Rodolphe Ruffy

Treatment of paroxysmal reentrant supraventricular tachycardia with flecainide acetate

The electrophysiologic effects and therapeutic efficacy of intravenous and oral flecainide were studied in 15 patients with spontaneous and inducible sustained paroxysmal supraventricular tachycardia (SVT). Twelve patients had atrioventricular (AV) reentrance using an accessory pathway for retrograde conduction and 3 had AV nodal reentrance. Fourteen patients received intravenous flecainide (2 mg/kg body weight over 15 minutes) during an initial electrophysiologic study. Nine patients were restudied during oral flecainide administration (200 to 400 mg/day). After intravenous or oral flecainide therapy, reentrant SVT was noninducible in 6 patients with AV reentrance and in the 3 with AV nodal reentrance. In these 9 patients, intravenous flecainide prevented induction of reentrant SVT by depressing conduction over the retrograde limb of the reentry circuits. In the 6 patients with inducible sustained AV reentrant SVT before and after flecainide therapy, the cycle length of tachycardia increased significantly, mainly as the result of an increase in ventriculoatrial conduction time. There was concordance between the intravenous and the oral effects of flecainide on the mechanism of the SVT. Twelve patients continued oral flecainide treatment for a mean of 16 months (range 5 to 28). Tachycardia recurred in 3 of 4 patients whose arrhythmia remained inducible after flecainide therapy and in 1 of 8 patients whose SVT was suppressed. It is concluded that flecainide is an effective and convenient antiarrhythmic agent to treat patients who have AV nodal or AV reentrant SVT.

Flecainide and amiodarone interaction.

Oral amiodarone therapy was given to seven patients already taking oral flecainide regularly. In one additional patient, administration of flecainide was temporarily discontinued when amiodarone therapy was begun, and then resumed. Amiodarone produced a rise in mean dose-adjusted flecainide plasma level (trough plasma level at steady state/daily dose) from 2.3 +/- 0.8 to 3.4 +/- 0.9 (ng/ml)(mg/day) (p less than 0.01). Accordingly, the mean dose of flecainide required to maintain similar plasma levels of the drug was one-third lower during combined treatment than during therapy with flecainide alone. This drug interaction must be accounted for when amiodarone and flecainide are used concomitantly.

Short- and long-term experience with flecainide acetate in the management of refractory life-threatening ventricular arrhythmias

Thirty-eight patients with organic heart disease and history of sudden cardiac arrest or recurrent sustained ventricular tachycardia were treated with flecainide. Coronary artery disease was present in 33 patients. Previous antiarrhythmic therapy consisted of two to eight drugs (mean four). Fourteen patients were resuscitated from sudden cardiac death and 24 patients had chronic recurrent sustained ventricular tachycardia. Twenty-eight patients had electrophysiologic testing before and during flecainide treatment. Sustained ventricular tachycardia became noninducible in 5 patients, nonsustained in 5 patients and slowed in 13 patients (cycle length increased from 278 +/- 64 to 395 +/- 91 ms; p = 0.002). Three of the 14 patients with sudden cardiac death and 15 of the 24 patients with recurrent sustained ventricular tachycardia remained on long-term flecainide treatment. The mean left ventricular ejection fraction in 16 of these 18 patients was 37%. Nonlimiting side effects occurred in seven patients (18%). Proarrhythmic effects were seen in four patients (10%). At a mean follow-up time of 11 +/- 3 months, 15 patients (39%) had had no recurrence, including 5 who had inducible sustained ventricular tachycardia and 5 who did not on retesting during treatment. In the 18 patients who received long-term therapy, 3 late deaths occurred, 1 of which was of arrhythmic origin. These data suggest that flecainide is effective in about 40% of patients with severe refractory ventricular arrhythmias. Its value as a single drug in the treatment of sudden cardiac death remains to be defined.

