血运重建对急性心肌梗死患者心脏胶原重塑的影响

目的:探讨血运重建对急性心肌梗死(AMI)患者心脏胶原合成和降解代谢的影响。方法:对65例AMI患者分别予以常规强化内科保守治疗(常规治疗组,20例)或在此基础上的血运重建治疗(血运重建组,45例),应用酶联免疫法分别检测AMI后1周、3个月及6个月的血清Ⅰ型前胶原羟基端肽(PⅠCP)、Ⅲ型前胶原(PCⅢ)、基质金属蛋白酶-1(MMP-1)及基质金属蛋白酶组织抑制剂因子-1(TIMP-1)含量,并计算PⅠCP/PCⅢ的比值。以48例正常人为对照组。结果:与对照组比较,常规治疗组各亚组和血运重建组6个月亚组的PⅠCP及常规治疗组和血运重建组各亚组的PCⅢ明显增高(P<0.05),而2组的PⅠCP/PCⅢ、MMP-1及TIMP-1显著降低(P<0.05)。血运重建组各亚组的PⅠCP、1周亚组的PCⅢ及6个月亚组的MMP-1低于常规治疗组相应时点亚组(P<0.05)。结论:AMI后出现心脏胶原重塑的表现。在常规治疗的基础上,血运重建可进一步抑制AMI后心脏胶原的合成与降解。     

急诊与择期血运重建对急性心肌梗死后心脏胶原重塑的影响

目的评价急诊与择期血运重建对急性心肌梗死（AMI）后心脏胶原重塑的影响差异。方法45例AMI患者依据不同干预方法分为择期血运重建组（急诊组,25例）和急诊血运重建组（择期组,20例）,采用酶联免疫法测定患者在AMI发病后1周、3个月及6个月时的血清Ⅰ型前胶原羧基端肽（PICP）、Ⅲ型前胶原（PCⅢ）。结果急诊组3个月和6个月的PⅠCP及1周时点的PCⅢ浓度分别为（7．61±4．05）ng／ml、（10．44±4．36）ng／ml和（27．91±8．71）ng／ml,均低于择期组的（10．79±4．17）ng／ml、（13．20±4．42）ng／ml和（37．71±13．64）ng／ml,均P〈0．05。结论急诊血运重建对AMI后半年内心脏胶原合成代谢的抑制作用强于择期血运重建。     

AMI患者血浆BNP的水平与组织纤维化血清指标关系的研究

目的:观察血浆脑钠尿肽(BNP)的水平以及血清Ⅰ型前胶原羧基端肽(PⅠCP)、Ⅲ型前胶原(PCⅢ)在急性心肌梗死(AMI)后的改变,了解BNP与心脏胶原代谢的关系。方法:AMI患者组37例,仅接受强化内科保守治疗,正常对照组为32例健康体检者[平均年龄50~72(62.42±11.37)岁],分别在AMI后72 h、1个月及3个月,采用免疫荧光法测定血浆BNP的水平,ELISA测定血清PⅠCP和PCⅢ的含量。结果:AMI后1个月、3个月的患者血清PⅠCP的含量和AMI后72 h、1个月、3个月的患者血清PCⅢ的含量均高于正常对照组。AMI后1个月、3个月的患者血清PⅠCP的含量和AMI后各时间段血清PCⅢ的含量与AMI后各时间段血浆BNP的水平之间均呈正相关(PⅠCP与BNP正相关:1月,r=0.394;3月,r=0.328。PCⅢ与BNP正相关:72 h,r=0.389;1月,r=0.413;3月,r=0.396)。结论:AMI患者心脏胶原代谢活跃,与AMI后心功能不全关系密切,BNP可能参与了AMI患者心脏胶原代谢的调节。     

