Premature Atrial Stimuli Research Articles

Dexmedetomidine Depresses Sinoatrial and Atrioventricular Nodal Function Without Any Change in Atrial Fibrillation Inducibility.

It has been reported that dexmedetomidine (dex) has an impact on the cardiac conduction system and even has potential antiarrhythmic actions. We examined the influence of dex on the cardiac electrophysiological properties and atrial fibrillation (AF) inducibility. Adult paroxysmal AF patients were randomly assigned to receive (N = 107) or not receive (N = 108) dex during cardiac electrophysiological studies. The corrected sinus node recovery time (558 ± 331 vs. 459 ± 260 milliseconds; P = 0.02), Wenckebach cycle length (P < 0.001), atrioventricular nodal effective refractory period (317 ± 76 vs. 252 ± 54 milliseconds; P < 0.001), and atrio-His interval (P < 0.001) were longer in patients with dex than in those without. We tested the induction of repetitive atrial firing (RFA) defined as the occurrence of ≥2 successive atrial activities induced by single premature atrial stimuli to determine the AF inducibility. RFA was seen with a similar proportion (41.1% vs. 44.4%), yet it was evoked at a longer stimulus coupling interval in the dex patients, which was potentially attributed to the longer atrial effective refractory period (237 ± 36 vs. 213 ± 27 milliseconds; P < 0.001) and more prolonged atrial conduction delay seen in the dex group. In conclusion, dex may depress the sinus and atrioventricular nodal function, however, it may not reduce the AF inducibility.

263 Junctional tachycardia in the mouse can be prevented by pacemaker channel (If) blockade with Ivabradine hydrochloride

Atrioventricular nodal re-entrant tachycardia (AVNRT) and junctional tachycardia (JT) are common, electrocardiographically similar, arrhythmias. AVNRT is described as re-entry conduction between the fast (FP) and slow (SP) AV nodal pathways. JT occurring following cardiac surgery in neonates increases mortality risk by 5.6-14%. JT mechanisms are unknown, but may include autonomic nervous system involvement. Pacemaking mechanisms utilize a membrane clock, involving the pacemaker funny channel (If), and an intracellular calcium clock involving rhythmic oscillations in calcium release from ryanodine receptors. The SP, formed by the inferior extension of the compact AV node (INE), contains the dominant AVN pacemaker, expresses If, and may be involved in JT. We investigated the mechanisms of junctional arrhythmia in male wild type C57BL/6 mice. Studies utilized an intracardiac octapolar electrode catheter in anaesthetized mice. Programmed electrical stimulation elicited antegrade AVN conduction and SP conduction in 8/18 mice, single re-entrant beats in 3/18, but rarely AVNRT (1/18). Rapid ventricular pacing (RVP, 50 Hz, 400 ms, 10-30 bursts), induced junctional arrhythmia in 14/18 mice (83%) producing a 32% increase in rate (325 ± 15 vs 429 ± 19 BPM, P < 0.001). Response of arrhythmia to single premature atrial stimuli distinguish AVNRT from JT. Premature FP activation did not terminate the arrhythmia (0/14) indicating JT. RVP caused decreases (46 ± 2.6%) in minimum end-diastolic blood pressure and enhanced nodal conduction following 10 bursts (pre-pacing AH = 31 ± 1ms vs post-pacing AH = 28 ± 1ms, P < 0.001, n = 14) prior to JT initiation, suggesting involvement of a baroreflex response. Vagal nerve stimulation (5/5, X2 = 10, P < 0.002) and propranolol (7/7, X2 = 14, P < 0.001) prevented JT induction, confirming a role for the autonomics. Ivabradine hydrochloride, a selective If blocker, prevented JT (8/9, X2 = 14.4, P < 0.001). Ruthenium red, a potent inhibitor of intracellular calcium release also prevented JT (5/5, X2 = 10,P < 0.002). Forskolin (an adenylyl cyclase activator) and caffeine (a stimulator of intracellular calcium release) together produced long lasting (>2 mins) spontaneous JT (5/5, X2 = 10, P < 0.002) that was terminated by Ivabradine (5/5, X2 = 10,P < 0.002). AVNRT was infrequent, but the mouse is susceptible to JT. JT may rely on an interaction of membrane and intracellular events which can be prevented by If channel blockade. Ivabradine might be useful in neonatal patients with post-operative JT.

