Reentrant Supraventricular Tachycardia Research Articles

Effectiveness of oral sotalol for treatment of pediatric arrhythmias

Sotalol is a β blocker with class III activity. Few investigators have reported its use in pediatric patients. From August 1985 to May 1990, 66 patients (mean age 8.7 years; range 9 days to 24 years), including 14 infants aged <3 months, were treated with oral sotalol alone (n = 46) or in association with digoxin (n = 20). Supraventricular reentrant tachycardia was present in 38 patients (20 with documented preexcitation), atrial flutter in 10 and atrial ectopic tachycardia in 7. Three patients had other types of supraventricular tachycardia. Tachycardia was of ventricular origin in 6 patients and both of supraventricular and ventricular origin in the remaining 2. Mean dose of oral sotalol was 135 mg/m 2/day given in 2 doses. Congenital heart disease was present in 28 patients, 14 with previous cardiac surgery, mostly at the atrial level. Prior treatment with 1 or more antiarrhythmic agent had been unsuccessful in 83% of patients. Mean duration of treatment was 13.3 months (range 2 months to 5 years). Overall, treatment was successful in 79% of cases. Highest rate of success was observed in patients with supraventricular reentrant tachycardia with or without preexcitation (89%) and in those with atrial ectopic tachycardia (85.5%). Atrial flutter could be controlled in 60% of cases. Sotalol seemed less effective in ventricular tachycardia with a complete control of the arrhythmia being achieved in only 17%; however, it decreased the number of runs of ventricular tachycardia and the number of ventricular premature complexes in 50% of patients. There were no adverse effects in 89% of patients. Two patients with previous sick sinus syndrome had worsening of their bradycardia necessitating implantation of a pacemaker in 1. Sotalol is a very effective drug for the treatment of the various Pediatric arrhythmias, in particular supraventricular arrhythmias, without significant adverse effects.

Adenosine's effectiveness in long RP' re‐entrant tachycardia: Additional evidence of the decremental qualities of the retrograde limb

Adenosine's ability to terminate atrioventricular (AV) re-entrant supraventricular tachycardia is well documented. Typically, termination occurs as a consequence of transient conduction block in the atrioventricular node, a tissue with decremental qualities. However, the atrioventricular node is not always the site of action when adenosine is used on the re-entrant types of long RP' tachycardias. These tachycardias are, in part, characterized by the decremental qualities of the retrograde limb of the tachycardia circuit, which, in turn, are typically exemplified by retrograde Wenckebach during ventricular (VVI) pacing during intracardiac electrophysiology studies. This case report involves adenosine's ability to block conduction in the retrograde limb of the permanent form of junctional reciprocating tachycardia to provide further evidence as to the AV "nodelike" decremental qualities of this limb.

Efficacy of intravenous sotalol for suppressing inducibility of supraventricular tachycardias at rest and during isometric exercise

The efficacy of intravenous sotalol (1 mg/kg) for suppressing inducibility of supraventricular tachycardias (SVT) with different electrophysiologic mechanisms was studied in 30 consecutive patients referred for an electrophysiologic study because of paroxysmal SVT. Orthodromic SVT using accessory atrioventricular (AV) connection was inducible in 14 patients, AV nodal reentrant SVT in 8, and intraatrial SVT in 8 before administration of sotalol. Isometric handgrip exercise facilitated the inducibility of SVT in 8 patients who were noninducible at rest. After intravenous sotalol, 7 of 14 patients (50%) with orthodromic SVT, 8 of 8 (100%) with AV nodal reentrant SVT, and 8 of 8 (100%) with intraatrial reentrant SVT became noninducible into sustained SVT. Isometric exercise facilitated the inducibility of only 3 nonsustained SVT runs after sotalol infusion, and exercise did not reverse the prolongation of refractory periods of the atrium, AV node, accessory pathway and ventricle caused by sotalol. During a mean follow-up period of 18 ± 7 months, none of the 14 patients who remained noninducible into sustained SVT during the stress test after intravenous sotalol and tolerated long-term oral sotalol therapy had recurrence of symptomatic SVT. Thus, sotalol is efficacious for suppressing SVT with AV nodal or intraatrial reentrant mechanism, but less efficacious in patients with accessory AV pathway. The β-blocking and cellular antiarrhythmic effects of sotalol are not significantly reversed by exercise.

