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

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

Programmed Electrical Stimulation Protocols: Variations on a Theme

A series of prospective protocols were designed to determine the yield ratio (true positives vs. false positives = nonclinical) in various patient groups using a variety of programmed electrical stimulation (PES) variables. First, a PES protocol was used in 772 patients. Single, double, and triple extrastimuli were delivered in sequence (leaving each successive extrastimulus just beyond its refractory period before moving to the next extrastimulus) during sinus rhythm and two ventricular paced rates at the RV apex, before moving to the outflow tract and repeating the sequence and then moving on to isoproterenol infusion with the PES sequence repeated at the apex. This protocol met NASPE standards for induction of VT in patients with coronary artery disease and a history of VT, while failing to induce monomorphic VT in any control patient. The best yield ratios combined with the greatest likelihood of inducing clinical tachycardia were achieved with sinus rhythm and three extrastimuli, and pacing at the lower rate and three extrastimuli. Pacing at the faster rate and triple extrastimuli was highly inductive of clinical arrhythmias, but had a low yield ratio due to induction of more nonclinical arrhythmias than other steps. The next protocol was performed in 61 patients with inducible ventricular tachycardia. In each case, the protocol described above was completed at the RV apex, even if tachycardia was also induced at an earlier point in the protocol. This allowed for more accurate yield ratios to be established for each step in the protocol, since each patient was exposed to each of these steps. The results confirmed those of the first protocol described above. The next protocol compared extrastimuli delivered (1) in a straight sequential fashion (each extrastimulus decremented to its refractory period and then left just late enough to capture while the next extrastimulus was added and decremented in a similar fashion); versus (2) the tandem method, in which after reaching refractoriness, each extrastimulus was moved 50 msec beyond the refractory period and then decremented in tandem with the next extrastimulus. Preliminary analysis of this protocol in > 30 subjects indicates no significant difference in the number of clinical or nonclinical arrhythmias induced with these methods, although the tandem method was much more time consuming. We conclude that a simple sequential PES protocol, taken to refractoriness, is efficient and effective, and is not at a disadvantage compared to more complex or cumbersome protocols.     

Extended Protocol for Demonstration of Dual AV Nodal Physiology

The incidence of dual atrioventricular (AV) nodal physiology was evaluated in 22 patients (14 males, 8 females, age 52 ± 18 years) undergoing electrophysiology studies for evaluation of ventricular tachycardia/honsustained ventricular tachycardia (n = 11), supraventricular tachycardia (n = 5), and syncope (n = 6). Patients with AV node reentrant tachycardia were excluded. Thirteen patients had riormal left ventricular function and nine patients (seven with coronary artery disease, two with dilated cardiomyopathy) had depressed left ventricular function. Single atrial extrastimuli (A2) were introduced after eight-beat drives at paced cycle lengths of 550 msec and 400 or 450 msec beginning at coupling intervals of 650 and 500 or 550 msec, respectively. The coupling interval was decreased at 10-msec intervals until AV node or atrial refractoriness. A second atrial extrastimulus (A3) was then added. A2 was fixed at 50 msec greater than the atrial or AV nodal refractory period. A3 was coupled to A2 at 650 and 500 or 550 msec and decremented as with single extrastimulation. Dual AV nodal physiology was defined by a 50-msec increase in A2H2 or A3H3 with a 10-msec decrement in the coupling interval or a discontinuous H1H2 versus A1A2 or H2H3 versus A2A3 curve. Using a single extrastimulus, 1 of 22 patients demonstrated dual AV nodal physiology. Using double extrastimuli, an additional four patients with dual AV nodal physiology were identified. The occurrence of dual AV nodal physiology determined using double extrastimuli is increased compared to using only a single extrastimulus (P = 0.03). In conclusion, dual AV nodal physiology can be demonstrated with greater frequency using an extended rather than a standard protocol.     

