快速三维MR血管壁成像评估急性脑梗死及颈动脉粥样硬化的研究

本研究探讨在脑梗死及颈动脉粥样硬化斑块评估中,快速三维MR血管壁成像技术的应用价值。选取颈动脉粥样硬化斑块患者78例,共计斑块112个,其中发生脑梗死患者36例,未发生脑梗死患者42例。与病理结果比较,快速三维MR血管壁成像评估颈动脉斑块性质一致性Kappa值为0.790(P<0.05);不稳定性斑块MR积分明显高于稳定性斑块(P<0.05);脑梗死患者甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)和平均MR积分明显高于无脑梗死患者(P<0.05),而高密度脂蛋白胆固醇(HDL-C)明显低于无脑梗死患者(P<0.05);平均MR积分预测脑梗死的ROC曲线下面积为0.852(P<0.05)。因此,快速三维MR血管壁成像技术能有效评估颈动脉粥样硬化斑块性质,对预测脑梗死有一定应用价值。     

冠心病患者血清钙、镁、铁、铜、铬、铝变化的临床观察

观察血清钙、镁、铁、铜、铬、铝与不同类型冠心病的关系,将冠心病患者分为三组:(1)冠状动脉痉挛30例;(2)稳定型心绞痛(SAP)患者27例;(3)急性冠脉综合症(ACS)患者35例,以34例健康者为对照组(NC),利用ICP-AES法测定了其血清钙、镁、铁、铜、铬、铝。结果表明,与正常对照组比较,钙水平在冠状动脉痉挛组和稳定型心绞痛组偏低(P<0.05或P<0.01),男性急性冠脉综合症组血清铝偏低(P<0.05)。提示血清钙水平下降可能与稳定型心绞痛及冠状动脉痉挛有关,而男性血清铝水平下降可能与急性冠脉综合症有关。     

冠状动脉CTA定量评估稳定型心绞痛患者斑块进展及其在心血管事件中的预测价值

本文对非创伤性血管成像技术(CTA)定量评估稳定型心绞痛患者的冠状动脉斑块进展及其在心血管事件中的预测价值进行了分析。选取2017年1月~2017年12月我院心血管科142例因新发症状或症状加重随访行两次冠状动脉CT血管造影(CCTA)的稳定型心绞痛患者作为研究对象,根据后期随访患者是否有主要不良心脏事件发生进行分组,其中82例发生主要不良心脏事件的患者作为观察组,60例未发生主要不良心脏事件的患者作为对照组,定量评估稳定型心绞痛患者斑块的进展情况。结果显示:观察组患者有糖尿病、高血脂、吸烟史的比例均高于对照组,差异有统计学意义(P<0.05)。两组随访CCTA总体斑块负荷率、冠状动脉直径狭窄率比较差异有统计学意义(P<0.05);两组斑块进展方面,脂质斑块负荷率、纤维斑块负荷率、钙化斑块负荷率、总体斑块负荷率、冠状动脉直径狭窄率比较差异有统计学意义(P<0.05)。通过多因素Logisitic回归分析,脂质斑块负荷进展与基线高血脂有关(P<0.05),总体斑块负荷进展与基线高血脂具有相关性(P<0.05),冠状动脉直径狭窄率进展与糖尿病、高血脂、吸烟史具有相关性(P<0.05)。本文证实了CCTA检查是检测稳定型心绞痛患者斑块负荷进展的一种有效方法,且心血管危险因素能加快稳定型心绞痛患者负荷进展。     

脑胶质瘤磁共振弥散张量成像定量参数与VEGF、MMP-9表达的相关性

本研究旨在分析脑胶质瘤患者的磁共振弥散张量成像(DTI)参数与病变组织血管内皮生长因子(VEGF)和基质金属蛋白酶-9(MMP-9)表达的相关性,以及DTI参数对脑胶质瘤进行分级诊断的价值。根据病理分级将102例脑胶质瘤患者分为低级别组(47例)和高级别组(55例),均行MRI和DTI检查,定量测定表观弥散系数(ADC)、各向异性分数(FA)、相对ADC(rADC)、相对FA(rFA)值及相对轴向扩散系数(rAD)值;用免疫组化法检测VEGF和MMP-9表达情况。结果显示,高级别组患者的rADC、ADC、rAD、FA、rFA均低于低级别组(P<0.05);高级别组患者的VEGF和MMP-9阳性表达均高于低级别组(P<0.05)。rADC、ADC、rAD、FA、rFA与VEGF和MMP-9表达均呈负相关(P<0.05);rADC、ADC、rAD、FA、rFA对脑胶质瘤分级诊断的AUC均具有一定诊断价值(P<0.05)。本研究结果提示DTI定量参数与脑胶质瘤VEGF和MMP-9表达具有相关性,且有助于脑胶质瘤的分级诊断。     

