Control of tachycardia with intravenous amiodarone in acute left heart failure

The treatment of atrial tachycardia in critically ill patients can be difficult. Nine cases were presented with atrial tachyarrhythmias (mean heart rate > 130 beats/min) and left heart failure. Congestive heart failure was diagnosed in 6 patients (ejection fraction < 25%) and hypertensive heart failure in 3 patients (ejection infarction > 55%). The infusion of amiodarone (450 mg over 10 min and 0.5 mg/min after the bolus administration) was associated with a decrease in heart rate 31 beats/min and an increase in systolic blood pressure of 13 mm Hg after one hour. There was only one adverse effect secondary to amiodarone therapy. In this case the sinus rhythm converted within 24 hours but T-waves alternans and short running torsade de pointes ventricular tachycardia was observed and amiodarone therapy was discontinued.     

A case of concealed WPW syndrome with three different reciprocal tachycardias due to triple AV nodal pathways.

Triple atrioventricular nodal pathways (TAVNP) occur occasionally, but it is rare for them to produce more than two different tachycardias. Here we report a case of concealed WPW syndrome with three different tachycardias. During electrophysiologic studies, three different reciprocal tachycardias were induced. Tachycardia #1 was characterized by a cycle length of 230 msec and an A'-H interval of 70 msec. For tachycardia #2, these parameters were 300 msec and 140 msec, while they were 370 msec and 200 msec for tachycardia #3. During all three tachycardias, the earliest atrial activity was observed in the left atrium. Ventriculoatrial conduction occurred following ventricular stimulation, and the earliest atrial activity was observed in the left atrium, indicating the existence of left-sided accessory pathway. Persistence of tachycardia for 15-30 min caused marked pulmonary congestion. The heart rate was very high (260 beats/min) during tachycardia #1, and the pulmonary arterial pressure rose to 40/30 mmHg, with the pulmonary arterial diastolic pressure remaining at about 30 mmHg throughout the tachycardia. It seems that the pulmonary venous pressure rises abnormally during paroxysmal supraventricular tachycardia with a very high heart rate and that pulmonary congestion can easily occur during a short period of tachycardia.     

不同起源部位局灶性房性心动过速的心电图P波形态分析及导管消融

目的：评价局灶性房性心动过速（房速）心房内不同起源部位的心电图房性P波形态特征及导管消融疗效。方法：通过三维电解剖标测系统的精确定位17例局灶性房速的起源部位，并回顾性分析体表心电图房性P波的形态特点，探讨二者的联系。结果：17例房速起源部位均获得精确定位并成功行导管消融。9例右心房起源房速包括上腔静脉房间隔侧1例，中上部界嵴1例，房间隔右侧3例，冠状静脉窦口内1例，希氏束旁2例，右心耳1例；8例左心房起源房速包括左上肺静脉2例，右上肺静脉1例，二尖瓣环2例，左心耳1例，房间隔左侧1例，无冠窦1例。V1导联P波负向者房速多起源于右心房；P波正向者，房速除起源于左心房外，尚可能起源于右心房上部、后部；P波等电位线者，房速多起源于Koch三角附近的相关解剖结构，如冠状静脉窦口、房间隔以及希氏束。结论局灶性房速常起源于肺静脉附近、瓣环、房间隔等心房内有特殊解剖结构的部位，心电图P波形态，尤其是V1导联可初步定位房速起源部位，而三维标测系统可快速对此作进一步精确定位，缩短导管消融及放射线透视时间。     

Life-threatening ventricular tachycardia during flecainide treatment for symptomatic atrial fibrillation in a patient with a structural cardiac disorder

A 37-year-old man with symptomatic acute atrial fibrillation and a low-voltage electrocardiogram was treated with flecainide intravenously. Instead of conversion to sinus rhythm, he developed a wide-complex tachycardia suggestive of ventricular tachycardia. The patient recovered following electric cardioversion. First-choice therapy for symptomatic atrial fibrillation of recent onset (duration < 48 hours) is chemical conversion with a class IC antiarrhythmic drug (e.g. flecainide, propafenone). However, in patients with structural heart disorders, these drugs may induce ventricular tachycardia. A low-voltage electrocardiogram is suggestive of left ventricular damage. For these patients, electric cardioversion is a better alternative.     