Effects of Semotiadil (SD-3211), a Benzothiazine Calcium Antagonist, on Blood Pressure and Atrioventricular Conductivity in Anesthetized Dogs

We investigated the effects of semotiadil (SD-3211), a novel calcium antagonist, on blood pressure and the atrioventricular (AV) conduction time and functional refractory period (FRP) of the AV conduction system (AV conductivity) in anesthetized open-chest dogs. The heart was electrically stimulated at a constant rate. In dogs with an intact nerve supply to the heart, i.v.-injections of semotiadil (0.03 to 0.3 mg/kg) produced a fall of blood pressure in a dose-dependent manner. AV conduction time and FRP were prolonged by rather higher doses (0.3 mg/kg), and second-degree AV block occurred only with the highest dose (1 mg/kg). In dogs with the nerve supply to the heart interrupted, the vasodepressor effects and suppressant effects of semotiadil on AV conductivity were slightly enhanced. The suppressant effects on AV conductivity became marked as pacing rates were increased. These results suggest that semotiadil at appropriate doses produces a vasodepressor effect without affecting AV conductivity even in the heart deprived of nervous control, e.g., the heart with β-adrenoceptors blocked. The frequency-dependent suppressant effect on FRP of semotiadil is also noteworthy in the treatment of reentrant supraventricular tachycardia that involves the AV node.

Successful radiofrequency catheter ablation of medically resistant reentrant supraventricular tachycardia in an infant

SummaryThe feasibility and efficacy of radiofrequency catheter ablation of medically resistant supraventricular tachycardia is a promising technique with applications in the pediatric age group. The limitations of this procedure in the pediatric population, however, have yet to be delineated. We herein report a case of incessant reentrant supraventricular tachycardia in a two month old infant which was resistant to pharmacologic therapy, yet successfully treated by radiofrequency catheter ablation.

Usefulness of the ΔHA interval to accurately distinguish atrioventricular nodal reentry from orthodromic septal bypass tract tachycardias

Surface electrocardiographic criteria may be inadequate to distinguish some cases of atrioventricular (AV) nodal reentrant supraventricular tachycardia (SVT) from those with orthodromic SVT incorporating a posterior septal bypass tract (orthodromic SVT) because of similarities in P-wave morphology and timing during SVT. Invasive electrophysiologic studies may occasionally leave uncertainty in the correct diagnosis, using currently accepted criteria. A new criterion for distinguishing these 2 forms of SVT was therefore devised and tested based on differences in the sequence of activation of the His bundle and atrium during SVT and ventricular pacing. Eighty-four patients underwent invasive electrophysiologic studies (60 with proved AV nodal SVT, 24 with proved orthodromic SVT), during which His to atrial (HA) intervals were measured during SVT as well as ventricular pacing at the same rate. The newly devised criterion, the delta HA interval (HA pace − HA svt) was found to accurately distinguish AV nodal SVT (ΔHA >0 ms) from orthodromic SVT (ΔHA < −27 ms). An intermediate value of ΔHA = −10 ms was chosen which had a 100% sensitivity, specificity and predictive accuracy in differentiating the 2 forms of SVT. A clear retrograde His potential during ventricular pacing, which is essential for application of this criterion, was present in 78 of 84 (93%) cases. In summary, patients with ΔHA intervals >−10 ms separate AV nodal reentry from orthodromic SVT incorporating a septal bypass tract, and no overlap exists between the 2 groups. This criterion may be useful in differentiating the mechanism of SVT in cases in which distinction is not possible by other methods.

Intravenous 3‐Methoxy‐O‐Desmethyl‐Encainide in Reentrant Supraventricular Tachycardia: A Randomized Double‐Blind Placebo‐Controlled Trial in Patients Undergoing EP Study

