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Flecainide-Induced Sustained Ventricular Tachycardia Successfully Treated with Lidocaine

1987; Elsevier BV; Volume: 92; Issue: 3 Linguagem: Inglês

10.1378/chest.92.3.573

1931-3543

Jerry L. Bauman, Jose Gallastegui, Seth R. Tanenbaum, Robert J. Hariman,

Ion channel regulation and function

A 69-year-old man had new sustained ventricular tachycardia caused by flecainide which promptly responded to intravenous lidocaine therapy. Discontinuation of the lidocaine infusion resulted in the reappearance of ventricular tachycardia which again immediately terminated after lidocaine was given. In this case, lidocaine effectively reversed the proarrhythmic effects of flecainide. A 69-year-old man had new sustained ventricular tachycardia caused by flecainide which promptly responded to intravenous lidocaine therapy. Discontinuation of the lidocaine infusion resulted in the reappearance of ventricular tachycardia which again immediately terminated after lidocaine was given. In this case, lidocaine effectively reversed the proarrhythmic effects of flecainide. In addition to successfully suppressing arrhythmogenic foci, antiarrhythmic drugs may also paradoxically precipitate new rhythm disturbances or worsen existing arrhythmias.1Ruskin JN McGovern B Garan H DiMarco JP Kelly E Antiarrhythmic drugs: a possible cause of out-of-hospital cardiac arrest.N Engl J Med. 1983; 309: 1302-1306Crossref PubMed Scopus (161) Google Scholar, 2Bauman JL Bauernfeind RA Hoff JV Strasberg B Swiryn S Rosen KM Torsades de pointes due to quinidine: observations in 31 patients.Am Heart J. 1984; 107: 425-430Abstract Full Text PDF PubMed Scopus (176) Google Scholar Indeed, antiarrhythmic agents have been causally related to out-of-hospital cardiac arrest in patients who do not have underlying sustained ventricular tachycardia or ventricular fibrillation.1Ruskin JN McGovern B Garan H DiMarco JP Kelly E Antiarrhythmic drugs: a possible cause of out-of-hospital cardiac arrest.N Engl J Med. 1983; 309: 1302-1306Crossref PubMed Scopus (161) Google Scholar Flecainide is a new type 1C antiarrhythmic agent recently approved for the treatment of serious ventricular arrhythmias. The proarrhythmic potential of flecainide has received considerable attention in the medical literature.3Morganroth J Horowitz LN Flecainide: its proarrhythmic effect and expected changes on the surface electrocardiogram.Am J Cardiol. 1984; 53: 89-94Abstract Full Text PDF PubMed Scopus (229) Google Scholar, 4Griffith L Platia E Ord S Reid P Persistent ventricular tachycardia/fibrillation: a possible adverse interaction between flecainide and class I antiarrhythmic drugs (abstract).J Am Coll Cardiol. 1984; 3: 583Google Scholar However, there is little information regarding the therapeutic approach to patients with flecainide-induced arrhythmias. We report a case of new sustained ventricular tachycardia related to flecainide therapy which terminated immediately after intravenous administration of lidocaine. A 69-year-old black man was admitted to the University of Illinois Hospital for numerous episodes of palpitations associated with mild dizziness. An ambulatory Holter recording prior to admission showed sinus bradycardia with preexcited ventricular complexes and occasional episodes of a slightly irregular rhythm with wide QRS complexes (rate 120 bpm, 9 beats maximum). On admission, physical examination was not remarkable. Blood pressure was 146/90 mm Hg. Laboratory examination revealed normal findings except for a blood urea nitrogen value of 31 mg/dl and a serum creatinine concentration of 2.2 mg/dl. Chest roentgenogram revealed a normal heart size. Ejection fraction by gated nuclear angiography was 51 percent. Twelve-lead ECG showed sinus bradycardia (rate 56 bpm) with evidence of ventricular preexcitation. Electrocardiographic monitoring for 48 hours revealed occasional premature ventricular complexes and several episodes of a self-terminating wide QRS tachycardia (four to nine beats) (Fig 1A). Intravenous and oral procainamide failed to suppress recurrences of this rhythm, and the patient was subsequently taken to the electrophysiology laboratory. During this study, nonsustained ventricular tachycardia was confirmed as the cause of the wide QRS tachycardia (Fig 2A) and the effective refractory period of the accessory atrioventricular pathway was determined to be 200 ms. Oral flecainide, 100 mg twice daily, was started (48 hours after the last dose of procainamide) in an attempt to control the nonsustained ventricular tachycardia and to depress conduction through the accessory pathway.5Kim SS Lal R Ruffy R Treatment of paroxysmal reentrant supraventricular tachycardia with flecainide acetate.Am J Cardiol. 