心脏康复治疗对缺血性心肌病室性心律失常的影响

目的:探讨心脏康复治疗对缺血性心肌病(ischemic cardiomyopathy,ICM)患者QT间期离散度(QT dispersion,QTd)、T波峰-末间期(the interval from the peak to the end of the T wave,Tp-e)及室性心律失常的影响。方法:取心内科2012年3月—2014年11月住院的ICM患99例,随机分为对照组(常规治疗)54例和治疗组(在常规治疗的基础上给予心脏康复治疗)45例。治疗前后应用超声心动图检测左心室射血分数(left ventricular ejection fraction,LVEF)和短轴缩短率(fractional shortening,FS),心电图(electrocardiogram,ECG)和动态心电图(dynamic electrocardiogram,Holte)检测室性心律失常发生情况并计算心电图QTd、Tp-e。结果:与对照组相比较,治疗组对室性心律失常的有效率显著提高(82.2%比74.1%,P0.05),LVEF和FS显著增高[(49.2±6.6)%比(42.5±5.9)%,(34.8±8.1)%比(25.8±6.2)%,均P0.05],QTd和Tp-e显著减小([45.5±7.5)ms比(51.2±7.9)ms,(118.7±13.1)ms比(129.8±12.6)ms,均P0.01]。结论:心脏康复治疗可改善ICM患者心功能,降低ICM患者QTd、Tp-e及室性心律失常的发生率。     

扩张型心肌病患者QT间期与室性心律失常及心功能的关系

目的:探讨扩张型心肌病患者QT间期(QTc) 室性心律失常及心功能的关系.方法:通过回顾性分析56例扩张型心肌病患者,测量心电图中QT间期,并计算QTc,按QTc分为两组:QTc>440 ms组36例和QTc≤440 ms组20例,观察两组室性心律失常的发生及超声心动图中左室射血分数(LVEF)变化.结果:56例扩张型心肌病患者,QTc>440 ms组36例患者中有30例并发了室性心律失常,QTc≤440 ms组20例患者有11例并发了室性心律失常,X<'2>=5.263,P=0.022,两组相应的LVEF分别为(31.17±4.607)%、(35.80±8.250)%(P=0.029).分析QTc与LVEF的相关性,r=-0.320,P=0.016.结论:扩张型心肌病患者QTc>440 ms时,室性心律失常的发生率明显增加,同时心功能显著降低,QTc与LVEF呈负相关,随着QTc的延长,LVEF逐渐降低,心功能减低.QTc可作为预测室性心律失常发生和心功能变化的一个指标.     

老年室性心律失常患者QTd与心室晚电位的关系

目的 :探讨 QT离散度 (QTd)和心室晚电位之间的关系 ,以及它们对预测定性心律失常发生的意义。方法 :分别检测 34例老年室性心律失常患者 ,30例正常老年人的 QTd和心室晚电位 (VL P)。结果 :正常组和心律失常组患者的QTd值分别为 (76 .94± 2 2 .19) ms和 (38.88± 11.46 ) ms,具有显著性差异。VL P阳性人数分别为 6例和 2 0例 ,有显著性差异 ,而 VL P阳性者和阴性者 QTd值分别为 (6 2 .72± 30 .6 7) ms和 (43.86± 17.39) ms,经检验 ,t<3.143,P<0 .0 0 5。结论 :VL P和 QTd结合起来对预测老年室性心律失常 ,乃至猝死的发生均有意义     

扩张型心肌病QT间期离散度测定及临床意义

目的探讨扩张型心肌病(DCM)、QT间期离散度(QTd)、校正QT间期(QTcd)水平及临床意义.方法测量60例DCM同步12导联心电图,分析QTd、QTcd变化,并与60例正常人对照.结果QTd、QTcd比较,DCM组高于对照组(P＜0.01);心源性猝死组高于存活组和进行性心力衰竭死亡组(P＜0.05);室性心动过速组显著高于室性早搏组(P＜0.05)和无室性心律失常组(P＜0.01),而室性早搏组又高于无室性心律失常组(P＜0.05);NYHAⅢ～Ⅳ级患者高于NYHAⅠ～Ⅱ级患者.QTd＞110ms组室速、心源性猝死和NYHAⅢ～Ⅳ级发生率显著高于QTd≤110ms组(P＜0.01或P＜0.05),而射血分数、短轴缩短率无差异;多元线性回归分析示QTd、QTcd与NYHA分级、室性心律失常、心源性猝死相关,与射血分数、短轴缩短率不相关.结论DCM患者存在QTd、QTcd变化,QTd、QTcd的增加可作为预测DCM恶性室性心律失常的敏感指标,也是发生心源性猝死的重要预测指标.QTd与NYHA分级相关而与射血分数、短轴缩短率无关.     

