Mechanoelectrical feedback: role of beta-adrenergic receptor activation in mediating load-dependent shortening of ventricular action potential and refractoriness.

BACKGROUND: Augmented preload increases myocardial excitability by shortening action potential duration (APD). The mechanism governing this phenomenon is unknown. Because myocardial stretch increases intracellular cAMP, we hypothesized that load-dependent changes in myocardial excitability are mediated by beta-adrenergic stimulation of a cAMP-sensitive K(+) current. METHODS AND RESULTS: The effects of propranolol on load-induced changes in electrical excitability were studied in 7 isolated ejecting canine hearts. LV monophasic APD at 50% and 90% repolarization (MAPD(50) and MAPD(90)) and refractoriness were determined at low (9+/-3 mL) and high (39+/-4 mL) load before and after beta-adrenergic blockade. During control, the MAPD(50) decreased from 193+/-26 to 184+/-26 ms with increased load, as did the MAPD(90) (238+/-28 to 233+/-28 ms), P

Cardiac sympathetic denervation after transmyocardial laser revascularization.

BACKGROUND: Transmyocardial laser revascularization (TMR) has been shown to improve refractory angina not amenable to conventional coronary interventions. However, the mechanism of action remains controversial, because improved myocardial perfusion has not been consistently demonstrated. We hypothesized that TMR relieves angina by causing myocardial sympathetic denervation. METHODS AND RESULTS: PET imaging of resting and stress myocardial perfusion with [13N]ammonia (NH3) and of sympathetic innervation with [11C]hydroxyephedrine (HED) was performed before and after TMR in 8 patients with class IV angina ineligible for CABG or PTCA. A mean of 50+/-11 channels were created in the left ventricle (LV) with a holmium:YAG laser. A semiautomated program was used to determine NH3 uptake and HED retention in the LV. Perfusion and innervation defects were defined as the percentage of LV with tracer uptake or retention >2 SD below normal mean values. All patients experienced improvement in their angina by 2.4+/-0.5 angina classes after surgery, P=0.008. Sympathetic innervation defects exceeded resting perfusion defects in all patients before TMR (34.6+/-27.3% for HED versus 9.4+/-10.8% for NH3, P=0.008). TMR did not significantly affect resting or stress myocardial perfusion but increased the extent of sympathetic denervation in 6 of 8 patients by 27.5+/-15.9%, P=0.03. In the remaining 2 patients, both sympathetic denervation and stress perfusion defects decreased after surgery. CONCLUSIONS: TMR causes decreased myocardial HED uptake in most patients without significant change in resting or stress myocardial perfusion, suggesting that the improvement in angina may be at least in part due to sympathetic denervation.

Interactions between electronic article surveillance systems and implantable cardioverter-defibrillators.

BACKGROUND: In patients with implantable cardioverter-defibrillators (ICDs). inappropriate shocks have been reported with exposure to electronic article surveillance systems. The risk to patients with ICDs of walking through or lingering near surveillance systems requires further investigation. METHODS AND RESULTS: We evaluated the response in ICD function in 170 subjects during a 10- to 15-second midgate walk-through of and during extreme (2 minutes within 6 in of the gate) exposure to 3 common article surveillance systems. Complete testing was done in 169 subjects. During a 10- to 15-second (very slow) walk-through of the 3 surveillance systems, no interactions were observed that would negatively affect ICD function. During extreme exposure (169 subjects) and during extreme exposure and pacing via the ICD (126 subjects), interactions between the ICD and the article surveillance systems were observed in 19 subjects. In 7 subjects, this interaction was clinically relevant and would have likely (3 subjects) and possibly (4 subjects) resulted in ICD shocks. In 12 subjects, the interaction was minor. CONCLUSIONS: It is safe for a patient with an ICD to walk through electronic article surveillance systems. Lingering in a surveillance system may result in an inappropriate ICD shock.

Posterior fast atrioventricular node pathways: implications for radiofrequency catheter ablation of atrioventricular node reentrant tachycardia.

