国产瑞替普酶和进口阿替普酶对ST段抬高型心肌梗死的溶栓疗效比较

目的 比较国产瑞替普酶和进口阿替普酶对急性ST段抬高型心肌梗死（STEMI）的溶栓效果.方法 回顾性分析100例STEMI患者,根据溶栓药物不同分为国产瑞替普酶治疗组52例,进口阿替普酶治疗组48例,比较两组患者再通率、心功能、出院存活率、住院天数、出血率、低血压、休克、恶性心律失常发生率、心脏骤停、心衰发生率的差别.结果 两组在再通率、心功能恢复、出院存活率、住院天数、出血率、低血压、休克、恶性心律失常发生率、心脏骤停发生率、心衰发生率方面差异无统计学意义（P＞0.05）.结论 国产瑞替普酶和进口阿替普酶治疗STEMI均有良好的疗效,但国产瑞替普酶使用简便、易操作,更适合在临床使用.     

瑞替普酶溶栓治疗老年ST段抬高型心肌梗死的疗效观察

目的观察瑞替普酶治疗老年(60岁)ST段抬高型急性心肌梗死患者的溶栓效果及安全性。方法选取2013年1月至2016年12月在我院治疗的急性ST段抬高型心肌梗死患者73例为研究对象,采用随机数字表法随机分为瑞替普酶组(38例)和尿激酶组(35例),分别采用瑞替普酶和尿激酶进行静脉溶栓治疗。比较两组患者梗死相关血管的血管再通率、出血并发症发生率以及住院病死率。结果瑞替普酶组患者溶栓治疗后30 min、60 min、90 min、120 min的血管再通比例,即临床再灌注成功率均显著高于尿激酶组,差异有统计学意义(P0.05)。在溶栓后1~2周行冠脉造影检查,瑞替普酶组患者冠脉血管再通率,即冠脉造影再灌注成功率,无论是TIMI 2级还是TIMI 3级均显著高于尿激酶组,差异有统计学意义(P0.05)。瑞替普酶组患者出血并发症发生率(10.5%)显著低于尿激酶组(34.3%),差异有统计学意义(P0.05)。结论瑞替普酶治疗老年急性ST段抬高型心肌梗死患者的溶栓效果优于尿激酶,安全性高于尿激酶。     

瑞替普酶与阿替普酶在急性ST段抬高型心肌梗死溶栓治疗中的疗效比较

目的 研究瑞替普酶(r-PA)和阿替普酶(rt-PA)在急性ST段抬高型心肌梗死患者溶栓治疗中的疗效及安全性.方法 选择2011年8月-2012年8月心内科收治的80例无溶栓禁忌证急性ST段抬高型心肌梗死患者,按照随机分组原则,平均分为两组.瑞替普酶治疗组40例,给予静脉推注瑞替普酶.阿替普酶治疗组40例,给予先静脉推注后静脉泵入阿替普酶.溶栓治疗后观察患者溶栓再通时间、再通率、不良反应发生率、病死率等.评价两种药物的临床疗效和安全性.结果 瑞替普酶组与阿替普酶组临床资料情况相比较无统计学意义(P>0.05);r-PA组与rt-PA组血管再通率分别为85%和80%(P>0.05);在心肌损伤程度、改善心功能方面两药无统计学意义;安全性上两种药都有轻度出血,差异无统计学意义.结论 瑞替普酶与阿替普酶治疗急性ST段抬高型心肌梗死的疗效及安全性相同,但瑞替普酶更经济、操作更简便、更适合临床使用.     

