Paced Beats Research Articles

Effects of disopyramide on repolarisation and intraventricular conduction in man

Right ventricular repolarisation and refractoriness after therapeutic doses of disopyramide have been studied in 10 patients with coronary artery disease by recording monophasic action potentials (MAP) during programmed stimulation. Using 2 catheters, with the tip of one in the apex and the other in the outflow tract of right ventricle, conduction intervals for propagation of stimuli in the ventricle were also measured. Disopyramide increased the duration of MAP signals at 90% repolarisation (MAP90), the QT-interval and the right ventricular effective refractory period (V-ERP). The ratio refractoriness/action potential duration was slightly increased. Early premature action potentials were more markedly prolonged in relation to steady-state action potentials. The differences between the shortest and longest premature action potentials, however, were not changed significantly. The conduction intervals of the normal and premature paced beats were significantly prolonged. The observed effects of disopyramide on conduction and action potential duration may be of major importance for its effect on termination and slowing ventricular tachycardias. Its influence on the duration of premature action potentials in man is consistent with the results of in vitro studies.

Observations on rapid ventricular pacing during reentrant ventricular tachycardia in canine myocardial infarction--the use of epicardial mapping in demonstrating the modes of resetting, concealed perpetuation and termination of reentry.

The changes in activation sequences in and around the epicardial reentrant circuit were analyzed during rapid pacing against ventricular tachycardia by using a canine infarction model. In 13 episodes of sustained ventricular tachycardia induced by a premature stimulation technique in eight dogs, reentry circuits were located in the superficial subepicardial myocardium in eight. Pacing stimuli were clearly demonstrated to enter the reentrant circuit in two directions: one wavefront collided with the orthodromic reentrant wavefront and the other entered prematurely into the reentrant circuit to reset the tachycardia (resetting phenomenon). With a faster pacing rate, stimuli failed to reset the tachycardia due to slower entry into the circuit despite the fact that most epicardial recording sites were activated by pacing wavefronts (concealed perpetuation). Termination of tachycardia was achieved by a local conduction block in the center of the reentrant circuit. A pacing impulse which encountered the local block was also shown to reinitiate the tachycardia using a different reentrant pathway. These different phenomena could be observed in consecutive pacing beats. These epicardial mapping data provided a direct electrophysiological basis for the mechanisms of reentrant ventricular tachycardia and the mode of its termination.

Decline in ventricular fibrillation threshold after successive premature extrastimuli: a possible explantation for the induction of ventricular fibrillation during programmed stimulation with multiple extrastimuli.

To examine the relation between the ventricular fibrillation threshold and the number of premature extrastimuli delivered to the right ventricle during programmed ventricular stimulation, a clinical stimulation protocol was performed in nine normal, anaesthetised, closed chest dogs. In addition, the ventricular fibrillation threshold was measured in each dog after a train of eight paced (S1) beats (VFT-S2), after a single premature extrastimulus (VFT-S3), and after two extrastimuli (VFT-S4). The VFT-V3 was 32% lower than the VFT-S2 (16(7) mA vs 24(9) mA, p less than 0.001). The VFT-S4, or the current required by the S4 extrastimulus to induce ventricular fibrillation, was 25% lower than the VFT-S3 (12(8) mA vs 16(7) mA, p less than 0.05). The cumulative reduction in the ventricular fibrillation threshold measured by the S1S2S3S4 stimulation protocol was approximately 50%. Although in most dogs the VFT-S4 was still considerably higher than twice threshold current intensity, the results of the study suggest that a possible mechanism for the induction of non-clinical ventricular fibrillation in the clinical electrophysiology laboratory may be the progressive lowering of the ventricular fibrillation threshold caused by the addition of multiple extrastimuli. This may be particularly relevant in patients with an already reduced fibrillation threshold.

Demonstration of coronary artery myogenic vasoconstriction in the awake dog.

