用户名: 密码: 验证码:
冠心病合并糖尿病患者血小板参数与炎症反应的相关性研究
详细信息    本馆镜像全文|  推荐本文 |  |   获取CNKI官网全文
摘要
第一部分冠心病合并糖耐量减低患者血小板参数与hsCRP的相关性研究
     目的:
     冠心病患者具有较高的糖代谢受损及糖尿病发生率。近年来研究表明,血小板除具有凝血功能外,尚有调控免疫反应和参与炎症反应的功能。有学者将糖尿病时活性增强的血小板称为“糖尿病血小板”。C反应蛋白(C reactive protein, CRP)是全身炎症反应的非特异性标志,也是目前最可靠的动脉粥样硬化的炎症的标记物,是疗效评估以及预后监测指标。C反应蛋白是一种急性时相蛋白,由肝脏合成。动脉粥样硬化的炎性变化,可以促使肝脏内C反应蛋白合成增加,血清中C反应蛋白含量增加。同时C反应蛋白能增强其他炎性物质的作用,是炎性反应的重要参与者。目前有关冠心病并糖耐量减低人群中血小板参数变化与相互关系的研究国内外报道较少,本研究通过检测冠心病合并糖耐量减低患者血小板四项参数、hsCRP及其相关性,了解冠心病合并糖耐量减低患者炎症程度及血小板的功能状态,为加强糖耐量减低人群心血管并发症的防治提供一定的理论依据。
     方法:
     研究病例分为二组:A组(冠心病同时合并糖耐量减低)及B组(正常对照组)。A组39名已确诊冠心病(CHD)同时合并糖耐量减低(IGT)的病例来自“阿卡波糖心血管评价(ACE)试验”武汉大学人民医院研究分中心。该试验选自2009年12月~2012年9月在武汉大学人民医院心内科2科住院治疗的冠心病并糖耐量减低(IGT)患者,男25例,女14例;年龄50~76岁,平均63±8岁。B组(病例对照组)来源于武汉大学人民医院心内科二科2011年9月~2012年9月住院患者,均因阵发性室上性心动过速而行射频消融术,年龄之50岁。共收集病例对照组17例,其中男性10例,女性7例,年龄,平均年龄62±5岁(50-71岁)。
     观察内容包括:
     1.病人性别、年龄、相关危险因素,包括既往冠心病、高血压病、高脂血症及糖尿病史;
     2.入院后实验室检查:心肌酶(CTnI, CK-MB,Myo)、糖耐量试验、血小板参数、血脂(TC, TG, HDL,LDL,Lpa)及高敏感度C反应蛋白(hs-CRP);
     3.心电图检查;
     4.冠状动脉造影或冠脉CTA结果;
     统计学:
     采用SPSS inc的SPSS10.0软件包进行统计学分析,所有指标均先进行正态性检验。符合正态分布且方差齐的计量资料以均数±标准差(x±SD)表示。不符合正态分布的指标以中位数表示。计数资料采用χ2检验。计量资料组间比较采用One-Way ANOVA检验,组内比较采用t检验。变量间相关性采用Spearman's rho等级相关分析。以p<0.05为差异具有显著性意义。
     结果:
     1.冠心病合并糖耐量减低患者与对照组患者一般临床特征及实验室检测指标比较:冠心病合并糖耐量减低组与病例对照组比较,空腹血糖高于病例对照组,高密度脂蛋白胆固醇则低于病例对照组,差异显著有统计学意义;体重指数、血压、甘油三酯、总胆固醇、低密度脂蛋白胆固醇差异无统计学意义。
     2.血小板参数及hsCRP的比较:A组血小板三项参数MPV、PDW、P-LCR及hsCRP高于B组,PLT则低于B组,差异有统计学意义。
     3.糖尿病合并糖耐量减低患者血小板参数及其与hsCRP之间的相关性分析:Spearman's rho等级相关分析表明,在冠心病合并糖耐量减低组PLT与MPV、PDW及P-LCR负相关,P-LCR、PDW、MPV之间正相关。hsCRP与PLT呈负相关,与MPV、PDW及P-LCR呈正相关。
     结论:
     1.冠心病合并糖耐量减低患者存在较高的血小板活性及C反应蛋白水平。血小板体积增大、活性增加以及C反应蛋白水平增加可能与冠状动脉粥样硬化的形成、血栓的形成有关。
     2.冠心病合并糖耐量减低患者血小板活性及C反应蛋白存在相关性,提示二者存在相互作用,并且对冠心病动脉粥样硬化的影响是协同的。
     第二部分
     冠心病合并糖尿病患者血小板参数与hsCRP的相关性研究
     目的:
     中国冠心病患者糖代谢紊乱较西方国家更为显著,高达80%的冠心病患者合并糖代谢紊乱。在急性心肌梗死患者中,合并糖代谢异常的比例也非常高,有相当比例是糖代谢紊乱引起的持续性高血糖,而不是应激引起的一过性高血糖。近年来研究表明,血小板除具有凝血功能外,尚参与炎症反应。C反应蛋白(C reactive protein, CRP)是全身炎症反应的非特异性标志。血清C反应蛋白浓度可反映体内炎症介质活动情况,与炎症和组织损伤程度成正比,也是目前最可靠的动脉粥样硬化的炎症的标记物。
     目前有关冠心病合并糖尿病人群中血小板参数变化及其与C反应蛋白相互关系的研究国内外报道较少。在本研究的第一部分,我们进行了冠心病合并糖耐量减低患者血小板参数与hsCRP的相关性研究,发现冠心病合并糖耐量减低患者存在较高的血小板活性及C反应蛋白水平,并且血小板活性与C反应蛋白存在相关性,提示二者对冠心病动脉粥样硬化的影响是交互的。本研究将进一步检测冠心病合并糖尿病患者血小板四项参数、hsCRP及血脂等,探讨冠心病合并糖尿病人群血小板参数的变化及其与C反应蛋白的相互关系,掌握其血小板炎症程度及功能状态的变化,为防治糖尿病心血管并发症提供一定的理论依据。
     方法:
     研究病例分为二组:A组(冠心病同时合并糖尿病),B组(单纯冠心病)。98名冠心病(CHD)合并2型糖尿病(T2DM)患者以及112例冠心病不合并2型糖尿病患者,选自2009年08月~2012年08月在武汉大学人民医院心内科2科住院治疗的冠心病患者,男173例,女37例;年龄34~87岁,平均61±12岁。
     临床资料包括:
     1.病人性别、年龄、相关危险因素,包括既往冠心病、高血压病、高脂血症及糖尿病史;
     2.入院后实验室检查:心肌酶(CTnI, CK-MB, Myo)、糖耐量试验、血小板参数、血脂(TC, TG, HDL, LDL, Lpa)及高敏感度C反应蛋白(hs-CRP);
     3.心电图检查;
     4.冠状动脉造影或冠脉CTA结果。
     统计学方法:
     采用SPSS inc的SPSS10.0软件包进行统计学分析,所有指标均先进行正态性检验。符合正态分布且方差齐的计量资料以均数±标准差(x±SD)表示。不符合正态分布的指标以中位数表示。计数资料采用χ2检验。计量资料组间比较采用One-Way ANOVA检验,组内比较采用t检验。变量间相关性采用Spearman's rho等级相关分析。以p<0.05为差异具有显著性意义。
     结果:
     1.冠心病合并糖尿病患者与对照组患者一般临床资料和实验检测指标比较:
     冠心病合并糖尿病组与冠心病组相比,空腹血糖、女性比例高于病例对照组,其差异有统计学意义;年龄、高血压病、吸烟率、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇、甘油三醋及总胆固醇差异无统计学意义。
     2.血小板参数及hsCRP的比较:
     血小板三项参数MPV、PDW、P-LCR及hsCRP在A组高于B组,PLT则低于B组,差异有统计学意义。
     3.血小板参数之间及其与其他变量之间的相关分析:
     Spearman's rho等级相关分析表明,在冠心病合并糖尿病组血小板数目与MPV、PDW及P-LCR呈负相关,MPV、PDW及P-LCR之间呈高度正相关。hsCRP与血小板计数呈负相关,与MPV、PDW及P-LCR呈负相关。
     结论:
     1.冠心病合并糖尿病患者存在较高的血小板活性及C反应蛋白水平。
     2.冠心病合并糖尿病患者血小板活性及C反应蛋白存在相关性,提示二者对糖尿病性动脉粥样硬化的发生及发展是相互、协同作用的,应该引起临床研究及临床实践的重视。
     第三部分急性心肌梗死合并糖尿病患者全身炎症反应及其对院内主要不良事件的预测价值
     目的:
     在急性心肌梗死患者中,合并糖代谢异常的比例非常高,有相当比例是糖代谢紊乱引起的持续性高血糖,而不是应激引起的一过性高血糖。急性心肌梗死患者病情发生变化快,极其容易并发心律失常、心力衰竭及猝死,所以预后一般很差。急性心肌梗死合并糖尿病患者相比不合并糖尿病急性心肌梗死患者,其长期预后更差。急性心肌梗死患者的预后评估越来越受到重视。对新入院的急性心肌梗死患者,早期预测危险程度,可以指导下一步的检查及治疗方案,减少住院期间并发症的发生,指导医务工作者有重点地有目的地开展工作,有效地提高生存率。
