Unmasking of Retrograde Conduction by Isoproterenol in a Concealed Accessory Pathway

A 52-year-old female with no structural heart disease presented with a right bundle branch block (RBBB)/right axis deviation tachycardia with a cycle length of 300 msec. P waves were not discernible on the surface ECG. Baseline electrophysiology study in the drug-free state revealed no evidence for anterograde or retrograde conducting accessory pathways (APs) or for dual AV node physiology. Retrograde VA block with AV dissociation was present at a ventricular paced cycle length of 600 msec (sinus cycle length of 635–700 msec). AV nodal Wenckebach occurred during decremental atrial pacing at a cycle length of 300 msec. During isoproterenol administration, a left lateral AP with retrograde only conduction became manifest with 1:1 VA conduction to 380 msec. No anterograde AP conduction was present. Orthodromic reciprocating tachycardia with a cycle length of 285–315 msec was easily induced. We conclude that total functional conduction block can exist in APs, and unmasking of total conduction block can be accomplished with isoproterenol. All patients with undiagnosed tachycardias should have full repeat stimulation studies during adrenergic stimulation if the initial baseline evaluation is nondiagnostic.     

Effects of Verapamil on Electrophysiological Properties in Paroxysmal Atrial Fibrillation

Verapamil is used to control ventricular response during atrial fibrillation (AF). Limited data is available on the effects of verapamil on atrial vuinerability in human AF. The effects of intravenous verapamil (0.15 mg/kg) on electrophysiological properties of the atrium were investigated in 12 patients with documented paroxysmal AF by electrophysiological studies. Sinus cycle length, sinus node recovery time, and the effective refractory period of the right atrium were not significantly affected by verapamil. The intraatrial conduction delay zone was significantly increased (33 ± 20 msec before verapamil versus 50 ± 22 msec after verapamil, P < 0.01, and the maximal intraatrial conduction delay was also significantly prolonged by verapamil, both to the His bundle region (30 ±12 msec before verapamil versus 42 ± 15 msec after verapamil. P < 0.01) and to the coronary sinus (40 ± 15 msec before verapamil versus 53 ± 17 msec after verapamil, P < 0.01). The fragmented atrial activity zone was significantly increased (15 ± 14 msec before verapamil versus 25 ± 22 msec after verapamil, P < 0.02), and the percentile fragmented atrial activity was also significantiy increased by verapami] (149 ± 18 msec before verapamil versus 174 ± 44 msec after verapamil, P < 0.05). The repetitive atriaJ firing zone remained unchanged. Sustained AF spontaneousiy occurred in only one patient after the administration of verapamil. Thus, verapamil may modulate the abnormal atrial electrophysiology in paroxysmal AF, and wouid favor production of atrial reentry.     

New Observations on Decremental Atriofascicular and Nodofascicular Fibers: Implications for Catheter Ablation

Introduction: The purpose of this study was to characterize the anatomy and physiology of accessory pathways that exhibit anterograde decremental conduction. Results: Among 100 consecutive patients with an accessory pathway undergoing electrophysiological study, six individuals with decremental anterograde accessory pathway conduction were identified. Anterograde accessory pathway effective refractory periods and conduction curves were assessed by atrial extrastimulus testing. Atrial pace mapping and ventricular activation sequence mapping were used to define accessory pathway origin and insertion. Surgical ablation (N = 1) or radiofrequency catheter ablation (N = 3) was performed based on accessory pathway anatomy as determined during electrophysiological study. Four of 6 patients had gaps in anterograde accessory pathway conduction. Two patients had evidence of functional longitudinal dissociation in the accessory pathway. Five of 6 patients had atriofascicular fibers with an atrial rather than AV nodal site of origin of their decrementally conducting accessory pathway and with distal insertions in the right bundle branch. Among these five patients, a right posterior atrial origin was nearly as common as a right anterior atrial origin. One patient had a true nodofascicular fiber that arose from the AV node, inserting distally into the left bundle branch. Conclusion: Most accessory pathways with anterograde decremental conduction arise from the right anterior or right posterior atrium, not the AV node. A gap in anterograde accessory pathway conduction and functional longitudinal dissociation are common in such accessory pathways. Surgical or catheter ablation of such pathways is effective when directed at the atrial origin of the accessory pathway. True nodofascicular fibers arising from the AV node are rare. These may insert distally in the left ventricle. Catheter ablation of the proximal origin of such fibers is likely to result in complete AV block.     