Encainide is an agent effective in atrioventricular and atrioventricular nodal reentrant tachycardia. The metabolites O-desmethyl encainide and 3-methoxy-O-desmethyl encainide (MODE) are responsible for the clinical effects of encainide in most patients. In this study, intravenous MODE was evaluated in eight patients with reentrant supraventricular tachycardia undergoing electrophysiological testing. After tachycardia was induced at least twice to ensure reproducibility, MODE (30 micrograms/kg/min x 15 min, then 7.5 micrograms/kg/min) or placebo was administered in a double-blind fashion. If tachycardia remained inducible, the infusion was unblinded; in nonresponding subjects who received placebo, MODE was then administered. Placebo was ineffective in 3/3 patients. MODE prevented tachycardia induction in 5/8 patients and increased the tachycardia cycle length from 302 +/- 38 to 413 +/- 67 msec in the other three. At a mean concentration of 774 +/- 229 ng/ml, MODE prolonged PR, AH, HV, QRS, and QT intervals, right ventricular and accessory pathway effective refractory periods, and slowed or blocked antegrade accessory pathway conduction. Changes in intracardiac conduction were rate independent between cycle lengths 400 to 600 msec, while changes in ventricular effective refractory periods were most pronounced at rapid pacing rates. No adverse effects, hemodynamic changes, or conduction disturbances occurred. Thus, MODE can modify or suppress induction of reentrant atrioventricular or atrioventricular nodal tachycardia. The study design used here is well suited for the evaluation of newer antiarrhythmic agents by electrophysiological testing.

Efficacy and safety of intravenous sotalol for termination of paroxysmal supraventricular tachycardia

A double-blind, placebo-controlled, crossover, multicenter study was conducted to study the efficacy and safety of a single intravenous dose of sotalol (1.5 mg/kg over 10 minutes) in achieving normal sinus rhythm in paroxysmal supraventricular tachycardia (SVT) lasting ≥15 minutes. Patients were randomized to either sotalol or placebo as initial treatment, and if the SVT was not terminated a crossover was performed after 20 minutes. A total of 43 patients were enrolled, 38 of whom with spontaneous (n = 14) or induced (n = 24) SVT were analyzed for sotalol efficacy. Most patients (n = 27) had atrioventricular (AV) nodal reentrant tachycardia, and an important subgroup (n = 11) had circus movement tachycardia, using an accessory pathway for retrograde conduction. The number of patients converting to sinus rhythm as a result of the initial treatment was significantly higher in the sotalol group than in the placebo group, for spontaneous (p < 0.005) as well as for induced tachycardia (p < 0.001). Sinus rhythm was achieved within 30 minutes in 83% of all patients who received sotalol as the first drug, compared with 16% of the patients first receiving placebo (p < 0.0001). For sotalol safety analysis, 42 patients were included. A total of 37 patients received sotalol, 19 as the first treatment, and 18 as the second treatment, while 25 patients received placebo. A total of 15 possible adverse effects were reported, occurring in 10 patients with sotalol versus 4 with placebo. The only severe side effect (hypotension) necessitating termination of drug administration occurred with placebo. No proarrhythmic effects were observed. The intravenous administration of sotalol appears to be safe and effective for acute termination of supraventricular reentrant tachycardia.

Antiarrhythmic and proarrhythmic properties of diazepam demonstrated by electrophysiological study in humans

We evaluated the electrophysiological parameters before and after the intravenous infusion of diazepam (0.2 mg/kg) in 20 cardiac patients to investigate the drug's antiarrhythmic effect. Diazepam did not significantly change the arterial pressure. After the intravenous infusion of diazepam, the sinus cycle length significantly shortened from 847 +/- 132 to 747 +/- 155 ms (p less than 0.01). No significant change in the maximal sinus node recovery time was noted. The AH interval at the atrial pacing length of 600 ms shortened significantly from 140 +/- 40 to 127 +/- 39 ms (p less than 0.05). However, there was no significant change after the administration of diazepam in the longest atrial pacing rate associated with Wenckebach conduction in the atrioventricular (AV) node, effective and functional refractory periods of the AV node, HV interval, and QRS width during ventricular pacing at the cycle length of 600 ms. The atrial and ventricular effective refractory periods remained unchanged after the administration of diazepam. Six of the eight patients who showed dual AV nodal refractory period curves in the control study did not demonstrate them after diazepam administration by increasing the atrial or AV node effective refractory period. Thus, diazepam showed significant electrophysiological effects of the heart including shortening of the sinus cycle length, improvement in AV node conduction, and no significant effect on the His-Purkinje or intraventricular conduction and refractoriness of the atrium, AV node and ventricle. On the other hand, diazepam may influence the inducibility of supraventricular reentrant tachycardia incorporating the AV node.

