冠心病患者胰岛素抵抗与冠脉狭窄程度的关系

选择冠心病(ACS)患者114例,其中稳定型心绞痛(SAP)24例、不稳定型心绞痛(UAP)33例、急性心肌梗死(AMI)26例、冠状动脉造影无狭窄或狭窄小于25%者31例(对照组),测定其血清胰岛素及血糖水平,计算胰岛素敏感指数(ISI),分析冠状动脉狭窄程度与ISI的关系.结果:①UAP组、AMI组ISI较对照组、SAP组明显降低( P＜0.05),SAP组较对照组、AMI组较UAP组降低,但均无统计学意义(P＞0.05);②ISI与其相应的冠状动脉狭窄积分呈显著负相关(r=-0.472,P＜0.05).提示胰岛素抵抗程度可能作为预测急性冠脉综合征及冠状动脉狭窄程度的参考指标之一.     

ACS患者血浆MMP-9及hs-CRP水平与冠状动脉病变的相关性

目的:探讨急性冠状动脉综合征(ACS)患者外周血浆基质金属蛋白酶-9(MMP-9)、超敏C反应蛋白(hs-CRP)水平与冠脉病变的相关性。方法:选择ACS患者60例,其中急性心肌梗死(AMI)30例(AMI组),不稳定型心绞痛(UAP)30例(UAP组);另选同期住院的稳定型心绞痛(SAP)30例(SAP组)及非冠心病患者30例(对照组);采用酶联免疫吸附(ELISA)法分别测定各组患者外周血浆MMP-9及hs-CRP水平,并与冠状动脉造影Gensini积分行相关性分析。结果:各组血浆MMP-9与hs-CRP水平均差异有统计学意义,其中AMI组>UAP组>SAP组>对照组(均P<0.05);与对照组比较,AMI组、UAP组及SAP组Gensini评分均增大(均P<0.05);血浆MMP-9水平与hs-CRP水平呈显著正相关性(r=0.881,P<0.05),血浆MMP-9水平与Gensini评分之间无相关性(r=0.392,P>0.05)。结论:急性ACS患者血浆MMP-9和hs-CRP水平可以预测冠状动脉病变的稳定性,但不能预测病变程度。     

不同类型冠心病患者心率减速力的变化及临床意义

目的定量检测不同临床类型冠心病患者的心率减速力(deceleration capacity of rate,DC)并探讨其临床意义。方法 ?选择经冠状动脉造影明确的冠心病患者72例,其中急性心肌梗死(AMI)28例,不稳定型心绞痛(UAP)28例,稳定型心绞痛(SAP)26例,选择同期在我院冠状动脉造影正常的年龄相当的非冠心病患者25例为对照组,入院后均进行24小时动态心电图检查,应用DC处理软件,计算各组患者的DC值。结果冠心病患者DC值较对照组降低(P<0.05),不同类型冠心病患者中DC值AMI(2.55±1.82)ms相似文献   

不同类型冠心病患者心率减速力的变化及临床意义

目的定量检测不同临床类型冠心病患者的心率减速力(deceleration capacity of rate,DC)并探讨其临床意义。方法 ?选择经冠状动脉造影明确的冠心病患者72例,其中急性心肌梗死(AMI)28例,不稳定型心绞痛(UAP)28例,稳定型心绞痛(SAP)26例,选择同期在我院冠状动脉造影正常的年龄相当的非冠心病患者25例为对照组,入院后均进行24小时动态心电图检查,应用DC处理软件,计算各组患者的DC值。结果冠心病患者DC值较对照组降低(P<0.05),不同类型冠心病患者中DC值AMI(2.55±1.82)ms相似文献   

冠心病患者血清同型半胱氨酸、高敏C-反应蛋白、胱抑素C水平变化及临床意义

目的:探讨冠心病患者血清同型半胱氨酸(Hcy)、高敏C-反应蛋白(hs-CRP)、胱抑素C(CysC)水平变化及临床意义。方法:将临床诊断为冠心病的142例患者分为急性心肌梗死(AMI)组58例、不稳定型心绞痛(UAP)组42例、稳定型心绞痛(SAP)组42例,测定其血清Hcy、hs-CRP、CysC水平,以112例非冠心病患者作对照组。结果:冠心病组血清Hcy、hs-CRP和CysC浓度明显高于对照组;AMI组患者血清Hcy和hs-CRP水平较UAP及SAP组高,而AMI组患者血清CysC水平较UAP及SAP组低。结论:Hcy、hs-CRP和CysC 3者联合检测对预测冠心病发生和发展有一定指导意义。     