Problems of Sensing Tachyarrhythmias by an Antitachycardia Pacemaker (Symbios 7008)

Atrial burst pacing is an effective method of terminating supraventricular tachycardia. In the patient presented in this report, a Symbios 7008 pacemaker (Medtronic Inc., Minneapolis, MN, USA) was implanted for two reasons: (1) severe AV conduction defect (AH, 230 msec; HV, 150 msec) and bifascicular block following anterior myocardial infarction; and (2) paroxysmal atrial flutter. The conduction defect ruled out programming other than atrial burst in DDD mode. Activation of burst pacing required appropriate programming of the "tachycardia detection window" on the basis of the cycle length of the flutter waves. In the case reviewed, episodes of atrial flutter with variable cycle lengths of 230 to 280 msec necessitated reprogramming of the AV interval, the refractory period, and the upper rate interval. The use of an antitachycardia device in automatic mode may be limited by variations in tachycardia cycle length.     

Variable Effects of Adenosine on Retrograde Conduction in Patients with Atrioventricular Nodal Reentry Tachycardia

Adenosine has been demonstrated to reliably produce transient block of atrioventricular nodal (AVN) conduction, and has been advocated as a method of differentiating retrograde conduction via the atrioventricular node from accessory pathway conduction. However, the response of retrograde AVN to adenosine in patients with typical atrioventricular nodal reentry tachycardia (AVNRT) remains unclear. We evaluated 13 patients (mean age 45 ± 20 years) with typical AVNRT prior to AVN modification. During right ventricular pacing, a rapid bolus of adenosine (0.2 mg/kg; maximum 18 mg) was administered. Adenosine sensitivity, defined by transient ventriculoatrial block, was observed in six patients, while in seven patients ventriculoatrial conduction was unaffected. An adenosine bolus administered during sinus rhythm or atrial pacing resulted in antegrade atrioventricular block in all the adenosine resistant patients in whom this was performed (n = 6). Comparisons of AVN electrophysiological characteristics between the adenosine sensitive and adenosine resistant patients were performed. There was no difference with respect to ventriculoatrial effective refractory period, ventriculoatrial Wenckebach, AVNRT cycle length, and His to atrial echo interval in AVNRT. However, there was a trend toward a longer antegrade fast pathway ERP in the adenosine sensitive group (P = 0.07). Electrophysiological properties do not predict retrograde AVN adenosine sensitivity. Adenosine does not cause retrograde AVN block in all patients with AVNRT, and therefore cannot reliably distinguish between retrograde conduction via the AVN or an accessory pathway.     

Atrial standstill with subnodal conduction defect and diffuse ventricular fibrosis managed with low right atrial pacing

In patients with congenital heart disease presenting with bradyarrhythmia, many electrophysiological abnormalities are found. This report presents a case of a man with surgically corrected single atrium and pulmonary valve stenosis, atrial standstill, delayed AV node conduction, first-degree intra- and second-degree infra-His block, who was permanently paced from a restricted excitable area of the low right atrium, as the pacing threshold was unacceptable at any ventricular site.     

AV junctional ablation allowing more effective delivery of cardiac resynchronization therapy in patients with intra- and interatrial conduction delay

We report two patients with cardiac resynchronization therapy (CRT) devices and evidence of refractory heart failure in whom impaired intraatrial conduction in one patient, and interatrial conduction in the other, prohibited optimization of the atrioventricular (AV) timing sequence. The patient with intraatrial conduction delay exhibited late right atrial sensing and latency during right atrial pacing that required programming of a short-sensed AV delay and long-paced AV delay (wide differential AV delay). In both patients AV junctional ablation and echocardiography-guided device optimization significantly improved heart failure.     