Subthreshold electrical stimulation for termination and prevention of reentrant tachycardias.

Subthreshold electrical stimulation (STS) was used to terminate and prevent reentrant supraventricular and ventricular (VT) tachycardia. Of 12 patients with SVT, 8 had atrioventricular nodal (AVN) reentry, and 4 had orthodromic tachycardias. Trains of STS applied close to the AVN area terminated the tachycardias in five of the eight patients with AVN re-entry and two of the patients with orthodromic tachycardia. In 13 patients with recurrent sustained hemodynamically stable VT (mean cycle length 370 +/- 40 ms), trains of STS were delivered at the site of early activity during the tachycardia. Number of train cycles ranged between 3 to 8 pulses and their cycle lengths ranged between 20 and 70 ms. In 7 of the 13 patients VTs were effectively terminated by STS application close to the site of early activity and in the remaining 6 patients it did not. In nine patients the effect of STS applied at the site of early activity on VT induction from the right ventricular apex was examined. In four of the nine patients STS prevented VT induction and in the remaining five patients it did not. These observations suggest that STS applied in proximity to the area critical for initiation and maintenance of reentry can terminate or prevent induction of the tachycardia.

Transcutaneous Cardiac Pacing for Termination of Tachyarrhythmias

Transcutaneous cardiac pacing (TCP) was used for interruption of tachyarrhythmias in 31 patients: 20 with ventricular tachycardia (VT); eight with atrioventricular reentrant tachycardia (AVRT) and three had atrioventricular nodal tachycardia (AVNT). The stimulators used (Pace Aid 50/52) allow pacing at programmable rates (50-160 ppm) and output (10-200 mA at 20-msec pulse duration), when possible overdrive pacing was used. Short bursts of stimuli were delivered with increasing current intensity until interruption of the arrhythmia or to the maximum energy tolerated by the patient. VTs were interrupted in eight of the 20 patients: four of the six (67%) treated by overdrive pacing and four of the 14 (29%) were treated by underdrive pacing. Supraventricular tachycardias (SVT) were terminated in eight of the 11 patients: seven out of eight (88%) AVT, and one out of three AVNT (33%). We observed two cases of arrhythmia worsening: a VT acceleration and induction of ventricular fibrillation in a patient with AVNT. TCP was well tolerated by the majority of the patients. We conclude that TCP is an effective method for interruption of ventricular and supraventricular reentrant tachycardias, but the risk of arrhythmia worsening must be considered.

Transcutaneous Cardiac Pacing: Evaluation of Cardiac Activation

The effects of transcutaneous cardiac pacing (TCP) on cardiac activation were evaluated by endocavitary recording (HRA, RVA) in eight patients, in order to test the possibility to obtain a simultaneous atrial and ventricular stimulation. The transcutaneous pacemaker used was the Pace Aid 52 (pacing rate 50-160 ppm, current output 10-150 mA, pulse width 20 sec). The two skin electrodes (surface area 50 cm2) were placed on the chest in anteroposterior position. Ventricular capture was observed in all patients (threshold = 74 +/- 14 mA), simultaneous atrial capture was obtained in only four cases (threshold = 138 +/- 25 mA). In conclusion, our data show that four-chamber simultaneous stimulation by TCP is possible, but only with pacing energies much higher than those usually required to capture the ventricle. The ability of TCP to simultaneously pace the atria and ventricles, though not relevant in the emergency cardiac stimulation for symptomatic severe bradyarrhythmias, could be useful in the treatment of reentrant supraventricular tachycardias.

Electrophysiological effects of nicainoprol in patients with paroxysmal supraventricular tachycardias

