Right atrial perforation secondary to implantable cardioverter defibrillator insertion.

Implantable cardioverter defibrillator (ICD) placements can be associated with serious complications. This paper reports a patient in whom percutaneous placement of an ICD resulted in a hemopneumothorax. This was due to an active fixation lead that perforated the right atrial wall and injured the adjacent lung parenchyma. The hemothorax was drained thoracoscopically, and the atrial injury was covered with fibrin glue.

Reducing mortality from sudden cardiac death in the community: lessons from epidemiology and clinical applications research.

The reduction of mortality from sudden cardiac death (SCD) in the community remains a challenge. Clinical-epidemiologic studies have identified a range of factors that are associated with an increased risk of SCD. While of potential etiologic and prognostic importance, these factors have limited sensitivity and a low positive predictive value for SCD. On the other hand, clinical trials have suggested that a variety of interventions, including risk factor reduction, nutritional interventions, drug therapies, cardiac procedures, and new technologies, have the potential to reduce mortality from SCD. In this review, we examine what is known about the epidemiology and clinical application of interventions to reduce mortality from SCD; and, we consider the impact of both prevention and clinical interventions on mortality from SCD from a community perspective. There is mounting evidence that supports both public health and clinical efforts to prevent the occurrence of SCD. There also is evidence suggesting that new technologies, such as automated external defibrillators, have the potential to reduce case-fatality from SCD. Further progress will depend on improved methods to identify persons-at-risk, reduction of risk factors, and application of techniques -- both simple and advanced -- to improve survival in victims of SCD.

Implantable defibrillators and antiarrhythmic drugs in patients at risk for lethal arrhythmias.

The high mortality rate and frequency of ventricular arrhythmias in patients with congestive heart failure has prompted numerous clinical trials aimed at reducing mortality by addressing arrhythmic death. Recently completed trials have suggested that for patients who have survived cardiac arrest, the preferred treatment may be an implantable cardioverter defibrillator (ICD). From the standpoint of primary prevention, implantable defibrillators and amiodarone have received the most attention. It remains unclear, however, to which patients these studies apply, and if and how the results might be generalized. No available studies confirm an additional benefit of pharmacologic or device-based antiarrhythmic therapy beyond that offered by optimal treatment with beta blockers, angiotensin-converting enzyme inhibitors, and lipid-lowering drugs in the majority of patients with cardiomyopathy. Clinical trials are ongoing to address these issues.

Emergency extracorporeal membrane oxygenation (ECMO)-supported percutaneous coronary interventions in the fibrillating heart.

We describe two cases of refractory ventricular fibrillation complicating transcatheter interventional procedures. Extracorporeal membrane oxygenation was used in each to support percutaneous coronary revascularization in the fibrillating heart as a means of facilitating successful restoration of sinus rhythm. Cathet. Cardiovasc. Intervent. 48:402-405, 1999.

Relationship between shock energy and postdefibrillation ventricular arrhythmias in patients with implantable defibrillators.

BACKGROUND: The relationship between postdefibrillation ventricular arrhythmias and shock strength is poorly understood in patients with implantable defibrillators. The purpose of this study was to characterize the relationship between postdefibrillation ventricular arrhythmias and shock strength. METHODS AND RESULTS: Forty-three patients with an implanted defibrillator underwent six separate inductions of ventricular fibrillation (VF) after a step-down defibrillation energy requirement (7.3 +/- 4.6 J) was determined. For each of the first three inductions of VF, the first two shocks were low energy and equal to approximately 75% of the defibrillation energy requirement (5.4 +/- 3.3 J), or to the defibrillation energy requirement plus 10 J (17.5 +/- 4.3 J). After the first two shocks, subsequent shocks were programmed to the maximum available energy (29.0 +/- 2.5 J). The alternate technique was used for the subsequent three inductions of VF. Postdefibrillation ventricular arrhythmias were noted. Postdefibrillation ventricular arrhythmias with a cycle length < or = 300 msec were more frequent after a low-energy shock (19%), than after a high-energy shock (1.5%; P = 0.005). Postdefibrillation ventricular arrhythmias with a cycle length < or = 300 msec were more frequent after a high-energy shock (32%), than after a low-energy shock (7.1%; P = 0.002). A relationship between the cycle length of the postdefibrillation ventricular arrhythmias and the absolute defibrillation energy was observed (P < 0.001; r = 0.6), and ventricular arrhythmias with a cycle length > 300 msec were uncommon after shocks < or = 10 J (P = 0.001). The characteristics of ventricular arrhythmias after maximum-energy shocks were similar to those that occurred after high-energy shocks. CONCLUSIONS: Postdefibrillation ventricular arrhythmias with a cycle length < or = 300 msec are more common after shocks of strength associated with a low probability of successful defibrillation. Postdefibrillation ventricular arrhythmias with a cycle length of > 300 msec are more common after high- and maximum-energy shocks, and are directly related to the absolute defibrillation energy.

