极短联律间期室性早搏引起多形性室性心动过速六例分析

极短联律间期室性早搏引起多形性室性心动过速六例分析温晓红陈文珍⒇极短联律间期室性早搏引起的多形性室性心动过速（ＶＴ），其ＱＲＳ波群形态、振幅、频率及极性变化虽和尖端扭转型室性心动过速（ＴｄＰ）无异，但其ＱＴ间期，Ｔ或Ｕ波正常，必须注意鉴别。本科近年来...     

非持续性室性心动过速患者心率变异的研究

对非持续性室性心动过速（ＮＳＶＴ）患者进行心率变异（ＨＲＶ）分析。记录２４ｈ动态心电图分析６个ＨＲＶ时域指标，并对照分析ＮＳＶＴ发作前、后的窦性Ｒ－Ｒ间期标准差（ＳＤ）。结果：ＮＳＶＴ患者（ｎ＝３５）之ＨＲＶ时域指标中２４ｈ平均Ｒ－Ｒ间期（ＭＲＲＩ）、ＳＤ、５ｍｉｎ节段Ｒ－Ｒ间期均值的标准差（ＳＤＡ）、５ｍｉｎ节段Ｒ－Ｒ间期标准差的均值（ＭＳＤ）较正常对照组（ｎ＝１０５）明显下降（其中ＳＤ为９０．８８±３７．７７ｍｓｖｓ１４３．１８±３１．００ｍｓ，Ｐ＜０．０１），与病例对照组（ｎ＝４４）比较无显著性差异（Ｐ＞０．０５）。ＮＳＶＴ发作前、后５ｍｉｎ和１ｈ的ＳＤ（５ｍｉｎＲ－Ｒ节段）无显著性差异。结论：ＮＳＶＴ患者ＨＲＶ较正常对照组下降，但ＨＲＶ下降与ＮＳＶＴ无明显关系。     

洋地黄诱发混乱性房—室律伴扭转性室性心动过速

患者女 ,2 9岁。临床诊断 :风心病 ;亚急性细菌性心内膜炎 ;心衰三度。血培养 :白葡萄球菌。长期服用洋地黄。图 1示同一导联Ｐ波有多种形态 ,Ｐ -Ｐ周期不等 ,Ｐ -Ｒ间期多变。Ⅱ导联Ｐ波有 6种形态 :高宽型、高尖型、窄尖型、较钝型、低尖型、倒置型。以上Ｐ波形成多源性房性心动过速(ＡＴ)。Ⅱ导联室性早搏 (ＰＶＳ)形态有 3种 ,联律间期不等 ,第1种Ｒｓ型 ,第 2种ＱＳ型 ,第 3种宽Ｒ型 ,Ｖ1 导联是呈多源性ＰＶＳ二联律。Ｖ3导联可见短阵性扭转性室性心动过速 (ＶＴ)。图 1　混乱性房 -室律　　讨论　本图多源性ＡＴ的Ｐ波 5、6种形态十…     

多形性室性心动过速的心电学特征及临床意义

为观察多形性室性心动过速（ＰＶＴ）的临床意义，对１８例ＰＶＴ与３４例单形性室性心动过速（ＭＶＴ）的心电学和临床特征对比分析后发现：１．ＰＶＴ组的室性心动过速（ＶＴ）≥６阵／日的发生率高、频率快、ＱＲＳ波的时限宽，两组差异显著（Ｐ〈０．０５）；２．两组室性早搏总数、３组以上和ＱＲＳ波类型≥３种的发生率差异显著（Ｐ〈０．０５）；３．ＰＶＴ组左室射血分数≤４０％、左心室肥大、心力衰竭和心性死亡的发生率均     