瑞替普酶治疗急性ST段抬高性心肌梗死疗效观察

目的：观察瑞替普酶（r PA）治疗急性 ST段抬高性心肌梗死的临床疗效及出血不良反应发生情况。方法选取2011年6月—2013年6月我院住院的90例急性 ST段抬高性心肌梗死病人,随机分为瑞替普酶组（47例）和尿激酶组（43例）。观察两组的临床溶栓再通率及出血不良反应。结果瑞替普酶组30 min、60 min、90 min、120 min临床冠状动脉再通率分别为12.76%、61.70%、74.47%、80.85%。尿激酶组临床冠状动脉再通率分别为2.32%、23.25%、51.16%、55.81%。瑞替普酶组各时间段冠脉再通率均高于尿激酶组,差异有统计学意义（P〈0.05）。瑞替普酶组早期溶栓与晚期溶栓冠状动脉再通率高于对照组（P〈0.05）。两组出血不良反应比较差异无统计学意义。结论瑞替普酶治疗急性 ST段抬高性心肌梗死疗效显著,是一种高效安全的溶栓药。     

急诊应用瑞替普酶、重组链激酶溶栓治疗ST段抬高型心肌梗死临床分析

目的 比较第三代静注溶栓药物瑞替普酶和重组链激酶对ST段抬高型心肌梗死患者进行静脉溶栓治疗的临床疗效.方法 静脉溶栓治疗ST段抬高型心肌梗死患者40例,其中瑞替普酶组22例,重组链激酶组18例,观察血管再通率、死亡率、心力衰竭及休克等并发症和出血不良反应.结果 瑞替普酶组和重组链激酶组的临床再通率分别为86.36%和66.66%,其中60 min及90 min再通率瑞替普酶组高于重组链激酶组,差异有统计学意义(P<0.05).溶栓后30 d内再闭塞率、心力衰竭及梗死后心绞痛发生率两组差异无统计学意义(P>0.05),死亡率分别为4.55%和5.55%,差异有统计学意义(P<0.05),出血发生率瑞替普酶组高于重组链激酶组,差异有统计学意义(P<0.05).结论 瑞替普酶、重组链激酶均适合急诊室内急性心肌梗死惠者的静脉溶栓治疗,瑞替普酶早期再通率高于重组链激酶.     

瑞替普酶与尿激酶在急性ST段抬高心肌梗死溶栓治疗中的疗效比较

目的 研究瑞替普酶和尿激酶在急性ST段抬高心肌梗死患者溶栓治疗中的疗效及安全性.方法 选用符合溶栓标准的急性心肌梗死患者65例.随机分为观察组(瑞替普酶)33例与对照组(尿激酶)32例.观察两组血管再通率、肌钙蛋白达峰时间、出血率、病死率.结果 观察组再通率82.1%明显,优于对照组的62.5%(P＜0.05)、出血发生率6.1%、肌钙蛋白达峰时间13.4 h±2.3 h,明显低于对照组,两组比较差异有统计学意义(P＜0.05);两组病死率无统计学意义.结论 瑞替普酶在急性心肌梗死溶栓治疗中再通率安全性优于尿激酶.     

瑞替普酶与尿激酶静脉溶栓治疗急性ST段抬高型心肌梗死的效果和安全性

目的探究瑞替普酶与尿激酶静脉溶栓治疗急性ST段抬高型心肌梗死的效果和安全性。方法选取2015年3月~2016年3月期间,我院接受治疗的48例急性ST段抬高型心肌梗死患者作为研究对象,按照治疗药物的不同分为治疗组(n=24)和对照组(n=24),对照组采用尿激酶进行治疗,治疗组采用瑞替普酶联合尿激酶还原型谷胱甘肽进行治疗,观察分析两组患者的治疗效果,CK(肌酸激酶)、cTnT(肌钙蛋白)和SOD(超氧化物歧化酶)的水平,出血发生率和临床再通率。结果治疗组的临床效果优于对照组,CK、cTnT和SOD的水平改善情况好于对照组,出血发生率和临床再通率与对照组相比存在较大差异,两组患者差异显著(P0.05),有统计学意义。结论采用瑞替普酶与尿激酶静脉溶栓治疗急性ST段抬高型心肌梗死患者具有较大的意义。     

