣化組織面積[OR(95%CI):0.000(0.000~0.120),P=0.008]的增高是SVG介入治療出現(xiàn)慢復(fù)流或無復(fù)流現(xiàn)象的危險因素。將具有共線性的病變SVG纖維組織比例、病變SVG壞死核心組織比例、病變SVG致密鈣化組織比例、病變SVG狹窄最重處壞死核心組織面積及病變SVG狹窄最重處致密鈣化組織面積合并成VH-IVUS影響因子之后,應(yīng)用多因素Logistics回歸分析顯示,VH-IVUS影響因子[OR(95%CI):3.800(1.103~13.085),P=0.034]是SVG介入治療出現(xiàn)慢復(fù)流或無復(fù)流現(xiàn)象的獨立危險因素。應(yīng)用Kaplan-Meier生存曲線Log-rank檢驗顯示:中期隨訪慢復(fù)流或無復(fù)流組患者對比正常復(fù)流組患者,無MACE生存率(66.7%vs.88.5%,P=0.118)、無致命性MI生存率(66.7%vs.92.3%,P=0.056)及無嚴(yán)重心絞痛生存率(66.7%vs.88.5%,P=0.118)均存在下降趨勢,差異無統(tǒng)計學(xué)意義(P0.05),慢復(fù)流或無復(fù)流組與正常復(fù)流組比較,無嚴(yán)重心力衰竭生存率(83.3%vs.100%,P=0.037)差異存在統(tǒng)計學(xué)意義(P0.05)。單因素Cox回歸分析顯示:患者病變SVG纖維組織比例[OR(95%CI):0.832(0.706~0.980),P=0.028]增高是SVG介入治療后MACE事件發(fā)生的保護(hù)因素,病變SVG壞死核心組織比例[OR(95%CI):1.262(1.066~1.493),P=0.007]、病變SVG狹窄最重處壞死核心組織面積[OR(95%CI):3.201(1.396~7.336),P=0.006]的增高是SVG介入治療后MACE事件發(fā)生的危險因素,多因素Cox回歸分析顯示:患者病變SVG壞死核心組織比例[OR(95%CI):1.439(1.055~1.962),P=0.022]增高是SVG介入治療后MACE事件發(fā)生的獨立危險因素。結(jié)論:病變SVG狹窄最重處的斑塊負(fù)荷同纖維組織的比值負(fù)相關(guān)而同纖維脂質(zhì)組織的比值呈正相關(guān);病變SVG狹窄最重處的斑塊面積同纖維組織的比值呈負(fù)相關(guān)。單因素Logistic回歸分析提示,患者更高的收縮壓水平以及更高病變SVG纖維組織比例是SVG介入治療慢復(fù)流或無復(fù)流的保護(hù)因素,而患者總膽固醇水平、病變SVG壞死核心組織比例、病變SVG致密鈣化組織比例、病變SVG狹窄最重處壞死核心組織面積以及病變SVG狹窄最重處致密鈣化組織面積的增高是SVG介入治療出現(xiàn)慢復(fù)流或無復(fù)流現(xiàn)象的危險因素。多因素Logistic回歸分析提示,VH-IVUS影響因子是SVG介入治療出現(xiàn)慢復(fù)流或無復(fù)流現(xiàn)象的獨立危險因素。Kaplan-Meier生存曲線Log-rank檢驗提示,中期隨訪慢復(fù)流或無復(fù)流組患者的無嚴(yán)重心力衰竭生存率低于正常復(fù)流組。檢驗同時提示慢復(fù)流或無復(fù)流組患者的無MACE生存率、無致命性MI生存率及無嚴(yán)重心絞痛生存率均較正常復(fù)流組有下降趨勢。單因素Cox回歸分析提示,患者病變SVG纖維組織比例增高是SVG介入治療后MACE事件發(fā)生的保護(hù)因素,病變SVG壞死核心組織比例、病變SVG狹窄最重處壞死核心組織面積的增高是SVG介入治療后MACE事件發(fā)生的危險因素,多因素Cox回歸分析顯示:患者病變SVG壞死核心組織比例增高是SVG介入治療后MACE事件發(fā)生的獨立危險因素。
[Abstract]:Objective: to select the coronary artery bypass graft (Percutaneous Coronary Intervention, PCI) for the coronary artery bypass grafting (Percutaneous Coronary Intervention, PCI) under the guidance of Intravenous Ultrasound (IVUS) in the Tianjin Thoracic Hospital and to select Saphenous Vein Graft (SVG) for the coronary artery bypass grafting (Percutaneous Coronary Intervention, PCI). CABG) patients with recurrent angina pectoris were studied by studying the clinical baseline data, laboratory test indicators, Coronary Arteriography (CAG) reexamination results, previous CABG basic situation and the examination results of the virtual histologic intravascular ultrasound (Virtual Histology Intravascular Ultrasound, VH-IVUS). The risk factors of slow reflow or non reflow phenomenon in SVG intervention, and the predictive value of VH-IVUS in the slow reflow or reflow phenomenon, and the predictive value of the prognosis of VH-IVUS in the SVGD patients with SVG intervention according to the follow-up results. Methods: CABG operation in Tianjin Thoracic Hospital from April 2015 to September 2016. In the patients with recurrent angina pectoris, 32 patients with SVG stenosis greater than or equal to 50% were selected through coronary artery and angiography reexamination. The clinical baseline data of the subjects were collected, the basic information of previous CABG, cardiac color Doppler and left ventricular ejection fraction (LVEF), admission blood routine, biochemical routine, and so on were collected. The results of laboratory test, and SVG intervention under the guidance of IVUS, all patients performed IVUS and VH-IVUS before PCI, and measured the most severe transverse area of the lumen of SVG stenosis (Lumen Cross-sectional Area, Lumen CSA), the transverse area of the outer elastic membrane, and the patch load. The total length of SVG lesions, the total plaque volume, the absolute value of the total volume of the necrotic core tissue, the proportion of the tissue composition in the total volume of the tissue, the absolute value of the total volume of the dense calcified tissue, the proportion of the tissue composition in the total volume of the plaque, the absolute volume of the fibrous tissue, were measured. The absolute value of the total volume of the tissue, the absolute value of the total volume of the fibrous tissue and the proportion of the tissue in the