高分辨MRI 3D黑血技术诊断颈动脉斑块的研究

本研究探讨高分辨磁共振成像(MRI)3D黑血技术判断颈动脉斑块位置及预测脑卒中的应用价值。选取缺血性脑卒中患者68例(观察组),同时选取健康体检者50例作为对照组,给予高分辨MRI 3D黑血技术检查,分析两组黑血技术参数差异,同时采用ROC曲线分析参数预测脑卒中的价值。共检出颈动脉粥样硬化斑块82处;高分辨MRI 3D黑血技术颈动脉斑块检出率为95.12%;观察组颈动脉血管总面积(TVA)、管壁面积(WA)及管壁标准化指数(NWI)明显高于对照组(P<0.05);观察组缺血侧TVA明显高于非缺血侧(P<0.05);TVA、WA及NWI预测脑卒中的ROC曲线下面积分别为0.801、0.825和0.842(P<0.05)。高分辨MRI 3D黑血技术判断颈动脉斑块位置有较好的价值,颈动脉定量指标在脑卒中预测中有一定应用价值。     

双源CT双能量参数联合血清miR-126、miR-204检测对肺癌诊断价值及与临床病理特征关联性

回顾性选取肺癌患者86例为肺癌组,同期肺良性结节患者86例为对照组,患者均行双源CT双能量、血清miR-126、miR-204水平检测,发现静脉期标准化碘浓度(NIC)、动脉期NIC、miR-204、miR-126水平在肺癌组中呈异常表达,并与肺癌组病理类型、临床分期、淋巴结转移存在一定相关性,三者联合对肺癌具有一定诊断价值。同时经Kaplan-Meier生存分析可知,肺癌组静脉期NIC、动脉期NIC高水平患者生存率低于低水平患者,而miR-126、miR-204高水平患者生存率高于低水平患者(P<0.05)。早期采用双源CT双能量、血清miR-126、miR-204联合诊断,可为临床诊治、预后评估提供循证指导。     

超微血管成像及超声造影技术评价慢性肾功能不全患者颈动脉粥样硬化斑块稳定性的研究

应用超微血管成像(SMI)和超声造影(CEUS)技术对慢性肾功能不全患者颈动脉粥样硬化斑块内新生血管进行评估。选取318例慢性肾功能不全患者为研究对象,利用SMI及CEUS技术,对322个斑块进行检查,评估其新生血管的检出情况。结果显示,颈动脉粥样硬化斑块的新生血管在低回声或以低回声为主导的混合性回声斑块中出现较多,斑块内新生血管的显现明显高于强回声斑块组(P<0.01),两种方法对于新生血管的评估基本一致。超微血管成像及超声造影技术可以发现更多的不稳定性斑块,CEUS中超声增强强度越大,SMI中新生血管越多,则斑块不稳定的风险就越大,慢性肾功能不全患者发生缺血性脑病的风险也越高。     

颈动脉超声筛查脑卒中高危人群颈动脉易损斑块与ACR、ALBU的相关性研究

本研究探讨颈动脉超声筛查脑卒中高危人群颈动脉易损斑块与尿微量白蛋白/肌酐(ACR)、尿微量白蛋白(ALBU)的相关性。选取307例脑卒中高危患者,根据颈动脉超声检查将其分为:无颈动脉斑块组112例、颈动脉稳定斑块组45例和颈动脉易损斑块组150例。研究发现,各组年龄≥60岁占比、有脑卒中家族史占比以及颈动脉内中膜厚度(IMT)、ACR、ALBU水平对比存在明显差异(P0.05);脑卒中高危人群IMT与ACR、ALBU呈正相关(P0.05);年龄、脑卒中家族史、IMT、ACR、ALBU均为脑卒中高危人群颈动脉斑块发生的影响因素(P0.05);IMT、ACR、ALBU联合在颈动脉斑块诊断、易损斑块鉴别诊断方面均具有较高效能。这些结果可以证实,脑卒中高危人群IMT与ACR、ALBU呈正相关,早期联合IMT、ACR、ALBU检查,可辅助临床诊断颈动脉斑块、鉴别诊断易损斑块。     