The aim of this study was to determine whether or not coronary vasoconstriction occurs in response to a transient increase in coronary perfusion pressure. Eleven awake dogs with formalin-induced heart block, chronically instrumented with aortic and left ventricular catheters and left circumflex coronary and aortic electromagnetic flowprobes, were studied at a paced heart rate of 60 beats/min. A transient increase in aortic diastolic pressure of 17.3 +/- 1.5% for 330 +/- 20 ms and of 33.6 +/- 2.2% for 520 +/- 20 ms, via the inflation of an intra-aortic balloon, resulted in an increase in diastolic coronary vascular resistance index in the first response beat of 6 +/- 1% and 11 +/- 1%, respectively. An identical increase in diastolic coronary flow produced by the omission of a single paced beat resulted in no significant change in diastolic coronary vascular resistance index in the first response beat. Thus, the increase in diastolic coronary vascular resistance index following diastolic pressure augmentation is related to the increase in aortic diastolic pressure and not to the increase in diastolic coronary flow. These data are consistent with that of a brief myogenic response.

Significance of pacing cycle lengths in manifest entraiment of orthodromic circus movement tachycardia by ventricular pacing

The physiology of entrainment of orthodromic circus movement tachycardia (CMT) was studied using ventricular pacing during 18 episodes of induced CMT in 7 patients with atrioventricular (AV) accessory pathways. The first paced impulse was delivered as late as possible in the tachycardia cycle (mean 88 ± 5% of the spontaneous cycle length [CL]). Entrainment was demonstrated by the following criteria: 1:1 retrograde conduction via the accessory pathway; capture of atrial, ventricular and His bundle electrograms at the pacing rate; and resumption of tachycardia at its previous rate after cessation of pacing. The number of ventricular paced impulses ranged from 5 to 14 (mean 8 ± 3), and entrainment occurred in 2 to 7 paced cycles (mean 4 ± 2). Orthodromic activation of a major part of the reentry circuit (manifest entrainment) was demonstrated during 9 episodes by the occurrence of His bundle electrogram preceding the first CMT QRS at the time anticipated from the last paced beat. In the 9 other episodes, persistent retrograde His bundle activation and AV nodal penetration by each paced impulse caused a delay (mean 79 ± 25 ms) in activation of the His bundle preceding the first CMT QRS after the last paced beat. The mean pacing CL achieving manifest entrainment was 92 ± 3% of the tachycardia CL, compared with 84 ± 3% for retrograde AV nodal penetration (p < 0.01). In conclusion, manifest entrainment of orthodromic CMT can be demonstrated by ventricular pacing at very long CLs; shorter CLs may cause CMT termination due to retrograde AV nodal penetration.

Complete sinoatrial block in two patients with bradycardia-tachycardia syndrome

Electrophysiologic studies with recordings of sinus node electrograms were performed in two patients with bradycardia-tachycardia syndrome. In both patients, the rest electrocardiogram showed apparent sinus bradycardia. Patient 1 had frequent paroxysms of atrial tachycardia with long pauses of up to 10 seconds; Patient 2 had paroxysmal atrial flutter and atrial pauses of up to 8 seconds. Multiple, repetitive, low frequency deflections, with a cycle length ranging from 730 to 960 ms in Case 1 and 570 to 750 ms in Case 2, suggestive of sinus node electrograms, were recorded at a critical area at the junction between the superior vena cava and the right atrium. These low frequency deflections had no relation to spontaneous junctional beats or the spontaneous atrial beats that showed high frequency deflections on the atrial electrogram. However, they could be suppressed by spontaneous or paced atrial beats. Pharmacologic interventions in Case 2 showed that the cycle length of the low frequency deflections shortened after administration of isoproterenol and did not change after propranolol or atropine. Thus, complete sinoatrial exit block with intact entrance conduction can occur in patients with bradycardia-tachycardia syndrome. Under such circumstances, the surface electrocardiographic manifestation of sinus bradycardia may not be of sinus origin.

