冠脉搭桥术后炎症反应与心肌标志物的关系

目的：探讨非体外循环与并行循环方法对心肌损伤和全身炎症反应的差异。方法：选择2009年6月～2010年1月在我院行冠脉搭桥术患者30例,其中选取采用并行循环下不停跳冠脉搭桥术（OnP-BH CABG）和非体外循环冠脉搭桥术（OPCABG）患者各15例,即A组和B组。检测T1（术前）、T2（手术结束时）、T3（术后6小时）、T4（术后12小时）、T5（术后24小时）不同时间点白细胞数量（WBC）、中性粒细胞（PMN）百分比、血浆肿瘤坏死因子-α（TNF-α）、白介素-6（IL-6）、白介素-8（IL-8）、肌钙蛋白I（cTn I）含量,并记录桥血管数量、精神状况、引流量及ICU入住时间。结果：两组血浆WBC总数、PMN%、TNF-α、IL-6、IL-8、cTn I含量T1时无统计学意义（P〉0.05）,T2、T3、T4、T5时均呈升高趋势。A组较B组T2、T3、T4、T5各时间点WBC总数、PMN%、TNF-α、IL-6、IL-8指标升高差异显著（P〈0.01）;cTn I升高幅度略缓,T4、T5差异无统计学意义。比较患者术后精神状况及ICU入住时间,B组均优于A组（P〉0.05）。术中搭桥血管支数无统计学差异、A组引流量较B组多,有统计学意义（p=0.02）。结论：并行循环下不停跳冠脉搭桥术与非体外循环冠脉搭桥术相比,心肌组织损伤略重;体外循环可加重机体全身炎性反应程度,增加神经系统并发症机率。     

冠状动脉TF/TFPI 与急性冠脉综合征关系的研究

目的:研究急性冠脉综合症患者冠状循环局部血液TF/TFPI改变。方法:入选40名冠状动脉造影患者,其中不稳定心绞痛(Unstable pectoris,UP)20例,稳定性心绞痛(Stable pectoris,SP)和正常对照组各10例。所有受试者在冠状动脉造影时,同时经导管抽取主动脉根部、冠状静脉窦和股静脉血样,采用ELISA法测定血浆TF、TFPI水平,计算TF/TFPI比值。结果:三组受检者基本情况均相似,UA组和SA组冠心病危险因素无统计学差异。股静脉血中TF、TFPI浓度及TF/TFPI比值比较:UA组和SA组血TF水平显著高于对照组,UA组血TF水平显著高于SA组。UA组血TFPI水平低于SA组及对照组;SA组血TFPI水平略低于对照组,但未达到统计学意义;UA组血TF/TFPI比值显著高于对照组和SA组,SA组与对照组比较差异无统计学意义。不同部位血TF、TFPI水平及TF/TFPI比值比较:UA组冠状静脉窦血中TF水平较主动脉根部显著升高,CS-AO差值显著高于FV-AO差值;UA组冠状静脉窦血TFPI水平较主动脉根部有升高趋势,但差异无统计学意义,而TF/TFPI比值较主动脉根部升高,差异有统计学意义,CS-AO差值显著高于FV-AO差值。血TF、TFPI水平及TF/TFPI比值在股静脉与主动脉根部之间差异无统计学意义(P>0.05)。SA组和对照组血TF、TFPI水平及TF/TFPI比值三部位间差异无统计学意义。结论:冠脉循环TF/TFPI比值能较敏感地反映ACS的情况。     

