射频消融治疗室性早搏触发特发性室性心动过速／心室颤动的病例分析

目的探讨射频消融治疗在室性早搏（室早）触发特发性室性心动过速／心室颤动（室速／室颤）中的作用。方法总结3例由室早触发室速／室颤的治疗经验,1例对室早进行射频消融（RF—CA）并植入心律转复除颤器（ICD）,另1例经射频消融未完全消除室早而选择植入ICD,第3例经射频消融成功消除室早,未再发室颤。结果随访2年,3例患者均存活,ICD未再记录到室速／室颤。结论在室早触发室速／室颤病例中,应分析室早与室速／室颤的相关性,给予个体化治疗,射频消融室早可以消除／减少晕厥和室颤的发作。     

Ablation of premature ventricular contraction triggering ventricular fibrillation in a patient with early repolarization syndrome

Early repolarization syndrome is associated with an increased risk of arrhythmic death caused by ventricular fibrillation (VF). VF is usually initiated by premature ventricular contractions (PVCs), and PVCs commonly arise from Purkinje system, the ventricular outflow tract, and papillary muscles. We report the case of a patient with J wave syndromes and recurrent VF, triggered by PVCs originating from the tricuspid annular region. VF was successfully suppressed by catheter ablation of the triggering PVCs, and there has been no recurrence of VF during a follow-up period of 6 months.     

Mode of initiation and ablation of ventricular fibrillation storms in patients with ischemic cardiomyopathy

OBJECTIVES: We report on the initiation of ventricular fibrillation (VF) storm in patients with ischemic cardiomyopathy (ICM) and the results of targeted ablation to treat VF storm. BACKGROUND: Monomorphic premature ventricular contractions (PVCs) have been shown to initiate VF in patients without structural heart disease. METHODS: A total of 29 patients with ICM and documented VF initiation were identified. In 21 patients, VF storm was controlled with antiarrhythmic drugs and/or treatment of heart failure. Eight patients with VF (mean 52 +/- 25 episodes) refractory to medical management required ablation. All patients underwent three-dimensional electroanatomical mapping using CARTO (Biosense-Webster Inc., Diamond Bar, California), and PVCs were mapped when present. Scarred areas were identified using voltage mapping. RESULTS: Monomorphic PVCs initiated VF in all 29 identified patients. Five of eight patients requiring ablation had frequent PVCs that allowed PVC mapping. The earliest activation site was consistently located in the scar border zone. The PVCs were always preceded by a Purkinje-like potential (PLP). Ablation was successfully performed at these sites. In three patients, infrequent PVCs prevented mapping, but PLPs were recorded around the scar border. Ablation targeting these potentials along the scar border was successfully performed. During follow-up (10 +/- 6 months), one patient had a single VF episode and another developed sustained, monomorphic ventricular tachycardia. There was no recurrence of VF storm. CONCLUSIONS: Ventricular fibrillation in ICM is triggered by monomorphic PVCs originating from the scar border zone with preceding PLPs; targeting these PVCs may prevent VF recurrence. In the absence of PVCs, both substrate mapping and ablation appear to be equally effective.     

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。     

Catheter ablation of ventricular fibrillation storm in patients with infiltrative amyloidosis of the heart

Recent studies have demonstrated that premature ventricular contractions (PVCs) originating from the Purkinje system are responsible for initiation of ventricular fibrillation (VF) in patients with and without structural heart disease. Ablation of the PVCs has been shown to be feasible. We report 2 patients with repetitive VF associated with cardiac amyloidosis. Each episode of ventricular arrhythmia was preceded by monomorphic PVC. The electrical storms were drug resistant. Electrophysiological testing was performed and the sites of earliest activation were localized within the left ventricle in the absence of significant scar tissue. After ablation, PVCs subsided and there were no further VF recurrences.     

Repolarization abnormalities in survivors of out-of-hospital ventricular fibrillation.