药物与择期经皮冠状动脉介入治疗对急性心肌梗死后MMP-1及TIMP-1的影响

目的 评价药物与择期经皮冠状动脉介入治疗(PCI)对急性心肌梗死(AMI) 基质金属蛋白酶-1(MMP-1)及其抑制物-1(TIMP-1)的影响.方法 对2005年3月至2007年11月贵州省人民医院心内科的41例AMI患者在分别于强化内科药物(药物组,22例)和在此基础上行择期PCI介入(PCI组,19例)治疗.应用酶联免疫法检测AMI患者发病1周、3个月、6个月及12个月时的血清MMP-1和TIMP-1质量浓度.结果 与对照组比较,药物组与PCI组各组MMP-1均显著降低;除12个月外,各时点组TIMP-1均显著降低(P＜0.05).两组组内比较,药物组12个月组TIMP-1较3个月及6个月组均显著升高(P＜0.05).两组同期各时点组比较,PCI组3个月及6个月TIMP-1较同期药物组显著升高,同时其6个月组MMP-1/TIMP-1比值较同期药物组显著降低(P＜0.05).结论 从抑制原有胶原网络降解的角度而言,择期PCI在AMI后6个月内明显优于药物治疗.而至12个月时择期PCI未进一步显示出此方面的优越性.     

药物治疗与择期PCI对急性心肌梗死后心肌细胞外基质重塑的对比研究

目的对比药物治疗与择期冠状动脉介入治疗（PCI）对急性心肌梗死（AMI）后心肌细胞外基质重塑的影响。方法将41例AMI患者分成两组,药物治疗组给予优化达标的内科药物治疗,择期PCI组在优化达标的内科药物治疗基础上行择期PCI治疗。应用酶联免疫法检测两组发病1周及6、12、24个月时的血清基质金属蛋白酶-1（MMP-1）、基质金属蛋白酶组织抑制剂（TIMP-1）、Ⅰ型前胶原羧基端肽（PICP）及Ⅲ型前胶原（Pcm）水平。结果与对照组比较,药物治疗组与择期PCI组MMP-1各亚组均显著降低;TIMP-1在1周及6个月时较对照组显著降低,药物治疗组的TIMP-1在12个月时较6个月显著升高,择期PCI组TIMP-1在6个月时较同期药物治疗组显著升高;药物组与PCI组各时点PICP水平及PCⅢ水平均较对照组显著升高（P均〈0．05）,两组AMI后6个月内均逐渐升高,至12个月呈下降趋势;PCI组6个月时PⅠCP水平与药物组同时点相比均显著降低（P〈0．05）。结论AMI后发生心肌细胞外基质重塑,其可被药物和择期PCI抑制;从抑制胶原合成代谢亢进及原有胶原网络降解的角度而言,择期PCI在AMI后6个月内明显优于药物治疗,而12～24个月时择期PCI未进一步显示出此方面的优越性,故对于未实施PCI而临床状况又稳定的AMI患者应立足于优化达标的内科药物治疗。     

急性心肌梗死患者心脏胶原代谢和左室重构与心功能的关系

目的观察急性心肌梗死（AMI）患者血清Ⅰ型前胶原羧基端肽（PⅠCP）和Ⅲ型前胶原（PCⅢ）水平,探讨AMI后心脏胶原代谢与左室重构及心功能的变化规律。方法应用酶联免疫法检测AMI患者发病后1周和3月的血清PⅠCP和PCⅢ含量,超声心动图同期检测左室舒张末期内径（LVEDD）、左室舒张末期容积（LVEDV）、左室射血分数（LVEF）和二尖瓣血流舒张早期流速（VE）与心房收缩期流速（VA）的比值。结果AMI后3月患者血清PⅠCP和发病后各时点血清PCⅢ均高于对照组,而AMI后3月患者PⅠCP高于AMI后1周。与正常对照组比较,AMI后各时点的LVEDD、LVEDV均增高,而LVEF和VE/VA比值降低。AMI发病后1周和3月PCⅢ分别与LVEDD和LVEDV呈正相关,与LVEF呈负相关;AMI发病后1周PⅠCP分别与LVEDD和LVEDV呈正相关,AMI发病后3月PⅠCP与LVEF呈负相关。结论AMI患者心脏胶原代谢活跃,血清PⅠCP和PCⅢ含量明显持续升高,参与左室重构,与AMI后心功能不全密切相关。     

