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PubMed1968

Atrial reciprocal rhythm and reciprocating tachycardia in Wolff-Parkinson-White syndrome.

In an infant with type A Wolff-Parkinson-White syndrome, atrial reciprocal beats and attacks of reciprocating tachycardia were repeatedly recorded. Their dependence on a prolongation of the P-R interval could be well demonstrated during Wenckebach periods. Because of the normal aspect of the QRS complex during arrhythmia, the short ventriculo-atrial conduction time (0.08 sec), and the vectorial orientation of the secondary P wave, it was concluded that retrograde reactivation of the atria probably took place via the anomalous bundle. The versatility of the conduction through the accessory bundle is shown by the fact that its direction may change from antegrade in one beat to retrograde in the next. The importance of a circus movement in the genesis of some types of tachycardia in the WPW syndrome is discussed.

Atrioventricular Node↗
PubMed1975

Electrophysiological evaluation of the Wolff-Parkinson-White syndrome: problems in assessing antegrade and retrograde conduction over the accessory pathway.

The effect of atrial pacing and recording site and ventricular pacing site on assessment of conduction over the accessory pathway (AP) was examined in a group of patients with the Wolff-Parkinson-White syndrome. The importance of initial localization of the AP by recording the sequence of retrograde atrial activation during circus movement tachycardia is demonstrated. Inability to record or pace near the AP may lead to significant errors in the assessment of the antegrade and retograde conduction properties of the AP. During ventricular pacing, retrograde atrial fusion was consistently demonstrated with laterally located APs.

Cardiac Catheterization↗
PubMed1980

Characteristics of reflection as a mechanism of reentrant arrhythmias and its relationship to parasystole.

A model of "reflection" was developed in a sucrose gap preparation of Purkinje fibers. In this preparation, a driven impulse on the proximal side of a sucrose gap is electrotonically transmitted after a delay to the tissue distal to the gap. When the delay is long enough, electrotonic transmission in the reverse direction over the same blocked segment can reexcite the proximal segment. Frequency-dependent alterations of patterns of ectopic activity were qualitatively similar to those of a parasystolic model and to those described in previous in vivo demonstrations presumed to represent circus movement reentry. Moderate changes of frequency or in the degree of block were shown to convert a manifest bigeminal rhythm to a trigeminal or more complex rhythm with or without intervening periods of silence. Our observations suggest that reflection and parasystolic pacemaker activity are examples of a continuous spectrum of ectopic impulse generation.

Animals↗
PubMed1980

Serial electrophysiologic testing of multiple drugs in patients with atrioventricular nodal reentrant paroxysmal tachycardia.

Serial electrophysiologic testing of multiple drugs was performed in 21 patients with recurrent atrioventricular (AV) nodal reentrant paroxysmal supraventricular tachycardia (PSVT). All patients had reproducible sustained PSVT induced before drug administration. Serial daily PSVT induction was attempted after administration of i.v. ouabain (0.01 mg/kg) (16 patients), i.v. propranolol (0.1 mg/kg (17 patients), i.v. ouabain + propranolol (same dosages) (12 patients), i.v. procainamide (600-1000 mg) (17 patients) and oral quinidine (1600-2400 mg/day) (nine patients). In two of 21 patients (10%), no tested drug prevented induction of sustained PSVT. In 19 of 21 patients (90%), one or more drugs prevented induction of sustained PSVT: ouabain--seven patients, propranolol--seven patients, ouabain + propranolol--seven patients, procainamide--11 patients, quinidine--seven patients. The site of action of ouabain and/or propranolol was either the antegrade limb or the retrograde limb (RL) of the circus movement. The site of action of procainamide or quinidine was always the RL. These 19 patients were treated with oral drugs, based on results of serial testing. Eighteen patients were successfully followed for 6-50 months. In 13 of these 18 patients PSVT did not recur. Two patients (11%) had > 95% reduction in frequency of PSVT recurrences, and three (17%) did not respond to chosen oral drugs. Serial electrophysiologic testing of multiple drugs is feasible in patients with AV nodal reentrant paroxysmal tachycardia. Drug responses are variable. In most but not all patients, serial electrophysiologic testing defines effective prophylactic drug therapy. This method of defining prophylactic drug therapy appears most suitable for patients with poorly tolerated tachycardias that occur only sporadically.