A technique for the rapid diagnosis of atrial tachycardia in the electrophysiology laboratory.

OBJECTIVE: The purpose of this study was to determine if the atrial response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction during paroxysmal supraventricular tachycardia is a useful diagnostic maneuver in the electrophysiology laboratory. BACKGROUND: Despite various maneuvers, it can be difficult to differentiate atrial tachycardia from other forms of paroxysmal supraventricular tachycardia. METHODS: The response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction was studied during four types of tachycardia: 1) atrioventricular nodal reentry (n = 102), 2) orthodromic reciprocating tachycardia (n = 43), 3) atrial tachycardia (n = 19) and 4) atrial tachycardia simulated by demand atrial pacing in patients with inducible atrioventricular nodal reentry or orthodromic reciprocating tachycardia (n = 32). The electrogram sequence upon cessation of ventricular pacing was, categorized as "atrial-ventricular" (A-V) or "atrial-atrial-ventricular" (A-A-V). RESULTS: The A-V response was observed in all cases of atrioventricular nodal reentrant and orthodromic reciprocating tachycardia. In contrast, the A-A-V response was observed in all cases of atrial tachycardia and simulated atrial tachycardia, even in the presence of dual atrioventricular nodal pathways or a concealed accessory atrioventricular pathway. CONCLUSIONS: In conclusion, an A-A-V response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction is highly sensitive and specific for the identification of atrial tachycardia in the electrophysiology laboratory.

Acute changes in spontaneous echo contrast and atrial function after cardioversion of persistent atrial flutter.

With use of transesophageal echocardiography, the short-term effects of transthoracic electrical cardioversion of atrial flutter (AFI) on atrial mechanical function and spontaneous echo contrast were determined. Thirty patients who had AFI for a mean of 6.4 +/- 12.2 months underwent transthoracic cardioversion. A transesophageal echocardiogram was recorded immediately before cardioversion, and left atrial appendage emptying velocity and spontaneous contrast were assessed serially at 1, 3, and 5 minutes after cardioversion in 28 patients, and also at 8, 10, and 15 minutes after cardioversion in a subgroup of 13 patients. Cardioversion was deferred in 2 patients (7%) because a thrombus was found in the left atrial appendage. Before cardioversion, spontaneous contrast was present in the left atrium in 7 of 28 patients (25%) who underwent cardioversion. The mean left atrial appendage emptying velocity of 54 +/- 22 cm/s before cardioversion fell by 26% to 40 +/- 25 cm/s at 1 minute after restoration of sinus rhythm (p <0.01). There were no significant changes in the mean left atrial appendage-emptying velocity between 1 and 15 minutes after cardioversion. Within 5 minutes after conversion to sinus rhythm, left atrial spontaneous echo contrast developed de novo or worsened in 12 of the 28 patients (43%). In conclusion, the results of this study demonstrate that persistent AFI may be associated with left atrial thrombi before cardioversion and that cardioversion of AFI is associated with a significant degree of atrial stunning and formation of spontaneous echo contrast.

Use of adenosine in patients hospitalized in a university medical center.

