Ventricular tachycardia due to sustained bundle branch reentry: Diagnostic and therapeutic considerations

We have identified bundle-branch reentry (BBR) as the mechanism of ventricular tachycardia (VT) during electrophysiologic studies in 48 patients at our institution. All but three patients had significant structural heart disease, that is, dilated ischemic or idiopathic cardiomyopathy, the most common of anatomic substrates. Syncope and sudden death were the modes of presentation in up to 70% of these patients. The critical prerequisite for the development of this arrhythmia is conduction delay in the His-Purkinje system, which was present in all patients and manifests as a nonspecific conduction delay or a left bundle-branch block (LBBB) in the surface electrocardiogram (ECG) and a prolonged HV interval in the intracardiac recordings. VT with an LBBB morphology is the most common form of BBR, present in 98% of patients. Transcatheter ablation of the right bundle branch (RBB) with the use of radiofrequency current is the treatment of choice, as it effectively eliminates BBR. During long-term follow-up, recurrent tachycardia due to BBR was not documented in any patient; however, congestive heart failure was a common cause of death in this population.     

特发性束支折返性室性心动过速的临床特点(附二例报道)

通过对两例特发性束支折返性室性心动过速 (BBR VT)的临床、心电图及电生理特性进行分析 ,提出该类病人的临床特点。两例病人均无器质性心脏病的证据。例 1男性 ,VT发作最长持续达 2 7h ,体表心电图呈近似心室扑动的图形 ,心内电生理检查证实为类左束支阻滞图形 ,QRS波宽 2 6 0ms。平时体表心电图QRS波正常 ,心内电图提示HV间期延长 ,VT可稳定诱发和终止 ,存在V3 现象 ,右束支消融成功。例 2女性 ,VT发作病史 7年 ,呈无休止性VT发作 ,平时体表心电图为完全性右束支传导阻滞伴左前分支阻滞图形 ,VT可稳定诱发和终止 ,发作时其QRS波宽为 14 0ms ,呈类完全性右束支传导阻滞伴左前分支阻滞图形 ,V波前有稳定的H波 ,消融左后分支后可导致Ⅲ度房室阻滞而终止VT。结论 :束支折返性VT可见于无器质性心脏病病人 ,有独特的电生理特性 ;是一种特殊类型的特发性VT     

Sustained bundle branch reentry as a mechanism of clinical tachycardia

The incidence of sustained bundle branch reentrant (BBR) tachycardia as a clinical or induced arrhythmia or both continues to be underreported. At our institution, BBR has been the underlying mechanism of sustained monomorphic ventricular tachycardia in approximately 6% of patients, whereas mechanisms unrelated to BBR were the cause in the rest. Data gathered from 20 consecutive patients showed electrophysiologic characteristics that suggest this possibility. These include induction of sustained monomorphic tachycardia with typical left or right bundle branch block morphology or both and atrioventricular dissociation or ventriculoatrial block. On intracardiac electrograms, all previously published criteria for BBR were fulfilled, and in addition, whenever there was a change in the cycle length of tachycardia, the His to His cycle length variation produced similar changes in ventricular activation during subsequent complexes with no relation to the preceding ventricular activation cycles. Compared with patients with ventricular tachycardia due to mechanisms unrelated to BBR, patients with BBR had frequent combination of nonspecific intraventricular conduction defects and prolonged HV intervals (100% vs. 11%, p less than 0.001). When this combination was associated with a tachycardia showing a left bundle branch block pattern, BBR accounted for the majority compared with mechanisms unrelated to BBR (73% vs. 27%, p less than 0.01). The above finding in patients with dilated cardiomyopathy should raise the suspicion of sustained BBR because dilated cardiomyopathy was observed in 95% of the patients with BBR. Twelve of the 20 patients were treated with antiarrhythmic agents, and the other eight were managed by selective catheter ablation of the right bundle branch with electrical energy. Our data suggest that sustained BBR is not an uncommon mechanism of tachycardia; it can be induced readily in the laboratory and is amendable to catheter ablation by the very nature of its circuit. The clinical and electrophysiologic features outlined in this study should enable one to correctly diagnose this important arrhythmia.     

