Critical Cycle Length Research Articles

A comparative study on pantograph-catenary models and effect of parameters on pantograph-catenary dynamics under crosswind

This paper is aimed at selecting a suitable pantograph-catenary model for investigations under crosswind and investigating parameter influences on pantograph-catenary dynamics, including the friction, the rising angle, the value of zigzag and the sliding plate irregularity. One spatial-beam pantograph model is proposed and its governing equations are obtained. Combining with the catenary, the 3-D pantograph-catenary model is established. Comparing with the other models, the 3-D pantograph-catenary model is more probable to obtain accurate results in the standard deviation (STD) of the contact force and the rate of contact loss (RCL) under crosswind. Based on it, the effects of parameters mentioned above are discussed. The calculation results indicate that the friction affects little on mean contact force and STD of the contact force but greatly on RCL when the crosswind attack angles are large. This great effect on RCL depends on the directions of crosswind and the rising angle. The larger value of zigzag means smaller STD of the contact force and larger RCL. There is a critical cycle length corresponding to a certain wear depth. Less than it, the pantograph-catenary interaction may well be tremendous. Severe wear and crosswind can lengthen the critical cycle length.

Real-time Traffic Signal Settings at an Isolated Signal Control Intersection

In this paper, we present a method for traffic signal control including simultaneously signal plan design and signal timing optimization with real-time information on the network dynamics. The problem is formulated so as to find the signal plan design, the green and inter-green time for each signal group in response to recurrent traffic flow demand at an intersection. The approach used was the group-based Akçelik method for determining critical path, cycle length and green time split for each possible signal plan design. The signal plan design selection was formulated to minimize the total delay.The resulting algorithm was coded in Java and used TraSMAPI to dynamically link it to Aimsun's API, which allows an automatic change of the signal settings at an isolated signal control intersection.A theoretical three arms intersection with a time varying origin-destination demand example is tested to demonstrate the proposed method.The paper contributes to the development of an integrated design of signal plan design and signal timings. The proposed method aims to be sufficiently general for its application in different networks, with few inputs dependent on the local geometry layout. This strategy is able to react to non-schedulable events or unpredictable events without requiring human manipulation.

Sensitivity analysis of optimization models for isolated intersections with short left‐turn lanes on approaches

SUMMARYShort left‐turn lanes are often channelized to improve capacity and level of service at signalized intersections. On the basis of previous achievements, this paper improves the joint optimization models for isolated signalized intersections with short left‐turn lanes and aims to analyze the sensitivity of the optimization results to the parameters (critical cycle length and maximum short‐lane length). To further clarify the effects of these models on traffic flow operations, several better optimization scenarios are simulated together with the existing one. The models and the methods are illustrated via the field data from Dalian, China. According to the analysis results, the optimum models and parameter values or ranges are recommended. Finally, the procedure of the model application is also proposed to apply in practice. Copyright © 2012 John Wiley & Sons, Ltd.

Atrial fibrillatory cycle length: computer simulation and potential clinical importance

Atrial fibrillatory cycle length (AFCL) is generally accepted as a surrogate marker for local refractoriness. In this study, a computer model and clinical data on human subjects undergoing catheter ablation for paroxysmal and persistent AF were used to determine the clinical potential of AFCL. Simulations were performed in a biophysical computer model of AF, induced from eight simultaneously active focal sources. Atrial fibrillatory cycle length persistence and termination were assessed in response to successively switching off the involvement of the eight sources. Electrophysiological data were obtained from 178 subjects undergoing catheter ablation of AF. Atrial fibrillatory cycle length, measured in the atria appendages using automated monitoring software, was studied to determine its clinical correlation, the complexity of the ablation procedure, and the AF termination success rate. Computer simulations showed an inverse relationship between the number of sources participating in AF maintenance and AFCL. Clinical data demonstrated a strong relationship between duration, degree of ablation, and AFCL, with shorter AFCL associated with more extensive ablation to terminate AF. Atrial fibrillatory cycle length was prolonged exponentially at each stage, with a critical cycle length of approximately 200 ms for AF conversion. Atrial fibrillatory cycle length is inversely associated with the number of sources participating in AF maintenance observed in the computer model. In addition, AFCL is an important predictor of baseline duration of the arrhythmia, type of AF, and ease of catheter ablation therapy to terminate AF.