冠状动脉TF/TFPI与急性冠脉综合征关系的研究

目的：研究急性冠脉综合症患者冠状循环局部血液TF/TFPI改变。方法：入选40名冠状动脉造影患者,其中不稳定心绞痛（Unstable pectoris,UP）20例,稳定性心绞痛（Stable pectoris,SP）和正常对照组各10例。所有受试者在冠状动脉造影时,同时经导管抽取主动脉根部、冠状静脉窦和股静脉血样,采用ELISA法测定血浆TF、TFPI水平,计算TF/TFPI比值。结果：三组受检者基本情况均相似,UA组和SA组冠心病危险因素无统计学差异。股静脉血中TF、TFPI浓度及TF/TFPI比值比较：UA组和SA组血TF水平显著高于对照组,UA组血TF水平显著高于SA组。UA组血TFPI水平低于SA组及对照组;SA组血TFPI水平略低于对照组,但未达到统计学意义;UA组血TF/TFPI比值显著高于对照组和SA组,SA组与对照组比较差异无统计学意义。不同部位血TF、TFPI水平及TF/TFPI比值比较：UA组冠状静脉窦血中TF水平较主动脉根部显著升高,CS-AO差值显著高于FV-AO差值;UA组冠状静脉窦血TFPI水平较主动脉根部有升高趋势,但差异无统计学意义,而TF/TFPI比值较主动脉根部升高,差异有统计学意义,CS-AO差值显著高于FV-AO差值。血TF、TFPI水平及TF/TFPI比值在股静脉与主动脉根部之间差异无统计学意义（P〉0.05）。SA组和对照组血TF、TFPI水平及TF/TFPI比值三部位间差异无统计学意义。结论：冠脉循环TF/TFPI比值能较敏感地反映ACS的情况。     

胆固醇酯转运蛋白基因多态性与冠心病关系的研究进展

胆固醇酯转运蛋白(CETP)是杀菌蛋白基因家族的重要成员,其主要功能是介导血浆中的胆固醇酯逆向从外周组织转运至肝脏中。目前,CETP基因被广泛认为是冠状动脉疾病(CHD)易感基因之一,CETP基因位点的遗传差异表明其与高密度脂蛋白浓度的变化有关,而高密度脂蛋白的浓度高低与冠心病的形成有很大的关系。因此,CETP的功能、遗传差异及与冠心病的关系是当前心血管疾病研究中的一个热点。本文较全面地阐述了CETP的生物学特性、功能以及CETP基因多态性与冠心病的关系。     

The Relationship Between Serum Levels of Zn and Cu and Severity of Coronary Atherosclerosis

The essential trace elements play important roles in the maintainance of the normal structure and physiology of cells. Several research groups have demonstrated that they also play important roles in states of cardiovascular diseases. Our aim is to investigate whether there is a relationship between trace elements (Zn and Cu) and the degree of atherosclerosis. The sample consisted of 67 patients with coronary artery disease and 26 clinically healthy individuals. Ninety-three subjects were separated into four groups according to their Gensini scores, the number of diseased vessels, the presence of acute coronary syndrome, and ejection fraction. Each group was divided into three subgroups, and serum zinc and copper levels were measured for each individual. The serum levels of zinc and copper were found to be significantly lower in patients with atherosclerosis than in the control group, but there were no significant differences in the serum levels of Cu and Zn between severe atherosclerosis and mild atherosclerosis. In Spearman's rank correlation, the zinc and copper levels were correlated with the Gensini score and the number of diseased vessels. The present study revealed a relationship between the serum levels of zinc and copper and atherosclerosis, but not between these levels and the severity of the disease.     

C反应蛋白、低密度脂蛋白、尿微量白蛋白与冠心病病变程度关系的探讨

炎症在冠心病的发生、发展中起着重要作用,C反应蛋白作为炎症敏感指标是心血管的一个危险标志物;低密度脂蛋白水平升高是冠心病的一个危险因子;尿微量白蛋白作为早期肾损害的独立指标,综合三者或许可从不同方面对冠心病的发生或预后有一定的预测价值.     