左室特发性室速射频消融术后T波改变的临床观察

目的观察左室特发性室速射频消融术后T波的改变。方法 10例左室特发性室速患者射频消融术后每日行心电图检查。结果 10例左室特发性室速患者射频消融术后心电图均显示不同程度的T波倒置改变。结论左室特发性室速射频消融术后T波倒置属于电张调整,是心肌正常的电生理特性,一般持续7～16天自动恢复正常。     

Electroanatomical mapping and radiofrequency ablation of tachycardia originating in pulmonary vein in an adult patient

A 29-year-old male was admitted to our outpatient clinic because of palpitation and documented narrow QRS arrhythmia. Based on the ECG, supraventricular tachycardia was diagnosed, electrophysiological examination was indicated and ablation therapy was recommended. During positioning of the catheter the patient developed arrhythmia. On the coronary sinus catheter the activation spread from distal to proximal electrodes, suggesting left atrial origin. During atrial entrainment pacing long return cycle was observed and distal coronary sinus pacing resulted in a 15 ms longer cycle length than the arrhythmia. Therefore, the left atrial origin of the arrhythmia was confirmed and double transseptal puncture was performed. Lasso and irrigated tip catheter were introduced into the left atrium and electroanatomical mapping was performed with CARTO3 system. After electroanatomical mapping the origin of tachycardia was located proximally in the left superior pulmonary vein. Ablation was started at the earliest activation point, where acceleration was observed and the arrhythmia stopped after the first ablation. Pulmonary vein isolation was completed, and bidirectional block could be confirmed. After 30 minutes the arrhythmia was not inducible. During follow-up, Holter-examination was negative and the patient remained asymptomatic. The pulmonary vein tachycardia is a supraventricular arrhythmia that can occur at any age, but the diagnosis based on the ECG is not always simple. Detailed electroanatomical mapping is very important in the diagnosis of this type of arrhythmia, although it can be verified with conventional electrophysiological methods as well. Focal ablation may be a therapeutic option; however, total isolation of pulmonary veins can be more effective.     

Alcohol consumption of patients with supraventricular tachyarrhythmias other than atrial fibrillation

We studied the recent alcohol consumption and other possible precipitating factors in 99 consecutive patients (53 men and 46 women) all under 65 years of age with sustained re-entry and automatic supraventricular tachyarrhythmias and compared them with those of two groups of controls. One control group was derived from the Emergency Room patients and matched for age and sex; the other group (44 men, 22 women, mean age 48.7 years) was randomly selected from the general out-of-hospital population. There were 50 patients with supraventricular tachycardia, 30 with atrial flutter, and 19 with paroxysmal atrial tachycardia. Coronary heart disease (14% of patients), hypertension (10%), and dilated cardiomyopathy (6%) were the most prevalent cardiovascular diseases associated with the arrhythmias. The self-reported alcohol consumption of patients with arrhythmias during the week preceding the arrhythmia did not differ significantly from that of hospital or population controls, although significantly more patients than controls had liver enzyme levels above normal; neither were there any significant differences between the groups regarding prevalence for alcoholism as judged by the CAGE questionnaire. The results were essentially similar when patients with supraventricular tachycardia and those with intra-atrial tachyarrhythmias (flutter and paroxysmal tachycardia) were separately compared with the controls. We conclude that alcohol consumption, although a risk factor for atrial fibrillation, is not associated with the induction of other supraventricular tachyarrhythmias in patients of working age.     