Survivors of out-of-hospital ventricular fibrillation (VF) are at high risk for recurrent VF, probably reflecting continued myocardial electrical instability. In this study 12-lead ECGs of 125 VF survivors with coronary heart disease were examined and compared to those of 98 ambulatory post-MI patients. The study was part of an effort to define clinical identifiers of patients likely to develop sudden cardiac death. Ventricular fibrillation survivors were commonly had premature ventricular complexes (PVCs):30% versus 13% (P less than 0.01). In addition, ECGs of VF survivors showed a significantly greater prevalence of ST-segment depression (46% versus 10%), T wave flattening (52% versus 26%), and QTc prolongation (35% versus 18%). It is proposed that these repolarization abnormalities represent asynchronous repolarization, which together with frequent PVCs, may set the stage for re-entrant ventricular dysrhythmias and ultimately VF. It is also possible that repolarization abnormalities together with premature ventricular contractions might serve as markers of patients with coronary heart disease who are at increased risk for sudden cardiac death.     

Successful radiofrequency catheter ablation for electrical storm of ventricular fibrillation in a patient with Brugada syndrome.

The case of a 41-year-old man with Brugada syndrome (BS) who suffered electrical storms (ES) of ventricular fibrillation (VF) is presented. Although intravenous infusion of isoproterenol (ISP) suppressed the VF occurrence, he consistently experienced recurrence of VF following discontinuation of ISP infusion. Quinidine and cilostazol were ineffective. An analysis of VF episodes on electrocardiogram monitoring revealed that the QRS morphology of the first beat of all VF episodes was identical to that of premature ventricular complexes (PVCs) with a left bundle branch-block morphology and inferior axis, which occurred repetitively before the episodes of VF and were recorded throughout the day. In addition, stored electrograms from the implantable cardioverter defibrillator showed that the first beat of all VF episodes had the same morphology. On electrophysiological study, the VF-triggering PVC was found to originate from the posterior portion of the right ventricular outflow tract area and their elimination, which was achieved with radiofrequency catheter ablation (RFCA), resulted in the suppression of ES. Although several other PVCs were still observed, the patient has been free of VF during the 29-month follow-up period. This case indicates that RFCA of VF-triggering PVCs may be useful in the treatment of drug-resistant ES in patients with BS.     

Idiopathic ventricular fibrillation associated with long-coupled Purkinje ectopy

Introduction

Idiopathic ventricular fibrillation (IVF) is mainly associated with and triggered by short-coupled (R-on-T) ventricular ectopics. However, little is known about the risk of VF associated with long-coupled premature ventricular complexes (LCPVCs).

Objective

To examine the prevalence and characteristics of IVF patients presenting with LCPVCs.

Methods

Consecutive patients with IVF and PVCs from five arrhythmia referral centers were reviewed. We included patients presenting LCPVCs, defined as PVCs falling after the end of the T wave, with a normal QTc interval. We evaluated demographics, medical history, and clinical circumstances associated with PVCs and VF episodes. The origin of PVCs was determined by invasive mapping.

Results

Seventy-nine patients with IVF were reviewed. Among them, 12 (15.2%) met the inclusion criteria (8 women, age 36 ± 14 years). Eleven patients had documented LCPVCs initiating repetitive PVCs or sustained VF, whereas 1 had only documented isolated PVCs. In 10 of 12 patients, PVCs were recorded showing both long and short coupling intervals of 418 ± 46 and 304 ± 33 ms, respectively. Mapping showed that PVCs originated from the left Purkinje in 10 patients, from the right Purkinje in 1 patient, and both in 1 patient. Compared to other patients from the initial cohort, IVF with LCPVCs was associated with a left-sided origin of PVCs (92% in long-coupled IVF vs. 46% of left Purkinje PVCs in short-coupled IVF, p = .004).

Conclusion

Long-coupled fascicular PVCs, traditionally recognized as benign, can be associated with IVF in a subset of patients. They can induce IVF by themselves or in association with short-coupled PVCs.     