急性心肌梗死患者QT离散度与室性心律失常的关系

目的探讨急性心肌梗死(AMI)患者QT间期离散度(QTd)与室性心律失常的关系。方法测量42例AMI患者心电图的QTd,对有室性心律失常组与无室性心律失常组进行比较。结果AMI有室性心律失常组的QTd高于无室性心律失常组的QTd。结论AMI患者发生室性心律失常与QTd增大有关。     

小剂量胺碘酮联合倍他乐克在肥厚型心肌病伴恶性室性心律失常治疗中的应用研究

目的探讨和分析小剂量胺碘酮联合倍他乐克治疗肥厚型心肌病伴恶性室性心律失常治疗中的临床效果。方法将94例肥厚型心肌病伴恶性室性心律失常患者按照住院时间先后顺序分组为对照组和观察组;对照组:采用倍他乐克治疗;观察组:采用小剂量胺碘酮联合倍他乐克治疗。对两组患者进行为期6~12个月随访。结果观察组和对照组的治疗有效率分别为95.7%(45/47)、80.9%(38/47)。除QT间期最大值以外,两组心电图指标和LVEF治疗后均较治疗前显著改善(P0.05),观察组治疗后心率和QT间期最小值以及QT散度、LVEF、再住院率、猝死率等方面均优于对照组(P0.05)。治疗和随访期间均没有发现明显性不良反应。结论采用小剂量胺碘酮联合倍他乐克治疗肥厚型心肌病伴恶性室性心律失常,可有效地改善患者的临床症状,效果明确。     

56例扩张型心肌病患者QT离散度变化

目的:探讨扩张型心肌病(DCM)QT离散度(QTd)与恶性室性心律失常的关系。方法:选择32例恶性室性心律失常DCM,24例非恶性室性心律失常DCM和43例非心脏疾病患者,测定QTd,QTcd。结果:DCM恶性室性心律失常组及非恶性室性心律失常组QTd,QTcd明显高于对照组(P<0.05);DCM恶性室性心律失常组QTd,QTcd明显高于非恶性室性心律失常组。结论:QTd及QTcd可能是DCM恶性室性心律失常的监测指标。     

心室复极指标对急性心肌梗死恶性室性心律失常的预测价值

目的:探讨J波、ST段墓碑型抬高、Q-T间期离散度(QTd)、J-T间期离散度(JTd)预测急性心肌梗死(AMI)后恶性室性心律失常的价值.方法:回顾性分析2000年1月至2010年12月住院临床确诊的173例急性ST段抬高型心肌梗死患者的心电图(ECG)及其相关资料,根据ECG结果分为J波组(n=57)、ST段墓碑型抬高组(n=52,其中26例兼有J波出现)和通常组(n=90),J波组、ST段墓碑型抬高组分别与通常组比较QTd、JTd及恶性室性心律失常的发生率.结果:J波组、ST段墓碑型抬高组的QTd、JTd分别为(75.1+22.0)ms、(72.9±23.9)ms和(71.4±21.3)ms、(69.0±25.0),均明显高于通常组的(59.0±17.9)ms和(53.3±18.4)ms,P均＜0.01;J波组、ST段墓碑型抬高组的恶性室性心律失常的发生率分别为31.6％、28.8％,均明显高于通常组的10％,P均＜0.01.结论:心电图心室复极异常指标J波、ST段抬高、QTd、JTd延长均可作为AMI患者恶性室性心律失常的预测指标.     

胺碘酮治疗对50例心律失常QT间期离散度的影响

目的:研究胺碘酮治疗心律失常对QT间期及QT间期离散度(QTd)的影响.方法:随机选取心律失常患者50例,予以胺碘酮治疗6周,比较治疗前后心律失常的疗效及QT间期与QTd的变化.结果:治疗后心律失常均明显减少,有效率85.2%,QTd明显缩短,由(61.03±9.20)ms减至(32.8±14.1)ms(P<0.01).结论:胺碘酮能有效减少恶性心律失常发生,而且使患者QTd明显缩小.     

