抗心律失常药物致尖端扭转性室速5例

抗心律失常药物应用后导致原有心律失常加重或诱发新的心律失常，称为抗心律失常药物的致心律失常作用。尖端扭转性室速(TPVT)是典型的药物导致的心律失常。导致TPVT最常见于IA类和Ⅲ类抗心律失常药物，如奎尼丁、普鲁卡因酰胺、双异丙吡胺、胺碘酮等。现将我们收集到的5例报道如下。     

极短联律距多形性室性心动过速1例报告

极短联律距多形性室速临床上为特殊的室性心动过速,我院收治1例该病患者,现报告如下。1　病例报告患女,45岁,无诱因一天内出现心慌、反复晕厥伴抽搐发作5次于1999年8月9日16时入院。晕厥每次持续1分钟许自行缓解,既往无心脏病、癫痫病史,查体除早搏外无阳性体征。血液化验:Ｋ 4.32ｍｍｏｌ/Ｌ,Ｎａ 147.3ｍｍｏｌ/Ｌ,Ｃｌ-105.4ｍｍｏｌ/Ｌ,ｉＣａ1.18ｍｍｏｌ/Ｌ,ＴＣａ2.42ｍｍｏｌ/Ｌ,ＴＧ1.00ｍｍｏｌ/Ｌ,Ｃｈ3.69ｍｍｏｌ/Ｌ,ＨＤＬ1.36ｍｍｏｌ/Ｌ,ＥＳＲ75ｍｍ/ｈ。胸片:心肺膈正常。心电监护示室早ＲｏｎＴ,1～2次/分,短阵室速心室…     

极短联律间距室性心动过速临床分析

目的:探讨极短联律间距室性心动过速的治疗.方法:本组10例,男4例,女6例,年龄16～62岁,平均42±12岁.本类室性心动过速以正常QT伴极短联律间距(平均300ms)为心电图特征,临床上反复发作晕厥,无器质性心脏病.通常对Ⅰ、Ⅱ、Ⅲ类抗心律失常药物无效,但维拉帕米治疗有效.结果:维拉帕米静脉注射能终止本类室性心动过速,用量5～39mg,平均22mg.结论:维拉帕米治疗本类室性心动过速安全、有效,使用剂量宜个体化.     

伴极短联律间期的多形性室性心动过速—附2例报告

报道2例心电图特征具有正常QT、极短联律问期的伟短暂晕厥的多形性空性心动过速。2例患者对维拉帕米治疗反应不佳，而对胺碘酮或合用利多卡因治疗有效，不同于文献报道的无器质性心脏病基础，对维拉帕米治疗十分敏感的同类型多形性室速。提示该类型室速可能有不同的病理基础，容易误诊，当对维拉帕米治疗反应不佳时，应及时换用其他抗心律失常药物。     

抗精神病药致长Q-T间期综合征6例临床分析

获得性长Q-T间期综合征常由药物引起,以抗心律失常药、抗精神病药物为多见,常伴尖端扭转型室性心动过速,严重者可危及生命.作者报道本院10年来收住6例因抗精神病药致长Q-T间期综合征的临床资料,以探讨可能的防治措施.     

1例抗精神病药物诱导长QT综合征并发尖端扭转型室性心动过速患者的护理

总结1例由抗精神病药物诱发获得性QT间期延长伴尖端扭转型室性心动过速患者的救治与护理经验。对患者进行24 h的心电监护,严密关注患者的意识、生命体征、心律及心电图的变化,在第一时间进行除颤,配合医生进行电复律,及时识别临时起搏器的异常工作情况,正确使用抢救药物以及补钾补镁药物;对患者及家属进行心理护理,出院时进行健康指导。该患者在发生尖端扭转型室性心动过速后得到及时有效的救治,经过15 d的治疗与护理后,患者康复出院。     

抗心律失常药导致室性心律失常187例临床分析

目的分析抗心律失常药导致室性心律失常的原因。方法应用动态心电图分析187例抗心律失常药致室性心律失常。结果各种抗心律失常药都有不同程度致心律失常不良反应,尤其Ic类抗心律失常药致室心律失常作用较强。结论当左室射血分数降低(LVEF40%),联合应用利尿剂及/或地高辛,和/或应用抗精神类药物,用药后QT间期离散度增加等都可出现致室性心律失常不良反应。     