瑞替普酶与尿激酶对急性心肌梗死患者院内治疗有效性及安全性的多中心随机对照研究

目的对比观察瑞替普酶与尿激酶用于急性ST段抬高型心肌梗死患者溶栓治疗的疗效及安全性。方法2014年河南省34家医院参加本研究,356例急性ST段抬高型心肌梗死患者符合入排标准入选,随机分组给予瑞替普酶(n=178)或尿激酶(n=178)溶栓治疗。溶栓后通过监测临床症状、心电图、心肌酶及心律变化判断溶栓再通率,并观察住院期间心血管事件及出血事件的发生率,出血事件采用全球梗死相关动脉开通策略(GUSTO)分级。结果瑞替普酶组溶栓后2 h临床标准判断血管再通率为88.6%(156/176),尿激酶组为51.1%(91/178)(P0.001),瑞替普酶组血管再通时间较尿激酶组平均提早18 min(IC95%11~25)(P0.001)。瑞替普酶组溶栓后住院期间死亡率为0.6%(1/176),尿激酶组为3.4%(6/178)(P0.05)。瑞替普酶组与尿激酶组均无GUSTO严重出血事件发生,GUSTO中度出血率分别为1.7%(3/176)、0.0%(0/178)(P0.05);GUSTO轻度出血率分别为6.8%(12/176)、2.8%(5/178)(P0.05)。结论与尿激酶相比,瑞替普酶具有更高的血管再通率,不良反应少,是一种安全有效的溶栓药物。     

瑞替普酶在急性ST段抬高型心肌梗死溶栓治疗中的有效性及安全性研究

目的观察瑞替普酶与尿激酶用于急性ST段抬高型心肌梗死病人溶栓治疗的有效性及安全性。方法将113例急性ST段抬高型心肌梗死病人随机分为瑞替普酶组(57例)与尿激酶组(56例),观察两组溶栓冠脉血管再通率、心血管事件的发生情况、出血并发症及住院期间死亡情况,比较两种药物溶栓治疗的有效性及安全性。结果瑞替普酶组治疗后30min,1h及2h血管再通率均高于尿激酶组,差异有统计学意义(P0.01);发病距溶栓时间在6h以内和(6~12)h再通率相比较,瑞替普酶组均高于尿激酶组,差异有统计学意义(P0.05);两组溶栓后住院期间心血管事件及并发症的发生情况,无统计学意义(P0.05)。结论瑞替普酶较尿激酶有更高的血管再通率,能够早期快速开通血管,是一种安全有效的溶栓药物。     

基层医院应用瑞替普酶治疗急性心肌梗死的疗效观察

目的 观察基层医院应用瑞替普酶治疗急性ST段抬高心肌梗死的疗效和安全性.方法 对入选的87例急性心肌梗死患者进行瑞替普酶静脉溶栓治疗,利用患者ST段回落、肌酸激酶同工酶、再灌注心律失常及胸痛症状间接判断梗死血管是否再通,观察疗效.结果 瑞替普酶治疗急性心肌梗死30 min、60 min和90 min的血管再通率分别是37.9%、67.8%和92.0%,随访35 d死亡率为6.9%.所有患者均未出现严重不良反应.结论 在基层医院应用瑞替普酶溶栓治疗急性ST段抬高心肌梗死有较好疗效和安全性.     

