超负荷量氯吡格雷对急性心肌梗死急诊PCI后心肌微循环再灌注的影响

目的:观察急性心肌梗死(AMI)患者急诊经皮冠脉介入(PCI)前超负荷量应用硫酸氢氯吡格雷(简称氯吡格雷)对PCI术后患者心肌微循环再灌注和心功能的影响。方法:将52例成功急诊PCI的急性心梗患者随机平分为氯吡格雷超负荷剂量组(600mg组)及氯吡格雷负荷剂量组(300mg组),每组26例,术后第7天比较两组患者左室射血分数(LVEF)、术后24h的ST段抬高总和回落百分比(sumSTR%)、术后即刻的心肌呈色显像(Blush)3级获得率。结果:600mg组LVEF、sumSTR%和Blush 3级获得率均高于300mg组(P均0.05)。结论:急性心梗患者PCI术前应用超负荷量氯吡格雷可以改善术后心功能及心肌微循环再灌注。     

择期经皮冠脉介入术对急性心肌梗死心肌微循环的作用

目的应用心肌声学造影(MCE)评价急性心肌梗死(AMI)患者择期经皮冠脉介入术(PCI)前后的心肌微循环。方法选择20例AMI患者,在择期PCI治疗前、后分别应用声诺维(SonoVue)静脉注射,行间歇触发、二次谐波MCE检查,应用声学密度分析软件(AD)定量测定心肌微循环内造影剂的声学峰值强度(PI)、曲线下面积(AUC)。结果治疗前梗死相关节段的PI、AUC明显低于正常灌注节段(P<0.001);择期PCI治疗后梗死节段的PI、AUC仍明显低于正常节段(P<0.001),但较PCI前明显升高(P<0.001),校正后的PIr、AUCr亦明显升高(P<0.001);而正常灌注节段的PI、AUC在PCI前后无明显变化(P>0.05)。结论MCE可定量评定AMI患者的心肌微循环;择期PCI可改善AMI患者梗死节段的微循环。     

早期复极综合征与心肌梗死超急性损伤期临床表现及心电图特点对比分析

目的对比分析早期复极综合征与心肌梗死超急性损伤期的临床表现及心电图特点。方法选择早期复极综合征患者与心肌梗死超急性损伤期患者各42例,分别设为ERS组与AMI组,对比分析两组的临床症状与体征及心电图特点。结果 ERS组患者临床表现以无明显症状(76.19%)为主,AMI组以心悸(42.86%)、胸痛(57.14%)与压榨感(26.19%)为主,组间差异具有统计学意义(P0.05);ERS组患者的心电图以J波明显(76.19%)为主,AMI组主要表现为ST段下移(85.71%)、QRS形态改变(85.71%)、出现心律失常(83.33%)等,其差异具有统计学意义(P0.05)。结论早期复极综合征患者多无明显症状且心电图以J点太高为主,可与心肌梗死超急性损伤期进行区分,建议广泛应用。     

心电图aVR导联ST段改变在急性心肌梗死中的应用

目的：探讨心电图aVR导联ST段改变在急性心肌梗死（AMI）预测中的应用价值。方法：回顾性分析宜春市第二人民医院2020年1月至2022年1月收治的189例AMI患者临床资料,依据心电图aVR导联ST段改变分为ST段抬高组（ST段抬高≥0.5 mm,90例）、无偏移组（ST段抬高不足0.5 mm及下移不足0.5 mm,64例）、下移组（ST段下移≥0.5 mm,35例）。所有患者均行心电图及冠脉造影检查,比较3组患者冠脉病变数量、梗死相关血管部位、全球急性冠脉事件注册（GRACE）风险评分及不良心血管事件差异。结果：ST段抬高组、下移组三支病变发生率高于无偏移组,单支病变发生率低于无偏移组,差异有统计学意义（P<0.05）。ST段抬高组左主干、左前降支近端梗死率高于下移组、无偏移组,左前降支远端梗死率低于无偏移组,右冠状动脉梗死率低于下移组、无偏移组（P均<0.05）;ST段下移组左回旋支梗死率高于抬高组、无偏移组（P<0.05）。ST段抬高组、下移组GRACE危险评分高于无偏移组（P<0.05）。ST段抬高组、下移组不良心血管事件总发生率高于无偏移组（P<...     