联合应用抗精神病药物致恶性症状群

1　病例资料男 ,34岁。精神分裂症病史 8年 ,长期服用氯氮平2 5 0～ 30 0ｍｇ/ｄ。否认高血压、癫病史。因精神症状加重住院 ,予氯氮平、氯丙嗪各 2 75ｍｇ/ｄ口服 ,约 1个月后出现发热、咳嗽、气促。查体 :体温 39 5℃ ,脉搏14 0 /ｍｉｎ ,呼吸 5 0 /ｍｉｎ ,血压 195 / 75ｍｍＨｇ。急性病容 ,烦躁不安 ,大汗淋漓 ,面色苍白 ,唇甲发绀 ,三凹征明显 ,双肺可闻及大量干湿性罗音及痰鸣音 ,心脏未见异常 ,腹部无特殊 ,双下肢无水肿 ,四肢肌张力呈齿轮样强直 ,病理反射未引出。Ｘ线胸片示肺部感染 ;心电图示窦性心动过速。血白细胞 12 1× 1…     

分子生物学与室性心动过速

心脏病患者存在从心脏大体结构到心肌细胞、蛋白分子的病理和病理生理改变．其中包括与心电生理异常有关的结构和功能改变。在这些病理基础上，经诱发，患者可出现包括室性心动过速（室速）在内的多种心律失常。近年来，随着分子生物学、细胞生物学、     

Relationship Between QT Interval Duration and Electrical Induction of Ventricular Tachycardia

The relation of inducible ventricular tachycardia (VT) to QT interval duration of ventricular paced rhythm has not been evaluated. To clarify this relation we measured corrected QT interval duration (QT_C) during sinus rhythm and QT interval duration during ventricular paced rhythm (QT-V) in patients with coronary artery disease without (non-VT group = group B) and with inducible VT (VT group = group A). Duration of QT-V was greater in the VT group (n = 20) compared with non-VT group (n = 20) during ventricular pacing at cycle lengths of 600 ms (424 ± 26 vs 396 ± 19 ms, P < 0.01), of 500 ms (407 ± 20 vs 383 ± 21 ms, P < 0.01), and of 400 ms (390 ± 21 vs 362 ± 17 ms, P < 0.001). During sinus rhythm the mean values of QT_C were similar in both groups (408 ± 25 vs 413 ± 20 ms, NSJ. During ventricular stimulation the percentage of patients with values of QT-V exceeding 380 ms was 35% in non-VT group and 95% in VT group (P <0.01) at cycle length of 500 ms and 5% versus 60%, respectively, (P < 0.01), at cycle length of 400 ms. Thus, a trend toward longer QT values of ventricular paced rhythm exists in patients with inducible VT.     

Fusion with the Prolonged First Postpacing Interval in Pacing of Ventricular Tachycardia

In cases of recurrent sustained ventricular tachycardia (VT), constant fusion and progressive fusion in fhe surface electrogram were observed during overdrive pacing of VT. However, following cessation of pacing, the return cycle of VT (stimulus to the first nonpaced QRS) was longer than the VT cycle length. This phenomenon can be explained by orthodromic capture of the exit site of the VT current with a conduction time (stimulus to QRS) exceeding the VT cyde length. This site can therefore be activated during entrainment of VT during the mid-to-terminal portion of the paced QRS complex, resulting in constant fusion.     

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.     

Ventricular Tachycardia and Ventricular Fibrillation in Patients with Short P-R Intervals and Narrow QRS Complexes

Eleven patients with short P-R Intervals and narrow QRS complexes had ventricular tachycardia due to organic heart disease: mitral valve prolapse with mitral insufficiency (2 patients); alcoholic (?) cardiomyopathy (2 patients); and coronary artery disease (7 patients). Intracardiac studies showed short A-H intervals during sinus rhythm in all cases. The onset of ventricular fibrillation (which, to our knowledge, has not been observed in patients having short P-R and A-H intervals coexisting with narrow QRS complexes) was documented in 4 cases. Only 1 patient (with quinidine syncope) had been premedicated. In the 3 other patients the episodes of ventricular fibrillation appeared during bouts of atrial fibrillation with rapid ventricular rates which could have been an expression of the “enhanced A-V conduction” that had been manifested in sinus beats by short P-R and A-H intervals. In clinical settings and physiological conditions proven to be hemodynamicaliy unstable (such as transient ischemia or acute myocardial infarction) these rapid ventricular rates could have led to ventricular fibrillation; directly because of the R-on-T phenomenon, and/or indirectly due to decreased coronary perfusion. Ventricular tachycardia and ventricular fibrillation due to organic heart disease probably occur more often than suggested by the few reported cases in the literature. Its significance, however, has to be clarified by further prospective studies     