冠心病患者冠状动脉病变与免疫细胞的相关研究

目的冠状动脉粥样硬化性心脏病(冠心病)患者冠状动脉粥样硬化病变与免疫细胞的关系。方法选取2014年1月~2016年1月于济宁医学院附属医院治疗的冠心病患者100例,其中急性心肌梗死(AMI)组患者35例、不稳定型心绞痛(UAP)组患者40例、稳定型心绞痛组(SAP)患者25例。同时选取30例健康者作为对照组。采用流式细胞仪检测各组外周血CD4+CD25+调节性T细胞(Treg)和单核细胞CD36比例,同时检测高敏C反应蛋白(hs-CRP)、白细胞介素-17(IL-17)和肿瘤坏死因子-α(TNF-α)水平。结果 AMI组和UAP组外周血CD4+CD25+Treg比例分别为(8.60±1.55)%和(8.17±1.43)%,低于对照组的(10.40±1.43)%和SAP组的(10.72±1.66)%,差异有统计学意义(P均0.05)。与对照组比较,SAP组、AMI组和UAP组单核细胞CD36比例均升高;AMI组和UAP组高于SAP组,差异有统计学意义(P均0.05)。对照组、SAP组、UAP组以及AMI组hs-CRP、IL-17和TNF-α水平均呈升高趋势,差异有统计学意义(P均0.05)。相关性分析结果显示,冠心病患者CD4+CD25+Treg和单核细胞CD36比例与hs-CRP、IL-17、TNF-α等炎症因子水平无明显相关(P均0.05)。结论冠心病患者冠状动脉粥样斑块的不稳定与炎症和免疫反应有关,外周血单核细胞CD36比例明显增加,CD4+CD25+Treg比例明显减低,炎症因子水平升高。     

妊娠相关蛋白-A与冠状动脉斑块形态关系的临床研究

目的 探讨冠心病患者妊娠相关蛋白-A(PAPP-A)与冠状动脉斑块形态的关系及斑块的稳定性.方法 42例冠心病患者分为急性心肌梗死(AMI)组12例,不稳定型心绞痛(UAP)组15例,稳定型心绞痛(SAP)组15例,均行冠状动脉造影(CAG)确诊,16例CAG结果正常者为对照组.采用酶联免疫吸附法(ELISA)测定其PAPP-A水平,分析与冠状动脉斑块形态的关系.结果 PAPP-A在AMI组、UAP组、SAP组和对照组中浓度分别为(16.85±10.30)mIU/L、(15.24±10.51)mIU/L、(8.51±3.10)mIU/L和(8.35±2.01)mIU/L;在AMI和UAP组PAPP-A水平明显高于SAP和对照组(P＜0.01),但在AMI组与UAP组、SAP和对照组之间差异无统计学意义(P＞0.05).PAPP-A在Ⅱ型斑块组明显高于Ⅰ型、Ⅲ型斑块组(P＜0.01),Ⅱ型斑块在AMI组、UAP组中的发生率明显高于SAP组(P＜0.01).结论 PAPP-A参与动脉硬化粥样斑块的发生发展过程,可作为预测斑块稳定性的标志物.Ⅱ型斑块易破裂.     

冠心病病人non-HDL-C、D-D、Fg、EPCs的变化及其与病情的关系

目的探讨非高密度脂蛋白胆固醇(non-HDL-C)、D-二聚体(D-D)、纤维蛋白原(Fg)、循环内皮祖细胞(EPCs)在冠心病病人中的变化及其意义。方法选取2015年1月—2017年10月确诊的冠心病病人200例作为CHD组,其中稳定型心绞痛(SAP)病人90例、不稳定型心绞痛(UAP)病人70例、急性心肌梗死(AMI)病人40例;单支冠状动脉狭窄90例,双支冠状动脉狭窄72例,三支冠状动脉狭窄38例。另选取健康者100名为对照组。对比CHD组与对照组non-HDL-C、D-D、Fg、EPCs水平,并根据冠心病类型、冠状动脉病变支数进行分层分析。结果 CHD组non-HDL-C、D-D、Fg水平均高于对照组(P 0.05),EPCs水平低于对照组(P 0.05);AMI组non-HDL-C、D-D、Fg水平高于SAP组(P 0.05),UAP组与AMI组EPCs水平低于SAP组(P 0.05);AMI组non-HDL-C、D-D、Fg水平均高于UAP组(P 0.05),AMI组EPCs水平低于UAP组(P 0.05);双支冠状动脉病变组、三支冠状动脉病变组non-HDL-C、D-D、Fg水平均高于单支冠状动脉病变组(P 0.05),双支冠状动脉病变组、三支冠状动脉病变组EPCs水平均低于单支冠状动脉病变组(P 0.05);三支冠状动脉病变组non-HDL-C、D-D、Fg水平均高于双支冠状动脉病变组(P 0.05),三支冠状动脉病变组EPCs水平低于双支冠状动脉病变组(P 0.05)。结论冠心病病人的non-HDL-C、D-D、Fg水平均升高,EPCs水平降低,并且与冠状动脉病变程度、冠心病病情变化有关。     