Mode of onset of ventricular fibrillation in patients with Brugada syndrome detected by implantable cardioverter defibrillator therapy

OBJECTIVES: We sought to demonstrate the mode of spontaneous onset of ventricular fibrillation (VF) in patients with Brugada syndrome. BACKGROUND: The electrophysiologic mechanisms of VF in Brugada syndrome have not been fully investigated. METHODS: Nineteen patients (all male, mean age 47 +/- 12 years) with Brugada syndrome were treated with an implantable cardioverter defibrillator (ICD). The implanted devices were capable of storing electrograms during an arrhythmic event. We investigated the mode of spontaneous onset of VF according to the electrocardiographic features during the episode of VF, which were obtained from stored electrograms of ICDs and/or electrocardiographic (ECG) monitoring. RESULTS: During a follow-up of 34.7 +/- 19.4 months (range 14 to 81 months), 46 episodes of spontaneous VF attacks were documented in 7/19 (37%) patients. The event-free period between ICD implantation and the first spontaneous occurrence of VF was 14.6 +/- 12.1 months (range 3.7 to 27.4 months). We investigated 33/46 episodes of VF, for which electrocardiographic features (10 to 20 s before and during VF) were obtained from ICDs and/or ECG monitoring in five patients. A total of 22/33 episodes of VF were preceded by premature ventricular contractions (PVCs), which were almost identical to the initiating PVCs of VF. Furthermore, in three patients who had multiple VF episodes, VF attacks were always initiated by the same respective PVC. The coupling interval of the initiating PVCs of VF was 388 +/- 28 ms. CONCLUSIONS: Spontaneous episodes of VF in patients with Brugada syndrome were triggered by specific PVCs. These findings may provide important insights into the pathophysiological mechanisms causing VF in Brugada syndrome.     

Short-term normalization of ventricular repolarization by transcatheter ablation in a patient with suspected Brugada Syndrome

We report a 30 year old male without structural heart disease who presented with recurrent nocturnal syncope and aborted sudden cardiac death. 12-lead ECG showed elevated ST in inferior leads and short coupled premature ventricular complexes (PVCs). Propafenone challenge suggested a diagnosis of an atypical Brugada syndrome. Two morphological types of PVCs and ventricular fibrillation (VF) were induced during propafenone challenge test. He underwent two ablation procedures in right ventricular inflow tract and left ventricular post-inferior septum region by pace-mapping, respectively. After ablation, VF could not be induced and the elevated ST segments normalized. Two subsequent propafenone challenge tests were also negative. Nonetheless, elevated ST segments and PVCs reappeared by 1 month follow-up. An implantable defibrillator was recommended, but the patient declined for financial reasons. Unfortunately, he suffered a sudden cardiac death at home 10 weeks post-ablation. These findings suggest that short-term normalization of ventricular repolarization possibly due to radiofrequency ablation may occur in Brugada syndrome. However, the transient nature of this finding suggests that it is not a reliable indicator of protection against sudden cardiac death.     

射频导管消融治疗特发性室性期前收缩触发的心室颤动／多形性室性心动过速

目的：探讨特发性室性期前收缩（早搏,PVC）触发心室颤动和（或）多形性室性心动过速（VF／PVT）的临床特点及射频导管消融治疗效果。方法：313例无器质性心脏病接受射频导管消融治疗的特发性PVC患者,其中6例发生了由PVC触发的VF／PVT,分析该6例患者的临床资料及射频导管消融治疗效果。结果：该6例患者动态心电图可记录到频发PVC[（16303±5854）次／d],PVC联律间期及基础QT间期分别为（412±44）ms和（407±10）ms。这些参数值在另外307例特发性PVC患者中分别为（15570±4743）次／d、（419±36）ms和（404±8）ms,两组间无显著性差异。313例患者中,有88例记录到由PVC触发的单形态室性心动过速（VT）。PVC触发VF／PVT患者中晕厥发生率（3／6）高于由PVC触发的单形态VT患者（4／88,4．5％,P〈0．05）,PVT的周长[（235±22）ms]则短于单形态VT组[（324±29）ms,P〈0．05]。针对触发VF／PVT的PVC消融后随访的10～36个月期间,所有6例患者未再发生晕厥、VF及心脏骤停。结论：恶性VF／PVT可能由一些特发性PVC诱发,射频导管消融PVC治疗可作为一项有效的治疗选择。     

Electrocardiographic determinants of the polymorphic QRS morphology in idiopathic right ventricular outflow tract tachycardia