急性心肌梗死PCI术后尼可地尔治疗对心肌循环再灌注及预后康复的影响

目的:观察尼可地尔对急性心肌梗死冠状动脉(Percutaneous coronary intervention,PCI)术后心肌循环再灌注及预后康复的影响.方法:回顾性分析2018年1月至2019年12月于本院进行急性心肌梗死PCI治疗的103例患者资料.根据治疗方法将其分为对照组(51例,单硝酸异山梨酯治疗)和观察组(52例,单硝酸异山梨酯+尼可地尔治疗).分析对比两组心肌微循环灌注指标、预后情况以及不良反应.结果:观察组患者心肌微循环灌注指标高于对照组(P<0.05);两组患者术后6 m内,观察组再灌注心律失常发生率低于对照组(P<0.05);两组不良反应比较无明显差异(P>0.05).结论:在急性心肌梗死PCI患者术后应用尼可地尔能扩大心脏表面血管面积,改善血流速度以及心肌供血,还能降低再灌注心律失常的发生,具有良好的安全性.     

老年女性急性心肌梗死合并2型糖尿病临床特征分析

目的 探讨老年女性急性心肌梗死(AMI)合并2型糖尿病的临床特点.方法 将60例老年女性AMI分为合并2型糖尿病(T2DM)组(糖尿病组)及不合并2型糖尿病组(对照组),观察两组的危险因素、临床表现、住院期间并发症的发生率.结果 与对照组比较,糖尿病组高脂血症多,非典型心绞痛及非ST段抬高型心肌梗死(NSTEMI)比例高于对照组(P均<0.05),易发生肺部感染及心力衰竭(P<0.05).结论 老年女性AMI合并2型糖尿病者,临床表现不典型,并发症多,预后差.     

冠心病患者心肌复极异常心电图表现与cTnI及CK-MB的关系

目的 探讨冠心病心肌复极异常心电图表现与肌钙蛋白Ⅰ(cardiac troponin Ⅰ,cTnI)及磷酸肌酸激酶心型同工酶(creatine kinase,CK-MB)的关系.方法 选择2018年2月至2020年2月于我院就诊的冠心病患者120例,并根据临床表现,将患者分为3组:稳定型心绞痛组(stable angina pectoris,SAP)、不稳定型心绞痛组(unstable angina pectoris,UAP)、急性心肌梗死组(acute myocardial infarction,AMI),每组40例.此外选择40例健康的体检者作为对照组.收集患者临床资料,检测心肌酶谱和生化指标,分析心电图特征与cTnI及CK-MB的关系.结果 SAP、UAP、AMI组总胆固醇(total cholesterol,TC)、三酰甘油(triglyceride,TG)、低密度脂蛋白(low density lipoprotein,LDL-C)明显大于对照组,高密度脂蛋白(high density lipoprotein,HDL-C)明显小于对照组(P＜0.05),AMI组TC、TG、LDL-C明显大于UAP、SAP组,HDL-C明显小于对照组(P＜0.05).4组受试者V2导联Tp-Te间期差异具有统计学意义(P＜0.05),SAP、UAP、AMI组患者T波异常、ST段异常的发生率明显大于对照组(P＜0.05).AMI、UAP组cTnI、CK-MB、CK、谷草转氨酶(glutamic oxaloacetic transaminase,AST)明显高于对照组与SAP组(P＜0.05),AMI组cTnI、CK-MB、CK、AST水平均明显高于UAP组(P＜0.05).ST段异常、T波异常组患者cTnI、CK-MB明显高于ST段正常、T波正常组患者(P＜0.05).结论 冠心病患者血清cTnI及CK-MB表达增加,且cTnI及CK-MB与心电图复极异常存在一定的关系,可为临床治疗提供一定的参考.     