普罗帕酮与洋地黄转复慢性心房颤动的临床观察

目的观察普岁帕酮与洋地黄转复慢性心房颤动的作用。方法将心房颤动发作时间大于3周的患者随机分为普罗帕酮组和洋地黄组,普罗帕酮组先静脉椎注2mg／kg,再以5mg/kg维持24h,后改口服每天450mg治疗4周。洋地黄组先静脉推注毛花甙C0．4mg,然后每6h静脉推注0．2mg,24h后改口服地高辛每日0.25mg。结果普罗帕酬组17例（48．6％）转复为窦性心律,洋地黄组仅2例转复成功。普岁帕酮组转复成功者与未转复者卡甘比,左房内径明旺较小（P〈0．001）,心房颤动持续时间显著较短（P〈0．001）。结论普罗帕酮可有效地转复慢性心房颤动,洋地黄转复慢性心房颤动疗效不佳;左房内径、心房颤动持续时间是影响转复成功的重要因素。     

瑞舒伐他汀治疗高血压并发阵发性心房颤动效果研究

目的观察瑞舒伐他汀治疗高血压并发阵发性心房颤动的效果。方法选择2012年6—12月就诊的高血压并发阵发性心房颤动患者80例,随机分为对照组和治疗组各40例。患者均于心房颤动复律后24 h内开始服药,对照组口服阿司匹林100 mg,1次/d;硝苯地平控释片30 mg,1次/d;胺碘酮第1周200 mg/次,3次/d,第2周200 mg/次,2次/d,第3周起200 mg,1次/d。治疗组在对照组治疗基础上加服瑞舒托伐他汀10 mg,1次/d。若血压不能达标则加用吲达帕胺片2.5~5 mg,1次/d。两组均治疗12个月,对比两组疗效、阵发性心房颤动再发率、持续性心房颤动发生率,治疗前后对比两组左房内径、血脂、hsCRP、肾素、AngⅡ的表达水平及肝肾功能。计量资料采用t检验,计数资料采用x~2检验,P0.05为差异有统计学意义。结果总有效率、阵发性心房颤动复发率、持续性心房颤动发生率对照组分别为67.5%、32.5%、15.0%,治疗组分别为92.5%、7.5%、2.5%,比较差异均有统计学意义(均P0.05)。治疗后对照组左房内径及血脂指标(TC、LDL-C、HDL-C、TG)[(35.42±0.36)mm、(4.33±0.79)、(2.80±0.21)、(0.99±0.21)、(2.04±0.48)mmol/L]与治疗组[(33.10±0.45)mm、(3.24±0.60)、(1.44±0.20)、(1.26±0.17)、(1.13±0.35)mmol/L]比较差异均有统计学意义(均P0.05)。治疗后对照组hs-CRP、肾素、AngⅡ水平[(3.52±0.12)mg/L、(0.47±0.27)ng·ml~(-1)·h~(-1)、(60.94±21.44)pg/ml]与治疗组[(2.98±0.11)mg/L、(0.36±0.32)ng·ml~(-1)·h~(-1)、(50.89±30.22)pg/ml]比较差异均有统计学意义(均P0.05)。结论高血压并发阵发性心房颤动的患者应用瑞舒伐他汀治疗,能够降低阵发性心房颤动的再发率,减少持续性心房颤动的发生率,减小左房内径,降低血清hs-CRP、肾素、AngⅡ的水平,从而提高疗效,值得临床应用。     