total volume of the plaque, the absolute value of the necrotic core area of the most serious SVG stenosis and the ratio of the area in the most serious area of the stenosis, and the absolute value of the compact calcified tissue area and its absolute value. The ratio of the area of the most severe plaque, the absolute value of fibrous tissue area and the ratio of the area of the most serious area of the stenosis, the absolute value of the area of the fibrous tissue and the ratio of the most serious area of the plaque, were measured by the corrected TIMI frame (Corrected TIMI Frame Count, CTFC) by the evaluation of the evaluation of PCI after the operation. CTFC28 is defined as normal blood flow. When CTFC > 28 is defined as slow flow, no forward flow is defined as no complex flow, and the patients are divided into slow reflow or non reflow group (n=6) and normal reflow group (n=26), and the risk factors that lead to slow reflow or non reflow phenomenon in SVG intervention therapy, and VH-IVUS in the slow reflow or no reflow phenomenon are analyzed. The predictive value of VH-IVUS was also evaluated according to the follow-up results. Results: the prognostic value of VH-IVUS in patients with SVG intervention was investigated. Results: 32 patients were enrolled, including 6 patients with slow reflow or no reflow group and 26 patients in normal reflow group. The clinical baseline data of the two groups were compared with the normal reflow group, the slow reflow group or the non reflow group. The difference of systolic blood pressure level (SBP:136.92 + 19.75 vs.116.50 + 12.23) was statistically significant (P0.05). The average volume of red blood cells (94.25 + 9.20 vs.88.96 + 4.55) and total cholesterol level in patients with slow reflow or non reflow group and normal reflow group were compared with those of two groups. (TC:4.79 The difference between 0.89 vs.4.01 + 0.74) and high density lipoprotein cholesterol (HDL-C:1.25 + 0.40 vs.0.98 + 0.23) had statistical significance (P0.05). According to the linear regression results, the plaque load in the most severe SVG stenosis was negatively correlated with the ratio of fibrous tissue (R2=0.234, P= 0.005), and was positively correlated with the ratio of fibrous tissue (R2=0.123) (R2=0.123). P=0.049); the plaque area in the most severe SVG stenosis was negatively correlated with the ratio of fibrous tissue (R2=0.192, P=0.012). The pathological changes of the patients with slow reflow or no reflow group and normal reflow group were (79.43 + 48.68 vs.47.28 + 29.14), and the proportion of SVG necrotic core tissue (23) in the two groups of patients with the lesion of SVG (23 .12 + 10.09 vs.14.39 + 7.79), the proportion of SVG dense calcified tissue in the lesion (7.33 + 4.66 vs.3.09 + 3.42), the proportion of SVG fibrous tissue (58.82 + 6.53 vs.66.32 + 5.55), the most severe necrotic core area (2.07 + 1.57 vs.0.75 +) in the lesion of SVG stenosis, and the ratio of the most serious necrotic core tissue in the lesion of SVG stenosis (23.38 + 12.72 vs.12.52 +%). The densest calcified tissue area of the most severe SVG stenosis (0.30 + 0.17 vs.0.07 + 0.13) and the ratio of dense calcified tissue in the most severe SVG stenosis (3.85 + 2.18 vs.1.30 + 2.44) were different, and all were statistically significant (P0.05). The single factor Logistic regression analysis showed that the systolic pressure level of the patients was [OR (95%CI): 1.093 (1.007~1.186). The proportion of P=0.033] and pathological SVG fibrous tissue [OR (95%CI): 1.241 (1.038~1.484), the increase of P=0.018] is the protective factor of SVG interventional therapy, and the total cholesterol (TC) level of the patient is [OR (95%CI): 0.311 (0.096~1.000) and P=0.050]. (95%CI): 0.786 (0.627~0.985), P=0.036], [OR (95%CI) of the most severe necrotic core area of the lesion of SVG: 0.328 (0.118~0.915), P=0.033], and the dense calcified tissue area of the most severe SVG stenosis, [OR (95%CI): 0 (0.000~0.120), which is a risk factor for the slow reflow or no reflow phenomenon in the interventional therapy. The proportion