Serial Cardioversion by Class IC Drugs During 4 Months of Persistent Atrial Fibrillation in the Goat

The success rate of pharmacological cardioversion of atrial fibrillation (AF) in patients depends on the duration of AF. It is unknown to what extent AF-induced structural atrial remodeling contributes to this loss of efficacy. In 10 goats, persistent AF was induced by repetitive burst pacing. During a time period of 16 weeks, the efficacy of flecainide and cibenzoline to cardiovert AF was investigated by serial cardioversion. The drugs were administered intravenously at a rate of 0.1 mg/kg/min. AF cycle length (AFCL) was continuously monitored. Drug infusion was continued until AF was successfully cardioverted or the QRS duration was prolonged about twofold. The average atrial cycle length during persistent AF was 104 +/- 10 msec and did not change during the 16-week period. The success rate of cardioversion by flecainide and cibenzoline decreased with the duration of AF from 60% to 17% and from 80% to 63%. In goats that failed to cardiovert, sinus rhythm was not restored despite a twofold prolongation of the AF cycle length (respectively from 96 +/- 5 msec to 168 +/- 30 msec (flecainide) and 203 +/- 26 msec (cibenzoline)). The sensitivity of AF for Class IC drugs was not altered with time, and the dose-dependent effect on AFCL remained the same (flecainide: 8 +/- 5 vs 7 +/- 2 msec/mg/kg (P = 0.70) and cibenzoline: 13 +/- 3 vs 13 +/- 5 msec/mg/kg (P = 0.95)). In animals in which cardioversion remained possible, the critical AFCL at which cardioversion occurred increased from 96 +/- 5 msec to 211 msec (flecainide) and 189 +/- 24 msec (cibenzoline). The progressive loss of efficacy of Class IC drugs to cardiovert AF of longer duration is not due to a decrease in the sensitivity of remodeled atrial myocardium for Class IC drugs. Failure of cardioversion was due to an increase in the critical AF cycle length required for pharmacological cardioversion.

Variability of AV nodal potentials recorded, in vivo: direct demonstration of dual AV nodal physiology.

We developed a method to record extracellular A-V nodal potentials in the beating dog heart, in vivo. In eleven Na-pentobarbital anesthetized, open-chest dogs, an octapolar electrode catheter (2 mm rings, 2 mm spacing) was inserted through a purse-string suture in the coronary sinus (CS) distal to the ostium and positioned electrographically so that the tip electrode recorded a His bundle (Hb) potential. Stable recordings of A-V nodal potentials (amplitude, 178 +/- 94 microV; duration 78 +/- 26 msec) were consistently made during sinus rhythm from the second and/or third bipolar pairs of electrodes. Programmed atrial stimulation and vagal stimulation resulted in loss of amplitude and increased duration of the A-V nodal potentials associated with A-H prolongation. In another series of experiments, crushing the sinus node in 6 dogs resulted in AV nodal rhythms with AV nodal potentials of varying amplitudes (132 to 840 microV) and durations (range 25 to 71 msec) as the earliest activation which preceded the Hb, atrial and ventricular deflections. One dog, showing dual AV nodal physiology as documented from the AV nodal function curve, had two distinctly different AV nodal potentials. The low-level, longer duration potentials were associated with longer (slow pathway) A-H intervals; whereas the shorter higher amplitude potentials (fast pathway) showed shorter A-H intervals, each occurring at a critical paced cycle length. We conclude that consistent extracellular AV nodal electrograms can be recorded in vivo although the configuration of these potentials varies depending on heart rate, autonomic stimulation and different arrhythmic conditions such as AV nodal escape rhythms and dual AV nodal physiology.

Abrupt loss of constant fusion during entrainment of ventricular tachycardia at a critical paced cycle length.