Administration, Oral↗
PubMed1981

Effects of oral disopyramide phosphate on induction of paroxysmal supraventricular tachycardia.

The effects of oral disopyramide phosphate on laboratory induction of paroxysmal supraventricular tachycardia (PSVT) were studied in 16 patients with clinical PSVT. After control electrophysiologic study to determine the inducibility and mechanism of PSVT, patients were given 200-300 mg (275 +/- 45 mg, mean +/- SD) of disopyramide for three to five doses over 24 hours and were then restudied. All patients had inducible, sustained PSVT during the control study. After disopyramide, PSVT was noninducible in eight patients (50%), including six of nine with atrioventricular nodal reentrance and two of seven with atrioventricular reentrance; inducible but nonsustained in two (12.5%) (both with atrioventricular reentrance); and inducible and sustained in six (37.5%). The benefit of disopyramide seemed predominantly to reflect depression of conduction in the retrograde limb of the circus movements, although effects upon the antegrade limb were also observed. In the eight patients with inducible PSVT before and after disopyramide, tachycardia cycle length increased from 348 +/- 33 to 404 +/- 29 msec (mean +/- SEM) (p less than 0.001). These results suggest that disopyramide would be effective in preventing recurrence of clinical PSVT in selected patients.

Administration, Oral↗
PubMed1983

Reentrant ventricular arrhythmias in the late myocardial infarction period. Interruption of reentrant circuits by cryothermal techniques.

Both sustained and nonsustained ventricular tachycardias were reproducibly induced in dogs 3 to 5 days after ligation of the left anterior descending coronary artery. Isochronal maps of ventricular activation were constructed from close bipolar electrograms recorded from the entire epicardial surface and selected intramural sites by a computerized multiplexing technique. The electrophysiologic data were correlated with the anatomic characteristics of the infarction. The induced tachycardias were due to reentrant activation in the surviving epicardial layer overlying the infarction. Cooling or cryoablation was applied to localized epicardial sites along the reentrant circuit to reversibly or permanently interrupt reentrant activation. The reentrant circuit could be consistently interrupted when cooling or cryoablation was applied to the distal part of the common reentrant wave front proximal to the site of earliest reactivation. Localized cooling of the site of earliest reactivation usually failed to interrupt reentry because the common reentrant wave front reactivated other sites close to the original reactivation site. Before interruption of reentry, cooling resulted in characteristic changes in conduction of the reentrant wave front. The study (1) fulfills Mines' criteria that circus movement reentry is the mechanism of the induced rhythms in this canine experimental model and (2) identifies the critical site along the reentrant circuit at which cryothermal ablation (or surgical interruption) of reentrant activation could be successfully accomplished.

Animals↗
PubMed1984

A comparison of the electrophysiologic effects of intravenous and oral amiodarone in the same patient.

In 12 patients (nine with Wolff-Parkinson-White syndrome and three with ventricular tachycardia) the electrophysiologic effects of intravenous (5 mg/kg body weight in 1 min) and oral (total dose 9800 to 11,200 mg) amiodarone were studied with programmed stimulation of the heart. Intravenous and oral amiodarone had a similar (p less than .05) effect of lengthening on the effective refractory period of the atrioventricular node. Only intravenous amiodarone prolonged (p less than .05) the AH interval. Oral amiodarone was more effective than intravenous amiodarone in lengthening the anterograde effective refractory period of the accessory atrioventricular pathway. Only oral amiodarone prolonged the effective refractory period of atrium and ventricle and the HV interval, all significantly (p less than .05). Intravenous amiodarone slowed (p less than .05) the rate of circus-movement tachycardia in patients with Wolff-Parkinson-White syndrome, and further slowing was observed after oral amiodarone. Termination of tachycardia by intravenous amiodarone predicted prevention of reinitiation of tachycardia during oral amiodarone. These data indicate that intravenous and oral amiodarone do not have the same electrophysiologic effects. It is not clear whether cumulative effects, active metabolites, or both are responsible for these differences.

Administration, Oral↗
PubMed1985

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.

Adolescent↗
PubMed1987

Effects of activation sequence and anisotropic cellular geometry on the repolarization phase of action potential of dog ventricular muscles.