of collinear SVG fibrous tissue, the proportion of SVG necrotic core tissue, the proportion of SVG dense calcified tissue in the lesion, the most heavy necrotic core area of the lesion of SVG stenosis and the densest calcified tissue area of the SVG stricture of the lesion into VH-IVUS influencing factors, the multiple factor Logistics regression analysis should be used to show the influence of VH-IVUS. Factor [OR (95%CI): 3.800 (1.103~13.085), P=0.034] is an independent risk factor for slow reflow or no reflow phenomenon in SVG intervention therapy. The Kaplan-Meier survival curve Log-rank test showed that patients with slow reflow or no reflow group were compared with normal reflow patients at medium term follow-up, without MACE survival (66.7%vs.88.5%, P=0.118), and no fatal MI survival. The rate (66.7%vs.92.3%, P=0.056) and the survival rate of no severe angina (66.7%vs.88.5%, P=0.118) had a downward trend, the difference was not statistically significant (P0.05). There was a significant difference between the slow reflow or the non reflow group and the normal reflow group (83.3%vs.100%, P= 0.037) (P0.05). Single factor Cox regression analysis showed that there was a significant difference (P0.05). The proportion of SVG fibrous tissue in patients with [OR (95%CI) was 0.832 (0.706~0.980), and the increase of P=0.028] was the protective factor of MACE event after SVG intervention. The proportion of SVG necrotic core tissue was [OR (95%CI): 1.262 (1.066~1.493), P=0.007], and the increase of necrotic core tissue area of the lesion: 3.201 The risk factors of MACE event after SVG interventional therapy. Multiple factor Cox regression analysis showed that the proportion of SVG necrotic core tissue in patients with [OR (95%CI): 1.439 (1.055~1.962) and P=0.022] increased as an independent risk factor for MACE event after SVG interventional therapy. Conclusion: the ratio of plaque load to fibrous tissue is negative in the heaviest stenosis of disease variable SVG stenosis. The correlation was positively correlated with the ratio of fibrous tissue; the area of the most severe SVG stenosis was negatively correlated with the ratio of fibrous tissue. Single factor Logistic regression analysis suggested that higher systolic blood pressure and higher SVG fibrous tissue ratio were protective factors for slow reflow or non reflow of SVG interventional therapy. Total cholesterol level, the proportion of SVG necrotic core tissue, the proportion of SVG dense calcified tissue, the most heavy necrotic core area of SVG stenosis and the increase of the densest calcified tissue area in the most severe SVG stenosis are the risk factors for the slow reflow or no reflow phenomenon in the SVG interventional therapy. Multifactor Logistic regression analysis The VH-IVUS impact factor was an independent risk factor.Kaplan-Meier survival curve Log-rank test for slow reflow or no reflow phenomenon in SVG intervention therapy. The survival rate of no severe heart failure in patients with slow reflow or non reflow group was lower than that of normal reflow group at the mid-term follow-up. The test also indicated that there was no MACE in patients with slow reflow or no reflow group. The survival rate, the non fatal MI survival rate and the survival rate of no severe angina were all lower than those of the normal reflow group. The single factor Cox regression analysis suggested that the increase in the proportion of SVG fibrous tissue in the patients was the protective factor of the MACE event after SVG intervention, the proportion of the necrotic core tissue in the pathological changes, and the most serious necrosis core of the necrotic SVG stenosis. The increase of the product was a risk factor for the occurrence of MACE events after SVG intervention. Multiple factor Cox regression analysis showed that the increase in the proportion of SVG necrotic core tissue in the patients was an independent risk factor for the occurrence of MACE events after SVG intervention.
【學(xué)位授予單位】：天津醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R541.4