Coupling Intervals and Polymorphic QRS Morphologies . Introduction: Premature ventricular contractions (PVCs) arising from the right ventricular outflow tract (RVOT) can trigger polymorphic ventricular tachycardia (PVT) or ventricular fibrillation (VF) in patients with no structural heart disease. We aimed to clarify the ECG determinants of the polymorphic QRS morphology in idiopathic RVOT PVT/VF. Methods and Results: The ECG parameters were compared between 18 patients with idiopathic PVT/VF (PVT‐group) and 21 with monomorphic VT arising from the RVOT (MVT‐group). The coupling interval (CI) of the first VT beat was comparable between the 2 groups. However, the prematurity index (PI) of the first VT beat was smaller in the PVT‐group than in the MVT‐group (P < 0.001). Furthermore, the QT index, defined as the ratio of the CI to the QT interval of the preceding sinus complex, was also smaller for the PVT/VF in the PVT‐group than that for the VT in the MVT‐group (P < 0.01). In the PVT‐group, the CI of the first VT beat was comparable between that of VT and isolated PVCs, but the PI of the first VT beat was shorter for VT than isolated PVCs (P < 0.05). The PI was the only independent determinant of the polymorphic QRS morphology (odd ratio = 2.198; 95% confidence interval = 1.321–3.659; P = 0.002). Conclusion: The smaller PIs of the first VT beat may result in a polymorphic QRS morphology. (Cardiovasc Electrophysiol, Vol. 23, pp. 521‐526, May 2012)     

特发性右室流出道心律失常患者J波的发生率及其临床特征

目的 调查J波在特发性右室流出道室性心动过速或室性早搏（RVOT-VT/PVCs）病人的发生率及其临床特征。方法 该研究纳入143例特发性 RVOT-VT/PVCs的患者和285例年龄和性别匹配的健康体检者作为对照组。 评估、比较两组间 J-波的发生率。 依据J波的存在与否,将患者分为伴有J波的 RVOT-VT/PVCs组（J-VT/PVCs组）和不伴有J波的 RVOT-VT/PVCs组（non-J-VT/PVCs组）,对两组的临床和电生理数据进行比较。 结果 与对照组比较,J波在特发性 RVOT-VT/PVCs患者中更为常见（39. 9% vs 16. 1% ,P〈0. 01）。 与 non-J-VT/PVCs组比较,J-VT/PVCs组持续性VT、晕厥有较高的发生率,分别为24. 6% vs 4. 7% ;26. 3% vs 2. 3% ,P均〈0.01。 而且VT的周期更短[（304±56）ms vs（350±56）ms,P〈0. 01]。 两组中无心室颤动或心脏猝死发生。 结论 特发性RVOT-VT/PVCs患者,有较高的J波发生率;有J波的患者伴随有较严重的心律失常 。     

Brugada综合征室性心律失常发作的时间特征及其临床意义

目的运用Holter和置入式心脏复律除颤器(ICD)研究Brugada综合征(BrS)患者室性心律失常发作的时间特征。方法8例BrS患者和6例特发性BrS心电图征者均为男性,平均年龄(41.07±11.49)岁,根据临床表现分为心室颤动(室颤)组和无室颤组各7例,行Holter检查比较两组间室性早搏(室早)发作的时间特征。根据ICD的随访资料,分析室颤发作的时间特征。结果Holter显示,多数患者室早总数在0~74(9.61±17.23)个/24h,两组间室早的数量差异无统计学意义[(108±269)个/24h与(8±19)个/24h,P>0.05]。室颤组的98.67%的室早发作集中在夜间2200至凌晨700,而无室颤组为44.14%,室颤组明显高于无室颤组(χ2=1480,P<0.01)。5例患者ICD置入后随访9~54(23.80±17.96)个月,75次室颤发作中93.3%集中在夜间2200至凌晨700。结论高危的BrS患者的室早具有夜间和凌晨集中发作的特征,可能是新的无创性危险分层指标。BrS患者的室颤发作多集中在夜间和凌晨,可据此设计给药方案以减少副作用。     