Long-term outcome of patients with syncope associated with coronary artery disease and a nondiagnostic electrophysiologic evaluation

Syncope in the patient with structural heart disease and a nondiagnostic noninvasive workup is a generally accepted indication for an invasive electrophysiologic study. However, if the electrophysiologic evaluation is not highly sensitive, arrhythmic causes of syncope may not be discovered. In these patients, recurrent syncope and even sudden death may be observed at follow-up. Thus, we evaluated long-term follow-up in 68 consecutive patients who presented with syncope, coronary artery disease, and who had a negative invasive electrophysiologic evaluation. At a mean follow-up of 30 +/- 18 months (range 1 to 65), there have been 2 sudden deaths and 1 episode each of ventricular fibrillation and ventricular tachycardia in patients treated with an implantable cardioverter-defibrillator. All 4 arrhythmias occurred in patients with left ventricular fractions < or = 25%. Seventeen patients had recurrent presyncope or syncope. Bradycardia causing syncope was found in 8 of these patients. A bundle branch block at the initial evaluation predicted for the occurrence of bradycardia at follow-up. We conclude that in patients with coronary artery disease and syncope, noninducibility at electrophysiologic study predicts a lower risk of sudden death and ventricular arrhythmias. However, in patients with a reduced ejection fraction, the risk of sudden death and ventricular arrhythmias remains up to 10%/year and these patients may warrant treatment with implantable cardioverter-defibrillators. Recurrent syncope is common, and frequently a bradyarrhythmia is found to be the cause. Treatment of selected patients (especially those with bundle branch blocks) with permanent pacemakers may be justified.     

Adenosine-Sensitive Bundle Branch Reentry

Adenosine-Sensitive Bundle Branch Reentry. Introduction: Bundle branch reentry is an uncommon mechanism for ventricular tachycardia. More infrequently, both fascicles of the left bundle may provide the substrate for such macroreentrant bundle branch circuits, so-called interfascicular reentry. The effect of adenosine on bundle branch reentrant mechanisms of tachycardia is unknown.
Methods and Results : A 59-year-old man with no apparent structural heart disease and history of frequent symptomatic wide complex tachycardias was referred to our center for further electrophysiologic evaluation. During electrophysiologic study, a similar tachycardia was reproducibly initiated only during isoproterenol infusion, which had the characteristics of bundle branch reentry, possibly using a left interfascicular mechanism. Intravenous adenosine reproducibly terminated the tachycardia. Application of radiofrequency energy to the breakout site from the left posterior fascicle prevented subsequent tachycardia induction and rendered the patient free of spontaneous tachycardia during long-term follow-up.
Conclusions : Patients with ventricular tachycardia involving a bundle branch reentrant circuit may be sensitive to adenosine. These results suggest that adenosine may not only inhibit catecholamine-mediated triggered activity but also some catecholamine-mediated reentrant ventricular arrhythmias.     

Radiofrequency catheter ablation of left ventricular tachycardia in the normal heart

Background: Radiofrequency (RF) catheter ablation is a safe and effective cure for many forms of supraventricular tachycardia. Its efficacy in the cure of right ventricular outflow tract tachycardia, and some forms of left ventricular tachycardia in patients with left ventricular dysfunction, has also been shown. In contrast limited data are available to assess the role of RF catheter ablation in treating idiopathic left ventricular tachycardia (ILVT), an unusual form of tachycardia occurring in patients without demonstrable heart disease.
Aim: To examine the efficacy and safety of RF catheter ablation in patients with ILVT.
Methods: Three patients without structural heart disease and with recurrent drug-refractory ILVT (right bundle branch block and left axis morphology) underwent electrophysiologic study (EPS) to initiate and localise the site of origin of their VT. RF catheter ablation of the VT focus was performed, with success being defined as failure to reinduce VT during incremental infusion of isoprenaline.
Results: In all three patients VT was inducible by rapid right atrial pacing and/or programmed ventricular stimulation, and could be terminated by intravenous verapamil. RF catheter ablation was successful in all patients. The site of successful ablation was common to each patient and was localised to the infero-apical aspect of the left ventricular septum. It was characterised by the recording of the earliest presystolic 'P' potential during both sinus rhythm and induced ILVT. No complications occurred during the procedure. During follow-up periods ranging from six to 12 months there were no symptomatic or documented episodes of recurrent ILVT.
Conclusions: We conclude that ILVT can be safely and effectively cured by RF catheter ablation.     