磷酸肌酸钠对急性心肌梗死后室性心律失常的影响

目的探讨磷酸肌酸钠对急性心肌梗死（AMI）后室性心律失常的影响,为临床治疗提供依据。方法选择2012年1月至2012年11月住院的AMI患者112例,随机分为两组,各56例。所有患者均给予AMI常规治疗（抗血小板、抗凝、他汀类药物、β受体阻滞剂、血管紧张素转化酶抑制剂、硝酸酯类药物）,有适应证者应用尿激酶溶栓。治疗组在此基础上静脉应用磷酸肌酸钠。观察治疗期间两组患者室性心律失常的发生情况及治疗前后QT间期离散度（QTd）和校正的QT间期离散度（QTcd）的变化。结果治疗组频发室早、短阵室速、持续性室速和室颤发生率均稍低于对照组,但差异无统计学意义（P均﹥0.05）。两组治疗后QTd和QTcd均低于治疗前（P均〈0.05）。治疗组治疗后QTd和QTcd为（64.17±4.14）ms及（71.33±6.52）ms,低于对照组治疗后的（71.30±5.22）ms及（77.82±7.65）ms,差异具有统计学意义（P均〈0.05）。结论磷酸肌酸钠可使AMI患者QTd和QTcd显著降低,能否确实减少AMI后室性心律失常的发生,有待扩大样本量进一步观察。     

Chest Thump and Ventricular Tachycardia

Chest thump is a simple method of treatment of some paraxysmal arrhythmias. Its therapeutic efficacy, electrophysiological bases and clinical utility have been studied in 17 patients during 45 episodes of ventricular tachycardia (VT). Thumping the precordium interrupted the VT in 22 episodes. Three types of interruption of VT have been observed: (1) In 15 episodes, single ventricular premature beats induced by the blow, occurring randomly in the cycle, stopped the arrhythmia; (2) In 5 episodes, a run of premature beats, induced by a rapid succession of blows, interrupted the tachycardia; (3) In 2 episodes, chest thump caused a short period of asystole followed by sinus rhythm. Chest thump is an antiarrhythmic treatment of definite clinical utility. The complications are rare, although there is a possibility of ventricular fibrillation. Therefore, it should be performed only under careful supervision.     

Amiodarone in the Management of Patients with Ventricular Tachycardia and Ventricular Fibrillation

Fifty-eight patients with symptomatic ventricular tachycardia (VT) or ventricular fibrillation (VF) were treated with amiodarone. All had clinical episodes of VT/VF or inducible VT during electropharmacologic testing despite treatment with maximumtolerated doses of conventional antiarrhythmic agents. Chronic treatment with amiodarone was begun at a dose of 800–1000 mg per day. Thirty-two patients were also treated with a previously ineffective conventional agent. Thirty patients underwent programmed ventricular stimulation after 2.6 ± 1.7 months (mean ± S. D.) of treatment with amiodarone at a mean daily dose of 588 ± 155 mg. VT was induced in 25 patients (sustained in 20, nonsustained in five). Seventeen patients had a recurrence of VT or VF after 0.5–9 months of treatment with amiodarone (fatal in seven, non-fatal in 10). Forty-one patients (71%) had no recurrence of symptomatic VT or VF while being treated with amiodarone (mean follow-up period, 17.1 ± 12.4 months). Among the 25 patients who had inducible VT with programmed ventricular stimulation while being treated with amiodarone, 19 patients (76%) have had no recurrence of symptomatic VT or VF overa follow-up period of 21.5 ± 7.3 months. Ambulatory electrocardiographic recordings obtained after one week of treatment with amiodarone were not helpful in predicting clinical response. Twenty-two patients (38%) developed ataxia and/or an intention tremor which improved with a decrease in the amiodarone dose. Amiodarone, either by itself or in combination with conventional antiarrhythmic drugs, has a significant therapeutic effect in high risk patients with refractory VT. The finding of inducible VT during electropharmacologic testing in patients taking amiodarone does not preclude a favorable clinical response. Neurologic toxicity is common in patients treated with 600–800 mg per day of amiodarone.     

Ventricular Pacing Induced Ventricular Tachycardia in Patients with Implantable Cardioverter Defibrillators

Appropriately timed noncompetitive ventricular pacing potentially may initiate ventricular tachycardia in patients prone to these arrhythmias. The combination of bradycardia pacing and stored electrograms in a currently available cardioverter defibrillator provides an opportunity to evaluate the occurrence of such pacing induced ventricular tachycardia. During a surveillance period of 18.7 ± 11.4 months, stored electrograms documented 302 episodes of ventricular tachycardia in 77 patients. Five patients (6.5%) demonstrated 25 episodes (1–16 per patient) of ventricular tachycardia that were immediately preceded by an appropriately paced ventricular beat (8.3% of all episodes of ventricular tachycardia). All five patients had prior myocardial infarctions and a history of monomorphic ventricular tachycardia occurring both spontaneously and in response to programmed electrical stimulation. Antitachycardia pacing terminated pacing induced ventricular tachycardia in 22 episodes; in one episode antitachycardia pacing accelerated ventricular tachycardia. In two cases shock therapy was aborted for nonsustained ventricular tachycardia. We conclude that, in selected postinfarction patients with recurrent sustained monomorphic ventricular tachycardia treated with implantable cardioverter defibrillators, appropriately timed ventricular pacing may induce ventricular tachycardia.     