Atrial Septal Pacing to Synchronize Atrial Depolarization in Patients with Delayed Interatrial Conduction

The current method of pacing the right atrium from the appendage or free wall is often the source of delayed intraatrial conduction and discoordinate left and right atrial mechanical function. Simultaneous activation of both atria with pacing techniques involving multisite and multilead systems is associated with suppression of supraventricular tachyarrhythmias and improved hemodynamics. In the present study we tested the hypothesis that pacing from a single site of the atrial septum can synchronize atrial depolarization. Five males and two females (mean age 58 ± 6 years) with drug refractory paroxysmal atrial fibrillation (AF) were studied who were candidates for AV junctional ablation. All patients had broad P waves (118 ± 10 ms) on the surface ECG. Multipolar catheters were inserted and the electrograms from the high right atrium (HRA) and proximal, middle, and distal coronary sinus (CS) were recorded. The atrial septum was paced from multiple sites. The site of atrial septum where the timing between HRA and distal CS (d-CS) was ≤ 10 ms was considered the most suitable for simultaneous atrial activation. An active fixation atrial lead was positioned at this site and a standard lead was placed in the ventricle. The interatrial conduction time during sinus rhythm and AAT pacing and the conduction time from the pacing site to the HRA and d-CS during septal pacing were measured. Atrial septal pacing was successful in all patients at sites superior to the CS os near the fossa ovalis. During septal pacing the P waves were inverted in the inferior leads with shortened duration from 118 ± 10 ms to 93 ± 7 ms (P < 0.001), and the conduction time from the pacing site to the HRA and d-CS was 54.3 ± 6.8 ms and 52.8 ± 2.5 ms, respectively. The interatrial conduction time during AAT pacing was shortened in comparison to sinus rhythm (115 ± 18.9 ms vs 97.8 ± 10.3 ms, P < 0.05). In conclusion, simultaneous activation of both atria in patients with prolonged interatrial conduction time can be accomplished by pacing a single site in the atrial septum using a standard active fixation lead placed under electrophysiological study guidance. Such a pacing system allows proper left AV timing and may prove efficacious in preventing various supraventricular tachyarrhythmias.     

Hemodynamic Consequences of Atrioventricular and Ventriculoatrial Pacing

The effect of atrialventricular versus ventricular pacing and contraction were studied in seven open-chest dogs. Cardiac output, left ventricular, left atrial, right atrial and pulmonary artery pressures were recorded. The right or left ventricular apical areas were consistently superior as ventricular pacing sites.
Appearance of cannon A waves within the pre- or ejection period produced a significant decrease in left ventricular and systemic blood pressure, and cardiac output with a concomitant increase in right atrial, ventricular and pulmonary pressures. Prominent "v" waves were also observed during these periods.
Reducing the basic driving cycle length from 400 to 300 msec caused a marlted deterioration of all hemodynamic parameters with the appearance of mechanical alternans. Random VA conduction or ventricular pacing in the presence of com-plete AV and VA heart block appeared to offer a more favorable hemodynamic result than constant 1:1 VA conduction. It is concluded that maintenance of a physiologic AV interval permitting atrial contraction to appear outside of pre- or ejection period of ventricular systole is an important determinant or ventriculor function during cardiac pacing.     

Evidence for adenosine mediation of atrioventricular block in the ischemic canine myocardium.

Adenosine levels in oxygen-deprived myocardium can rise to 10- 100 microM concentrations known to cause atrioventricular (AV) conduction delay and block. We reported that the AV conduction delay and block caused by hypoxia is markedly attenuated by 10 microM aminophylline, and adenosine competitive antagonist. THe purpose of the present study was to investigate adenosine's role in ischemic AV conduction disturbances. Dogs were anesthetized and instrumented for His bundle and surface electrogram recordings. The total AV conduction time was subdivided in to atrial-His bundle (AH) and His bundle-ventricle intervals. The atrioventricular node artery (AVNA) was cannulated for selective injection of drugs in the AV node region. Adenosine (10 to 100 microgram), as a 2-ml bolus injection, rapidly produced a dose-dependent, transient increase in the AH interval; a 1,000-microgram dose caused second degree AV block. The duration of the increase in AH interval was also dose-dependent. Dipyridamole, and inhibitor of nucleoside transport, potentiated the negative dromotropic effects of adenosine, whereas aminophylline attenuated them. In some dogs, after cannulation of the AVNA, first and second degree AV block occurred spontaneously or were induced by rapid atrial pacing. Injection of the aminophylline (5 mg/kg, i.e.) or theophylline (100-1,000 microgram) into the AVNA rapidly reversed the AV blocks. Upon washout of the drugs the AV blocks recurred. We conclude that endogenously released adenosine may account for a major fraction of the AV conduction delay and block associated with impaired blood supply to the AV node, and the theophylline and aminophylline reverse the AV conduction defect by antagonizing the effects of adenosine.     