1986; 58: 80-85Abstract Full Text PDF PubMed Scopus (42) Google Scholar After three doses of flecainide, the patient developed a sustained wide QRS tachycardia which resulted in dizziness and nausea. This tachycardia (Fig 1B) was considerably different from any previously documented tachycardia in that it was sustained, much faster in rate (200 bpm), and caused more severe symptoms. Systolic blood pressure recorded at the time of the tachycardia was 80 to 100 mm Hg. Flecainide was discontinued, and a repeat electrophysiologic study was performed. During this study, the diagnosis of sustained ventricular tachycardia was confirmed (Fig 2B). Intravenous lidocaine was administered as a 75 mg bolus followed by another 50 mg bolus, ten minutes later and a continuous infusion of 2 mg/min. Eight minutes after the second lidocaine bolus, the tachycardia ceased and sinus rhythm returned. Systolic blood pressure increased to 100 to 120 mm Hg. The lidocaine infusion was continued for 24 hours and then discontinued. However, sustained ventricular tachycardia returned 20 hours after the discontinuation of lidocaine. Again, lidocaine administration resulted in the rapid restoration of sinus rhythm. The patient was eventually treated with amiodarone and discharged from the hospital. During a follow-up of six months, he did not have any recurrence of the tachycardia. Recently, the proarrhythmic potential of antiarrhythmic drugs has been emphasized. In particular, it has been estimated that 7 to 20 percent of patients treated with the new type 1 agent, flecainide, exhibit proarrhythmic effects of this drug.3Morganroth J Horowitz LN Flecainide: its proarrhythmic effect and expected changes on the surface electrocardiogram.Am J Cardiol. 1984; 53: 89-94Abstract Full Text PDF PubMed Scopus (229) Google Scholar Griffith and co-workers4Griffith L Platia E Ord S Reid P Persistent ventricular tachycardia/fibrillation: a possible adverse interaction between flecainide and class I antiarrhythmic drugs (abstract).J Am Coll Cardiol. 1984; 3: 583Google Scholar reported that six of 31 (19 percent) patients died because of ventricular tachycardia degenerating into ventricular fibrillation shortly after the initiation of flecainaide therapy. In this study, flecainide was reported to precipitate ventricular arrhythmias that were resistant to resuscitative efforts and that occurred in proximity of the administration of other type 1 antiarrhythmic drugs such as aprindine or procainamide. Ventricular tachycardia also occurred, in our case, shortly after procainamide was discontinued and flecainide was initiated. There is little information available regarding the appropriate management of flecainide-induced ventricular arrhythmias. Certainly, direct current cardioversion should be attempted if severe symptoms or hemodynamic deterioration arise. However, previous reports allude to an unusual resistance to countershock and difficulties in overdrive pacing techniques.4Griffith L Platia E Ord S Reid P Persistent ventricular tachycardia/fibrillation: a possible adverse interaction between flecainide and class I antiarrhythmic drugs (abstract).J Am Coll Cardiol. 1984; 3: 583Google Scholar, 6Hohnloser S Zeiher A Hust MH Wollschlager H Just H Flecainide-induced aggravation of ventricular tachycardia.Clin Cardiol. 1986; 6: 130-135Crossref Scopus (14) Google Scholar, 7Spivack C Gottlieb S Miura DS Somberg JC Flecainide toxicity.Am J Cardiol. 1984; 53: 329-330Abstract Full Text PDF PubMed Scopus (20) Google Scholar In view of these reports, we decided to try intravenous lidocaine therapy first. The impressive temporal relationship between lidocaine administration and restoration of sinus rhythm on two separate occasions implies that lidocaine therapy was effective in this patient Further, since the elimination rate of flecainide (mean half-life 20 hours) is much longer than the elimination rate of lidocaine (mean half-life 1.5 hours), recurrence of flecainide-induced ventricular tachycardia may occur if lidocaine is discontinued prior to the systemic elimination of flecainide. This happened in the present case as ventricular tachycardia recurred less than 24 hours after the lidocaine infusion was stopped. The suppression of flecainide-induced sustained ventricular tachycardia by lidocaine has been briefly mentioned in two previous case reports.3Morganroth J Horowitz LN Flecainide: its proarrhythmic effect and expected changes on the surface electrocardiogram.Am J Cardiol. 1984; 53: 89-94Abstract Full Text PDF PubMed Scopus (229) Google Scholar, 8Lui HK Lee G Dietrich P Low RI Mason DT Flecainide-induced QT prolongation and ventricular tachycardia.Am Heart J. 1982; 103: 567-569Abstract Full Text PDF PubMed Scopus (49) Google Scholar Recently, Wynn and co-workers9Wynn J Fingerhood M Keefe D Maza S Miura D Somberg JC Refractory ventricular tachycardia with flecainide.Am Heart J. 1986; 112: 174-175Abstract Full Text PDF PubMed Scopus (7) Google Scholar reported two cases of sustained ventricular tachycardia due to flecainide that were resistant to direct current cardioversion and pacing techniques, respectively. In both of these patients, lidocaine promptly restored sinus rhythm. However, in view of the rather limited information available regarding the treatment of flecainide-induced ventricular tachycardia, we cannot yet recommend the routine use or comment on the overall effectiveness of lidocaine in this setting. As clinical experience with flecainide increases, further insight into the management of the proarrhythmic actions of this drug will become apparent.