血栓抽吸联合替罗非班对急性下壁心肌梗死的介入治疗作用

目的:观察血栓抽吸导管(ZEEK)抽吸血栓及注入抗栓药物替罗非班对急性下壁心肌梗死介入治疗的效果。方法:需经皮冠状动脉介入治疗(PCI)的急性下壁心肌梗死患者174例,随机分为两组:ZEEK组(n=75),用ZEEK反复抽吸血栓后,经ZEEK注入替罗非班至梗死相关血管(IRA)后行PCI;对照组(n=99),除不进行血栓抽吸外,其余同ZEEK组。比较两组患者的血流改善情况及预后。结果:与对照组比较,ZEEK组术后ST段回落(STR)70%比例(85.33%vs 58.59%)和远端血流分级(TIMI)3级比例(89.33%vs 60.61%)均高于对照组(P0.05);肌酸激酶同工酶(CK-MB)峰值(71.28±10.92V/L vs 98.63±12.71V/L)、峰值时间(11.67±3.23hvs 14.85±3.75h)和校正的TIMI帧数(CTFC)(25.60±6.10vs33.10±6.20)均显著低于对照组(P0.05);两组术后STR50%比例(97.33%vs 93.94%)无明显差异(P0.05),术后3个月两组均未发生主要不良心脏事件(MACE)。结论:在急性下壁心肌梗死患者行PCI前采用ZEEK抽吸血栓和注入替罗非班可改善心肌再灌注和减少心脏损伤。     

左心室肥厚并急性心肌梗死患者室性电风暴心电图特征及对预后的影响

目的:研究左心室肥厚并急性心肌梗死患者室性电风暴心电图特征及对预后的影响。方法:选择2018年1月至2019年1月就诊于青海红十字医院的左心室肥厚并急性心肌梗死室性电风暴患者100例作为观察组,另选取无左心室肥厚的急性心肌梗死室性电风暴患者作为对照组,两组患者均进行心电图检查以及持续心电监护,对心电图特征和患者预后进行分析,比较两组患者ST段抬高导联数、QTc间期、对应导联ST段下移发生率、冠脉病变支数及并发症发生率。结果:观察组ST段抬高导联数(4.17±1.07),QTc间期(431.0±13.2)mm、对应导联ST段下移发生率(36.0%)与对照组比较,差异具有统计学意义(P0.05)。观察组冠脉病变支数(1支49例、2支30例、3支21例)与对照组(1支7例、2支13例、3支10例)比较,差异具有统计学意义(P0.01)。观察组并发症发生率高于对照组(7.0%比2.0%,P0.05)。结论:左心室肥厚并急性心肌梗死室性电风暴患者心电图多项指标发生异常,对患者预后具有预测价值。     

NT-proBNP在急性心肌梗死中的应用

目的：分析不同部位急性心肌梗死(AMI)NT-proBNP的关系及急诊PCI术对前壁AMI NT-proBNP的影响。方法选取2012年3月~2014年7月入住中南大学湘雅二医院心内科的急性AMI患者共263例,按梗死部位分为：非ST段抬高型、下壁和前壁三组。选取无器质性心脏病患者为对照组,选取行急诊PCI术的急性前壁AMI患者为PCI组;各组均测定血清NT-proBNP。结果各AMI组的NT-proBNP均高于对照组(P<0.05)。前壁AMI组的NT-proBNP最高(P<0.05)。前壁AMI,行PCI术组的NT-proBNP低于未行PCI术组(P<0.05)。结论血清NT-proBNP可作为评价急性AMI梗死部位的指标。 PCI术可降低急性AMI患者的NT-proBNP。     

Myocardial signs of cardiotoxicity

The myocardium have been get from 70 died patients suffered from schizophrenia and treated by neuroleptic drugs. The cardiotoxic effect of neuroleptic drugs was characterized as adaptive, degenerative, and fibrous changes in the miocardium. In the extracellular matrix of the myocardium the processes of microcirculation and the collagenogenesis were damaged. As a result of the using neuroleptic drugs a compensatory hypertrophy of cardiomyocytes was transformed into their degeneration and atrophy that could be reason of a heart failure.     