阵发性心房颤动患者血清炎性因子水平及其来源

目的 探讨阵发性心房颤动患者肿瘤坏死因子（TNF）-α、白细胞介素（IL）-6和可溶性肿瘤坏死因子受体1 （sTNFR1）的变化及其可能来源.方法 连续采集30例行射频消融术治疗的阵发性心房颤动患者（阵发性心房颤动组）股静脉、高位右房、冠状窦及左房血液样本,酶联免疫吸附法检测血清TNF-α、sTNFR1和IL-6水平,与相同部位采血的20例阵发性室上性心动过速患者（阵发性室上性心动过速组,左侧旁路）进行比较.结果 阵发性心房颤动组股静脉、高位右房、冠状窦及左房血清TNF-α和IL-6水平较阵发性室上性心动过速组增高[TNF-α：（4.45±1.76） ng/L比（0.59±0.36） ng/L、（6.67±1.43） ng/L比（0.51±0.30） ng/L、（8.35±2.03） ng/L比（0.85±0.50） ng/L、（9.97±2.70） ng/L比（0.28±0.29） ng/L;IL-6：（2.02±0.87） ng/L比（1.04±0.63） ng/L、（1.51±0.68） ng/L比（0.74±0.26） ng/L、（2.00±0.51）ng/L比（0.88±0.35） ng/L、（1.32±0.47） ng/L比（0.48±0.28） ng/L],差异有统计学意义（P=0.000）.阵发性心房颤动组高敏C反应蛋白（hs-CRP）水平高于阵发性室上性心动过速组[（2.41±1.35） mg/L比（1.10±0.53） mg/L,P=0.002].阵发性心房颤动组左房TNF-α水平较其他三个部位增高,差异有统计学意义（P=0.000）;IL-6水平在股静脉和冠状窦增高,与高位右房和左房比较差异有统计学意义（P＜ 0.05）; sTNFR1水平在股静脉、高位右房、冠状窦比较差异无统计学意义（P＞0.05）,但均高于左房,差异有统计学意义（P＜0.05）.各部位血清TNF-α、IL-6水平及肘静脉hs-CRP水平与左房内径（LAD）存在相关性（P＜ 0.01或＜0.05）;左房sTNFR1水平与LAD呈正相关,而右房sTNFR1水平与LAD呈负相关（P＜0.01）.结论 阵发性心房颤动患者血清hs-CRP、TNF-α及IL-6水平增高,心房颤动患者TNF-α、IL-6水平增高可能来源于心肌分泌,并与左房增大有关.     

Effectiveness of amiodarone in resistant arrhythmias

Amiodarone is used in the treatment of previously drug-resistant supraventricular and ventricular arrhythmias. We report our experience with amiodarone in 8 patients. Five patients had paroxysmal atrial flutter, one had paroxysmal atrial fibrillation, one had supraventricular tachycardia, and one ventricular tachycardia. Considerable improvement, both objectively and subjectively, was observed in all patients. Side effects were as follows: all patients had corneal microdeposits, one developed left bundle branch block which resolved on stopping amiodarone, and one reported constipation and abdominal pains. Six patients have been treated for 10–28 months; 3 developed tolerance at 4–14 months after the introduction of amiodarone therapy, but symptoms improved with increased dosage. It is important to watch for the development of tolerance to this drug.     

缬沙坦对持续性心房颤动复律后的干预治疗

目的 通过观察血管紧张素Ⅱ受体拮抗剂(ARB)缬沙坦在持续性心房颤动患者复律后对窦性心律的维持作用及对左心房收缩功能的影响,探讨ARB是否能够逆转心房重构,从而消除心房颤动的复发.方法 选择72例持续性心房颤动患者,按随机数字表法分为对照组和缬沙坦组,每组36例.两组复律当日均给予胺碘酮200 mg口服,每8 h 1次,5 d后减量为200mg,每12 h 1次,5 d后再次减量为200 mg,每日1次,持续至1个月,之后以100 mg每日1次维持至8个月,两组患者复律前后均给予正规抗凝治疗,缬沙坦组同时给予缬沙坦80 mg每日1次维持至8个月.复律后当日及复律后8个月时分别行超声心动图检查,比较两组左心房内径(LAD)、舒张末期面积(EDA)、舒张末期容量(EDV)、收缩末期面积(ESA)及收缩末期容量(ESV)的变化.结果 72例患者中,59例经胺碘酮复律成功,时间(18±6)h,3例72 h未成功,经电复律1次成功,10例直接电复律1次成功.72例中3例未完成随访,2例意外死亡被剔除,共67例完成随访,其中对照组33例,缬沙坦组34例,均无发生显著心动过缓而退出试验.随访8个月,对照组12例(36.4%,12/33)复发,缬沙坦组6例(17.6%,6/34)复发,两组心房颤动复发率比较差异有统计学意义(P＜0.05).缬沙坦组复律后8个月LAD、EDA、ESA、EDV、ESV与复律后当日比较均显著下降,差异有统计学意义(P＜0.05或＜0.01),而对照组各项指标比较差异均无统计学意义(P＞0.05).复律后8个月,两组收缩压、舒张压均较复律前有所下降,但差异无统计学意义(P＞0.05).结论 缬沙坦联合胺碘酮用于持续性心房颤动复律后,对维持窦性心律、改善心功能较单用胺碘酮更有效.

