Reversing the direction of paced ventricular and atrial wavefronts reveals an oblique course in accessory AV pathways and improves localization for catheter ablation.

BACKGROUND: The purpose of this study was to determine how often accessory atrioventricular (AV) pathways (AP) cross the AV groove obliquely. With an oblique course, the local ventriculoatrial (VA) interval at the site of earliest atrial activation (local-VA) and the local-AV interval at the site of earliest ventricular activation (local-AV) should vary by reversing the direction of the paced ventricular and atrial wavefronts, respectively. METHODS AND RESULTS: One hundred fourteen patients with a single AP were studied. Two ventricular and two atrial pacing sites on opposite sides of the AP were selected to reverse the direction of the ventricular and atrial wavefronts along the annulus. Reversing the ventricular wavefront increased local-VA by >/=15 ms in 91 of 106 (91%) patients. With the shorter local-VA, the ventricular potential overlapped the atrial potential along a 17.2+/-8.5-mm length of the annulus. No overlap occurred with the opposite wavefront. Reversing the atrial wavefront increased local-AV by >/=15 ms in 32 of 44 (73%) patients. With the shorter local-AV, the atrial potential overlapped the ventricular potential along an 11.9+/-8.9-mm length of the annulus. No overlap occurred with the opposite wavefront. Mapping during longer local-VA or local-AV identified an AP potential in 102 of 114 (89%) patients. Catheter ablation eliminated AP conduction in all 111 patients attempted (median, 1 radiofrequency application in 99 patients with an AP potential versus 4.5 applications without an AP potential). CONCLUSIONS: Reversing the direction of the paced ventricular or atrial wavefront reveals an oblique course in most APs and facilitates localization of the AP potential for catheter ablation.

Characterization of reentrant circuit in macroreentrant right atrial tachycardia after surgical repair of congenital heart disease: isolated channels between scars allow "focal" ablation.

BACKGROUND: The purpose of this study was to characterize the circuit of macroreentrant right atrial tachycardia (MacroAT) in patients after surgical repair of congenital heart disease (SR-CHD). METHODS AND RESULTS: Sixteen patients with atrial tachycardia (AT) after SR-CHD were studied (atrial septal defect in 6, tetralogy of Fallot in 4, and Fontan procedure in 6). Electroanatomic right atrial maps were obtained during 15 MacroATs in 13 patients, focal AT in 1 patient, and atrial pacing in 2 patients without stable AT. A large area of low bipolar voltage (/=2 scars forming narrow channels. Ablation within the channels eliminates MacroAT.

The predictive value of electrophysiologic studies in untreated patients with Wolff-Parkinson-White syndrome.

The ability of invasive electrophysiologic studies to predict future arrhythmic events in patients with minimally symptomatic Wolff-Parkinson-White syndrome is not known. To assess this ability, 42 patients with evidence of atrioventricular (AV) pre-excitation on the surface electrocardiogram underwent electrophysiologic studies and were then followed up as outpatients taking no medications. The patients were classified into three groups on the basis of prestudy symptoms: group I, 15 asymptomatic patients; group II, 10 patients with infrequent symptoms but no documented arrhythmias; and group III, 17 patients with one documented episode of supraventricular tachycardia or atrial fibrillation, or both. At electrophysiologic study, the number of patients with short anterograde accessory pathway effective refractory periods and rapid ventricular responses during induced atrial fibrillation did not differ statistically among the three groups. During a mean follow-up period of 7.5 +/- 4.9 years, 11 of the 42 patients had documented arrhythmias: 2 patients from group II and 2 patients from group III had supraventricular tachycardia and 7 patients from group III had atrial fibrillation. All nine patients from group III with subsequent arrhythmias had had clinical atrial fibrillation before study. No patient from group I had an arrhythmia during follow-up. There were no episodes of ventricular fibrillation or sudden cardiac death during follow-up in any of the patients. The only predischarge variables that correlated with the subsequent occurrence of arrhythmias were a history of documented arrhythmias before electrophysiologic study (p less than 0.01) and inducible supraventricular tachycardia at electrophysiologic study (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Life-threatening ventricular arrhythmias due to transient or correctable causes: high risk for death in follow-up.