The influence of activation sequences on action potential configuration, especially in the repolarization phase, was examined in isolated canine ventricular muscles. Action potentials were recorded from the epicardial surface in the center of a preparation having nearly uniform fiber orientation (25 X 25 mm). Stimuli applied just adjacent to the recording site produced nearly centrifugal propagation. An activation sequence either parallel (longitudinal) or perpendicular (transverse) to the long axis of the muscle fibers was produced by peripheral stimulation. Action potential duration at -60 mV (APD-60 mV) during centrifugal propagation was significantly longer than that during longitudinal propagation. Further shortening of APD-60 mV was observed during transverse propagation. When a collision of longitudinal or transverse wavefronts (longitudinal or transverse collision) was produced at the action potential recording site, the shortest APD was recorded. During centrifugal propagation, action potential mapping around the stimulating electrodes revealed that APD-60 mV shortened gradually as the recording site was moved further from the stimulation site. The spatial gradient of APD was steeper in the transverse than in the longitudinal direction, causing a distortion in the repolarization sequence and the recovery of excitability near the center of the tissue. Premature stimuli applied to an area near the central stimulation site induced one-way block and circus movement of the wavefront, indicating reentry of excitation. We concluded that the activation sequence and anisotropic cellular geometry substantially affect APD, and that such a change contributes to the spatial inhomogeneity of refractoriness leading to reentrant arrhythmias.

Action Potentials↗
PubMed1988

A fourth criterion for transient entrainment: the electrogram equivalent of progressive fusion.

Prior data pertaining to transient entrainment and associated phenomena have been best explained by pacing capture of a reentrant circuit. On this basis, we hypothesized that rapid pacing from a single site of two different constant pacing rates could constantly capture an appropriately selected bipolar electrogram recording site from one direction with a constant stimulus-to-electrogram interval during pacing at one rate, yet be constantly captured from another direction with a different constant stimulus-to-electrogram interval when pacing at a different constant pacing rate. To test this hypothesis, we studied a group of patients, each with a representative tachycardia (ventricular tachycardia, circus-movement tachycardia involving an atrioventricular bypass pathway, atrial tachycardia, and atrial flutter). For each tachycardia, pacing was performed from a single site for at least two different constant rates faster than the spontaneous rate of the tachycardia. We observed in these patients that a local bipolar recording site was constantly captured from different directions at two different pacing rates without interrupting the tachycardia at pacing termination. The evidence that the same site was captured from a different direction at two different pacing rates was supported by demonstrating a change in conduction time to that site associated with a change in the bipolar electrogram morphology at that site when comparing pacing at each rate. The mean conduction time (stimulus-to-recording site electrogram interval) was 319 +/- 69 msec while pacing at a mean cycle length of 265 +/- 50 msec, yet only 81 +/- 38 msec while pacing at a second mean cycle length of 233 +/- 51 msec, a mean change in conduction time of 238 +/- 56 msec. Remarkably, the faster pacing rate resulted in a shorter conduction time. The fact that the same electrode recording site was activated from different directions without interruption of the spontaneous tachycardia at pacing termination is difficult to explain on any mechanistic basis other than reentry. Also, these changes in conduction time and electrogram morphology occurred in parallel with the demonstration of progressive fusion beats on the electrocardiogram, the latter being an established criterion for transient entrainment.(ABSTRACT TRUNCATED AT 400 WORDS)

Atrial Flutter↗
PubMed1989

Activation mapping of reentry around an anatomic barrier in the canine atrium. Observations during entrainment and termination.

We determined total right atrial activation sequences during entrainment and termination of flutter induced in dogs with a surgically induced atrial lesion. This type of atrial flutter is due to circus movement of an impulse around the tricuspid valve orifice. We recorded simultaneously from 96 bipolar intracavity electrodes in the right atrium of the isolated, perfused heart. By constructing isochronal maps, we demonstrated the pattern of atrial activation during atrial pacing protocols that either entrained or entrained and then terminated the reentrant rhythm. We show that during pacing the antidromic wavefront from the paced impulse (An) collides with the orthodromic wavefront from the previous paced impulse (On-1). During entrainment, the site of collision of the orthodromic and antidromic wavefronts was constant during pacing at a fixed rate but shifted in the antidromic direction as the pacing rate increased. Furthermore, the last paced beat was entrained only up to the site of collision of the previous paced beat. During one period of entrainment, termination of the reentrant arrhythmia occurred because On-1 blocked in the reentrant pathway due to refractory tissue left by On-2. However, subsequent An did not collide directly with On as was expected, but rather On blocked by an interaction with tissue left refractory by An. Because On was blocked, no reentry occurred when pacing ended.