Abstract：

Objective To observe the influences of valsartan on maintenance of sinus rhythm and left atrial contraction function after cardioversion of permanent atrial fibrillation, and discuss if angiotensin Ⅱ (AT-Ⅱ)receptor blockade could reverse atrial remodeling and remove the basis of permanent atrial fibrillation relapse. Methods Seventy-two patients with permanent atrial fibrillation were divided into control group (36 patients)and valsartan group(36 patients)by random digits table. The two groups were given amiodarone of 200 mg oral once every 8 hours on the eardioversion day. Five days later, the dose was decreased to 200 mg once every 12 hours. And another 5 days later, the dose was again decreased to 200 mg once a day. And 1 month later, the dose was decreased to 100 mg once a day which would be kept for 8 months. On the electrical conversion day and after 8 months, the patients of the two groups were performed echocardiography, and the left atrial dimension(LAD), end diastolic area(EDA), end diastolic volume (EDV), end systolic area(ESA)and end systolic volume(ESV)were compared. Results In 72 patients,59 patients were successful in recovering from sinus rhythm, and duration time was(18±6)h,3 patients were given electrical conversion after 72 h, and 10 patients were directly given electrical conversion and successful. Three patients didn't finish follow-up,and 2 patients died. Sixty-seven patients finished follow-up,among whom 33 patients were in control group and 34 patients were in valsartan group. After followed up for 8 months, 36.4%(12/33)patients recurred in control group, and 17.6%(6/34)patients recurred in valsartan group(P＜0.05).The levels of LAD, EDA, ESA, EDV and ESV in valsartan group were significantly decreased(P＜0.05 or＜0.01), but they showed no significantly difference in control group(P ＞ 0.05). The systolic pressure and diastolic pressure decreased in two groups, but there were no significant difference (P＞0.05). Conclusion Valsartan combines with amiodarone is superior to amiodarone in maintaining sinus rhythm and improving left atrial contraction function after cardioversion of permanent atrial fibrillation.     

无休止性心动过速的临床研究

目的通过8例无休止性心动过速合并心律失常性心肌病患者的临床、心电图及超声心动图的特点及射频消融术后的观察,提高对无休止性心动过速合并心律失常性心肌病的再认识。方法全组8例患者,男3例,女5例,年龄12～32岁。24h动态心电图记录中心动过速所占比例可达50%～90%。超声心动图检查左室舒张末径56～74mm,EF值28%～45%。心律失常类型(1)无休止性房性心动过速2例;(2)持续性反复性交界区心动过速(PJRT)5例;(3)无休止性室性心动过速1例。结果7例患者经射频消融术得以根治。随访6个月～2年半,心动过速均未复发,射频消融术后3个月超声心动图报告心脏各腔大小正常或接近正常,EF值明显提高。心功能恢复正常。     

Successful hybrid therapy combined with oral bepridil and ICD in a patient with amiodarone refractory life-threatening ventricular tachyarrhythmia associated with ischemic cardiomyopathy

A 68-year-old man was admitted to our hospital for the treatment of angina and ventricular tachyarrhythmia. A coronary and left ventricular angiography showed coronary artery disease and ischemic cardiomyopathy with severe left ventricular dysfunction. A percutaneous transluminal coronary angioplasty was performed successfully in the right coronary artery and his angina symptoms disappeared. However, ventricular tachycardia (VT)/ventricular fibrillation (VF) occurred spontaneously and converted to sinus rhythm with direct current shock (300 J). Oral amiodarone (200 mg/day) and continuous intravenous infusion of nifekalant and lidocaine were started. In addition, a dual chamber implantable cardioverter defibrillator (ICD) for his VT/VF was implanted. However, VT/VF occurred repeatedly after discontinuation of nifekalant. After the administration of bepridil (200 mg/day), VT/VF was completely prevented without nifekalant administration. The hybrid therapy with ICD and oral bepridil is very useful for the treatment of amiodarone resistant ventricular tachyarrhythmia.     