Comparison of Ventricular Refractory Periods Determined by Incremental and Decremental Scanning of an Extrastimulus

This study compared the ventricular effective refractory periods measured by scanning diastole with an extrastimulus in incremental and decrementaJ steps of 5 msec. The subjects of the study were 80 patients undergoing a clinically indicated electrophysiological test. Eight beat basic drive trains at a cycle length of 600 msec and an intertrain pause of 4 seconds were used to measure the ventricular effective refractory period (VERP). In the incremetal method, the extrastimulus initially was positioned at a coupling interval shorter than the VERP and the coupling interval then was progressively increased until ventricular capture occurred. In the decremental method, the initial extrastimulus coupling interval was longer than the VERP and the coupling interval was progressively shortened until ventricular capture was lost. In 50 subjects, the mean VERP determined by the incremental method, 252 ± 18 (± standard deviation), was significantly longer than the mean VERP determined in the same patients by the decremental method, 248 ± 18 msec (P < 0.0001). In ten subjects, a subthreshold stimulus (S') positioned 10 msec earlier than the VERP had an inhibitory effect that lengthened the VERP by an average of 7 msec; however, when S' was positioned after the seventh beat of an eight heat drive train, no inhibitory effect could be demonstrated. In 20 subjects, VERP's were determined by the incremental and decremental methods using intertrain pauses of 1, 4, 8, 12, and 20 seconds. The mean VERP measured by the incremental method was significantly less than the mean VERP measured by the decremental method when the intertrain pause was 1,4, or 8 seconds, but not when the pause was 12 or 20 seconds. The results of this study demonstrate that incremental scanning of an extrastimulus with eight beat basic drive trains yields a longer VERP than when the extrastimulus is scanned in decremental fashion. The discrepancy between the two methods is not attributable to inhibition by noncapturing extrastimuli in the incremental method, but rather to a decrease in the VERP caused by an effect of extrastimuli that capture the ventricle in the decremental method. Therefore, when a conventional eight beat driye train and 4 second intertrain pause are used to measure ventricular refractoriness, incremental scanning of an extrastimulus yields a more accurate VERP than does decremental scanning.     

Strength-Interval Curves in Canine Myocardium at Very Short Cycle Lengths

While ventricular electrophysiological properties have been intensively studied at normal heart rates, little is known about these properties at the very short cycle lengths (approximately 100 msec), which are present in ventricular fibrillation. We examined refractoriness in the right ventricles of six dogs at stimulation intervals of 80 to 300 msec. Starting at 300 msec, the basic (S₁) cycle length was decremented by 10 msec each beat to 200, 150, or 125 msec. A 1-msec premature (S₂) stimulus of 1, 5, 10, or 20 mA was then introduced. The S₁-S₂ interval was decremented until capture was lost. The refractory period was considered to be the shortest interval that captured the heart for each S₂ strength. Only pacing episodes that did not induce fibrillation were included. Strength-interval curves maintained the same hyperbolic shape but shifted to very short refractory periods as the S₁-S₁ interval was decreased. At the shortest S₁-S₁ intervals, premature stimuli were capable of capturing the heart without inducing ventricular fibrillation for S₁-S₂ intervals as short as 83 ±3 msec. Thus, decremental rapid pacing can produce refractory periods shorter than the cycle length during ventricular fibrillation. This finding suggests that there is no need to postulate a discontinuous jump to new electrophysiological properties or relationships at the onset of fibrillation, but that the capability for fibrillation is an integral part of normal electrophysiological parameters when they are pushed to values that do not occur normally. The results of this study should be useful in the further development of active membrane models and cellular automata models of cellular electrical behavior.     

Quantitative Relationship Between Atrial Refractoriness and the Dispersion of Refractoriness in Atrial Vulnerability

We investigated the quantitative relationship between the atrial refractory period and the dispersion of refractoriness with respect to atrial vulnerability in 19 adult mongrel dogs. The atrial effective refractory period (AERP) was measured at the sinus node area (SNA), the low posterior right atrium (LRA), and the distal coronary sinus. The study was performed under the following conditions: (1) control status; (2) hypothermia (30°C); (3) vagus nerve stimulation; and (4) a combination of (2) and (3). The subjects were separated into two groups: atrial fibrillation (AF) (+) group (n = 23), which developed AF by atrial extrastimulus due to increased vulnerability, and AF (−) group (n = 39), which did not develop AF. The mean AERP was 97 ± 23 msec (mean ± SD) in the AF (+) group and 124 ± 23 msec in the AF (−) group, with a significantly shorter refractory period seen in the former (P < 0.001). The dispersion of refractoriness was 59 ± 24 msec in the AF (+) group and 29 ± 18 msec in the AF (−) group, with a significant increase noted in the former (P < 0.001), On X-Y coordinates (where X denotes the AERP, and Y denotes the dispersion of refractoriness) the data from the AF (+) group were clustered in the upper left region of the graph while the data from the AF (−) group were clustered in the lower right region. These two groups were separated by a linear equation of Y = 0.86X - 57 with a predictability of 90.3%. No difference in the time from SNA stimulation to LRA excitation was found between the groups. On the basis of these results, we suggest that increased atria) vulnerability can be predicted from an analysis of the quantitative relationship between the atrial refractory period and the dispersion of refractoriness.     