Animals↗
PubMed1991

Proarrhythmic effects of flecainide. Experimental evidence for increased susceptibility to reentrant arrhythmias.

BACKGROUND: The goal of this study was to investigate the nature and electrophysiological mechanisms of the proarrhythmic effects of flecainide in Langendorff-perfused rabbit hearts. METHODS AND RESULTS: A thin layer of epicardium was obtained by an endocardial cryotechnique in 10 Langendorff-perfused rabbit hearts. Six other hearts were kept intact. Programmed electrical stimulation using up to three closely coupled premature stimuli and burst pacing was used to test the inducibility of arrhythmias both during control and administration of 1 micrograms/ml flecainide. During control, in the thin layer of epicardium, application of one to three premature stimuli induced nonsustained ventricular tachycardia in out of 10 hearts, and burst pacing induced nonsustained ventricular tachycardia in four hearts and sustained ventricular tachycardia in two hearts. During administration of 1 microgram/ml flecainide, application of one to three premature stimuli induced sustained ventricular tachycardia in five hearts, and burst pacing induced sustained ventricular tachycardia in nine hearts. All tachycardias were based on circus movement of the impulse around arcs of functional block. During administration of flecainide, different locations of the arc of block could be found in the same heart, leading to different reentrant circuits with different cycle lengths. In the control group of six intact hearts, application of up to three closely coupled premature stimuli in all cases induced ventricular fibrillation both during control and administration of flecainide. CONCLUSIONS: Flecainide alters propagation of the impulse in thin surviving layers of myocardium in a manner that facilitates the induction of functionally determined reentry.

Animals↗
PubMed1992

Echo-wave termination of ventricular tachycardia. A common mechanism of termination of reentrant arrhythmias by various pharmacological interventions.

BACKGROUND: Based on epicardial mapping, different mechanisms of termination of reentrant ventricular tachycardia by various pharmacological interventions are described. METHODS AND RESULTS: In 40 Langendorff-perfused rabbit hearts, rings of anisotropic left ventricular epicardium were made by a cryoprocedure. Sustained monomorphic ventricular tachycardia based on continuous circus movement of the impulse around the ring was induced by programmed stimulation. Increasing doses of heptanol (n = 10), potassium (n = 10), tetrodotoxin (n = 6), RP62719 (a new class III drug) (n = 4), flecainide (n = 5), and propafenone (n = 5) were administered to terminate ventricular tachycardia. Epicardial mapping (248 points) was used to study the mechanism of termination of ventricular tachycardia. In 28 of 40 hearts, ventricular tachycardia terminated because the drugs produced complete conduction block of the impulse in a segment of the reentrant pathway. In the remaining 12 hearts (heptanol, n = 2; potassium, n = 3; tetrodotoxin, n = 2; RP62719, n = 2; flecainide, n = 1; and propafenone, n = 2), termination of ventricular tachycardia occurred by collision of the circulating impulse with a spontaneous antidromic wave front reflected within the circuit. This phenomenon occurred when the circulating impulse encountered an arc of functional conduction block that did not extend along the whole width of the ring. As a result, the impulse dissociated into a continuing orthodromic circulating wave and a returning antidromic echo-wave caused by microreentry within the ring. CONCLUSIONS: Independent of their mechanisms of action, sodium channel blockers, electrical uncouplers, and class III drugs terminate reentrant ventricular tachycardia either by complete conduction block or by collision of the impulse with an echo-wave.

Animals↗
PubMed1994

Surgical treatment of ventricular tachycardia after surgical repair of tetralogy of Fallot. Relation between intraoperative mapping and histological findings.