Diagnosis and treatment of haemodynamically significant fetal tachycardia--in 33 cases

INTRODUCTION: Fetal tachycardia may lead to an increased pre- and postnatal morbidity and mortality rate particularly if it is complicated by cardial decompensation and hydrops fetalis. AIM AND METHODS: In this study 33 fetal tachycardia cases diagnosed and treated between 1993 and 2004 in the fetal echocardiography unit of the I. Department of Obstetrics and Gynecology of the Semmelweis University, Budapest are reviewed. The data of postnatal care of the newborns delivered in the author's department from these pregnancies, and the follow up data provided by the National Institute of Cardiology are examined as well. RESULTS: Mean gestational age at diagnosis of fetal tachycardia was 30 weeks (21-41 weeks). The tachyarrhythmias were classified into atrial flutter (n = 8), supraventricular tachycardia (n = 18), arrhythmia absoluta (n = 5), parasystole (n = 1) and brady-tachyarrhythmia (n = 1). Six cases were complicated by hydrops fetalis, 13 cases by cardial dysfunction. Transplacental antiarrhythmic therapy was applied in 22 cases, in 8 cases the newborns were delivered because of advanced gestational age, in 3 cases tachyarrhythmia resolved spontaneously or therapy was not indicated. The drug of first choice for transplacental therapy was digoxin, which was combined with amiodarone or verapamil (n = 10). Transplacental therapy led to cardioversion in 13/22 cases. The outcome of the 33 examined pregnancies was live birth in 27 cases, in utero death in 3 cases and 3 newborns were delivered elsewhere. The postnatal documentation of 24 newborns out of the 27 born in the author's department is available. At the time of birth 15/24 newborns were in sinus rhythm--out of whom 5 developed tachyarrhythmia later during the neonatal period--, 9/24 were tachycardic. Out of the 14 cases of tachyarrhythmia detected in the neonatal period altogether 3 resolved spontaneously, in 7 cases antiarrhythmic therapy was successful, in 4 cases unsuccessful. In 2 of these latter cases electrical cardioversion led to sinus rhythm. Neurological disorder was not detected in any case. In the early postnatal period 2 in utero severely decompensated newborns died. The follow-up data of 10 children is available, the follow-up period ranges between 6 weeks and 5 and a half years. All 5 children with history of supraventricular tachycardia are in sinus rhythm, 3 of them after suspending antiarrhythmic treatment, while the other 2 still on antiarrhythmic medication. Four out of 5 children with history of atrial flutter are in sinus rhythm, 2 of them left antiarrhythmic therapy, and 2 of them still take antiarrhythmic agents after electrical cardioversion. The atrial flutter of a 3 month old child could not be controlled yet permanently, despite several drug combinations applied. CONCLUSIONS: Survival and late prognosis of tachycardic fetuses treated in utero is good. A prospective study of even more cases is required to establish uniform therapeutic guidelines and to provide appropriate follow-up data.     

老年人群12导联动态心电图应用的研究

目的探讨老年心律失常给予动态心电图(Holter)诊断的临床价值。方法选取2018年3月-2019年3月天津东丽医院收治的152例老年心律失常患者为研究对象,均行常规心电图与12导联Holter检查,比较两种检查方法对冠心病的检出率。结果 Holter的心肌缺血检出率为78.95%,高于常规心电图的31.58%,差异有统计学意义(P<0.05)。Holter对房、室性早搏成对,间歇左、右束支阻滞,短阵房、室速,房室阻滞等的检出率高于常规心电图,差异有统计学意义(P<0.05);两种方法对房、室性早搏单发,持续性心房扑动,房颤的检出率比较差异无统计学意义(P>0.05)。结论Holter是心电信息学的重要组成部分,对冠心病心律失常的诊断实用、高效、准确、重复性强,是重要的无创性心电检测技术。     