Site-specific arrhythmogenesis in patients with Brugada syndrome

INTRODUCTION: It has been believed that electrophysiologic abnormality of the epicardial region of the right ventricular free wall may play an important role in arrhythmogenesis of phase 2 reentry in Brugada syndrome, but clinical evidence of the occurrence of ventricular arrhythmias at the right ventricular free wall has not been evaluated. In this study, we evaluated the site-specific inducibility of ventricular fibrillation (VF) and the origin of spontaneous premature ventricular contractions (PVCs) in patients with Brugada syndrome. METHODS AND RESULTS: Forty-five patients with Brugada-type ECG were enrolled in this study. Spontaneous PVCs were recorded in 9 patients. Programmed electrical stimulation (PES) was performed at the right ventricular apex (RVA), the free wall and septal region of the right ventricular outflow tract (RVOT), and the left ventricle (LV). The inducibility of PVT/VF was evaluated at each ventricular site, and the origin of PVC was determined by pace mapping. Sustained VF was induced in 17 patients. VF was induced in all 17 patients by PES at RVOT. Although PES at the septal region of the RVOT induced VF in only 5 patients (29%), PES at the free-wall region of the RVOT induced PVT/VF in 13 patients (76%). PES at RVA induced VF in only 2 patients (12%), and PES at LV failed to induce any arrhythmic events. Ventricular pace mapping showed that 64% of PVCs occurred at the free-wall region of the RVOT, 18% at the septal region of the RVOT, 9% at RVA, and 9% at LV. CONCLUSION: VF in patients with Brugada syndrome frequently is induced at the free-wall region of the RVOT area. The origin of PVC appears to be related to the site of PVT/VF induction by PES.     

Mode of Onset of Malignant Ventricular Arrhythmias in Idiopathic Ventricular Fibrillation

Mode of Onset of Idiopathic VF. Introduction : The mode of onset of malignant ventricular arrhythmias (ventricular tachycardia [VT] or ventricular fibrillation [VF] has been well described in patients with organic heart disease and in patients with the long QT syndromes. Less is known about the mode of onset of VF in patients with out-of-hospital VF who have no evidence of organic heart disease or identifiable etiology.
Methods and Results : We reviewed the ECGs of all our patients with Idiopathic VF. Documentation of the onset of spontaneous arrhythmias was available for 22 VK episodes in 9 patients (6 men and 3 women; age 41 ± 16 years). In all instances, spontaneous VF followed a rapid polymorphic VT, which was initiated by premature ventricular complexes (PVCs) with very short coupling intervals. The PVC initiating VF had a coupling interval of 302 ± 52 msec and a prematurity index of 0.4 ± 0.07. These PVCs occurred within 40 msec of the peak of the preceding T wave. Pause-dependent arrhythmias were never observed.
Concltision : Cardiac arrest among patients with idiopathic VF has a very distinctive mode of onset. Documentation of a polymorphic VT that is not pause dependent is of diagnostic value.     

Electrophysiologic and antiarrhythmic effects of sotalol in patients with life-threatening ventricular tachyarrhythmias

Sotalol is a unique beta-blocker that lengthens cardiac repolarization and effective refractory period (ERP). Its efficacy after intravenous (1.5 mg/kg) and oral (160 to 480 mg bid) administration was therefore evaluated in 37 patients with refractory recurrent ventricular tachycardia/fibrillation (VT/VF). Thirty-five patients, 33 with inducible VT/VF, underwent electrophysiologic testing. Intravenous sotalol lengthened the ERP in the atrium (+24.6%, p less than .01), atrioventricular node (+24.9%, p less than .01), and ventricle (+14.9%, p less than .01). It also significantly lengthened sinus node recovery time, corrected QT interval (QTc), and the AH interval, but not the HV interval. Sotalol prevented reinduction of VT/VF in 15 patients (45.5%). Twenty-five of the 33 patients (15 with positive results of electrophysiologic tests; 10 with negative results) were given oral sotalol. The drug was ineffective in seven (26.9%) and aggravated arrhythmia in one (3.8%). In four patients sotalol was withdrawn because of side effects; arrhythmias recurred late in two (7.7%). Eleven patients (42.3%) have continued on oral sotalol over a mean follow-up period of 9.2 +/- 8.6 months. Sotalol reduced (n = 21) total premature ventricular complex (PVC) count on the Holter electrocardiogram by 73% (p less than .01), paired PVCs by 89% (p less than .01), and beats of ventricular tachycardia by 95% (p less than .01). In 52% (n = 11), total reduction in PVCs was at least 85%, and incidence of paired and tachycardiac beats was reduced at least 90% (group A). In the remainder (n = 10), PVC suppression was not significant (group B). Group A included nine patients with nonreinducible VT/VF and two in whom it was reinducible; in group B, eight of 10 patients had reinducible VT/VF. The difference between the two groups (Fisher exact test) was significant (p less than .01). The prevention of reinduction of VT/VF by intravenous sotalol and suppression of spontaneously occurring arrhythmias by the oral drug were both predictive of long-term drug efficacy. Sotalol is a significant advance in the short- and long-term management of life-threatening ventricular tachyarrhythmias.     