低血钾致巨大倒置U波电交替及室性心律失常1例

患者女 ,35岁 ,因呕吐腹泻 2ｄ ,全身无力心悸 ,胸闷加重1ｄ入院。临床诊断 :急性胃肠炎 ,低血钾。心电图示 (图 1) :窦律 ,ＰＰ间期 0 .92～ 0 .96ｓ,ＰＲ间期 0 .16ｓ ,ＱＲＳ时限 0 .0 9ｓ,ＳＴⅠ、ａＶＬ、Ｖ5、Ｖ6 轻度下移 ,ＴⅠ、Ⅱ、ａＶＬ、ａＶＦ低平 ,ＴＶ3～Ｖ6 倒置 ,巨大倒置Ｕ波呈交替出现 ,伴极性电交替 ;倒置Ｕ波深达 1.6ｍＶ ,尤其在Ｖ3、Ｖ4 导联显著。深倒置Ｕ波与Ｔ波融合使ＴＵ界限不清 ,ＱＴｕ间期 0 .88ｓ,并伴有室性早搏 (ＰＶＳ)及短阵室速。随后患者出现短阵昏厥及轻度抽搐 ,心电监护出现尖端扭转性室速及室颤 ,…     

食管心房调搏对儿童室上性心动过速的诊断

３４例阵发性室上性心动过速（室上速）患儿经食管心房调搏检查，诊断为房室结折返１３例。快慢径有效不应期分别为３３７±５９．４６ｍｓ和２７８±７１．２４ｍｓ（Ｐ＜０．０５）；传导时间分别为２２０±５０ｍｓ和３０８±５８．０９ｍｓ（Ｐ＜０．０５）。旁室旁道折返１９例，其中６例为隐性，旁道前向有效不应期２００～３２０ｍｓ，与年龄呈正相关，但无显著性。自律性房住心动过速２例。儿童ＳＶＴ以房室折返为主，测定ＰＶ１－ＰＥ时距及ＲＰＥ间期有助于鉴别折返性室上速的类型及旁道位置。房室结折返ＰＶ１－ＰＥ时距近于零，房室折返为３４．２９±８．５ｍｓ．左侧旁道为正值，右侧为负值。但ＰＶ１有时辨认不满意，有局限性。房室结折返ＲＰＥ间期＜７０ｍｓ．而旁路折返则＞７０ｍｓ。     

急性血栓性心肌缺血室性心律失常的实验研究(I.方法学)

目的　用三维标测方法观察急性冠状动脉血栓性心肌缺血室性心律失常的机制。方法　向左冠状动脉回旋支（ＬＣＸ）近端释放阳极电流刺激血栓形成。结果　９ 例发生非持续性室速（ＮＳｕＶＴ）,其激动的起源和维持在心室的不同部位。６例发生持续性室速（ＳｕＶＴ）,其诱发是由于局灶性机制。Ｓｕ－ＶＴ的维持在３／６ 例是由于局灶性机制,另３ 例ＳｕＶＴ的维持,是由于心肌内的一个大折返径路,即以前壁缺血区心内膜下经间隔作为快径,而左室后壁心外膜并经心肌内返回心内膜下作为慢径。４／６ 例Ｓｕ－ＶＴ在１０～４１ｓ内蜕变成心室颤动（室颤,ＶＦ）。１ 例ＳｕＶＴ自行终止,但于１４ ｍ ｉｎ 后出现４ 个连续的室性激动诱发ＶＦ。ＶＦ诱发是由于多发的折返波形成。平均总的心肌激动时间（ＡＴ）在缺血前是（４０±４）ｍ ｓ,缺血后增加达２７～１０２ ｍ ｓ。ＳｕＶＴ发作前ＡＴ值（１０１±２８）ｍ ｓ比１ ｍ ｉｎ 前的ＡＴ值（７９±１５）ｍ ｓ明显延长（Ｐ＜ ０．０１）。ＶＦ前１０ 个持续性室速激动的平均ＡＴ值为（１６９±２９）ｍ ｓ,比ＳｕＶＴ没有发展为ＶＦ的犬的ＡＴ值明显延长。结论　ＬＣＸ的血栓栓塞可导致９０％ 的犬出现ＮＳｕＶＴ,６０％ 的ＳｕＶＴ及５０％ 的ＶＦ。     