Atrioventricular Nodal Reentrant Tachycardia

Atrioventricular nodal reentrant tachycardia (AVNRT) represents the most common regular supraventricular arrhythmia in humans.1 The precise anatomic site and nature of the pathways involved have not yet been established, and several attempts to provide a reasonable hypothesis based on anatomic or anisotropic models have been made.2 There has been considerable evidence that the right and left inferior extensions of the human atrioventricular (AV) node and the atrionodal inputs they facilitate may provide the anatomic substrate of the slow pathway, and a comprehensive model of the tachycardia circuit for all forms of AVNRT based on the concept of atrionodal inputs has been proposed.2 Still, however, the circuit of AVNRT remains elusive. Recently, time-honored conventional schemes for the diagnosis and classification of the various forms of the arrhythmia have been refuted in part by evolving evidence. Recognition of the various types of AVNRT is important, however, to expedite diagnosis and allow implementation of appropriate ablation therapy without complications. We present an update on AVNRT with a particular emphasis on electrophysiological criteria used for the differential diagnosis of regular, supraventricular tachycardias. Typically, AVNRT is a narrow-complex tachycardia, ie, QRS duration <120 ms, unless aberrant conduction, which is usually of the right bundle-branch type, or a previous conduction defect exists. Tachycardia-related ST depression and RR-interval variation may be seen. RR alternans in AVNRT has been attributed to the proposed model of a figure of 8 reentry with continuous crossing over of antegrade activation through an inferior input to the contralateral superior input via the node.2 In the typical form of AVNRT (slow-fast), abnormal (retrograde) P′ waves are constantly related to the QRS and in the majority of cases are indiscernible or very close to the QRS complex (RP′/RR <0.5). Thus, P′ waves are either masked by the QRS complex or …

Decremental Accessory Pathway Conduction After Ablation and Antidromic Atrioventricular Reciprocating Tachycardia 8 Years After Successful Radiofrequency Ablation

This is a rare case of antidromic reciprocating tachycardia developing 8 years after successful catheter ablation. A 15-year-old girl had recurrence of palpitations 8 years after the ablation of manifest right posteroseptal accessory pathway. Atrial burst pacing revealed Wenckebach atrioventricular conduction with preexcitation. Wide QRS tachycardia with identical morphology to sinus rhythm associated with retrograde His potential recorded immediately after the V-wave was induced by isoproterenol infusion. Atrial premature stimulus applied at the identical timing of His potential advanced the subsequent ventricular beat and His potential. Catheter ablation may produce decremental accessory pathway conduction and rarely cause antidromic atrioventricular reciprocating tachycardia. This may be explained by a presence of "de novo" accessory pathway with decremental conduction properties that became manifest after the first ablation.

Antifibrillatory Actions of Cisatracurium: An Atrial Specific M2 Receptor Antagonist

Muscarinic receptor antagonists are proposed to prevent atrial fibrillation (AF), but also facilitate AV conduction, limiting clinical usefulness. Cisatracurium, a neuromuscular blocker, was administered to anesthetized dogs (0.05-0.8 mg/kg IV) and was administered to superfused pulmonary vein (PV) tissues in vitro. Dose-dependent suppression of AF induced by premature atrial stimuli was observed under control conditions (n = 3), right vagus nerve stimulation (n = 7), and anterior right ganglionated plexus stimulation (n = 3). AF was prevented (P < 0.0001) concurrent with suppression of the decreased atrial MAP duration/ERP accompanying vagus nerve stimulation without altering AH intervals or sinus cycle length. Although atropine (0.001-0.016 mg/kg, n = 4) suppressed AF (P < 0.04) in association with suppression of atrial MAP shortening induced by vagus nerve stimulation, atropine also prevented sinus cycle length and AH interval prolongation with vagus nerve stimulation, and decreased AV effective and functional refractory periods. In vitro, both cisatracurium and atropine prevented (1) action potential shortening produced by acetylcholine administration and (2) action potential shortening and arrhythmia triggering within PV sleeves produced by local autonomic nerve stimulation, atropine producing competitive inhibition, and cisatracurium producing noncompetitive M(2) muscarinic receptor blockade. Cisatracurium demonstrates a dose-dependent (1) suppression of AF and atrial action potential shortening accompanying vagus nerve stimulation without facilitating sinus or atrioventricular nodal function and (2) noncompetitive blockade of action potential shortening and triggered firing induced in isolated PVs by local autonomic nerve stimulation. The data are consistent with allosteric binding of cisatracurium to the M(2) muscarinic receptor in canine atrium.