Sustained monomorphic ventricular tachycardia (VT) can be frequently entrained and interrupted with rapid pacing and the mechanism of the pacing-induced interruption is considered to be due to orthodromic block. This study focused on the incidence of VT which was interrupted at a critical cycle length and was characterized by an abrupt loss of constant fusion in the surface electrocardiogram (ECG), and the role of orthodromic block as the cause of such characteristic change and interruption of VT was analyzed. Among 45 consecutive patients with symptomatic VT, rapid pacing was performed in 43 VTs of 39 patients. The exit was mapped as the earliest site of the activation during VT and an electrode catheter was located at the site. Rapid pacing was performed at progressively shorter cycle lengths in steps of 10 msec until VT was interrupted and the timing of the orthodromic and direct capture was compared at the exit. Abrupt loss of constant fusion was observed in 25 of 39 patients (64.1%): and the loss was invariably associated with interruption of VT. When the timings of the activation of the exit were compared, which were measured from the preceding (n-1) stimulus as the time reference, the direct capture was relatively delayed compared to that of the orthodromic capture. This finding suggests that orthodromic block is the cause of the direct capture as well as the pacing-induced interruption of VT. In the remaining 13 patients (35.9%), the surface ECG showed a gradual transition into the fully paced QRS morphology. The direct capture was confirmed in the non-fused beats, but it was not necessarily associated with interruption of VT. The interval from the stimulus to the entrained electrogram at the exit showed a gradual prolongation until the exit was finally captured directly from the pacing site. The confirmation of constant fusion followed by abrupt loss in ECG can be a reliable hallmark of orthodromic block as the cause of the interruption of VT during transient entrainment at a critical paced cycle length.

Cardiac alternans: mechanisms and pathophysiological significance.

Time for primary review 31 days. Mechanical alternans (pulsus alternans) is a condition in which there is a beat-to-beat oscillation in the strength of cardiac muscle contraction at a constant heart rate. Since the first description of pulsus alternans by Traube in 1872 [1], there has been continuing interest in understanding the mechanisms and clinical manifestations of this phenomenon [2,3]. Initially observed in the hearts of laboratory animals, the phenomenon has been reported frequently in patients particularly those with severe heart failure and aortic valve disease. Although much is known about the cellular mechanisms of alternans in isolated cardiac muscle preparations, little is known about the mechanisms by which changes in preload or afterload evoke alternans in the intact heart. The purpose of this review article is to discuss the mechanisms of alternans at both the cellular level and in the intact heart. The relationship between mechanical and electrical alternans is reviewed. The role of sympathetic nervous system is discussed as a means of protecting the heart from alternans during accelerations of heart rate. Since pulsus alternans has been reported in patients with cardiac disease, the diagnostic and prognostic significance of mechanical and electrical alternans is also discussed. The ability to induce mechanical alternans by rapid driving frequencies appears to be a fundamental property of mammalian ventricular muscle. Experimental studies have shown that by varying the pacing cycle length over a wide range, it is possible to define a critical cycle length (threshold) for the induction of sustained mechanical alternans [4–7]. Driving the heart at cycle lengths shorter than the threshold cycle length may increase the amplitude of the beat-to-beat oscillations in contraction strength (Fig. 1). Driving the heart at cycle lengths just longer than the threshold may produce transient alternans [4,6]. Transient alternans may also … * Tel.: +1-612-315-2155; fax: +1-612-315-2199

Effects of class I and III antiarrhythmic drugs on ventricular tachycardia-interrupting critical paced cycle length with rapid pacing.

