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.

Acute conversion of paroxysmal supraventricular tachycardia with intravenous diltiazem. IV Diltiazem Study Group.

Diltiazem has electrophysiologic effects similar to those of verapamil. Its efficacy and safety in 4 doses for treatment of induced supraventricular tachycardia (SVT) were examined and compared with those of placebo in 87 patients (25 with atrioventricular [AV] nodal reentry tachycardia, 60 with AV reentry associated with an accessory AV connection, and 2 with atrial tachycardia). Conversion to sinus rhythm occurred in 4 of 14 patients (29%) with 0.05 mg/kg of diltiazem, 16 of 19 (84%) with 0.15 mg/kg, 13 of 13 (100%) with 0.25 mg/kg, and 14 of 17 (82%) with 0.45 mg/kg compared with 6 of 24 (25%) treated with placebo. Conversion rates in groups receiving doses of 0.15 to 0.45 mg/kg of diltiazem were superior to that in the placebo group (p less than 0.001). Time to conversion was 3.0 +/- 2.6 minutes in responding diltiazem patients compared with 5.9 +/- 6.1 minutes in responding control patients. Diltiazem administration resulted in significant lengthening of SVT cycle length, AH interval, and AV nodal effective refractory period and block cycle length. The most frequent adverse response to diltiazem was hypotension (7 of 63 patients); however, only 4 patients had symptoms related to hypotension. Thus, intravenous diltiazem in doses of 0.15, 0.25 and 0.45 mg/kg is an effective and safe treatment for the acute management of SVT.

Comparison of sustained-release formulations of nicardipine and verapamil for mild to moderate systemic hypertension.

In this double-blind, parallel, multicenter study, sustained-release (SR) preparations of 2 calcium antagonists, nicardipine and verapamil, were compared for the treatment of mild to moderate systemic hypertension. Two hundred eighteen patients with supine diastolic blood pressures (BP) 95 to 114 mm Hg were randomly assigned to receive nicardipine-SR 45 mg twice daily (n = 73), nicardipine-SR 60 mg twice daily (n = 73) or verapamil-SR 240 mg once daily in the morning (n = 72). All 3 regimens significantly reduced supine and sitting systolic and diastolic BPs compared with baseline values (p < 0.005). The efficacy of drugs became apparent after 2 weeks of therapy, and was sustained throughout the 12-week study. Reductions in sitting diastolic BP and supine and sitting systolic BPs were statistically greater with nicardipine-SR 60 mg twice daily compared with verapamil, and nicardipine-SR 45 mg twice daily was equivalent to verapamil. Asthenia and constipation occurred more frequently in patients treated with verapamil (9.7 and 11.1%, respectively, compared with 6.8 and 4.1% in either nicardipine group). Adverse events reported more frequently with nicardipine were headache (17.8% with nicardipine-SR 60 mg and 15.1% with nicardipine-SR 45 mg vs 13.9% with verapamil) and edema (15.1% in the nicardipine-SR 60 mg group, 8.2% with nicardipine-SR 45 mg vs 4.2% with verapamil). Verapamil, but not nicardipine, produced significant reductions in heart rate. SR preparations of calcium antagonists offer options for effective monotherapy of systemic hypertension. Side-effect profiles differ and may affect choice of therapy.

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)

Ventricular tachyarrhythmias in the long QT syndromes.

Marked prolongation of the electrocardiographic QT interval often is associated with a distinctive form of ventricular tachycardia characterized by the gradual oscillation around the baseline of the peaks of successive QRS complexes. This was named torsades de pointes, or "twisting of the points." This form of ventricular tachycardia tends to be rapid and self-terminating and often occurs in clusters, leading afflicted patients to present with recurrent dizziness and syncope. Ventricular fibrillation and sudden death are common.

Termination of ventricular tachycardia by single extrastimulation during the ventricular effective refractory period.

Termination of ventricular tachycardia by low-energy shocks delivered during the ventricular refractory period has been reported. We describe a case of reproducible termination of multiple episodes of sustained ventricular tachycardia by a low-current extrastimulus delivered during the effective refractory period of the right ventricle, from the distal bipole of a quadripolar electrode catheter.

Evaluation of the efficacy and safety of oral nicardipine in treatment of urgent hypertension: a multicenter, randomized, double-blind, parallel, placebo-controlled clinical trial.