Incidence of the coexistence of left ventricular false tendons and premature ventricular contractions in apparently healthy subjects

The incidence of the coexistence of left ventricular false tendons and premature ventricular contractions (PVCs) was evaluated prospectively. Over 14 months, left ventricular false tendons were found in 71 (6.4%) of 1117 consecutive patients examined echocardiographically. Two types of false tendons were observed: longitudinal, from the ventricular septum to the posteroapical wall (n = 62), and transverse, between the septum and the lateral wall (n = 9). Among 62 patients with PVCs and no underlying heart disease, false tendons were detected in 35 (56%); 28 had unifocal and seven had bifocal PVCs. Episodes of ventricular tachycardia were documented in one of the 28 patients with unifocal PVCs and in one of the seven patients with bifocal PVCs. These PVCs were poorly controlled by antiarrhythmic drugs but easily suppressed by exercise. Left ventricular false tendons were detected in 36 patients on routine echocardiographic examinations performed in the other 1055 subjects, and 10 of these patients were judged to have no underlying heart disease. PVCs were detected in two (20%) of these 10 patients. Although a definite conclusion that left ventricular false tendons are arrhythmogenic cannot be derived from these results, the unexpectedly high incidence of the coexistence suggests that left ventricular false tendons may be an etiologic factor in the development of PVCs, especially the rate-dependent and medically uncontrollable PVCs seen in apparently healthy individuals.     

射频消融治疗起源于左室流出道的非持续性室性心动过速和频发性室性早搏

目的观察左室流出道非持续性室性心动过速（室速）和频发性室性早搏患者的射频消融治疗结果,探讨此类患者的射频消融指证。方法５例患者因非持续性室速和频发性室性早搏而引起明显临床症状,药物治疗无效。采用起搏标测法确定室速和室性早搏的起源部位,并射频消融治疗。结果在升主动脉瓣左窦下方的左室流出道记录到提前（３１±４）ｍｓ的心室激动,起搏心电图１２导联ＱＲＳ波形与室速和室性早搏形态完全相同者４例,１１导联相同者１例,该部位消融后５例患者的室速和室性早搏不被诱发。随访１３±６个月,除１例患者复发,另４例的临床症状明显改善。结论射频消融治疗左室流出道非持续性室速和室性早搏安全有效,但应严格掌握适应证。     

Coupling interval and types of ventricular ectopic activity associated with ventricular runs

Repetitive 10-hour ECG recordings of 289 patients obtained within a year after myocardial infarction were analyzed for the presence of ventricular runs, and their association with various types of ventricular ectopic activity (VEA), average rate of premature ventricular complexes (PVCs), and coupling interval of PVCs initiating the runs. Tapes which contained complex VEA (bigeminy, multiform PVCs, couplets, or runs), early PVCs (coupling interval less than 400 msec), or late PVCs (coupling interval greater than 600 msec) had a substantially higher average PVC rate than those without them. The occurrence of ventricular runs was significantly more likely in tapes having other complex VEA or late PVCs than in those without them, and when tapes were stratified by PVC rates the presence of these dysrhythmias appeared to have an independent predictive value for the occurrence of runs. In contrast, the influence of early PVCs on the occurrence of runs was rather minimal, and this seemed to be related to their common association with the PVC rate. Furthermore, a larger percentage of isolated PVCs had coupling intervals between 400 msec and 600 msec, and most couplets (77%) and runs (67.8%) were initiated by PVCs with coupling intervals in this range. However, the proportion of either short (less than 400 msec) or long (greater than 600 msec) coupling interval PVCs initiating couplets or runs was significantly higher than those with intermediate coupling intervals (between 400 and 600 msec).