BACKGROUND: The mechanism of ventricular tachycardia (VT) after correction of tetralogy of Fallot (TF) is poorly understood. The purpose of this study was to examine the histopathology of the arrhythmogenic area detected by intraoperative mapping. METHODS AND RESULTS: The patients were three men who underwent radical surgery for TF at age 3, 3, or 5 years, respectively. VT developed at 8, 9, or 11 years, respectively, after surgery, and shock developed during VT in every case. The ECG revealed monomorphic VT in two cases and polymorphic VT in one case. Induction of VT resulted in a wide left-axis deviation-pattern QRS with cycle lengths varying between 260 and 330 milliseconds. The VT origin was identified at the right ventricular outflow tract (RVOT). A radical operation was performed with the patient under cardiopulmonary bypass. On epicardial mapping, delayed activation of the RVOT was recorded during sinus rhythm, and clockwise circus movement of the macroreentry current during VT on the right ventricular free wall was documented in each case. The VTs were treated successfully by surgical resection and cryoablation of the myocardium. In every patient, histology of the myocardial specimens showed degeneration, adiposis, fibrosis, inflammatory cell infiltration, and scattered myocyte islets. These lesions corresponded anatomically to the area of myocardium in which delayed activation was evident during epicardial mapping. CONCLUSIONS: The results of this study indicate that patients with VT after radical correction of the TF have abnormal histopathological findings at the site of the prior right ventriculotomy scar. These lesions were noted within the region of delayed activation found during epicardial mapping and were found to be a part of the reentrant circuit.

Adult↗
PubMed1996

Cycle length dynamics and spatial stability at the onset of postinfarction monomorphic ventricular tachycardias induced in patients and canine preparations.

BACKGROUND: The aim of this study was to determine whether cycle length (CL) variations at the onset of monomorphic ventricular tachycardias follow distinctive patterns. METHODS AND RESULTS: We retrospectively analyzed 59 monomorphic ventricular tachycardias induced in 40 patients in whom intraoperative mapping was performed with 63 epicardial and 64 endocardial electrograms recorded simultaneously. Activation times and CL were determined at each electrode site over several beats (36+/-10 beats, mean+/-SD) starting with the first after programmed stimulation. In the majority of the tachycardias, CL variations were accounted for by fitting to an exponential function: CL=CLs+Ae-b/tau, where CLs is the stable CL, b is beat number, tau is the time constant (in beat number), and A is the magnitude of CL relaxation. A decelerating trend (with reference to rate) (negative A) accounted for 21 tachycardias, an accelerating trend in rate (positive A) accounted for 12 tachycardias, and 4 others displayed a double dynamic behavior, with an initial acceleration followed by a decelerating trend in rate. Among the ventricular tachycardias that were not fitted to exponential models, 12 showed a constant trend and 10 others showed irregular CL fluctuations. The monomorphic character of the tachycardias was established by principal-component analysis, which also indicated that CL dynamics associated with the accelerating and decelerating trends may be related to shortening and prolongation of activation times, respectively, occurring in equal proportion at all recording sites. In canine preparations in which reentry circuits could be mapped with high resolution, CL showed an accelerating trend in rate when circus movement of excitation occurred around a transmural scar in muscle generating unipolar electrograms with relatively high -dV/dtmax, and a decelerating trend in rate occurred when functional reentry occurred in muscle generating unipolar electrograms with depressed -dV/dtmax. CONCLUSIONS: Beat-to-beat CL variations may occur at the onset of sustained monomorphic ventricular tachycardia as a result of uniform acceleration or deceleration of activation times while the overall activation pattern remains constant. The associated initial trends in the rate of sustained monomorphic ventricular tachycardia follow typical patterns that might provide "signatures" corresponding to reentry substrates with distinctive functional properties.

Adult↗
PubMed1996

Electrophysiological mechanisms of spontaneous termination of sustained monomorphic reentrant ventricular tachycardia in the canine postinfarction heart.