Paroxysmal nonreentrant supraventricular tachycardia due to simultaneous fast and slow pathway conduction in dual atrioventricular node pathways

Electrophysiologic studies were performed on a 49 year old woman who had paroxysmal nonreentrant supraventricular tachycardia due to simultaneous anterograde conduction through dual atrioventricular (AV) node pathways. Slow pathway conduction was inversely related to the preceding sinus cycle length and fast pathway conduction was determined by the Hs-A interval (measured from the His potential due to slow pathway conduction to the onset of the subsequent atrial electrogram). Major determinants of sustained simultaneous anterograde fast and slow pathway conduction during sinus rhythm were 1) a retrograde unidirectional block in both fast and slow pathways, and 2) a critical conduction delay in the slow pathway and a long enough Hs-A interval to allow sequential conduction of impulse from both pathways. Flecainide was successful in preventing recurrences of the tachycardia by eliminating slow pathway conduction during long-term follow-up.

Treatment of atrial tachyarrhythmias and preexcitation syndrome with flecainide acetate

Sixteen consecutive patients who had ventricular preexcitation complicated by atrial fibrillation or flutter were treated with intravenous flecainide acetate after treatment with as many as 5 unsuccessful trial regimens with other drugs. In 15 patients who had atrial fibrillation, the shortest RR interval during spontaneous episodes was 210 +/- 39 ms (mean +/- standard deviation), and the average ventricular rate was 208 +/- 37 beats/min. Intravenous flecainide prevented induction of atrial fibrillation in 4 of 9 patients and eliminated anterograde accessory pathway conduction in 9 of the 16 patients. In 5 patients whose atrial fibrillation remained inducible and who continued to have preexcitation, the shortest preexcited RR interval increased from 185 +/- 29 to 281 +/- 46 ms (p less than 0.01). Fourteen patients who had favorable responses to intravenous flecainide were given an oral regimen of the drug. Oral treatment was discontinued early because of proarrhythmic effects in 2 patients, and after 2 1/2 months because of headaches in 1 patient. Eleven patients, 5 receiving concomitant beta-blockade therapy, have continued to receive a regimen of flecainide for a mean of 21 months (range 3 to 48). Seven patients have had no clinical recurrence of arrhythmias. Recurrences in 4 patients have been rare and brief with no changes in therapy required.

Combined bipolar dual chamber pacing and automatic implantable cardioverter/defibrillator

A 67 year old man with recurrent hypotensive ventricular tachycardia, amiodarone-induced bradyarrhythmias and severe cardiac dysfunction underwent simultaneous implantation of an automatic cardioverter/defibrillator and bipolar atrioventricular (AV) pacemaker. The pacing electrodes were placed epicardially near the right atrial appendage and on the lateral right ventricular wall. The rate detector of the automatic defibrillator was placed epicardially on the posterobasal left ventricular wall. Effective bipolar AV pacing produced no false counting of the heart rate by the automatic cardioverter/defibrillator, and ventricular tachycardia properly inhibited the pacemaker. Long-term follow-up study confirmed the safety of this treatment. With proper precautions, bipolar AV pacing can be safely combined with an automatic cardioverter/defibrillator.

Paroxysmal fascicular tachycardia: Electrophysiologic characteristics and treatment by catheter ablation

A 69 year old man with ischemic heart disease underwent electrophysiologic evaluation for paroxysmal wide QRS tachycardia, the configuration of which was identical to that recorded during sinus rhythm, that is, right bundle branch block, left anterior fascicular block and anterior myocardial infarction. Electrocardiographic recordings during tachycardia showed atrioventricular dissociation and His bundle activation occurring 5 ms after the onset of the QRS complex recorded on the surface electrocardiogram, consistent with a left posterior fascicular tachycardia. All traditional therapeutic attempts failed to prevent frequent recurrences of tachycardia, which was finally ablated by three 300 J shocks delivered through an electrode catheter positioned in the posterobasal region of the left ventricular septum.

Treatment of life-threatening ventricular arrhythmias with nonguided surgery supported by electrophysiologic testing and drug therapy.