The most common mechanism of sustained ventricular tachycardia (VT) is re-entry with an excitable gap, but the electrophysiologic properties and response to antiarrhythmic drugs in the area of slow conduction are not yet fully known. The purpose of this study was to assess the effects of a class I antiarrhythmic drug (procainamide) and class III agents (amiodarone, E-4031, and MS-551) on re-entrant VT using the width of the zone of entrainment. The cycle length (CL) of VT (VTCL), the block CL that was the longest paced CL that interrupted the VT, and the width of the zone of entrainment, defined as the difference between VTCL and block CL, were compared before and after treatment with antiarrhythmic drugs. The VTCL was prolonged significantly from 308+/-63 to 410+/-77 msec after procainamide (p<0.005) but was not changed after the administration of the class III agents: from 294+/-50 to 292+/-13 msec after amiodarone, and from 305+/-47 to 313+/-31 msec after E-4031 or MS-551 (p=NS). The block CL was prolonged from 255+/-61 to 331+/-70 msec after procainamide (p <0.01), from 256+/-20 to 260+/-25 msec after amiodarone, and unchanged after E-4031 or MS-551 (253+/-31 msec before and 270+/-43 msec after) (p=NS). The width of the zone of entrainment as a representative of the width of the excitable gap was changed from 52+/-26 to 79+/-35 msec (p<0.05) after procainamide, whereas it was unchanged after amiodarone (48+/-7 msec before and 43+/-7 msec after) and after E-4031 or MS-551 (50+/-10 msec before and 40+/-9 msec after). Therefore, amiodarone, E-4031, and MS-551 did not affect VTCL and block CL whereas procainamide increased these parameters. The excitable gap substituting as the zone of entrainment was increased by procainamide but slightly reduced by amiodarone, E-4031, and MS-551. The effects of these antiarrhythmic drugs on the excitable gap of re-entrant VT were variable and should be examined further.

Contraction-excitation feedback in human atrial fibrillation.

Contraction-excitation feedback, that is, electrophysiologic changes that are caused or preceded by mechanical changes of the myocardium, has been extensively studied in the ventricles. The role of contraction-excitation feedback in the atria, and more particularly in the genesis and maintenance of atrial fibrillation, has been less adequately investigated. The aim of the present study was to determine whether increased right atrial pressure (RAP) facilitates the induction of atrial fibrillation (AF) in patients with a history of lone AF. Sixteen patients with a history of paroxysmal AF but without structural heart disease were included in the study. All patients underwent electrophysiologic study at both a lower (3.1 +/- 2.0 mmHg) and (in 13 cases) a higher (6.4 +/- 2.5 mmHg) RAP. "Higher" was considered the pressure following rapid (in about 30 min) intravenous administration of normal saline or before the administration of a diuretic. Rapid atrial pacing induced AF in 19 of 29 attempts. At a lower pressure, rapid pacing induced brief (3 s to 3 min) AF in 3 of 16 patients, long-lasting (> 3 min) AF in 3 of 16 patients, and no AF in 10 of 16 patients. At a higher pressure, brief AF was induced in 3 of 10 patients in whom no AF could be induced at a lower pressure, and long-lasting AF in 10 patients in whom either brief AF (3 cases) or no AF (7 cases) was induced at a lower pressure. In 11 patients, in whom Wenckebach periodicity was determined at both higher and lower pressure, the critical cycle length at which atrioventricular block appeared was significantly (p < 0.001, paired t-test) longer (349.1 +/- 44.4 ms, i.e., +15.5 +/- 11.3 ms) at higher than at lower atrial pressure (333.6 +/- 41.0 ms). In nine patients, in whom Wenckebach periodicity was determined and two rhythms occurred at different pressures, the critical cycle length was 332.2 +/- 45.8 ms when associated with sinus rhythm, and significantly (p < 0.01) longer (344.4 +/- 48.0 ms, i.e., +12.2 +/- 8.3 ms) when associated with induction of AF. In patients with lone atrial fibrillation, modest increases in atrial pressure may facilitate the induction of atrial fibrillation.

Discrepant effects of mexiletine on cycle length of ventricular tachycardia and on the effective refractory period in the area of slow conduction.