血清C-反应蛋白、可溶性CD40配体、基质金属蛋白酶-2水平与冠心病的相关性

目的:观察不同类型冠心病(CHD)患者血清中C-反应蛋白(CRP)、可溶性细胞分化抗原40配体(sCD40L)、基质金属蛋白酶-2(MMP-2)水平的变化情况,探讨炎性指标与冠状动脉狭窄程度之间的关系及与急性冠状动脉综合征(ACS)间的关系。方法:选取CHD患者65例,包括稳定型心绞痛(SAP)组21例、不稳定型心绞痛(UAP)组22例、急性心肌梗死(AMI)组22例。按Gensini评分法评定其冠状动脉狭窄程度。另16例冠状动脉造影正常者列为对照组。结果:UAP组和AMI组的血清CRP水平均均明显高于SAP组和对照组(均P<0.01),SAP组与对照组差异无统计学意义(P>0.05),AMI组较UAP组明显增高(P<0.01);血清sCD40L水平在对照组、SAP组、UAP组、AMI组逐渐增高,其中AMI组和UAP组较SAP组和对照组的差异有统计学意义(均P<0.01),而在AMI组和UAP组之间以及SAP组和对照组之间,差异无统计学意义(P>0.05);血清MMP-2水平在对照组、SAP组、UAP组、AMI组逐渐升高,且各组间均差异有统计学意义(均P<0.01)。这3个指标与冠状动脉狭窄程度间无相关性(P>0.05)。多元Logistic逐步回归分析显示CRP的风险比值(OR)为1.452,P<0.05;sCD40L的OR值为1.071,P>0.05;MMP-2的OR值为1.152,P<0.05。结论:血清CRP、sCD40L、MMP-2水平能反映CHD的严重程度,并可间接反映冠状动脉斑块的稳定性。CRP、MMP-2可能是ACS发生发展的重要危险因子。     

急性冠状动脉综合症患者血清肿瘤坏死因子-α变化的临床意义

目的探讨肿瘤坏死因子-α(TNF-α)在急性冠状动脉综合征(ACS)患者血清中浓度变化及其意义。方法选取40例ACS患者,其中不稳定型心绞痛(UAP)患者19例,急性心肌梗死(AMI)患者21例。60例非ACS患者,其中稳定型心绞痛(SAP)患者21例,陈旧性心肌梗死(OMI)患者19例。冠状动脉造影正常者20例为正常对照组,采用放射免疫法测定上述病例的血清TNF-α浓度。结果SAP、UAP、AMI、OMI患者血清TNF-α浓度均显著高于正常对照组。ACS组血清TNF-α水平显著高于非ACS组;AMI组血清TNF-α水平显著高于UAP组;SAP组与OMI组血清TNF-α水平无显著性差异;SAP与UAP患者冠状动脉狭窄程度比较无显著性差异。结论TNF-α参与冠心病的形成,并且在ACS的发病中起重要作用。检测血清TNF-α浓度将有助于诊断和预测ACS的发生、发展和预后。     

A heart within a heart

A 44‐year‐old man with a history of end‐stage dilated cardiomyopathy status‐post orthotopic cardiac transplant 14 years ago presented for coronary angiography in preparation for re‐operative tricuspid valve replacement. Coronary angiography revealed an anomalous origin of the left coronary artery, with a common coronary trunk arising from the right coronary cusp and bifurcating into right and left main coronary arteries. Interestingly, the right and left coronary arteries coursed to form the shape of a heart, hence, a heart within a heart! © 2017 Wiley Periodicals, Inc.     