Atrial Tachycardia Facilitating Initiation of Ventricular Tachycardia

A 17-year-old male was studied because of clinically documented tachycardias showing narrow and wide QRS complexes. He was found to suffer from an atrial and a ventricular tachycardia. It was demonstrated that initiation of ventricular tachycardia occurred on reaching a critical ventricular rate during atrial tachycardia. Our study illustrates the value of electrophysiological studies in patients suspected of suffering from double or multiple tachycardias. It also shows that the occurrence of one type of tachycardia may be critically related to another type of tachycardia.     

Use of Cardioplegia to Guide Alcohol Ablation for Incessant Ventricular Tachycardia

Incessant scar‐related reentrant ventricular tachycardia is an important cause of morbidity and mortality. In patients not amenable to emergent radiofrequency catheter ablation, selective transcoronary alcohol ablation has been successfully performed. In our case study, we introduce the novel use of cardioplegia as a mapping technique for identification of the critical ventricular tachycardia isthmus to guide efficient transcoronary alcohol ablation and prevent unnecessary myocardial damage.     

Diagnostic Value of Comparison of Ventriculoatrial Interval During Junctional Tachycardia and Right Ventricular Apical Pacing

We postulated that comparison of ventriculoatrial intervals during junctional tachycardia and during right ventricular apical pacing may provide similar diagnostic information to that obtained from the insertion of ventricular extrasystoles during tachycardia. We studied 39 patients with either atrioventricular reentrant tachycardia (AVRT) (23 patients) using a single atrioventricular accessory pathway or atrioventricular nodal reentrant tachycardia (AVNRT) (16 patients). Ventriculoatrial [VA] intervals were measured during tachycardia, during right ventricular apical pacing at the same rate as that of the tachycardia and following a ventricular extrasystole delivered at the minimum reset interval (minimum prematurity of a ventricular extrasystole required to advance the subsequent atrial complex by more than 10 msec). The difference between the minimum VA interval during tachycardia and during ventricular pacing was closely related to both the minimum reset interval (r = 0.92, P less than 0.001) and the difference between the minimum VA interval during tachycardia and following a ventricular extrasystole delivered at the minimum reset interval (r = 0.97, P less than 0.001) in the 23 patients in whom the minimum reset interval could be determined. The ratio between the minimum ventriculoatrial interval during tachycardia and ventricular pacing could be determined in all cases and was between 1.53 and 1.68 in AVRT with right free wall (two patients), 0.94 and 1.29 with anteroseptal (three patients), 0.91 and 1.08 with posteroseptal (five patients) and 0.48 and 0.71 with left free wall (13 patients) pathways, while it was between 0.32 and 0.27 in AVNRT (16 patients). The ratio was more discriminative when corrected for ventricular latency and was also useful when calculated from the high right atrial electrogram. We concluded that comparison of ventriculoatrial intervals during junctional tachycardia and during right ventricular apical pacing can discriminate between the mechanisms of tachycardia and the site of pathway. It provides similar information to that obtained from ventricular extrasystoles during tachycardia with the advantage that it can be determined in all cases.(ABSTRACT TRUNCATED AT 400 WORDS)     

持续性特发性室性心动过速误诊为室上性心动过速的探讨

1病例资料男,25岁。因胸闷、心悸2小时入院。患者缘于2小时前搬重物时突然出现心悸、心前区憋闷、头晕、恶心,伴全身乏力,无头痛、呕吐、视物旋转及晕厥,休息后无缓解,自摸脉搏190~200/m in,急诊来我院。既往体健。查体:脉搏195/m in,血压110/60 mmHg。听诊心律齐,未闻及病理性杂音。心电图示:心率187/m in,QRS增宽,时限0.12秒,电轴异常右偏260,°QRS波V1导联呈宽大伴顶端切迹的R形波,呈rS形,Ⅰ、Ⅱ、Ⅲ、aVF、V5导联呈rS形,aVL呈Rs形,连续描记各导联中均未见窦性P波,R-R节律规整。初诊为阵发性室上性心动过速伴室内差异性传导,见图…