Myocardial Revascularization in High-Risk Coronary Patients

It is recognized that postoperative mortality, infarction and the need for inotropic support are increased following myocardial revascularization in highrisk patients. Operations were carried out in 57 such patients in whom one or more of the following factors were present: ventricular dysfunction—ejection fraction less than 0.4 (17), unstable (8) or preinfarction angina (29), evolving infarction (8), recent infarction (less than two weeks before) (5) and refractory ventricular tachyarrhythmia (4). Combined risk factors were present in nine patients. The following principles were utilized to minimize ischemic injury: (1) avoidance of prebypass hypertension and hypotension, (2) avoidance of extreme hemodilution, (3) avoidance of ventricular fibrillation, (4) maintenance of beating empty heart, when possible, (5) the limiting of ischemic periods to less than 12 minutes (hypothermia 32°C) and (6) repaying myocardial oxygen debt with total (vented) bypass, when necessary. The following results were obtained: inotropic support was required in five patients (9 percent), “new” postoperative infarction occurred in five patients (9 percent) and one patient died (2 percent). These results are comparable to those reported in good-risk patients, and indicate that optimal myocardial protection will allow safe revascularization in a high-risk patient.     

血浆IIA 分泌型磷脂酶A2 水平与冠脉支架术后再狭窄关系

目的:测定稳定型冠心病患者支架植入术(percutanous coronary intervention,PCI)前血浆IIA分泌型磷脂酶A2(group IIAsecretory phospholipase A2,ⅡA-sPLA2)的水平,以探讨该酶与冠脉支架术后再狭窄的可能关系。方法:稳定型冠心病行PCI患者63例,非冠心病患者39例,健康正常对照组42例,分别取外周静脉血测定血浆ⅡA-sPLA2酶浓度。PCI患者6个月后复查造影。结果:PCI患者术前该酶浓度显著高于正常对照组(P<0.05),支架内再狭窄率34.9%,再狭窄(restenosis,RS)患者支架术前该酶水平与无再狭窄患者该酶水平无统计学差异(P>0.05)。结论:PCI患者术前血浆ⅡA-sPLA2酶浓度显著高于正常对照组,但可能与支架术后再狭窄无关。     

血浆IIA分泌型磷脂酶A2水平与冠脉支架术后再狭窄关系

目的：测定稳定型冠心病患者支架植入术（percutanous coronary intervention,PCI）前血浆IIA分泌型磷脂酶A2（group IIA secretory phospholipase A2,IIA-sPLA2）的水平,以探讨该酶与冠脉支架术后再狭窄的可能关系。方法：稳定型冠心病行PCI患者63例,非冠心病患者39例,健康正常对照组42例,分别取外周静脉血测定血浆IIA-sPLA2酶浓度。PCI患者6个月后复查造影。结果：PCI患者术前该酶浓度显著高于正常对照组（P〈0．05）,支架内再狭窄率34．9％,再狭窄（restenosis,RS）患者支架术前该酶水平与无再狭窄患者该酶水平无统计学差异（P〉0．05）。结论：PCI患者术前血浆IIA-sPLA2酶浓度显著高于正常对照组,但可能与支架术后再狭窄无关。     

RDW和hs-CRP水平在急性心肌梗死中的表达及与冠状动脉狭窄程度的关系

目的:研究红细胞分布宽度(RDW)和高敏C反应蛋白(hs-CRP)水平在急性心肌梗死中的表达及与冠状动脉狭窄程度的关系。方法:选取2010年1月到2015年1月我院收治的急性心肌梗死患者300例(研究组),另选取单纯心绞痛患者300例(对照组),比较两组RDW、hs-CRP、Gensini评分和冠状动脉病变支数,并分析RDW、hs-CRP和Gensini评分、冠状动脉病变支数的关系。结果:研究组RDW、hs-CRP、Gensini评分和冠状动脉病变支数均显著高于对照组,两组比较差异具有统计学意义(P0.05);冠状动脉Gensini评分和病变支数与RDW、hs-CRP呈正相关关系(r=0.58,0.69,0.49,0.57,P0.05),同时RDW和hs-CRP呈正相关关系(P0.05)。结论:急性心肌梗死患者会出现RDW和hs-CRP水平增高现象,和冠状动脉狭窄程度呈正相关关系。     

白细胞与心肌缺血的关系

炎症是引发心血管疾病的一个重要的危险因子.白细胞数量增多的患者更容易患上急性心肌梗塞、急性冠状动脉等疾病.对临床上白细胞数量高的数据与疾病预测之间的关系,这其中可能有几种机制.测量白细胞的数量和亚群可能是区分急性血管疾病患者危险程度的一种更好的方法.     