增强CT联合血清指标诊断结直肠癌的价值

本文探讨癌胚抗原(CEA)、糖类抗原19-9(CA19-9)、胰岛素样生长因子结合蛋白-3(IGFBP-3)及增强CT在结直肠癌中的联合诊断效果。选取100例结直肠癌患作为观察组,同时选取结直肠良性肿瘤患者60例作为对照组,检测血清CEA、CA19-9、IGFBP-3,同时给予增强CT检查。观察组血清CEA和CA19-9高于对照组(P<0.05),而IGFBP-3低于对照组(P<0.05);TNM分期Ⅲ~Ⅳ和Ⅰ~Ⅱ患者血清CEA、CA19-9和IGFBP-3差异比较有统计学意义(P<0.05);增强CT联合血清指标联合诊断灵敏性为89.00%、特异性为90.00%;增强CT诊断结直肠癌T分期、N分期与病理结果Kappa值分别为0.696和0.790(P<0.05)。CEA、CA19-9、IGFBP-3联合增强CT是一种具有较高效能的结直肠癌诊断方法。     

MSCTP参数及基质金属蛋白酶在急性脑缺血介入治疗前后的变化和对预后的预测价值分析

选取急性脑缺血患者122例,均采取介入治疗,治疗前后均行多层螺旋CT灌注成像(MSCTP)检查,并检测患者血清基质金属蛋白酶-9(MMP-9)和基质金属蛋白酶抑制剂-1(TIMP-1)水平。结果发现,介入治疗后7 d,患者缺血边缘区和缺血中央区的相对脑血流量(rCBF)高于介入治疗前,相对平均通过时间(rMTT)短于介入治疗前,血清MMP-9、TIMP-1低于介入治疗前;缺血边缘区和缺血中央区rCBF及血清MMP-9联合预测急性脑缺血预后不良的曲线下面积为0.933。由本研究结果可知,介入治疗后7 d,急性脑缺血患者缺血边缘区和缺血中央区rCBF升高,rMTT缩短,血清MMP-9和TIMP-1水平下调,而且联合预测对评估急性脑缺血患者预后具有一定价值。     

Upregulation of extracellular matrix metalloproteinase inducer (EMMPRIN) and gelatinases in human atherosclerosis infected with Chlamydia pneumoniae: the potential role of Chlamydia pneumoniae infection in the progression of atherosclerosis

Chlamydia pneumoniae infection implicated as an important etiologic factor of atherosclerosis, especially in coronary artery disease (CAD), was found in vitro to be associated with the induction of matrix metalloproteinases (MMPs). An extracellular matrix metalloproteinase inducer (EMMPRIN)/ membrane-type 1 matrix metalloproteinase (MT1-MMP) system which induces and activates MMPs, is suggested to be functional and were upregulated in the failing myocardium. However, the upstream regulation of MMPs by C. pneumoniae within atheroma itself remains unclear. We evaluated the seroepidemiologic study of C. pneumoniae infection in CAD patients (n= 391) and controls (n=97) and performed histopathological and in vitro analysis in atherosclerotic vascular tissues obtained from patients with seropositive to C. pneumoniae (n=20), by using immunochemistry for C. pneumoniae, EMMPRIN/MT1-MMP, MMP-2, and MMP-9. The seropositive rates of both anti-C. pneumoniae IgG and IgA were 56.7% in CAD group and 43.3% in control group (P=0.033). Seropositive rate was increased in subgroups of CAD patients without conventional coronary risk factors compared to those with conventional risk factors. Immunoreactivities of EMMPRIN, MT1-MMP, MMP-2, and MMP-9 were increased in the atheromatous plaque itself, predominantly in immunoreactive macrophages/mononuclear cells to C. pneumoniae. Furthermore, Western blot analysis showed that EMMPRIN and MMP-2 were detected more prominently in atherosclerotic tissues infected with C. pneumoniae compared to control tissues. Zymographic analysis revealed that activities of MMP-2 and MMP-9 were more increased in atherosclerotic tissues infected with C. pneumoniae compared to control tissues. The present study demonstrated upstream regulation of MMPs can be induced by C. pneumoniae within atheromatous plaque itself. These findings help to understand the potential role of C. pneumoniae in the progression of atherosclerosis.     