     本研究将检测急性心肌梗死合并糖尿病患者早期全身炎症反应指标(体温、心率、呼吸频率及血液白细胞计数),绘制ROC曲线来确定各系统性炎症反应对院内主要不良事件的预测价值,同时进行多变量(多项测量指标)观察值的ROC曲线分析,探讨四种全身炎症反应指标联合预测急性心肌梗死预后的优点。
     方法:
     67例均为武汉大学人民医院心内科住院患者,2007年12月~2012年9月住院治疗的急性心肌梗死合并糖尿病患者,男53例,女14例;年龄34~83岁,平均63±15岁。所有病例均为ST段抬高心肌梗死,发病至入院8h内,排除了入院时伴有感染的情况或已经行溶栓治疗。发生院内主要心脏事件(即研究终点:心跳骤停、心脏室速及室颤等高危心律失常、呼吸骤停、急性左心衰、心源性休克、再次心肌梗死及死亡等)的患者,分为A组;未发生院内主要不良事件的患者,分为B组。记录患者入院时病人年龄、性别、发病至入院时间(h)、住院时间(d);相关危险因素,包括既往高血压病、高脂血症;一般查体项目:入院后记录体温(腋下BT)、心率(HR)、呼吸频率(RR);入院后实验室检查:肌酐(Cr)、hs-CRP、血糖(GS)、血脂(TC, TG, HDL, LDL, Lpa)、心肌酶(CTnI,CK-MB,Myo)及白细胞计数(WBC);心电图检查等。
     统计学
     采用SPSS inc的SPSS10.0软件包进行统计学分析,所有指标均先进行正态性检验。不符合正态分布的指标以中位数表示。符合正态分布且方差齐的计量资料以均数±标准差(x±SD)表示。CRP经对数转换达近似正态分布后进行数据分析(为使结果简明仍以变换前数据表示)。计量资料组间比较采用One-Way ANOVA检验,组内比较采用t检验,不符合正态分布的指标采用Manner Whitney u检验。计数资料采用χ2检验。变量间相关性采用Spearman相关系数定量法。以p<0.05为差异具有显著性意义。
     采用SPSS10.0软件包绘制应用受试者工作特征ROC曲线(receiver operating characteristic curve, c-statistic),并比较和计算曲线下面积(area under the curve,AUC)。采用Z检验(MedCalc)比较各参数ROC曲线下面积。采用两样本率比较的正态近似法比较各个预测指标的敏感度、特异度及诊断准确度。采用函数法确定各指标的最佳截断点(cutoff point),即敏感度和特异度之和取最大值时所代表的诊断截断值作为最佳截断点(cutoff point)。AUC在0.5-0.7时有较低的准确性,AUC在0.7-0.9时有一定的准确性,AUC超过0.9有较高准确性。AUC=0.5时,说明诊断方法完全不起作用,无诊断价值。应用多变量观察值logistic回归的ROC曲线分析评价四种炎症反应指标联合预测价值。
     结果:
     1.一般临床资料和实验检测指标
     67例急性心肌梗死合并糖尿病患者住院期间共有18例(A组,27%)发生主要不良事件,其中心源性猝死8例,心源性休克2例,急性左心衰2例,需要干预的室速1例、Ⅲ°房室传导阻滞1例,室颤3例,再次心肌梗死1例。A、B二组间年龄、高血压史、吸烟史、血脂、hs-CRP等无显著性差异。患者入院时体温、心率、呼吸频率、WBC、GS、Cr与主要不良事件发生率存在相关性。入院时单次测量心肌酶谱(cTnI, CK-MB及Myo)亦不能预测主要不良事件的发生。
     2.体温对AMI近期预后的预测价值
     ROC曲线下面积=0.757±0.064,P=0.000,表明预测准确性较高,具有较高的临床预测价值。最佳界点(T<=36.0℃)预测急性心肌梗死合并糖尿病患者院内主要不良事件的敏感度为77.8%,特异度70.0%。
     3.心率对AMI近期预后的预测价值
     ROC曲线下面积=0.712±0.077,P=0.01,表明预测准确性较高,具有一定的临床预测价值。最佳界点(HR>83bpm)预测急性心肌梗死合并糖尿病患者院内主要不良事件的敏感度为66.7%,特异度67.5%。
     4.呼吸频率对AMI近期预后的预测价值
     ROC曲线下面积AUC=0.779±0.071,P=0.045(与AUC=0.5比较),表明预测准确性较高,具有较高的临床预测价值。最佳界点(RR>21bpm)预测急性心肌梗死合并糖尿病患者院内主要不良事件的敏感度为50.0%,特异度97.5%。
     5.WBC对AMI近期预后的预测价值
     AUC=0.664±0.080,P=0.01,(与AUC=0.5比较),表明有一定的预测能力,具有临床预测价值。最佳界点(WBC>11.5万/μl)预测急性心肌梗死合并糖尿病患者院内主要不良事件的敏感度为38.9%,特异度100.0%。
     6.四个协变量对急性心肌梗死合并糖尿病患者院内主要不良事件的预测价值
     作为急性心肌梗死合并糖尿病预后的预测指标,四个协变量(T、HR、RR、WBC)联合预测的ROC曲线下面积为0.88,且差异有统计学意义(与AUC0.5比较),说明诊断准确性较高,具有极高的临床预测价值。相比单指标(单协变量WBC AUC为0.66),联合指标提高了预测效能。二者AUC比较,p=0.026,差异有显著性。
     7.炎症反应积分与住院期间主要不良事件发生率的关系
     炎症反应积分:按照以上ROC曲线获得的最佳界点值,将病人入院时T、HR、RR及WBC进行计分,存在其中一项为1分,将炎症反应严重度评为0~4分。
     卡方检验发现炎症反应积分与住院期间主要不良事件发生率存在相关性。炎症反应积分0~1组主要不良事件发生率为18.2%,炎症反应积分2~4组主要不良事件发生率为71.4%,二组之间比较,p=0.000,有统计学差异。炎症反应积分2~4组院内主要不良事件发生率明显高于炎症反应积分0~1组,优势比(odds ratio)为11.25(2.80,45.16),p=0.000。炎症反应积分0~1可判别为低危病人,炎症反应积分2~4可预测高度危险病人。
     结论:
     1.入院时体温、心率、呼吸频率及外周血白细胞计数可以预测急性心肌梗死合并糖尿病患者院内主要不良事件的发生率。
     2.本研究首次建立的评价方法简单、易行。炎症反应积分0~1可判别为低危病人,炎症反应积分2~4可判别为高危病人。采用本研究建立的全身炎症反应积分预测急性心肌梗死患者院内预后,给护理人员开展健康教育与心理指导提供显而易见的数据,使病情风险预警时间提前,便于医生早期采取治疗措施。
     3.体温、心率、呼吸频率及外周血白细胞计数联合指标预测预后准确性较高,具有极高的临床预测价值。与单一指标相比,联合指标提高了预测效能。
PART I Relationship between Platelet Parameters and C-reaction Protein in Patients with Coronary Heart Disease and Impaired Glucose Tolerance
     Objective:
     Impaired Glucose Tolerance and Type2diabetes are very frequent in Coronary Heart Disease. Activated platelet plays an important role in atherosclerosis, thrombosis, and inflammation. The platelet in patients with Type2diabetes also called "diabetic platelet".C-reaction protein plays an important role in the developmental progress of atherosclerosis and type2diabetes. There were few reports on platelet function and C-reaction protein in the stage of impaired glucose tolerance in patients with coronary artery disease. The aim of this study was to investigate the change of platelet parameters and C-reaction protein in patients with coronary Heart disease and impaired glucose tolerance.