Identification and ablation of three types of ventricular tachycardia involving the his-purkinje system in patients with heart disease

INTRODUCTION: Ventricular tachycardia (VT) with involvement of the His-Purkinje system (HPS) can be difficult to recognize in patients with heart disease, but it may be particularly susceptible to ablation targeting the HPS. This study defines the incidence and types of HPS involvement in VT. METHODS AND RESULTS: Involvement of the HPS was sought during electrophysiologic study with catheter mapping in 234 consecutive patients referred for catheter ablation of recurrent VT associated with heart disease. HPS VT was observed in 20 (8.5%) patients (mean ejection fraction 29%+/- 17%); in 9 (11%) of 81 patients with nonischemic heart disease and 11 (7.1%) of 153 patients with coronary artery disease (P = NS). Three types of HPS VT were observed: 16 patients (group 1) had typical bundle branch reentry, 2 patients (group 2) had bundle branch reentry and interfascicular reentry, and 2 patients (group 3) had VT consistent with a focal origin in the distal HPS. In all three groups, the VT QRS had morphologic similarity to the sinus rhythm QRS. Ablation of HPS VT was successful in all patients in whom it was attempted but produced high-degree AV block in 6 (30%). In 12 patients (60%), other VTs due to reentry through scar also were inducible. CONCLUSION: Involvement of the HPS in VT associated with heart disease has three distinct clinical forms, all of which are susceptible to ablation. Ablation often is not sufficient as the sole therapy due to other induced VT's and conduction abnormalities, requiring pacemaker and/or defibrillator implantation.     

隐匿性束室纤维介导的心动过速(附一例报告)

目的 阐明隐匿性束室纤维介导的心动过速的电生理机制及其导管消融方法。方法 研究病例为男性、29岁,心动过速病史7年余。心动过速不能被腺苷三磷酸和维拉帕米终止,但可被普罗帕酮终止。曾在院外拟诊房室结折返性心动过速,两次行慢径改良术,但心动过速仍反复反作。在我院行电生理检查一次并在非接触球囊导管标测系统（即EnSite,3000）指导下标测和消融。结果 电生理检查示窦性心律时AH为75ms,HV 44ms,心房增频刺激及程序刺激未见心室预激现象。心室600ms起搏示室房分离,RS2程序刺激无逆传A波,提示室房逆传功能较弱。心房与心室均能诱发心动过速,但心室更易诱发。心动过速时室房分离。心动过速可呈窄QRS图形、左束支传导阻滞（LBBB）图形及右束支传导阻滞（RBBB）图形。LBBB和RBBB心动过速可自行转为窄QRS心动过速。窄QRS心动过速及RBBB图形时,心动周期为300ms;LBBB图形时,心动周期为316ms,明显长于前。三种心动过速时,希氏束激动均领先于右束支激动。维拉帕米和腺苷三磷酸不能终止心动过速。专房程序刺激及超速抑制不能终止心动过速,但可被心室程序刺激终止。EnSite 3000标测系统分析发现三种心动过速的最先激动点均位于心动过速的最先活动点均位于右室间隔上部,此处行环状消融后心动过速不再诱发。随访4个月,临床无心动过速发作。结论 该患的心动过速由隐匿性束室纤维介导,其折返环路包括正常的希－浦传导系统、心室和束室纤维,其消融方法与室性心动过速相似;EnSite3000标测系统指导此类心动过速的消融有极大的优越性。     

Bundle branch reentrant tachycardia in patients with apparent normal His-Purkinje conduction: the role of functional conduction impairment

INTRODUCTION: His-Purkinje conduction delay, manifested by bundle branch block QRS complex configuration or by HV interval prolongation, is considered an essential condition for maintenance of bundle branch reentrant tachycardia (BBRT). METHODS AND RESULTS: Of 178 patients with different types of ventricular tachycardia (VT), 13 were found to have BBRT as the underlying electrophysiologic mechanism. Of these 13 patients (9 men and 4 women; mean age 64 +/- 13 years), 6 had an HV interval < or = 55 msec (group A), and 7 had a prolonged HV interval (> 55 msec; group B) during sinus rhythm (SR). PR interval (169 +/- 32 vs 339 +/- 138 msec, P = 0.01) and QRS duration (116 +/- 17 vs 167 +/- 29 msec, P = 0.003) during SR were significantly shorter in group A than in group B. In group A, the HV interval was significantly longer during VT than during SR (73 +/- 18 vs 47 +/- 7 msec, P = 0.007). There were more patients with functional His-Purkinje block (split His potentials, a jump of HV interval induced by programmed atrial stimulation or burst pacing) or phase 3 block in group A than group B (6/6 patients vs 0/7 patients, P < 0.001). Successful ablation of the right bundle branch was performed in all 13 patients without deteriorating AV block. Two patients died in each group, and VTs (other than BBRT) or ventricular fibrillation were documented by ICD electrogram storages in 4 patients during follow-up of 27 +/- 17 months. CONCLUSION: A prolonged HV interval during SR is not a prerequisite for BBRT. Functional His-Purkinje system abnormalities appear to be the electrophysiologic substrate for this specific type of BBRT.     