冠心病和心力衰竭

冠心病心力衰竭（简称冠心病心衰）顾名思义是指由于冠心病引起的心力衰竭,据统计大约65％的心力衰竭由冠状动脉疾病引发的。冠心病心衰在临床上分急性和慢性两种,急性心衰主要由急性心肌梗死和急性冠脉缺血诱发的心肌收缩或舒张功能异常所致,慢性心衰主要是心肌梗死后心肌重塑和心肌的血供长期不足,心肌组织发生营养障碍和萎缩,以致纤维组织增生所致。由于冠心病导致心衰的成因不同,因此治疗上的侧重点就会有所不同,下面就对冠心病心衰发病机制及诊治作一浅谈。     

Congenital heart disease and heart failure

The syndrome of heart failure in adult non-congenital heart disease patients includes myocardial disease and ventricular dysfunction. In the presence of congenital abnormalities the cause of heart failure is often multi-factorial and can be a result of the underlying anomaly, surgical intervention, or ventricular dysfunction. Despite the possible clinical similarities, the two conditions are fundamentally different. In congenital heart disease the neurohormonal system is already abnormal even in the absence of clinical manifestations of heart failure and, in many cases, exercise intolerance is related to cyanosis. The approach to heart failure management in the two etiologies might be similar. Preventative attempts to preserve ventricular function in coronary or valve disease parallels early reparative therapy in congenital heart disease Pharmacological therapy is common for the two conditions, despite the limited number of evidence-based recommendations for congenital diseases. In drug-resistant patients, cardiac electrical resynchronization is an established therapy for treating ventricular asynchrony in non-congenital heart failure sufferers, but has only recently been adopted in selected congenital cases. Due to this, congenital heart disease patients are managed in highly specialized unites in close cooperation with cardiologists and surgeons. The ideal follow-up protocol for such patients remains to be determined, particularly in those individuals with subclinical signs of residual cardiac dysfunction. Heart Fail Monit 2008;6(1):2-8.     

Ischemic heart disease and heart weight

Separate weights for heart ventricle walls and interventricular septa were analyzed in 110 hearts with autopsy findings of ischemic heart disease (coronary atherosclerosis, recent or old myocardial infarcts) and with no other cardiac or systemic causes of cardiac enlargement. In hearts with coronary atherosclerosis alone (without old or recent myocardial infarcts) no weight increase was observed in the left ventricle when compared to 29 controls. Patients having infarcts associated with nonstenosing atherosclerosis (less than 50% of the luminal diameter narrowed) of the coronaries had normal heart weights as well. On the contrary, infarcts associated with stenosing coronary sclerosis (narrowing more than 50%) showed significant signs of left ventricular weight increase, which is interpreted as compensatory heart hypertrophy. The greatest degree of hypertrophy was observed in hearts with left ventricular aneurysms.     

Athletes' heart and echocardiography: athletes' heart

Sudden death of competitive athletes is rare. However, they continue to have an impact on both the lay and medical communities. These deaths challenge the perception that trained athletes represent the healthiest segment of modern society. There is an increasing frequency of such reported deaths worldwide and the visibility of this issue is underlined by the high-profile nature of each case. Differential diagnosis between pathological and the physiologic (nonpathological) responses to high levels of physical training has become clinically more important. The purpose of this review is to highlight the main echocardiograph characteristics related to different types of training/sports participation and to highlight already recognized and newer concepts in their clinical assessment.     

The right heart in congenital heart disease

The clinical presentation of right ventricular (RV) dysfunction due to congenital heart disease (CHD) is similar to that of cor pulmonale. RV volume and pressure loads, and primary RV myocardial dysfunction are mechanisms by which CHD affects right heart function. RV volume load may arise from pre-tricuspid left to right shunts (e.g., atrial septal defect) or regurgitant lesions in the right heart (e.g., Ebstein's anomaly of the tricuspid valve and pulmonary insufficiency after repair of tetralogy of Fallot). RV pressure load may be caused by anatomic obstruction to RV outflow and by pulmonary arteriolar hypertension. The latter can result from Eisenmenger syndrome secondary to congenital and postoperative left to right shunts or from defects that cause pulmonary venous hypertension (e.g., pulmonary vein stenosis, cor triatriatum, or mitral stenosis). The RV myocardium may be affected by a primary cardiomyopathy or by congenital abnormalities of the coronary vessels. Finally, CHD may be associated with airway obstruction, scoliosis, or pulmonary emboli, which, in turn, may lead to the development of cor pulmonale. Congenital heart disease, therefore, must be included in the differential diagnosis of patients who present with right ventricular dysfunction.