Supraventricular tachycardia with simultaneous atrial and ventricular activation: What is the mechanism?

A 50-year-old man underwent an electrophysiologic study for very frequent episodes of supraventricular tachycardia. He had a left bundle branch block with a baseline sinus cycle length, atrial-His (AH) interval, and His-ventricular (HV) interval of 670, 100, and 65 ms, respectively. Atrial pacing induced a regular supraventricular tachycardia with a cycle length of 540 ms. Ventricular pacing at a cycle length of 500 ms was performed during the tachycardia (Figure 1). A premature atrial stimulus was introduced in the high right atrium during tachycardia (Figure 2).

Right Ventricular Pressure Shows Greater Sensitivity Than Left Ventricular Pressure to Dual Chamber Coupled Pacing in Ischemic Heart Failure Dogs

Dual chamber coupled pacing (DCCP) has potential as a therapy for patients with heart failure by increasing atrial and ventricular contractility and reducing the mechanical heart rate (MHR). DCCP has global effects on the heart due to the propagated depolarization and, therefore, it is likely that the increase in contractility is similar in the left and right ventricle. The objective of this study was to evaluate the effects of DCCP on right ventricular and left ventricular hemodynamics. Methods: Eight dogs were given serial intracoronary injections of microspheres until their ejection fraction dropped to # 35% (biplane echocardiography). The animals were then anesthetized with isoflurane and fentanyl and instrumented with pressure sensors in the RV, LV and aorta during closed-chest surgery. Pacing leads were placed in the right atrial appendage and RV apex. DCCP was performed with stimuli that were delivered to the RV 10, 30, 50, 100 and 150 ms after the effective refractory period. The order of the different coupling intervals was randomized. An atrial premature stimulus was delivered 60 ms prior to the ventricular stimulus. Hemodynamic data during normal sinus rhythm (NSR) and DCCP were gathered for one minute. The median of the final 30 seconds of each period was used to calculate the following parameters for both the RV and LV: maximum change in pressure with respect to time (dPdtmax), maximum pressure (max), pulse pressure (pulse), mechanical heart rate (MHR), and mean arterial pressure (mABP). Results: Significant differences between the right and left ventricular responses to DCCP were seen when potentiation was greatest at the shortest coupling interval (10 ms). At this setting the percent change in RVPmax and RVPpulse was significantly greater than LVPmax and LVPpulse. As shown in the Figure below, dPdtmax was not significantly different. Discussion: DCCP has always been assumed to affect the left and right heart equally. These data suggest that there may be significant differences in the effects of DCCP on the left and right heart. These differences might be due to the site of delivery of the premature ventricular stimulus.

Suppression of Autonomic‐Mediated Triggered Firing in Pulmonary Vein Preparations, 24 Hours Postcoronary Artery Ligation in Dogs

Rapid arrhythmia originating within pulmonary veins (PVs) precipitates atrial fibrillation (AF) in man. To determine a possible basis for an increased incidence of AF observed peri-myocardial infarction in man, we compared AF induction in vivo and triggered arrhythmia formation within isolated PVs in vitro in normal dogs and dogs studied 24 hours postcoronary artery ligation. The incidence of AF initiated by atrial premature stimuli was increased in dogs postcoronary artery ligation (6/9) versus normal (2/12) (P = 0.03). In isolated PVs from normal hearts, pause-dependent early afterdepolarizations (EADs) were enhanced by catecholamines. Rapid arrhythmia (1,182 +/- 213 beats/min) was triggered during isoproterenol/norepinephrine (32 nM) + acetylcholine (100 nM) (N = 16/23) using the same pacing pauses eliciting EADs. Rapid arrhythmia (802 +/- 161 beats/min) was also triggered by local autonomic nerve stimulation (ANS; N = 18/23). Despite equivalent pause-dependent afterdepolarization formation in PVs from infarcted hearts, a rightward 45-fold and 28-fold shift in the dose-response curve for afterdepolarization enhancement was observed for isoproterenol and norepinephrine, respectively (P < 0.02). ANS (N = 1/19) and isoproterenol/norepinephrine (32 nM) + acetylcholine (100 nM) (N = 0/9 and 0/12, respectively) (P = 0.0001) failed to elicit arrhythmia formation. Beta-adrenergic receptor desensitization was associated with a 2.5-fold increase in PV beta-adrenergic receptor kinase (ARK). The data demonstrate decreased susceptibility of isolated canine PVs for arrhythmia triggered by local ANS, or pacing pauses in the presence of a catecholamine + acetylcholine, postmyocardial infarction, despite a greater susceptibility of the intact heart to AF. The decreased arrhythmia susceptibility was observed coincident with an increase in beta-ARK and a decreased responsiveness to beta-adrenergic receptor agonists.