阈下刺激定位慢径消融靶点的临床应用研究

目的 :探讨利用阈下刺激 (STS)定位房室结折返性心动过速 (AVNRT)的慢径消融靶点的临床应用价值。方法 :选择AVNRT患者 6例 ,经常规电生理检查明确诊断后 ,将大头电极放在冠状窦口下缘与希氏束之间的中下区域进行标测 ,测定该点的起搏阈值后 ,诱发AVNRT ,然后发放STS终止AVNRT ,在终止位点处试消融 ,观察STS标测消融的有效性 ;在非终止位点处 ,结合局部心内电图判断是否进行试消融 ,如在非终止位点处试消融 ,观察STS标测的可靠性。同时观察STS标测定位的安全性。结果 :在 6例患者中 ,有 3例STS终止了持续性AVNRT ,且在终止位点处试消融并获得成功 ;有 5例共在 10个位点处发放了STS ,其中在 9个位点未终止心动过速 ,在这些非终止位点处试消融均未获得成功 ,非 1个位点出现了心房夺获。所有患者在STS标测过程中 ,未出现心房颤动、心动过速的加速或心室颤动等现象。结论 :STS终止AVNRT的位点是判断消融靶点的一个良好的电生理学指标。STS标测定位是安全、有效和可靠的一种方法 ,值得进一步地深入研究     

Refractory ventricular tachycardia secondary to cardiac sarcoid: Electrophysiologic characteristics, mapping, and ablation

BACKGROUND: Cardiac sarcoidosis is a recognized cause of ventricular tachycardia (VT) and sudden death that has not been well studied. OBJECTIVES: The purpose of this study was to describe the clinical characteristics of a consecutive series of eight patients with recurrent monomorphic VT due to cardiac sarcoidosis and to define the electrophysiologic characteristics of the VT and its electrophysiologic substrate. METHODS/RESULTS: Of 98 patents with nonischemic cardiomyopathy and VT referred for ablation over a 7-year period, sarcoid was the etiology in 8%. Mean age was 42 +/- 8 years, and all but one patient had a reduced left ventricular ejection fraction (mean 34% +/- 15%). VT was the initial manifestation of sarcoid disease in 5 of 8 cases based on retrospective analysis. All patients had not responded to therapy with multiple antiarrhythmic drugs (mean 2.5 +/- 1). Cardiac biopsy initially was negative in 3 of 7 patients, and in 2 patients the diagnosis was not made until posttransplant examination of the heart. Two patients (25%) had a previous presumptive diagnosis of arrhythmogenic right ventricular dysplasia. Electrophysiologic study revealed evidence of scar-related reentry with multiple monomorphic VTs induced (4 +/- 2 VTs per patient) with both right bundle branch block and left bundle branch block QRS configurations. Areas of low-voltage scar were present in the right ventricle in all 8 of 8 patients, in the left ventricle in 5 (63%) of 8 patients, and in the epicardium in 2 patients undergoing epicardial mapping. Ablation abolished one or more VTs in 6 (75%) of 8 patients, but other VTs remained inducible in all but one patient. Postablation, some form of sustained VT recurred in 6 of 8 patients within 6 months. However, at longer follow-up (range 6 months to 7 years), 4 of 8 patients currently are free of VT with antiarrhythmic drugs and immunosuppression. Cardiac transplantation eventually was required in 5 of 8 patients because of either recurrent VT (n = 4) or heart failure (n = 1). CONCLUSION: Sarcoid is an important diagnostic consideration in scar-related VT. Sarcoid can be misdiagnosed as idiopathic or arrhythmogenic right ventricular cardiomyopathy. Arrhythmia control can be difficult, although ablation can be helpful in some patients.     