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.     

Changes in Ventricular Effective Refractory Periods After Two Extrastimuli and Ventricular Electrical Instability

Using programmed stimulation with one and three extrastimuli delivered in the right ventricular apex, we compared the effective refractory period (ERP) during sinus rhythm (ERP-SR) and during the third extrastimulus (EHP-S₃) in patients without ventricular tachycardias (control group, n = 87) and in patients with documented ventricular tachycardia (VT group, n = 76). The protocol was not completed to determine ERP-S₃ in one patient in the control group and in 15 patients in the VT group. We observed a significantly greater change (i.e., shortening) in ERP after two extrastimuli in the VT group compared with patients without VT (ΔERP = 45 ± 20 msec in the control group and 70 ± 16 msec in the VT group, P < 0.001), This electrophysiological phenomenon, along with conduction delay, may play an important role in VT induction.     

Effect of the Atrioventricular Relationship on Atrial Refractoriness in Humans

Atrial arrhythmias occur frequently in the setting of increased atrial size and pressure. This may result from contraction-excitation feedback. The objective of this study was to investigate the effect of alterations in atrial pressure, induced by varying the atrioventricular (AV) interval, on atrial refractoriness, and on the frequency of induction of atrial fibrillation. Twenty-seven patients without structural heart disease participated in the study. In each patient the atrial effective (ERP) and absolute refractory period (ARP) were measured during AV pacing at a cycle length of 400 msec and AV intervals of 0, 120, and 160 msec. 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 during continuous pacing using the incremental extrastimulus technique. A subset of patients had the pacing protocol performed during autonomic blockade. As the AV interval was increased from 0 to 160 msec, the peak right atrial pressure decreased from 16 +/- 4 mmHg to 7 +/- 3 mmHg and the mean right atrial pressure decreased from 7 +/- 3 mmHg to 3 +/- 22 mmHg (P less than 0.001). The atrial ERP and ARP did not change with alterations in the AV interval. There was no difference in the frequency of induction of atrial fibrillation. Similar results were obtained during autonomic blockade. These findings suggests that the phenomenon of contraction-excitation feedback may not be of importance in the development of atrial arrhythmias in patients without structural heart disease.     

Detection of rapid changes in ventricular refractoriness in human studies

Conventional determination of the ventricular effective refractory period (VERP) is unsuitable for detection of rapid fluctuations in the effective refractory period (ERP). A programmed stimulation system was developed that adapts continuous atrioventricular sequential pacing, incremental extrastimulus interval (S1S2) scanning, and automatic detection of extrastimulus capture which is followed by shortening of S1S2 to execute repeated scanning. The accuracy of ERP determination was tested using variable incremental (2 and 4 ms) and decremental (4-16 ms) steps of the S1S2 interval. Based on a mean of 82 determinations in eight patients, the average VERP values stayed at 249.8-251.0 ms except during the highest capture frequency. Standard deviation of ERP values ranged from 1.1 to 2.5 ms on average at the tested incremental and decremental steps. One determination was accomplished within 7.8-15.6 seconds on average. The ability to track changes in ERP was tested by changing the drive cycle length. Time constants for the adaptation rate of VERP and ventricular monophasic action potential duration at a 90% level of repolarization were determined from each test, and were similar, 51 +/- 8 seconds (mean +/- SEM) for ERP and 51 +/- 6 seconds for the action potential duration. Thus, the developed method provides accurate ERP measurements during rapid variation in ventricular refractoriness. It allows studying the recovery of excitability and the action potential duration simultaneously, and would be valuable particularly in pathological conditions and pharmacologic interventions where these electrophysiological variables become dissociated.     