OBJECTIVES: This study evaluated the prognosis of patients resuscitated from ventricular tachycardia (VT) or ventricular fibrillation (VF) with a transient or correctable cause suspected as the cause of the VT/VF. BACKGROUND: Patients resuscitated from VT/VF in whom a transient or correctable cause has been identified are thought to be at low risk for recurrence and often receive no primary treatment for their arrhythmias. METHODS: In the Antiarrhythmics Versus Implantable Defibrillators (AVID) trial, patients with a potentially transient or correctable cause of VT/VF were not eligible for randomization. The mortality of these patients was compared with the mortality of patients with a known high risk of recurrence of VT/VF in the AVID registry. RESULTS: Compared with patients having high risk VT/VF, those with a transient or correctable cause for their presenting VT/VF were younger and had a higher left ventricular ejection fraction. These patients were more often treated with revascularization as the primary therapy, more commonly received a beta-blocker, less often required therapy for congestive heart failure and less commonly received either an antiarrhythmic drug or an implantable cardioverter defibrillator. Nevertheless, subsequent mortality of patients with a transient or correctable cause of VT/VF was no different or perhaps even worse than that of the primary VT/VF population. CONCLUSIONS: Patients identified with a transient or correctable cause for their VT/VF remain at high risk for death. Further research is needed to define truly reversible causes of VT/VF. Meanwhile, these patients may require more aggressive evaluation, treatment and follow-up than is currently practiced.

Cryothermal mapping of the sinus node in dogs: a simple method of localising dominant and latent pacemakers.

To investigate the potential use of cryothermal mapping to localise the sites of the dominant and latent pacemakers of the sinus node, we compared the results of cryothermal and electrical mapping of the sinus node in 16 dogs. In all dogs, cooling (-5 to +5 degrees C) of a localised epicardial area of about 3 X 3 mm2 close to the sulcus terminalis (area 1) resulted in a decrease in heart rate and a change in the P wave configuration. Cooling of an additional area of up to 15 X 3 mm2 (area 2) while cooling of area 1 was maintained resulted in a further decrease in heart rate and a further change in P wave configuration until junctional rhythm occurred. In all dogs areas 1 and 2 could be identified within 5 min. The heart rate and P wave configuration returned to control following cooling suggesting no adverse effect of cooling on the sinus node in this temperature range. In dogs with sufficiently slow heart rates, recording from area 1 showed diastolic and upstroke slopes followed by primary negativity, indicating that area 1 was the area of the dominant pacemaker. Recording from area 2 showed only diastolic slopes indicating that area 2 was the area of the latent pacemaker. Compared to electrical mapping for identifying diastolic slope, upstroke slope and primary negativity or earliest atrial activation, cryothermal mapping is a simple, quick and safe procedure for localisation of the sinus pacemakers. Unlike recording of sinus nodal electrograms, cryothermal mapping can be performed in the presence of rapid heart rates.(ABSTRACT TRUNCATED AT 250 WORDS)

Impact of food on the pharmacokinetics and electrocardiographic effects of sustained release verapamil in normal subjects.