扩张型心肌病猝死高危因素分析

收治１２２例扩张型心肌病（ＤＣＭ），其中１２例住院期间发生猝死（猝死组），１１０例存活（存活组）。结果发现，持续性室速（ＳＶＴ）的猝死率为５２．９％，非持续性室速（ＮＳＶＴ）为８．１％；心室晚电位（ＶＬＰ）阳性者猝死率为３０％，阴性者为１１％；猝死组生前平均ＱＴ离散度（ＱＴｄ）、右室流出道分别为９６．２２±２２．２３ｍｓ、３．５４±０．１８ｃｍ，存活组分别为５４．２０±１２．１１ｍｓ、２．８８±０．２８ｃｍ。提示ＳＶＴ、ＶＬＰ阳性、ＱＴｄ显著增加、右室流出道扩张为ＤＣＭ的猝死高危因素     

多形性室速临床分型与治疗的探讨

多形性室速临床分型与治疗的探讨叶国良（浙江省义乌市人民医院３２２０００）关键词多形性室速ＱＴ间期联律间期多形性室速（ＰＶＴ）即尖端扭转型室速（Ｔｄｐ）是一种介于室速与室颤之间的特殊类型的室速［１］。根据其病因与类型不同，治疗方法差异很大，预后与之关系...     

平板运动试验诱发尖端扭转性室速1例

心电图上ＱＴ间期不长者 ,由运动试验诱发尖端扭转性室速 (ＴｄＰ)较为少见 ,现报告 1例如下。患者女 ,5 1岁。阵发性胸痛 ,劳累时加重 1月余。血常规、肝肾功能均正常 ;胸片、常规心电图正常 ,拟诊劳累性心绞痛 ,行活动平板心电运动试验 (ＴＥＴ)。采用Ｂｒｕｃｅ方案 ,共运动了 7′10″,达 3级 ,在恢复期 2ｍｉｎ时出现冠状Ｔ波 ,3′44″患者发生晕厥。心电图示 :成对室早 (ＰＶＳ)、短阵室速 (ＶＴ) ,后自行终止 ,恢复神志。经分析系少见的ＱＴ间期正常 ,短联律ＰＶＳ(ＲｏｎＴ现象 )诱发ＴｄＰ见图 1。讨论　ＴｄＰ多在ＱＴ间期延长基础…     

特发性右室流出道室性早搏触发多形性室性心动过速或心室颤动四例的临床特点

目的报道4例特发性右室流出道(RVOT)室性早搏(PVC)触发多形性室性心动过速/心室颤动(PVT/VF)的临床特点。方法 76例起源于RVOT的VT患者,其中4例为PVC触发PVT/VF,总结4例的临床资料并与另72例有关资料相比较。结果所有4例触发PVT/VF时的PVC与孤立PVC的形态一致,但2种PVC的联律间期发生了明显改变,其改变幅度均≥70 ms,其中2例缩短,2例延长。1例孤立PVC时的联律间期亦不恒定。72例PVC触发的单形VT患者每天PVC次数为15 427±1 109,QT间期为404±15 ms,孤立PVC联律间期为419±22ms。4例PVC触发PVT/VF患者中3例1天的PVC次数与72例PVC触发的单形VT患者平均PVC次数相当。4例患者的QT间期及孤立PVC联律间期与另72例患者相当。而4例PVT/VF的周长均小于280 ms,明显短于72例VT的平均周长(324±59 ms)。72例单形VT患者发生晕厥比率4.1%;4例PVT/VF患者中发生晕厥者2例。采用激动标测和起搏标测证实4例患者PVC均起源于RVOT间隔侧,经射频导管消融PVC取得成功。结论起源于RVOT的PVC触发PVT/VF具有PVC联律间期不恒定及PVT/VF的周长短的临床特征,射频导管消融治疗有效。     