Ibutilide Induced Intraatrial Wenckebach Periodicity in the Neonatal Canine Heart

PICKOFF, A.S., et al. : Ibutilide Induced Intraatrial Wenckebach Periodicity in the Neonatal Canine Heart. In nine anesthetized canine neonates, the high right atrium was paced at progressively shorter cycle lengths while recording high right atrial electrograms and left atrial appendage monophasic action potentials before and after the administration of the new Class III agent, ibutilide. Prior to ibutilide administration, 1:1 conduction was maintained from the high right atrium to the left atrial appendage at all paced cycle lengths, down to 160 ms. Following ibutilide, a pattern of intraatrial conduction was observed in two of nine neonates at a cycle length of 160 ms that was consistent with the development of intraatrial Wenckebach periodicity. This represents one of the only demonstrations of drug induced intraatrial Wenckebach periodicity in vivo and suggests that this rarely reported form of atrial conduction block might play a role in ibutilide's clinical efficacy against atrial arrhythmias.     

Effects of An Acute Increase in Atrial Pressure on Atrial Refractoriness in Humans

Contraction-excitation feedback has been studied extensively in mammalian ventricles. In contrast, little is known about contraction-excitation feedback in mammalian atria. The objective of this study was to investigate the effect of acute alterations in atrial pressure, induced by varying the atrioventricular (AV) interval, on atrial refractoriness. Twenty patients without structural heart disease participated in the study. In each patient the atrial effective (ERP) and absolute refractory periods (ARP) were measured during AV pacing at a cycle length of 500 msec and an AV interval of 120 msec. Acute increases in atrial pressure were induced by pacing the atrium and ventricle simultaneously for the final two beats of the drive train. The ERP was defined as the longest extrastimulus coupling interval that failed to capture with an extrastimulus current strength of twice the stimulation threshold. The ARP was defined in a similar manner with an extrastimulus current strength of 10 mA. The ERP and ARP were determined using the incremental extrastimulus technique. A subset of patients had the pacing protocol performed during autonomic blockade. As the AV interval of the final two beats of the drive train was shortened from 120 msec to 0 msec, the peak right atrial pressure increased from 7 ± 3 mmHg to 15 ± 5 mmHg (P < 0.001). The increase in atrial pressure associated with simultaneous pacing of the atrium and ventricle resulted in shortening of the atrial ERP and ARP by 7.3 ± 5.2 and 6.2 ± 3.5 msec, respectively (P < 0.0011). Similar results were obtained during autonomic blockade. These findings confirm the presence of contraction-excitation feedback in normal human atria.     

Adenosine-Sensitive Atrial Tachycardia

Limited data suggest that adenosine termination of atrial tachycardia is uncommon. To investigate further the effect of adenosine on atrial tachycardia, adenosine (6–12 mg) was administered during sustained atrial tachycardia in 17 patients. All patients underwent electrophysiological study to exclude other mechanisms of supraventricular tachycardia. Mean patient age was 51 ± 20 years (range 18–82 years). Seven patients had no structural heart disease. The mean atrial tachycardia cycle length was 390 ± 80 msecs (range 260–580). Sustained atrial tachycardia was induced with atrial extrastimuli in 8 patients, and was either incessant at baseline or developed spontaneously during isoproterenol infusion in 9 patients. Adenosine terminated atrial tachycardia in 3 patients (18%), transiently suppressed atrial tachycardia in 4 patients (23%), and produced AV block without affecting tachycardia cycle length in the remaining 10 patients. Adenosine sensitivity was observed in 3 of 8 patients with tachycardias initiated and terminated by atrial extrastimuli, and in 4 of 9 patients with spontaneous, but not inducible tachycardias including 3 of 4 patients with isoproterenol facilitated tachycardias. Of multiple clinical and electrophysiological variables examined as potential predictors of adenosine sensitivity, only isoproterenol facilitation of spontaneous or inducible sustained tachycardia predicted adenosine sensitivity (P = 0.02). These observations suggest that adenosine-sensitive atrial tachycardia may be more common than previously recognized. Adenosine sensitivity does not appear to be specific for tachycardia mechanism and cannot be predicted by response to pacing. Atrial tachycardias dependent on β-adrenergic stimulation are most likely to be terminated by adenosine.     

