Pacing in right ventricular dysplasia after disconnection surgery.

This report describes a 33-year-old patient with arrhythmogenic right ventricular (RV) dysplasia who had a dual chamber pacemaker implanted at age 23 years for drug-induced bradycardia. Pacing was continued after right ventricular free-wall disconnection (RVFWD) at age 24 years. Her pacemaker was not replaced after battery depletion 7 years later. She presented the following year in severe right-sided heart failure. Her old pacemaker generator was replaced. This was followed by rapid resolution of her clinical failure and return to a full, active, physical lifestyle. This observation suggests the potential benefit of dual chamber pacing in patients with RV dysplasia after RVFWD.

Initial experience with a co-radial bipolar pacing lead.

A new type of endocardial bipolar pacing lead has been designed to overcome the potential drawbacks of the conventional coaxial bipolar pacing lead. We prospectively evaluated the new co-radial bipolar pacing leads (Intermedics Thin-Line), which are thinner (5 Fr vs 6-8 Fr) than standard coaxial bipolar leads. X-ray visibility and lead handling were subjectively assessed (excellent, good, adequate, or poor) at implant; lead impedance, sensitivity threshold, and pacing threshold were measured at implant, then at 1, 3, 6, 12, and 18 months. The results were as follows: 103 patients (51 M; age 63.8 +/- 17.4 years) received 71 atrial (A) and 89 ventricular (V) leads. X-ray visibility was excellent in 59/103; good in 23/103; adequate in 11/103; and poor in 10/103. Overall handling was excellent in 56/71 A and 69/89 V; good in 11/71 A and 18/89 V; adequate in 3/71 A and 1/89 V; poor in 1/71 A and 1/89 V. There were two perioperative complications. At implant: impedance in A and V were 370.1 +/- 74.7 and 501.5 +/- 124.4 omega, sensing thresholds in A and V were 3.0 +/- 1.5 and 9.9 +/- 5.0 mV, pacing thresholds at 0.45 ms in A and V were 0.59 +/- 0.21 and 0.41 +/- 0.15 volt, respectively. At 1, 3, 6, 12, and 18 months of follow-up: no pacing lead related complications were reported; pacing lead characteristics remained outstanding and stable. This new lead appears to have significant clinical advantages over the conventional coaxial bipolar pacing lead. Long-term follow-up is required to confirm its reliability and chronic performance characteristics.

Atrial diagnostics in a tiered therapy implantable defibrillator.

Dual chamber sensing has been proposed in implantable defibrillators as an additional diagnostic modality for enhanced differentiation of ventricular and supraventricular tachycardias. A patient with different rates of wide QRS complex tachycardias is described in whom a tiered therapy implantable defibrillator with atrial sensing capability was implanted. Atrial diagnostic data in this patient enabled definitive diagnosis of his ventricular tachycardias and guided management decisions of his arrhythmia.

Characteristics of restitution kinetics in repolarization of rabbit atrium.

The study was designed to characterize restitution kinetics in atrial repolarization of rabbits and to examine effects of K+ or Ca2+ channel blockers on restitution. Action potentials were recorded from rabbit atrial tissue. Restitution curves of phase I amplitude and action potential duration at 50 and 90% repolarization (APD50, APD90) were defined at a basic cycle length of 0.5 s during control and with interventions. Restitution of phase I amplitude had a monoexponential function with a time constant of 2.8 +/- 0.2 s. The curves of APD50 frequently had a monoexponential function and time constants were 1.8 +/- 0.1 s. Restitution curves of APD90 were biphasic: a descending phase followed by an ascending phase. The blocker of Ito1 (a 4-aminopyridine-sensitive component of the transient outward current), 4-aminopyridine, flattened the restitution curves of phase I amplitude, and APD50 and APD90 curves became monophasic. Sotalol, a selective IKr (a rapid component of the delayed rectifier K+ current) blocker, did not alter curves of phase I amplitude and APD50 but shifted APD90 curves upward. Cadmium, a Ca2+ blocker shifted curves of phase I amplitude and APD50 downward and abolished the ascending phase of APD90 curves. We conclude that kinetics of Ito1 and ICa (calcium current) may account for characteristics of restitution of atrial repolarization in rabbit.

