Atrial and Ventricular Vulnerability in a Patient with the Wolff-Parkinson-White Syndrome

An electrophysiologic study was carried out in a patient with the Wolff-Parkinson-White syndrome and a history of spontaneous atrial fibrillation but with no evidence of organic cardiac disease. A single induced premature ventricular depolarization resulted in ventricular tachycardia followed by ventricular fibrillation. Similarly, atrial pacing or premature atrial stimulation resulted in frequent episodes of atrial fibrillation or flutter, The atrial and ventricular effective refractory periods were 180 ms and < 160 ms, respectively, at a driven cycle length of 480 ms. Intravenous administration of procainamide resulted in lengthening of the refractory periods and failure to induce either atriaJ or ventricular arrhythmias with pacing. In most patients with enhanced atrioventricular nodal or accessory atrioventricular nodal bypass, the mechanism of ventricular tachycardia is related to an inordinately rapid ventricular response during supraventricular arrhythmias. In our patient, a unique mechanism was apparent: atrial and ventricular vulnerability to fibrillation was associated with extremely short myocardial effective refractory periods. The relationship of this finding to sudden cardiac death bears further study.     

Usefulness of Intravenous Propofol Anesthesia for Radiofrequency Catheter Ablation in Patients with Tachyarrhythmias: Infeasibility for Pediatric Patients with Ectopic Atrial Tachycardia

General anesthesia is sometimes required during radiofrequency catheter ablation (RFCA) of various tachyarrhythmias because of an anticipated prolonged procedure and the need to ensure stability during critical ablation. In this study, we examine the feasibility of using propofol anesthesia for RFCA procedure. There were 150 patients (78 male, 72 female; mean age 30 years, range 4-96 years) in the study. Electrophysiologic study was performed before and during propofol infusion in the initial 20 patients and was performed only during propofol infusion in the remaining 130 patients. In the initial 20 patients, propofol infusion increased the sinus rate and facilitated AV nodal conduction. The accessory pathway effective refractory period, as well as the sinus node recovery time, atrial effective refractory period, and ventricular effective refractory period were not significantly changed. There were 152 tachyarrhythmias in 150 patients (24 atrial flutter, 31 AV nodal reentrant tachycardia, 68 AV reciprocating tachycardia, 12 ventricular tachycardia, and 17 atrial tachycardia). Most (148/152) tachycardias remained inducible after anesthesia and RFCA was performed uneventfully. However, in four of the seven pediatric patients with ectopic atrial tachycardia, the tachycardia terminated after propofol infusion and could not be induced by isoproterenol infusion. Consequently, RFCA could not be performed. Intravenous propofol anesthesia is feasible during RFCA for most tachyarrhythmias except for ectopic atrial tachycardia in children.     

Effects of Procainamide and dl-Sotalol on the Changes of Atrial Electrophysiology Induced by High Current Stimulation

The relation between high current atrial stimulation and antiar-rhythmic drugs was not clear. We evaluated the effects of procainamide and dl-sotalol on the electrophysiological changes induced by high current stimulation. Effects of high current atrial stimulation on effective refractory period, dispersion of refractoriness, conduction velocity, and wavelength of the earliest atrial premature beat were evaluated at baseline and after infusion of procainamide (10 patients) and dl-sotalol (10 patients). High current atrial stimulation shortened effective refractory period locally (−12%± 4.0%, −7.0%± 3.0%, −5.1 ± 3.3%, and −3.0 ± 2.0%, at 0, 7, 14, and 21 mm from the S1 stimulation site, respectively; P < 0.001); increased the dispersion of refractoriness (from 17.8 ± 8.5 to 27.4 ± 12.5 ms, P < 0.001); decreased conduction velocity of the earliest premature beat (from 0.58 ± 0.10 to 0.52 ± 0.09 ms, P = 0.01); and decreased wavelength of the earliest atrial premature beat (from 10.9 ± 2.4 to 8.8 ± 2.1 cm, P < 0.001). These effects of high current stimulation persisted after procainamide infusion. However, after dl-sotalol infusion, high current atrial stimuli did not change the dispersion of refractoriness (23.1 ± 10 ms vs 26.4 ± 10.4 ms; P > 0.05, twice diastolic threshold vs 10 mA); conduction velocity of the earliest premature beat (0.54 ± 0.06 ms vs 0.50 ± 0.06 ms, P > 0.05); or wavelength of the earliest premature atrial beat (11.5 ± 1.6 m/s vs 10.1 ± 1.7 cm; P > 0.05). Although high current atrial stimulation shortened effective refractory period locally, increased dispersion of refractoriness, and decreased the wavelength of the earliest premature atrial impulse, these effects were abolished by dl-sotalol but not procainamide.     