Long-term efficacy of antitachycardia pacing for treatment of ventricular tachycardia in patients with implantable cardioverter/defibrillator]

Antitachycardia pacing techniques (ATP) have proved useful for termination of ventricular tachycardia (VT). However, little is known about the efficacy and safety off ATP during long-term follow-up in a larger study population. We analyzed the data of 80 ICD patients (pts) with spontaneous monormorphic VT, mean age 59 +/- 12 years, the mean follow-up was 26 +/- 17 months. 50 pts (62.5%) had coronary artery disease, 18 (22.5%) dilative cardiomyopathy (DCM), the remaining 12 pts (15%) had no or other cardiac diseases. 2926 episodes of ventricular tachycardia (cycle length 349 +/- 51 ms, 240-520 ms) occurred in 64/80 pts (80%), overall efficacy of ATP was 89.9%, acceleration occurred in 4.1% of VTs. Success of ATP did not correlate with positive ATP testing on induced arrhythmias, LVEF, NYHA class or aneurysm. Neither underlying heart disease nor antiarrhythmic medication had an impact on the ATP success rate. ATP efficacy was linked significantly to short VT cycle length (VTCL, 240-300 ms, p < 0.01) and long coupling intervals (91-97%), p < 0. 01). Acceleration occurred in 32% of pts and in 4.1% of VT episodes; it was also dependent on short VT cycle length (< 300 ms vs > 300 ms, p < 0.04) and short coupling intervals (< 81% vs >/= 81%, p 相似文献   

Comparison of coupling intervals that induce clinical and nonclinical forms of ventricular tachycardia during programmed stimulation

Coupling intervals of extrastimuli that induced 57 previously documented unimorphic ventricular tachycardias (VTs) were compared with coupling intervals that induced 57 episodes of polymorphic VT or ventricular fibrillation (VF) in patients without a documented or suspected history of polymorphic VT or VF. Programmed stimulation was performed with the patient in the drug-free state, with 1 to 3 extrastimuli and 2 basic drive cycle lengths (600 or 500 ms, and 400 ms) at 2 right ventricular sites; stimuli were twice diastolic threshold. The mean coupling intervals of the first, second and third extrastimuli that induced nonclinical VT/VF (241 +/- 19, 185 +/- 19 and 173 +/- 24 ms, respectively, mean +/- standard deviation) were significantly shorter than the corresponding coupling intervals that induced the clinical VTs (266 +/- 25, 228 +/- 32 and 214 +/- 27 ms, respectively, p less than 0.001 for each). Regardless of the basic drive cycle length, the shortest coupling interval required to induce a clinical VT was 180 ms. Depending on the drive cycle length, 29 to 70% of nonclinical VT/VF induced by 3 extrastimuli required a coupling interval of less than 180 ms to induce. Therefore, a lower limit of coupling intervals may be identified below which only nonclinical VT/VF is induced by programmed stimulation. Restriction of coupling intervals to this lower limit may allow for significant improvement in specificity without compromise in the sensitivity of programmed ventricular stimulation protocols.     

Respective role of sympathetic tone and of cardiac pauses in the genesis of 62 cases of ventricular fibrillation recorded during Holter monitoring