Effects of a blocked atrial beat on the atrioventricular nodal recovery property in patients with dual nodal pathways.

Dual AVN physiology can be demonstrated by a variety of maneuvers. To determine whether AVN recovery times following a blocked extrastimulus facilitate or obscure detection of dual AVN physiology, 11 patients (9-17 years) were studied with dual AVN pathways by using single and double atrial extrastimuli. With a single atrial extrastimuli, the premature atrial stimulus (A2) was coupled to basic atrial beats (A1). The fast and slow AVN recovery curves were constructed with plots of the nodal conduction time against the recovery time (A1A2,A2H2). With double atrial extrastimuli, a fixed blocked A2 beat (A2B) was followed by a scanning atrial beat (A3). The nodal recovery property post-A2B was studied by plots of A2BA3,A3H3. In all patients the recovery curve of the fast pathway post-A2B had a leftward shift when compared to that of the pre-A2B curve (i.e., the AH was shortened at the same recovery time). The window of slow pathway conduction post-A2B disappeared totally in five patients and decreased significantly in six patients (post-A2B: 26 +/- 42 ms; pre-A2B: 80 +/- 65 ms, P < 0.05). In the six patients that still had slow pathway conduction post-A2B, the slow pathway effective refractory period post-A2B was significantly less than that of pre-A2B (215 +/- 38 vs 268 +/- 16 ms, P < 0.05). The fast pathway effective refractory period post-A2B was also diminished significantly (235 +/- 62 vs 357 +/- 76 ms, P < 0.0001). The authors conclude that blocked atrial beats decrease the visibility of the slow pathway conduction.

Effects of adenosine on local stimulus-response latency and induction of atrial fibrillation by premature stimuli.

Premature atrial stimuli delivered during the relative refractory or "vulnerable" period exhibit increased local stimulus-response latency and may occasionally induce atrial arrhythmias. The use of adenosine to treat supraventricular tachycardias may also provoke atrial arrhythmias. In this study we investigated the effects of adenosine on the latency of premature complexes in relation to repolarization and induction of atrial arrhythmias in 14 patients without structural heart disease. A monophasic action potential catheter was used for recording in the right atrium and introducing premature stimuli (S2) at twice diastolic threshold after eight paced (S1) complexes. At short coupling intervals, S2 latency increased relative to S1 latency. S2 was delivered repeatedly at a fixed coupling interval (producing maximal local response latency) and adenosine (6 mg) was given intravenously. Adenosine decreased S2 latency significantly (23+/-5 to 11+/-3 ms, P<0.01), to values similar to S, latency. However, despite the decrease in S2 latency, the combination of adenosine and S2 more often resulted in transient atrial arrhythmias (11 of 14 patients vs 2 of 14 patients without adenosine, P<0.05). Adenosine had no effect on S, latency (9+/-2 vs. 9+/-2 ms) but decreased monophasic action potential duration from 202+/-37 to 158+/-38 ms (P<0.01). Adenosine was also given to 10 patients with S2 introduced at a coupling interval 40-50 ms less than the baseline effective refractory period. This resulted in a decrease in atrial refractoriness and capture of S2 in all cases. Latency for S2 was significantly greater than Si latency (21+/-12 vs. 9+/-2 ms, P<0.01) and transient atrial arrhythmias were induced in 9 of 10 patients. We conclude that for a given S2 coupling interval, adenosine decreases local stimulus-response latency but increases atrial vulnerability to transient atrial arrhythmias. Decreased latency may be related to a shift in the zone of relative refractoriness associated with an adenosine-mediated decrease in monophasic action potential duration. Induction of atrial arrhythmias in the presence of adenosine occurs independently of increased latency and is therefore not dependent on S2 falling within the relative refractory period at the site of stimulation.