PURPOSE: Adenosine is a useful agent for the diagnosis and termination of tachycardias. The purpose of this study was to identify the rhythms for which adenosine is prescribed in hospitalized adults and to identify the reasons for its misuse. PATIENTS AND METHODS: Data were collected from the medical records of 100 patients who received intravenous adenosine while hospitalized at a university medical center. The characteristics of the patients, rhythms treated with adenosine, and dosages of adenosine were analyzed. In addition, internal medicine house officers were administered a questionnaire referring to an electrocardiogram of atrial fibrillation with a rapid ventricular response. RESULTS: The arrhythmias for which adenosine was administered consisted of regular, narrow-QRS complex tachycardias in 33% of patients; atrial fibrillation in 32% of patients; regular, wide-QRS complex tachycardias in 23% of patients; atrial flutter in 10% of patients, and multifocal atrial tachycardia in 2% of patients. The mean (+/-SD) number of doses of adenosine given to each patient was 1.6+/-0.8, and the mean dose of adenosine was 7.8+/-2.8 mg. Internal medicine house officers prescribed 70% of the doses of adenosine and were as likely to use it for patients with atrial fibrillation as were surgical house officers. There was a 2% incidence of proarrhythmia, including asystole and polymorphic ventricular tachycardia. Thirty-one percent of the 100 house officers in our survey misdiagnosed a 12-lead electrocardiogram of rapid atrial fibrillation as paroxysmal supraventricular tachycardia, suggesting that adenosine may have been misused for atrial fibrillation because of errors in rhythm diagnosis. Only 5% of those who correctly diagnosed atrial fibrillation also answered that adenosine would be likely to terminate the arrhythmia, suggesting that a misunderstanding that adenosine terminates atrial fibrillation is not a common reason for its misuse. CONCLUSIONS: Approximately 40% of hospitalized adults who are treated with adenosine receive the medication unnecessarily for atrial fibrillation or atrial flutter, and this misuse results in unnecessary expenses and risks of adverse effects. The primary reason that adenosine is misused for atrial fibrillation is the inability to recognize that rhythm on an electrocardiogram. House officers need additional education on the electrocardiographic recognition of atrial fibrillation.

Long-term evaluation of the ventricular defibrillation energy requirement.

INTRODUCTION: Defibrillation energy requirements in patients with nonthoracotomy defibrillators may increase within several months after implantation. However, the stability of the defibrillation energy requirement beyond 1 year has not been reported. The purpose of this study was to characterize the defibrillation energy requirement during 2 years of clinical follow-up. METHODS AND RESULTS: Thirty-one consecutive patients with a biphasic nonthoracotomy defibrillation system underwent defibrillation energy requirement testing using a step-down technique (20, 15, 12, 10, 8, 6, 5, 4, 3, 2, and 1 J) during defibrillator implantation, and then 24 hours, 2 months, 1 year, and 2 years after implantation. The mean defibrillation energy requirement during these evaluations was 10.9+/-5.5 J, 12.3+/-7.3 J, 11.7+/-5.6 J, 10.2+/-4.0 J, and 11.7+/-7.4 J, respectively (P = 0.4). The defibrillation energy requirement was noted to have increased by 10 J or more after 2 years of follow-up in five patients. In one of these patients, the defibrillation energy requirement was no longer associated with an adequate safety margin, necessitating revision of the defibrillation system. There were no identifiable clinical characteristics that distinguished patients who did and did not develop a 10-J or more increase in the defibrillation energy requirement. CONCLUSION: The mean defibrillation energy requirement does not change significantly after 2 years of biphasic nonthoracotomy defibrillator system implantation. However, approximately 15% of patients develop a 10-J or greater elevation in the defibrillation energy requirement, and 3% may require a defibrillation system revision. Therefore, a yearly evaluation of the defibrillation energy requirement may be appropriate.

Effect of ventricular shock strength on cardiac hemodynamics.

INTRODUCTION: The effect of implantable defibrillator shocks on cardiac hemodynamics is poorly understood. The purpose of this study was to test the hypothesis that ventricular defibrillator shocks adversely effect cardiac hemodynamics. METHODS AND RESULTS: The cardiac index was determined by calculating the mitral valve inflow with transesophogeal Doppler during nonthoracotomy defibrillator implantation in 17 patients. The cardiac index was determined before, and immediately, 1 minute, 2 minutes, and 4 minutes after shocks were delivered during defibrillation energy requirement testing with 27- to 34-, 15-, 10-, 5-, 3-, or 1-J shocks. The cardiac index was also measured at the same time points after 27- to 34-, and 1-J shocks delivered during the baseline rhythm. The cardiac index decreased from 2.30 +/- 0.40 L/min per m2 before a 27- to 34-J shock during defibrillation energy requirement testing to 2.14 +/- 0.45 L/min per m2 immediately afterwards (P = 0.001). This effect persisted for > 4 minutes. An adverse hemodynamic effect of similar magnitude occurred after 15 J (P = 0.003) and 10-J shocks (P = 0.01), but dissipated after 4 minutes and within 2 minutes, respectively. There was a significant correlation between shock strength and the percent change in cardiac index (r = 0.3, P = 0.03). The cardiac index decreased 14% after a 27- to 34-J shock during the baseline rhythm (P < 0.0001). This effect persisted for < 4 minutes. A 1-J shock during the baseline rhythm did not effect the cardiac index. CONCLUSION: Defibrillator shocks > 9 J delivered during the baseline rhythm or during defibrillation energy requirement testing result in a 10% to 15% reduction in cardiac index, whereas smaller energy shocks do not affect cardiac hemodynamics. The duration and extent of the adverse effect are proportional to the shock strength. Shock strength, and not ventricular fibrillation, appears to be most responsible for this effect. Therefore, the detrimental hemodynamic effects of high-energy shocks may be avoided when low-energy defibrillation is used.