The electrophysiological effects of nicainoprol, a new class I antiarrhythmic drug, were evaluated in 29 patients with supraventricular reentrant tachycardias, due to accessory pathways in 15 and dual atrioventricular nodal pathways in 14 patients. Nicainoprol was administered intravenously as a bolus followed by continuous infusion of 1.5 mg/kg in two and of 2 mg/kg in 27 patients over one hour. Nicainoprol was given as a bolus of 1.5–2 mg/kg during sinus rhythm in 11 patients or during induced supraventricular tachycardia in 18. The drug successfully terminated the tachycardia in 17 patients due to block in the retrograde tachycardia limb in 15 and the antegrade limb in 2 patients. Prolongation of the cycle length preceded the termination in each case. In one case, the termination could not be achieved despite the administration of 3 mg/kg. The sinus cycle length, heart rate corrected QT interval as well as right atrial and right ventricular effective refractory periods remained unchanged. In contrast, the intranodal and infranodal conduction times, as well as QRS duration, were prolonged significantly. In patients with dual atrioventricular nodal pathways, there was a significant ( P < 0.05) increase of the effective refractory periods of the anterograde slow pathways. The changes of the anterograde fast pathways, however, did not reach significance level. More pronounced effects were found on effective refractory periods of the retrograde pathways, which were blocked in 4 patients and significantly ( P < 0.05) prolonged in the remainder. Similarly, in patients with accessory pathways the effect on the retrograde conduction was more marked with complete block in 5 patients and significant prolongation of effective refractory periods and shortest paced cycle lengths in the remainder. Antegrade block occurred in 5 patients, two of whom had short (< 250 msec) effective refractory period. It is concluded that nicainoprol is highly effective in termination of supraventricular reentrant tachycardias and prevents reinducibility in the majority of the patients. Nicainoprol was well tolerated without any relevant side effects.

Long‐Term Antitachycardia Pacing Experience for Supraventricular Tachycardia

A pacemaker was used to control drug-resistant reentrant supraventricular tachycardia (SVT) in 40 patients. An antitachycardia pacemaker was implanted in 37 for SVT; in one for ventricular tachycardia that could also be used to terminate SVT; in one SVT could be terminated with an activity rate variable pacemaker; and in one a DDD pacemaker was used for prevention and termination of SVT. Twenty patients had AV nodal reentrant tachycardias, eight had tachycardias due to a concealed accessory pathway, eight had a Wolff-Parkinson-White syndrome, three had reentrant atrial tachycardias, and one had atrial flutter. Twenty-two patients were paced from the right atrium, five from the coronary sinus, ten from the right ventricle, and three had a DDD pacemaker. During a total follow-up period of 1,503 (mean 38) months an estimated 16,240 episodes of tachycardia were terminated promptly at home, 58 required several attempts, 57 episodes lasted longer than 30 minutes but did not require medical attention, and 11 required hospital admission. Hospital admission for SVT decreased from one per patient-month (in the 3 months before implantation) to 1 per 137 patient-months after implantation. Additional reentrant tachycardias occurred in 13 patients. Antiarrhythmic drug therapy in combination with a conservative antitachycardia pacing mode was required in four patients paced from the atrium to avoid pacing induced atrial fibrillation. Antiarrhythmic drug therapy was used in 42% of patients to help control SVT. (1) Drug-resistant SVTs can be safely and effectively managed on the long-term with antitachycardia pacemakers. (2) Rapid termination of SVT improved the quality-of-life significantly by avoiding prolonged episodes of tachycardia and repetitive hospital admissions.

Short-term Control of Supraventricular Tachycardia with Verapamil Infusion and Calcium Pretreatment

Nineteen consecutive patients with atrial fibrillation/flutter or other types of supraventricular tachycardia were given intravenous (IV) calcium salts (1 g) followed by verapamil infusion at a rate of 1 mg/min. Successful treatment was defined as control of ventricular response to less than or equal to 100 beats per minute (bpm) or conversion to sinus mechanism in patients with atrial arrhythmias: 11 patients had atrial fibrillation; three had atrial flutter; four had reentrant supraventricular tachycardias (SVT); and one had paroxysmal SVT. Therapy was successful in all patients. The mean dose of verapamil required to achieve desired outcome was 20 mg. Heart rate showed no significant change as a result of calcium pretreatment (160 bpm v 151 bpm). However, heart rate was significantly decreased, to 95 bpm, after treatment with verapamil. Blood pressure showed no change from baseline with either calcium or verapamil therapy. Verapamil infusion following IV calcium successfully treats atrial fibrillation/flutter or SVTs without depressing systemic blood pressure.