新生儿心律失常的临床分析及随访与预后

目的 研究新生儿心律失常的病因、发病机制、心律失常类型、临床表现及预后。 方法 对1986年1月～1998年12月入院并诊断为心律失常的20例新生儿进行临床分析和随访。结果 房性早搏7例,室性早搏7例,各占35％(7/20);室性心动过速2例,窦房结功能不良2例,各占10％(2/20);房扑1例,Ⅰ度房室传导阻滞1例,各占5％(1/20)。转归:心律失常消失16例,占80％(16/20);失访2例,死亡2例,各占10％(2/20)。结论 新生儿心律失常以房性早搏或窒性早搏最常见,常不需要治疗,预后良好。室性心动过速若原发病严重,则预后很差。     

Designing clinical trials for paroxysmal atrial tachycardia and other paroxysmal arrhythmias

Paroxysmal atrial tachycardia may be useful as a model for designing clinical trials of paroxysmal tachycardia. Individual occurrences of paroxysmal atrial tachycardia are clinically independent events, and the time periods between events follow an exponential probability distribution; i.e. paroxysmal atrial tachycardia behaves like a Poisson process. We propose that treatment of paroxysmal atrial tachycardia can be studied efficiently using a clinical trial with a two period cross-over design in which placebo and investigational therapy are delivered in random order. A screening phase, dose ranging phase, and both limbs of a cross-over plane can be completed in 180 days or less in each patient.     

白介素—11在乙肝肝硬化所致的血小板减少症中的临床应用

目的 探讨白介素-11（rhIL-11）治疗肝硬化血小板减少的疗效与副作用。方法 对16例乙肝肝硬化血小板〈20×109/L患者应用IL-11治疗,8例剂量为1.5mg/d,8例剂量为3mg/d,iH,7-14天,观察血小板升高情况、副作用及剂量相关性。结果 13例应用5天内血小板开始升高,平均7天达高峰,14例显效,10例血小板上升〉60×109/L,4例〉20×109/L,主要副作用为：发热、乏力、全身肌肉酸痛、浮肿、心率失常（房速、房颤）,其中,3mg/d剂量副作用表现更突出。结论 IL-11能有效治疗乙肝肝硬化所致的血小板减少,耐受性较好,对老年人需注意其心脏毒性。     

多普勒联合超声评价心房颤动复律后心房顿抑的临床研究

目的 应用心肌组织多普勒成像(TDI)技术结合M型超声、脉冲多普勒及心尖搏动图测定二尖瓣环运动速度及幅度、跨二尖瓣血流速度及压力变化,评价心房颤动复律后心房顿抑的发生.方法 38例心房颤动患者于复律后1 h行超声检查.采用TDI技术测量二尖瓣环游离壁舒张晚期心肌组织运动峰速(Am)、舒张早期心肌组织运动峰速(Em),M型超声测量二尖瓣环游离壁舒张晚期心肌最大运动幅度(DAD)、舒张早期心肌最大运动幅度(DED),脉冲多普勒测量舒张早期跨二尖瓣血流速度(E)和舒张晚期跨二尖瓣血流速度(A),心尖搏动网记录心房收缩压力波.根据有无心房顿抑分为顿抑组和非顿抑组.结果 复律后1 h,11例患者发生心房顿抑.复律方式两组比较差异无统计学意义(P>0.05);顿抑组复律前心房颤动持续时间及左房内径与非顿抑组比较差异有统计学意义(P<0.05).心房收缩期A、Am及DAD值顿抑组均为0,非顿抑组分别为(43±34)cm/s、(6±4)cm/s、(0.27 ±0.18)cm,两组比较差异均有统计学意义(P<0.05).结论 心房颤动复律后有心房顿抑发生.左房内径越大、心房颤动持续时间越长,越容易发生心房顿抑.