Bipolar leads for use with permanently implantable cardiac pacing systems: a review of limitations of traditional and coaxial configurations and the development and testing of new conductor, insulation, and electrode designs.

The unacceptable rate of mechanical failures, threshold problems, and recalls experienced with many coaxial bipolar cardiac pacing lead designs are reviewed in detail. To address these problems, redundant insulation coradial atrial and ventricular tined leads (AL and VL, respectively) with iridium oxide electrodes were developed and subjected to extensive accelerated testing. There were no mechanical failures. The new lead body design proved to be much more durable than widely used trifilar MP35N configurations. The data reviewed and early and current test results are strongly supportive of tightly coupled insulation being a major factor in improving lead durability as long as the insulating material is not stressed. In addition to improving flex life, insulation adherence to the conductor may reduce the potential for ionic degradation. Pacing and sensing thresholds in animal studies of the new leads were within the reported range for leads with steroid eluting electrodes. A multicenter Canadian clinical trial was initiated with the first implant in early January 1994. By November 1995, 110 VL and 82 AL had been placed in 124 patients and followed for a mean of 11 +/- 6 months; maximum 21, total 1355. There were 60 males and 64 females with a mean age of 64 +/- 16 years, range 15-88. Primary indications for pacing were AV block in 61 patients, sick sinus syndrome in 53, vasovagal syncope in 4, and congestive heart failure in 7. Many patients had associated or primary tachyarrhythmias, including 111 with supraventricular and 12 with ventricular. Forty-two percent of patients (52/124) had prior cardiac procedures, including 18 open heart surgeries and 20 AV nodal ablations. At implant, 8 lead characteristics were rated good or excellent in 90% (746/829) of evaluations. X-ray visibility was of concern in 10% of patients (12/124). Three perioperative complications occurred, including displacement of one AL (1.2%) and one VL (0.9%). There were no subsequent mechanical (connector, conductor, or insulation) or functional (exit block, micro or macro displacement, or over- or undersensing) problems. Implant pacing thresholds (PT) at 0.45 ms were AL, 0.6 +/- 0.2 (74) and VL 0.4 +/- 0.2 V; impedance (Z) at 3.5 V output AL 373 +/- 77 (82) and VL 497 +/- 117 omega. Sensing thresholds (ST) were AL 3.1 +/- 1.6 (74) and VL 10.3 +/- 4.9 mV. Ventricular lead data were obtained for all patients (N = 110). Atrial lead data are incomplete, because some patients were in atrial fibrillation during implantation. After 12 months, AL PT at 1.5 V output was 0.18 +/- 0.10 ms (21) and at 2.5 V was 0.10 +/- 0.053 (22). Associated AL ST was 3.3 +/- 0.9 mV (21) AL Z 500 +/- 65 omega (25). After 18 months VL PT at 1.5 V was 0.15 +/- 0.10 ms (9) and at 2.5 V output was 0.09 +/- 0.04 ms (9). Associated VL ST was > 7.5 +/- 2.4 mV (9) and VL Z 497 +/- 105 omega (9). Follow-up time discrepancy is due to the VL being available 6 months earlier than the AL. There were no 30-day deaths and only one late death at 10 months in a patient with chronic atrial fibrillation. Death was unrelated to pacer or lead function. At 1 year, 68% AL (15/22) and 62% (24/39) captured at 0.5 V and < or = 1 ms pulse width output. Innovative adherent insulation coradial bipolar lead conductors of the design studied combined with coated iridium oxide electrodes provide for a negligible incidence of mechanical or functional failure with clinical follow-up now approaching 3 years. Excellent acute and chronic sensing and pacing thresholds have been documented. Late thresholds have continued to improve gradually. Long-term clinical pacing at < or = 1.5 V output with a large safety margin is feasible in essentially all patients. This coradial design produces very flexible < 5 French bipolar redundantly insulated lead bodies allowing both AL and VL to simultaneously pass through a single 10 French introducer sheath. (ABSTRACT TRUNCATED)

pH-dependent actions of 4-aminopyridine on atrial repolarization: effects on the transient outward current.