     Methods:
     This study cohort included39consecutive patients with patients with coronary Heart disease and impaired glucose tolerance. These patients come from the (Acarbose Cardiovasculer Evaluation)ACE test in Renmin hospital of Wuhan University from Dec2009~Sep2012. These patient was divided into group A included25men and14women, aged50~76years(63±8ys). Group B (normal control group) included patients with PSVT (Paroxysmal supraventricular tachycardia),10men and7women, aged50~71years(62±5ys).These patients received RFCA(Catheter radiofrequency Ablation operation in2nd department of Cardiology, Renmin Hospital of Wuhan university from Sep2011to Sep2012, with age above50ys. The observed parameters were collected at initial admission. These parameters included sex,age,history,CTnI, CK-MB, Myo)、oral glucose tolerance tes、TC, TG, HDL, LDL, Lpa,hs-CRP,blood parametes,EKG,reports of SCA or coronary CA.
     Statistical analysis:Results were presented as±SD for continuous normally distributed variables, as median for continuous non-normally distributed data, and as percentages for categorical data. Significance was assumed with a two-sided p value of below0.05. We tested continuous variables by one-way ANOVA for between-group comparisons and Student's t-test for within-group comparisons. If a normal distribution of variables was not presented, the Mann-Whitney Test was used for testing treatment-group differences and the Coefficients of correlation (r) were calculated by the Spearman's rho correlation analysis. The data were analyzed using SPSS for windows10.0(SPSS Inc.).
     Results:
     1. The subjects in group A had higher levels of fasting plasma glucose and lower levels of high-density lipoprotein cholesterol compared with subjects in group B.
     2. The subjects in group A had higher levels of MPV、PDW、P-LCR and hsCRP and lower levels of PLT compared with subjects in group B.
     3. Spearman's rho correlation analysis revealed that there were relationships between platelet parameters and hsCRP in patients with coronary Heart disease and impaired glucose tolerance, respectively. PLT was negatively related to MPV、PDW and P-LCR. There were positive relationships between P-LCR、PDW and MPV. The levels of hsCRP were negatively related with PLT and positively related with MPV、 PDW and P-LCR.
     Conclusions:
     1. There are higher levels of platelet activity and hsCRP in patients with coronary Heart disease and impaired glucose tolerance compared with normal control group. The high levels of platelet activity and hsCRP may induce coronary atherosclerosis and thrombosis.
     2. The relationships between platelet parameters and hsCRP in patients with coronary Heart disease and impaired glucose tolerance imply cooperative effects in the development of atherosclerosis. This should be paid attention.
     PART Ⅱ:Relationship between Platelet Parameters and C-reaction Protein in Patients with Coronary Heart Disease and Diabetes Mellitus
     Objective:
     The disorders of glucose metabolism in coronary heart disease are more frequent in P.R.China than in west countries. The combined presence of disorders of glucose metabolism and coronary heart disease is up to80%. The proportion of abnormal glucose metabolism in patients with acute myocardial infarction is very high. The most glucose metabolism disorders are caused by persistent hyperglycemia, rather than a transient hyperglycemia induced by stress. Activated platelet plays an important role in atherosclerosis, thrombosis, and inflammation. The platelet in patients with Type2diabetes also called "diabetic platelet". In recent years, studies have shown that platelet coagulation is still involved in the inflammatory response. C-reactive protein is a non-specific marker of the systemic inflammatory response. Serum C-reactive protein concentrations may reflect inflammatory mediator activities in vivo. And they are proportional to the degree of inflammation and tissue damage. CRP is the most reliable atherosclerosis inflammatory markers. The study on platelet parameters and C reactive protein in patient with coronary heart disease combined with diabetes mellitus is few. In the first part of this study, we performed the study on the relationship between platelet parameters and hsCRP in patients with coronary heart disease and abnormal glucose tolerance, and we found high platelet activity and C reactive protein levels, and the relationship in patients with coronary heart disease and impaired glucose tolerance. This part of study will further detect blood platelet parameters, hsCRP and serum lipids in patients with coronary artery disease combined with type2diabetes.
     Methods:
     This study included group A (patients with coronary artery disease combined with type2diabetes) and group B (patients with coronary artery disease and without type2diabetes).98consecutive patients with patients with coronary heart disease and T2MD and112consecutive patients with coronary heart disease and without T2MD. These patients come from the inpatients in2nd department of Cardiology, Renmin hospital of Wuhan University from Aug2009-Aug2012. These210patients included173men and37women, aged34~87years(61±12ys). The observed parameters were collected at initial admission. These parameters included sex,age,history,CTnI, CK-MB, Myo)、 oral glucose tolerance test, TC, TG, HDL, LDL, Lpa, hs-CRP,blood parametes,EKG, reports of SCA or coronary CA. Statistical analysis:Results were presented as x±SD for continuous normally distributed variables, as median for continuous non-normally distributed data, and as percentages for categorical data. Significance was assumed with a two-sided p value of below0.05. We tested continuous variables by one-way ANOVA for between-group comparisons and Student's t-test for within-group comparisons. If a normal distribution of variables was not presented, the Mann-Whitney Test was used for testing treatment-group differences and the Coefficients of correlation (r) were calculated by the Spearman's rho correlation analysis. The data were analyzed using SPSS for windows10.0(SPSS Inc.).
     Results:
     1. The subjects in group A had higher levels of fasting plasma glucose, higher proportion of women compared with subjects in group B.
     2. The subjects in group A had higher levels of MPV、PDW、P-LCR and hsCRP, and lower levels of PLT compared with subjects in group B.
     3. Spearman's rho correlation analysis revealed that there were relationships between platelet parameters and hsCRP in patients with coronary Heart disease and T2DM, respectively. PLT was negatively related to MPV、PDW and P-LCR. There were positive relationships between P-LCR、PDW and MPV. The levels of hsCRP were negatively related with PLT and positively related with MPV、PDW and P-LCR.
     Conclusions:
     1. There are higher levels of platelet activity and hsCRP in patients with coronary Heart disease and T2DM compared with normal control group. The high levels of platelet activity and hsCRP may induce coronary atherosclerosis and thrombosis.
     2. The relationships between platelet parameters and hsCRP in patients with coronary heart disease and T2DM imply cooperative effects in the development of atherosclerosis. This should be paid attention.
     Part III:A New Simplified Immediate System Inflammatory Score for Type2Diabetic Patients Presenting with ST-segment Elevation Acute Myocardial Infarction
     Objective:
     Patients with diabetic mellitus have worse outcomes after acute myocardial infarction (AMI) occurs than non-diabetics. The body condition changes fast in patients with T2DM and AMI and the arrhythmia, heart failure and sudden death extremely easily occur, so the prognosis is usually poor. The prognosis assessment for patients with T2MD and acute myocardial infarction should be paid more and more attention. Early prediction of the degree of risk for new admissions of patients with acute myocardial infarction can guide the next step of the examination and treatment programs and help to reduce the incidence of complications during hospitalization. The early systemic inflammatory response variables (body temperature, heart rate, respiratory rate, and white blood cell count) were collected in diabetic patients with acute myocardial infarction in this study. The ROC curves were drawn to evaluate the power of various systematic inflammatory response variables and discriminatory combining power of4variables to predict the prognosis of patients with acute myocardial infarction.
     Methods:
     This study cohort included67consecutive diabetic patients with STEMI during8hours from symptom onset. These diabetic patients with STEMI,53men and14women, aged34~83years(63±15ys), were admitted to the department of cardiology in Renmin Hospital of Wuhan University between Dec2007and Sep2012. An inflammatory score model was developed for predicting in-hospital major adverse events using parameters available at initial admission. These parameters including sex,age,history,CTnI, CK-MB, Myo、TC, TG, HDL, LDL, Lpa, hs-CRP,blood parametes, EKG, reports of SCA or coronary CA.body temperature, heart rate and respiratory rate were collected at admission.
     Statistical analysis:Results were presented as x±SD for continuous normally distributed variables, as median for continuous non-normally distributed data, and as percentages for categorical data. Significance was assumed with a two-sided p value of below0.05. We tested continuous variables by one-way ANOVA for between-group comparisons and Student's t-test for within-group comparisons. If a normal distribution of variables was not presented, the Mann-Whitney Test was used for testing treatment-group differences and the Coefficients of correlation (r) were calculated by the Spearman's rho correlation analysis. The data were analyzed using SPSS for windows10.0(SPSS Inc.). ROC(receiver operating characteristic) curves analysis was used to analyze the efficacy of the body temperature, heart rate, respiratory rate and white cell count in the prognosis in diabetic acute myocardial infarction.