恶性室性心律失常埋藏式心脏复律除颤器与药物治疗的对比研究

观察埋藏式心脏复律除颤器 (ICD)与药物对恶性室性心律失常的治疗效果 ,探讨其对心源性猝死的预防。94例患者 ,均有室性心动过速 (简称室速 )和 /或心室颤动等恶性室性心律失常发作史 ,其中冠心病 68例、原发性扩张型心肌病 2 6例。根据电生理心室程序刺激结果将患者分为药物治疗组 (A组 )、ICD组 (B组 )和慢频率室速药物治疗组 (C组 )。分别给予胺碘酮和 /或阿替洛尔药物治疗和ICD治疗。观察随访 1 ,2 ,5年的总生存率 ,不同左室射血分数 (EF)值亚组的生存率和心律失常性死亡的发生率。结果显示 ,随访 5年的总生存率C组明显低于A、B两组(P <0 .0 5 ) ,B组的低EF(≤ 0 .40 )值亚组的 5年生存率明显高于A、C两组的低EF值亚组 (P <0 .0 5 )。B组随访期间无心律失常死亡者 ,其心律失常性死亡事件的发生率明显低于A、C两组 (P <0 .0 5 )。结论 :ICD对于合并有恶性室性心律失常的心脏病人预防猝死的总体效果优于 β 阻断剂和胺碘酮等药物治疗。这尤其见于长期随访 (≥ 5年 )和伴有心功能不全 (EF值≤ 0 .40 )的病人。对于有过恶性室性心律失常发作史的患者 ,若心电生理检查不能诱发室速 ,在没有条件安装ICD时 ,胺碘酮与 β 阻断剂联合应用仍可在一定程度上减少心源性猝死的发生。     

急性ST段抬高心肌梗死24h内死亡原因分析

目的:探讨急性ST段抬高心肌梗死(STEMI)患者早期24h内死亡的原因。方法:对STEMI523例患者中24h内死亡17例的死亡病因、梗死部位、治疗方法、临床特征等临床资料进行分析。结果:死因为心脏破裂12例,占总病死率70.6%;心力衰竭合并心源性休克4例,占23.5%;恶性心律失常1例,占5.9%;心脏破裂的病死率高于心力衰竭合并心源性休克、恶性心律失常(P0.01)。心脏破裂死亡的12例中溶栓9例,未溶栓2例,急诊介入术1例。结论:心脏游离壁破裂是STEMI患者早期24h内死亡的主要病因;静脉溶栓治疗可能增加心脏破裂的发生率,尤其对于老年STEMI患者,宜尽早行急诊介入术或冠状动脉搭桥术以减少心脏破裂的发生。     

The impact of transtelephonic documentation of arrhythmia on morbidity and mortality rate in sudden death survivors

A post hospital follow-up system based on predetermined antiarrhythmic strategies and telephone transmitters used to record ECGs was helpful in managing post hospital course and improved survival in patients with a history of out-of-hospital sudden death. All patients underwent therapy guided by serial electrophysiologic testing. Of the 47 patients, 19 used the telephone transmitter system and 28 did not. During follow-up, residual symptomatic and silent ventricular arrhythmia was documented in 78% of patients using telephone transmitters. Ventricular tachycardia was transmitted in six patients--all survived. During an average 15-month follow-up, 1 of 19 patients using the telephone transmitter system died vs 12 deaths among the 28 patients who did not use the system (p less than 0.005). These results were independent of ejection fraction, presence of congestive heart failure, amiodarone therapy, and the outcome on electrophysiologic therapy. Thus, patients with a history of out-of-hospital sudden death, discharged following electrophysiologic guided therapy, require repeated antiarrhythmic dose titration for side effects or residual ventricular arrhythmia. Prompt diagnosis and treatment of potentially fatal arrhythmia is crucial and feasible, especially with regular ECG checks through telephone transmission.     