Effects of extracellular pH (pHo) were examined on the changes in atrial repolarization induced by 4-aminopyridine (4AP), which is a selective blocker of the transient outward potassium channel, I(to). Action potential parameters were measured, using the conventional microelectrode technique, in the absence and presence of 4AP (0.1-3.0 mM) at pHo 6.5, 7.25, and 8.0. Phase 1 amplitude served as an index of I(to). The onset and recovery kinetics of phase 1 amplitude were assessed at a basic cycle length of 0.5 s, and time constants (tau on and tau r) were computed. Both onset and recovery kinetics had monoexponential functions. Tonic blockade was influenced by external pH, and Kd for half block was 0.19, 0.44, and 2.43 mM for pHo 8.0, 7.25, and 6.5, respectively. Phasic block was defined and exhibited cycle length dependence. Phasic block was also modified by external pH with the greatest effect at pHo 8.0. 4AP (0.3 mM) accelerated tau on, 0.62 +/- 0.2, 0.55 +/- 0.1, and 2.0 +/- 0.8 beats for pHo 8.0, 7.25, and 6.5 compared with control 6.8 +/- 1.9, 6.3 +/- 1.9, and 5.1 +/- 1.4 beats. In contrast, 4AP slowed tau r by about 1 s from control value to 1.5 +/- 0.5 s at pHo 6.5, 4.8 +/- 1.5 s at pHo 7.25 (p < 0.05), and 5.7 +/- 2.0 s at pHo 8.0. We conclude that an increase in extracellular pH enhances block of Ito induced by 4AP, whereas low pHo attenuates the block.

Characterization of junctional rhythm after atrioventricular node ablation.

BACKGROUND: Catheter ablation of the atrioventricular (AV) node with radiofrequency current (RFC) is associated with the short-term onset of a junctional escape rhythm (JER) in nearly all patients. However, the origin of the JER and short-term thermal effects of RFC on this junctional pacemaker activity are ill defined. METHODS AND RESULTS: Short-term and noninvasive long-term follow-up studies were performed to examine the electrophysiological characteristics of the underlying JER in 45 patients who had undergone AV nodal ablation with RFC. Baseline characteristics and responses to overdrive ventricular pacing and intravenous atropine followed by an incremental isoproterenol infusion were determined. Short- and long-term responses were compared. HV intervals before and after ablation were 49 +/- 9 and 48 +/- 9 milliseconds, respectively (P = NS). Follow-up was 11 +/- 8.3 months. JER cycle length was 1526 +/- 298 milliseconds in the short-term setting and was present in 44 patients (98%) in the long-term setting, measuring 1426 +/- 223 milliseconds (P < .005). Junctional recovery times increased exponentially as overdrive pacing rates increased-there was no difference between short-term and long-term responses. Drug responses within each study were all significant when compared with baseline. However, there was no significant difference between short- and long-term responses, except at the highest dose of isoproterenol. Intravenous atropine (1 mg) caused an 8.6 +/- 9.3% decrease in JER cycle length in the short-term setting compared with a 7.6 +/- 7.3% decrease in the long-term setting. The decreases in JER cycle length with isoproterenol infusion (short-term versus long-term) were 10.1 +/- 9.6% versus 9.6 +/- 7.4% with 1 microgram/min, 15.8 +/- 11.7% versus 17.4 +/- 8.5% with 2 micrograms/min, 17.9 +/- 11.2% versus 21.4 +/- 9.1% with 3 micrograms/min (all P = NS), and 20.6 +/- 12.1% versus 24.8 +/- 9.1% with 4 micrograms/min (P < .01). CONCLUSIONS: Radiofrequency ablation of the AV node is associated with development of a JER that is stable in the long-term setting. The lack of change in HV interval after ablation locates the junctional pacemaker proximal to the central fibrous body. The pattern of drug responses suggests an origin within the proximal His bundle at its junction with the AV node rather than the AV node itself. The overall similarity between short- and long-term characteristics of junctional pacemaker activity mitigates against any reversible thermal effects of RFC on this pacemaker focus.

Electrophysiologic properties of a narrow isthmus in rabbit atrial tissue: cycle length dependent effect of quinidine.