Cycle Length Alternation During Supraventricular Tachycardia: Occurrence and Mechanism in a Canine Model of AV Reentrant Tachycardia

Cycle length alternation (CLA) is commonly observed during supraventricular tachycardia (SVT) onset and termination. The present study was designed to gain insights into the mechanism and potential clinical relevance of CLA by comparing computer simulations of tachycardia to directly observed behavior in a canine model of AV reentrant tachycardia (AVRT). The computer model was based on the hypothesis that CLA is secondary to feedback between AV nodal output during SVT and subsequent AV nodal input, and used the measured anterograde AV nodal recovery curve (AV vs A1A2) to predict sequential AV and RR intervals during SVT. Orthodromic AVRT was created experimentally in 11 open-chested, autonomically-blocked (atropine plus nadolol) dogs using a sensing and pacing circuit that mimicked a retrograde-conducting accessory pathway. Steady-state cycle length and AV interval during experimental AVRT closely paralleled predictions made by the computer model. CLA appeared consistently at the onset of experimental AVRT at programmed VA intervals less than or equal to 100 msec (corresponding to VA less than or equal to 150 msec as measured clinically) in all dogs. The amplitude and duration of CLA increased as the VA interval decreased, and closely paralleled predictions based on the computer model. Abrupt accelerations in atrial pacing to the same rate as AVRT did not result in alternation of cycle length. In conclusion, alternation of cycle length results from feedback between AV nodal output and subsequent AV nodal input at the onset of reentrant supraventricular tachycardia, and does not require changes in autonomic tone or dual AV nodal pathways. CLA occurrence, amplitude, and duration are predictable based on AV node recovery properties, and depend on retrograde conduction properties of the reentrant circuit. The presence of CLA suggests that the AV node is an integral component of the SVT reentry circuit, and may be useful clinically to identify the mechanism of supraventricular tachycardias.

Prospective evaluation of parenteral magnesium sulfate in the treatment of patients with reentrant AV supraventricular tachycardia

This study prospectively assessed the electrophysiologic effects of parenteral magnesium sulfate administration on paroxysmal atrioventricular (AV) reentrant supraventricular tachycardia and the efficacy of magnesium to terminate these arrhythmias. Eleven normomagnesemic patients, seven with orthodromic reentrant supraventricular tachycardia that used an accessory AV pathway, and four with typical AV nodal reentry were examined. All patients had a history of sustained supraventricular tachycardia requiring pharmacologic therapy or electrical cardioversion for termination of tachycardia. After baseline electrophysiologic study, including documentation of sustained supraventricular tachycardia that was reproducibly induced, parenteral magnesium sulfate (a bolus of 0.3 mEq/kg of elemental magnesium infused over a 10-minute period followed by a maintenance infusion of 0.2 mEq/kg/hr) was administered during sustained supraventricular tachycardia. The serum magnesium concentration increased from (mean +/- standard deviation) 1.9 +/- 0.2 mg/dl to 4.0 +/- 0.6 mg/dl (p = 0.0001). Except for flushing and mild diaphoresis during infusion of the magnesium sulfate bolus, and dry heaves in one patient, there were no untoward effects or significant changes in systolic blood pressure. During administration of magnesium, the tachycardia cycle length increased from 319 +/- 39 msec to 348 +/- 43 msec (p = 0.0001). Slowing of the tachycardia occurred predominantly in the antegrade limb of the circuit at the level of the AV node with the AH interval increasing from 171 +/- 66 msec to 197 +/- 68 msec (p = 0.0001), whereas there was no significant change in the HV interval (43 +/- 3 msec to 43 +/- 4 msec, p = NS) or the VA interval (106 +/- 43 msec to 110 +/- 47 msec, p = NS) during tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Transvenous Ablation with High Frequency Energy for Atrioventricular Junctional (AV Nodal) Reentrant Tachycardia

We performed transcatheter AV junction ablation with high frequency energy in four patients with AV nodal reentrant tachycardia where extensive trials of several antiarrhythmic drugs failed to prevent further recurrences of tachycardia. Initially high frequency catheter ablation induced complete AV block in all patients. A recuperation of AV 1:1 conduction followed some time later, persisting in follow-up. No complications have been encountered in either the acute phase or the follow-up (from 6 to 8 months; mean +/- SD: 8.7 +/- 2.5 months). The electrophysiological study was carried out 6 weeks following ablation, and all patients showed AV 1:1 conduction. No dual nodal pathway was encountered and no tachycardia could be triggered. With refinement of the method, the potential application of high frequency energy to interrupt intranodal or perinodal connections responsible for reentrant supraventricular tachycardia or to retard AV nodal conduction appears promising.