Forty-six patients who had coronary artery disease, left ventricular aneurysm and life-threatening ventricular tachyarrhythmia underwent surgical treatment to eliminate or facilitate control of the arrhythmia. Surgery was performed without the assistance of intraoperative mapping techniques. Forty-three patients underwent preoperative or postoperative electrophysiologic testing, or both, and antiarrhythmic therapy was added, when indicated, postoperatively. The patients had a mean age of 63 years, a mean preoperative left ventricular ejection fraction of 27 +/- 9% and a mean preoperative left ventricular end-diastolic pressure of 23 +/- 9 mm Hg. Twenty-one patients (46%) underwent surgical treatment within 2 months of their last myocardial infarction. The overall operative mortality rate was 6.5% (three patients). Eighteen of the 43 operative survivors were discharged from the hospital on no antiarrhythmic therapy, whereas 25 received additional antiarrhythmic treatment. During a mean follow-up period of 36 months (range 2 to 88), there were 13 deaths; eight patients died suddenly, three died of congestive heart failure, one of myocardial reinfarction and one from a noncardiac cause. The overall cumulative cardiac mortality rate at 1, 2 and 3 years was 16, 22 and 35%, respectively, whereas the sudden cardiac death rate was 5, 12 and 20%, respectively. This experience suggests that high risk patients who undergo nonguided surgery for life-threatening ventricular arrhythmia and left ventricular aneurysm have a relatively low surgical mortality and a better long-term survival than previously reported. However, if utilized, such an approach must be systematically supported by perioperative electrophysiologic testing to determine the need for supplemental antiarrhythmic therapy.

Flecainide in the Treatment of Nonsustained Ventricular Tachycardia

Thirty-two patients received flecainide acetate for nonsustained ventricular tachycardia after having had unsuccessful treatment with a mean of four antiarrhythmic drugs. The mean left ventricular ejection fraction was 41% in 27. Thirty-one patients had organic heart disease, and 22 patients had arrhythmia-related symptoms. Total suppression of ventricular tachycardia occurred in 22 patients. Thirty patients were discharged from the hospital receiving flecainide at a mean (+/- SD) dosage of 315 +/- 76 mg/d and 26 of these patients attained a mean trough plasma drug level of 567 +/- 254 ng/mL. One patient had proarrhythmia and 3 had worsening of heart failure. Twenty-two patients remained in the trial for a mean follow-up of 13 +/- 7 months. Five patients died (1 suddenly) during the follow-up period. Our data indicate that flecainide suppresses refractory nonsustained ventricular tachycardia in 69% of patients who have organic heart disease. Serious adverse effects were minimized by initiation of treatment in the hospital and careful surveillance of electrocardiograms and plasma drug levels.

Flecainide acetate for treatment of bypass tract mediated reentrant tachycardia.

Flecainide acetate was administered to 19 patients who had inducible sustained orthodromic atrioventricular reentrant tachycardia. Eleven of 18 patients had no inducible tachycardia and 7 patients continued to have inducible tachycardia while receiving flecainide. The effects of flecainide could not be evaluated because of hypotension during intravenous infusion in 1 patient. The main effect of the drug was a selective depression of retrograde conduction over the bypass tract, resulting in abolition of reentry or prolongation of tachycardia cycle length. The electrophysiologic effects of intravenous flecainide were concordant with those of oral flecainide in 5 patients who were studied during both regimens. Fifteen patients were discharged from the hospital on a regimen of flecainide. One patient received concomitant beta-blocking therapy. During an average follow-up of 18.5 months (range 2 to 48), 9 patients remained symptom free. Recurrences were observed in 5 patients, 3 of whom still had inducible tachycardia during electrophysiologic testing. Treatment had to be discontinued in 1 patient because of drug intolerance. Thus, flecainide is likely to be effective and well tolerated in the long-term treatment of at least 50% of patients who present with bypass tract mediated orthodromic reentrant tachycardia.