To evaluate the impact of food on the pharmacokinetics and electrocardiographic effects of sustained release (SR) verapamil tablets, 9 healthy men each received 3 single doses of verapamil in a randomized, crossover manner: 10 mg of intravenous verapamil, 240 mg SR verapamil on an empty stomach, and 240 mg SR verapamil with a standardized meal. PR intervals and racemic verapamil serum concentrations were measured serially over 30 hours after administration. The time to peak concentration was longer (7.5 +/- 3.0 vs 4.4 +/- 2.3 hours), resulting in a lower peak verapamil serum concentration (118 +/- 43 vs 175 +/- 50 ng/ml) when SR verapamil was administered with food (p < 0.05). Food tended to decrease the bioavailability of SR verapamil (34 +/- 12 vs 49 +/- 14%), although this difference did not reach statistical significance (p = 0.065). Precipitous or exaggerated release of verapamil from the SR tablet was not observed in any subject during the fasting state. Prolongation of the PR interval paralleled these alterations in serum concentration. The maximal change in the PR interval was greater (21 +/- 8 vs 14 +/- 5%; p < 0.05) when SR verapamil was given in the fasting state. Although an exaggerated verapamil release or effect was not observed, food significantly altered the absorption and electrocardiographic effects of a single dose of SR verapamil. Manipulation of the administration condition may be helpful in achieving desired outcomes.

Long-term follow-up in patients with incessant ventricular tachycardia.

Seventeen patients with coronary artery disease, idiopathic dilated cardiomyopathy or no organic heart disease who presented with incessant ventricular tachycardia (VT) were studied and followed for a mean period of 51 +/- 35 months. In these patients the incessant VT included greater than or equal to 3 episodes of sustained VT at a rate of greater than or equal to 120 beats/min and frequent episodes of nonsustained VT over a 24-hour period. No patient had electrolyte disorder, prolonged QT interval, drug-induced arrhythmia or myocardial infarction less than 2 weeks old. Six patients died within 27 months of follow-up; 4 from sudden death and 2 from acute myocardial infarction. Three of the 11 surviving patients had remission of their VT within 1 week after the diagnosis of incessant VT. In 3 other patients in whom antiarrhythmic drugs were discontinued during follow-up because of adverse effects of the drugs or other medical reasons, 2 were found in remission. In the remaining 5 alive patients, deliberate attempts were made to discontinue the antiarrhythmic drugs; 4 of these patients were found in remission when the drugs were discontinued. Thus, 9 of these patients (53%) with incessant VT had remission over a mean follow-up of 55 +/- 34 months after discontinuation of the antiarrhythmic drugs. The probability of remission in patients surviving incessant VT warrants trials of discontinuation of antiarrhythmic drugs in these patients.

Evaluation of the pharmacokinetics and electrocardiographic effects of intravenous verapamil with intravenous calcium chloride pretreatment in normal subjects.

To evaluate the effects of calcium pretreatment on the disposition and electrocardiographic effects of verapamil, 8 healthy male volunteers received treatment in each of 3 phases in a randomized, double-blind, crossover manner. Phase I denoted 10 ml of 0.9% intravenous sodium chloride followed by 10 mg of intravenous verapamil; phase II denoted 10 ml of 10% intravenous calcium chloride followed by 4 ml of 0.9% intravenous sodium chloride; and phase III denoted 10 ml of 10% intravenous calcium chloride followed by 10 mg of intravenous verapamil. Blood samples for the determination of verapamil concentrations were drawn at 5, 10, 15, 20, 30, 45, 60 and 90 minutes, and at 2, 4, 6, 10 and 24 hours. Blood pressure, heart rate and PR intervals were also measured at these times. Pretreatment of verapamil with intravenous calcium did not alter the disposition of intravenous verapamil. Blood pressure was not significantly altered in any treatment phase, although calcium tended to increase mean arterial pressure and verapamil abolished this effect. Calcium had no significant affect on verapamil-induced PR prolongation (maximum percent change in PR interval: phase I = 19 +/- 11%, phase III = 18 +/- 7%; time to maximal prolongation: phase I = 0.38 +/- 0.21 hours, phase III = 0.37 +/- 0.26 hours; and area under the percent change in PR vs time curve: phase I = 15.5 +/- 10, phase III = 21 +/- 9). Verapamil caused a reflex increase in heart rate of similar magnitude in both phases I and III (24 +/- 10% and 21 +/- 7%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute hemodynamic effects of intravenous ibutilide in patients with or without reduced left ventricular function.