多普勒组织成像评价择期与急诊血运重建对急性心肌梗死患者左心室收缩和舒张功能的影响

目的:应用二维超声心动图及多普勒组织成像(DTI)技术评价择期与急诊血运重建对急性心肌梗死(AMI)患者左心室收缩和舒张功能影响的差异.方法:根据AMI后不同的治疗方案,将54例首次AMI患者分为常规药物治疗组(常规组,n=18)、择期血运重建组(择期组,n=16,在常规药物治疗基础上接受择期冠状动脉支架置入术)和急诊血运重建组(急诊组,n=20,在常规药物治疗基础上接受静脉溶栓、急诊冠状动脉支架置入术).应用二维超声心动图检测患者AMI后1周、3个月、6个月及12个月的左心室射血分数、二尖瓣口血流舒张早期流速和心房收缩期流速比值;应用DTI检测二尖瓣环6个节段的收缩期运动速度峰值、舒张早期运动速度峰值和舒张晚期运动速度峰值的平均值.以20名健康体检者为正常对照组.结果:①左心室射血分数:与正常对照组比较,常规组、择期组、急诊组各时点均降低;与常规组同时点比较,择期组(3、6个月)、急诊组(6、12个月)时点均升高,差异均有统计学意义(P<0.05).②二尖瓣口血流舒张早期流速/心房收缩期流速:与正常对照组比较,常规组和急诊组各时点、择期组3、6、12个月均降低,差异均有统计学意义(P<0.05).③二尖瓣环收缩期运动速度峰值:与正常对照组比较,常规组、择期组、急诊组各时点均降低;急诊组6个月较常规组同时点升高,差异均有统计学意义(P<0.05).④二尖瓣环舒张早期运动速度峰值/舒张晚期运动速度峰值:与正常对照组比较,常规组和择期组各时点、急诊组(1周,6、12个月)均降低,差异均有统计学意义(P<0.05).⑤二尖瓣口血流舒张早期流速/二尖瓣环舒张早期运动速度峰值:与正常对照组比较,常规组各时点、择期组3、12个月及急诊组12个月均升高(P<0.05);择期组3个月和急诊组1周、3、6个月较常规组相应同时点降低,差异有统计学意义(P<0.05).结论:AMI后出现左心室收缩和舒张功能减退,急诊和择期血运重建均可改善患者左心室收缩功能,而择期血运重建对舒张功能的改善作用尚不明显;DTI可较二维超声心动图更敏感、准确地反映AMI后的左心室收缩和舒张功能变化.     

经皮冠状动脉介入治疗对急性心肌梗死患者胶原Ⅰ、Ⅲ和Fibulin-5的影响

目的:观察经皮冠状动脉介入治疗(PCI)对心肌细胞外基质重构的影响。方法:选择急性ST段抬高型前壁心肌梗死患者47例,按照是否行急诊PCI分为急诊PCI组(n=32)和非PCI组(n=15),并设置同期稳定性冠状动脉粥样硬化性心脏病患者30例为对照组。比较3组患者入院即刻,PCI术后1、7、30、45d血清胶原Ⅰ型C端胶原前肽(PⅠCP)、Ⅲ型N端胶原前肽(PⅢNP)及Fibulin-5水平。结果:不同处理方法对患者心肌细胞外基质重构有显著影响。对照组血清中PⅠCP、PⅢNP及Fibulin-5水平无显著变化;急诊PCI组及非PCI组PⅠCP、PⅢNP及Fibulin-5水平升高,7d后达到峰值,但急诊PCI组上述指标较非PCI组在同一时间窗明显降低(P均0.05)。结论:急诊PCI可减轻患者心肌细胞外基质重构,改善心脏功能。     