     Results:
     ROC curves (receiver operating characteristic curve, c-statistic) analysis revealed that body temperature, heart rate, respiratory rate and white cell count can predict in-hospital major adverse events with AUC0.757±0.064,0.712±0.077,0.779±0.071, and0.664±0.080, p<0.05, respectively. ROC curves analysis also revealed that the combining predictive ability of the four parameters was strong (c=0.88) and it is better than single variable predictive ability.
     An inflammatory score model was developed using the four parameters above to predict in-hospital major adverse events according to the best cutoff values as fellow:(1) BT<=36.℃;(2) HR>83bpm;(3) RR>21bpm; and (4) WBC>11.5×109/L. There was a relationship between inflammatory scores and in-hospital major adverse events (p=0.000)。The rate of major adverse events with score2~4was higher than that with score0~1,71.4%vs.18.2%, p=0.000. The odds ratio(OR) was11.25(2.80,45.16),p=0.000。These patients with score0~1could be classified into low-risk person, while these patients with score2~4could be classified into high-risk person.
     Conclusions:
     1. The parameters including body temperature, heart rate, respiratory rate and white cell count which were collected on admission can predict major adverse events post-AMI in Type2diabetics.
     2. The simple systematic inflammatory score for major adverse events post-AMI in Type2diabetics showed excellent predictive capacity in a population based on cohort of patients with STEMI during8hours from symptom setup.
引文
[1]Shi Q, Rafii S, Wu MH, et al. Evidence for circulating bone marrow-derived endothelial cells. Blood 1998;92(2):362-7.
    [2]中华医学会糖尿病学分会.中国2型糖尿病防治指南.中华医学杂志2008;8(18):1227-45.
    [3]Norhammar A, Tenerz A, Nilsson G, et al. Glucose metabolism in patients with acute myocardial infarction and no previous diagnosis of diabetes mellitus:a prospective study. Lancet 2002;359(9324):2140-4.
    [4]Koek HL, Soedamah-Muthu SS, Kardaun JW, et al. Short-and long-term mortality after acute myocardial infarction:comparison of patients with and without diabetes mellitus. Eur J Epidemiol 2007;22(12):883-8.
    [5]张呈,马丽萍.血小板与炎症-血栓网络.血栓与止血学2008;14(3):136-8.
    [6]Hekimsoy Z, Payzin B, Ornek T, Kandogan G. Mean platelet volume in Type 2 diabetic patients. J Diabetes Complications 2004; 18(3):173-6.
    [7]苏娜,魏桂琴,朱瑾宏.糖尿病患者血小板参数的调查分析..2006,27(2):188-189.国际检验医学杂志2006;27(2):188-9.
    [8]Furman MI, Benoit SE, Barnard MR, et al. Increased platelet reactivity and circulating monocyte-platelet aggregates in patients with stable coronary artery disease. J Am Coll Cardiol 1998;31(2):352-8.
    [9]郑植荃.血小板激活及其机制.见:汪钟,郑植荃.现代血栓病学.第4版.北京:北京医科大学,中国协和医科大学联合出版社,.1997:212-3.
    [10]高原,肖谦.超敏C-反应蛋白与心血管疾病.西藏医药杂志2003;24(2):16-8.
    [11]国乾,张金梅.急性冠脉综合征炎症标记物及抗炎治疗研究进展.中华医学研究杂志2007;7(10):100-1.
    [12]Bernard GR, Vincent JL, Laterre PF, et al. Efficacy and safety of recombinant human activated protein C for severe sepsis. N Engl J Med 2001;344(10):699-709.
    [13]Biasucci LM. CDC/AHA Workshop on Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice:clinical use of inflammatory markers in patients with cardiovascular diseases:a background paper. Circulation 2004; 110(25):e560-7.
    [14]de Winter RJ, Heyde GS, Koch KT, et al. The prognostic value of pre-procedural plasma C-reactive protein in patients undergoing elective coronary angioplasty. Eur Heart J 2002; 23(12):960-6.
    [1]Bartnik M, Ryden L, Ferrari R, et al. The prevalence of abnormal glucose regulation in patients with coronary artery disease across Europe. The Euro Heart Survey on diabetes and the heart. Eur Heart J 2004;25(21):1880-90.
    [2]Murthy SN, Sukhanov S, McGee J, et al. Insulin glargine reduces carotid intimal hyperplasia after balloon catheter injury in Zucker fatty rats possibly by reduction in oxidative stress. Mol Cell Biochem 2009;330(1-2):1-8.
    [3]Norhammar A, Tenerz A, Nilsson G, et al. Glucose metabolism in patients with acute myocardial infarction and no previous diagnosis of diabetes mellitus:a prospective study. Lancet 2002;359(9324):2140-4.
    [4]中华医学会糖尿病学分会.中国2型糖尿病防治指南.中华医学杂志2008;8(18):1227-45.
    [5]Blanco M, Nombela F, Castellanos M, et al. Statin treatment withdrawal in ischemic stroke:a controlled randomized study. Neurology 2007;69(9):904-10.
    [6]Glucose tolerance and cardiovascular mortality:comparison of fasting and 2-hour diagnostic criteria. Arch Intern Med 2001;161(3):397-405.
    [7]Hanefeld M. Postprandial hyperglycaemia:noxious effects on the vessel wall. Int J Clin Pract Suppl2002(129):45-50.
    [8]张呈,马丽萍.血小板与炎症-血栓网络.血栓与止血学2008;14(3):136-8.
    [9]Hekimsoy Z, Payzin B, Ornek T, Kandogan G. Mean platelet volume in Type 2 diabetic patients. J Diabetes Complications 2004; 18(3):173-6.
    [10]苏娜,魏桂琴,朱瑾宏.糖尿病患者血小板参数的调查分析..2006,27(2):188-189.国际检验医学杂志2006;27(2):188-9.
    [11]Furman MI, Benoit SE, Barnard MR, et al. Increased platelet reactivity and circulating monocyte-platelet aggregates in patients with stable coronary artery disease. J Am Coll Cardiol 1998;31(2):352-8.
    [12]郑植荃.血小板激活及其机制.见:汪钟,郑植荃.现代血栓病学.第4版.北京:北京医科大学,中国协和医科大学联合出版社,.1997:212-3.
    [13]高原,肖谦.超敏C-反应蛋白与心血管疾病.西藏医药杂志2003;24(2):16-8.
    [14]Hu CL, Li YB, Tang YH, et al. Effects of withdrawal of Xuezhikang, an extract of cholestin, on lipid profile and C-reactive protein:a short-term time course study in patients with coronary artery disease. Cardiovasc Drugs Ther 2006;20(3):185-91.
    [15]毛焕元,曹林生.心脏病学.第2版.北京:人民卫生出版社,2001:738.
    [16]Age, body mass index and glucose tolerance in 11 European population-based surveys. Diabet Med 2002;19(7):558-65.
    [17]向红丁,刘纬,刘灿群.1996年全国糖尿病流行病学特点基线调查报告.中国糖尿病杂志1998(6):131-3.
    [18]李光伟.糖尿病一级预防任重道远.中华内科杂志2006;45(2):91-2.
    [19]潘长玉.国际糖尿病联盟召集糖耐量低减/空腹血糖受损专家研讨会的背景和意义.中华内分泌代谢杂志2003(19):77.
    [20]Unwin N, Shaw J, Zimmet P, Alberti KG. Impaired glucose tolerance and impaired fasting glycaemia:the current status on definition and intervention. Diabet Med 2002;19(9):708-23.
    [21]Kim YI, Kim CH, Choi CS, et al. Microalbuminuria is associated with the insulin resistance syndrome independent of hypertension and type 2 diabetes in the Korean population. Diabetes Res Clin Pract 2001;52(2):145-52.
    [22]Gabir MM, Hanson RL, Dabelea D, et al. Plasma glucose and prediction of microvascular disease and mortality:evaluation of 1997 American Diabetes Association and 1999 World Health Organization criteria for diagnosis of diabetes. Diabetes Care 2000;23(8):1113-8.
    [23]Coban E, Bostan F, Ozdogan M. The mean platelet volume in subjects with impaired fasting glucose. Platelets 2006;17(1):67-9.
