Ventricular fibrillation in patients without recognizable heart disease is uncommon and electrophysiologic data on such patients is limited. Over a 7 year period, five patients (three men and two women, ranging in age from 24 to 52 years) without demonstrable heart disease underwent electrophysiologic studies with pharmacologic drug testing because of single (four patients) or multiple (one patient) documented episodes of ventricular fibrillation. The arrhythmic event was unrelated to myocardial ischemia or infarction, metabolic or electrolyte disturbances, drug toxicity, preexcitation, or prolonged QT syndromes. In all three patients receiving no antiarrhythmic drugs and in two pretreated with amiodarone, a rapid poorly tolerated ventricular tachyarrhythmia requiring cardioversion was induced by programmed ventricular stimulation with up to two extrastimuli. In all instances, addition of either oral quinidine or oral disopyramide prevented the induction of sustained ventricular arrhythmias. All five patients were placed on antiarrhythmic drug regimens found effective during electrophysiologic studies and remained asymptomatic during follow-up periods ranging from 12 to 93 (mean 52) months. We conclude that in the patients with idiopathic ventricular fibrillation in our study: (1) programmed ventricular stimulation reliably replicated the spontaneous arrhythmia, (2) class I antiarrhythmic agents effectively prevented induction of the arrhythmia in the laboratory, and (3) in contrast to the severity of the presenting arrhythmia, a benign clinical course was observed during longterm therapy with class I antiarrhythmic agents. Circulation 75, No. 4, 809-816, 1987.

Simultaneous AV nodal reentrant and ventricular tachycardias were observed during the course of an electrophysiological study in a 51-year-old patient who suffered from recurrent attacks of sustained ventricular tachycardia. Occurrence of simultaneous tachycardias was facilitated by the fact that both tachycardias had a similar cycle length. Ventricular tachycardia was most probably initiated by AV nodal tachycardia previously induced by atrial extrastimulation following the administration of atropine.

Baseline and single-dose captopril scintigraphy with 1 mCi of ^99mTc-diethylene-triamine-pentaacetic acid (or ^99mTc-glucoheptonate) was performed in 5 neonates with renovascular hypertension. Unilateral renal artery thrombosis and/or renal infarction was associated with severe impairment or lack of function on both studies (3 patients). Renal ischemia due to aortic thrombus manifested itself as lack of function only following captopril (2 patients). This approach predicted renal failure as a side effect of captopril therapy in 2 patients, 1 with unilateral (contralateral kidney infarcted) and the other with bilateral renal ischemia from aortic thrombus. Single-dose captopril scintigraphy may be a useful tool to predict tolerance to captopril therapy.

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