QT dispersion in premature beats produced by extrastimuli from the right atrium and right ventricle

The difference between the maximum and minimum QT interval measured from a 12-lead electrocardiogram was defined as an index of spatial inhomogeneous repolarization of the ventricular myocardium. The causal relationship between QT dispersion and incidence of ventricular arrhythmias has been pointed out in various heart diseases, but until now it was discussed mainly related to sinus rhythm. QT dispersion in extrasystole may be more important in the development of arrhythmias. We examined 5 cases (mean age 34 +/- 12 years) with a history of paroxysmal supraventricular tachycardia, who underwent electrophysiologic study. Both atrial and ventricular premature stimuli were given at a basic cycle length of 600 msec respectively. The QT interval and the ventricular activation time (VAT) (period from premature test stimulus to the summit of QRS) of the premature beats were measured in a simultaneously recorded 12-lead electrocardiogram. QT dispersion (the difference between the longest QT interval and the shortest QT interval) and VAT dispersion (the difference between the longest VAT and the shortest VAT) were measured. In atrial premature beats, there were no significant changes in the QT dispersion or VAT dispersion when the coupling interval of the premature beats was shortened. In the ventricular premature beats, however, both the QT dispersion and the VAT dispersion tended to increase with the shortening of the coupling interval. We concluded that only a short coupled ventricular premature beat induces greater QT and VAT dispersion. A ventricular couplet with short coupling interval may contribute to the development of ventricular tachyarrhythmias.

724-6 Resetting Responses During Atrioventricular Nodal Reentrant Tachycardia Suggest an Anisotropic Mechanism

We hypothesized that an anatomically determined circuit should have an identical excitable gap regardless of the site of stimulation, while a functional anisotropic circuit could show differences depending on stimulation site. In order to explore the nature of the reentrant circuit, and to characterize the excitable gap during atrioventricular nodal reentrant tachycardia (AVNRT), we determined the resetting response patterns in eight patients with typical AVNRT (meantachycardia cycle length (TCl) 346 ± 18 msec). Premature atrial stimuli were delivered during tachycardia from the area of the slow pathway (SPI in 7 patients, the fast pathway (FP) in 6 patients, and the ventricle (V) in 7 patients and the subsequent return cycles (As-Ar) were analyzed. In all patients, two or more sites were stimulated. Ventricular extrastimulation employed double extrastimuli such that the first extrastimulus did not interact with the circuit and acted as a conditioning stimulus. The excitable gap was defined as the range of coupling intervals from first reset to tachycardia termination. Duration of Excitable Gap (msec) by Stimulation Site Patient 1 2 3 4 5 6 7 8 Mean %TCL FP 10 * 65 20 30 20 10 * 26 ± 21 7 SP 35 80 90 40 * 20 20 20 43 ± 30 12 V 35 75 45 * 50 50 10 20 42 ± 19 12 AVNRT could be reset from the atrium and from the ventricle at all sites studied. In all cases, when the coupling intervals of premature extrastimuli were plotted against the return cycle (As-Ar), an increasing resetting response pattern was obtained. There was no decremental conduction over the retrograde FP with V stimulation. 1) The reentrant circuit of AVNRT can be reset from multiple sites. 2) The circuit as a whole demonstrates partial excitability with heterogenicityof conduction over individual pathways. 3) A difference in the measured excitable gap of &gt; 20 msec dependent on stimulation site was seen in 5/8 patients and suggests a functionally determined circuit and anisotropic reentry.