This study was a prospective, randomized, double-blind, placebo-controlled clinical trial designed to evaluate the safety and efficacy of oral nicardipine for the treatment of urgent hypertension in the emergency department. Of 57 patients with urgent hypertension 53 patients were enrolled: 36 men and 17 women, 43 black and 10 white, age range 48 +/- 11 years, and diastolic blood pressure 128 +/- 7 mm Hg. Patients were randomly assigned to receive 30 mg nicardipine or placebo in blind fashion followed by 30 mg open-label nicardipine in nonresponders. Responders to one or two doses of nicardipine received 30 or 40 mg nicardipine three times a day for 1 week after discharge from the emergency department. Adequate blood pressure reduction, defined as a reduction of diastolic blood pressure to less than 100 mm Hg or by at least 20 mm Hg, was achieved in 65% and 22% of patients who received 30 mg nicardipine or placebo (p = 0.002). Adequate blood pressure reduction after administration of open-label nicardipine occurred in 76% of the nonresponders to placebo. Blood pressure reductions were maintained at 1 week after discharge. The drug was well tolerated, and no significant adverse events occurred. We conclude that oral nicardipine is a safe and effective drug for the initial treatment of urgent hypertension.

Electrogram patterns predicting successful catheter ablation of ventricular tachycardia.

Ventricular tachycardia in patients with remote myocardial infarction is thought to be due to reentry. To improve the efficacy of catheter ablation, we sought to identify electrograms identifying essential components of the reentrant circuit. In this study we compared the efficacy of shocks delivered at sites of early ventricular activation during tachycardia (presumably exit sites from the reentrant circuit) with that of shocks delivered at sites recording mid-diastolic potentials that were not continuous with the main ventricular potential recorded during the QRS complex, but that always remained associated with the tachycardia during initiation, termination, and resetting with extrastimuli (presumably activation of a segment of the slowly conducting region of the reentrant circuit). A total of 20 attempts was made to ablate 14 monomorphic ventricular tachycardias in 10 patients with remote myocardial infarction with use of one to five shocks of 50 to 370 J (200 J in 70%). All seven tachycardias in which isolated mid-diastolic potentials were targeted were successfully ablated, although one required a second attempt. Twelve attempts were made to ablate seven tachycardias by delivering shocks at sites of early activation during tachycardia when mid-diastolic potentials were not identified. Only three attempts (25%) were successful. Activation preceded the QRS complex by 60, 85, and 120 msec in the three successful attempts and by 20 to 110 msec (median 55 msec) in the nine unsuccessful attempts. For the total 20 attempts, there was no significant difference between successful and nonsuccessful ablation in the number of shocks or total energy delivered.(ABSTRACT TRUNCATED AT 250 WORDS)

Sites of conduction block in accessory atrioventricular pathways. Basis for concealed accessory pathways.

Catheter recordings of accessory pathway (AP) activation were used to identify the site of antegrade and retrograde AP conduction block in 126 consecutive patients undergoing electrophysiological testing. Activation was recorded from 89 of 121 left free-wall and posteroseptal pathways (left APs) and from 12 of 24 right free-wall, midseptal, and anteroseptal pathways (right APs). The recorded APs were further subdivided into those exhibiting consistent antegrade conduction during sinus rhythm (overt APs: 50 left APs, eight right APs), those exhibiting intermittent antegrade conduction (intermittent APs: six left APs, two right APs), and those exhibiting only retrograde conduction (concealed APs: 33 left APs, two right APs). The sites of block were recorded during decremental atrial and ventricular stimulation. The sites of both antegrade and retrograde block were determined in 40 of 50 overt left APs and six of eight overt right APs. Antegrade and retrograde block occurred at or near the AP-ventricular (AP-V) interface in 37 of 40 overt left APs and two of six overt right APs and at the atrial-AP (A-AP) interface in one of 40 overt left APs and four of six overt right APs. In three of three overt left APs with no retrograde conduction, retrograde block occurred at or near the AP-V interface. The site of antegrade and retrograde block differed in only two of 58 overt pathways. There was no difference between overt APs limited at the A-AP or the AP-V interface in the shortest atrial or ventricular pacing cycle length maintaining 1:1 antegrade or retrograde AP conduction, respectively. Both antegrade and retrograde block occurred near the AP-V interface in four of six intermittent left APs and zero of two intermittent right APs and near the A-AP interface in two of six intermittent left APs and one of two intermittent right APs. The sites of both antegrade and retrograde block were determined in 28 of 33 concealed left APs, and both occurred at or near the AP-V interface in 26 and A-AP interface in two APs. In two of two concealed right APs, antegrade block occurred at the AP-V interface. These findings suggest that both antegrade and retrograde conduction are limited by factors operating near the AP-V interface in overt left APs and at the A-AP or AP-V interface in overt right APs. Factors limiting antegrade conduction in concealed APs appear to be located almost always near the AP-V interface.