BACKGROUND: The electrophysiological mechanisms of spontaneous termination of sustained monomorphic ventricular tachycardia (SMVT), in the postinfarction heart, generally considered secondary to a reentrant mechanism, have not been fully investigated. METHODS AND RESULTS: Epicardial activation maps of spontaneous termination of 20 different episodes of SMVT (lasting 30 seconds to 10 minutes) from 8 dogs, 4 to 5 days after one-stage ligation of the left anterior descending coronary artery, were analyzed with the use of 254 bipolar electrode recordings with high density (2.5 to 2.8 mm between bipolar electrodes) in the ischemic zone. All ventricular tachycardias (VTs) were due to circus movement reentry with a characteristic figure-8 configuration. Termination always occurred when the two circulating wave fronts blocked in the central common pathway (CCP). Two basic mechanisms of spontaneous termination were observed: (1) In 15 episodes, acceleration of conduction occurred in parts of the reentrant circuit and was associated with slowing of conduction and finally conduction block in the CCP. Acceleration of conduction occurred in the last few cycles of VT both at the outer border of the arcs of functional conduction block in the "normal" myocardial zone and at the pivot points to the entrance to the CCP. When acceleration of conduction was compensated on a beat-to-beat basis by an equal degree of slowing in the CCP, there was no discernible change in the cycle length of the VT in the ECG. In some episodes, the termination of the original reentrant circuit was followed by the development of a different, slower reentrant pathway that lasted for one or a few cycles prior to termination. (2) In 5 VT episodes, the activation wave front in the CCP abruptly broke across a stable arc of functional conduction block, resulting in premature activation of the CCP and conduction block. CONCLUSIONS: Distinct electrophysiological changes always preceded spontaneous termination of stable SMVT. The electrophysiological basis for acceleration of conduction in parts of the reentrant circuit during the last few beats prior to termination and of the abrupt reactivation across a stable arc of block remains to be determined.

Animals↗
PubMedDate not supplied

Longitudinal dissociation within the posterior AV nodal input of the rabbit: a substrate for AV nodal reentry.

BACKGROUND: Longitudinal dissociation of an anatomic pathway into 2 electrophysiologically distinct pathways has been hypothesized as a basis for localized AV nodal reentry and supraventricular arrhythmias. METHODS AND RESULTS: Extracellular bipolar and intracellular microelectrodes were used to record activation in the superfused rabbit AV junction. A subset of rabbit hearts (n=19 of 72) demonstrated dissociation of the posterior AV nodal input into >/=2 functional pathways. Antegrade AH conduction was maintained by a pathway just inferior to the tendon of Todaro. Rate-dependent conduction block was observed in a second pathway just superior to the tricuspid annulus, allowing retrograde activation of the distal portion of the inferior posterior AV nodal input and leading to the formation of apparent "dead-end" pathways. The superior (antegrade) and inferior (retrograde) pathways were separated by a band of well-polarized but poorly excitable transitional cells. Additional decreases in the atrial cycle length progressively increased the AH interval, further delaying retrograde activation of the inferior pathway, and progressively moved the site of conduction block in the inferior pathway proximally, thus extending the length of the retrograde conduction pathway and allowing circus movement within the transitional cells of the posterior AV nodal connection. CONCLUSIONS: Longitudinal dissociation within the posterior AV nodal input can give rise to localized reentry and AV nodal reentrant tachycardia.

Action Potentials↗
PubMed1983

Triggered ventricular rhythms in 1-day-old myocardial infarction in the dog.

Triggered activity developed in depolarized Purkinje fibers (maximum diastolic potential -59.3 +/- 9.9 mV) during superfusion with normal Tyrode's solution in 84% of subendocardial preparations from 1-day-old canine infarct. Triggered activity occurred when a delayed afterdepolarization attained threshold potential and spontaneously terminated after a subthreshold delayed afterdepolarization. Triggered activity was initiated either by stimulated beats or by the background slow Purkinje automaticity. When multiple stimulated beats were required, the amplitude of the afterdepolarization increased and the coupling interval decreased when the stimulation frequency and/or the number of stimulated beats increased. Varying degrees of entrance and exit block around sites of triggered activity were common, and some triggered activity manifested as a parasystolic rhythm. In preparations showing subthreshold delayed afterdepolarizations, both epinephrine (2.5 x 10(-6) M) and increasing [Ca++]o, (from 2.7 to 8.1 mM) increased the amplitude of afterdepolarizations and resulted in triggered activity. On the other hand, verapamil (2.2 x 10(-6) M) resulted in exit block around sites of triggered activity and/or completely suppressed afterdepolarizations and triggered activity. Isochronal mapping of endocardial activation during the initiation and perpetuation of triggered activity elucidated a focal site of origin from Purkinje fibers overlying the infarct and showed no evidence of a circus movement of excitation. The in vitro triggered activity may explain the spontaneous multiform ventricular rhythms seen in the intact heart.

Action Potentials↗