The modulation of quinidine's effect by pacing cycle lengths was assessed over an isthmus of atrial myocardium, simulating the Wolff-Parkinson-White syndrome. Isolated rabbit atria were dissected so that two tissue blocks, A and B, were linked by an isthmus, 1 mm in width. Effective refractory period in the tissue blocks and over the isthmus was measured at cycle lengths of 1,000, 600, and 400 ms, and the minimum cycle length to sustain 1:1 conduction over the isthmus was measured before treatment, during quinidine superfusion (4 mg/L), and after washout. Longitudinal velocity over the isthmus was also measured. The increment in the effective refractory period in the tissue blocks by quinidine appeared to be similar, about 10% at three pacing cycle lengths (p > 0.05). However, the increment of the effective refractory period over the isthmus was modulated by pacing cycle lengths: greater increase at shorter cycle lengths (p < 0.001). Quinidine prolonged the minimum cycle length over the isthmus by 44 +/- 17%. Regression analysis showed that after quinidine there was a correlationship between conduction velocity and refractoriness over the isthmus (R = 0.85, p < 0.001). Intracellular implements showed stable action potentials, confirming the integrity of the preparation. We conclude that (i) quinidine preferentially prolongs refractoriness over the isthmus and (ii) quinidine's effect on refractoriness over the isthmus is cycle length dependent.

Efficacy of sotalol guided by programmed electrical stimulation for sustained ventricular arrhythmias secondary to coronary artery disease.

Sotalol is a class III antiarrhythmic drug with additional beta-blocker activity that has been shown to be effective in supraventricular and ventricular arrhythmias. Its long-term efficacy for ventricular arrhythmias is not as well described. Patients with documented sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) who had their clinical arrhythmia inducible at baseline electrophysiologic study received sotalol 320 to 640 mg/day. Repeat programmed stimulation was performed after a minimum of 72 hours while receiving the final dose. Of 28 patients (25 men and 3 women) whose arrhythmias were inducible at baseline, 15 had their arrhythmias suppressed with sotalol. Sotalol had greater success in suppressing arrhythmias in those with VF (8 of 9, 89%) than in those with VT (7 of 19, 37%, p < 0.01). In patients with a history of coronary artery disease but no history of myocardial infarction the arrhythmia was suppressed in 7 of 8 (88%) compared with 8 of 20 (40%, p < 0.05) patients with a history of myocardial infarction. All 15 patients in whom ventricular arrhythmias were suppressed continued to take long-term sotalol, and at a follow-up of 10.3 +/- 6.4 months none has had arrhythmia recurrence. Thus, sotalol is an effective drug for the suppression of ventricular arrhythmias as judged by programmed electrical stimulation. It appears to be more effective in patients in whom the clinical arrhythmia is VF rather than VT.

Atrioventricular nodal reentrant tachycardia in patients with ventriculo-atrial conduction block.

OBJECTIVE: To demonstrate the reversibility of retrograde ventriculo-atrial block by isoproterenol in patients with atrioventricular nodal reentrant tachycardia (AVNRT). DESIGN: Three case reports and their electrophysiological features. PATIENTS: Three patients with documented or suspected paroxysmal supraventricular tachycardia. INTERVENTIONS: At routine electrophysiology study, no supraventricular tachycardia was inducible in the baseline state. Infusion of isoproterenol (1 to 5 micrograms/min) was given and stimulation procedures were repeated. RESULTS: At baseline, all three patients had discontinuous antegrade atrioventricular (AV) nodal conduction, but very poor (two patients) or absent (one patient) ventriculo atrial conduction prevented induction of AVNRT. During infusion of isoproterenol, retrograde conduction was enhanced so that 1:1 retrograde occurred to cycle lengths of 300, 340 and 260 ms. AVNRT was then inducible in all patients, reproducing their clinical symptoms. CONCLUSION: Absent or poor ventriculo-atrial conduction in patients with suspected AV node reentry does not preclude the development of tachycardia with sympathomimetic enhancement. Isoproterenol should be given to attempt reversal of retrograde block in these patients.

Regional differences in rabbit atrial repolarization: importance of transient outward current.