Monomorphic sustained ventricular tachycardia (VT) can often be entrained and interrupted at a critical paced cycle length. The aim was to evaluate a possible determinant of this phenomenon by observing the action of mexiletine on the critical paced cycle length and other variables. Nine consecutive patients with symptomatic VT were studied. After induction of VT, the area of slow conduction was mapped as the earliest site of the activation or the site with mid-diastolic potential during the tachycardia. Rapid pacing was performed at a site distant from the tachycardia circuit to entrain the tachycardia, starting at a cycle length 10-20 ms shorter than the VT cycle length, and repeated after a decrement of the cycle length in steps of 10 ms to obtain the longest paced cycle length that interrupted the tachycardia: the block cycle length. The effective refractory period (ERP) was measured at the pacing site at which the myocardium was presumed to be normal and also in the area of slow conduction. The effects of mexiletine on the cycle length of VT, the block cycle length, and the ERP at two sites were obtained before and after mexiletine administration. The relation between the cycle length of VT and block cycle length and their changes were also analysed. 11 VTs with the same morphology were induced before and after mexiletine administration. The VT cycle length was prolonged by mexiletine from 309 (SD 53) to 361 (47) ms, and it was interrupted at block cycle lengths of 247 (37) and 307 (41) ms, respectively, the changes being 18 (12)% and 23 (8)% (both P < 0.001). All VTs were entrained, and during pacing at the block cycle length there was abrupt loss of fusion and change in the presystolic electrogram, always associated with interruption of VT on cessation of rapid pacing. A good correlation was observed between the VT cycle length and the block cycle length (r = 0.77 to 0.80). The ERP at the pacing site (normal myocardium) and in the area of slow conduction showed no significant change: 241 (21) v 240 (22) ms and 262 (9) v 252 (9) ms, respectively. The block cycle length was longer than the ERP after mexiletine administration: 362 (55) v 252 (9) ms (P < 0.02). Mexiletine prolonged the cycle length of VT and the VT-interrupting critical cycle length but not the ERP. The prolongation of the VT cycle length and the block cycle length by mexiletine seemed to be unrelated to the action potential duration, but related to depressed intercellular conduction.

Characterization of return cycle responses predictive of successful pacing-mediated termination of ventricular tachycardia

Objectives. The purpose of this study was to characterize response patterns during overdrive pacing that predict successful termination of ventricular tachycardia.Background. Overdrive pacing during ventricular tachycardia typically results in entrainment at slow pacing rates and in termination or acceleration at faster rates. The factors that determine the critical paced cycle length that results in tachycardia termination have not been extensively studied.Methods. Ventricular tachycardias in 14 patients with coronary artery disease were studied with overdrive pacing at several cycle lengths. Return cycles were measured after each additional paced beat at each paced cycle length. The return cycle responses during pacing trials that resulted in tachycardia termination and those that resulted in entrainment were compared.Results. Three return cycle responses were identified: flat, plateau and increasing. Twenty trials of overdrive pacing resulted in tachycardia termination; all were characterized by an increase in the return cycle with the delivery of each successive beat in the pacing drive until the tachycardia terminated (increasing response). Thirty-four pacing trials resulted in entrainment and not termination; these were characterized either by a constant return cycle (flat response) or an initial increase in return cycle followed by a longer, constant return cycle (plateau response) with the delivery of additional paced beats. The longest paced cycle length that resulted in tachycardia termination correlated with the relative refractory period of the circuit, defined as the tachycardia cycle length minus the fully excitable gap (r2= 0.764, p = 0.0001). Tachycardia termination was not observed unless the paced cycle length was shorter than the relative refractory period of the circuit.Conclusions. The critical paced cycle length that causes termination of ventricular tachycardia depends on the relative refractory period of the circuit because this factor determines whether the nth + 1 beat of the pacing drive will encounter partially recovered tissue. These data provide insights into the mechanism of pacing-mediated tachycardia termination and entrainment and are applicable to the development of improved antitachycardia pacing algorithms.

Procainamide-induced changes in reentrant ventricular tachycardia with special reference to the tachycardia-interrupting critical paced cycle length during transient entrainment with rapid pacing.