Many antiarrhythmic agents have adverse hemodynamic effects which limit their use in patients with impaired ventricular function or during tachyarrhythmias. Ibutilide is an intravenous, selective class III antiarrhythmic agent that is effective for conversion of atrial fibrillation or flutter. This multicenter, randomized, placebo-controlled, dose-ranging study evaluated the effects of intravenous ibutilide on hemodynamic parameters during invasive monitoring in 47 patients with or without reduced left ventricular ejection fraction (LVEF) > 35% or < or = 35%. Patients received either placebo or ibutilide as a 10-minute loading and a 30-minute maintenance infusion using 1 of the following dosing regimens: placebo then placebo (n = 12); 0.01 then 0.002 mg/kg (n = 12); 0.02 then 0.004 mg/kg (n = 12); or 0.03 then 0.006 mg/kg (n = 11). Ibutilide significantly increased QT and QTc intervals in a dose-related manner with mean increases ranging from 51 to 99 ms, but did not alter the PR interval or QRS duration. During ibutilide infusion, a few small but statistically significant changes from baseline in several hemodynamic variables were present. However, the changes in cardiac output, pulmonary artery or capillary wedge pressures, blood pressure, or heart rate in patients receiving ibutilide were not significantly different from the changes in patients receiving placebo. Thus, ibutilide did not cause clinically important adverse hemodynamic effects, even in patients with depressed ventricular function. One patient developed 2 episodes of nonsustained torsades de pointes during ibutilide. These results demonstrate that with careful monitoring for proarrhythmia, ibutilide can be used safely from a hemodynamic standpoint in the acute treatment of arrhythmias, even in patients with reduced ventricular function.

Proarrhythmia: a paradoxic response to antiarrhythmic agents.

Antiarrhythmic drugs may effectively terminate and prevent symptomatic tachycardias, but they may also provoke life-threatening rhythm disturbances. The electrophysiologic mechanisms responsible for proarrhythmia can be extrapolated from the existing models of reentry and abnormal automaticity. Although all antiarrhythmic drugs may cause proarrhythmia with seemingly similar frequency, the profile of the disturbance with each class of agents appears somewhat distinct. All agents may cause an increased frequency of premature beats or new or worsened ventricular tachycardia, but the classic form of proarrhythmia due to type la agents is torsades de pointes. Recent information has provided clues to the underlying mechanism of drug-induced torsades de pointes and has provided a clinical picture of patients with this adverse effect. Types lb and lc agents only rarely precipitate torsades de pointes. The latter, however, may cause a rapid, sustained, monomorphic ventricular tachycardia in certain high-risk patients that can be resistant to resuscitation efforts. Amiodarone may cause a broad variety of arrhythmias that are complicated by their extended duration and difficulty in distinguishing proarrhythmia from simple inefficacy. Proarrhythmia is a relatively common, paradoxic side effect that necessitates the clinician to make careful risk-benefit decisions in choosing antiarrhythmic drug therapy.

A functional approach to the preexcitation syndromes.

Electrophysiologic studies have been used to elicit the mechanisms of the preexcitation syndromes and have become a therapeutic tool over the past decade. A thorough understanding of the physiology and anatomy of accessory pathways that are responsible for preexcitation and the associated arrhythmias is necessary before considering the various forms of intervention. The approach to patients with preexcitation syndromes is discussed, with an emphasis on the functional properties of accessory pathways and the associated arrhythmias.

Transseptal left heart catheterization for cardiac ablation procedures.