Sudden cardiac death

Opinion statement Sudden cardiac death is often due to a ventricular arrhythmia. When a patient presents with a malignant arrhythmia unrelated to a transient reversible cause, there is a high probability of recurrent arrhythmia and sudden death. Clinical trials have shown a uniform survival benefit from implantable cardioverter-defibrillator (ICD) therapy in survivors of a malignant arrhythmia when compared with drug therapy. However, only 1% to 5% of patients survive an out-of-hospital cardiac arrest, emphasizing the need for primary prevention of sudden death. Clinical trial data available in this regard are largely limited to patients with coronary artery disease (CAD). Mortality can be reduced by the ICD in patients with CAD and depressed left ventricular ejection fraction (LVEF) less than 30%. If left ventricular function is only moderately depressed (LVEF between 30% and 40%), the presence of nonsustained ventricular tachycardia with inducible ventricular arrhythmia at electrophysiologic testing identifies patients who benefit from an ICD. The role of the ICD in primary prevention of sudden death in patients with nonischemic dilated cardiomyopathy is less clear at this time. Preliminary data indicate that the presence of heart failure symptoms in this population increases risk of sudden death that can be prevented by an ICD. Antiarrhythmic drugs have little role in prevention of sudden death; however, drugs that block the effects of β-adrenergic stimulation, angiotensin, and aldosterone reduce mortality partly through their salutary effects on sudden death. Finally, a number of inherited defects of genes coding for ion channels, contractile sarcomeric proteins, and cell-to-cell junction proteins can result in primary electrical abnormalities and sudden death. The ICD is effective for secondary prevention, but its role in primary prevention is controversial and should be based on individual risk factors.     

Determinants of survival in patients with malignant ventricular arrhythmia associated with coronary artery disease

The long-term survival data in patients with coronary artery disease and a history of malignant ventricular arrhythmia, defined as noninfarction ventricular fibrillation (VF) or hemodynamically compromising ventricular tachycardia (VT) followed for up to 9 years, were analyzed. In this group of 161 patients there was a total of 57 deaths, of which 35 (63%) were sudden. Life-table analysis demonstrated a 10% sudden death rate for all patients in the first year and a 7% annual rate in the subsequent 4 years. In patients managed noninvasively, the overall mortality rate was 27% over 9 years, or 3% per year. Suppression of ventricular tachycardia on both ambulatory monitoring and exercise testing was associated with improved survival. In patients evaluated by electrophysiologic testing the sudden death rate was 1.4% per year over an average of 5 years. This survival rate was not different compared with the noninvasive group (p = 0.09). Measures of left ventricular dysfunction and the frequency of ventricular arrhythmia before and after drug therapy were associated with a risk of sudden cardiac death by univariate analysis. Multivariate regression analysis identified 4 variables as independent predictors of sudden cardiac death: rales (p = 0.009), the number of runs of VT during exercise testing while receiving antiarrhythmic drug therapy (p = 0.0003), a history of congestive heart failure (p = 0.0009) and the number of premature beats on Holter monitoring (p = 0.01). These findings support the concept that suppression of repetitive arrhythmia on Holter monitor and exercise testing is a marker for improved survival among patients with malignant ventricular arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)     

113例急性心肌梗死心率变异性与恶性心律失常相关性的研究

目的:探讨急性心肌梗死(AMI)患者的心率变异性(HRV)情况与恶性室性心律失常发生率及猝死率的相关性,预测AMI患者的病情及预后。方法:对113例已确诊AMI患者进行24 h动态心电图检查,对HRV进行时域分析(主要参数为全部正常窦性心动周期的标准差-SDNN),监测恶性室性心律失常的发生率,然后随访患者1年。结果:SDNN<50 ms,预测高危险水平的患者31例;SDNN介于50 ms～100 ms,预测中危险水平患者36例;SDNN介于100 ms～150 ms,预测低危险水平患者46例。高危险水平患者组发生恶性室性心律失常19例,猝死6例;中危险水平患者组发生恶性室性心律失常9例,猝死1例;低危险水平患者组发生恶性室性心律失常5例,无猝死。3组患者恶性室性心律失常发生率比较,P<0.05,心脏猝死率比较,P<0.01。结论:HRV减小程度与恶性室性心律失常及猝死发生率有正相关性,HRV在预测AMI患者的危险性及预后起着重要作用。     