Localization of left free-wall and posteroseptal accessory atrioventricular pathways by direct recording of accessory pathway activation.

With the advent of catheter ablation techniques, precise localization of accessory AV pathways (AP) assumes greater importance. In an effort to define the course of AP fibers, we attempted to record activation of 56 left free-wall and 23 posteroseptal APs in 62 patients undergoing electrophysiological study. The coronary sinus (CS) and great cardiac vein (GCV) were mapped using orthogonal catheter electrodes, which provide a recording dipole perpendicular to the AV groove. The tricuspid annulus (TA) was mapped using a 2 mm spaced octapolar electrode catheter. Potentials were considered to represent AP activation only if they could be dissociated from both atrial and ventricular activation by programmed stimulation. Orthogonal catheter electrodes in the CS and GCV were advanced beyond the site of earliest retrograde atrial activation and/or earliest antegrade ventricular activation in 45 of the 56 left free-wall APs, and AP potentials were recorded from 42 (93%). An oblique course was identified in 36 APs, with the ventricular insertion being recorded 4-30 mm (median 15 mm) distal or anterior to the atrial insertion. In three patients, antegrade and retrograde conduction proceeded over different (but close) parallel fibers. AP potentials were recorded from 19 of 23 posteroseptal pathways. Ten pathways (left posteroseptal) were recorded from the CS, beginning 5-11 mm (median 9 mm) distal to the os, with potentials extending 8-18 mm (median 11 mm) distally. Four pathways (mid-septal) were recorded along the TA, anterior to the CS ostium and posterior to the His bundle catheter. Five pathways (right posteroseptal) were recorded along the TA, directly opposite or immediately posterior to the CS ostium. One of the patients had both midseptal and left posteroseptal pathways and three patients had both right posteroseptal and left posteroseptal pathways. We conclude: 1) left free-wall APs transit the AV groove obliquely and may be comprised of multiple, closely spaced, parallel fibers; 2) the anatomical location of "posteroseptal" pathways is variable and the presence of fibers at multiple sites is common; and 3) direct recordings of AP activation facilitate tracking of the accessory pathway along its course from atrium to ventricle and help identify the presence of multiple fibers.

New catheter technique for recording left free-wall accessory atrioventricular pathway activation. Identification of pathway fiber orientation.

The ability to record accessory atrioventricular (AV) pathway activation consistently may be uniquely beneficial in improving pathway localization, identifying anatomic relations, and providing insight into unusual conduction properties. For the purpose of recording left AV accessory pathway activation, an electrode catheter was specially designed for use in the coronary sinus. The orthogonal catheter has three sets of four electrodes spaced evenly around the circumference. Electrograms were recorded at low gain (less than 1 cm/mV) between adjacent electrodes on the same set (interelectrode distance, 1.5 mm, center to center). This provides a recording dipole perpendicular to the atrioventricular groove to enhance recording of accessory pathway activation while minimizing overlapping atrial or ventricular potentials. The orthogonal electrode catheter was used in the electrophysiological study of 48 consecutive patients with 59 left AV accessory pathways. The catheter could be advanced along the coronary sinus beyond the site of earliest retrograde atrial activation in 49 of the 59 accessory pathways. Activation potentials were recorded from 45 of the 49 (92%) accessory pathways accessible to the catheter (5 of 5 anterior, 8 of 8 anterolateral, 15 of 16 lateral, 5 of 5 posterolateral, 5 of 5 posterior, and 7 of 10 posteroseptal). Accessory pathway potentials were validated by dissociating them from both atrial and ventricular activation by programmed-stimulation techniques. During surgery, accessory pathway potentials were identified from orthogonal catheter electrodes in the coronary sinus in 14 of 16 accessory pathways (12 patients). Epicardial mapping confirmed the location of the accessory pathway, and direct pressure over the orthogonal catheter electrode that recorded the accessory pathway potential resulted in transient conduction block in nine of the 14 accessory pathways. Orthogonal electrode maps of the coronary sinus identified an oblique course in 39 of 45 recorded accessory pathways. Thirty-two of 38 left free-wall accessory pathways were oriented with atrial insertion 4-30 mm (median, 14 mm) proximal (posterior) to the ventricular insertion. In the remaining six free-wall accessory pathways, the lateral excursion could not be determined because either only the atrial end of the accessory pathway was recorded or activation of multiple pathway fibers prevented tracking of individual strands. The seven recorded posteroseptal pathways exhibited accessory pathway potentials throughout an 8-18-mm (median, 10 mm) length of the proximal coronary sinus, but fiber orientation was difficult to determine.(ABSTRACT TRUNCATED AT 400 WORDS)

Catheter ablation of atrioventricular junction using radiofrequency current in 17 patients. Comparison of standard and large-tip catheter electrodes.