The Response of Regular Re-entrant Supraventricular Tachycardia to Right Heart Stimulation

The study was designed to assess the effect of various forms of right atrial or ventricular stimulation on the termination of re-entrant "supraventricular" tachycardias. Standard electrophysiological techniques were used in 81 patients to study 86 stable tachycardias. All tachycardias were initiated by single or double atrial or ventricular premature stimuli or incremental atrial pacing. Eight groups of tachycardia circuit were defined in terms of the anterograde and retrograde pathways. Termination of each tachycardia was studied by atrial underdrive, ventricular underdrive, rapid atrial stimulation and single or double atrial and ventricular premature extrastimuli. Intranodal re-entrant tachycardias formed 33% of the total and WPW tachycardias as a whole formed 55% of the total number of arrhythmias. The remainder were comprised of atrial tachycardia (5%), tachycardias in association with a partial AV nodal bypass (3%) and pre-excited tachycardias (5%). A single atrial extrastimulus was most effective where the circuit involved the right atrium. Atrial underdrive was consistently less successful than a single atrial extrastimulus in all groups. Rapid atrial pacing was effective in all groups, but caused transient atrial flutter or fibrillation in a proportion of each group except one. Ventricular underdrive stimulation was most effective in those groups where the right ventricle was involved in the circuit, but tended to be less effective than programmed single or double ventricular extrastimuli. Pacemakers designed to deliver appropriately timed single or double extrastimuli may offer an important alternative to other pacing modalities.     

Acute effects of lidocaine on repolarization and conduction in patients with coronary artery disease

Right ventricular repolarization and refractoriness were studied during continuous infusion of lidocaine in patients with coronary artery disease. Compared with baseline the duration of monophasic action potential was shortened (p less than 0.01) at constant and premature stimulation. Early premature action potentials were less shortened (p less than 0.05). Therefore the difference between the longest and shortest action potential duration elicited 2 to 150 msec after refractoriness decreased during lidocaine infusion (p less than 0.01). The right ventricular effective refractory period was shortened similarly to the action potential duration. Lidocaine did not change the conduction of constant paced beats, whereas the more rapid conduction of the midrange premature beats was inhibited (p less than 0.01). The inhibition of premature conduction 50 to 150 msec from the right ventricular effective refractory period may be attributed to the effect of lidocaine on the rate-dependent recovery from inactivation. The effect on the restitution curve indicates that lidocaine may influence the dispersion of premature action potentials in human beings.     

Ventriculoatrial Conduction: A Cause of Atrial Malpacing in AV Universal Pacemakers. A Report of Two Cases

Retrograde atrial activation during ventricular pacing has often been a cause of intermittent or persistent arrhythmias (pacemaker-mediated tachycardia) in AV universal pacemakers. We recently encountered two cases in which VA conduction was responsible for atrial malpacing in patients with an implanted AV universal pacemaker, one programmed in DDD and one in DVI mode. Atrial malpacing was induced by the atrial refractoriness due to retrograde activation. In the first patient, it was observed when the pacemaker was programmed to a rate of 110 ppm (lower rate) and an AV interval of 200 ms in order to check crosstalk. In the second patient, it was observed after ventricular premature contractions.     

Use of a New Fallback Function to Prevent Endless-Loop Tachycardias: First Clinical Results

The methods used for preventing endless-loop tachycardias (ELTs) most often consist of initiating a long postventricular atrial refractory period (PVARP) with the sensing of every event likely to induce ELTs, such as sensed premature ventricular contractions (PVCs). A new fallback function may be useful to prevent the initiation of ELTs. A window of atrial rate acceleration detection (WARAD) is initiated with the sensing of every sinus event and equals 75% of the preceding PP interval. If an atrial event is sensed during this period, as are premature atrial contractions (PACs), no atrioventricular (AV) delay is initiated, but an atrial puise output is delivered and a subsequent 31-msec AV delay is started. Theoretically retrograde P waves are premature compared to sinus rhythm. They are therefore detected as PACs, and do not initiate AV delay, thus prohibiting the induction of ELTs. This function was tested in six patients, using external or implanted Chorus 2 pacemakers. Short PVARP (203 msec) and high atrial sensibility were programmed. Retrograde conduction was induced either by inefficient atrial pacing or a long programmed AV delay. Two different dual chamber settings were tested: dual chamber pacing with the fallback function On or Off. In every situation, the function proved effective in preventing ELTs: the number of tachycardia episodes went from 124 with the function programmed Off to 5 with the function programmed On for comparable durations. More than 75 ELTs effectively prevented by fallback have been recorded.     