UNLABELLED: Transseptal left heart catheterization has been performed as an alternative to the retrograde approach since 1958. However, this procedure can result in life-threatening complications, some of which may occur because of insufficient anatomical landmarks. Accordingly, we sought to assess the safety and efficacy of a new transseptal left heart catheterization technique designed for ablation procedures. Specifically, we examined whether electrode catheters could be used as anatomical landmarks, permitting identification of the aortic root and other critical structures. RESULTS: One hundred and eight consecutive patients underwent transseptal left heart catheterization under biplane fluoroscopy during catheter ablation. Electrode catheters positioned in the right atrial appendage, His bundle region, and coronary sinus were used as anatomical landmarks to guide the transseptal unit to the fossa ovalis. The angles of the right anterior and left anterior oblique projections were selected in each patient based on the orientation of the His bundle and coronary sinus catheters. Transseptal left heart catheterization was successfully performed in all patients without complications. In contrast to previous reports, the direction of the needle at the successful puncture site in the last 96 patients varied substantially: 2 o'clock in 13 patients (13 %); 3 o'clock in 43 patients (45 %); and 4 o'clock in 40 patients (42 %). CONCLUSION: The use of electrode catheters as anatomical landmarks and biplane fluoroscopy facilitates transseptal catheterization. This approach can be used safely during catheter ablation procedures.

Unexpectedly high defibrillation thresholds in an active can implantable cardioverter defibrillator system.

This case report describes a patient undergoing defibrillator generator replacement in whom the defibrillation thresholds were significantly higher with a can-active system than with a non-active can system.

Hemodynamic and electrophysiological actions of cocaine. Effects of sodium bicarbonate as an antidote in dogs.

BACKGROUND: Cocaine abuse has been implicated as a cause of death due to sudden cardiac arrest. METHODS AND RESULTS: We examined the hemodynamic and electrophysiological effects of cocaine administered as a series of 5-mg/kg i.v. boluses coupled with a continuous infusion in anesthetized dogs. Sodium bicarbonate (50 meq i.v.) was administered as a potential antidote in 11 of 15 dogs, and intravenous 5% dextrose was given in the remaining four. In a dose-dependent fashion, cocaine significantly decreased blood pressure, coronary blood flow, and cardiac output; increased PR, QRS, QT, and QTc intervals and sinus cycle length; and increased ventricular effective refractory period and dispersion of ventricular refractoriness. No afterdepolarizations were noted in the monophasic action potential recording. Nonsustained monomorphic ventricular tachycardia occurred spontaneously in two dogs, and sustained ventricular tachycardia could be induced by programmed stimulation at the end of the dosing protocol in five of 11 animals. Sodium bicarbonate promptly decreased cocaine-induced QRS prolongation to nearly that measured at baseline but had no effect on the other electrocardiographic or hemodynamic variables. In one dog, sodium bicarbonate administration was associated with reversion of ventricular tachycardia to sinus rhythm. CONCLUSIONS: We conclude that high-dose cocaine possesses negative inotropic and potent type I electrophysiological effects. Sodium bicarbonate selectively reversed cocaine-induced QRS prolongation and may be a useful treatment of ventricular arrhythmias associated with slowed ventricular conduction in the setting of cocaine overdose.

Microwave ablation of the atrioventricular junction in open-chest dogs.

The use of microwave energy for ablation of the atrioventricular (AV) junction was examined in open-chest dogs. Using a specially designed microwave catheter and a 2450 MHz generator, microwave energy was delivered to the AV junction according to one of two protocols. In protocol 1, increasing amounts of energy were delivered until irreversible AV block occurred. In protocol 2, only two applications of energy were used, one at low energy and the other at an energy found to be high enough to cause irreversible AV block. Each dog received between one and six applications of microwave energy. The amount of energy delivered per application ranged from 25.6 to 311.4 J. No AV block was seen at 59.4 +/- 28.3 J. Reversible AV block was seen with an energy of 120.6 +/- 58 J. Irreversible AV block was seen at 188.1 +/- 75.9 J. Irreversible AV block could be achieved in each animal. There was no difference in the energy required to cause irreversible AV block between the two protocols. The tissue temperature measured near the tip of the microwave catheter was correlated with both the amount of energy delivered and the extent of AV block caused. Histologic examination demonstrated coagulation necrosis of the conduction system. Microwave energy is a feasible alternative energy source for myocardial ablation. Since tissue damage is due exclusively to heating and the resulting rise in temperature can be measured, microwave energy may have advantages over currently existing energy sources in terms of both titrating delivered energy and monitoring the extent of tissue destruction.