Prolongation of the averaged QRS complex. A simple prognostic factor in patients with post-infarction bundle branch block and a history of syncope

Patients with a history of myocardial infarction and complete bundle branch block with syncopal episodes have a high risk of sudden death: the identification of the cause of the syncope is therefore essential. The aim of the study was to assess the diagnostic value of non-invasive techniques used in the investigations of syncope: 24 hour Holter recording, high amplification ECG and measurement of left ventricular ejection fraction. The results of these investigations were compared with those of complete electrophysiological investigation evaluating atrioventricular conduction and the inducibility of tachycardia. The patient population was 134 patients, 83 with right bundle branch block and 51 with left bundle branch block. Ninety one patients had inducible sustained ventricular tachycardia and 24 had atrioventricular conduction defects: of these, 14 also had ventricular tachycardia. During follow-up, there were 12 sudden deaths and 13 deaths from cardiac failure. Uni- and multivariate analysis showed induction of ventricular tachycardia to be a significant risk factor for global mortality and sudden death but prolongation of the averaged QRS complex (> 165 msec) was also an independent risk factor of global cardiac mortality. The authors conclude that simple prolongation of the averaged QRS duration > 160 ms in patients with right bundle branch block and > 170 ms in patients with left bundle branch block after myocardial infarction and syncope is a significant poor prognostic factor. However, this sign is not predictive of sudden death.     

Usefulness of clinical characteristics in predicting the outcome of electrophysiologic studies in unexplained syncope.

Guidelines for the use of electrophysiologic studies in syncope have not yet been formulated. To confirm the sensitivity and specificity of a previously derived model to predict the results of electrophysiologic testing in syncope, the importance of 6 clinical predictors was assessed in a new data set of 141 consecutive patients with unexplained syncope who were referred for electrophysiologic studies. The 6 predictors were: organic heart disease; premature ventricular beats, sinus bradycardia, first-degree heart block and bundle branch block by electrocardiogram; and nonsustained ventricular tachycardia by Holter monitor. Organic heart disease and nonsustained ventricular tachycardia by Holter monitoring were highly sensitive for serious ventricular tachyarrhythmias at electrophysiologic study (sensitivity 100%), whereas sinus bradycardia, first-degree heart block or bundle branch block by electrocardiogram were sensitive for bradyarrhythmic outcomes (sensitivity 79%). Because these variables are so sensitive for serious outcomes of electrophysiologic testing in syncope, invasive studies in patients without these clinical predictors are likely to be of very low diagnostic yield.     

Sustained ventricular tachycardia: induced polymorphism. Clinical and electrophysiological aspects; therapeutic implications

By induced polymorphism (I.P.) we mean the electrical induction during endocavitary electrophysiologic study (E.E.S.) either of two or more morphologically distinct types of Sustained Ventricular Tachycardia (S.V.T.) (i.e. different bundle branch block patterns or with shifting of QRS by greater than or equal to 90 degrees) or of one type of sustained ventricular tachycardia other than the spontaneous one. Twenty-two patients with clinical sustained ventricular tachycardia, in whom at least one episode of sustained ventricular tachycardia was induced during endocavitary electrophysiologic study, were divided into 2 groups depending on the presence or not of induced polymorphism: Group I consisted of 13 patients with induced polymorphism; Group II consisted of 9 patients without induced polymorphism. All the patients of the Group I had chronic ischemic heart disease (C.I.H.D.); 12/13 previously had myocardial infarction. Only 1 patient of the Group II had chronic ischemic heart disease. Intraventricular conduction defect was present in 9 patients of the Group I and in 2 of the Group II. An overall of 26 sustained ventricular tachycardia episodes were induced in patients of the Group I: 9 with RBBB, 10 with LBBB and 7 with "bizarre" QRS morphology. Sustained ventricular tachycardia reinduction was attempted in 10 patients of the Group I after acute drug testing (Ajmaline, Propafenone, Amiodarone): sustained ventricular tachycardia was no longer inducible in 6, but in 3 of those 4 in whom it was, a marked increase in polymorphism was observed as compared to pre-test pattern. Of the 11 alive patients of Group I, 10 are on Amiodarone alone or in combination with other antiarrhythmic drugs. We conclude as follows: different morphological types of sustained ventricular tachycardia can be quite commonly induced during endocavitary electrophysiologic study; according to our cases induced polymorphism is observed only in patients with chronic ischemic heart disease; patients with induced polymorphism often have intraventricular conduction defect; induced polymorphism furtherly accounts for reentry as the mechanism of sustained ventricular tachycardia in patients with chronic ischemic heart disease; a prevalent morphology of the endocavitary electrophysiologic study induced sustained ventricular tachycardia in patients with chronic ischemic heart disease was not observed at least in our patients; Amiodarone is the drug of choice for the treatment of induced polymorphic sustained ventricular tachycardia patients.     