Regional differences in rabbit atrial repolarization were investigated using a conventional microelectrode technique. A more rapid phase 1 repolarization (lower phase 1 amplitude) was seen in the left atrial (LA) roof area compared with the right atrial (RA) roof area: 54 +/- 10 vs. 82 +/- 6 mV at 1,000 ms (P < 0.001). In addition, action potential duration at 40 mV above the resting potential (APD40) was shorter in LA and was associated with a slower phase 3 repolarization rate. Furthermore, the recovery time constant of phase 1 amplitude at 500 ms was 0.9 +/- 0.2 s in LA and 3.5 +/- 1.5 s in RA (P < 0.001). Pacing cycle lengths (2,000, 1,500, 1,000, 800, and 500 ms) modulated phase 1 amplitude, APD40, and phase 3 rate in both regions. 4-Aminopyridine (4-AP; 1 mM), a selective transient outward current (I(to)) blocker, abolished cycle length dependence of the above action potential parameters and diminished the differences in electrophysiological properties between the two regions. 4-AP also flattened the restitution curve of phase 1 amplitude in both regions. In conclusion, the findings suggest that the different kinetics of I(to) play an important role in regional differences of atrial repolarization.

Successful treatment of deglutition syncope with oral beta-adrenergic blockade.

A case of deglutition syncope of 20 years' duration in a patient without cardiac or esophageal disease is presented. The therapeutic efficacy of beta-blockade is documented by symptomatic improvement, repeat esophageal balloon inflation and tilt-table testing. This suggests the Bezold-Jarisch reflex or sympathetic nervous system may be involved in the pathogenesis of deglutition syncope.

Propafenone-mexiletine combination for the treatment of sustained ventricular tachycardia.

OBJECTIVES: The purpose of this study was to explore the efficacy of combined therapy with propafenone and mexiletine for control of sustained ventricular tachycardia. BACKGROUND: Combination antiarrhythmic drug therapy may enhance efficacy and lead to control of ventricular arrhythmias in some patients. Few reports have studied the combination of class IB and class IC drugs. Thus, this study was designed to investigate a combination of mexiletine and propafenone in patients with refractory ventricular tachycardia. METHODS: Sixteen patients with sustained ventricular tachycardia had their clinical arrhythmia induced by programmed stimulation. Procainamide and propafenone alone failed to prevent reinduction of tachycardia in all. Mexiletine was subsequently added to propafenone and programmed stimulation was repeated. RESULTS: With combination therapy ventricular tachycardia was noninducible in three patients (19%). A fourth who had presented with polymorphic ventricular tachycardia had slow bundle branch reentry (cycle length 500 ms) induced. In the other 12, tachycardia cycle length increased from 262 +/- 60 ms at baseline to 350 +/- 82 ms with propafenone and to 390 +/- 80 ms with propafenone plus mexiletine (p less than 0.0001 compared with baseline). Hemodynamic deterioration requiring defibrillation occurred in six patients at baseline study, in five taking propafenone and in two taking both drugs. CONCLUSIONS: The combination of propafenone and mexiletine is effective in suppressing the induction of ventricular tachycardia in some patients refractory to procainamide and propafenone alone. In those in whom ventricular tachycardia could still be induced, the rate was slower and hemodynamically tolerated.

Effect of pacing on epinephrine-stimulated atrial natriuretic factor release.

Previous in vitro studies showed that epinephrine stimulation can induce atrial natriuretic factor (ANF) release only form the right atrium but not from the left. In addition, sinus node has been shown to play an important role in the release of ANF. In vitro studies were done in isolated left and right rat atria to determine if pacing can induce the left atria to release ANF during epinephrine stimulation. ANF concentrations in the perfusate were measured by a radioimmunoassay method. Epinephrine increased ANF release in the right atria (from 6.3 +/- 0.8 to 10.8 +/- 0.9 pg/min/mg), but not in the unpaced left atria (4.2 +/- 0.4 and 4.2 +/- 0.3 pg/min/mg). However, when the atria were paced, ANF release rose in both the left (from 6.2 +/- 0.5 to 11.5 +/- 1.4 pg/min/mg) and right (from 8.4 +/- 1.15 to 16.6 +/- 1.8 pg/min/mg) atria with epinephrine addition. These results suggest that atrial contraction and tension play an important role in epinephrine-stimulated ANF release.