Two different patterns of entrainment of ventricular tachycardia

In a patient with two morphologic forms of ventricular tachycardia, rapid pacing from different ventricular sites produced two distinctively different patterns of entrainment. Pacing from sites contralateral to the site of emergence of ventricular tachycardia caused progressive fusion. Following pacing, the interval (return interval) between the first tachycardia beat (return beat) and the preceding beat was equal to the pacing cycle length. Near the site of emergence, the local electrogram of the return beat was morphologically identical to that of the preceding paced beats. In contrast, pacing from sites ipsilateral to the site of emergence did not cause fusion. The return intervals increased with decreasing pacing cycle lengths. The local electrogram of the return beat was morphologically different from that of the preceding paced beats. Using a model of ventricular reentrance, both patterns of responses can be explained. Pacing impulses arising from sites contralateral to the site of emergence activate the latter orthodromically. Fusion occurs between the emerging tachycardia wavefront and the next pacing wavefront. In contrast, pacing impulses arising from sites ipsilateral to the site of emergence activate the latter antidromically. Fusion is not observed because collision within the area of slow conduction prevents the emergence of the tachycardia during pacing.

Reactive hyperemia following one-beat coronary occlusions in the awake dog.

This study was performed to examine the effect of alterations of cardiac activity during brief coronary artery occlusions on the subsequent reactive hyperemic response. Reactive hyperemia following coronary occlusions equal in duration to one cardiac cycle were examined in 12 chronically instrumented awake dogs while heart rate was maintained constant by cardiac pacing. During continuous pacing, one-beat coronary occlusions resulted in reactive hyperemia with excess flow equal to 220 +/- 23% blood flow debt repayment. When coronary occlusions of identical duration were performed while a single cycle of pacing was omitted during the interval of occlusion, the subsequent reactive hyperemia was decreased. Conversely, when coronary occlusion was produced during the first potentiated beat following a single cycle of paired ventricular stimulation, the reactive hyperemia was increased. Since, in the absence of coronary occlusion, omitting a single paced beat caused a transient decrease in coronary flow, while a single cycle of paired ventricular stimulation caused a brief increase in coronary flow, the reactive hyperemic responses were corrected for these perturbations in flow. Despite these corrections, the influence of alterations of myocardial activity during the interval of occlusion persisted, with the decreased reactive hyperemia when occlusion occurred during an omitted beat and increased hyperemia when occlusion was performed during a potentiated beat. These data indicate substantial coupling between myocardial activity during coronary occlusions as brief as one cardiac cycle in duration and the subsequent reactive hyperemic response.

“Isolength” postextrasystolic potentiation as a predictor of functional restoration following surgical revascularization for myocardial ischemia

A previously developed method of programmed postextrasystolic potentiation (PESP) was assessed in eight patients with medically refractory unstable angina, as a predictor of functional restoration resulting from surgical revascularization. Prior to coronary arteriography, left ventricular segmental wall motion was determined during ventricular pacing and the first postextrasystolic beat following an extrasystole. The postextrasystole was induced at an interval calculated to occur at a time where ventricular preload was identical to the regular paced beat (isolength interval). The left ventricular wall was divided into six segments, each subscribing one area of the ventriculogram, and correction for rotation during systole was made. Of 48 segments, 21 were considered "jeopardized," due to greater than 70% reduction in cross-sectional lumen of the serving coronary arteries. Fifteen of these 21 responded to PESP, increasing their segmental area ejection fraction from 44 +/- 5 (paced "normal" beat) to 56 +/- 6 (postextrasystolic beat) (p less than 0.05). Following surgical revascularization, these segments showed an improvement in their baseline area ejection fraction from 44 +/- 6 to 58 +/- 5 (p less than 0.05). Six jeopardized segments that failed to respond to PESP prior to revascularization showed functional deterioration after revascularization. The 27 non-jeopardized segments (which were not revascularized) also showed functional improvement, suggesting improved collateral flow. This study demonstrates that isolength postextrasystolic potentiation obtained with a standardized pacing protocol may be used to predict the potential for improvement in cardiac function following surgical revascularization. Our results also show that lack of PESP predicts loss of left ventricular myocardial function following revascularization.

Further observations on transient entrainment: importance of pacing site and properties of the components of the reentry circuit.