【參考文獻(xiàn)】

相關(guān)期刊論文 前9條

1 陳偉偉;高潤霖;劉力生;朱曼璐;王文;王擁軍;吳兆蘇;李惠君;顧東風(fēng);楊躍進(jìn);鄭哲;蔣立新;胡盛壽;;《中國心血管病報告2015》概要[J];中國循環(huán)雜志;2016年06期

2 吳海波;徐殊;王強;都業(yè)君;趙科研;王輝山;;冠狀動脈旁路移植術(shù)中應(yīng)用內(nèi)窺鏡采集大隱靜脈的技術(shù)要點及近期效果評價[J];中國胸心血管外科臨床雜志;2015年01期

3 梁國慶;姜鐵民;陳少伯;張建起;趙季紅;;冠狀動脈分叉病變的血管內(nèi)超聲虛擬組織學(xué)影像特點[J];介入放射學(xué)雜志;2012年04期

4 Vincent G DeMarco;Adam T Whaley-Connell;James R Sowers;Javad Habibi;Kevin C Dellsperger;;Contribution of oxidative stress to pulmonary arterial hypertension[J];World Journal of Cardiology;2010年10期

5 梁國慶;陳少伯;趙季紅;姜鐵民;李玉明;;血管內(nèi)超聲虛擬組織學(xué)成像的技術(shù)原理與臨床應(yīng)用的探討[J];醫(yī)療衛(wèi)生裝備;2010年04期

6 陳鑫;徐明;石開虎;蔣英碩;汪黎明;邱志兵;肖立瓊;趙海鵬;劉培生;王睿;鄭林;;再次冠狀動脈旁路移植術(shù)的臨床應(yīng)用[J];中國胸心血管外科臨床雜志;2007年06期

7 胡曉鵬;許建屏;胡盛壽;宋云虎;孫寒松;徐波;;冠狀動脈旁路移植術(shù)后橋血管造影特點分析[J];中國心血管病研究雜志;2007年02期

8 李世康;龍村;何巍;彭青云;周華富;郭建極;;高鉀停搏液中鎂離子對冠狀動脈張力的影響[J];中華胸心血管外科雜志;2006年04期

9 李世康,龍村,程邦昌,劉唐威,何巍,陳銘伍,史世勇;組氨酸-色氨酸-酮戊二酸與威斯康星大學(xué)溶液對冠狀動脈內(nèi)皮細(xì)胞的影響[J];中華實驗外科雜志;2003年04期

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