Failure of coronary sinus pacing in reducing local atrial conduction delay in patients with atrial fibrillation after successful internal cardioversion

Recent studies suggested that distal coronary sinus (CS) pacing may prevent atrial fibrillation (AF) by reducing site dependent intraatrial conduction delay. The aim of this study was to investigate the effect of high right atrial (HRA) and distal CS pacing on local conduction delay in patients with AF. The study population consisted of 10 patients with persistent AF after transvenous atrial defibrillation and 10 control subjects. The local conduction delays along the anterolateral right atrium (RA), in the CS, and at the right atrial septum (RAS), and the incidence of AF in response to an atrial extrastimulus during HRA and distal CS pacing at a drive cycle length of 400, 500, and 600 ms were evaluated. In patients with AF, distal CS and HRA pacing are associated with more prominent and similar extent of conduction delay within the atria, without any significant difference in the dispersion of conduction delay and susceptibility to AF induction (70% vs 60%, P = 0.9). In normal controls, distal CS pacing reduces the conduction delay at the RAS and CS ostium and decreases the dispersion of conduction delay and the propensity for AF induction (0% vs 50%, P = 0.03) compared to HRA pacing. The pacing drive cycle length has no significant effect on conduction delay in patients with AF and normal controls (P > 0.05). Compared to normal controls, patients with AF have significantly longer conduction delay at the RAS and along the anterolateral RA during HRA and distal CS pacing. The result of this study demonstrates that the effect of HRA and distal CS pacing on the local atrial conduction delay in patients with and without AF differ significantly. These patients with AF may have more diffuse atrial anisotropy causing the changes in conduction, and pacing from distal CS in these patients dose not reduce the propensity for AF.     

Atrial Vulnerability and Electrophysiology Determined in Patients With and Without Paroxysmal Atrial Fibrillation

For elucidation of atrial electrophysiology and vulnerability an electrophysiological study was performed in 45 patients with documented paroxysmal atrial fibrillation and a control group (n = 46). Atrial vulnerability was assessed by programmed atrial stimulation with up to two extrastimuli during sinus rhythm and paced cycle lengths of 600 msec, 430 msec and 330 msec. Sustained atrial fibrillation or flutter was induced in 37/45 patients with paroxysmal atrial fibrillation in contrast to 9/46 patients in the control group (P less than 0.001). Left atrial diameter (M-mode echocardiogram), P wave duration, sinus cycle length, sinus node recovery time, and the effective refractory period of the right atrium were not significantly different between the two study groups. Intraatrial conduction time from the high right atrium (HRA) to the basal right atrium (A) and the functional refractory period of the right atrium were significantly longer in patients with paroxysmal atrial fibrillation.     

Interatrial Conduction in Patients Undergoing AV Stimulation: Effects of Increasing Right Atrial Stimulation Rate

To evaluate the frequency of spontaneous or rate dependent interatrial blocks, the interatrial conduction time (IACT) was studied on 100 consecutive patients (mean age 78.3 ±7.8 years) during a transvenous dual chamber pacemaker implant. The spontaneous interatrial conduction time (SIACT) was measured from the intrinsic deflection (ID) of the unipolar right atrial signal to the ID of the left atrial signal recorded in a bipoiar way by an esophageal lead. The paced interatrial conduction time (PIACT) was measured from the stimulus artifact to the left atrial ID, when the atrium was paced at a slightly higher rate than the spontaneous rate and during incremental atrial pacing. From these measurements, the maximum increase ofPIACT (MIPIACT) was deduced. In this elderly population, the PIACT was similar (117 ± 26.9 msec) to the data in the literature. However, there were large interindividual variations that were also found in SIACT. We found a close correlation between SIACT and PIACT (P < 0.0001). PIACT was on average 50 msec longer than SIACT. SIACT increased with age (P < 0.03). The MIPIACT was 15.3 ± 15.2 msec. In the majority of patients, the MIPIACT was > 10 msec, and even reached 90 msec in one patient. MIPIACT was longer in patients with a PIACT exceeding 110 msec (P < 0.004). Based on IACT alone, the AV interval must be lengthened on average by 50 msec when changing from atrial tracking-ventricular pacing to atrial pacing-ventricular pacing, but large individual differences must be kept in mind. Elderly people should probably have a longer AV delay.     