Transient entrainment of circus-movement tachycardia utilizing an atrioventricular (AV) bypass pathway was studied in 13 patients (nine with the orthodromic form, two with the antidromic form, and two with both the orthodromic and antidromic forms). All patients had a left-sided AV bypass pathway. Pacing at selected rates faster than the spontaneous rate was performed during the tachycardia at a site proximal or distal to the AV node, an area of slow conduction within the reentry loop. Rapid pacing from a site proximal to the AV node (from the right atrium during the orthodromic form of the arrhythmia or the right ventricle during the antidromic form of the arrhythmia) always demonstrated at least one of the three entrainment criteria: constant fusion beats except for the last captured beat, which was entrained but not fused (first criterion); progressive fusion (second criterion); localized conduction block to a site(s) for 1 paced beat associated with interruption of the tachycardia followed by activation of that site(s) by the next paced beat from a different direction and with a shorter conduction time (third criterion). In contrast, rapid pacing from a site distal to the AV node (from the right ventricle during the orthodromic form of the arrhythmia, or the right atrium during the antidromic form of the arrhythmia) transiently entrained the tachycardia, but never demonstrated any entrainment criteria because the antidromic wave front from the pacing impulse always blocked in the AV node (concealed entrainment). We conclude that the location of the pacing site relative to the components of a reentry loop is critical to the demonstration of the criteria of transient entrainment; i.e., if it is proximal to an area of slow conduction and/or unidirectional block within a reentry loop, transient entrainment should be demonstrable, but if it is distal, it will not be demonstrable.

Pseudosimultaneous fast and slow pathway conduction: A common electrophysiologic finding in patients with dual atrioventricular nodal pathways

Two ventricular responses following termination of rapid atrial pacing were noted in 24 of 87 patients with dual atrioventricular (AV) nodal pathways and supraventricular tachycardia. In all 24 patients, the AH intervals of the first and second ventricular responses were comparable with those of the fast and slow pathways, respectively. Careful analysis of the whole pacing sequence revealed that, in 21 patients, this phenomenon resulted from sustained slow pathway conduction with long AH intervals. In these patients, as the AH interval of each paced beat was progressively lengthened during pacing, the corresponding His bundle and ventricular responses were pushed one cycle behind the current atrial paced beat, so that the last paced beat was followed by two His bundle and ventricular responses. In only three patients did double ventricular responses result from simultaneous fast and slow pathway conduction. One of these three patients also showed two ventricular responses resulting from sustained slow pathway conduction. Several factors predispose to the occurrence of this phenomenon in patients with dual AV nodal pathways. These include an ability to sustain slow pathway conduction, a longer slow pathway AH interval, a shorter sinus AH interval (fast pathway) and a shorter atrial paced cycle length that sustains slow pathway conduction. In conclusion, sustained slow pathway conduction with resultant long AH intervals is the mechanism of two ventricular responses following termination of atrial pacing in most patients with dual AV nodal pathways. This phenomenon should be distinguished from the rare occurrence of double ventricular responses to an atrial impulse due to simultaneous fast and slow pathway conduction.

The Use of Programmed Electrical Stimulation to Assess the Fibrillatory Propensity of Ionic and Nonionic Contrast Media

Coronary angiography occasionally results in ventricular fibrillation. To compare the fibrillatory propensity of conventional ionic and nonionic contrast media, we measured QT intervals and performed programmed electrical stimulation during intracoronary injection of Renografin 76 (R76), Hypaque 76 (H76), and iopamidol (IOP) in 16 open chest dogs. In ten dogs the incidence of ventricular fibrillation following induction of a single premature ventricular beat after every fourth atrial paced beat was 19/20 with R76, 8/20 with H76, and 0/20 with IOP (P less than .001). When two premature beats were induced, the incidence of ventricular fibrillation was 20/20 with R76, 19/20 with H76, and 1/20 with IOP (P less than .001). In six additional dogs, the mean prolongation of the QT interval was 170 +/- 20 msec with R76, 105 +/- 14 msec with H76, and 63 +/- 9 msec with IOP (P less than .001). Thus, programmed electrical stimulation readily induces ventricular fibrillation during intracoronary injection of conventional ionic contrast media. The incidence of ventricular fibrillation parallels the amount of QT interval prolongation produced. H76, which lacks EDTA and sodium citrate, is less fibrillatory than R76. However, the nonionic medium IOP appears far less fibrillatory than either R76 or H76.