BACKGROUND: Two catheter electrode systems were compared for delivering radiofrequency current for ablation of the atrioventricular junction. Seventeen patients with drug-resistant supraventricular tachyarrhythmias were studied. METHODS AND RESULTS: A 6F or 7F catheter with six or eight standard electrodes (1.25 mm wide, 2.5-mm spacing) was used in the first seven patients (group 1). A 7F quadripolar catheter with a large-tip electrode (4 mm long; surface area, 27 mm2) was used in the final 10 patients (group 2). Both ablation catheters were positioned to record a large atrial potential and a small but sharp His bundle potential from the distal bipolar electrode pair. Radiofrequency current was applied between a large skin electrode on the left posterior chest and either 1) each individual electrode on the standard-tip electrode catheter at 40 V (group 1) or 2) the large-tip electrode at 50-60 V (group 2). Radiofrequency current was limited to 40 V in group patients because of the strong potential for an early impedance rise when higher voltage is applied through standard electrodes. Complete atrioventricular block was achieved in six of seven group 1 patients and all 10 group 2 patients. A junctional escape rhythm followed ablation in five or six group 1 patients (mean cycle length, 1,066 +/- 162 msec) and eight of 10 group 2 patients (mean cycle length, 1,281 +/- 231 msec). Atrioventricular block was produced in a mean of 4.7 +/- 4.6 radiofrequency current applications delivered over a period of 42 +/- 45 minutes using the large-tip electrode (group 2) compared with 46 +/- 22 applications using standard electrodes (15.9 +/- 10.2 applications delivered through the standard-tip electrode) over a period of 147 +/- 59 minutes (group 1). For the application producing atrioventricular block, the large-tip electrode used higher voltage (58 +/- 17 versus 38 +/- 5 V, p less than 0.03) and had lower impedance (103 +/- 22 versus 148 +/- 40 omega, p less than 0.01), resulting in greater power (33.0 +/- 13.0 versus 10.2 +/- 0.6 W, p less than 0.003) and shorter time to block (8 +/- 3 versus 22 +/- 3 seconds, p less than 0.001). Current delivery through standard electrodes was limited by an impedance rise occurring 7 +/- 7 seconds after the onset of one or more radiofrequency current applications at 10 +/- 1 W in six of seven patients. Using the large-tip electrode, an impedance rise occurred in five of 10 patients, but at 25 +/- 10 W and after 21 +/- 9 seconds. Atrioventricular block occurred before the impedance rise in three of these five patients. Complete atrioventricular block persisted in 15 of 16 patients at a mean follow-up of 8.7 months. Atrioventricular conduction returned at 1 month in one group 2 patient and was successfully ablated by a second procedure. Three group 1 patients died 0.5-2 months after ablation, and a fourth patient underwent cardiac transplantation after 10 months. Pathological examination of the heart in two of these patients showed necrosis of the atrioventricular node and origin of the His bundle, without injury to the middle or distal His bundle. All 10 group 2 patients are alive and subjectively improved after ablation. CONCLUSIONS: We conclude that catheter-delivered radiofrequency current effectively produces complete atrioventricular block (94%) without requiring general anesthesia or the risk of ventricular dysfunction or cardiac perforation. The large-tip electrode allows a threefold increase in delivered power and markedly decreases the number of pulses and time required to produce atrioventricular block.

Catheter ablation of accessory atrioventricular pathways (Wolff-Parkinson-White syndrome) by radiofrequency current.