Sixty-two Holter recordings of sudden death due to ventricularfibrillation (VF) were analysed by full disclosure and computerizedprocessing. Thirteen sudden deaths were due to torsades de pointesin non coronary subjects (11/13), related to quinidine-likedrugs and/or hypokalaemia: they were always initiated by a longRR cycle due to a post-extrasystolic pause, and announced bya progressive decrease of mean heart rate (from 77.5 ±2.5 to 60.6 ± 2.7 beats min^–1, P<0.001), inthe three preceding hours. The other cases occurred in coronarypatients (45/49), with acceleration of ventricular tachycardia( VT), monomorphic in 24 cases, polymorphic in 13, the ventricularrate increasing from 220.6 ±55 to 241.5 ±69 beatsmin^–1, rather than with primary VF (12 cases). A cardiacpause (RR cycle exceeding 125% of the mean five preceding cycles)was present in 22/49 cases immediately before the onset of VT/VF.The coupling interval of the extrasystole initiating VT/ VFwas shorter than the shortest value encountered before: 377.6±± 94.5 ms vs 421.4 ± 92.3. The prematurityindex (coupling interval/preceding RR cycle ratio) was lowerin primary VF than in VT leading to VF. In the last hour precedingVF, ST changes were unusual (five cases), whereas heart rateincreased from82.8±20 to 92.0 ± 26.7 beats min^–1,(P<0001).This acceleration was in fact present only in caseswithout pauses before the onset of VT/VF: from 85.0±22.8to 99.1 + 31.1 (n = 27, P<0.001) whereas no changeoccurredin cases with preceding pause: from 79.8 ±15.5 to 80.8±16.3 (n = 22, P = NS). As a result, VT/VF without apreceding pause occurs in the setting of a higher heart rate,most probably reflecting a higher sympathetic drive. Preventionof these two main determinants by pacing and beta-blocking therapyshould bemore efficient than the use of antianginal or antiarrhythmicdrugs.     

短QT间期综合征发生室性心律失常机制探讨

目的:探讨吡那地尔(pinacidil)建立的短QT间期综合征模型致室性心律失常的机制,并观察缝隙连接激动剂抗心律失常肽(AAP10)对该模型电生理参数的影响.方法:利用pinacidil灌注家兔楔形心肌块建立短QT间期综合征模型. 将20只新西兰长耳白兔随机分成pinacidil组和AAP10组,每组10只.pinacidil组灌流10 μmol/L的pinacidil,AAP10组灌流AAP10 500 nmol/l和pinacidil 10 μmol/L的混合液,同步记录灌流前后内外膜动作电位和容积心电图,观察灌流前后QT间期,跨室壁离散度(TDR),程序性刺激观察心肌组织不应期和室性心律失常的诱发情况.结果:灌流pinacidil后,QT间期从(291±19)ms缩到(232±19) ms (P<0.05),TDR从(44±12)ms减少到(22±7)ms(P<0.05),而不应期从(164±8)ms减少到(112±14)ms(P<0.05),室性心律失常发生率从0/10增加至8/10(P<0.05).AAP10 组和pinacidil组的TDR、QT间期、不应期及室性心律失常的诱发率无显著差别.结论:TDR减小和不应期的缩短可能是pinacidil建立的短QT间期模型致室性心律失常的基础,AAP10对pinacidil诱导的短QT间期综合征模型电不稳定性无明显影响.     

Triggers of Sustained Monomorphic Ventricular Tachycardia Differ Among Patients with Varying Etiologies of Left Ventricular Dysfunction

Background: The mechanisms underlying the initiation of sustained ventricular tachycardia (VT) have not been fully elucidated. The extent to which reentry, abnormal automaticity, and triggered activity play a role in VT differs depending on the etiology of left ventricular dysfunction. By analyzing electrograms from implantable cardioverter defibrillator (ICD), we sought to determine whether there were differences in VT initiation patterns between patients with ischemic and nonischemic cardiomyopathy. Methods: We analyzed ICD electrograms in patients with ejection fractions < 40% who had sustained VT over a 27‐month period. The trigger for VT onset was classified as a ventricular premature beat (VPB), supraventricular tachycardia, or of “sudden onset.” The baseline cycle length, VT cycle length, coupling interval, and prematurity ratio were recorded for each event. The prematurity ratio was calculated as the coupling interval of the VT initiator divided by the baseline cycle length. Results: Sixty‐three VT events in 14 patients met the inclusion criteria. A VPB initiated the VT in 58 episodes (92%), 1 episode (2%) was initiated by a supraventricular tachycardia, and 4 episodes (6%) were sudden onset. The prematurity ratio was significantly higher (P < 0.05) in patients with ischemic cardiomyopathy (0.751 ± 0.068) as compared to patients with nonischemic cardiomyopathy (0.604 ± 0.139). Conclusion: VPBs initiated most sustained VT episodes. A significantly higher prematurity ratio was observed in the ischemic heart disease group. This may represent different mechanisms of VT initiation in patients with ischemic versus nonischemic heart disease.     