OBJECTIVES: This study sought to present evidence that fast atrioventricular (AV) node pathways with posterior exit sites may participate in typical AV node reentry. BACKGROUND: Catheter ablation of the slow AV node pathway in the posteroseptal right atrium is the preferred therapeutic approach in patients with AV node reentrant tachycardia. Despite the success achieved with this approach, electrophysiologic changes consistent with fast pathway ablation are occasionally observed. One potential explanation is the presence of an aberrant posterior fast pathway. METHODS: The location of fast and slow AV node pathways was determined by atrial activation mapping along the tricuspid valve annulus during tachycardia and was further confirmed by the effect of radiofrequency catheter ablation. RESULTS: Seven patients with AV node reentrant tachycardia had evidence of a posterior fast pathway near the coronary sinus os. Abolition of anterograde and retrograde fast pathway conduction followed radiofrequency ablation in the posteroseptal region in six patients. Consistent with fast pathway ablation, the AH interval increased from 70 +/- 24 to 195 +/- 35 ms (mean +/- SD), and tachycardia was no longer inducible. Selective slow pathway ablation was performed in one other patient with a posterior fast pathway. CONCLUSIONS: Functionally fast AV node pathways may be located in the posteroseptal right atrium, where slow pathway modification is performed. These data delineate the limitation of an anatomically guided slow pathway ablative approach and emphasize the importance of detailed mapping and localization of the retrograde fast pathway exit site before ablation. Failure to recognize the presence of posterior fast AV node pathways may account for sporadic examples of AV block, complicating posteroseptal ablation in patients with AV node reentry.

Limitations of adenosine in assessing the efficacy of radiofrequency catheter ablation of accessory pathways.

Adenosine has been shown to reliably confirm the success of accessory pathway catheter ablation by producing transient atrioventricular (AV) block during atrial and ventricular pacing. This is due to the insensitivity of accessory pathway conduction to adenosine (with the rare exception of accessory pathways with decremental conduction properties). However, 4 of 204 consecutive patients who underwent successful accessory pathway ablation (as shown by adenosine-induced transient AV block) had recurrent AV reciprocating tachycardia involving a second, previously nonmanifest accessory pathway. In each case, the second accessory pathway was localized to a site disparate from the original pathway. No pathway showed decremental anterograde or retrograde conduction properties. In 2 patients, adenosine initially did not show the presence of the second concealed accessory pathway, because the refractory period of the accessory pathway was longer than the pacing cycle length used to assess ventriculoatrial conduction. Only when the refractory period of this second accessory pathway was shortened by infusion of isoproterenol did adenosine reveal the presence of the pathway during follow-up electrophysiologic study. In another patient, a non-decremental accessory pathway was shown to be sensitive to adenosine. In the remaining patient, the second accessory pathway may have been transiently injured during the initial study, thereby simulating adenosine sensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine induced intraatrial block.

Adenosine, an endogenous nucleoside with potent negative chronotropic and dromotropic effects on the sinus and AV nodes, is thought to have little if any antiarrhythmic effect on normal atrial tissue. However, there may be an electrophysiological basis for an adenosine effect on atrial tissue with atypical conduction properties. We examined the electrophysiological effects of adenosine in a patient with decremental atrial conduction properties. During incremental pacing from the high right atrium there was gradual prolongation of the intraatrial interval between the high right atrium and the low septal atrium, from 180 to 280 msec, until 2:1 intraatrial block occurred at a pacing cycle length of 280 msec. Adenosine (6 mg IV) resulted in transient intraatrial block followed by prolonged intraatrial conduction during high right atrial pacing at a cycle length of 400 msec. Thus, similar to its effects on the AV node and decremental AV accessory pathways, adenosine may also slow and abolish conduction in decremental atrial issue, an effect that is likely attributed to adenosine induced hyperpolarizing K+ current in partially depolarized atrial tissue.

Increased defibrillation threshold due to ventricular fibrillation duration. Potential mechanisms.

The duration of ventricular fibrillation (VF) that precedes a high energy shock has been recognized as a critical determinant of defibrillation outcome. Factors such as metabolic acidosis or alkalosis do not affect outcome. The authors hypothesized that release of myocardial adenosine during VF could potentially mediate the time-dependent effects of VF duration on defibrillation. Defibrillation threshold (DFT) was therefore determined in dogs during concurrent infusion of adenosine and dipyridamole (a nucleoside transport blocker). Transthoracic DFT increased by approximately 50%, whereas transmyocardial DFT increased by approximately 100% in a separate group of dogs. These effects of adenosine on DFT were abolished when the dogs were autonomically denervated, suggesting that the deleterious effects of adenosine on DFT are due to its antiadrenergic mechanism of action. These data indicate that adenosine release during VF can markedly increase DFT. Since adenosine myocardial release during VF is time dependent, it is likely that adenosine plays a significant role in mediating the increase in threshold that is dependent on the duration of VF.