尿激酶联合氯吡格雷阿司匹林治疗急性ST段抬高型心肌梗塞疗效

目的：观察尿激酶溶栓联合氯吡格雷、阿司匹林治疗急性ST段抬高型心肌梗塞（STEMI）的临床疗效及安全性。方法：87例STEMI符合溶栓治疗患者,被随机分为两组,常规治疗组（40例）和氯吡格雷组（47例）,两组溶栓前均给予阿司匹林0．3g口服,氯吡格雷组于入院后即刻口服氯吡格雷300mg,次日改为75mg,1次／d,口服。观察两组治疗的血管再通率,30d内的主要心血管不良事件（死亡、AMI、恶性心律失常、肺水肿等）的发生率。结果：较之对照组,氯吡格雷组梗塞相关血管再通率明显提高（60．3％：74．5％,P〈0．05）,梗塞后心绞痛发生率、30d死亡及再发心肌梗塞率、严重心律失常发生率、肺水肿发生率均显著下降（P〈0．05）。结论：尿激酶溶栓联合氯吡格雷、阿司匹林治疗急性ST段抬高型心肌梗塞是安全有效的。     

心肌缺血后适应对老人急性心肌梗死临床及预后的影响

目的探讨心肌缺血后适应对老人急性心肌梗死临床及预后的影响。方法选择首次发生急性心肌梗死老年患者65例，分为缺血后适应组（适应组）及对照组，均接受急诊经皮冠状动脉介入术（percutaneous coronary intervention，PCI）。对照组行常规PCI。测定两组术前及术后肌酸激酶及心肌型肌酸激酶同工酶水平；测量术后左心室舒张末期容积指数、左心室收缩末期容积指数、左心室射血分数：观察术后严重心律失常、心力衰竭、心源性休克发生率及住院期间病死率。结果与对照组比较．适应组术后肌酸激酶及心肌型肌酸激酶同工酶峰值水平明显减低；术后3个月左心室容积减小，左心室舒张末期容积指数升高[（65．2±6.7）ml／m^2与（70.4±6.3）ml／m^2，P〈O．05]，左心室收缩末期容积指数升高1（31．4±3.2）ml／m^2与（35.5±3.5）ml／m^2，P〈0.051，左心室射血分数升高（0.52±0.03与0．49±0．02，P〈0．05）；但严重心律失常、心力衰竭、心源性休克发生率减低、住院期间病死率的差异无统计学意义。结论心肌缺血后适应可以改善老年人急性心肌梗死的体征，对梗死后心肌具有一定的保护作用。     

Value of beta blockers in the treatment of recurrent ventricular tachycardia in cardiac insufficiency

Beta-blockers were used to treat 20 patients (mean age 55 +/- 12 years) presenting with severe ventricular arrhythmia on chronic heart failure (NYHA stages II to IV; mean ejection fraction 29.7 +/- 7.8%) due to coronary disease (18 cases) or to cardiomyopathy (2 cases). Ventricular tachycardia sustained (7.6 +/- 6.3 attacks/patient) in 19 patients, unsustained in 18, monomorphous in 8 and polymorphous in 12, had been present for 12.4 +/- 18 months. In all but one hitherto untreated patient, the condition had failed to respond to amiodarone combined with a type Ia (19 patients) and type Ic (16 patients) antiarrhythmic drug. Short-term results were: 17 successes, 2 failures and 1 death due to cardiogenic shock. Fifteen patients were followed up for 14 +/- 6.7 months. Thirteen of them benefited from smaller doses of a formerly ineffective treatment; there was one failure, and one patient in whom the attacks of tachycardia, but not the numerous and polymorphous extrasystoles, were controlled by the beta-blockers suddenly died at night. The actuarial mortality rate was 11.4% as against an expected figure of 30% in such a high risk group. Although no significant changes in ejection fraction were observed, heart failure became worse in 8 patients, but it was compensated by diuretics and/or vasodilators. The effects of beta-blockers in resistant ventricular arrhythmia on heart failure suggest that an adrenergic factor is involved in the mechanism of arrhythmia. Provided treatment is progressive and its haemodynamic consequences carefully monitored, beta-blockade is well tolerated. Its effectiveness on severe arrhythmia and on mortality rate seems to confirm that it prevents sudden death by an anti-arrhythmic mechanism.