Novel mechanism of postinfarction ventricular tachycardia originating in surviving left posterior Purkinje fibers

BACKGROUND: Other than bundle branch reentry and interfascicular reentry, monomorphic postmyocardial infarction (post-MI) reentrant ventricular tachycardia (VT) including the His-Purkinje system has not been reported. Verapamil-sensitive idiopathic left VT includes the left posterior Purkinje fibers but develops in patients without structural heart disease. OBJECTIVES: The purpose of this study was to describe a novel mechanism of reentrant VT arising from the left posterior Purkinje fibers in patients with a prior MI. METHODS: The study consisted of four patients with a prior MI and symptomatic heart failure who underwent electrophysiologic study and catheter ablation for VT showing right bundle branch block (n = 3) or atypical left bundle branch block (n = 1) morphology with superior axis. In two patients, the VT frequently emerged during the acute phase of MI and required emergency catheter ablation. RESULTS: Clinical VT was reproducibly induced by programmed stimulation. In three patients, both diastolic and presystolic Purkinje potentials were sequentially recorded along the left ventricular posterior septum during the VT, whereas in the fourth patient, only presystolic Purkinje potentials were observed. During entrainment pacing from the right atrium, diastolic Purkinje potentials were captured orthodromically and demonstrated decremental conduction properties, whereas presystolic Purkinje potentials were captured antidromically and appeared between the His and QRS complex. Radiofrequency energy delivered at the site exhibiting a Purkinje-QRS interval of 58 +/- 26 ms successfully eliminated the VTs without provoking any conduction disturbances. CONCLUSION: Reentrant monomorphic VT originating from the left posterior Purkinje fibers, which is analogous to idiopathic left VT, can develop in the acute or chronic phase of MI. Catheter ablation is highly effective in eliminating this VT without affecting left ventricular conduction.     

Spontaneous automaticity arising from a successfully ablated Mahaim fiber

The authors describe a 22-year-old woman with regular and irregular arrhythmias exhibiting left bundle branch block (LBBB) morphology at various heart rates. An atriofascicular fiber was diagnosed as the underlying mechanism for the antidromic reciprocating tachycardia. In addition, spontaneous automaticity of the Mahaim fiber was present during electrophysiologic study. The accessory pathway was ablated successfully, targeting a Mahaim potential at the supero-anterior tricuspid valve annulus. Relatively slow automatic rhythms with identical LBBB morphology were recorded immediately after ablation, as well as during long-term follow-up in a more sporadic and subclinical form. Abnormal automaticity arising from the distal portions of the remnant pathway was considered to be the origin of the slow ventricular rhythms in this peculiar case.     

Repetitive beating after single ventricular extrastimuli: Incidence and prognostic significance in patients with recurrent ventricular tachycardia

The incidence of repetitive ventricular beating in response to programmed single ventricular extrastimuli delivered during spontaneous rhythm was tabulated in 59 patients with recurrent ventricular tachycardia. Repetitive beating occurred in only nine patients (15 percent). The repetitive response seemed to be a result of bundle branch reentry in four subjects and possibly a result of other mechanisms in five. There was no difference in the incidence of repetitive beating or type of repetitive response in patients with and without ischemic heart disease. During an average patient follow-up period of 13.6 months, there were eight sudden and six nonsudden deaths. Life table analysis revealed a significantly greater incidence of sudden death in patients with ischemic than in patients with nonischemic heart disease. There was no significant difference in the incidence of sudden death in patients with and without repetitive beating. It is concluded that the repetitive response to single ventricular extrastimulation is infrequent in patients with recurrent ventricular tachycardia, and that repetitive beating is not a prognostic indicator or an indicator of vulnerability to ventricular tachycardia.     