Observations on the Initiation of Sustained Ventricular Tachycardia by Programmed Stimulation

We analyzed the initiation of sustained monomorphic ventricular tachycardia (VT) by programmed ventricular stimulation (PVS) in 50 consecutive patients who had clinical VT or aborted sudden cardiac death with remote myocardial infarction. In 25 of 50 patients, the first induced QRS complex of VT was morphologically identical to the succeeding QRS complexes of VT (type I). In 25 other patients, the first VT beat had a different morphology (type II). Type I had a significantly longer VT cycle length than type II (333 +/- 65 msec and 293 +/- 66 msec, P = 0.036). Type II VT initiation required more aggressive stimulation protocol than type I (type I: type II; number of extrastimulus required for induction 2.5 +/- 0.9 : 3.0 +/- 0.6, P = 0.026; shortest extrastimuli coupling interval 244 +/- 28 msec : 220 +/- 23 msec, P = 0.002). The interval between the last extrastimulus and the onset of the first VT beat was 408 +/- 88 msec in type I and 336 +/- 75 msec in type II (P = 0.004). Furthermore, there was good correlation between the VT cycle length and the interval from last extrastimulus to the onset of nonpaced beat in type I but not in type II.(ABSTRACT TRUNCATED AT 250 WORDS)     

Atrial Refractory Periods after Atrial Premature Beats in Patients with Paroxysmal Atrial Fibrillation

To study the effects of an atrial premature beat on atrial refractory periods, we investigated 11 patients (group A) who were the control group, 12 patients suffering from paroxysmal atrial fibrillation (group B), and 10 patients (group C) without arrhythmias but with cardiopathy or cardiomyopathy. At every eighth complex of a constant atrial electrostimulated rhythm a fixed premature extrastimulus was introduced, and effective and functional refractory periods (ERP and FRP) were measured in three different sites of the right atrium, before and after introduction of this extrastimulus. Average ERP and FRP shortened respectively in group A, from 220.28 ± 25.68 msec and 281.17 ± 28.15 msec before extrastimulation, to 190.58 ± 22.74 msec and 245.88 ± 19.86 msec after; in group B, from 219.44 ± 27.38 msec and 284 ± 30.06 msec to 191.66 ± 28.72 msec and 253.23 ± 34.01 msec; and in group C from 229.03 ± 29.65 msec and 289.67 ± 51.62 msec to 194.19 ± 24.6 msec and 237.74 ± 39.59 msec. The average dispersions of ERP and FRP in group A were, respectively: 41.81 ± 21.36 msec and 36.36 ± 18.04 msec before extrastimulation, 28.18 ± 18.14 msec and 35.45 ± 15.72 msec after. In group B: 26.66 ± 19.46 msec and 41.66 ± 16.96 msec versus 45.83 ± 23.91 msec and 45 ± 34.77 msec and in group C: 27 ±11.59 msec and 45 ± 29.15 msec versus 29 ± 18.52 and 27 ± 18.88. It is concluded that an atrial premature beat tends to shorten the dispersion of atrial refractory periods when patients are free of arrhythmias, and to lengthen them when paroxysmal atrial fibrillation are documented.     

Quantitative Analysis of Concealed Conduction into Accessory Atrioventricular Pathways in Wolff-Parkinson-White Syndrome

Concealed conduction is demonstrated to occur in an accessory AV pathway (AP). To test the hypothesis that anterograde and retrograde concealed conduction in the AP would have different characteristics, 35 consecutive patients with single APs were studied. The anterograde or retrograde ERP of the AP could be determined in 23 of those patients. Anterograde concealed conduction in the AP was assessed in the first 13 patients with retrograde AP conduction (8 APs with retrograde conduction only and 5 with both directions) (group A). Retrograde concealed conduction in the AP was evaluated in the remaining 10 patients with anterograde AP conduction (6 APs with anterograde conduction only and 4 with both directions) (group B). The concealed conduction in the AP was quantified by determining the ERP of the AP using a “probe” extrastimulus (S_p) introduced in the opposite chamber. The ERP was determined both during conventional extrastimulus (S₁S₂ method; ERP_c) and during that with an S_p (S₁S_pS₂ method; ERP_p). The S_p was delivered before or after the last S₁ with various S₁S_p intervals. The ERP_p was determined at each S₁S_p interval. Three distinct patterns in concealed conduction in the AP were noted. In the first pattern, the ERP_p was always shorter than the ERP_c, whereas the reverse relation was noted in the second pattern. The third pattern showed a combination of the two. In group A, only the first pattern was noted. In group B, the first, second, and third patterns were noted in 4, 2, and 4 patients, respectively. The first pattern was noted only in septal APs and the second and third were seen only in left free-wall APs. The second pattern was seen in patients with retrograde AP conduction, whereas the third one was mainly noted in patients without retrograde AP conduction. These observations indicate that anterograde and retrograde concealed conduction in the AP have different characteristics. Shortening of the ERP_p might be due to the “peeling back” phenomenon, and its lengthening might be caused by the presence of the inhomogeneous refractory periods of the AP. (PACE 1997; 20[Pt. I]:1342-1353)     