急性心肌梗死患者冠状动脉病变严重性与脉压和脉压指数的关系

目的:探讨急性心肌梗死(AMI)患者冠状动脉病变严重程度与脉压和脉压指数的关系.方法:对185例AMI患者进行冠状动脉造影术,冠状动脉病变严重程度用冠状动脉病变支数和Gensini积分来表示,并测定收缩压(SBP)和舒张压(DBP)并计算脉压(PP)及脉压指数(PPI).结果:与脉压＜65mmHg的患者相比,脉压≥65mmHg的患者冠状动脉3支血管病变的患病率和Gensini积分显著增高(P＜0.01).与PPI＜0.500的患者相比,PPI≥0.500的患者冠状动脉3支血管病变的患病率和Gensini积分亦显著增高(P＜0.01).结论:PP和PPI与AMI患者冠状动脉病变程度密切相关,在临床上具有指导作用.     

前列环素、神经肽Y与冠状动脉临界病变的关系及对近期功能性心肌缺血的预测研究

摘要 目的：探讨与研究前列环素（PGI）、神经肽Y（NPY）与冠状动脉临界病变的关系及对近期功能性心肌缺血的预测价值。方法：选择2018年8月到2021年9月本院诊治的80例冠状动脉临界病变患者与80例冠状动脉病变患者分别作为临界组与病例组,同期选择在本院体检的正常冠状动脉人群80例作为正常组,检测三组前列环素、神经肽Y表达水平并进行相关性分析。随访冠状动脉临界病变患者的近期预后并进行功能性心肌缺血的预测分析。结果：病例组、临界组的血清前列环素含量低于正常组,血清神经肽Y含量高于正常组,病例组与临界组对比有明显差异（P<0.05）。病例组、临界组的生理维度、社会维度、心理维度、环境维度等生命质量评分明显低于正常组,病例组也低于临界组（P<0.05）。在240例人群中,Pearson相关性分析显示血清前列环素、神经肽Y含量与冠状动脉临界病变的发生存在相关性（P<0.05）。多因素logistic回归分析显示前列环素、神经肽Y为导致冠状动脉临界病变发生的重要因素（P<0.05）。所有临界组患者预后随访到2022年4月,平均随访时间为31.02±2.58个月,发生功能性心肌缺血21例,发生率为26.3 %。接收者操作特征（ROC）曲线分析显示血清前列环素、神经肽Y预测功能性心肌缺血的曲线下面积分别为0.828、0.836。结论：冠状动脉临界病变患者多伴随有前列环素、神经肽Y表达异常,可导致生命质量下降,前列环素、神经肽Y与冠状动脉临界病变存在相关性,两者预测近期功能性心肌缺血的发生具有很好的价值。     

急性心肌梗死PCI术后早期T波倒置与左室功能的关系

目的:探讨急性ST段抬高心肌梗死直接PCI术后早期T波倒置与左心室功能的关系.方法:对急性ST段抬高心肌梗死直接PCI术后78例患者,以24小时抬高的T波是否倒置分组,采用超声心动描记术检测左室射血分数、心肌活动指数,评价早期T波倒置与左室功能的关系.结果:早期T波倒置组左心功能优于T波未倒置组(P＜0.01),T波深倒置组左心功能优于浅倒置组(P＜0.05).结论:急性ST段抬高心机梗死早期T波倒置可早期评估左心功能、判断预后.     