Electrophysiologic effects of E-4031, a class III antiarrhythmic agent, on re-entrant ventricular arrhythmias in a canine 7-day-old myocardial infarction model

Effects of E-4031, a class III antiarrhythmic agent, on re-entrant ventricular arrhythmias were studied in eight dogs with a 7-day-old myocardial infarction. Epicardial mapping and local refractory periods were obtained using 47-channel bipolar electrodes attached to the epicardium. The induction of sustained ventricular tachycardia by programmed electrical stimulation was not suppressed by i.v. infusion of E-4031 at 1 microgram/kg/min, but was suppressed markedly by infusion at 10 micrograms/kg/min in six of seven dogs. During the infusion of E-4031 at 10 micrograms/kg/min, epicardial conduction velocity in the normal ventricle did not change (0.7 +/- 0.12 to 0.71 +/- 0.13 m/sec, n = 6), whereas slowed conduction in the infarct zone improved (0.58 +/- 0.10 to 0.77 +/- 0.13 m/sec, n = 6). E-4031 at 10 micrograms/kg/min prolonged effective refractory periods (ERP) in the normal zone (139 +/- 8 to 164 +/- 18 msec, P less than .01, n = 8), nontransmural infarct zone (145 +/- 7 to 177 +/- 15 msec, P less than .01, n = 8) and transmural infarct zone (156 +/- 14 to 191 +/- 22 msec, P less than .01, n = 8). The degrees of ERP prolongation were almost equal in all zones. On epicardial mapping, the areas of longer ERP and delayed conduction were observed to become inexcitable after the administration of E-4031. These results demonstrated that E-4031 effectively prevented the induction of re-entrant ventricular tachycardia in canine myocardial infarction model, and suggested that E-4031 rendered re-entrant circuits inexcitable by marked ERP prolongation in both normal and infarct zones.     

Spontaneous Endless Loop Tachycardia

Pacemaker-mediated endless loop tachycardia is usually caused by a P wave displaced from the physiologic position preceding a QRS complex to a time of atrial channel sensitivity after the QRS. Five cases are described of endless loop tachycardia starting after a normally-timed P wave, either spontaneous and preceding a ventricular stimulus or a P wave produced by an atrial channel stimulus followed by a ventricular stimulus and QRS complex. In each instance, the atrial refractory interval (ARI) was shorter than the retrograde conduction time. In four of the cases, prolongation of the atrial refractory interval after the ventricular event ended the tachycardias. In the fifth, in which the pulse generator could not be so programmed, the ventricular inhibited mode was required.     

Fast-Slow Type of Atrioventricular Nodal Reentrant Tachycardia: Horizontal Dissociation of the AV Node During Tachycardia

Two patients with recurrent supraventricular tachycardia are presented. The tachycardia was initiated and terminated by atrial extrastimulation beyond the atrial relative refractory period and the atrial activation sequence during the tachycardia was low to high. The induction of tachycardia was dependent on a critical AH interval. In patient 1 who had ventriculoatrial conduction, the tachycardia was initiated by the premature ventricular stimulation followed by double atrial response. In patient 2 the ventriculoatrial conduction was not observed. In both patients, the unchanged atrial cycle length during the tachycardia with antegrade Wenckebach AH block was observed. When AH block occurred during tachycardia the first AH interval was shorter than the subsequent HA interval. In patient 2 verapamil (5 mg) prolonged the atrial cycle length during tachycardia and rapid intravenous injection of adenosine triphosphate (10 mg) terminated the tachycardia. Oral diltiazem (280 mg/day) suppressed the tachycardia in patient 1. These findings suggest that the mechanism of tachycardia may be fast-slow type of AV nodal reentry in the upper portion of the AV node and this type of arrhythmia has tendency to show incessant form.     