Mechanisms determining sudden death. A cooperative study of 69 cases recorded using the Holter method

A cooperative study involving 23 centres enabled review of 69 cases of sudden death occurring less than one hour after onset of symptoms recorded by the Holter method and not related to recent, clinically documented myocardial infarction or to class IV cardiac failure. The 15 cases of asystole (22 p. cent) were observed in elderly patients (73.3 +/- 2.7 years) whose known ischaemic heart disease (12/15) was confirmed in 10 cases as the direct cause by the preceding acute ST changes. In 2 cases, death resulted from AV block presumed to be iatrogenic. The 13 episodes of torsades de point (19 p. cent) occurred mainly in younger women (58.8 +/- 6 years) without apparent cardiac disease (8 cases) and were provoked by a Group IA antiarrhythmic drug (7 cases) or by hypokalemia (3 cases). Apart from 1 case of congenital long QT syndrome, slowing of the sinus rhythm was observed (78.3 +/- 2.6 to 60.2 +/- 2.7 bpm, p less than 0.001) in the 3 hours preceding these episodes, and ventricular bigeminy with a long coupling interval was recorded in the lasts seconds before the torsades. The 41 (59 p. cent) cases of ventricular fibrillation (VF) were observed in men aged 64.9 +/- 2 years with coronary artery disease (39/41). However signs of acute ischaemia were only found in 5 cases. The VF was primary in 8 cases and secondary to ventricular tachycardia (VT in 33 cases). An acceleration of the cardiac rhythm (83.3 +/- 3.4 to 90 +/- 4.1 bpm, p less than 0.01) was recorded in the hour preceding VF and other arrhythmias were common: atrial tachycardia (4 cases), atrial extrasystoles (4 cases), a new type of ventricular extrasystoles (VES). The VF and VT were preceded by a long cycle in 17 cases. The first complex was different from previous VES in 10 cases and identical to the previous VES in 16 cases; in 4 cases this feature could not be identified and in 11 cases there were no premonitory VES. The coupling interval of the initial VES was shorter than that of the most premature preceding VES (368 +/- 13 ms vs 442 +/- 19 ms, p less than 0.001), especially in primary VF (335 +/- 9 ms, N = 8) compared to polymorphic VT (360 +/- 12 ms, N = 11) or monomorphic VT (384 +/- 18 ms N = 22).(ABSTRACT TRUNCATED AT 250 WORDS)     

Morphological findings in apparently idiopathic ventricular tachycardia. An echocardiographic haemodynamic and histologic study

In order to investigate the anatomic substrate of ‘idiopathic’ventricular tachycardia (VT) 10 patients with chronic recurrentVT and no apparent sign of heart disease underwent an echocardiographic,haemodynamic and histologic study (5 males, 5 females: meanage=40±11 years). In the patients with a left bundle branch block morphology ofVT (7 cases), four showed findings compatible with an arrhythmogenicright ventricular dysplasia or a right ventricular cardiomyopathy.In the other three all examinations were normal with the exceptionof endomyocardial biopsy, which showed slight non specific changesin two. Of the remaining 3 cases (characterized by a right bundlebranch block morphology of VT or by the presence of polymorphicVT) one had histologic evidence of myocarditis while anotherdeveloped dilated cardiomyopathy. Macroscopic and/or microscopic ventricular abnormalities arefrequently found in patients with VT which appears idiopathic.In these cases myocardial disease is frequently progressive,despite optimal control of VT.     