Flecainide acetate for resistant arrhythmias in the young: Efficacy and pharmacokinetics

Drug efficacy and pharmacokinetics were assessed in 63 patients, aged 5 days to 30 years (mean 8 years), who received flecainide acetate for control of resistant arrhythmias. Doses of flecainide ranged from 59 to 225 mg/m2 body surface area per day (mean 141) in divided doses every 8 to 12 h and serum trough levels ranged from 0.10 to 0.99 μg/ml (mean 0.36).Flecainide controlled or partially controlled arrhythmia in 53 (84%) of the 63 patients: 7 of 7 patients who had the permanent form of junctional reciprocating tachycardia, 12 of 13 who had an atrial ectopic tachycardia, 10 of 10 who had ventricular tachycardia and 18 of 25 patients who had reentrant supraventricular tachycardia. Five of seven patients who had the latter arrhythmia were unsuccessfully treated with flecainide. They had Wolfl-Parkinson-White syndrome and developed asymptomatic, incessant, slower orthodromic reciprocating tachycardia while receiving the drug. Transient blurred vision was reported in three patients and two patients had transient hyperactivity. No significant hemodynamic side effects were seen in any patient.Twenty-five patients underwent oral pharmacokinetic investigation. Young infants (<1 year of age) had a mean plasma elimination half-life (11/2) approximating that (11 to 12 h) found in older children and healthy adults; children aged I to 12 years had a shorter mean t 1/2 of 8 h. Dosing schedules based on milligrams per square meter body surface area correlated better with plasma flecainide levels than did dosing based on milligrams per kilogram body weight.In conclusion, 1) flecainide was effective pediatric therapy for permanent junctional reciprocating tachycardia, atrial ectopic and chaotic atrial tachycardia, ventricular tachycardia and, in most patients, reentrant supraventricular tachycardia; 2) some patients with WolffParkinson-White syndrome developed asymptomatic incessant slow supraventricular tachycardia while receiving flecainide; 3) flecainide resulted in rare side effects and no negative hemodynamic effects in any patient; 4) despite a shorter elimination half-life, every 12 h dosing schedule (with lower flecainide trough levels than usually seen in adults) provided adequate arrhythmia control in 80% of young patients aged 1 to 12 years; and 5) further study of oral flecainide pharmacokinetics is needed for patients < 1 year of age.

Intravenous diltiazem in patients with paroxysmal re-entrant supraventricular tachycardia

The electrophysiologic effects and efficacy of diltiazem were evaluated with programmed electrical stimulation of the heart in 12 patients with supraventricular re-entrant tachycardia (five with atrioventricular nodal tachycardia and seven with circus movement tachycardia the accessory pathway being concealed in 4). Diltiazem was infused over 1 minute at the dose of 0.25 mg/kg and the electrophysiologic parameters were evaluated at 5 and 30 minutes. Diltiazem prolonged the AH interval from 83.5 ± 58 to 99 ± 55 msec ( P < 0.05), effective and functional refractory periods of atrioventricular node from 244 ± 40 to 268 ± 56 msec ( P < 0.05) and from 432 ± 124 to 468 ± 130 msec ( P < 0.005) respectively, lowered the atrial pacing rate inducing second-degree atrioventricular block from 159 ± 32 to 134 ± 33 beats/min ( P < 0.005) and decreased systolic and diastolic blood pressure from 143.5 ± 33 to 132.5 ± 22 mm Hg ( P < 0.05) and from 90 ± 15 to 82.5 ± 9 ( P < 0.05), respectively. Diltiazem prevented the reinduction of the tachycardia in 4 of 5 patients with atrioventricular nodal tachycardia and in 4 of 7 with circus movement tachycardia. The mechanism of action of diltiazem consisted of depression of conduction in atrioventricular node in anterograde fashion while there were no effects on refractoriness of the accessory pathway. The drug was well tolerated with no adverse effects. Diltiazem, therefore, appears an effective and safe drug in the acute treatment of re-entrant supraventricular tachycardia.