Volume 114 Number 5 10. enalase is a molecular marker for peripheral and central neuroendocrine ceils. Nature 197X$276:834-6. Glancey DL, Roberts WC. The heart in malignant melanoma: a study of 70 autopsy cases. Am J Cardiol 1968;21:555-71. Berge T, Sievers J.-Myocardial metaatases: a pathological and electrocardiographic studv. Br Heart J 1967:30:383-90. Waller BF, Gotidiener Js, Virmani R, et ai. The “charcoal heart”: melanoma of the car. Chest 1980,77:671-6. Hanley PC, Shub C, Seward JB, et al. Intracavitary cardiac melanoma diagnosed by endomyocardial left ventricular biopsy. Chest 1983;84:195-8. Amparo EG, Higgins CB, Farmer D, Gordon G, McNamara M. Gated MRI of cardiac and paracardiac masses: initial experience. Am J Roentgen01 1984;143:1151-6. Localization of slow conduction in a ventricular tachycardia circuit: Implications for catheter ablation William G. Stevenson, M.D., James Weiss, M.D., Isaac Wiener, M.D., Daniel Wohlgelernter, M.D., and Lawrence Yeatman, M.D. Los Angeles, Calif. Reentry is the likely mechanism of ventricular tachycar- dia arising from an area of healed myocardial infarction’s2 For reentry to occur, unidirectional conduction block and an area of slow conduction must be present in the tachycardia circuit.2 Reports of entrainment of ventricular tachycardia have suggested that an area of slow conduc- tion is present during ventricular tachycardia in hu- mans.2-5 Canine studies6 have suggested that damaging the area of slow conduction is likely to be successful in controlling reentrant ventricular tachycardia. This report describes a patient with ventricular tachycardia in whom an area of slow conduction participating in the tachycar- dia circuit was identified by programmed electrical stimu- lation at that site. A 54-year-old man was referred to UCLA for manage- ment of recurrent sustained ventricular tachycardia that had developed 4 years after an anterior myocardial infarc- tion. Ventricular tachycardia had occurred during therapy with procainamide, quinidine, tocainide, mexiletine, amiodarone, and combinations of these agents. At the time of study he had been on amiodarone for 7 months (most recent dose 600 mg/day). Contrast ventriculography demonstrated a left ventricular ejection fraction of 20% with akinesis of the anterior wall. Following informed consent, left ventricular mapping and endocardial cathe- ter ablation were performed according to the protocol approved by the UCLA Human Subjects Protection Com- mittee. A No. 5 French quadripolar catheter was posi- From The Division of Cardiology, UCLA School of Medicine and Center for the Health Sciences. Reprint requests: William G. Stevenson, M.D., Division of Cardiology, UCLA, CHS 47-123, Los Angeles, CA 90024. Brief Communications 1253 tioned in the right ventricular apex and a No. 6 French quadripolar catheter with a 1 cm interelectrode distance (USCI, Billerica, Mass.) was inserted into the right femo- ral artery and advanced into the left ventricle. Surface ECG leads and intracardiac electrograms were recorded at paper speeds of 100 to 150 mm/set on an Electronics for Medicine VR-12 chart recorder (Electronics for Medicine/ Honeywell Inc., Pleasantville, N.Y.). Full standard 12- lead ECGs were recorded on a separate three-channel recorder (Marquette Electronics Inc., Milwaukee, Wise.). Programmed electrical stimulation was performed by the use of stimuli with a 2 msec pulse width and amplitude of twice the late diastolic threshold in the right ventricle or an amplitude of 10 mA in the left ventricle (Bloom Associates Ltd., Reading, Pa.). Sustained monomorphic ventricular tachycardia with a cycle length of 420 msec and right bundle branch block superior axis QRS morphology identical to the patient’s spontaneous tachycardia was initiated by single ventricu- lar extrastimuli delivered during pacing from the right ventricular apex (Fig. 1). During tachycardia, continuous electrical activity was recorded at a site on the inferior aspect of the apical left ventricular septum (site l-2). As shown in Fig. 1, initiation of tachycardia by a premature stimulus was associated with a sudden increase in the interval between the initial portion of the ECG at site l-2 and the late fractionated portion of the electrogram. Bipolar left ventricular stimulation was performed at site l-2 from the distal pair of electrodes on the left ventricular catheter and a bipolar electrogram was record- ed from the proximal electrode pair. The 12-lead ECG recorded during pacing at this site demonstrated excellent concordance with the QRS morphology of the spontane- ous ventricular tachycardia (Fig. 2). In addition, the duration from the stimulus artifact to the onset of ventric- ular depolarization in all surface ECG leads was greater than 120 msec, suggesting that the pacing site was within an area of slow conduction even in the absence of ventric- ular tachycardia. More rapid ventricular pacing at site l-2 initiated a second morphology of ventricular tachycardia, which displayed a right bundle branch block configuration and right axis deviation. As shown in Fig. 3, during left ventricular pacing at a cycle length of 400 msec the interval between the stimulus artefact and left ventricular electrogram, recorded from the electrode pair 1 cm proxi- mal to the pacing electrodes, increased slightly from 170 to 180 msec on the first two beats shown. Following the third stimulus, the stimulus-to-electrogram interval increased markedly to 300 msec, the morphology of the left ventric- ular electrogram changed, and sustained ventricular tachycardia was initiated. The change in morphology of the left ventricular electrogram is consistent with activa- tion of that site from a different direction as a result of marked slowing or block of conduction in the pathway that had activated it in the previous beat, as shown schematically in Fig. 4. Fractionated electrical activity was recorded from the distal electrode pair at site l-2 during the second morphology of ventricular tachycardia (not shown). As shown in panel A of Fig. 5, overdrive pacing at a