The Dynamic Nature of Ventriculoatrial Conduction

An endless loop tachycardia starts when the atrial sensory amplifier of a dual chamber pacemaker identifies an early atrial signal originating from a ventricular or atrial premature depolarization or from myopotential noise. The tachycardia will continue as long as ventriculoatrial conduction is sustained. By selecting the appropriate atrial sensitivity setting, postventricular atrial refractory period, or upper rate limit, it is possible to eliminate sustained endless loop tachycardia. Electrophysiological data obtained at the time of dual chamber pacemaker implantation can assist the physician when selecting these settings. This report summarizes our intraoperative data on ventriculoatrial conduction obtained from 432 consecutive patients. One hundred sixty-two patients had evidence of ventriculoatrial conduction including 14% of patients with antegrade complete heart block and 32% with 2:1 AVB. The majority of patients with preserved antegrade conduction had sustained retrograde conduction. During incremental ventricular pacing, ventriculoatrial conduction prolonged in the majority of patients, and with faster ventricular pacing rates, ventriculoatrial block developed. Ventriculoatrial block developed in half of the patients at a ventricular pacing rate exceeding 120 bpm. Analysis of these data suggests that by selecting an upper rate limit of 140 bpm, a postventricular atrial refractory period of 300 msec, and an atrioventricular interval of 125 msec, approximately 90% of patients will not have sustained endless loop tachycardia.     

Computer Simulation of Dual Chamber Pacemaker Algorithms Using a Realistic Heart Model

Single and dual chamber pacing algorithms have been incorporated into a realistic computer model of cardiac electrical activation. The model enables different pacemaker algorithms to be tested, it allows prediction of their behavior, and it produces a simulated ECG record for each case. The computer model has been used to test eight different modifications of a simple DDD mode to prevent or terminate pacemaker-mediated "endless loop" tachycardia: (1) constant prolongation of the atrial channel refractory period; (2) prolongation of the atrial refractory period after a ventricular premature beat (VPB); (3) atrial pacing synchronously with a VPB; (4) simple rate control; (5) rate control in which the VA counter is not reset; (6) no ventricular pacing after an atrial premature beat; (7) rate limitation of atrial sensing; and (8) a combination of DDD and high frequency atrial stimulation modes. These modifications were tested with VPBs, atrial premature beats, atrial stimulation without capture, and accelerating sinus tachycardia. Only the pacemaker designed not to pace the ventricles following an atrial premature beat behaves satisfactorily in all four circumstances. Further possibilities for the development and use of a pacemaker-oriented computer heart model are discussed.     

Limitations to Activation of the Antitachycardia Burst Pacing Function of the Symbios 7008 Pacemaker in the Universal (DDD) Mode

The Symbios 7008 antitachycardia pacemaker was implanted in five patients for control of supraventricular tachycardia. Shortly after implantation in the first two patients, it was noted that the burst pacing sequence was not automatically activated by tachycardia when the pacemaker was in the DDD mode. Data from these two and the subsequent three patients were evaluated to explain this observation. The problem was primarily related to the operation of the device during the postventricular atrial refractory period. In all patients, the atrial electrogram encroached upon the programmed postventricular atrial refractory period because VA conduction during SVT was less than the lowest programmable interval (155 ms). Atrial events occurring during this interval will not trigger the tachycardia termination sequence. In all five patients, the size of the atrial electrogram decreased substantially (48 +/- 10%; mean +/- SD) during supraventricular tachycardia compared to sinus rhythm. In at least two of the five patients, decreased atrial size during supraventricular tachycardia may also have resulted in intermittent failure of atrial sensing during tachycardia, even at the most sensitive setting (0.6 mV). The latter may remain a problem even if the technical fault in SVT detection in the DDD mode were corrected. Two related problems were noted in the DDD mode: ventricular events during rapid SVT do not reset the low rate interval, resulting in random low rate pacing; and, automatic prolongation of atrial refractory period by two successive ventricular events without an intervening atrial sensed event compounds problems of atrial sensing. All of these problems were easily circumvented in all patients by noninvasive reprogramming to the DVI mode in which supraventricular tachycardia detection is based on ventricular sensing. These findings have implications for the future design of such devices.     

Effects of lidocaine on reperfusion arrhythmias and electrophysiological properties in an isolated ventricular muscle model of ischemia and reperfusion