Myocardial diseases of animals

In this review we have attempted a comprehensive compilation of the cardiac morphologic changes that occur in spontaneous and experimental myocardial diseases of animals. Our coverage addresses diseases of mammals and birds and includes these diseases found in both domesticated and wild animals. A similar review of the myocardial diseases in this broad range of animal species has not been attempted previously. We have summarized and illustrated the gross, microscopic, and ultrastructural alterations for these myocardial diseases; and, whenever possible, we have reviewed their biochemical pathogenesis. We have arranged the myocardial diseases for presentation and discussion according to an etiologic classification with seven categories. These include a group of idiopathic or primary cardiomyopathies recognized in man (hypertrophic, dilated, and restrictive types) and a large group of secondary cardiomyopathies with known causes, such as inherited tendency; nutritional deficiency; toxicity; physical injury and shock; endocrine disorders, and myocarditides of viral, bacterial, and protozoal causation. Considerable overlap exists between each of the etiologic groups in the spectrum of pathologic alterations seen in the myocardium. These include various degenerative changes, myocyte necrosis, and inflammatory lesions. However, some diseases show rather characteristic myocardial alterations such as vacuolar degeneration in anthracycline cardiotoxicity, myofibrillar lysis in furazolidone cardiotoxicity, calcification in calcinosis of mice, glycogen accumulation in the glycogenoses, lipofuscinosis in cattle, fatty degeneration in erucic acid cardiotoxicity, myofiber disarray in hypertrophic cardiomyopathy, and lymphocytic inflammation with inclusion bodies in canine parvoviral myocarditis. The myocardial diseases represent the largest group in the spectrum of spontaneous cardiac diseases of animals. Pericardial and endocardial diseases and congential cardiac diseases are seen less frequently; and, in contrast to man, coronary artery disease and myocardial ischemia are rather infrequent in animals. The present review shows clearly that the spectrum of myocardial diseases in animals is enlarging and that many newly recognized diseases are emerging and assuming considerable importance. For example, various heritable cardiomyopathies have recently been described in the KK mouse, cattle, and rats. Increasingly recognized myocardial diseases include cardiomyopathies in cats, dogs, and birds; anthracycline cardiotoxicity; furazolidone cardiotoxicity; ionophore cardiotoxicity; myocardial damage associated with central nervous system injuries; myocardial hypertrophy in     

Myocardial Rupture in Acute Myocardial Infarction: Report of Experience and Review

A review of eight cases of myocardial rupture following myocardial infarction confirmed the association of rupture with advanced age, a preponderance of females, hypertension, and physical exercise after infarction. In four patients, electrocardiograms recording the events of rupture showed further S-T elevation, supraventricular tachycardia, and conduction defects. One case of septal rupture showed increase in the amplitude of the P waves. The combination of these changes with sudden reappearance of chest pain, development or worsening of congestive cardiac failure with hypotension, and the appearance of a precordial systolic murmur should aid in the earlier diagnosis of this complication which may be amenable to surgery. Successful repair of rupture has been reported during the acute phase of infarction and after variable periods of delay.     

心肌微循环改变在缺血再灌注损伤中作用的探讨

目的探讨缺血与再灌注时心肌组织微循环的改变.方法采用家兔心肌缺血与再灌注模型,观察心肌组织毛细血管腔内和管壁的变化以及心肌细胞与间质的形态学改变,并测定血浆神经肽Y和内皮素水平及心肌组织微动脉、微静脉和毛细血管截面积.结果与对照组比较,实验组心肌组织毛细血管显著扩张(P＜0.001),微动脉、微静脉显著收缩(P＜0.05),实验组心肌缺血时血浆神经肽Y和内皮素水平显著上升(P＜0.001),再灌注时进-步上升(P＜0.001).心肌组织毛细血管内皮细胞脱落、固缩、变性和坏死,管腔内血细胞排列成串,心肌细胞水肿、变性、坏死,肌浆溶解,心内膜和心外膜下心肌间质广泛出血,心肌间质中性粒细胞呈小片状浸润,部分形成微脓肿.结论心肌组织微循环的改变在缺血再灌注损伤的发生机制中可能占重要地位.     

等容血液稀释对兔缺血—再灌注损伤时心肌细胞超微结构的影响

结扎兔冠脉左室枝45min，再灌注180min，复制急性心肌缺血－再灌注模型，观察等容血液稀释对再灌注损伤时心肌细胞超微结构的影响。20只兔随机分为两组：Ⅰ组（对照组）、Ⅱ组（稀释组）。结果：电镜下观察，Ⅰ组心肌细胞细胞器严重损伤，Ⅱ组心肌细胞超微结构有不同程度恢复。与此相对应，再灌注期间Ⅱ组心功能明显好于Ⅰ组，心肌梗塞面积亦小于Ⅰ组。提示：缺血－再灌注损伤时，心肌细胞的超微结构发生了异常改变，血液稀释疗法应用后细胞超微结构呈现出不同程度恢复且可缩小心肌梗塞范围，在心肌再灌注损伤的防治方面表现出良好的作用。