    [24]Carlsson M, Wessman Y, Almgren P, Groop L. High levels of nonesterified fatty acids are associated with increased familial risk of cardiovascular disease. Arterioscler Thromb Vasc Biol 2000;20(6):1588-94.
    [25]蒋晓真,邹宇峰,顾哲.炎症因子与胰岛素抵抗及糖尿病亚临床血管病变的关系研究.中国全科医学2010;13(9):2900.
    [26]刘燕,王红梅,亓文波.葡萄糖耐量减低人群血小板相关功能研究.山东大学学报(医学版)2009;47(11):9-13.
    [27]Taniguchi A, Nakai Y, Fukushima M, et al. Ultrasonographically assessed carotid atherosclerosis in Japanese type 2 diabetic patients:Role of nonesterified fatty acids. Metabolism 2002;51(5):539-43.
    [28]纪军,何胜虎.糖耐量异常对冠心病支架植入术后主要心脏事件的影响.中国基层医药2008;12(15):1946-7.
    [29]范泉,郭文怡,贾国良.冠心病合并高胰岛素血症患者血浆PAI-1与冠脉病变的相关性.第四军医大学学报2005;26(1):28-30.
    [30]张峻,陈纪林,顾晴.抗血小板药物抑制动脉粥样硬化进展及机制研究.中国循环杂志 2005;20:463-7.
    [31]Torzewski J, Torzewski M, Bowyer DE, et al. C-reactive protein frequently colocalizes with the terminal complement complex in the intima of early atherosclerotic lesions of human coronary arteries. Arterioscler Thromb Vasc Biol 1998;18(9):1386-92.
    [32]王卫明,单其俊,曹克将.C反应蛋白的研究进展.心血管病学进展2005;26(1):73-5.
    [33]Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997;336(14): 973-9.
    [34]Raj DS, Choudhury D, Welbourne TC, Levi M. Advanced glycation end products:a Nephrologist's perspective. Am J Kidney Dis 2000;35(3):365-80.
    [35]John AC. Inflammation and Diabetic Vascular Complicatons. Diabetes Care 1999;22(12): 1927-8.
    [1]中华医学会糖尿病学分会.中国2型糖尿病防治指南.中华医学杂志2008;8:1227-45.
    [2]Norhammar A, Tenerz A, Nilsson G, et al. Glucose metabolism in patients with acute myocardial infarction and no previous diagnosis of diabetes mellitus:a prospective study. Lancet 2002;359:2140-4.
    [3]张呈,马丽萍.血小板与炎症-血栓网络.血栓与止血学2008;14:136-8.
    [4]Hekimsoy Z, Payzin B, Ornek T, Kandogan G. Mean platelet volume in Type 2 diabetic patients. J Diabetes Complications 2004;18:173-6.
    [5]苏娜,魏桂琴,朱瑾宏.糖尿病患者血小板参数的调查分析..2006,27(2):188-189.国际检验医学杂志2006;27:188-9.
    [6]郑植荃.血小板激活及其机制.见:汪钟,郑植荃.现代血栓病学.第4版.北京:北京医科大学,中国协和医科大学联合出版社.1997:212-3.
    [7]Furman MI, Benoit SE, Barnard MR, et al. Increased platelet reactivity and circulating monocyte-platelet aggregates in patients with stable coronary artery disease. J Am Coll Cardiol 1998;31:352-8.
    [8]Hu CL, Li YB, Tang YH, et al. Effects of withdrawal of Xuezhikang, an extract of cholestin, on lipid profile and C-reactive protein:a short-term time course study in patients with coronary artery disease. Cardiovasc Drugs Ther 2006;20:185-91.
    [9]毛焕元,曹林生.心脏病学.第2版.北京:人民卫生出版社,2001:738.
    [10]Kamath S, Blann AD, Lip GY. Platelet activation:assessment and quantification. Eur Heart J 2001;22:1561-71.
    [11]Carlsson M, Wessman Y, Almgren P, Groop L. High levels of nonesterified fatty acids are associated with increased familial risk of cardiovascular disease. Arterioscler Thromb Vasc Biol 2000;20:1588-94.
    [12]安吉奥利洛.糖尿病的抗血小板治疗:当前治疗策略的效果和局限及未来方向.糖尿病天地·临床刊2010;4:18-29.
    [13]张淑贞,卢秀兰,欧丽丽.糖尿病合并冠心病患者高敏C反应蛋白与血小板参数的相关性研究.中国医药导报2012;9:60-2.
    [14]龚文胜,叶素丹,陈宁.糖尿病合并血管病变的血小板参数变化国际医药卫生导报2005;11:104-5.
    [15]武宗义.冠心病患者血小板参数变化及临床意义.山东医药2005;45:25-6.
    [16]Hankey GJ, Eikelboom JW. Aspirin resistance. Lancet 2006;367:606-17.
    [17]Zimmermann N, Wenk A, Kim U, et al. Functional and biochemical evaluation of platelet aspirin resistance after coronary artery bypass surgery. Circulation 2003; 108:542-7.
    [18]侍冬成,杨柳,封启明.平均血小板体积与阿司匹林抵抗的关系.上海交通大学学报(医学版)2008;28:222-7.
    [19]田耕.妊娠期糖尿病患者血小板参数变化意义的探讨.血栓与止血学2008;14:76-9.
    [20]陆紫敏,顾风英,吴金莺.流式细胞术检测活化血小板的临床应用.临床检验杂志2001;19:289-90.
    [21]咏梅,杜泽丽,陈岚.妊娠期血小板四项参数测定的临床意.华西医大学报2001;32:633-5.
    [22]Taniguchi A, Nakai Y, Fukushima M, et al. Ultrasonographically assessed carotid atherosclerosis in Japanese type 2 diabetic patients:Role of nonesterified fatty acids. Metabolism 2002;51:539-43.
    [23]Inoue N. Vascular C-reactive protein in the pathogenesis of coronary artery disease:role of vascular inflammation and oxidative stress. Cardiovasc Hematol Disord Drug Targets 2006;6: 227-31.
    [24]王茸,肖春洁.超敏C反应蛋白的变化在冠心病患者中的临床意义.中华现代内科学杂志2008;5:432-3.
    [25]张军霞,向光大,孙慧伶.2型糖尿病动脉硬化与血管内皮功能的关系.解放军医学杂志2011;36:547-8.
    [26]高原,肖谦.超敏C-反应蛋白与心血管疾病.西藏医药杂志2003;24:16-8.
    [27]陈琪,李胜涛,陈志伟,彭芳,张静.超敏C反应蛋白及肿瘤坏死因子与冠心病的关系及药物干预.实用中医药杂志2008;24:192-3.
    [28]Torzewski J, Torzewski M, Bowyer DE, et al. C-reactive protein frequently colocalizes with the terminal complement complex in the intima of early atherosclerotic lesions of human coronary arteries. Arterioscler Thromb Vasc Biol 1998;18:1386-92.
    [29]Pickup JC, Crook MA. Is Type Ⅱ diabetes mellitus a disease of the innate immune system? Diabetologia 1998;41:1241-8.
    [30]Raj DS, Choudhury D, Welbourne TC, Levi M. Advanced glycation end products:a Nephrologist's perspective. Am J Kidney Dis 2000;35:365-80.
    [31]John AC. Inflammation and Diabetic Vascular Complicatons. Diabetes Care 1999;22:1927-8.
    [32]都健曾,赵玉岩,赵晓娟,刘国良.空腹血糖受损人群血清C反应蛋白表达及临床意义探讨.中国实用内科杂志2006;26:431-2.
    [33]Pradhan AD, Manson JE, Rifai N, Buring JE, Ridker PM. C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. Jama 2001;286:327-34.
    [34]Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997;336:973-9.
    [35]王卫明,单其俊,曹克将.C反应蛋白的研究进展.心血管病学进展2005;26:73-5.
    [1]Norhammar A, Tenerz A, Nilsson G, et al. Glucose metabolism in patients with acute myocardial infarction and no previous diagnosis of diabetes mellitus:a prospective study. Lancet 2002;359:2140-4.
    [2]Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction--executive summary:a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction). Circulation 2004;110:588-636.
    [3]Lee GK, Lee LC, Chong E, et al. The long-term predictive value of the neutrophil-to-lymphocyte ratio in Type 2 diabetic patients presenting with acute myocardial infarction. QJM 2012.
