Junctional ectopic tachycardia has been described in infants but not in adults. Five adults with rapid symptomatic paroxysmal junctional tachycardia, distinct from the more common slower nonparoxysmal junctional tachycardia, were recently evaluated. The tachycardia was irregular (rate 120 to 250) and accompanied by periods of atrioventricular dissociation and narrow QRS complexes. A junctional origin was documented during electrophysiologic study in four of the five patients. Analysis of Holter recordings; the response to exercise, isoproterenol, and propranolol; and the effects of atrial and ventricular stimulation appeared to implicate abnormal automaticity of a high junctional focus that was catecholamine sensitive or dependent as the tachycardia mechanism. All patients responded somewhat to /3-blockers, although a combination of procainamide and propranolol proved to be the most effective therapy in one patient and another chose electrode catheter ablation of the atrioventricular junction rather than continued drug therapy. Thus, junctional ectopic tachycardia may occur in adults and its mechanism appears to be related to abnormal automaticity that is catecholamine sensitive or dependent. Initial therapy should include fl-blockers but selected patients may require more aggressive management.Circulation 73, No. 5, 930-937, 1986.

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Catheter electrical ablation of ventricular tachycardia (VT) was attempted in 33 patients who had recurrent unimorphic VT refractory to 3.7 1.2 (mean + SD) antiarrhythmic drugs. Their mean age was 56 + 14 years. Twenty-two patients had coronary artery disease, six had other types of heart disease, and five had no structural heart disease. The mean left ventricular ejection fraction was 0.34 + 0.17. Thirty patients had only one documented morphologic type of spontaneous VT, whereas three patients had more than one. One to four shocks of 100 to 300 J each were delivered to the endocardial exit site of VT, as identified by endocardial activation mapping and pace-mapping. In each patient endocardial activation at the exit site of VT preceded the onset of the QRS complex (mean activation time -50 30 msec). Pace-mapping was possible in 26 patients, and in all but two patients the QRS complexes during VT and during pacing at the exit site of VT were very similar in at least 10 of 12 electrocardiographic leads. In 29 patients, shocks were delivered between an endocardial electrode (cathode) and a patch electrode on the chest wall (anode). Seven patients (including three who first received shocks using an external anode) whose VT originated in the septum received transseptal shocks between two electrodes positioned on either side of the septum. The procedure was successful in 15 patients (45%), who had no recurrence of VT either on no antiarrhythmic therapy or on the same regimen that was ineffective before ablation, over a follow-up period of 15.5 + 10 months (range 5 to 35). The ablation attempt was unsuccessful in 18 patients (55%). There were no significant differences in clinical and electrophysiologic variables between patients with and without a successful outcome. Seven nonfatal complications occurred in six patients: sustained nonclinical VT immediately after the shock, ventricular fibrillation on days S and 6 after ablation, neurologic deficits (n = 2), atrioventricular block (n = 2), and brachial artery thrombosis. In conclusion, catheter electrical ablation of VT

A B S T R A C T To define the role of verapamil in the treatment of ventricular tachycardia (VT), we studied 21 patients with chronic recurrent VT. Electrophysiologic studies were performed before and during intravenous infusion of verapamil (0.15 mg/kg followed by 0.005 mg/kg per min). On the basis of the mode of VT initiation and termination, we identified three groups of patients: (a) 11 patients had VT suggestive of reentry, as VT could be initiated with ventricular extrastimulation and terminated with overdrive ventricular pacing. Verapamil did not affect the inducibility and cycle length of VT. (b) 7 patients had VT suggestive of catecholamine-sensitive automaticity as VT could not be initiated with programmed electrical stimulation but could be provoked by isoproterenol infusion. Moreover, the VT could not be converted to a sustained sinus rhythm with overdrive ventricular pacing and it resolved only with discontinuing isoproterenol infusion. Verapamil exerted no effects on VT. (c) 3 patients had VT with electrophysiologic characteristics suggestive of triggered activity related to delayed afterdepolarizations. Characteristically, after attaining a range of cycle lengths, the sinus, atrial or ventricular paced rhythm could initiate VT without ventricular extrastimulation. The first beat of VT invariably occurred late in the cardiac cycle with a premature coupling interval 0-80 ms shorter than the preceding QRS cycle length; the premature coupling interval gradually decreased as the sinus, atrial or ventricular paced cycle length progressively shortened. Of

One hundred and one patients with sustained unimorphic ventricular tachycardia underwent programmed ventricular stimulation with one of two protocols. Fifty patients underwent programmed stimulation with protocol A, which consisted of burst overdrive pacing, single, double, and triple extrastimuli at the right ventricular apex, right ventricular outflow tract, or septum, and then at the left ventricular apex. Fifty-one patients underwent programmed stimulation with protocol B, which consisted of burst overdrive pacing, single and double extrastimuli at the right ventricular apex, right ventricular outflow tract or septum, and at the left ventricular apex, followed by triple extrastimuli at these sites. The stimulation protocol was continued until sustained ventricular tachycardia or rapid, polymorphic ventricular tachycardia greater than 10 sec in duration was induced. With protocol A, clinical and nonclinical ventricular tachycardia was induced in 76% and 36% of patients, respectively; with protocol B, clinical and nonclinical ventricular tachycardia was induced in 85% and 38% of patients, respectively. Direct-current countershock for sustained polymorphic ventricular tachycardia was required in 10% of patients studied under protocol A, compared with in 2% of patients studied under protocol B. With protocol A, near-maximal yield of induced clinical (72%) and nonclinical ventricular tachycardia (30%) was attained after the use of triple extrastimuli at the first stimulation site. The yield of stimulation at a second right ventricular site and of left ventricular stimulation was only an additional 2% each. With protocol B, triple extrastimuli increased the yield of induced clinical ventricular tachycardia from 61% to 85%. In patients with sustained unimorphic ventricular tachycardia undergoing programmed ventricular stimulation, the use of triple extrastimuli at the first stimulation site (protocol A) resulted in a high yield of induced clinical ventricular tachycardia early in the protocol, but at the cost of a significant yield of nonclinical ventricular tachycardia. In the patient who has documented ventricular tachycardia, protocol A may be suitable since the nonclinical arrhythmias that are induced will be readily identifiable as such. The initial use of burst overdrive pacing and single and double extrastimuli in the right ventricle (protocol B) will obviate the need for triple extrastimuli and left ventricular stimulation in 53% of patients and result in a low yield of nonclinical arrhythmias, especially those that are polymorphic (4%). Protocol B may therefore be preferable in patients with sustained but undocumented ventricular tachycardia, to minimize uncertainty regarding the clinical significance of induced tachycardia. However, triple extrastimuli will still be required to induce clinical ventricular tachycardia in 24% of patients, and the overall yield of nonclinical ventricular tachycardia is similar with protocols A and B. Circulation 70, No. 1, 52-57, 1984.THE USE of triple extrastimuli...