High success rate of atrioventricular node ablation with radiofrequency energy.

Radiofrequency current was introduced as an alternative energy source for transcatheter ablation of cardiac arrhythmias to avoid the complications associated with direct current shocks. Initial use of radiofrequency current for complete ablation of the atrioventricular (AV) node yielded only moderate success rates, presumably because of the small size of electrodes and difficulty in localizing the AV node. The use of a larger 4-mm tip electrode for delivery of radiofrequency current and a method to better localize the AV node were prospectively studied in 32 patients undergoing catheter ablation of the AV node. There were 21 men and 11 women with a mean age of 62 +/- 12 years. Complete AV block was achieved immediately in 31 patients (97%) and it persisted in 28 patients (88%) during a mean follow-up period of 12 +/- 6 months. Three patients who had return of AV condition required no drug therapy for control of ventricular rate during atrial fibrillation. The number of radiofrequency pulses used to achieve complete AV block ranged from 1 to 5 (mean 1.9 +/- 1.1). In greater than 50% of the cases, only one radiofrequency pulse was required. The mean power and duration of radiofrequency pulses were 21.2 +/- 4.5 W and 33 +/- 15 s, respectively. All patients developed a stable junctional escape rhythm within 45 min of successful ablation. The QRS configuration was unchanged in 30 patients. One patient had a new right bundle branch block after ablation. There were no complications related to the ablation procedure.(ABSTRACT TRUNCATED AT 250 WORDS)

Long term efficacy of propafenone for prevention of atrial fibrillation.

OBJECTIVE: Propafenone, a class IC antiarrhythmic drug, has been successful in the treatment of ventricular and supraventricular arrhythmias. This study retrospectively evaluated the efficacy of propafenone in the prevention of recurrent atrial fibrillation. DESIGN: Propafenone was given to 81 patients (49 males and 32 females, mean age 61 +/- 16 years) with recurrent atrial fibrillation. The mean dose of propafenone was 701 +/- 235 mg. Patients were monitored for recurrent arrhythmias. MAIN RESULTS: Long term follow-up over 30 +/- 1.7 months showed 31 patients (38%) remained on propafenone with complete or partial control of atrial fibrillation. The drug was stopped in 35 due to inefficacy, in 12 due to adverse effects, and in three due to desire for ablation therapy. CONCLUSION: Propafenone may be effective in some patients for long term prevention of atrial fibrillation, although efficacy may decrease over time.

Nonsustained ventricular tachycardia arising from the right ventricular outflow tract.

Characteristics of left bundle branch block morphology, inferiorly directed frontal plane QRS axis and repetitive nonsustained salvos were used to define a discrete subgroup of patients with ventricular tachycardia (VT). The origin of this tachycardia was thought to be the right ventricular outflow tract. Twenty-six patients with this definition (group 1) were compared with 29 consecutive patients with all other forms of VT (group 2). When compared with patients in group 2, group 1 patients were younger (average age 37 vs 51 years, p less than 0.005), had less structural heart disease (2 of 26 vs 25 of 29 patients, p less than 0.005) and had a better prognosis (no deaths) after an average follow-up time of 28 months in comparison with 5 deaths after an average follow-up of 35 months (p less than 0.05). Induction of VT was possible using isoproterenol infusion in 14 of 20 group 1 patients, but no VT could be induced in 9 group 2 patients (p less than 0.05). Exercise stress testing induced VT in 11 of 21 group 1 patients and 2 of 9 group 2 patients (p greater than 0.05). Programmed electrical stimulation failed to induce VT in 9 group 1 patients, but did induce it in 15 of 20 group 2 patients (p less than 0.005). Successful therapy in group 1 patients was achieved by beta blockers alone (7 patients), beta blockers plus type 1A antiarrhythmic drugs (9 patients), procainamide alone (2 patients), sotalol (3 patients) and amiodarone (2 patients). Three patients were not treated.(ABSTRACT TRUNCATED AT 250 WORDS)

Use of intracardiac recordings to determine the site of drug action in paroxysmal supraventricular tachycardia.

