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Treatment of Atrioventricular Node Reentrant Tachycardia with Encainide: Reversal of Drug Effect with Isoproterenol

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Treatment of Atrioventricular Node Reentrant Tachycardia with Encainide: Reversal of Drug Effect with Isoproterenol View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector 904 JACC Vol. 13, No. 4 March 15, 1989:904-10 Treatment of Atrioventricular Node Reentrant Tachycardia With Encainide: Reversal of Drug Effect With Isoproterenol IMRAN NIAZI, MD, GERALD NACCARELLI, MD* ANN DOUGHERTY, MD,* ROBERT RINKENBERGER, MD,* PATRICK TCHOU, MD, MASOOD AKHTAR, MD, FACC Milwaukee, Wisconsin and Houston, Texas To determine the efficacy of encainide in the treatment of paced cycle length with 1:l ventriculoatrial conduction was atrioventricular (AV) node reentrant tachycardia, Holter 337 f 56 ms in the control study, 551 t 124 ms with electrocardiographic (ECG) monitoring, exercise treadmill encainide infusion (p < 0.01 versus control) and 354 f 72 testing and programmed electrical stimulation were per- ms during isoproterenol infusion in the encainide-loaded formed in 16 patients while they were taking no medication state (p < 0.01 versus both control and encainide). and after steady state levels were reached during treatment During a mean follow-up period of 19 + 10 months, with encainide (75 to 200 mg/day; mean 117 + 47). In significant clinical recurrences occurred in 4 of the 10 addition, to study the possible reversal of drug effects by patients in whom tachycardia could still be initiated with sympathetic stimulation, AV node conduction and tachy- encainide (with or without isoproterenol). In contrast, no cardia induction were reassessed during isoproterenol infu- significant episodes occurred in the six patients in whom sion (1 to 3 pg/min), a dose calculated to increase the rest tachycardia could not be induced with encainide despite heart rate by 25 + 10%. isoproterenol infusion. Suppression of atria1 or ventricular Sustained AV node reentrant tachycardia could be ectopic activity with encainide during Holter ECG moni- initiated in all 16 patients in the control state, in 2 patients toring did not appear to correlate with clinical recurrence. after encainide and in 10 patients during isoproterenol It is concluded that: 1) encainide is an effective agent for infusion. The shortest mean atria1 paced cycle length sus- control of AV node reentrant tachycardia, primarily by taining 1:l AV conduction was 358 -C 57 ms during the virtue of its depressant effect on retrograde pathways; and control study, which increased to 409 f 59 ms with 2) failure to induce tachycardia in the medicated state encainide (p < 0.01 versus control) and decreased to 313 r despite isoproterenol infusion predicts freedom from tachy- 31 ms during isoproterenol infusion (p < 0.01 versus cardia recurrence. control and encainide). The shortest mean ventricular (J Am Co11Cardiol1989;13:904-10) The clinical efficacy of encainide in paroxysmal atrioventric- control of tachycardia in the electrophysiology laboratory ular (AV) node reentrant tachycardia has not been exten- may not predict clinical control, possibly because of fluctu- sively studied, although a preliminary report (1) has sug- ations of autonomic tone in the ambulatory state (2,3). Both gested good results. Even though limited data indicate that sympathetic and vagal stimulation are known to influence this efficacy is related to a depressant effect on the AV node AV node conduction, and changes in autonomic modulation (l), the effect of the drug on AV node conduction and the could potentially negate the beneficial effects of the drug. manner in which this relates to clinical control of the The intent of the present study was to 1) determine the arrhythmia have never been closely scrutinized. Moreover, efficacy of encainide in treating AV node tachycardia with use of programmed electrical stimulation, Holter electrocar- From the Natalie and Norman Soref and Familv Electronhvsioloev diographic (ECG) monitoring, exercise treadmill testing and Laboratory, University of Wisconsin-Milwaukee Clinical Cam,&, Sin% long-term clinical follow-up; 2) examine the effect of encai- Samaritan Medical Center, Milwaukee, Wisconsin and the *Cardiology Divi- nide on anterograde and retrograde pathways in patients sion, University of Texas Medical School at Houston, Houston, Texas. Manuscript received July 25, 1988;revised manuscript received October with AV node tachycardia; 3) assess the reversal of drug 19, 1988;accepted November 2, 1988. effect on AV conduction by isoproterenol (used to simulate Address: lmran Niazi, MD, Sinai Samaritan Medical Center, Electrophysiology Department, 950 North Twelfth Street, G-31I. Milwaukee, intrinsic sympathetic stimulation); and 4) evaluate the clini- Wisconsin 53201. cal implications of such reversal. 