Short- and long-term experience with flecainide acetate in the management of refractory life-threatening ventricular arrhythmias

Thirty-eight patients with organic heart disease and history of sudden cardiac arrest or recurrent sustained ventricular tachycardia were treated with flecainide. Coronary artery disease was present in 33 patients. Previous antiarrhythmic therapy consisted of two to eight drugs (mean four). Fourteen patients were resuscitated from sudden cardiac death and 24 patients had chronic recurrent sustained ventricular tachycardia. Twenty-eight patients had electrophysiologic testing before and during flecainide treatment. Sustained ventricular tachycardia became noninducible in 5 patients, nonsustained in 5 patients and slowed in 13 patients (cycle length increased from 278 +/- 64 to 395 +/- 91 ms; p = 0.002). Three of the 14 patients with sudden cardiac death and 15 of the 24 patients with recurrent sustained ventricular tachycardia remained on long-term flecainide treatment. The mean left ventricular ejection fraction in 16 of these 18 patients was 37%. Nonlimiting side effects occurred in seven patients (18%). Proarrhythmic effects were seen in four patients (10%). At a mean follow-up time of 11 +/- 3 months, 15 patients (39%) had had no recurrence, including 5 who had inducible sustained ventricular tachycardia and 5 who did not on retesting during treatment. In the 18 patients who received long-term therapy, 3 late deaths occurred, 1 of which was of arrhythmic origin. These data suggest that flecainide is effective in about 40% of patients with severe refractory ventricular arrhythmias. Its value as a single drug in the treatment of sudden cardiac death remains to be defined.     

Clinical experience in patients with implantable cardioverter defibrillators

Forty patients (36 men and 4 women) with life-threatening arrhythmia received an implantable cardioverter defibrillator (ICD). Mean age was 63 years (range, 46 to 80 years). All patients had structural heart disease, with coronary artery disease in 32 patients, idiopathic cardiomyopathy in 7 patients, and hypertensive heart disease in 1 patient. Mean left ventricular ejection fraction was 29 +/- 13%. The clinical arrhythmia was out-of-hospital cardiac arrest in 14 patients (35%), symptomatic sustained ventricular tachycardia in 21 patients (53%), and episodes of syncope without documented spontaneous ventricular arrhythmia but ventricular tachycardia that was easily provoked at the time of electrophysiologic testing in 5 patients (13%). Sustained ventricular tachycardia was induced in 37 patients (93%) at basic electrophysiologic testing. The average number of drug failures was 2.9 +/- 1.4 per patient. One patient (2.5%) died perioperatively because of intractable ventricular tachycardia and ventricular fibrillation. During a median follow-up period of 5.5 months (range 2-21 months) 2 sudden deaths occurred. No patient had a serious complication during the follow-up period. Ten patients (25%) received antiarrhythmic drugs to suppress spontaneous ventricular tachycardia. Appropriate shock treatment was received by 18 patients (45%), and inappropriate shock treatment was received by 2 patients (5%). Several issues regarding use of the ICD must be considered, but the device seems to be useful, and it is associated with an acceptable rate of complications and good long-term success at the present time.     

Ventricular tachycardia and ventricular fibrillation in a young population.

In this study, we describe the findings in 18 young patients (age range 4 days to 24 years, mean 16.6 years) who had ventricular tachycardia and/or ventricular fibrillation and were followed for 4--70 months (mean 22.4 months). Patients had a variety of problems associated with their arrhythmia, including mitral valve prolapse, cardiomyopathy, myocarditis, prolonged QT syndrome and hypokalemia. Six patients had no clinically recognizable cardiac abnormality. The ventricular tachycardia showed a left bundle branch block contour in 10 of 17 patients, right bundle branch block in four, was multiform in two and had an indeterminate contour in one. Sustained ventricular tachycardia was initiated and terminated reproducibly by atrial and ventricular stimulation in three of seven patients who did not have spontaneous episodes of ventricular tachycardia during the electrophysiologic study. In one other patient, short bursts of ventricular tachycardia were induced. Patients who had ventricular fibrillation, those who died, and those who are still symptomatic with poorly controlled ventricular arrhythmias had significant heart disease. In one patient, a ventricular tachyarrhythmia that had required more than 100 electrical cardioversions spontaneously disappeared after requiring 1 year of antiarrhythmic therapy.