PATHOPHYSIOLOGY AND NATURAL HISTORY ELECTROPHYSIOLOGY Clinical and electrophysiologic characterization of automatic junctional tachycardia in adults

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. RAPID junctional ectopic tachycardia has been described in infancy, frequently in association with congenital cardiac defects, and may possibly occur in a familial pattern."' Typical features include rapid, irregular heart rates and atrioventricular dissociation. Junctional ectopic tachycardias of this sort generally respond poorly to drug therapy and are associated with a very poor prognosis.'-' To our knowledge, this arrhythmia has not been described in adults. The purpose of this report is to describe five adults with junctional ectopic tachycardia. Detailed analysis of the electrocardiograms, electrophysiologic studies, and response to therapy is provided. Material and methods Five patients with symptomatic, rapid, irregular tachycardias were referred for evaluation. Detailed medical histories, physical examinations, chest x-rays, and echocardiograms were obtained in all patients. In addition, multiple 24 hr Holter recordings were available for analysis in all and three of the patients From the Department of Medicine and Cardiovascular Research Institute, University of California, San Francisco. Dr. Ruder was supported by a Fellowship Grant from the North American Society of Pacing and Electrophysiology. Address for correspondence: Melvin M. Scheinman, M.D., Room 312 Moffitt Hospital, University of California, San Francisco, CA 94143. Received July 30, 1985; revision accepted Feb. 6, 1986. 930 had undergone cardiac catheterization before referral. Four of the five patients underwent invasive electrophysiologic studies for purposes of elucidating the mechanism of the arrhythmia, drug testing, and/or evaluation of nonpharmacologic therapy. Electrophysiologic studies. Patients were studied in the unsedated, postabsorptive state after informed consent was obtained. All antiarrhythmic drugs were discontinued for at least five half-lives before testing. Three quadripolar electrode catheters were inserted percutaneously into a femoral vein of each patient and positioned across the tricuspid valve, against the high lateral right atrium and the right ventricular apex. Electrocardiographic leads V,, I, and III, and the intracardiac recordings from the high right atrium, His bundle region, and right ventricle were displayed on the Electronics for Medicine VR12 oscilloscope and recorded simultaneously at a paper speed of 50 or 100 mm/sec. Atrial and ventricular stimulation were performed with a programmable digital stimulator (Bloom, Inc., Redding, PA). The stimuli were 2 msec in duration with current strength twice diastolic threshold for ventricular stimulation or 5 mA for atrial stimulation. Atrial overdrive pacing at cycle lengths of 600 to 270 msec and programmed atrial stimulation at a basic drive cycle length of 500 msec with the introduction of one and two extrastimuli were performed in all patients. Ventricular overdrive pacing at cycle lengths of 600 to 270 msec was then performed. Programmed ventricular stimulation at basic drive cycle lengths of 500 and 400 msec with the introduction of up to three ventricular extrastimuli was performed5; the tachycardia proved virtually incessant in patient 2. In three patients, isoproterenol was infused to increase the sinus rate to at least 130 beats/min. Isoproterenol was not infused in patient 2 because of documented initiation of tachycardia and acceleration with exercise. The effect of the infusion of propranolol (0.1 to 0.2 mg/kg) on CIRCULATION by gest on July 5, 2017 http://ciajournals.org/ D ow nladed from PATHOPHYSIOLOGY AND NATURAL HISTORY-ELECTROPHYSIOLOGY