Optimization of Ventricular Function by Improving the Activation Sequence During Ventricular Pacing

Abnormal electrical activation occurring during ventricular pacing reduces left ventricular (LV) pump function. Two strategies were compared to optimize LV function using ventricular pacing, minimal asynchrony and optimal sequence of electrical activation. ECG and hemodynamics aortic flowpmbe, thermodilution cardiac output, LV pressure and its maximal rates of rise (LVdP/dtpos) and fall (LVdP/dtneg) were measured in anesthetized open-chest dogs (n = 7) with healthy hearts. The QRS duration (a measure of asynchrony of activation) was 47 ± 5 ms during sinus rhythm and increased to 110 ± 12 ms during DDD pacing at the right ventricular (RV) apex with a short AV interval. During pacing at the LV apex and LV base, the QRS duration was 8%± 7% and 15%± 7% (P < 0.05) longer than during RV apex pacing, respectively. Stroke volumes, LVdP/dtpos and LVdP/dtneg, however, were higher during LV apex(15%± 16%, 10%± 12% [P<0.05], and 15%± 10%, respectively) and LV base pacing (11%± 12% [P<0.05], 3%± 12%, and 3%± 11%, respectively) than during RV apex pacing. Systolic LV pressure was not influenced significantly by the site of pacing. Biventricular pacing (RV apex together with one or two LV sites) decreased the QRS duration by approximately 20% as compared with RV apex pacing, however, it did not improve stroke volumes, LVdP/dtpos and LVdP/dtneg beyond those during pacing at the LV apex alone. In conclusion, the sequence of electrical activation is a stronger determinant of ventricular function than the synchrony of activation. For optimal LV function the selection of an optimal single pacing site, like the LV apex, is more important than pacing from multiple sites.     

Premature Ventricular Contractions Arising from the Intramural Ventricular Septum

A 68-year-old man with symptomatic idiopathic premature ventricular contractions (PVCs) underwent electrophysiological testing. Radiofrequency catheter ablation was unsuccessful at the earliest endocardial ventricular activation site in the left coronary cusp. Epicardial mapping via the cardiac veins was then performed. Balloon-occluded coronary sinus venography revealed the small branches of the anterior interventricular vein. Mapping with a microcatheter revealed the earliest ventricular activation and perfect pace map at the distal portion of the septal perforating branch, suggesting an intramural ventricular septal PVC origin. Catheter ablation was abandoned because of the inaccessibility of the ablation catheter to that site via the venous system.     

Entrainment of Ventricular Tachycardia in Arrhythmogenic Right Ventricular Tachycardia

In two patients with arrhythrnogenic right ventricular dysplasia (ARVDJ, sustained ventricular tachycardia (VT) was induced by programmed stimulations during serial drug testings. One patient had five and the other had two VT morphologies, and the sites of origin were determined by endocardial catheter mappings. When overdrive pacing was performed, constant fusion in the QflS complex was observed in the two patients. Constant fusion of a different degree was also observed at different paced cycle lengths. Both patients had dilated right ventricles and wall-motion abnormality, and the diagnosis of ARVD was further confirmed by the specimen resected at the site of origin of VT. Therefore, VT in ARVD can be entrained and reentry is the most likely mechanism of such VT.     

Beta Adrenergic Blockade in the Treatment of Sustained Ventricular Tachycardia or Ventricular Fibrillation

The value of β-blockers as antiarrhythmic drugs in patients with sustained VT or VF has received only little attention. This article summarizes the current state of knowledge regarding the identification of patients with sustained VT or VF with the highest benefit of β-blockade. The antiarrhythmic mechanisms of β-blockade and its efficacy as single or adjuvant therapy in patients with sustained VT or VF are reviewed. Current insights into the effects of β-blockade in patients suffering from VT, in particular in the setting of heart failure, are discussed and future directions are considered.     

健康人左室质量与舒张功能的关系

目的：探讨健康人左室质量与左室舒张功能的关系。方法：随机选取健康教师320名，行彩色多普勒超声心动图检查，结果：相关分析显示：伴随左室质量的增加E波的峰值速度下降，A波的峰值增加，二者比值下降，等容松驰时间延长，肺静脉收缩波峰值与舒峰值之比增加，但多元回归显示年龄增长、心率加快、体重指数大、血压高和男性是舒张功能减退的独立因素，左室质量指数进入多元回归方程，结论：决定健康人左室舒张功能的因素是年龄、心率、体重指数，血压和性别而不是左室质量。