Differential effect of adenosine on anterograde and retrograde fast pathway conduction in patients with atrioventricular nodal reentrant tachycardia.

INTRODUCTION: Several studies have shown that the fast pathway is more responsive to adenosine than the slow pathway in patients with AV nodal reentrant tachycardia. Little information is available regarding the effect of adenosine on anterograde and retrograde fast pathway conduction. METHODS AND RESULTS: The effects of adenosine on anterograde and retrograde fast pathway conduction were evaluated in 116 patients (mean age 47 +/- 16 years) with typical AV nodal reentrant tachycardia. Each patient received 12 mg of adenosine during ventricular pacing at a cycle length 20 msec longer than the fast pathway VA block cycle length and during sinus rhythm or atrial pacing at 20 msec longer than the fast pathway AV block cycle length. Anterograde block occurred in 98% of patients compared with retrograde fast pathway block in 62% of patients (P < 0.001). Unresponsiveness of the retrograde fast pathway to adenosine was associated with a shorter AV block cycle length (374 +/- 78 vs 333 +/- 74 msec, P < 0.01), a shorter VA block cycle length (383 +/- 121 vs 307 +/- 49 msec, P < 0.001), and a shorter VA interval during tachycardia (53 +/- 23 vs 41 +/- 17 msec, P < 0.01). CONCLUSION: Although anterograde fast pathway conduction is almost always blocked by 12 mg of adenosine, retrograde fast pathway conduction is not blocked by adenosine in 38% of patients with typical AV nodal reentrant tachycardia. This indicates that the anterograde and retrograde fast pathways may be anatomically and/or functionally distinct. Unresponsiveness of VA conduction to adenosine is not a reliable indicator of an accessory pathway.

Cardiac electrophysiologic effects of norepinephrine in human beings.

BACKGROUND: The electrophysiologic effects of norepinephrine (NE) in human beings have not been previously described. METHODS: The electrophysiologic effects of NE infused at a rate of 25 ng/kg/min were determined in 21 patients with a mean age of 41 +/- 11 years and without structural heart disease who underwent an electrophysiology procedure. In a subgroup of 10 patients electrophysiologic parameters were measured at baseline, after the infusion of NE, and after administration of beta-blockade while in continuous NE infusion. RESULTS: The baseline NE plasma concentration of 298 +/- 153 pg/ml increased to 708 +/- 419 pg/ml after the infusion of NE. NE significantly increased the mean blood pressure, sinus cycle length, corrected sinus node recovery time, ventriculoatrial block cycle length, and the atrial and ventricular effective refractory periods. In a subset of 10 patients 0.2 mg/kg propranolol administered during continued infusion of NE resulted in a further increase in sinus cycle length, atrial-His interval, and ventricular refractoriness. CONCLUSION: A physiologic elevation in the plasma NE concentration results in a depression of sinus node function and atrioventricular conduction and in prolongation of atrial and ventricular refractoriness. Some of NE's effects are partially offset by beta-adrenergic stimulation.

Changes in cardiac repolarization following short periods of ventricular pacing.