Metabolic determinants of defibrillation. Role of adenosine.

BACKGROUND: The single most important determinant of cardiac arrest outcome is the duration of ventricular fibrillation (VF) preceding delivery of a high-energy shock, because of the adverse effect of VF duration on defibrillation threshold (DFT). Although a metabolic mechanism has been proposed, hypoxia, metabolic acidosis, or alkalosis do not adversely affect DFT. However, since (1) catecholamines and adenosine levels are markedly increased during hypoxia, (2) exogenous catecholamines decrease DFT, and (3) adenosine is a potent antagonist of the electrophysiological effects of catecholamines on ventricular myocardium, we hypothesized that release of adenosine during prolonged VF adversely affects DFT and that this effect occurs through an antiadrenergic mechanism. METHODS AND RESULTS: DFT was determined in dogs during infusion of adenosine (300 micrograms.kg-1.min-1) and dipyridamole (0.25 mg/kg), an adenosine uptake blocker, a regimen that resulted in adenosine levels in the myocardial effluent equivalent to those achieved after 5 minutes of VF. Adenosine increased transthoracic DFT in each dog by 49 +/- 14% (n = 21) (mean +/- SEM) and transmyocardial DFT in a separate group of 10 dogs by 103 +/- 16%, P = .0003. Pretreatment with the specific A1 adenosine receptor antagonist 8-cyclopentyltheophylline (CPT) 5 mg/kg completely abolished the effects of adenosine on DFT. The effects of adenosine on DFT were also examined in the denervated state (propranolol 0.2 mg/kg plus bilateral vagotomy). In contrast to its effect in the innervated condition, adenosine had no effect on DFT in the same dogs when denervated, 49 +/- 11 versus 53 +/- 10 J (P = NS). CONCLUSIONS: Adenosine significantly increases transthoracic and transmyocardial DFT, effects that are mediated by the A1 adenosine myocardial receptor through an antiadrenergic mechanism. These results suggest that enhanced release of adenosine during VF may have a deleterious effect on defibrillation and that intramyocardial delivery of a specific A1 adenosine antagonist during VF may facilitate defibrillation and significantly reduce defibrillation threshold.

Mechanism-specific effects of adenosine on atrial tachycardia.

BACKGROUND: Recent reports suggest that adenosine, in addition to terminating supraventricular tachycardia involving the atrioventricular (AV) node, may have antiarrhythmic effects on atrial tachycardia. The electrophysiological effects of adenosine on supraventricular tissue include shortening of action potential duration in atrial myocytes mediated by the potassium current, IKACh,Ado; shortening of action potential duration and hyperpolarization in sinus node cells; and anti-adrenergic electrophysiological effects resulting from inhibition of adenylyl cyclase. We therefore hypothesized that the response of atrial tachycardia to adenosine would be mechanism specific, with termination of atrial tachycardia due to sinus node reentry or cAMP-mediated triggered activity, transient suppression of automatic atrial tachycardia, and an absence of antiarrhythmic effect on tachycardia due to intraatrial reentry. METHODS AND RESULTS: Adenosine (mean +/- SD, 143 +/- 54 micrograms/kg IV) was administered to 27 patients (55 +/- 19 years) in atrial tachycardia whose mechanism was confirmed by electrophysiological study. Adenosine terminated sinus node reentrant tachycardia in 6 of 6 patients and terminated atrial tachycardia due to triggered activity in the 1 patient in whom it was identified. Adenosine transiently suppressed automatic atrial tachycardia in 7 of 7 patients and had no effect in 13 patients with intra-atrial reentrant tachycardia, including 8 patients with atrial flutter. CONCLUSIONS: These findings demonstrate that adenosine's effects on atrial tachycardia are mechanism specific and can be used to differentiate between reentrant tachycardia confined to the region of the sinus node or atria and between nonreentrant atrial tachycardia due to either triggered activity or automaticity.

Role of arterial chemoreceptors in mediating the effects of endogenous adenosine on sympathetic nerve activity.