Influence of the cycle length of basic drive on induction of sustained ventricular tachycardia associated with coronary artery disease

The relation between the cycle length of basic drive during programmed ventricular stimulation and the coupling intervals at which sustained monomorphic ventricular tachycardia (VT) was initiated was analyzed in patients with coronary artery disease and documented sustained VT. The study included 28 patients in whom hemodynamically tolerable, monomorphic sustained VT was inducible at different cycle lengths of basic drive during the same electrophysiologic study. The stimulation protocol included single or double premature stimuli during paced ventricular rhythms at different cycle lengths of basic drive. The coupling intervals of premature stimuli for induction of VT (considered the outer margin of the echo zone) during step 1 of the stimulation protocol (basic drive at cycle lengths of 500 or 430 ms) were compared with those during step 2 (basic drive at cycle lengths of 370 or 330 ms). The mean cycle length of induced sustained VT was 370 +/- 79 ms. The mode of induction of VT remained the same in 23 patients (single or double premature stimuli); in 5 patients, fewer premature stimuli were required during step 2 than step 1. By moving from step 1 to step 2, VT could be induced at longer coupling intervals of the premature stimuli in 23 patients (82.1%). The mean increase in the sum of the coupling intervals was 52 +/- 37 ms. In 5 patients, the coupling intervals either did not change from step 1 to step 2 (n = 1) or decreased by an average of -40 +/- 14.1 ms. The results suggest that inducibility of VT is favored by a decrease in the cycle length of basic drive.(ABSTRACT TRUNCATED AT 250 WORDS)     

Increased variability of the coupling interval of premature ventricular beats may help to identify high-risk patients with coronary artery disease

OBJECTIVE: The purpose of this study was to determine the characteristics and predictive value of the variability of coupling interval of ventricular premature beats (VPBs) for cardiac mortality in patients with coronary artery disease (CAD). BACKGROUND: Frequent VPBs have been linked to an increased risk for cardiac death in patients with coronary artery disease. It is unknown whether analysis of coupling interval of VPBs from ambulatory ECG recordings can be used for risk statification in these patients. METHODS: In 78 consecutive symptomatic patients with documented CAD who presented with frequent VPBs (>720/24 h), the analysis of VPBs' coupling interval (SDNV) was performed. Left ventricular function, ventricular arrhythmias and simple measures of heart rate variability were assessed. Mean follow-up was 702+/-329 days. Cardiac mortality was the primary end-point of the study. RESULTS: During follow-up, 14 patients died-11 deaths were cardiac. Left ventricular ejection fraction (LVEF)<40%; no beta-blocker treatment and digoxin use were clinical variables showing a significant association with cardiac mortality. The presence of non-sustained ventricular tachycardia (nsVT), especially if more than five episodes were present; short mean sinus cycle (<750 ms) and SDNV were associated with cardiac deaths. Mean SDNV was 79+/-29 in victims and 63+/-29 in survivors (p<0.05). Univariate Cox regression analysis revealed that the presence of SDNV>80 ms carried a relative risk of 6.7 for cardiac mortality. The adjusted relative risk was 13.3 for nsVT and 4.4 for SDNV>80 ms. Among patients with nsVT, mortality rate was significantly higher with SDNV>80 ms (58%), compared to lower SDNV (14%, p<0.01). Sixty-four percent mortality rate was observed in patients with LVEF<40%, presence of nsVT and SDNV>80 ms, compared to 17% in similar patients with lower SDNV (p<0.05). CONCLUSION: The analysis of coupling interval of ventricular premature beats form the same 24-h ECG recordings may complement the standard Holter analysis for risk stratification. This seems especially promising in the subgroups of patients at highest risk-those with LV systolic dysfunction, non-sustained VT or both.