With rapid ventricular pacing, sustained ventricular tachycardia (VT) is often entrained and interrupted at a critical paced cycle length. In this paper, the possible mechanism and determinant of the critical cycle length interrupting VT are addressed. Sixteen consecutive patients underwent rapid ventricular pacing in 18 morphologically distinct sustained VTs before and after procainamide. The VT morphology was identical before and after the drug. The VT origin was determined by endocardial mapping as the earliest site of activation of VT and an electrode catheter was located at the site. Rapid pacing was performed to entrain VT and repeated in 10 msec decrements of cycle length until VT was interrupted at a critical paced cycle length which was defined as the block cycle length. The effective refractory period was measured at the pacing site. The paced QRS duration and the local conduction time were measured and used as indices of conduction time in the normal myocardium. VT was entrained and interrupted in all patients. At the block cycle length, initial constant fusion was replaced abruptly by the fully paced QRS complex. At the same time, the local electrogram at the site of VT origin showed changes in the morphology and the timing of activation which were identical to those of the fully paced beat. This loss of fusion and the changes in the local electrogram were considered to be a result of orthodromic block and the block cycle length was assumed to represent the cycle length at which 1:1 conduction fails in the area of slow conduction. After procainamide, both the VT cycle length and the block cycle length were prolonged to a similar degree (p < 0.001) but the relative degree of change varied from patient to patient. The paced QRS duration and the conduction time were prolonged by procainamide but in smaller degrees than the cycle length of VT or the block cycle length (p < 0.02-01). The effective refractory period at the pacing site and the QT interval showed small changes after procainamide. The postrepolarization refractoriness rather than the duration of action potential can be responsible for the procainamide-induced prolongation of the block cycle length, and the block cycle length might be used as a new index to characterize the electrophysiologic property of the VT circuit and also the action of antiarrhythmic drugs.

Early after/depolarizations and triggered activity: mechanisms and autonomic regulation.

An early after/depolarization (EAD) is an abnormality of the repolarization process of an action potential which causes an interruption or a retardation of normal repolarization. Two types were described: phase 3 EADs occur at a takeoff potential of approximately-60 mV and phase 2 EADs occur at the end of a prolonged plateau at a takeoff potential of between-10 and-30 mV. EADs can result from an increase in inward current, a reduction of outward current or both. EADs show cycle-length dependence: as cycle length increases and repolarization lengthens, EADs occur, and their magnitude increases, at a critical cycle length, can trigger the action potential of these EADs. The autonomic nervous system can also modulate EADs and trigger activity. In cesium-intoxicated Purkinje fibers, beta-adrenergic stimulation increases EAD magnitude and the occurrence of triggered activity. Cholinergic stimulation decreases EAD magnitude and suppresses triggered activity occurring after beta-adrenergic stimulation. Alpha 1-adrenergic stimulation has no effect on phase 3 EADs but induces phase 2 EADs. In normal Tyrode's solution (0 cesium), phenylephrine prolongs action potential and induces EADs. This effect seems to depend on alpha 1 A stimulation. These electrogenic abnormalities are supposed to be responsible for long QT and torsades de pointes. As our experimental data have shown that both the rate of stimulation and the autonomic nervous system could modulate EADs and trigger activity, we can speculate on the therapeutic implications of such modulations and the role of pacing as well as alpha- and beta-adrenergic antagonists.

Incidence and mechanism of interruption of reentrant ventricular tachycardia with rapid ventricular pacing.

Information concerning the electrophysiological characteristics of the reentrant circuit is still limited. To understand the incidence and mechanism of pacing-induced interruption of ventricular tachycardia (VT), rapid pacing was performed to entrain VT, and the local electrogram at the VT origin and the surface electrocardiogram were analyzed. Among 25 patients, evidence of transient entrainment was confirmed in 20 patients, but the critical paced cycle length at which VT was interrupted was obtained in 13 patients when the paced cycle length was decreased in steps of 10 msec. During pacing at the critical cycle length (defined as block cycle length), changes in the local electrogram at VT origin were confirmed in all of the 13 patients; that is, 1) a change in morphology and 2) a change in the timing of activation: a sudden shortening in the stimulus to local electrogram time (third entrainment criterion by Waldo). The two changes mean that the exit is activated from a different direction (retrograde capture) because of an orthodromic block in the slow conduction zone. The QRS complex in the surface electrocardiogram showed a change in configuration from the fusion complex to the fully paced one at the same time when the exit was captured antidromically. Based on our observations in these patients, ventricular tachycardia interruption is very often associated with orthodromic block in the reentrant circuit at a critical cycle length of rapid pacing.

Circus movement atrial flutter in canine sterile pericarditis model. Activation patterns during entrainment and termination of single-loop reentry in vivo.