肠道病毒71型感染小鼠心肌损害与CXCL12/CXCR4通路激活的关系

重症手足口病患儿中心肌损害常见,肠道病毒71型(Enterovirus 71,EV71)是引起手足口病的主要病原体之一,EV71感染小鼠可以出现心肌炎的病理改变,但EV71引起心肌损害的机制尚不明确。为了阐明EV71引起心肌损害的机制,本实验观察了EV71感染小鼠心肌损害与CXC趋化因子配体12(CXC chemokine ligand 12,CXCL12)/CXC趋化因子受体4(CXC chemokine receptor 4,CXCR4)通路激活的关系。BALB/c乳鼠随机分为对照组、EV71组、EV71+AMD3100组、AMD3100组,对照组、AMD3100组给予生理盐水腹腔注射,EV71组、EV71+AMD3100组给予EV71病毒液腹腔注射;而后EV71+AMD3100组、AMD3100组给予CXCR4抑制剂AMD3100腹腔注射、连续7d。比较四组间血清中CXCL12、磷酸肌酸激酶同工酶(CreatineKinase-MB,CK-MB)、乳酸脱氢酶(Lactate dehydrogenase,LDH)含量、心肌病理改变及细胞凋亡率、心肌中CXCR4、含半胱氨酸的天冬氨酸蛋白水解酶-3(caspase-3)表达及肿瘤坏死因子-α(Tumor necrosis factor,TNF-α)、白介素-6(Interleukin-6,IL-6)含量的差异。与对照组比较,EV71组血清中CXCL12、CK-MB、LDH的含量明显增加,心肌出现了典型的心肌炎病理改变且细胞凋亡率、CXCR4及caspase-3表达水平、TNF-α及IL-6含量明显增加;与EV71组比较,EV71+AMD3100组血清中CXCL12、CK-MB、LDH的含量明显降低,心肌的病理改变改善且细胞凋亡率、CXCR4及caspase-3表达水平、TNF-α及IL-6含量明显降低。以上结果表明EV71感染小鼠心肌中CXCL12/CXCR4通路过度激活,该通路的激活介导了心肌细胞凋亡及炎症反应。本研究创新点为阐明了CXCL12/CXCR4通路在EV71病毒感染引起心肌损害中的作用,CXCL12/CXCR4通路激活能够激活EV71感染小鼠心肌的炎症反应及细胞凋亡,这为今后研究手足口病发病过程中心肌损害的机制提供了依据。     

Obesity Affects Myocardial Vasoreactivity and Coronary Flow Response to Insulin

Objective: Obesity is associated with increased risk for cardiovascular diseases and peripheral endothelial dysfunction. We examined whether myocardial vasoreactivity and coronary‐flow response to insulin stimulation are altered in obesity. Research Methods and Procedures: Myocardial blood flow was quantitated in 10 obese men (body mass index, 33.6 ± 1.9 kg/m²) and 10 healthy matched non‐obese men (body mass index, 24.2 ± 1.9 kg/m²), using positron emission tomography and oxygen‐15‐labeled water. The measurements were performed basally and during adenosine infusion (140 μg/kg per minute), with or without simultaneous physiological (1 mU/kg per minute) and supraphysiological (5 mU/kg per minute) hyperinsulinemia. Results: Basal myocardial blood flow was not significantly different between obese and non‐obese subjects. Adenosine‐stimulated flow was blunted in obese (3.2 ± 0.6 mL/g per minute) when compared with non‐obese subjects (4.0 ± 1.1 mL/g per minute, p < 0.05). Simultaneous physiological hyperinsulinemia increased adenosine‐stimulated myocardial flow significantly in both groups (to 4.03 ± 1.24 and 4.85 ± 1.04 mL/g per minute in obese and non‐obese men, respectively; p < 0.05 vs. adenosine). Supraphysiological hyperinsulinemia further enhanced the adenosine‐stimulated flow in non‐obese subjects (to 5.56 ± 0.98 mL/g per minute; p < 0.05) but not in obese subjects. Discussion: Young obese, healthy men have reduced myocardial vasoreactivity, which may represent an early precursor of future coronary artery disease. Additionally, insulin‐induced enhancement of myocardial blood flow is blunted in obesity. Thus, endothelial dysfunction seems to also characterize myocardial vasculature of obese subjects.