Transmembrane electrical activity was recorded from endo- and epicardium of isolated segments of guinea pig right ventricles with standard microelectrode techniques. An ECG was also recorded by two electrodes placed at opposite ends of the tissue bath. Regular stimulation was delivered to the endocardium. Tissues were exposed to simulated ischemia for 15 min and then were reperfused with "normal" Tyrode's solution. Rapid sustained or nonsustained ventricular tachycardia, bigeminy or trigeminy with characteristics of transmural reentry occurred in early reperfusion in 14 of 20 hearts (70%). Arrhythmias were accompanied by prolongation of transmural conduction time and abbreviation of endocardial effective refractory period. With lidocaine, at 1, 5, 10 and 50 microM, reperfusion arrhythmias occurred in 53.3, 22.2, 20.8 and 14.3% of hearts, respectively. The decreased incidence of arrhythmias was statistically significant for 5 to 50 microM lidocaine (P less than .01). The antiarrhythmic effect did not correlate with changes in transmural conduction time, endocardial effective refractory period, or endocardial excitability. However, antiarrhythmic concentrations of lidocaine selectively depressed epicardial excitability and significantly increased endo- to epicardial conduction block during late ischemic and early reperfusion periods. Epicardial inexcitability extended to late diastole and conduction block was not restricted to premature beats. Thus, in transmural reentry in which the epicardium is an essential component of the circuit, lidocaine may interrupt the circuit by selectively rendering this component inexcitable.     

Programmed Electrical Stimulation of the Ventricle: An Efficient, Sensitive, and Specific Protocol

A relatively simple and evident ventricular programmed electrical stimulation (PES) protocol was developed, capable of achieving high degrees of sensitivity and specificity. In a series of 481 subjects, 1, 2, and 3 extrasfimuli (ES) were used successively during sinus rhythm and ventricular pacing at two drive cycle lengths, at one or more ventricular sites, together with rapid ventricular pacing, and other maneuvers such as isoproterenol infusion. Three ES were used immediately after two ES at each drive rate, rather than returning after completion of the protocol with two ES. Using the protocol, appropriate arrhythmias could be induced in 88% of all patients with ventricularfibrillation, 84% of all patients with sustained ventricular tachycardia (91% with underlying coronary disease), and 58% of patients with severe nonsus-tained ventricular tachycardia. There were significant differences in inducibility between patients whose ventricular arrhythmias were due to coronary artery disease and other causes. In contrast, sustained ventricular arrhythmias fall ventricular fibrillation) could be induced in only 5% of a control group of control patients, for a specificity of 95%. The protocol described is simpler and more efficient than those that use exhaustive testing of two ES before going to three ES. Three ES during sinus rhythm proved to be the most productive step, with a higher yield ratio (true:false-positives) than two ES or three ES during pacing, especially at fasterrates. Greater efficiency is also achieved by leaving the timing of an extrastimulus just beyond its effective refractory period when an additional extrastimulus is to be added, compared to protocols in which the extrastimulus is moved later in the cycle and then decremented in tandem with the additional extrastimulus. Coupling intervals < 200 msec produced some false-positives, but fewer overall than intervals < 200 msec, and with yield ratios comparable to other protocol steps. The protocol described meets NASPE standardsfor ventricular programmed stimulation protocols, and with its demonstrated specificity and relative simplicity and efficiency may be useful as a model for groups not yet committed to an alternative protocol.     

Comparison of Epicardial and Endocardial Programmed Stimulation in Patients at Risk for Ventricular Arrhythmias After Cardiac Surgery

Programmed ventricular stimulation was performed on 36 patients after recent cardiac surgery using implanted right ventricular epicardial temporary wires and with catheters positioned percutaneously at two right ventricular endocardial sites. Patients were followed for a mean of 18.5 months (range 3 to 36 months). Epicardial wires were nonfunctional in 10 patients (28%) due to excessively high pacing thresholds. Overall, 22 patients (61%) had inducible sustained ventricular tachycardia; epicardial wires were functional in 15 (68%) of these patients. Six patients without inducible ventricular tachycardia with epicardial stimulation were inducible using endocardial stimulation. Of the 24 patients in whom epicardial and endocardial ventricular stimulation could be performed, concordant results were obtained in only 17 (71%), despite similar epicardial and endocardial ventricular effective and functional refractory periods. A total of 14 arrhythmic events occurred during the follow-up period. Of the 22 patients with an inducible sustained ventricular tachycardia, 12 (64%) had subsequent arrhythmic events. Only 2 of the 14 noninducible patients had follow-up arrhythmic events, one of which was caused by medication proarrhythmia. Endocardial ventricular stimulation had a superior sensitivity (83% versus 30%, P < 0.0001) and an improved negative predictive value (86% versus 61%, P < 0.05) compared with epicardial ventricular stimulation. These results indicate that noninducibility using epicardial programmed ventricular stimulation does not reliably portend a low risk for recurrent ventricular tachyarrhythmias. Epicardial programmed stimulation, used alone, may be inadequate for postoperative electrophysiological evaluation of patients at risk for ventricular arrhythmias.     