BACKGROUND: Exogenous adenosine has been shown to increase muscle sympathetic nerve activity (MSNA), blood pressure, heart rate, and ventilation in conscious humans, effects attributed to peripheral chemoreceptor activation. METHODS AND RESULTS: To determine whether endogenous adenosine has similar effects and whether they are mediated through chemoreceptor activation, we examined the effects of dipyridamole, an inhibitor of adenosine reuptake, on sympathetic nerve activity and ventilation. Twenty studies were conducted on separate days in 15 healthy volunteers. We examined responses to dipyridamole 0.56 mg/kg during room air breathing (n = 7), during hyperoxia (100% O2, n = 6), and during room air breathing after pretreatment with aminophylline (n = 7). During room air breathing, dipyridamole increased MSNA from 231 +/- 42 to 504 +/- 136 U/min, heart rate from 65 +/- 3.8 to 96 +/- 4.7 beats per minute, and systolic blood pressure from 129 +/- 3.5 to 140 +/- 4.8 mm Hg; central venous pressure decreased from 5.5 +/- 0.4 to 4.5 +/- 0.3 mm Hg (P < .01), and minute ventilation increased from 7.8 +/- 0.6 to 9.1 +/- 0.5 L/min (P < .01). During peripheral chemoreceptor suppression (with hyperoxia), there was a dissociation of the effects of dipyridamole on ventilation and sympathoexcitation. Effects on ventilation were attenuated, but sympathoexcitatory effects were not. Pretreatment with aminophylline, an adenosine receptor antagonist, either abolished (blood pressure, minute ventilation, and end-tidal CO2) or markedly attenuated (MSNA and heart rate) the effects of dipyridamole during room air breathing. CONCLUSIONS: Augmentation of endogenous adenosine with dipyridamole increases sympathetic nerve activity and ventilation in conscious humans. The ventilatory effects of endogenous adenosine are mediated predominantly by chemoreceptor activation, but the sympathetic and hemodynamic responses to endogenous adenosine are probably mediated by an additional afferent mechanism that is independent of peripheral chemoreceptor activation.

Physiologic role of atrio-Hisian and nodo-Hisian bypass tracts in supraventricular tachycardia.

Atrio-Hisian bypass tracts are considered to be rare electrophysiologic curiosities. The prevalence and functional significance of these tracts are unknown. We examined the incidence of atrio-Hisian and nodo-Hisian bypass tracts, their electrophysiologic manifestations, and their physiologic role in supraventricular tachycardia in 200 consecutive patients referred for evaluation of supraventricular tachycardia. In one patient it was demonstrated for the first time that a concealed (retrograde only) nodo-Hisian bypass tract functioned as the retrograde limb of orthodromic reciprocating tachycardia. The VA interval was negative during tachycardia, similar to that sometimes observed in atrioventricular nodal reentry. In a second patient an anterograde and retrograde conducting pathway resulted in a pseudo Wolff-Parkinson-White electrocardiographic pattern and served as an "innocent bystander," permitting a rapid ventricular response during atrial flutter. In conclusion, although atrio-Hisian and nodo-Hisian bypass tracts are rare, they are sufficiently prevalent to make them observable in a larger referral series. Most importantly, they may participate as bystanders during supraventricular tachycardia or as either the anterograde or retrograde limbs of reciprocating tachycardia. They may possess features that mimic Wolff-Parkinson-White syndrome and/or AV nodal reentry.

AV nodal-His-Purkinje reentry: a novel form of tachycardia.

INTRODUCTION: Bundle branch reentry (BBR) typically occurs in patients with dilated cardiomyopathy and infra-Hisian conduction system disease. The macroreentrant circuit of BBR is confined to the His-Purkinje system (HPS) and ventricular myocardium. As such, the atrioventricular (AV) node plays no role in the tachycardia circuit. METHODS AND RESULTS: In the present study, we identified a novel form of wide complex tachycardia in a patient with coronary disease and severe aortic regurgitation. The tachycardia morphology was right bundle branch block with a left superior axis. Ventriculoatrial block was present during tachycardia. An unusual feature of this rhythm was two sequential His-bundle deflections (H and H') for each ventricular beat of tachycardia. The H'V interval was identical to the HV interval during supraventricular rhythm. Changes in the ventricular cycle length (VV) preceded changes in the HH interval, consistent with retrograde activation of the first His-bundle deflection. Changes in the H'H' interval preceded changes in the VV interval, consistent with anterograde activation of the second His-bundle deflection. Tachycardia could be terminated with ventricular extrastimuli that did not capture the proximal HPS as well as with ventricular extrastimuli that advanced the His deflection, consistent with block in the HPS and in the AV node, respectively. Reproducible termination of the tachycardia following the first His deflection was demonstrated with adenosine, consistent with an upper pivot in the AV node. CONCLUSIONS: We have identified a new form of reentrant tachycardia in which the AV node, HPS, and ventricular myocardium each obligatorily participates in the tachycardia circuit, with the left posterior fascicle and right bundle functioning as the anterograde and retrograde limbs, respectively. Unlike BBR, however, the His bundle is activated twice as the wavefront pivots in the AV node. This model requires longitudinal dissociation at the levels of the AV node and His bundle.