    [4]朱大乔,周秀华.急性心肌梗塞早期预后的临床危险因素.国外医学护理学分册1999;18:161-4.
    [5]Barthel, P, Wensel, P, Miiller A, et al. Risk Prediction Early After Myocardial Infarction: Resting Respiratory Rate Is Independent of GRACE Score Circulation 2011;124:A149.
    [6]Neumann FJ, Ott I, Gawaz M, et al. Cardiac release of cytokines and inflammatory responses in acute myocardial infarction. Circulation 1995;92:748-55.
    [7]杨春云,刘英,向群,周强.急性心肌梗死患者全身炎症反应综合征与预后的临床分析.现代医药卫生2003;19:137-8.
    [8]Bossowska A, Kiersnowska-Rogowska B, Bossowski A, Galar B, Sowinski P. Cytokines in patients with ischaemic heart disease or myocardial infarction. Kardiol Pol 2003;59:105-14.
    [9]Sakamoto T, Ogawa H, Takazoe K, et al. Effect of activated protein C on plasma plasminogen activator inhibitor activity in patients with acute myocardial infarction treated with alteplase: comparison with unfractionated heparin. J Am Coll Cardiol 2003;42:1389-94.
    [10]Suzuki M, Saito M, Nagai T, Saeki H, Kazatani Y. Systemic versus coronary levels of inflammation in acute coronary syndromes. Angiology 2006;57:459-63.
    [11]Kempf K, Haltern G, Futh R, et al. Increased TNF-alpha and decreased TGF-beta expression in peripheral blood leukocytes after acute myocardial infarction. Horm Metab Res 2006;38: 346-51.
    [12]Perski A, Olsson G, Landou C, de Faire U, Theorell T, Hamsten A. Minimum heart rate and coronary atherosclerosis:independent relations to global severity and rate of progression of angiographic lesions in men with myocardial infarction at a young age. Am Heart J 1992;123: 609-16.
    [13]Haverkate F, Thompson SG, Pyke SD, Gallimore JR, Pepys MB. Production of C-reactive protein and risk of coronary events in stable and unstable angina. European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group. Lancet 1997;349:462-6.
    [14]Gertz K, Laufs U, Lindauer U, et al. Withdrawal of statin treatment abrogates stroke protection in mice. Stroke 2003;34:551-7.
    [15]Chen YL, Bhasin A, Youssef AA, et al. Prognostic factors and outcomes in young Chinese patients with acute myocardial infarction undergoing primary coronary angioplasty. Int Heart J 2009;50:1-11.
    [16]Blanco M, Nombela F, Castellanos M, et al. Statin treatment withdrawal in ischemic stroke:a controlled randomized study. Neurology 2007;69:904-10.
    [17]de Winter RJ, Heyde GS, Koch KT, et al. The prognostic value of pre-procedural plasma C-reactive protein in patients undergoing elective coronary angioplasty. Eur Heart J 2002;23: 960-6.
    [18]Robertson CM, Coopersmith CM. The systemic inflammatory response syndrome. Microbes Infect 2006;8:1382-9.
    [19]Comstedt P, Storgaard M, Lassen AT. The Systemic Inflammatory Response Syndrome (SIRS) in acutely hospitalised medical patients:a cohort study. Scand J Trauma Resusc Emerg Med 2009;17:67.
    [20]Hu CL, Li YB, Tang YH, et al. Effects of withdrawal of Xuezhikang, an extract of cholestin, on lipid profile and C-reactive protein:a short-term time course study in patients with coronary artery disease. Cardiovasc Drugs Ther 2006;20:185-91.
    [21]毛焕元,曹林生.心脏病学.第2版.北京:人民卫生出版社,2001:738.
    [22]Botta F, Giannini E, Romagnoli P, et al. MELD scoring system is useful for predicting prognosis in patients with liver cirrhosis and is correlated with residual liver function:a European study. Gut 2003;52:134-9.
    [23]刘润幸.使用SPSS作多变量观察值的ROC曲线分析.中国公共卫生2003;19:1151-2.
    [24]Alexander RW. Inflammation and coronary artery disease. N Engl J Med 1994;331:468-9.
    [25]赵献明,李浪.急性心肌梗死心肌损伤的免疫学机制研究进展.临床荟萃2007;3:221-3.
    [26]Cusack MR, Marber MS, Lambiase PD, Bucknall CA, Redwood SR. Systemic inflammation in unstable angina is the result of myocardial necrosis. J Am Coll Cardiol 2002;39:1917-23.
    [27]Garcia Gonzalez MJ, Dominguez Rodriguez A, Santacreu Iniesta R, et al. [Systemic inflammatory response syndrome:incidence and influence on outcome in acute myocardial infarction treated with primary angioplasty]. Med Intensiva 2007;31:289-93.
    [28]凌燕,孟新科,李文广,何卫平,周丹SIRS评分对急性心肌梗死预后预测的研究.中国急救医学2004;24:63.
    [29]Kacprzak M, Kidawa M, Zielinska M. Fever in myocardial infarction:is it still common, is it still predictive? Cardiol J 2012;19:369-73.
    [30]Hale SL, Kloner RA. Elevated body temperature during myocardial ischemia/reperfusion exacerbates necrosis and worsens no-reflow. Coron Artery Dis 2002;13:177-81.
    [31]Lofmark R, Nordlander R, Orinius E. The temperature course in acute myocardial infarction. Am Heart J 1978;96:153-6.
    [32]李国芹.外科围手术期低体温及防治.中国临床保健杂志2008;11:333-4.
    [33]Ewing DJ, Campbell IW, Clarke BF. Heart rate changes in diabetes mellitus. Lancet 1981;1:183-6.
    [34]张晗,杨艳敏,朱俊,谭慧琼,刘力生,代表CREATE中国课题组.不同人院心率水平与ST段抬高型心肌梗死患者预后的关系.中华心血管病杂志2012;40:18-24.
    [35]王春梅,吴学思,韩智红,张倩.心率对急性心肌梗死患者住院期间病死率的影响.中华心血管病杂志2008;36:594-7.
    [36]Reil JC, Bohm M. The role of heart rate in the development of cardiovascular disease. Clin Res Cardiol 2007;96:585-92.
    [37]Kasahara Y, Izawa K, Omiya K, et al. Influence of autonomic nervous dysfunction characterizing effect of diabetes mellitus on heart rate response and exercise capacity in patients undergoing cardiac rehabilitation for acute myocardial infarction. Circ J 2006;70:1017-25.
    [38]Lanza GA, Fox K, Crea F. Heart rate:a risk factor for cardiac diseases and outcomes? Pathophysiology of cardiac diseases and the potential role of heart rate slowing. Adv Cardiol 2006;43:1-16.
    [39]Rouleau JL, Moye LA, de Champlain J, et al. Activation of neurohumoral systems following acute myocardial infarction. Am J Cardiol 1991;68:80D-6D.
    [40]de Gaetano G, Cerletti C, Evangelista V. Recent advances in platelet-polymorphonuclear leukocyte interaction. Haemostasis 1999;29:41-9.
    [41]Disegni E, Goldbourt U, Reicher-Reiss H, et al. The predictive value of admission heart rate on mortality in patients with acute myocardial infarction. SPRINT Study Group. Secondary Prevention Reinfarction Israeli Nifedipine Trial. J Clin Epidemiol 1995;48:1197-205.
    [42]Hjalmarson A, Gilpin EA, Kjekshus J, et al. Influence of heart rate on mortality after acute myocardial infarction. Am J Cardiol 1990;65:547-53.
    [43]Bonaa KH, Arnesen E. Association between heart rate and atherogenic blood lipid fractions in a population. The Tromso Study. Circulation 1992;86:394-405.
    [44]Palatini P. Elevated heart rate as a predictor of increased cardiovascular morbidity. J Hypertens Suppl 1999;17:S3-10.
    [45]陈炼.急性心肌梗塞的预后与白细胞计数及左心室射血分数关系探讨.中国血液流变学杂志2006;16:221-3.
    [46]杨海燕,佘强.粒细胞与急性心肌梗死预后的研究进展.心血管病学进展2007;28:723-5.
    [47]Shinozaki K, Tamura A, Watanabe T, et al. Significance of neutrophil counts after reperfusion therapy in patients with a first anterior wall acute myocardial infarction. Circ J 2005;69:526-9.
    [48]陈德容卢,蔡任军.急性心肌梗塞时白细胞增多与预后关系的探讨.国际医药导报2004;10:80-1.