Intravenous Adenosine Triphosphate Disodium: Its Efficacy and Electrophysiologic Effects on Patients with Paroxysmal Supraventricular Tachycardias

We studied the electrophysiologic effects of intravenous adenosine triphosphate disodium (ATP-2Na) on 17 patients with paroxysmal supraventricular tachycardias (PSVTs). One patient had sinus node (SN) reentry, two had intraatrial (IA) reentry, 7 patients had AV nodal reentry and seven had atrioventricular reentrant tachycardias (AVRTs) with accessory pathways (APs). ATP-2Na was injected during ventricular pacing in patients with AV nodal reentry and AVRTs with APs. A bolus injection of ATP-2Na terminated all the PSVTs within 50 s except for one case of IA reentry (case 2). The sites of block at termination were the atrium in SN reentry and IA reentry, between A and H (AH) or between H and A (HA) in AV nodal reentry, and AH block in all the PSVTs with APs. The sites of action on the patients with AV nodal reentry were both the antegrade and retrograde pathways, while the modes of block were Mobitz type I and type II, respectively. ATP-2Na during ventricular pacing in patients with AV nodal reentry produced Mobitz type II ventriculoatrial block (VAB) in four of seven cases. ATP-2Na during ventricular pacing in patients with AVRTs with APs produced changes of atrial activation sequences in two patients, induction of PSVT in two patients, and Mobitz type II VA block in three patients. The former two phenomena suggested a retrograde AV nodal block and raised the possibility of a simple test for retrograde atrial fusion during ventricular pacing in patients with WPW syndrome. Chest discomfort of short duration was most commonly noted after ATP-2Na administration.     

Intra- and interatrial conduction delay: implications for cardiac pacing

Atrial conduction disorders are frequent in elderly subjects and/or those with structural heart diseases, mainly mitral valve disease, hyperthrophic cardiomyopathies, and hypertension. The resultant electrophysiological and electromechanical abnormalities are associated with a higher risk of paroxysmal or persistent atrial tachyarrhythmias, either atrial fibrillation, typical or atypical flutter or other forms of atrial tachycardias. Such an association is not fortuitous because intra- and interatrial conduction abnormalities delays disrupt (spatial and temporal dispersion) electrical activation, thus promoting the initiation and perpetuation of reentrant circuits. Preventive therapeutic interventions induce variable, sometimes paradoxical effects as with the proarrhythmic effect of class I antiarrhythmic drugs. Similarly, atrial pacing may promote proarrhythmias or an antiarrhythmic effect according to the pacing site(s) and mode. Multisite atrial pacing was conceived to correct, as much as possible, abnormal activation induced by spontaneous intra- or interatrial conduction disorders or by single site atrial pacing, which are situations responsible for commonly refractory arrhythmias. Atrial electrical resynchronization can also be used to correct mechanical abnormalities like left heart AV dyssynchrony resulting from intraatrial conduction delays.     

Double Response of the Ventricle During Transient Entrainment in a Common Atrioventricular Nodal Reentrant Tachycardia

We report a patient with slow-fast atrioventricuiar (AV)nodal reentrant tachycardia, in which double ventricuJar response was demonstrated during rapid pacing at cycle length of 300 msec or less from the high right atrium. The determinants of double ventricular response during transient entrainment in the present case were: (1)a crucial conduction delay in the slow pathway; (2)the collision between the activation via the antegrade fast pathway (antidromically)of the last paced beat and the activation via the antegrade slow pathway (orthodromically)of the previous paced beat, instead of the unidirectional block in the slow pathway; and (3)the enhanced AV nodal conduction over the antegrade fast pathway.     

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)