INTRODUCTION: "Cardiac memory" (primary T wave change) is thought to occur after 15 minutes to several hours of right ventricular (RV) pacing. The two components of the temporal change in repolarization are memory and accumulation. The purpose of this study was to examine quantitatively the effect of short periods of ventricular pacing on the human cardiac action potential, using monophasic action potential (MAP) recordings. METHODS AND RESULTS: Thirty-one patients (ages 43+/-14 years) with structurally normal hearts undergoing a clinically indicated electrophysiologic procedure were enrolled. Catheters were placed in the right atrium (RA) and RV, and a MAP catheter was positioned at the RV septum. APD90 was calculated from digitized MAP recordings. MAP morphology comparisons were performed using the root mean square (RMS) of the difference between complexes. All pacing was at 500-msec cycle length. There were four pacing protocols: (1) RA pacing was performed for approximately 15 minutes to evaluate temporal stability of the MAP recordings (5 pts); (2) to evaluate the memory phenomenon, four successive 1-minute episodes of RV pacing were interspersed with 2 minutes of RA pacing (5 pts); (3) the accumulation phenomenon was evaluated by assessing the effects of 1, 5, 10, and 15 minutes of RV pacing on the MAP during RA pacing (16 pts); and (4) 20 minutes of RV pacing was followed by 10 minutes of RA pacing to correlate visually apparent T wave changes with changes in MAP recordings (5 pts). In the control patients, no changes in APD90 or RMS analysis were noted during 14.9+/-1.4 minutes of RA pacing. In the second protocol, RMS of the difference between the baseline MAP complexes and the signal average of the first 50 beats following each of four 1-minute RV pacing trains demonstrated progressively greater differences in morphology after successive episodes of RV pacing. In protocol 3, RMS analysis identified a progressively greater difference between the baseline MAP recording and the average of the first 50 beats after 1, 5, 10, and 15 minutes of RV pacing. In protocol 4, visually apparent changes in T waves occurred in parallel with the RMS of the difference between the baseline MAP recordings and the average of the first 50 beats after 20 minutes of RV pacing. Similar changes also were demonstrated by APD90 analysis. CONCLUSION: This study is the first to demonstrate that episodes of abnormal ventricular activation as short as 1 minute in duration may exert lingering effects on the repolarization process once normal ventricular activation resumes.

Incessant tachycardia using a concealed atrionodal bypass tract.

A case of incessant supraventricular tachycardia continuing despite AV block is reported. Atrial tachycardia and AV nodal reentrant tachycardia were excluded, as was orthodromic tachycardia using a concealed accessory AV pathway. The earliest retrograde atrial activation was at the posterolateral tricuspid annulus, and the tachycardia was eliminated by ablation at this site. The findings in this case are explained only by a concealed atrionodal pathway.

A prospective evaluation of two defibrillation safety margin techniques in patients with low defibrillation energy requirements.

INTRODUCTION: In patients undergoing defibrillator implantation, an appropriate defibrillation safety margin has been considered to be either 10 J or an energy equal to the defibrillation energy requirement. However, a previous clinical report suggested that a larger safety margin may be required in patients with a low defibrillation energy requirement. Therefore, the purpose of this prospective study was to compare the defibrillation efficacy of the two safety margin techniques in patients with a low defibrillation energy requirement. METHODS AND RESULTS: Sixty patients who underwent implantation of a defibrillator and who had a low defibrillation energy requirement (< or = 6 J) underwent six separate inductions of ventricular fibrillation, at least 5 minutes apart. For each of the first three inductions of ventricular fibrillation, the first two shocks were equal to either the defibrillation energy requirement plus 10 J (14.6+/-1.0 J), or to twice the defibrillation energy requirement (9.9+/-2.3 J). The alternate technique was used for the subsequent three inductions of ventricular fibrillation. For each induction of ventricular fibrillation, the first shock success rate was 99.5%+/-4.3% for shocks using the defibrillation energy requirement plus 10 J, compared to 95.0%+/-17.2% for shocks at twice the defibrillation energy requirement (P = 0.02). The charge time (P < 0.0001) and the total duration of ventricular fibrillation (P < 0.0001) were each approximately 1 second longer with the defibrillation energy requirement plus 10 J technique. CONCLUSION: This study is the first to compare prospectively the defibrillation efficacy of two defibrillation safety margins. In patients with a defibrillation energy requirement < or = 6 J, a higher rate of successful defibrillation is achieved with a safety margin of 10 J than with a safety margin equal to the defibrillation energy requirement.

Cost comparison of radiofrequency modification and ablation of the atrioventricular junction in patients with chronic atrial fibrillation.