螺内酯、氯沙坦对AMI大鼠血浆胶原代谢产物及心肌组织心钠素、醛固酮的影响

目的探讨螺内酯、氯沙坦对急性心肌梗死(AMI)大鼠血浆胶原代谢产物及心房利纳系统的影响。方法将AMI大鼠模型随机分成假手术组、AMI对照组、螺内酯组(S组)、氯沙坦组(L组)及合用组(S L组)。测定血浆Ⅲ型前氨基胶原末端肽(PⅢNP)、Ⅰ型前胶原羧基末端肽(PⅠ CP)、血浆和心肌血管紧张素Ⅱ(AngⅡ)、心钠素(ANP)、醛固酮(Ald)水平。结果①与AMI组比较,第2、6周L组、S组血浆PⅢNP、PⅠ CP均逐渐降低(P<0.05,P<0.01)。S组第2、6周血浆ANP逐渐下降(P<0.01);L组第2、6周血浆AngⅡ、ANP水平分别显著下降(P<0.01)。②与S及L组相比,S L各时间点血浆ANP均显著降低(P<0.01)。2与AMI组相比,第2、6周S组心肌ANP水平显著降低(P<0.01),L组与AMI组比、L组、S L组同S组相比,心肌AngⅡ、Ald和ANP均显著降低(P<0.01)。S L组与L组相比,心肌ANP显著降低(P<0.01)。结论螺内酯及氯沙坦可降低血浆PⅢNP、PⅠ CP和血浆、心肌组织ANP水平,二者联用有显著叠加效应。     

缬沙坦对自发性高血压大鼠血清PⅠCP、PⅢNP和MMP-1的影响

目的 探讨缬沙坦对自发性高血压大鼠(SHR)血清Ⅰ型前胶原羧基端肽(PⅠCP)、血清Ⅲ型前胶原氨基端肽(PⅢNP)和血清基质金属蛋白酶-1(MMP-1)的影响及意义.方法 16只12周龄雄性SHR随机分为2组,每组各8只,分别予以缬沙坦和生理盐水灌胃;同时选取8只同周龄的雄性Wistar-Kyoto大鼠(WKY)作为对照.给药8 w后采用ELISA法测定血清PⅠCP、PⅢNP和MMP-1浓度.结果 SHR对照组血清PⅠCP、PⅢNP浓度明显高于WKY组(P＜0.01);而SHR治疗组血清PⅠCP、PⅢNP浓度明显低于SHR对照组(P＜0.01);SHR治疗组血清PⅠCP、PⅢNP、MMP-1浓度与WKY组比较无显著性差异(P＞0.05).结论 缬沙坦可调控血清PⅠCP、PⅢNP及MMP-1的含量,恢复细胞外基质合成和降解的动态平衡,抑制心肌细胞外基质的增生,防止心室重构的发生.     

Anaerobic myocardial abscess following myocardial infarction

An anaerobic myocardial abscess due to Bacteroides fragilis developed in a 60-year-old man when he had an acute myocardial infarction while recuperating from surgery for a paracolonic abscess. Anaerobic bacteremia is a common event and may lead to infection in areas of low oxygen tension far removed from the original portal of entry.     

曲尼司特对心肌梗死后心肌间质纤维化的影响

目的探讨曲尼司特对兔心肌梗死后心肌间质纤维化干预作用。方法结扎左前降支制作兔心肌梗死模型,分实验组和对照组。3周后经胃管分别给予曲尼司特及安慰剂1月,心脏彩超评价心功能并检测血清转化生长因子（transform ing growth factor,TGF-β1）,I、III型胶原浓度及组织羟脯胺酸含量。结果实验组治疗前后心功能、心腔内径、室壁厚度明显改善,血清TGF-β1,I、III型胶原浓度及羟脯胺酸含量较对照组明显下降。结论曲尼司特可有效拮抗心肌梗死后心肌间质纤维化,预防心室重构。     

Transient myocardial ischaemia after acute myocardial infarction

The prevalence and characteristics of transient myocardial ischaemia were studied in 203 patients with recent acute myocardial infarction by both early (6.4 days) and late (38 days) ambulatory monitoring of the ST segment. Transient ST segment depression was much commoner during late (32% patients) than early (14%) monitoring. Most transient ischaemia (greater than 85% episodes) was silent and 80% of patients had only silent episodes. During late monitoring painful ST depression was accompanied by greater ST depression and tended to occur at a higher heart rate. Late transient ischaemia showed a diurnal distribution, occurred at a higher initial heart rate, and was more often accompanied by a further increase in heart rate than early ischaemia. Thus in the first 2 months after myocardial infarction transient ischaemia became increasingly common and more closely associated with increased myocardial oxygen demand. Because transient ischaemic episodes during early and late ambulatory monitoring have dissimilar characteristics they may also have different pathophysiologies and prognostic implications.     