Entrainment of ventricular tachycardia by atrial depolarizations

Four patients in whom rapid atrial pacing resulted in transient entrainment of a sustained ventricular tachycardia (VT) are reported. Ventricular fusion was seen in 3 of the 4. The following new observations were made: (1) A single atrial depolarization resulted in ventricular fusion and resetting of a VT, while atrial pacing at a faster rate entrained the same VT but without detectable fusion. This suggests that fusion during entrainment may be a rate-dependent phenomenon. (2) The interval between the last paced beat and the first nonpaced VT beat was different from the pacing cycle length in 3 patients. Two mechanisms accounted for this: the initial forces of each entrained QRS occurring as a result of the pacing wavefront, with fusion taking place only during the terminal forces, and the last entrained cycle exceeding the pacing cycle length by an amount related to the nonfused portion of the QRS, and delay in the presumed reentrant circuit responsible for the tachycardia. (3) One VT was entrained with atrial pacing while ventricular pacing at the same rate resulted in termination, suggesting “site specificity” for termination. It is concluded that entrainment can occur without the criteria previously described as characteristic of it and that additional phenomena may be observed after stimulation that further support reentry as the mechanism of VT.

Rate-responsive pacing: clinical experience.

Single chamber, rate-responsive pacing is emerging as a new modality in cardiac pacing and in the near future, dual chamber rate-responsive pacing may be the optimal solution for most pacemaker patients. In this report we describe our short- and long-term clinical experience with two different rate-responsive pacemakers: the RS4, an asynchronous atrial sensing ventricular pacemaker, and the TX-pacemaker, which senses the evoked QT after a ventricular paced beat, as an indicator of metabolic demand. Both systems use a single ventricular lead. Nine patients received RS4 and 10 patients received TX units. All of these patients had AV block and good ventricular function except for three patients with sinus node disease in the TX group. Between 1 and 3 months after implantation, a 24-hour Holter monitoring was performed, during which two maximal symptom-limited treadmill exercise tests (Bruce protocol) were conducted in VVI (70 bpm) and rate-responsive modes, in a random fashion. The mean follow-up was 25 months in RS4 group and 10 months in TX group. Significant improvements in patient exercise tolerance were found in the rate-responsive mode (9.0 vs. 6.6 METs in VVI) with similar results in both groups (RS4 and TX) despite higher ventricular pacing rates in the TX group (121 bpm vs. 102 bpm in RS4). An autolimited rate-responsive pacemaker-mediated tachycardia, induced by retrograde ventriculo-atrial conduction, was observed in a patient with an RS4.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventricular fibrillation during coronary angiography: An analysis of mechanisms