Significant variability in the mode of ventricular tachycardia induction and its implications for interpretation of acute drug testing.

Fifty-four patients with previous myocardial infarction and sustained ventricular tachycardia on fibrillation underwent two electrophysiologic studies in the drug-free state within 72 hours. Although the concordance of overall ventricular tachycardia induction over the 2 days was good (87% of patients), there was variability in the number of extrastimuli needed to induce sustained ventricular tachycardia on each day in 60% of patients. Of those in whom ventricular tachycardia was inducible on both days, 40% required additional extrastimuli and 20% required fewer extrastimuli. A change by two or more extrastimuli was found in 12% of patients. There was no correlation between the variability observed and multiple clinical and laboratory parameters (including the aggressiveness of the stimulation protocol); however, the direction of the variability (easier or harder to induce) correlated with changes in ventricular refractoriness. Inherent day-to-day variability may affect the reproducibility of electrophysiologic studies and influence the results of serial drug testing.

Comparison of in vivo tissue temperature profile and lesion geometry for radiofrequency ablation with a saline-irrigated electrode versus temperature control in a canine thigh muscle preparation.

BACKGROUND: It is thought that only a thin layer of tissue adjacent to the electrode is heated directly by electrical current (resistive heating) during radiofrequency ablation. Most of the thermal injury is thought to result from conduction of heat from the surface layer. The purpose of this study was to determine whether lesion depth could be increased by producing direct resistive heating deeper in the tissue with higher radiofrequency power, allowed by cooling the ablation electrode with saline irrigation to prevent the rise in impedance that occurs when the electrode-tissue interface temperature reaches 100 degrees C. METHODS AND RESULTS: In 11 anesthetized dogs, the thigh muscle was exposed and bathed with heparinized canine blood (36 degrees C to 37 degrees C). A 7F catheter, with a central lumen, a 5-mm tip electrode with six irrigation holes, and an internal thermistor, was positioned perpendicular to the thigh muscle and held at a constant contact weight of 10 g. Radiofrequency current was delivered to 145 sites (1) at high constant voltage (66 V) without irrigation (CV group, n = 31), (2) at variable voltage (20 to 66 V) to maintain tip-electrode temperature at 80 degrees C to 90 degrees C without irrigation (temperature-control group, n = 39), and (3) at high CV (66 V) with saline irrigation through the catheter lumen and ablation electrode at 20 mL/min (CV irrigation group, n = 75). Radiofrequency current was applied for 60 seconds but was terminated immediately in the event of an impedance rise > or = 10 omega. Tip-electrode temperature and tissue temperature at depths of 3.5 and 7.0 mm were measured in all three groups (n = 145). In 33 CV irrigation group applications, temperature was also measured with a separate probe at the center (n = 18) or edge (n = 15) of the electrode-tissue interface. In all 31 CV group applications, radiofrequency energy delivery was terminated prematurely (at 11.6 +/- 4.8 seconds) owing to an impedance rise associated with an electrode temperature of 98.8 +/- 2.1 degrees C. All 39 temperature-control applications were delivered for 60 seconds without an impedance rise, but voltage had to be reduced to 38.4 +/- 6.1 V to avoid temperatures > 90 degrees C (mean tip-electrode temperature, 84.5 +/- 1.4 degrees C). In CV irrigation applications, the tip-electrode temperature was not > 48 degrees C (mean, 38.4 +/- 5.1 degrees C) and the electrode-tissue interface temperature was not > 80 degrees C (mean, 69.4 +/- 5.7 degrees C). An abrupt impedance rise with an audible pop and without coagulum occurred in 6 of 75 CV irrigation group applications at 30 to 51 seconds, probably owing to release of steam from below the surface. In the CV and temperature-control group applications, the temperatures at depths of 3.5 (62.1 +/- 15.1 degrees C and 67.9 +/- 7.5 degrees C) and 7.0 mm (40.3 +/- 5.3 degrees C and 48.3 +/- 4.8 degrees C) were always lower than the electrode temperature. Conversely, in CV irrigation group applications, electrode and electrode-tissue interface temperatures were consistently exceeded by the tissue temperature at depths of 3.5 mm (94.7 +/- 9.1 degrees C) and occasionally 7.0 mm (65.1 +/- 9.7 degrees C). Lesion dimensions were smallest in CV group applications (depth, 4.7 +/- 0.6 mm; maximal diameter, 9.8 +/- 0.8 mm; volume, 135 +/- 33 mm3), intermediate in temperature-control group applications (depth, 6.1 +/- 0.5 mm; maximal diameter, 11.3 +/- 0.9 mm; volume, 275 +/- 55 mm3), and largest in CV irrigation group applications (depth, 9.9 +/- 1.1 mm; maximal diameter, 14.3 +/- 1.5 mm; volume, 700 +/- 217 mm3; P < .01, respectively). CONCLUSIONS: Saline irrigation maintains a low electrode-tissue interface temperature during radiofrequency application at high power, which prevents an impedance rise and produces deeper and larger lesions. A higher temperature in the tissue (3.5 mm deep) than at the electrode-tissue interface indicates that direct resistive heating occurred deeper