Vasodepressor syncope due to subclinical myocardial ischemia.

INTRODUCTION: Vasodepressor syncope is a common cause of syncope, but the initiating event that triggers the vasodepressor response remains incompletely understood. Although ischemia due to acute right coronary occlusion may precipitate hypotension and bradycardia through the Bezold-Jarisch reflex, an ischemic precipitant for the common vasodepressor faint has not been previously identified. In the present study, we present evidence for a causal relationship between myocardial ischemia and vasodepressor syncope. METHODS AND RESULTS: Two patients referred for evaluation of syncope underwent upright tilt table testing with either ST segment monitoring, sestamibi scintigraphy and echocardiography during the tilt test, or coronary angiography. Both patients had positive tilt table tests during the control study. Patient 1 was documented to have reproducible ischemic ECG changes during atypical chest pressure induced by upright tilt, despite a normal coronary angiogram with ergonovine provocation. Subsequent tilt testing with simultaneous sestamibi perfusion imaging and echocardiography revealed reversible anterolateral hypoperfusion corresponding with anterolateral hypokinesis during upright tilt that preceded syncope. Ischemic ECG changes during incremental rapid atrial pacing further suggested ischemia on the basis of microvascular disease. Follow-up tilt testing on verapamil was negative. Patient 2 developed ischemic ECG changes during the recovery phase of an exercise stress test, which was followed by a vasodepressor response and frank syncope. Coronary angiography revealed a 90% distal right coronary artery stenosis that was successfully dilated, after which follow-up tilt table testing off all other medication was negative. CONCLUSIONS: These two cases illustrate a previously unrecognized causality between myocardial ischemia and clinical vasodepressor syncope, and demonstrate that subtle manifestations of myocardial ischemia, associated with either atypical angina or silent ischemia, can provoke syncope.

Radiofrequency catheter ablation for postinfarct ventricular tachycardia.

Catheter mapping and radiofrequency ablation of postinfarct sustained ventricular tachycardia (VT) remain one of the greatest challenges for the electrophysiologist. Although there were no major breakthroughs during the past year, several refinements and clarifications of existing mapping criteria were published. In addition, initial reports appeared describing new mapping systems and ablation technologies that may significantly impact the way ablation studies are performed as well as the way in which they affect success rates. Uncertainties remain as to how effective catheter ablation will be as a longterm cure for this type of VT. For the foreseeable future, catheter ablation in postinfarct VT will remain adjunctive rather than primary therapy.

Autonomic changes and heart rate variability in children with neurocardiac syncope.

This study evaluated resting autonomic function and autonomic responses to head-up tilt-table testing in children who experienced neurocardiac syncope to determine whether predictable differences existed between these patients and normal volunteers. Neurocardiac syncope is a common cause of syncope in children. The mechanism, though related to abnormalities in autonomic function, has not been fully elucidated, particularly in pediatric patients. This study evaluated resting autonomic tone using noninvasive autonomic function tests (i.e., Valsalva, handgrip, and deep breathing) and 24-hour heart rate variability (HRV). In addition, heart rate and blood pressure were evaluated during head-up tilt examination. Values from patients who experienced neurocardiac syncope were compared to those from age-matched normal volunteers. No significant differences were noted during noninvasive testing. Some time domain HRV variables demonstrated a trend toward significant difference (p < 0.10). Tilt testing data were significantly different in sinus beat to sinus beat (RR) intervals between controls and syncope patients at 2, 5, and 10 minutes after tilting. In addition, significant differences were noted in RR interval and the standard deviation of RR interval 1 or 2 minutes prior to syncope when compared to controls at 5 and 10 minutes after tilting. Children with syncope exhibited abnormalities during tilt testing indicating an increased sympathetic or decreased parasympathetic tone, particularly prior to syncope. Some measures of HRV might constitute noninvasive parameters that correlate with the positive tilt table test.