Effects of adenosine on atrial refractoriness and arrhythmias

Transient atrial fibrillation is sometimes observed following adenosine administration and adenosine is known to shorten atrial action potential duration and refractory period. This study was designed to characterise the dose-response relationship of adenosine on these variables relative to arrhythmia induction with single atrial premature stimuli. The effects of adenosine during sustained atrial flutter were also determined. Intravenous bolus doses of adenosine were given to pentobarbitone anaesthetised dogs following cervical vagotomy and autonomic blockade with atropine and nadolol. Monophasic action potential catheter recordings were obtained from the right atrium and a programmable stimulator was used for pacing. Placebo had no effect on monophasic action potential duration (MAPD) or atrial effective refractory period (ERP) and no arrhythmias were observed. Adenosine (0.1-1.0 mg.kg-1) produced dose related decreases in MAPD and ERP and transient atrial fibrillation (5-122 s) was repeatedly and reproducibly induced in 12 dogs. In six dogs, intravenous dipyridamole (0.25 mg.kg-1) enhanced the effects of adenosine on MAPD and ERP and increased the incidence of atrial fibrillation. In another six dogs, 8-sulphophenyltheophylline (5.0 mg.kg-1, intravenously) markedly blunted the effects of adenosine, and atrial fibrillation could no longer be induced by premature stimuli. In a separate series of experiments the effects of adenosine were evaluated in seven dogs in which sustained atrial flutter could reproducibly be induced by rapid atrial pacing. Administration of placebo never caused termination of the arrhythmia, whereas intravenous boluses of adenosine (0.1-1.0 mg.kg-1) decreased and produced variation in atrial flutter cycle length, and then terminated the arrhythmia in all cases. These effects of adenosine were also enhanced by dipyridamole and antagonised by 8-sulphophenyltheophylline. Adenosine produces a receptor mediated shortening of monophasic action potential duration and refractoriness which increases vulnerability to transient atrial arrhythmias. During sustained atrial flutter, these effects may also contribute to destabilisation and termination of the arrhythmia.

Site of accessory pathway block after radiofrequency catheter ablation in patients with the Wolff-Parkinson-White syndrome.

Recent studies have demonstrated that the most common site of accessory pathway conduction block following the introduction of a premature atrial stimulus during atrial pacing is between the accessory pathway potential and the ventricular electrogram, consistent with block at the ventricular insertion of the accessory pathway. However, no prior study has evaluated the site of conduction block during radiofrequency catheter ablation procedures. Therefore, the objective of this study was to determine the site of conduction block after catheter ablation of accessory pathways by analyzing and comparing the local electrograms recorded before and after radiofrequency energy delivery at successful ablation sites. The electrograms evaluated in this study were obtained from 85 consecutive patients who underwent successful radiofrequency catheter ablation of a manifest accessory pathway. The 50 left free-wall accessory pathways were ablated using a ventricular approach and the 35 right free-wall or posteroseptal accessory pathways were ablated using an atrial approach. The characteristics of local electrograms recorded immediately before and immediately after successful ablation of the accessory pathway were determined in each patient. The site of accessory pathway block was determined by comparing the amplitude, timing, and morphology of the local electrograms at successful sites of radiofrequency catheter ablation before and after delivery of radiofrequency energy. A putative accessory pathway potential was present at the successful target site in 74 of the 85 patients (87%). Conduction block occurred between the atrial electrogram and the accessory pathway potential in 66 patients (78%) and between the accessory pathway potential and the ventricular electrogram in eight patients (9%). The site of block could not be determined in 11 patients (13%) in whom an accessory pathway potential was absent. Conduction block occurred most frequently between the atrial electrogram and the accessory pathway potential regardless of accessory pathway location. No electrogram parameter or accessory pathway characteristic was predictive of the site of conduction block. The results of this study demonstrate that conduction block occurs most frequently between the local atrial electrogram and the accessory pathway potential during radiofrequency catheter ablation of accessory pathways. This is true regardless of whether the accessory pathway is ablated from the atrial or ventricular aspect of the mitral or tricuspid annulus.