To investigate the mechanisms of ventricular fibrillation (VF) during coronary angiography, we assessed ventricular automaticity, local QT intervals, local conduction characteristics, and the ability to induce arrhythmias with premature ventricular stimulation in 30 dogs after intracoronary injections of 4 to 6 cc of Renografin 76 (RG 76). Ventricular automaticity was measured in six dogs as the idioventricular escape rate following intense vagal stimulation and was unchanged (51 ± 6 vs 52 ± 6 bpm, p > 0.05) with 6 cc of RG 76. In addition, 8 of 10 injections of 6 cc of RG 76 produced VF at a heart rate of 200 bpm compared to only 2 of 10 injections at a heart rate of 80 bpm ( p < 0.05). Composite and bipolar plunge electrodes were placed in the region perfused by the left anterior descending coronary artery (LAD) and circumflex coronary artery to assess QT intervals and conduction characteristics. RG 76, 4cc, produced a 116 ± 18 msec increase in the QT intervals recorded from the region perfused by the LAD, resulting in a marked dispersion in repolarization. Both local bipolar and composite electrograms showed minimal conduction delay, which rarely extended beyond the QRS of a lead II ECG during atrial paced rhythm. As premature beats (spontaneous or induced) conducted through the region of QT prolongation, marked conduction delay was recorded from bipolar electrograms, while composite electrograms recorded continuous fractionated electrical activity spanning the diastolic interval at the onset of VF. An early cycle premature impulse applied after every fourth atrial paced beat in the circumflex region produced VF in 23 of 25 injections of 4 cc of RG 76. The addition of CaCl 2 (40 mEq/L) to RG 76 markedly attenuated the QT prolongation, local fractionation, and conduction delay and totally prevented VF in response to premature stimulation. We conclude that the regional QT prolongation produced by RG 76 renders the myocardium vulnerable to VF by increasing the temporal dispersion of repolarization. VF appears to result from slow conduction of premature beats through incompletely repolarized myocardium leading to the formation of multiple reentrant pathways. However, the mechanism of the first premature beat in spontaneous VF remains unknown.

Post-pacing T loop abnormalities.

Vectorcardiograms of paced and unpaced beats were recorded from 18 patients with implanted pacemakers to investigate the characteristics of post-pacing T inversions. The intraventricular conduction during sinus rhythm of unpaced beats was normal in 13 of 18 patients and abnormal in the other 5 (RBBB in 3, LBBB in 2). The directions of the maximum QRS vector in paced beats (max QRSp.V) and maximum T vector in unpaced beats (max T unp.V) were studied. In 8 of 13 patients with normal intraventricular conduction (group A) and in 3 patients with right bundle branch block (RBBB), the differences between the directions of max QRSp.V and max T unp.V in both frontal and horizontal planes were less than 30 degrees, and in 5 of 13 patients with normal intraventricular conduction (group B) and 2 patients with left bundle branch block (LBBB), differences exceeded 30 degrees. The direction of max T unp.V tended to be superiorly, posteriorly and to the right regardless of max QRSp.V direction. The similarity in direction of max QRSp.V and max T unp.V supports the hypothesis by Rosenbaum et al that post-pacing T inversions may be, in part, explained on the basis of 'cardiac memory'. However the absence of correlation between the max QRSp.V and max T unp.V suggests that the post-pacing T inversions may be caused by other unknown mechanisms.

Effects of lidocaine, procainamide, metoprolol, digoxin and atropine on the conduction of premature ventricular beats in man

The acute electrophysiologic effects of clinical doses of procainamide, lidocaine, metoprolol, digoxin and atropine upon the conduction of ventricular premature beats, were studied in 48 healthy volunteers. The conduction time of the first premature beat, induced 1 ms after the ventricular effective refractory period (VERP) was longer than that of the basic paced beats in 41 of the 48 subjects (85%); in 31 (65%) the delay was greater than 5 ms, indicating subnormal conduction. Digoxin decreased the delay so that it became insignificant, while, after procainamide, the delay increased significantly. The other agents did not significantly affect the subnormal conduction. The mean conduction times of premature beats, induced 30-50 ms after the VERP, were shorter than the basic conduction time in 43 of the 48 subjects (90%), and in 25 (52%) the decrease was greater than 5 ms, showing supernormal conduction. Lidocaine abolished the supernormal conduction. The other agents did not significantly alter the supernormal conduction. In the healthy heart, sub- and supernormal conduction of premature beats seem to be common phenomena, and seem, with few exceptions, to be largely unaffected by clinical doses of procainamide, lidocaine, metoprolol, digoxin and atropine.

Shortening of ventriculoatrial conduction in patients with left-sided Kent bundles

In six patients with electrophysiologic evidence of ventriculoatrial conduction through a left Kent bundle, we documented that programmed right ventricular stimuli falling within an interval of 60 to 160 msec from the end of the T wave propagated to the left atrium (distal coronary sinus unipolar lead) 10 to 20 msec earlier than the basic paced beats. This phenomenon could be reproduced 24 hours later in two patients, and it was abolished by procainamide and amiodarone in one instance. During this interval we were unable to induce reciprocating tachycardia. Our observations outline a new pattern in ventriculoatrial conduction in patients with left-sided Kent bundles. The findings suggest in addition, that (1) supernormal conduction may be responsible for the observed shortening in retrograde conduction and (2) this phenomenon does not facilitate induction of reciprocating tachycardia.