Applicability of the Stimulus-T Interval for Antitachycardia Pacing

At (he onset of tachycardia, the refractory period (RP) changes together with the tachycardia terminal ion window. We evaluated dogs with total atrioventricular (AV) block lo determine if stimulus-T interval (STJ) can be used to adjust the coupling interval(s) of an antitachycardia pacemaker in relation to changes in HP. Endocardial STI was recorded continuously together with six surface EGG leads. Steady-state (> 2 miii) RP was determined for drive cycle lengths (DCL) 400 msec and 900 msec. The test pulse (TP) coupling interval, with DGL 900 msec, was chosen to be equal to (he RP of DCL 400 msec, DCL was then changed to 400 msec until TP captured. STI of DCL of beat before capture was gained was measured. DCL was then changed back to 900 msec and the interval determined when capture was lost. TP was then lengthened In 5 msec and the procedure repeated until TP captured immediately upon changing to DCL 400 msec. Results: The difference between RP at onset of pacing at DGL of 400 msec and RP when capture n us achieved with the shortest coupling interval was 35–50 (mean 40) msec. This required 35–90 (mean 62) seconds. The correlation coefficient RP to STI was > 0.95. Conclusions: (1) RP changed by as much as 35–50 msec at the: onset of an abrupt increase in rate in a 35–90-second period; and (2) STI enables estimation of RP on a beat-to-beat basis. Capture can therefore be preditrd from the previous beat mid the coupling interval adjusted accordingly in an antitachycardia pacing mode.     

Effect of the Intertrain Pause on the Ventricular Effective Refractory Period Measured by the Extrastimulus Technique

This study determined the effect of the duration of the intertrain pause on the ventricular effective refractory period (VERP) measured by the extrastimulus technique using conventional eight-beat basic drive trains. In 50 subjects, the VERP was measured using a basic drive train cycle length of 500 msec, 2-msec steps in the extrastimulus coupling interval, and intertrain pauses of 0, 1, 4, 8, 20, 40, 60, or 180 seconds. The VERP increased significantly with each stepwise increment in the intertrain pause up to 20 seconds, then reached a plateau. The VERP measured with an intertrain pause of 20 seconds was a mean of 13 msec longer than when measured with a conventional 4-second pause. The results of this study demonstrate a direct relationship between the VERP and the duration of the pause separating the eight-beat basic drive trains used to measure the VERP. When the cycle length of the basic drive train is 500 msec, the VERP lengthens as the duration of the intertrain pause increases from 1 to 20 seconds, demonstrating that the basic drive trains exert a cumulative effect on the VERP when the intertrain pause is shorter than 20 seconds. A cumulative effect of the basic drive trains on the VERP is lost when the intertrain pause is 20 seconds or more.     

Pacemaker Syndrome in a Patient with DDD Pacemaker for Long QT Syndrome

A patient with long QT syndrome was treated with beta blockers and had a permanent DDD pacemaker implanted. The lower rate was set to 85 beats/min because this provided the best shortening of QT interval at the lowest paced heart rate. The atrioventricular (AV) delay was programmed to 250 msec to allow native AV conduction. Patient returned complaining of symptoms suggestive of pacemaker syndrome. ECG during one of these episodes showed AV sequential pacing. Doppler echocardiography of hepatic vein flow suggested atrial contraction against a closed tricuspid valve. Endocardial electrogram telemetry demonstrated ventriculoatrial (VA) conduction with the retrograde atrial electrogram falling within the atrial refractory period and thus was not sensed. The following atrial stimulus did not capture because of the atrial refractoriness. Ventricular pacing proceeded after the programmed AV delay. Reprogramming the AV delay to 200 msec restored AV synchrony by allowing the atrial stimulus to capture by placing it outside of the refractory period of the atrium. No further symptoms reported during six months of follow-up.     