BACKGROUND: Surgical or catheter ablation of accessory pathways by means of high-energy shocks serves as definitive therapy for patients with Wolff-Parkinson-White syndrome but has substantial associated morbidity and mortality. Radiofrequency current, an alternative energy source for ablation, produces smaller lesions without adverse effects remote from the site where current is delivered. We conducted this study to develop catheter techniques for delivering radiofrequency current to reduce morbidity and mortality associated with accessory-pathway ablation. METHODS: Radiofrequency current (mean power, 30.9 +/- 5.3 W) was applied through a catheter electrode positioned against the mitral or tricuspid annulus or a branch of the coronary sinus; when possible, delivery was guided by catheter recordings of accessory-pathway activation. Ablation was attempted in 166 patients with 177 accessory pathways (106 pathways in the left free wall, 13 in the anteroseptal region, 43 in the posteroseptal region, and 15 in the right free wall). RESULTS: Accessory-pathway conduction was eliminated in 164 of 166 patients (99 percent) by a median of three applications of radiofrequency current. During a mean follow-up (+/- SD) of 8.0 +/- 5.4 months, preexcitation or atrioventricular reentrant tachycardia returned in 15 patients (9 percent). All underwent a second, successful ablation. Electrophysiologic study 3.1 +/- 1.9 months after ablation in 75 patients verified the absence of accessory-pathway conduction in all. Complications of radiofrequency-current application occurred in three patients (1.8 percent): atrioventricular block (one patient), pericarditis (one), and cardiac tamponade (one) after radiofrequency current was applied in a small branch of the coronary sinus. CONCLUSIONS: Radiofrequency current is highly effective in ablating accessory pathways, with low morbidity and no mortality.

Treatment of supraventricular tachycardia due to atrioventricular nodal reentry by radiofrequency catheter ablation of slow-pathway conduction.

BACKGROUND: Atrioventricular nodal reentrant tachycardia (AVNRT), the most common form of supraventricular tachycardia, results from conduction through a reentrant circuit comprising fast and slow atrioventricular nodal pathways. Antiarrhythmic-drug therapy is not consistently successful in controlling this rhythm disturbance. Catheter ablation of the fast pathway with radiofrequency current eliminates AVNRT, but it can produce heart block. We hypothesized that catheter ablation of the site of insertion of the slow pathway into the atrium would eliminate AVNRT while leaving normal (fast-pathway) atrioventricular nodal conduction intact. METHODS AND RESULTS: Eighty patients with symptomatic AVNRT were studied. Retrograde slow-pathway conduction (in which the earliest retrograde atrial potential was recorded at the posterior septum, close to the coronary sinus) was present in 33 patients. The retrograde atrial potential was preceded by a potential consistent with activation of the atrial end of the slow pathway (ASP). In 46 of the 47 patients without retrograde slow-pathway conduction, a potential with the same characteristics as the ASP potential was recorded during sinus rhythm. Radiofrequency current delivered through a catheter to the ASP site (in the posteroseptal right atrium or coronary sinus) abolished or modified slow-pathway conduction in 78 patients, eliminating AVNRT without affecting normal atrioventricular nodal conduction. In the single patient without ASP, the application of radiofrequency current to the proximal coronary sinus ablated the fast pathway and AVNRT: Atrioventricular block occurred in one patient (1.3 percent) with left bundle-branch block, after inadvertent ablation of the right bundle branch. AVNRT has not recurred in any patient during a mean (+/- SD) follow-up of 15.5 +/- 11.3 months. Electrophysiologic study 4.3 +/- 3.3 months after ablation in 32 patients demonstrated normal atrioventricular nodal conduction without AVNRT: CONCLUSIONS: Catheter ablation of the atrial end of the slow pathway using radiofrequency current, guided by ASP potentials, can eliminate AVNRT with very little risk of atrioventricular block.

Direct endocardial recording from an accessory atrioventricular pathway: localization of the site of block, effect of antiarrhythmic drugs, and attempt at nonsurgical ablation.

We recorded a discrete 0.95 mV potential consistent with accessory atrioventricular pathway (AP) activation during serial electrophysiologic studies in a patient with Ebstein's anomaly and Wolff-Parkinson-White syndrome. Bipolar pacing from the catheter electrode in which the AP potential was recorded resulted in a stimulus-ventricle interval identical to the AP-ventricle interval during antegrade conduction, and a stimulus-atrium interval identical to the AP-atrium interval during retrograde conduction. With the patient in the drug-free state, antegrade AP block during atrial pacing and retrograde AP block during ventricular pacing occurred distal to the AP potential (AP-ventricle junction and AP-atrium junction, respectively), supporting the "impedance mismatch" hypothesis. Procainamide and disopyramide each lengthened the antegrade AP effective refractory period by affecting the AP-ventricle junction (possibly by decreasing the current generated by the AP). Both drugs also lengthened the retrograde AP effective refractory period but produced a greater effect on the ventricle-AP junction than on the AP-atrium junction, suggesting marginal geometry of the former. R wave synchronous shocks of 160 and 320 W-sec delivered between the catheter electrode recording the largest unipolar AP potential and a skin electrode produced transient, complete, antegrade block over the AP, suggesting the feasibility of this new nonsurgical technique for AP ablation.