Effects of Epinephrine in Patients with an Accessory Atrioventricular Connection Treated with Quinidine Fred Morady, MD, William H. Kou, MD, Alan H. Kadish, MD, Lauri K. Toivonen, MD, Jeffrey A. Kushner, MD, and Stephen Schmaltz, MPH The purpose of this study was to determine whether physiologic doses of epinephrine reverse the electrophysiologic effects of quinidine in pa- tients with an accessory atrioventricular (AV) con- nection. Eighteen patients with an accessory AV connection who had inducible sustained orthodro- mic tachycardia underwent an electrophysiologic study in the baseline state and after at least 2 days of treatment with 1.4 to 1.9 g/day of quinidine glu- conate. The effects of epinephrine were then deter- mined. Epinephrine infusion rates of 25 and 50 ngl kg/min were used in 9 patients each because these doses of epinephrine previously have been demon- strated to result in elevated plasma epinephrine concentrations in the range that occurs during a va- riety of stresses in humans. Quinidine prolonged re- fractoriness in the atrium and accessory AV con- nection and slowed conduction through the acces- sory AV connection. These effects were partially or completely reversed by epinephrine. Among 8 pa- tients in whom quinidine resulted in orthodromic tachycardia becoming noninducible or nonsus- tained, sustained tachycardia became inducible again in 5 patients after infusion of epinephrine. After quinidine, atrial fibrillation was either non- inducible or nonsustained in 8 patients; however, sustained atrial fibrillation could be induced in 4 of these patients after infusion of epinephrine. The re- sults of this study demonstrate that the therapeutic effect of quinidine in patients who have an accesso- ry AV connection are often reversed by physiologic increases in circulating epinephrine. (AmJ Cardiol 1988;62:580-584) From the Division of Cardiology, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, Michigan. Manu- script received March 16,1988; revised manuscript received and accept- ed May 10,1988. Address for reprints: Fred Morady, MD, Division of Cardiology, University Hospital, 1500 East Medical Center Drive, UH Bl F245- 0022, Ann Arbor, Michigan 48109-0022. 580 THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 62 B eta-adrenergic stimulation with isoproterenol has been demonstrated to accelerate paroxysmal su- praventricular tachycardia’ and to antagonize the therapeutic effects of antiarrhythmic drugs in patients with the Wolff-Parkinson-White syndrome.2-6 How- ever, because isoproterenol is not produced endogenous- ly, the physiologic significance of the response to isopro- terenol in quantitative terms is unclear. In contrast to isoproterenol, epinephrine is produced endogenously and prior studies have determined that infusions of 25 and 50 ng/kg/min result in elevations of the plasma epi- nephrine concentration within a physiologic range.738 This study determines the effects of physiologic doses of epinephrine in patients with an accessory atrioventricu- lar (AV) connection and symptomatic tachycardias treated with quinidine. METHODS Patients studied: Eighteen patients with an accesso- ry AV connection underwent an electrophysiologic study because of recurrent, symptomatic tachycardia. A criterion for inclusion in this study was the ability to induce orthodromic reciprocating tachycardia in the baseline state. There were 15 men and 3 women, with a mean age of 40 f 18 years (& standard deviation). None had any evidence of structural heart disease. Six- teen patients had overt ventricular preexcitation and 2 patients had a concealed accessory AV connection. The accessory AV connection was located in the left free wall in 14 patients, in the right free wall in 2 patients and in the posterior septum in 2 patients. Electrophysiologic study: Electrophysiologic studies were performed in the fasting, unsedated state after informed consent had been obtained and at least 5 half-lives after all antiarrhythmic medications had been discontinued. The study protocol was approved by the Human Research Committee at the University of Michigan. Multiple quadripolar electrode catheters were positioned within the heart using conventional techniques. Leads Vi, I and III, and the intracardiac electrograms recorded at the right atrium, His bundle position, coronary sinus and right ventricular apex were displayed on an oscilloscope and recorded at a paper speed of 100 mm/s on a Siemens-Elema Mingograf 7 recorder. Pacing was performed with a programmable stimulator (Bloom Associates) using stimuli 2 ms in du- ration and twice the late diastolic threshold. Electrophysiologic parameters measured: The AV nodal (AH) and infranodal (HV) conduction times