BACKGROUND: Because it is not clear which technique is less expensive, the purpose of this study was to compare the cost of radiofrequency modification and ablation of the atrioventricular (AV) node in drug-refractory patients with atrial fibrillation and an uncontrolled ventricular rate. METHODS AND RESULTS: The initial nominal charges for a successful procedure were compared in 10 patients with chronic atrial fibrillation who underwent modification of the AV node ($13 109+/-2002) and 14 similar patients who underwent ablation and pacemaker implantation ($28 302+/-2023, P<.001). On the basis of the long-term follow-up of patients who underwent each procedure, it was assumed that 31% of patients selected for the modification procedure would require a permanent pacemaker for inadvertent AV block or because of AV nodal ablation after a failed modification procedure and that the recurrence rate after AV node ablation would be 2%. The annual charges during follow-up were predicted and adjusted for recurrences and the need for additional procedures. The adjusted total charges at 1 year of follow-up were significantly lower for the modification procedure ($19 389+/-2002) than for the ablation procedure ($28 485+/-2023, P<.001). After 10 years of follow-up, the cumulative, adjusted charges for modification were $20 016 (42%) less than for ablation. CONCLUSIONS: The initial charges generated by AV node modification are significantly lower than for AV node ablation in patients with chronic atrial fibrillation. Even when adjusted for higher failure and recurrence rates, the modification procedure retains a major cost advantage over ablation during long-term follow-up.

Accuracy of the unipolar electrogram for identification of the site of origin of ventricular activation.

INTRODUCTION: The purpose of this study was to determine the accuracy of the unipolar electrogram for identifying the earliest site of ventricular activation. The earliest site of ventricular activation may be identified with the unipolar electrogram by the absence of an R wave. However, the accuracy of this technique is unknown. METHODS AND RESULTS: A single ventricular premature complex was induced mechanically at the tip of an electrode catheter to simulate a ventricular premature depolarization site of origin. Unipolar electrograms were recorded from the right ventricular septum at the tip electrode and at 2, 5, 8, and 11 mm from the electrode tip in 20 patients. No R waves were detected at the ventricular premature depolarization site of origin. R waves were detected in 4 of 20 patients (20%) at 2 mm from the tip electrode and 7 of 20 patients (35%) at 5, 8, and 11 mm from the tip electrode. An R wave was not observed at distances < or = 11 mm from the site of tachycardia origin in 13 of 20 patients (65%). CONCLUSIONS: While an R wave in the unipolar electrogram can be seen as close as 2 mm from the site of impulse origin, the absence of an R wave as an indicator of the site of impulse origin in the right ventricle is highly inaccurate. Therefore, the absence of an R wave in the unipolar electrogram is unlikely to be an adequate guide for identification of an effective target site for ablation of right ventricular tachycardia.

Failure of single- and multisite high-frequency atrial pacing to terminate atrial fibrillation.

This study determined the efficacy of single- and multisite atrial pacing for terminating episodes of atrial fibrillation induced in patients in the electrophysiology laboratory. One- to 5-second bursts of atrial pacing at a cycle length of 20 ms were not effective in terminating atrial fibrillation, when delivered either in the high right atrium or when delivered simultaneously at the high right atrium, midseptum, and coronary sinus.

Idiopathic left ventricular tachycardia with left and right bundle branch block configurations.

INTRODUCTION: Idiopathic left ventricular tachycardia typically has a right bundle branch block configuration. The purpose of this case report is to demonstrate that idiopathic ventricular tachycardia arising in or near the left posterior fascicle also may have a left bundle branch block configuration. METHODS AND RESULTS: A 27-year-old woman underwent an electrophysiologic procedure because of recurrent, verapamil-responsive, wide QRS complex tachycardia. Two types of ventricular tachycardia (cycle lengths 330 to 340 msec) were reproducibly inducible, one with a right bundle branch block configuration and left-axis deviation that had been documented clinically, and the other with a left bundle branch block configuration and axis of zero. A Purkinje potential recorded at the junction of the left ventricular mid-septum and inferior wall preceded the ventricular complex by 40 msec in both tachycardias. A single application of radiofrequency energy at this site successfully ablated both ventricular tachycardias. CONCLUSION: The findings of this case report demonstrate that idiopathic ventricular tachycardia arising in or near the left posterior fascicle may have a left bundle branch block configuration.