链激酶治疗老年急性心肌梗塞患者的临床分析

目的探讨链激酶(SK)静脉溶栓治疗对老年患者的影响。方法对138例链激酶(SK)静脉溶栓治疗的患者进行临床分析,按年龄分组,对溶栓后冠状动脉再通率、心脏事件发生率、病死率及出血并发症作临床分析。结果 >65岁组的患者其血管再通率、心脏事件发生率、病死率及出血并发症与≤65岁的患者比较无显著性差异(70.5％ vs.77.7％ P>0.05;40.9％vs.40.4％ P>0.05;15.9％vs.10.6％ P>0.05;11.4％vs.10.6％ P>0.05)。结论 SK静脉溶栓治疗老年急性心肌梗塞患者是安全可行的,但要视每位患者具体情况而定。     

直接经皮冠脉内支架植入术治疗急性心肌梗死

目的：评价直接冠脉内支架植入术治疗急性心肌梗死的临床疗效。方法：１７例急性心肌梗死患者于症状发作后２～１４小时施行冠脉内支架术。结果：所有患者冠脉再通均获成功。ＴＩＭＩ血流均达到３级。无残余狭窄,血管再通距症状发作时间平均５．７小时,所有患者胸痛均在术后２小时内明显缓解;除２例ＳＴ段持续抬高外,其余病例均在术后２小时ＳＴ段下降〉５０％;心肌酶峰明显提前。１例左主干病变于术后１周发生严重泵衰竭死亡;     

急性脑梗塞的红细胞膜流动性及生化指标改变

目的 探讨急性脑梗塞（ＡＣＩ）的发病机制及治疗措施。方法 采用测定ＡＣＩ患者血浆粘度,纤维蛋白原含量,红细胞膜荧光偏振度Ｐ,过氧化脂质水平,超氧化物歧化酶活性等指标进行对比研究。结果 与同龄健康组比较,ＡＣＩ患者ηｐ,Ｆｇ,ＬＰＯ水平均显著升高,ＳＯＤ活性显著降低。红细胞膜流动性下降。     

脑梗塞患者脂蛋白(A)水平与肾脏早期损害

为探讨脑梗塞患者脂蛋白（Ａ）水平与肾脏早期损害的关系,应用ＥＬＩＳＡ法及化学显色终点法分别检测４０例梗塞患者血清ＬＰ（Ａ）水平和尿氨基葡萄糖苷酶活力。结果表明,脑梗塞组血ＬＰ（Ａ）及ＮＡＧ均明显高于正常对照组,且ＬＰ（Ａ）值与尿ＮＡＧ活力呈正相关。     

有否静脉溶栓的急性心肌梗死63例尸解病理分析

探讨溶栓治疗的并发症。方法急性心肌梗死住院死亡并行尸体解剖６３例,２６例曾给予溶栓治疗,３７例行常规治疗。结果两组性别、年龄、ＣＨＤ的危险因素,梗死次数,心肌酶学、梗死部位及血管狭窄程度均无明显差异。结论ＡＭＩ早期溶栓治疗心脏破 发生率较非溶栓组明显升高。     

脑梗死病人经颅磁刺激运动诱发电位初步研究

目的：探讨经颅磁刺激运动诱发电位（ＭＥＰ）在脑梗死中的应用价值。方法：对１０５例脑梗死患者进行检查。结果：患者瘫痪侧上肢ＭＥＰ潜伏期和中枢运动传导时间与健侧比较差异有高度显著性（Ｐ＜０．０１）。ＭＥＰ异常程度和临床症状呈正相关,且与治疗效果比较差异有显著性（Ｐ＜０．０１）。结论：ＭＥＰ反映中枢运动传导通路受损情况,对预测其预后亦有帮助。     

急性心肌梗塞溶栓治疗后血清超氧化物歧化酶活性和丙二醛的变化

为探讨溶栓治疗急性心肌梗塞(AMI)对血清超氧化物歧化酯(SOD)活性和丙二醛(MDA)的影响。将61例AMI患者分成溶栓再通组(37例)、溶栓未通组(24例)进行治疗观察。结果溶栓再通组,不同时问测定的血浆SOD和浓度高于对照组(P<0.01)。而MDA的浓度是下降的。结论提示只有使梗塞相关血管(IRA)再通,才能通过增加心肌细胞内SOD活性,降低MDA,对抗氧自由基对心肌细胞的损害作用。     

Release of chemoattractants and neutrophil activation in acute myocardial infarction immediately after successful recanalization of the infarct-related vessel by angioplasty

The study investigated inflamatory responses in evolving myocardialinfarction. Fifteen patients with acute myocardial infarction,who had undergone balloon recanalization of the infarct-relatedcoronary artery within 4 h after onset of symptoms, were examined.Blood samples were obtained through the guiding catheter andfrom the pulmonary artery before and immediately after successfulrecanalization. After recanalization, plas from the pulmonaryartery was 47% (quartiles: l9%, 78; P =0·001) more chemotacticto neutrophils from normal donors than before recanalization.Furthermore, significant changes in neutrophil function werefound in the pulmonary artery. Compared to the values beforerecanalization, the nitroblue tetrazolium score rose by 31%(quartiles: 4%, 37% P=0·003), FMLP-stimulated superoxideanion production by 10% (quartiles: 0%, 39% P=0·020),and chemotaxis by 46% (quartiles: 0%, 81%, P=0·011),while neutrophil filterability decreased by 28% (quartiles:15%, 47%; P=0·010). No significant changes in neutrophilparameters were found in the arterial blood The study indicatesthat chemoattractants are released in the early reperfusionperiod of evolving myocardial infarction. These chemoattractantsmay act as inflammatory mediators causing neutrophil activation.     

Myocardial infarction in an adult resulting from coronary ancurysms previously documented in childhood after an acute episode of Kawasaki's disease

Coronary aneurysms resulting from a previous episode of Kawasaki'sdisease are considered an important cause of myocardial infarctionin children. A case of a 19-year-old man presenting with anacute myocardial infarction associated with coronary aneurysmsis described. These coronary lesions were previously evaluatedangiographically and echocardiographically at the age of 13years, 5 months after the acute episode of a Kawasaki's disease.     

Reverse redistribution: fact or fiction?

It has been well documented that it is not uncommon for a thallium-201 perfusion defect to develop or become more evident on delayed exercise thallium scintigraphic imaging, as compared with the initial image immediately following stress. The pathophysiology and clinical significance of the phenomenon are currently unclear. Literature on this subject is reviewed, and it is concluded that reverse redistribution of ²⁰¹Tl in the post-myocardial infarction patient is indeed a fact. In this context it represents a low-risk condition and may imply successful thrombolysis, patent infarct-related coronary artery, improved wall motion at the infarct site and retained myocardial viability in that segment. Correspondence to: A. Labiri