Assessment of myocardial viability using myocardial contrast echocardiography

Myocardial contrast echocardiography (MCE) is a technique that uses microbubbles as a tracer during simultaneous ultrasound of the heart. The microbubbles can be used to provide quantitative information regarding the adequacy of myocardial blood flow (MBF), as well as the spatial extent of microvascular integrity. In acute myocardial infarction, MCE can identify the presence of collateral flow within the risk area, and can therefore predict preservation of myocardial viability and ultimate infarct size even prior to reperfusion. After reperfusion, the extent of microvascular no-reflow can be determined, and has significant implications for recovery of left ventricular function. In chronic ischemic heart disease, MCE has also been shown to successfully differentiate viable from necrotic myocardium. This technique can accurately predict recovery of function after revascularization. More importantly, MCE can be used to identify viable segments that may help to prevent infarct expansion and remodeling, and thus improve patient outcomes.     

Assessment of myocardial viability with myocardial contrast echocardiography

The application of noninvasive imaging techniques to assess myocardial viability has become an important part of routine management of patients with acute myocardial infarction and chronic coronary artery disease. Information regarding the presence and extent of viability may help identify patients likely to benefit from revascularization or therapy directed at attenuating left ventricular remodeling. Myocardial contrast echocardiography (MCE) is capable of defining the presence and extent of viability by providing an accurate assessment of microvascular integrity needed to maintain myocellular viability. It is especially suited for the spatial assessment of perfusion, even when myocardial blood flow is reduced substantially in the presence of severe epicardial stenoses or in a bed dependent on collateral perfusion. The routine use of MCE to evaluate viability in patients with acute and chronic coronary artery disease is now feasible with the advent of new imaging technologies and microbubble agents capable of myocardial opacification from venous injections. The utility of this technique for determining treatment strategies has not been established but is forthcoming.     

Transient myocardial ischaemia after acute myocardial infarction.

The prevalence and characteristics of transient myocardial ischaemia were studied in 203 patients with recent acute myocardial infarction by both early (6.4 days) and late (38 days) ambulatory monitoring of the ST segment. Transient ST segment depression was much commoner during late (32% patients) than early (14%) monitoring. Most transient ischaemia (greater than 85% episodes) was silent and 80% of patients had only silent episodes. During late monitoring painful ST depression was accompanied by greater ST depression and tended to occur at a higher heart rate. Late transient ischaemia showed a diurnal distribution, occurred at a higher initial heart rate, and was more often accompanied by a further increase in heart rate than early ischaemia. Thus in the first 2 months after myocardial infarction transient ischaemia became increasingly common and more closely associated with increased myocardial oxygen demand. Because transient ischaemic episodes during early and late ambulatory monitoring have dissimilar characteristics they may also have different pathophysiologies and prognostic implications.     

经静脉心肌声学造影评价心肌梗死后存活心肌的价值

目的　探讨经静脉心肌声学造影 (MCE)对心肌梗死后存活心肌的诊断价值。方法　 2 4例心肌梗死患者用二维超声评价室壁运动情况 ,同时经静脉进行MCE ,以 3个月后静态超声心动图左室心肌节段性运动改善为依据评价MCE对心肌梗死后存活心肌的诊断价值。结果　在 2 4例病人的 384个心肌节段中 ,运动异常节段 184个。在运动异常的 184个节段中 ,MCE1分 39段 ,0 5分 5 0段 ,0分 95段。 3个月复查 79个节段有运动改善 ,其中 39段来自MCE1分的心肌 ,4 0段来自MCE0 5分的心肌。MCE对预测心肌梗死后室壁运动改善的敏感性、特异性、阳性预测值、阴性预测值及准确率分别为 :10 0 %、89 7%、84 8%、10 0 %和 94 6 %。结论　MCE能比较准确地预测心肌梗死后心肌的存活性