An integrated overview of AV node physiology

The atrioventricular (AV) node generates half of the AV delay needed for blood pumping and filters atrial impulses that could otherwise induce life‐threatening ventricular arrhythmias. It is also a pacemaker and a key target in the treatment of cardiac arrhythmias. The special roles of the AV node primarily arise from its slow conduction, long refractory period, and cellular automaticity. However, efforts to establish the dynamics of these properties and their interaction led to many controversies. In fact, the AV node's behavior is so complex that it seems to escape broadly applicable rules. This review summarizes progresses made in resolving these issues and in integrating the multiple roles of the AV node within a common functional model. Presented evidence shows that the rate‐dependent conduction and refractory properties of the AV node can be reliably characterized and reconciled from nodal responses to S₁S₂S₃ protocols. It also supports the concept that dual pathways constitute a feature of the normal AV node and account for its overall conduction and refractory properties. In this model, the posterior extension and compact node provide the core of the slow and fast pathway, respectively. The transitional tissues and lower nodal bundle provide a common proximal and distal pathway, respectively. These pathways would also support bidirectional conduction. The dual pathway involvement can also be extended to widely variable AV nodal responses, such as Wenckebach cycles, hysteresis, and ventricular response to atrial fibrillation. In brief, the intricate AV nodal behavior may obey a limited set of accessible and definable rules.     

A Comparison of Intravenous Propafenone and Flecainide in the Treatment of Tachycardias Associated with the Wolff-Parkinson-White Syndrome

We compared the electrophysiological effects of intravenous propafenone andflecainide on accessory pathway conduction by a randomized crossover study in 16 patients with Wolff-Parkinson-While syndrome. The antegrade refractory period of the pathway increased from 256 ± 18 msec at baseline to 288 ± 13 msec on propafenone (P < 0.05) find to 296 ± 2 7 msec on flecainide (P = 0.075). The minimum preexcited HR interval during atrial fibrillation or incremental atrial pacing was prolonged from 225 ± 37 msec to 262 ± 22 msec by propafenone (P < 0.05) and to 301 ± 31 msec by flecainide (P < 0.005). The prolongation was significantly greater with flecainide than propafenone (P < 0.05). Both drugs increased tachycardia cycle length (TCL) from 310 ± 35 msec to 354 ± 37 msec (propafenone P < 0.005) and to 352 ± 37 msec (flecainide P < 0.01). Both propafenone and flecainide blocked antegrade conduction in the pathway in five patients. Both drugs rendered atrial fibrillation noninducifale in seven patients and orthodromic tachycardia nonindudble in five patients. Conclusions: (1) Fiecainide causes a greater prolongation of minimum preexcited RR interval than propafenone; (2) There is no significant difference between propafenone and flecainide on the inducibility of arrhythmias, TCL, or incidence of antegrade conduction block.     

Broad Applicability of Ultrarapid Train Stimulation as an Efficient Alternative to Conventional Programmed Electrical Stimulation

FISHER, J.D., et al.: Broad Applicability of Ultrarapid Train Stimulation as an Efficient Alternative to Conventional Programmed Electrical Stimulation. Background and study objective:Conventional programmed electrical stimulation (PES) is useful for establishing inducibility or noninducibility of clinical ventricular arrhythmias (VA), but is complex and time-consuming. This study compared a standard PES protocol with ultrarapid train stimulation (UTS) in a broad range of patients with and without a history of ventricular arrhythmias or structural heart disease. Methods: Patients prospectively underwent electrophysiologic testing with both UTS and conventional PES protocols in a randomized, crossover design. Results: The results were concordant in 79% of 150 matched pairs of comparisons in 104 patients (NS). There were no differences related to underlying heart disease or arrhythmia, or antiarrhythmic treatment. Induction of nonclinical arrhythmias with the two methods was similar   (P = 0.524)   . Inhibition phenomena were minor except in some patients receiving amiodarone. Fewer drive-extrastimuli sequences and less time were needed to complete the trains protocol   (P < 0.0001)   . Conclusions: In cases where the main intent is to induce ventricular arrhythmias, UTS yields results that are similar to those of conventional PES protocols in a shorter length of time. (PACE 2003; 26[Pt. II]:518–523)     

Transesophageal Measurement of Left Atrial Refractoriness

During electrophysiological evaluation of supraventricular arrhythmias the transesophageal (TEEP) approach may be the first step but is limited in information available. One difficulty is in measuring left atrial refractoriness as left atrial capture is seldom defectable either on ECG or via an esophageal lead. The problem may be eliminated and left atrial refractoriness measured via the esophagus, utilizing two or three extrastimuli to scan diastole to determine whether the atrial refractory period has been entered by the first extrastimulus. Measurement of left atrial and/or atrioventricular node or accessory pathway refractoriness then becomes possible.