Activation patterns in experimental canine atrial flutter produced by right atrial crush injury

Objectives. This study was designed to localize and characterize the atrial flutter reentrant circuit and the electrophysiologic effects of right atrial crush injury in a new canine model.Background. In previous studies sustained atrial flutter was induced in the canine heart by rapid atrial pacing after a linear crush injury was placed in the right atrial free wall.Methods. Eight dogs (group 1) with three electrode plaques on the right and left atria and Bachmann's bundle and seven dogs (group 2) with a single high density electrode plaque on the right atrium were studied with use of a 64-channel computerized mapping system.Results. At baseline, during sinus rhythm and right and left atrial pacing, activation spread uniformly without areas of slow conduction. Crush injury produced marked conduction delay or complete block during sinus rhythm, increasing the mean difference in activation times across the injury compared with control values (group 1, 31 ± 4 vs. 14 ± 5 ms, p < 0.01; group 2, 28 ± 10 vs. 7 ± 2 ms, p < 0.01). Rapid atrial pacing (S1S1200 ms) above and below the crush injury revealed a line of complete block across which adjacent electrodes recorded markedly different activation times (33 ± 5 and 38 ± 12 ms difference, respectively) and around which activation wave fronts proceeded, colliding opposite the stimulating electrodes, The mean atrial flutter cycle length of 11 episodes induced in group 1 and 14 episodes in group 2 was 157 ± 16 and 140 ± 16 ms, respectively (p = NS). Activation mapping revealed a reentrant circuit in the right atrium around the crush injury in all episodes. Although the reentrant circuit did not contain a discrete area of slow conduction, activation time below was longer than that above the crush injury (92 ± 14 vs. 66 ± 8 ms and 82 ± 12 vs. 59 ± 9 ms in groups 1 and 2, respectively, p < 0.01 for both). Rapid atrial pacing or premature stimuli produced progressive conduction delay and unidirectional block between the crush injury and the tricuspid anulus, inducing atrial flutter directly in 9 of 25 episodes. In 16 episodes, atrial flutter developed after transient induction of atrial fibrilation.Conclusions. 1) Atrial flutter in this model is due to reeentry in the right atrium; 2) the crush injury functions as an anatomic obstacle around which reentry may occur; and 3) the reentrant circuit does not contain a discrete area of slow conduction but, rather, generally slower conduction below the crush injury.

Effects of Verapamil on Postextrasystolic Potentiation

To assess the effects of verapamil on postextrasystolic potentiation (PESP), contrast left ventriculography was performed in ten healthy anesthetized dogs before and after the intravenous administration of verapamil, 0.1 mg/kg. During the contrast ventriculography, a single atrial premature stimulus was introduced. Ejection fractions of a control beat and postpremature beat were measured before and after verapamil. Before verapamil, the mean ejection fractions of the control beat and the postpremature beat were 60 +/- 10 percent and 67 +/- 10 percent, respectively (p less than 0.05). Following the administration of verapamil, the mean ejection fraction of the control beat decreased from 60 +/- 10 percent to 55 +/- 11 percent (p less than 0.05). However, the mean ejection fraction of the postpremature beats increased when compared with the control beats following intravenous verapamil (65 +/- 8 percent and 55 +/- 11 percent, respectively; p less than 0.05). These results suggest that PESP is not inhibited by the administration of intravenous verapamil.

Lack of prognostic implications of spontaneously occurring or stimulation induced atrial tachyarrhythmias in patients with dilated cardiomyopathy.

A prospective study was undertaken in 102 patients with idiopathic dilated cardiomyopathy to assess the significance of spontaneous and inducible atrial tachyarrhythmias (ATA). Twenty-six patients were in chronic atrial fibrillation (group I) and 76 patients were in sinus rhythm (group II); 14 patients in group II had a clinical history of ATA or episodes of ATA during Holter monitoring. An electrophysiological study was systematically performed. Programmed atrial stimulation was carried out in group II, and used up to two atrial premature stimuli from the right atrium at 2 cycle lengths (sinus cycle length--10%, 600 ms) and then one atrial extrastimulus under infusion of 1 to 4 micrograms. min-1 of isoproterenol. Programmed ventricular stimulation was performed in groups I and II. Sustained atrial tachyarrhythmia (ATA) was induced in 33 patients in group II (42%); isoproterenol infusion facilitated the induction of ATA in only one other patient, who had exercise-related ATA. Eleven patients in group II with spontaneous ATA had inducible sustained ATA. The sensitivity of programmed atrial stimulation to reproduce an ATA was 78.5% and its specificity 64.5%. Inducible ATA was related to a shorter atrial effective refractory period (209 +/- 25 ms vs 228 +/- 32, P less than 0.02). Inducible and spontaneous ATAs were related to older age but not to the existence of spontaneous or inducible ventricular tachycardia; they did not have prognostic significance: the left ventricular ejection fraction and the prognosis were similar in patients with spontaneous or inducible ATA and those without ATA.(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence suggesting time-dependent recovery of excitability in the in vivo human sinus node