Radiofrequency catheter ablation of idiopathic left ventricular tachycardia guided by a Purkinje potential.

BACKGROUND: Verapamil-sensitive, idiopathic left ventricular tachycardia (ILVT) with right bundle branch block configuration and left-axis deviation has been suggested to originate from the left posterior fascicle. The purpose of this study was to determine how frequently potentials generated by the Purkinje fiber network (P potential) can be recorded preceding ventricular activation, and the role of the P potential in guiding radiofrequency catheter ablation. METHODS AND RESULTS: Eight patients (mean age, 26 +/- 10 years) with ILVT (cycle length, 346 +/- 59 milliseconds) were studied. Right and left ventricular endocardial mapping during tachycardia identified earliest ventricular activation at the posteroapical left ventricular septum. In all patients, earliest ventricular activation during tachycardia was preceded by a distinct potential. This potential also preceded ventricular activation during sinus rhythm, consistent with activation of a segment of the left posterior fascicle (P potential). The earliest recorded P potential preceded the QRS during tachycardia by 15 to 42 milliseconds (mean, 27 +/- 9 milliseconds). The application of radiofrequency current at 1 to 4 sites (median, 1) eliminated ILVT in all eight patients. In the seven patients with P potentials recorded at multiple sites within the posteroapical septum, ablation was successful at the site of the earliest P potential and unrelated to the timing of ventricular activation. In the remaining patient, ablation was successful at a site recording a late P potential fusing with earliest ventricular activation. During follow-up (1 to 67 months; median, 10.5) ILVT recurred only in the latter patient. Pace mapping during tachycardia at the successful ablation site in four patients produced a similar QRS with stimulus-QRS interval equal to P-QRS interval during tachycardia. However, a similar QRS was obtained by pacing at nearby sites that recorded a later P potential. CONCLUSIONS: These findings support the hypothesis that ILVT originates from the Purkinje network of the left posterior fascicle. A P potential can be recorded at the posteroapical left ventricular septum during ILVT, and ablation is successful at the site recording the earliest P potential. Pace mapping with similar QRS is not specific due to capture of the Purkinje fiber network at a site remote from the origin of the tachycardia.