Reversal of Digoxin Toxicity with Specific Antibodies

To determine whether digoxin-specific antibodies can reverse established digoxin toxicity in the dog, digoxin intoxication was produced by the intramuscular administration of digoxin, 0.09 mg/kg, on each of 3 consecutive days. All animals developed toxic arrhythmias (atrioventricular block, ventricular premature contractions and/or ventricular tachycardia). In control animals not receiving antidigoxin antibodies, the arrhythmias persisted throughout a 6 hr study period. Seven of the nine control dogs were dead within 24 hr and one moribund animal was sacrificed at that time; the last animal died within 48 hr.In contrast, in six of eight dogs given digoxin-specific antibodies in canine plasma and/or rabbit serum, the arrhythmias reverted to a sinus mechanism within 30-90 min after the start of the infusion. At the end of a 6 hr period of study, these six dogs were in normal sinus rhythm and all eight were alive and in normal sinus rhythm at the end of 72 hr. This study provides evidence that digoxin-specific antibodies can reverse severe established digoxin toxicity in the dog.     

Catheter ablation of accessory pathway in the treatment of pacemaker-mediated tachycardia

Pacemaker-mediated tachycardia (PMT) remains a clinical problem in patients with dual-chamber pacemaker despite technological advances. The onset mechanism of this tachycardia is sensing of retrograde atrial activation after ventricular stimulation. Repeated retrograde conduction perpetuates tachycardia. Postventricular atrial refractory period prolongation has been used for prevention of PMT, but this is not the solution in all cases. We present a case with PMT where the retrograde limb is a left accessory pathway, which is treated with radiofrequency ablation successfully.     

Reciprocating tachycardia due to a right-sided unidirectional retrograde anomalous pathway (URAP).

An 8 year-old boy had extensive electrophysiological evaluation of his recurrent supraventricular tachycardias. His ECG never showed delta waves but intracardiac stimulation and recording disclosed the following (1) eccentric retrograde atrial activation; (2) increased cycle length and retrograde conduction time following the development of right bundle-branch block; (3) constant retrograde conduction time for increasingly premature ventricular stimuli; (4) atrial captures by ventricular stimuli when the atrioventricular-His pathways were refractory; and (5) no delta waves upon stimulation of the atrial input site of the anomalous pathway. A diagnosis of reciprocating tachycardia involving retrograde conduction through an accessory pathway was made. Reciprocating tachycardias involving a unidirectional retrograde anomalous pathway can be easily misdiagnosed as atrioventricular node reentrant tachycardias if no evidence of preexcitation can be found, particularly if the anomalous pathway is on the right side. In order to exclude the participation of a concealed unidirectional anomalous pathway in a patient's reentry tachycardia, a complete map must be made of right and left atrial endocardial activity.     

Clinical Electrophysiological Effects of Intravenous Recainam: An Antiarrhythmic Drug Under Investigation for the Treatment of Ventricular and Supraventricular Arrhythmias

This open-label, multicenter study was designed to assess the electrophysiological properties of intravenous recainam, an investigational Class I antiarrhythmic agent. In 25 patients undergoing electrophysiological studies for the evaluation of arrhythmias, recainam was administered intravenously in a loading infusion (0.1 mg/kg/min) for 40 minutes, followed by a maintenance infusion (0.02 mg/kg/min) until the completion of the study. Electrophysiological measurements were obtained at baseline, 30 minutes after initiation of the loading infusion, and 30 minutes after termination of the infusion during washout. Conduction intervals, refractory periods, and sinus node recovery times were measured during sinus rhythm and during atrial or ventricular pacing. Vital signs were obtained and recorded before, during, and after recainam infusion. The results showed no change in mean arterial pressure, but heart rate increased slightly by 4 beats/min following recainam infusion. Recainam produced a generalized slowing of intracardiac conduction. The mean intraatrial conduction time, measured at an atrial paced cycle length of 600 msec, increased during recainam loading infusion by 44%, from 38.8% +/- 2.8 to 53.0 +/- 5.4 msec; intranodal conduction time increased by 10%, from 102.0 +/- 5.5 to 112.1 +/- 5.2 msec; and infranodal conduction time increased by 31% from 53.1 +/- 3.0 to 70.7 +/- 3.8 msec. Slowed conduction persisted during washout. The mean right atrial effective refractory period was significantly prolonged (+7% at 600 msec cycle length and +8% at 450 msec cycle length, P less than 0.05 and P less than 0.01, respectively) during recainam loading and remained so during washout.(ABSTRACT TRUNCATED AT 250 WORDS)