Mechanism of repetitive monomorphic ventricular tachycardia.

BACKGROUND: The most common form of idiopathic ventricular tachycardia (VT) is repetitive monomorphic VT (RMVT), which is characterized by frequent ventricular ectopy and salvos of nonsustained VT with intervening sinus rhythm. Unlike most other forms of idiopathic VT, this tachycardia typically occurs at rest and is nonsustained. The mechanism of RMVT is undefined. Because of a common site of origin, the right ventricular outflow tract (RVOT), we hypothesized that RMVT is mechanistically related to paroxysmal sustained, exercise-induced VT, which has been shown to be consistent with cAMP-mediated triggered activity. Therefore, in this study, we sought to identify (1) the mechanism of RMVT at the cellular level by using electropharmacological probes known to activate either stimulatory or inhibitory G proteins and thereby modify intracellular cAMP levels, (2) potential autonomic triggers of RMVT through analysis of heart rate variability, and (3) whether well-characterized somatic activating mutations in the stimulatory G protein, G alpha s, underlie RMVT. METHODS AND RESULTS: Twelve patients with RMVT underwent electrophysiological study. Sustained monomorphic VT was reproducibly initiated and terminated with programmed stimulation and/or isoproterenol infusion in 11 of the 12 patients (the other patient had incessant RMVT). Induction of VT demonstrated cycle length dependence and was facilitated by rapid atrial or ventricular pacing. Termination of VT occurred in response to interventions that either lowered stimulated levels of intracellular cAMP (and thus decreased intracellular Ca2+)--ie, adenosine (12 of 12), vagal maneuvers or edrophonium (8 of 9), and beta-blockade (3 of 5)--or directly decreased the slow-inward calcium current--ie, verapamil (10 of 12). Analysis of heart rate variability during 24-hour ambulatory monitoring in 7 patients showed that the sinus heart rate is increased and accelerates before nonsustained VT (P < .05), whereas high-frequency heart rate variability is unchanged. These findings are consistent with transient increases in sympathetic tone preceding nonsustained VT. Finally, myocardial biopsy samples were obtained from the site of origin of the VT (typically the RVOT) and from the right ventricular apex from 9 patients. Genomic DNA was extracted from each biopsy sample, and three exons of G alpha s in which activating mutations have previously been described were amplified by polymerase chain reaction. All sequences from these regions were found to be identical to that of control. CONCLUSIONS: Although the arrhythmia occurs at rest, the constellation of findings in idiopathic VT that is characterized by RMVT is consistent with the mechanism of cAMP-mediated triggered activity. Therefore, the spectrum of VT resulting from this mechanism includes not only paroxysmal exercise-induced VT but also RMVT.

Ventricular tachycardias mimicking those arising from the right ventricular outflow tract.

INTRODUCTION: Ablation of ventricular tachycardia (VT) arising from the right ventricular outflow tract (RVOT) has proven highly successful, yet VTs with similar ECG features may originate outside the RVOT. METHODS AND RESULTS: We reviewed the clinical, echocardiographic, and ECG findings of 29 consecutive patients referred for ablation of monomorphic VT having a left bundle branch block pattern in lead V1 and tall monophasic R waves inferiorly. Nineteen patients (group A) had VTs ablated from the RVOT, and 10 patients (group B) had VTs that could not be ablated from the RVOT. The QRS morphology during VT or frequent ventricular premature complexes was the only variable that distinguished the two groups. During the target arrhythmia, ECGs of group B patients displayed earlier precordial transition zones (median V3 vs V5; P < 0.001), more rightward axes (90 +/- 4 vs 83 +/- 5; P = 0.002), taller R waves inferiorly (aVF: 1.9 +/- 1.0 vs 2.4 +/- 0.5; P = 0.020) and small R waves in lead V1 (10/10 vs 9/19; P = 0.011). Radiofrequency catheter ablation from the RVOT failed to eliminate VT in any group B patient, but ablation from the left ventricular outflow tract (LVOT) eliminated VT in 2 of 6 patients in whom left ventricular ablation was attempted. CONCLUSION: The absence of an R wave in lead V1 and a late precordial transition zone suggest an RVOT origin of VT, whereas an early precordial transition zone characterizes VTs that mimic an RVOT origin. The latter VTs occasionally can be ablated from the LVOT. Recognition of these ECG features may help the physician advise patients and direct one's approach to ablation.