Detection of altered extracellular matrix in surface layers of unstable carotid plaque: an optical spectroscopy, birefringence and microarray genetic analysis

Erosion and rupture of surface layers in atherosclerotic plaque can cause heart attack and stroke; however, changes in luminal surface composition are incompletely defined. Laser-induced fluorescence spectroscopy (LIFS), with limited tissue penetration, was used to investigate the surface of unstable carotid plaque and correlated with microscopy, birefringence and gene expression. Arterial matrix collagens I, III and elastin were assessed in unstable plaques (n = 25) and reference left internal mammary arteries (LIMA, n = 10). LIFS in addition to selective histological staining with picrosirius red, Movat pentachrome and immunostaining revealed decreased elastin and increased collagen I and III (P < 0.05) in carotid plaque when compared with LIMA. Within plaque, collagen I was elevated in the internal carotid region versus the common carotid region. Polarized light microscopy detected layers of aligned collagen and associated mechanical rigidity of the fibrous cap. Microarray analysis of three carotid and three LIMA specimens confirmed up-regulation of collagen I, III and IV, lysyl oxidase and MMP-12. In conclusion, LIFS analysis coupled with microscopy revealed marked regional differences in collagen I, III and elastin in surface layers of carotid plaque; indicative of plaque instability. Birefringence measurements demonstrated mechanical rigidity and weakening of the fibrous cap with complementary changes in ECM gene expression.     

Circulating Levels of Dephosphorylated-Uncarboxylated Matrix Gla Protein in Patients with Acute Coronary Syndrome

Vascular calcification contributes to the pathogenesis of coronary artery disease while matrix Gla protein (MGP) was recently identified as a potent inhibitor of vascular calcification. MGP fractions, such as dephosphorylated-uncarboxylated MGP (dp-ucMGP), lack post-translational modifications and are less efficient in vascular calcification inhibition. We sought to compare dp-ucMGP levels between patients with acute coronary syndrome (ACS), stratified by ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI) status. Physical examination and clinical data, along with plasma dp-ucMGP levels, were obtained from 90 consecutive ACS patients. We observed that levels of dp-ucMGP were significantly higher in patients with NSTEMI compared to STEMI patients (1063.4 ± 518.6 vs. 742.7 ± 166.6 pmol/L, p < 0.001). NSTEMI status and positive family history of cardiovascular diseases were only independent predictors of the highest tertile of dp-ucMGP levels. Among those with NSTEMI, patients at a high risk of in-hospital mortality (adjudicated by GRACE score) had significantly higher levels of dp-ucMGP compared to non-high-risk patients (1417.8 ± 956.8 vs. 984.6 ± 335.0 pmol/L, p = 0.030). Altogether, our findings suggest that higher dp-ucMGP levels likely reflect higher calcification burden in ACS patients and might aid in the identification of NSTEMI patients at increased risk of in-hospital mortality. Furthermore, observed dp-ucMGP levels might reflect differences in atherosclerotic plaque pathobiology between patients with STEMI and NSTEMI.     

Biomarker Discovery of Acute Coronary Syndrome Using Proteomic Approach

Acute coronary syndrome (ACS) is a condition in which the coronary artery supplying blood to the heart is infarcted via formation of a plaque and thrombus, resulting in abnormal blood supply and high mortality and morbidity. Therefore, the prompt and efficient diagnosis of ACS and the need for new ACS diagnostic biomarkers are important. In this study, we aimed to identify new ACS diagnostic biomarkers with high sensitivity and specificity using a proteomic approach. A discovery set with samples from 20 patients with ACS and 20 healthy controls was analyzed using mass spectrometry. Among the proteins identified, those showing a significant difference between each group were selected. Functional analysis of these proteins was conducted to confirm their association with functions in the diseased state. To determine ACS diagnostic biomarkers, standard peptides of the selected protein candidates from the discovery set were quantified, and these protein candidates were validated in a validation set consisting of the sera of 50 patients with ACS and 50 healthy controls. We showed that hemopexin, leucine-rich α-2-glycoprotein, and vitronectin levels were upregulated, whereas fibronectin level was downregulated, in patients with ACS. Thus, the use of these biomarkers may increase the accuracy of ACS diagnosis.