The sinus node (SN) possesses the properties of automaticity and conduction. Automaticity arises in its dominant and latent pacemaker cells and results from both time and voltage-dependent ionic currents as shown by in vitro studies. 1,2 Conduction is required for propagation of the generated impulse. Both automaticity and conduction can be assessed in vivo by way of clinical electrophysiologic studies, as well as in vitro. 3,4 The SN also displays excitability; i.e., the ability for an action potential to be produced by an applied stimulatory current. 1,2 In the SN, in vitro studies have shown that the recovery of excitability, the ability of a cell to be reexcited by a subsequent application of current, is also both voltage-dependent, typical of all cardiac tissues, and time-dependent, characteristic of only “slow response” fibers. 1,2 Time-dependent recovery outlasts voltage-dependent recovery; thus, SN cells cannot be reexcited by a stimulatory current (are “refractory”) despite a return of membrane potential to baseline voltage until time-dependent recovery has also been achieved. 1,2 Unlike automaticity and conduction, recovery of SN excitability has not been directly studied in humans since clinical electrophysiologic studies have not encompassed the ability to directly stimulate the SN and verify such stimulation. Nevertheless, one might expect that similar mechanisms would be operative in vivo as in vitro. In the 1980s, 2 developments occurred which bear on the ability to assess excitability in vivo. The first was the recognition and verification that SN refractoriness could be studied through retrograde activation 5–8 (i.e., the responses to atrial premature stimuli can be analyzed to determine the coupling interval at which retrograde penetration of the SN is lost and the complexes become interpolated). Interpolation has been shown to occur when SN refractoriness is encountered. 5 The second was the development of SN electrography 9–12 and the documentation that the extracellular, transcatheter SN electrogram truly reflects the action potentials occurring in the underlying SN. We believe these 2 developments could be combined to indicate whether time-dependent recovery of SN excitability exists in vivo. If SN refractoriness outlasts the voltage excursions of the SN depolarization on the SN electrogram, time dependence of recovery of excitability is suggested.

Atrial conduction: Effects of extrastimuli with and without atrial dysrhythmias

The effects of cycle length and stimulation site on intraatrial conduction and refractoriness were evaluated in patients with and without atrial flutter (AFI) or fibrillation (AF) using the extrastimulus technique. Nineteen patients with spontaneous sustained AFI or AF were compared with 19 control patients. Programmed stimulation was performed at the right atrium and coronary sinus at drive cycle lengths of 600 and 450 ms. The atrial effective refractory period was similar in the patients with atrial dysrhythmias and the control group. The right atrial effective refractory period at a drive cycle length of 600 ms was significantly shorter in patients with AF (211 ms) than in patients with AFI (235 ms, p = 0.05). The conduction time of late (coupling intervals more than 50% of the drive cycle length) premature impulses was similar in the patients with atrial dysrhythmias and the control group. However, early extrastimuli (coupling intervals less than 50% of the drive cycle length) at a drive cycle length of 600 ms produced significantly more intraatrial conduction delay in the patients with atrial dysrhythmias than in the control patients. At a drive cycle length of 450 ms, similar delays in intraatrial conduction occurred in the patients with and without atrial dysrhythmias because of an increase in the maximal-observed intraatrial conduction delay in the control patients. This study shows that delay in conduction of early premature atrial stimuli at a drive cycle length of 600 ms is a marker of patients with spontaneous AFI and AF.(ABSTRACT TRUNCATED AT 250 WORDS)

Dual atrioventricular nodal pathways associated with a gap phenomenon in atrioventricular nodal conduction

A 67 year old man underwent electrophysiologic study for evaluation of syncope. During atrial pacing at a basic cycle length of 600 ms, atrial premature stimuli were introduced at progressively shorter coupling intervals. The graph of atrial coupling intervals versus corresponding His bundle responses revealed an abrupt increase in atrioventricular (AV) nodal conduction time with coupling intervals from 320 to 340 ms. In an atrial coupling interval of less than 320 ms, conduction was again rapid until the effective refractory period of the atrium was reached. These unique findings are compatible with dual pathways and a gap phenomenon within the AV node.