    [49]Ishihara M, Inoue I, Kawagoe T, et al. Impact of prodromal angina pectoris and white blood cell count on outcome of patients with acute myocardial infarction. Int J Cardiol 2005; 103:150-5.
    [50]Ernst E. Fibrinogen, viscosity, and white blood cell count. Circulation 1992;85:1956.
    [51]Beard OW, Hipp HR, Robins M, Taylor JS, Ebert RV, Beran LG. Initial myocardial infarction among 503 veterans:five-year survival. Am J Med 1960;28:871-83.
    [52]张健,苏庆立,金英兰.急性心肌梗死时白细胞增多与近期预后关系的探讨.实用心脑肺 血管病杂志1996;4:10-1.
    [53]Barron HV, Cannon CP, Murphy SA, Braunwald E, Gibson CM. Association between white blood cell count, epicardial blood flow, myocardial perfusion, and clinical outcomes in the setting of acute myocardial infarction:a thrombolysis in myocardial infarction 10 substudy. Circulation 2000; 102:2329-34.
    [54]Sierra R, Rello J, Bailen MA, et al. C-reactive protein used as an early indicator of infection in patients with systemic inflammatory response syndrome. Intensive Care Med 2004;30:2038-45.
    [55]Williams BA, Wright RS, Murphy JG, Brilakis ES, Reeder GS, Jaffe AS. A new simplified immediate prognostic risk score for patients with acute myocardial infarction. Emerg Med J 2006;23:186-92.
    [56]Rott D, Behar S, Gottlieb S, Boyko V, Hod H. Usefulness of the Killip classification for early risk stratification of patients with acute myocardial infarction in the 1990s compared with those treated in the 1980s. Israeli Thrombolytic Survey Group and the Secondary Prevention Reinfarction Israeli Nifedipine Trial (SPRINT) Study Group. Am J Cardiol 1997;80:859-64.
    [57]Darbar D, Davidson NC, Gillespie N, et al. Diagnostic value of B-type natriuretic peptide concentrations in patients with acute myocardial infarction. Am J Cardiol 1996;78:284-7.
    [58]Halkin A, Singh M, Nikolsky E, et al. Prediction of mortality after primary percutaneous coronary intervention for acute myocardial infarction:the CADILLAC risk score. J Am Coll Cardiol 2005;45:1397-405.
    [1]Shi Q, Rafii S, Wu MH, et al. Evidence for circulating bone marrow-derived endothelial cells. Blood 1998;92:362-7.
    [2]Gotto AM, Jr., Brinton EA. Assessing low levels of high-density lipoprotein cholesterol as a risk factor in coronary heart disease:a working group report and update. J Am Coll Cardiol 2004;43:717-24.
    [3]Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). Jama 2001;285:2486-97.
    [4]Castelli WP. Lipids, risk factors and ischaemic heart disease. Atherosclerosis 1996; 124 Suppl:S1-9.
    [5]Alexander RW. Inflammation and coronary artery disease. N Engl J Med 1994;331:468-9.
    [6]杨春云,刘英,向群,周强.急性心肌梗死患者全身炎症反应综合征与预后的临床分析.现代医药卫生2003;19:137-8.
    [7]Kubica J, Kozinski M, Krzewina-Kowalska A, et al. Combined periprocedural evaluation of CRP and TNF-alpha enhances the prediction of clinical restenosis and major adverse cardiac events in patients undergoing percutaneous coronary interventions. Int J Mol Med 2005; 16:173-80.
    [8]赵献明,李浪.急性心肌梗死心肌损伤的免疫学机制研究进展.临床荟萃2007;3:221-3.
    [9]高原,肖谦.超敏C-反应蛋白与心血管疾病.西藏医药杂志2003;24:16-8.
    [10]Reynolds GD, Vance RP. C-reactive protein immunohistochemical localization in normal and atherosclerotic human aortas. Arch Pathol Lab Med 1987; 111:265-9.
    [11]Torzewski J, Torzewski M, Bowyer DE, et al. C-reactive protein frequently colocalizes with the terminal complement complex in the intima of early atherosclerotic lesions of human coronary arteries. Arterioscler Thromb Vasc Biol 1998;18:1386-92.
    [12]Pasceri V, Willerson JT, Yeh ET. Direct proinflammatory effect of C-reactive protein on human endothelial cells. Circulation 2000; 102:2165-8.
    [13]李鹏飞.C-反应蛋白的临床意义.中国全科医学2005;8:504-5.
    [14]Calabro P, Golia E, Yeh ET. CRP and the risk of atherosclerotic events. Semin Immunopathol 2009.
    [15]Ridker PM, Glynn RJ, Hennekens CH. C-reactive protein adds to the predictive value of total and HDL cholesterol in determining risk of first myocardial infarction. Circulation 1998;97:2007-11.
    [16]Ridker PM, Hennekens CH, Buring JE, Rifai N. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med 2000;342:836-43.
    [17]Mendall MA, Patel P, Ballam L, Strachan D, Northfield TC. C reactive protein and its relation to cardiovascular risk factors:a population based cross sectional study. Bmj 1996;312:1061-5.
    [18]Arroyo-Espliguero R, Avanzas P, Quiles J, Kaski JC. Predictive value of coronary artery stenoses and C-reactive protein levels in patients with stable coronary artery disease. Atherosclerosis 2009;204:239-43.
    [19]Gambino R. C-reactive protein-undervalued, underutilized. Clin Chem 1997;43:2017-8.
    [20]Haverkate F, Thompson SG, Pyke SD, Gallimore JR, Pepys MB. Production of C-reactive protein and risk of coronary events in stable and unstable angina. European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group. Lancet 1997;349:462-6.
    [21]Shimada K, Fujita M, Tanaka A, et al. Elevated serum C-reactive protein levels predict cardiovascular events in the Japanese coronary artery disease (JCAD) study. Circ J 2009;73:78-85.
    [22]Tomoda H, Aoki N. Prognostic value of C-reactive protein levels within six hours after the onset of acute myocardial infarction. Am Heart J 2000; 140:324-8.
    [23]叶忠平,宗金波,姜昌浩.血脂康胶囊对颈动脉粥样硬化斑块及高敏C-反应蛋白水平的影响.Herald of Medicine 2008;127:56-7.
    [24]Pickup JC, Crook MA. Is Type II diabetes mellitus a disease of the innate immune system? Diabetologia 1998;41:1241-8.
    [25]Raj DS, Choudhury D, Welbourne TC, Levi M. Advanced glycation end products:a Nephrologist's perspective. Am J Kidney Dis 2000;35:365-80.
    [26]John AC. Inflammation and Diabetic Vascular Complicatons. Diabetes Care 1999;22:1927-8.
    [27]都健曾,赵玉岩,赵晓娟,刘国良.空腹血糖受损人群血清C反应蛋白表达及临床意义探讨.中国实用内科杂志2006;26:431-2.
    [28]Pradhan AD, Manson JE, Rifai N, Buring JE, Ridker PM. C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. Jama 2001;286:327-34.
    [29]Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997;336:973-9.
    [30]王卫明,单其俊,曹克将.C反应蛋白的研究进展.心血管病学进展2005;26:73-5.
    [31]陈琪,李胜涛,陈志伟,彭芳,张静.超敏C反应蛋白及肿瘤坏死因子与冠心病的关系及 药物干预.实用中医药杂志2008;24:192-3.
    [32]车在前.血管外膜的结构与功能研究进展.血管病学进展2004;25:223-5.
    [33]Laine P, Naukkarinen A, Heikkila L, Penttila A, Kovanen PT. Adventitial mast cells connect with sensory nerve fibers in atherosclerotic coronary arteries. Circulation 2000;101:1665-9.
    [34]Khare VK, Albino AP, Reed JA. The neuropeptide/mast cell secretagogue substance P is expressed in cutaneous melanocytic lesions. J Cutan Pathol 1998;25:2-10.
    [35]Arniges M, Vazquez E, Fernandez-Fernandez JM, Valverde MA. Swelling-activated Ca2+entry via TRPV4 channel is defective in cystic fibrosis airway epithelia. J Biol Chem 2004;279: 54062-8.
    [36]Chubanov V, Waldegger S, Mederos y Schnitzler M, et al. Disruption of TRPM6/TRPM7 complex formation by a mutation in the TRPM6 gene causes hypomagnesemia with secondary hypocalcemia. Proc Natl Acad Sci U S A 2004; 101:2894-9.