Responses of an AV universal (DDD) pulse generator (Cordis 233D) to programmed single ventricular extrastimuli.

To evaluate factors playing a role in initiation and perpetuation of pacemaker-mediated tachycardias (PMTs), 22 consecutive patients with symptomatic conduction disorders were studied after implantation of an AV universal (DDD) pulse generator (Cordis 233D). Patients were divided into two groups, depending upon the presence or absence of ventriculo-atrial (VA) conduction during electrophysiological study (EPS) performed before pacemaker implantation. PMTs could be initiated in six of eight patients of Group I and in none of 14 patients of Group II. Initiation and perpetuation of PMTs during DDD pacing were dependent upon the capacity of the patient to conduct ventricular premature beats (VPBs) and subsequent paced ventricular beats retrogradely to the atria, and upon three programmable parameters of the pulse generator (AV delay period, upper rate limit, tachycardia response). Programmed single ventricular extrastimulation demonstrated that: (1) merely the presence of VA conduction during EPS, although necessary, was not sufficient to induce PMTs after DDD pacemaker implantation; (2) VPBs introduced late rather than early in the cardiac cycle initiated PMTs in a different way; (3) the initiation of PMTs could be prevented during study by adjusting the programmable parameters (AV delay period, upper rate limit, tachycardia response); (4) one of the two available tachycardia responses of the pulse generator (gradual fall-back response) was able to terminate and initiate PMTs consistently. These observations helped in understanding the responses of the Cordis 233D pulse generator to ventricular premature beats. They indicate that additional refinement of the pulse generator is necessary to solve the problem of PMT.

Induction and termination of triggered activity by pacing in isolated canine Purkinje fibers.

The clinical importance of delayed afterdepolarizations and resultant triggered activity as a cause of cardiac arrhythmias is uncertain. We studied the response of ouabain-induced delayed afterdepolarizations and triggered activity to a pacing protocol similar to those used clinically in an effort to quantify the types of responses to pacing that occur as a result of this arrhythmogenic mechanism. Isolated canine Purkinje fibers were superfused with 2 X 10(7)M ouabain until delayed afterdepolarizations occurred and attained an amplitude of 5 mV at a paced cycle length of 500 msec. We then studied the induction of triggered activity in these fibers by pacing. We found that: (1) As the pacing cycle length decreased, the coupling interval from the last paced beat to the first triggered beat decreased and 83% of fibers developed triggered activity. (2) The coupling interval of the first triggered beat after single (S2) or double (S2S3) premature beats was in part dependent on preceding pacing cycle lengths. S2 pacing induced triggered activity in 39% of fibers, and S2S3 pacing induced triggered activity in 48% of fibers. We then studied the termination of ouabain-induced sustained rhythmic activity by pacing: 89% of sustained rhythmic activity could be terminated by overdrive pacing at a cycle length less than or equal to 300 msec. The coupling interval of the first beat or first delayed afterdepolarization after the termination of overdrive decreased as pacing cycle length decreased. S2 premature beats reset the sustained rhythmic activity and terminated 14% of sustained rhythmic activity. The coupling interval of the first escape beat or delayed afterdepolarization after S2S3 premature beats decreased as the S2S3 interval shortened, and S2S3 terminated 26% of sustained rhythmic activity. Pacing at an S1S1 cycle length of 400 msec followed by an S2 terminated 50% of sustained rhythmic activity; S1S1 at a cycle length of 400 msec followed by S2S3 terminated 85% of sustained rhythmic activity. This quantitative demonstration of the responses of delayed afterdepolarizations, triggered activity, and sustained rhythmic activity to pacing may be useful in differentiating these from other mechanisms for arrhythmias.