Recently, we used a custom designed "jacket" electrode with 127 bipolar electrodes in a flexible nylon matrix to map the total atrial epicardial surface in the in situ canine heart. Atrial flutter in dogs with sterile pericarditis was shown to be due to a single wave front circulating around a combined functional/anatomic obstacle, with the arc of functional conduction block contiguous with one or more of the atrial vessels. In the present study, this model was used to analyze the activation pattern during pacing-induced entrainment and termination of single reentrant loops in a syncytium without anatomically predetermined pathways. Sustained atrial flutter was induced in five dogs with 3-5-day-old sterile pericarditis. Atrial pacing at a cycle length 5-30 msec shorter than the spontaneous cycle length entrained the arrhythmia and could result in a "classical" activation pattern, characterized by an antidromic stimulated wave that collided with the reentrant orthodromic wave front of the previous beat at a constant site. However, two variations of this classical activation pattern were also observed: 1) Pacing at short cycle lengths could lead to localized conduction block in antidromic direction, forcing a change in the pathway of the antidromic wave front. This could prevent the expected shift of the site of collision in antidromic direction. 2) The stimulated orthodromic wave front could also use a pathway different from that of the original reentrant impulse, so that a different circuit was active during the pacing period. Termination of atrial flutter by rapid atrial stimulation was associated with progressive slowing and finally blocking of the paced orthodromic wave front and a progressive shift of the site of collision in antidromic direction. The occurrence of conduction block was determined by the cycle length of stimulation and the number of stimulated beats. A longer train at the critical cycle length or the critical number of beats at a shorter cycle length could reinduce the same reentrant circuit or a different reentrant circuit, respectively, during stimulated cycles following the beat that terminated reentry. The epicardial activation sequence during entrainment of reentrant arrhythmias does not necessarily follow a standard activation pattern. Instead, the stimulated orthodromic as well as the antidromic wave front might use a pathway different from that of the original reentrant wave front. The mechanisms of termination, failure of termination, and reinitiation of single-loop reentry are similar to those in the "figure-eight" reentrant circuit.

Modification of atrioventricular node transmission properties by intraoperative neodymium-YAG laser photocoagulation in dogs

The purpose of this study was to test the feasibility of neodymium-yttrium-aluminum-garnet (Nd-YAG) laser photocoagulation of the atrioventricular (AV) node to control the ventricular rate during rapid atrial rhythms without creating AV block. In 12 dogs on normothermic cardiopulmonary bypass, short laser pulses were delivered to an area between the coronary sinus orifice and the site of the most proximally recorded His deflection until second degree AV block occurred at a paced atrial rate of 200 beats/min. Long-term effects on AV node function were followed up for 3 months. Three animals developed chronic high grade AV block. In nine animals with preserved 1:1 conduction, the mean (+/- SEM) critical atrial cycle length resulting in AV node Wenckebach periodicity increased from 183 +/- 6 to 261 +/- 24 ms (+43%), the mean RR interval during induced atrial fibrillation increased from 248 +/- 14 to 330 +/- 27 ms (+32%) and the shortest RR interval during atrial fibrillation increased from 215 +/- 11 to 275 +/- 20 ms (+28%). Laser effects were not reversed by isoproterenol infusion. Histologic examination of the irradiated area showed fibrotic changes in the AV node and fatty metamorphosis. This study suggests that 1) graded Nd-YAG laser photocoagulation of the AV node region in dogs results in long-term modification of anterograde AV node transmission properties; 2) 1:1 conduction during sinus rhythm usually remains preserved, but ventricular rate during rapid atrial rhythms is chronically reduced; and 3) progression to high grade AV block occurs in a minority of animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiologic effects of propranolol in intraventricular conduction disturbance

Sixteen patients underwent electrophysiologic studies before and after intravenous infusion of propranolol, 0.1 mg/kg. All of them had intraventricular conduction disturbances. A significant (p < 0.01) increase occurred after propranolol in the mean spontaneous cycle length (mean change 122 ms) and the AH interval (mean 28 ms). The HV interval did not change significantly. The effective refractory period of the His-Purkinje system increased in 4 of 5 patients (mean net change 44 ms, p > 0.10). In 7 patients with phase 3 infranodal block, the longest cycle length for producing block increased after propranolol in 5 and remained unchanged in 2 (mean increase 40 ms, p < 0.02). Two patients showed phase 4 atrioventricular block. Propranolol increased the critical cycle length by an average of 120 ms. Propranolol-induced bradycardia restored stable atrioventricular conduction in 2 patients with intermittent 2:1 block but facilitated the occurrence of high grade infranodal block in 1 patient. Thus, propranolol can impair His-Purkinje conduction in patients with preexisting infranodal abnormalities.