    [37]Agopyan N, Bhatti T, Yu S, Simon SA. Vanilloid receptor activation by 2-and 10-microm particles induces responses leading to apoptosis in human airway epithelial cells. Toxicol Appl Pharmacol 2003; 192:21-35.
    [38]Agopyan N, Head J, Yu S, Simon SA. TRPV1 receptors mediate particulate matter-induced apoptosis. Am J Physiol Lung Cell Mol Physiol 2004;286:L563-72.
    [39]Aarts M, Iihara K, Wei WL, et al. A key role for TRPM7 channels in anoxic neuronal death. Cell 2003;115:863-77.
    [40]陈炼.急性心肌梗塞的预后与白细胞计数及左心室射血分数关系探讨.中国血液流变学杂志2006;16:221-3.
    [41]杨海燕,佘强.粒细胞与急性心肌梗死预后的研究进展.心血管病学进展2007;28:723-5.
    [42]Shinozaki K, Tamura A, Watanabe T, et al. Significance of neutrophil counts after reperfusion therapy in patients with a first anterior wall acute myocardial infarction. Circ J 2005;69:526-9.
    [43]陈德容卢,蔡任军.急性心肌梗塞时白细胞增多与预后关系的探讨.国际医药导报2004;10:80-1.
    [44]Ishihara M, Inoue I, Kawagoe T, et al. Impact of prodromal angina pectoris and white blood cell count on outcome of patients with acute myocardial infarction. Int J Cardiol 2005;103:150-5.
    [45]Ernst E. Fibrinogen, viscosity, and white blood cell count. Circulation 1992;85:1956.
    [46]Beard OW, Hipp HR, Robins M, Taylor JS, Ebert RV, Beran LG Initial myocardial infarction among 503 veterans:five-year survival. Am J Med 1960;28:871-83.
    [47]张健,苏庆立,金英兰.急性心肌梗死时白细胞增多与近期预后关系的探讨.实用心脑肺血管病杂志1996;4:10-1.
    [48]Barron HV, Cannon CP, Murphy SA, Braunwald E, Gibson CM. Association between white blood cell count, epicardial blood flow, myocardial perfusion, and clinical outcomes in the setting of acute myocardial infarction:a thrombolysis in myocardial infarction 10 substudy. Circulation 2000; 102:2329-34.
    [49]Barthel, P, Wensel, P, Miiller A, et al. Risk Prediction Early After Myocardial Infarction: Resting Respiratory Rate Is Independent of GRACE Score Circulation 2011;124:A149.
    [50]Neumann FJ, Ott I, Gawaz M, et al. Cardiac release of cytokines and inflammatory responses in acute myocardial infarction. Circulation 1995;92:748-55.
    [51]de Gaetano G, Cerletti C, Evangelista V. Recent advances in platelet-polymorphonuclear leukocyte interaction. Haemostasis 1999;29:41-9.
    [52]Robertson CM, Coopersmith CM. The systemic inflammatory response syndrome. Microbes Infect 2006;8:1382-9.
    [53]Comstedt P, Storgaard M, Lassen AT. The Systemic Inflammatory Response Syndrome (SIRS) in acutely hospitalised medical patients:a cohort study. Scand J Trauma Resusc Emerg Med 2009; 17:67.
    [54]张呈,马丽萍.血小板与炎症-血栓网络.血栓与止血学2008;14:136-8.
    [55]Hekimsoy Z, Payzin B, Ornek T, Kandogan G. Mean platelet volume in Type 2 diabetic patients. J Diabetes Complications 2004; 18:173-6.
    [56]苏娜,魏桂琴,朱瑾宏.糖尿病患者血小板参数的调查分析..2006,27(2):188-189.国际检验医学杂志2006;27:188-9.
    [57]Furman MI, Benoit SE, Barnard MR, et al. Increased platelet reactivity and circulating monocyte-platelet aggregates in patients with stable coronary artery disease. J Am Coll Cardiol 1998;31:352-8.
    [58]郑植荃.血小板激活及其机制.见:汪钟,郑植荃.现代血栓病学.第4版.北京:北京医科大学,中国协和医科大学联合出版社,.1997:212-3.
    [59]Kamath S, Blann AD, Lip GY. Platelet activation:assessment and quantification. Eur Heart J 2001;22:1561-71.
    [60]Carlsson M, Wessman Y, Almgren P, Groop L. High levels of nonesterified fatty acids are associated with increased familial risk of cardiovascular disease. Arterioscler Thromb Vasc Biol 2000;20:1588-94.
    [61]安吉奥利洛.糖尿病的抗血小板治疗:当前治疗策略的效果和局限及未来方向.糖尿病天地.临床刊2010;4:18-29.
    [62]张淑贞,卢秀兰,欧丽丽.糖尿病合并冠心病患者高敏C反应蛋白与血小板参数的相关 性研究.中国医药导报2012;9:60-2.
    [63]龚文胜,叶素丹,陈宁.糖尿病合并血管病变的血小板参数变化国际医药卫生导报2005;11:104-5.
    [64]武宗义.冠心病患者血小板参数变化及临床意义.山东医药2005;45:25-6.
    [65]Kaplan ZS, Jackson SP. The role of platelets in atherothrombosis. Hematology Am Soc Hematol Educ Program 2011;2011:51-61.
    [66]华先平王.血小板活化在动脉粥样硬化中的作用.中国微循环2007;11:213-5.
    [67]Ross R. Atherosclerosis--an inflammatory disease. N Engl J Med 1999;340:115-26.
    [68]Frenette PS, Denis CV, Weiss L, et al. P-Selectin glycoprotein ligand 1 (PSGL-1) is expressed on platelets and can mediate platelet-endothelial interactions in vivo. J Exp Med 2000;191:1413-22.
    [69]McEver RP, Cummings RD. Perspectives series:cell adhesion in vascular biology. Role of PSGL-1 binding to selectins in leukocyte recruitment. J Clin Invest 1997;100:485-91.
    [70]侍冬成杨.平均血小板体积与阿司匹林抵抗的关系.上海交通大学学报(医学版)2008;28:223-7.
    [71]田耕.妊娠期糖尿病患者血小板参数变化意义的探讨.血栓与止血学2008;14:76-9.
    [72]陆紫敏,顾风英,吴金莺.流式细胞术检测活化血小板的临床
    [73]应用.临床检验杂志2001;19:289-90.
    [74]咏梅,杜泽丽,陈岚.妊娠期血小板四项参数测定的临床意.华西医大学报2001;32:633-5.
    [75]Taniguchi A, Nakai Y, Fukushima M, et al. Ultrasonographically assessed carotid atherosclerosis in Japanese type 2 diabetic patients:Role of nonesterified fatty acids. Metabolism 2002;51:539-43.
    [76]Bartnik M, Ryden L, Ferrari R, et al. The prevalence of abnormal glucose regulation in patients with coronary artery disease across Europe. The Euro Heart Survey on diabetes and the heart. Eur Heart J 2004;25:1880-90.
    [77]Murthy SN, Sukhanov S, McGee J, et al. Insulin glargine reduces carotid intimal hyperplasia after balloon catheter injury in Zucker fatty rats possibly by reduction in oxidative stress. Mol Cell Biochem 2009;330:1-8.
    [78]Norhammar A, Tenerz A, Nilsson G, et al. Glucose metabolism in patients with acute myocardial infarction and no previous diagnosis of diabetes mellitus:a prospective study. Lancet 2002;359:2140-4.
    [79]中华医学会糖尿病学分会.中国2型糖尿病防治指南.中华医学杂志2008;8:1227-45.
    [80]Blanco M, Nombela F, Castellanos M, et al. Statin treatment withdrawal in ischemic stroke:a controlled randomized study. Neurology 2007;69:904-10.
    [81]Glucose tolerance and cardiovascular mortality:comparison of fasting and 2-hour diagnostic criteria. Arch Intern Med 2001; 161:397-405.
    [82]Hanefeld M. Postprandial hyperglycaemia:noxious effects on the vessel wall. Int J Clin Pract Suppl 2002:45-50.
    [83]Hu CL, Xiang JZ, Hu FF, Huang CX. Adventitial inflammation:a possible pathogenic link to the instability of atherosclerotic plaque. Med Hypotheses 2007;68:1262-4.
    [84]胡艳超.血管外膜与动脉粥样硬化.国际内科学杂志2008;35:605-6.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700