01989 by the American College of Cardiology 073s1097/89/$3.50 JACC Vol. 13. No. 4 NlAZl ET AL. 905 March IS. 1989:904-10 ENCAINIDE FOR ATRIOVENTRICULAR NODE REENTRY Methods a maximal heart rate of 220 beatsimin. Refractory periods were determined with the extrastimulus technique at basic Patient characteristics and selection. The patient group drives of 400 and 600 ms cycle lengths. The electrophysio- consisted of 3 men and I3 women, having a mean age of 54 logic diagnosis of AV node reentrant tachycardia was based t 17 years. who were referred to either center for evaluation on previously published criteria (4-7). When two atria1 and treatment of difficult to control paroxysmal supraven- extrastimuli were required for induction of tachycardia. tricular tachycardia. A clinical history of supraventricular double stimuli were also used while the patient was taking tachycardia was present for an average duration of 1I .3 i- encainide, as well as during isoproterenol infusion. All 10.4 years (range 1 to 33). The frequency of clinical episodes episodes of induced AV node tachycardia. including those was occasional (> I but <4/years) in 3 patients, frequent (>I/ initiated during isoproterenol infusion, were terminated with month) in 11 patients and daily in 2 patients. None of the atrial or ventricular pacing. No complications occurred patients had incessant tachycardia. Four patients had expe- during any study. rienced syncopal episodes in the past, and one had required Atrio\~entricular node tuchyuwdia NWIS inducible Mith direct current cardioversion. An average of 2.6 2 1.7 drugs, programmed stimulation in ull patients \z,hile they were including a beta-adrenergic blocker, had been used unsuc- faking no medicution. Encainide was started at an initial cessfully before inclusion in this study. Atherosclerotic heart dose of 75 mgiday (administered in three divided doses). In disease and hypertension were each present in four patients, patients with very frequent episodes, the dosage was incre- and mitral valve prolapse was present in three patients: five mentally increased every 72 h until spontaneous tachycardia patients had no structural heart disease. episodes were completely suppressed. In the remaining Halter monitoring. Holter ECG monitoring was per- patients, the starting dosage (75 mgiday) was adhered to formed with use of an ACS Tech II recorder and Cardiac unless tachycardia recurred after loading. Once steady state Data Corporation Mark IV analyzer. All Holter recordings levels had been achieved on the lowest clinically effective were analyzed in a blinded fashion by Cardio Data Systems dose of encainide, programmed stimulation was repeated in (Haddonfield). A single 24 h Holter monitor was recorded in all patients. If sustained tachycardia was still inducible. the each patient after a 1 week washout of prior medications. dose of encainide was increased by 30 to 4.5 mgiday and Once adequate arrhythmic control with encainide had been programmed stimulation was repeated after steady state achieved (judged by noninducibility of the arrhythmia during levels had been achieved. If sustained tachycardia was no programmed electrical stimulation and absence of spontane- longer inducible with encainide or was inducible but slower. ous recurrences), another 24 h Holter monitor was repeated. isoproterenol infusion was started at a dose of I pgimin and Exercise stress testing. Maximal exercise stress testing titrated to achieve a minimal 15% increase in the rest heart was performed in II patients while they were taking no rate. A mean increase of 26 z 7% was achieved overall, with medication and was repeated after adequate arrhythmia use of an infusion rate of 1 to 3 pg/min. Programmed control had been achieved with encainide. The remaining stimulation was repeated during isoproterenol infusion. In- five patients could not undergo stress testing because of ducibility of tachycardia by programmed stimulation during arthritis or other physical limitations. After noninvasive isoproterenol infusion was not considered an indication for evaluation (in the drug-free state) had been completed, all increasing the encainide dose. patients underwent baseline electrophysiologic testing. Follow-up. Fourteen patients were discharged while re- Programmed stimulation. Right heart catheterization was ceiving the dose of encainide on which sustained AV node performed in the nonsedated postabsorptive state after in- tachycardia could not be induced by programmed electrical formed consent had been obtained. Under fluoroscopic stimulation. The remaining two patients were discharged guidance, multipolar electrode catheters were positioned in while taking encainide, even though tachycardia remained the region of the high right atrium. tricuspid valve and right inducible, because the induced rhythm was extremely slow. ventricular apex. When feasible, a fourth
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