Paroxysmal supraventricular tachycardia most often results from atrioventricular (AV) reentry using an accessory AV pathway (Wolff-Parkinson-White syndrome) or reentry within the region of the AV node. In AV reentry, using an accessory pathway, suppression of the tachycardia may be achieved by depressing either anterograde AV nodal conduction or retrograde accessory pathway conduction. Intracardiac recordings and programmed electrical stimulation have established that beta-adrenergic antagonists and calcium channel blockers principally affect AV nodal conduction (anterograde limb of the reentrant circuit), whereas class IA and IC agents principally affect the accessory AV pathway (retrograde limb). Pharmacologic therapy has been more effective when directed at the limb in which conduction is most marginal at the tachycardia rate (weak limb). In individual patients, intracardiac recordings and programmed electrical stimulation can be used to identify the weak limb, indicating the class of agents most likely to be effective. Specialized techniques allowing direct recording of accessory pathway activation suggest that limitations in accessory pathway conduction may be explained by anatomic impediments. Conduction is most limited at the atrial interface of the accessory pathway in some patients, whereas in others the ventricular interface may be the limiting factor. Class IA and IC agents appear to have the greatest effect at sites where conduction is most tenuous, i.e., at the anatomic impediments. Similar considerations apply to AV nodal reentry. Anterograde slow AV nodal pathway conduction is most often depressed by digitalis preparations, beta-adrenergic antagonists, and calcium channel blockers, whereas retrograde fast AV nodal pathway conduction is more often depressed by class IA and IC agents. Intracardiac recordings and programmed electrical stimulation can also be used in these patients to identify the weak limb and direct pharmacologic therapy. Direct catheter recordings of AV nodal conduction remain elusive, limiting knowledge of the different conduction properties of the anterograde and retrograde limbs and the site(s) of drug action. Studies in progress, comparing the retrograde AV nodal conduction time during tachycardia with that during ventricular pacing at the same rate, suggest that the His bundle may be incorporated in the reentrant circuit in some patients. It appears that verapamil more readily depresses retrograde fast pathway conduction in these patients than in those in whom the His bundle does not form part of the reentrant circuit, but the reasons for this are unknown.

Efficacy and electrophysiologic effects of encainide for atrioventricular nodal reentrant tachycardia.

To prospectively determine the clinical efficacy and electrophysiologic effects of encainide in atrioventricular nodal reentrant tachycardia (AVNRT), 49 patients refractory to 2.7 +/- 1.5 previous antiarrhythmic drug trials underwent electrophysiologic study before and 47 did so after administration of oral encainide (75 to 240 mg/day). Encainide prolonged the minimum atrial pacing cycle length maintaining 1:1 atrioventricular (AV) nodal conduction from 334 +/- 55 to 391 +/- 55 ms (p = 0.0001). Encainide induced ventriculoatrial (VA) block in 12 patients (25%) and slowed the minimum ventricular pacing cycle length maintaining 1:1 VA conduction from 315 +/- 46 to 485 +/- 89 ms (p = 0.0001) in the remaining 35 patients. After encainide, AVNRT was not inducible in 32 of 47 patients (68%) primarily because of the effects on retrograde AV nodal conduction. In the remaining 15 (32%) patients, AVNRT remained inducible; however, the tachycardia cycle length slowed from 397 +/- 86 to 492 +/- 90 ms (p = 0.0001). There was no significant difference in the baseline minimum ventricular pacing cycle length maintaining 1:1 VA conduction in patients whose inducible tachycardia was or was not suppressed. Forty-seven patients were treated for 18.9 +/- 12.9 months (range 1 to 50) with oral encainide. Encainide was completely effective in eliminating recurrences of supraventricular tachycardia in 26 of 47 patients (55%) and partially effective in an additional 42%. Recurrences of arrhythmia occurred in 15 of 32 patients (47%) whose inducible tachycardia was suppressed by encainide and 7 of 15 patients (47%) whose inducible tachycardia was not suppressed by encainide (p = not significant).(ABSTRACT TRUNCATED AT 250 WORDS)