Reentrant Ventricular Arrhythmias in the Late Myocardial Infarction Period: 14. Mechanisms of Resetting, Entrainment, Acceleration, or Termination of Reentrant Tachycardia by Programmed Electrical Stimulation

The mechanisms of resetting, entrainment, acceleration, or termination of reentrant ventricular tachycardia by programmed electrical stimulation were studied in the canine post-infarction model. In this model, reentrant circuits were localized in the epicardial layer overlying the infarction and were accessible to detailed mapping by multiplexer techniques. The reentrant circuit has a characteristic figure-eight configuration in the form of two circulating wavefronts around arcs of functional conduction block that coalesce into a slow common reentrant wavefront. Termination of reentrant tachycardia occurred when a stimulated wavefront arrived earlier to a strategically located area in the proximal portion of the zone of slow conduction, before refractoriness expired distally, resulting in conduction block. The three factors that determined if the stimulated wavefront could reach this zone in time for conduction block were: the cycle length of stimulation; the number of stimulated beats; and the site of stimulation. The most optimal situation for stimulated termination of reentry was a critically coupled single stimulus applied to the ischemic zone close to the proximal side of the zone of slow conduction that captured locally and conducted prematurely to the strategic zone for conduction block. When a single stimulated wavefront failed to terminate reentry, one or more subsequent wavefronts succeeded. However, the stimulated train had to be terminated following the beat that interrupted reentry. Otherwise, a subsequent stimulated beat could reinitiate the same reentrant circuit or induce a different circuit. The new circuit could have a shorter revolution time, resulting in tachycardia acceleration, and occasionally degeneration into ventricular fibrillation. Overdrive termination of reentry required both a critical cycle length of stimulation and a critical number of beats in a stimulated train. Otherwise, the stimulated train could establish a new balance of refractoriness and conduction velocity in the reentrant pathway. This could perpetuate the reentrant process at the shorter cycle length of the stimulated train and spontaneous reentry would resume on termination of the train (entrainment). The study provides better understanding of the mechanisms of action of programmed electrical stimulation on reentrant ventricular tachycardia.

Determinants of sustained slow pathway conduction and relation to reentrant tachycardia in patients with dual atrioventricular nodal transmission

In 24 patients with dual atrioventricular (AV) nodal pathways, multiple incremental atrial pacing studies were performed to obtain atrial (A) to His (H) basic driven (A 1 and H 1) and extrastimulus (A 2 and H 2) intervals. Discontinuous A 1-A 2 and H 1-H 2 intervals were analyzed for relations between initial coupling times and subsequent A-H responses, and to examine curves of sequential paced cycle lengths (A-A intervals) versus A-H intervals. Seventeen patients showed sustained slow pathway (SP) conduction with demonstration of discontinuous A-A and A-H curves. Sustained SP conduction occurred at critical atrial paced rates when the first paced beat was blocked in the fast pathway (FP) with conduction via the SP. Eleven of these 17 patients had inducible sustained supraventricular tachycardia (SVT). A-H interval during SVT in these 11 patients was closely related to SP A-H interval during atrial pacing at the paced rate comparable to SVT rate ( r = +0.89, p < 0.001). The seven remaining patients showed continuous A-A and A-H curves. In three of these seven patients, sustained SVT was inducible, suggesting ability to sustain SP conduction. All of these three patients had continuous A 1-A 2 and H 1-H 2 curves during sinus rhythm so that the first atrial paced beat could not be blocked in the FP for subsequent SP conduction. In the other four of the remaining seven patients, despite block of the first atrial paced beat in the FP with SP conduction, the second paced beat was blocked in the SP so that all subsequent beats resumed FP conduction. In conclusion, sustalned SP conduction in patients with dual AV nodal pathways requires (1) an initiating beat being blocked in the FP, (2) a critical rate cycle length, and (3) the ability of SP for repetitive conduction at critical rates.