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.
Method 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.
Sustained monomorphic ventricular tachycardia is not uncommon in patients with previous myocardial infarction and is generally considered to result from circus movement reentry.1 2 The arrhythmia can result in hemodynamic compromise and become life threatening. Spontaneous termination of SMVT is common and can ostensibly prevent potential complications of the arrhythmia. Several clinical studies of ECG changes associated with spontaneous termination of SMVT have been published1 2 but admittedly provide limited insight into the underlying electrophysiological mechanisms. Few studies have investigated the mechanism(s) of spontaneous termination of sustained circus movement reentry in atrial and ventricular models.3 4 The present study is the first to investigate the electrophysiological mechanisms of spontaneous termination of SMVT in a well-documented model of postinfarction circus movement VT in the dog.5 Understanding these mechanisms may help in designing appropriate therapeutic measures.
The studies were approved by the Animal Studies Committee of the local Institutional Review Board. Details of the procedure have been reported previously and will only be described briefly.6 Experiments were performed on 8 male, mongrel dogs weighing 15 to 25 kg that were preanesthetized with sodium thiopental (17.5 mg/kg IV) via the cephalic vein. The dogs were then anesthetized with inhalation anesthesia (1.0% to 2.0% isoflurane vaporized in 100% oxygen) via a positive ventilation anesthesia machine (F500, The Forreger Co). Under sterile conditions, a left thoracotomy was performed at the fourth intercostal space to expose the heart. The LAD coronary artery was dissected free and ligated in one stage, 1 to 2 cm from its origin. Coronary circulation and potential collateral blood flow were assessed. When necessary, large epicardial branches in the anterior left ventricular free wall and apex originating from the left circumflex or posterior descending coronary artery were also ligated. After the ligation, the dog was monitored in the open chest state for 20 minutes. The chest was then closed in layers and the pneumothorax evacuated. The dogs were allowed to recover and received antibiotic (Penicillin-G procaine, 20,000 U/kg IM) and analgesic (buprenorphine, 0.005 to 0.02 mg/kg) as required.
Four to 5 days after ligation, the dog was again preanesthetized with sodium thiopental (17.5 mg/kg IV) via the cephalic vein and anesthetized with inhalation (1.0% to 2.0% isoflurane vaporized in 100% oxygen) via positive ventilation. ECG lead II and aortic blood pressure (Statham, Gould, Inc) were continuously monitored on a VR12 monitor (PPG Industries). The heart was exposed through a left thoracotomy. Core temperature and intrathoracic temperature were monitored with the use of two electronic thermometers (Yellow Springs Instruments). To slow the sinus rate, a Grass S88 stimulator was used to stimulate the right and left vagosympathetic trunks through two pairs of Teflon-insulated silver wires (.010-in diameter) with square-wave pulses of 0.1- to 0.5-ms duration at a frequency of 20 Hz at 1 to 10 V.7
A sock electrode array was placed on the ventricular surface for simultaneous recording at 254 epicardial sites. Each bipolar electrode consisted of a pair of silver wires (125-μm diameter) sutured to the sock with an interpolar distance of 0.8 to 1.4 mm. The distance between electrodes ranged between 2.5 and 10 mm. A higher concentration of electrodes covered the zone of infarction and infarction border and consisted of 184 bipolar electrodes. These were arranged in 16 parallel rows, and the distance between rows was 2.5 mm. Each row consisted of alternating sets of 11 or 12 bipolar electrodes in which the distance between electrodes was 2.8 mm (Fig 1⇓). Additional details of the recording technique have been reported previously.8
Programmed electrical stimulation was provided by a digital stimulator (model DTU-101, Bloom Co) delivering square pulses (2 ms) through a bipolar plunge electrode consisting of two hooked stainless steel wires (enamel-coated, 125-μm diameter) placed in a 23-gauge hypodermic needle (0.64-mm outer diameter). The stimulation site was in the right ventricle, adjacent to the septal border of the infarct or near the right ventricular outflow tract.
After surgical preparation and sock electrode placement, the ribs were approximated and the chest cavity was closed. Once the core temperature had stabilized, programmed stimulation was applied to the control site to induce reentrant rhythms. The control stimulation sequence consisted of a train of 8 basic driven beats at two cycle lengths (S1S1, 400 and 300 ms) at twice diastolic threshold, followed by one or more premature stimuli that were introduced at decreasing coupling intervals. The end point of programmed stimulation was the induction of SMVT defined as VT with uniform QRS morphology lasting ≥30 seconds.
Electrogram recordings of activation during SMVT were obtained through the multiplexed data acquisition system (INET Corp).8 Each channel was sampled at 1 kHz with 12-bit resolution. To capture the spontaneous termination of SMVT, we used a circular memory buffer with an adjustable pretrigger of 0 to 15 seconds (16 Mbytes). Isochronal maps of epicardial activation were constructed with isochrones delineated by closed contours at 10-ms intervals. Activation times at each recording site were identified with the use of previously published criteria.8 The criteria used for activation detection in bipolar electrograms depend on electrogram configuration.9 In uniphasic and triphasic signals, the peak voltage is a reliable predictor of activation time.9 In biphasic signals, the activation time was selected at the maximum slope. Computer-derived activation times were edited by the operator. Arcs of functional conduction block were defined as an activation time difference between contiguous electrodes of more than 40 ms and by the recording of double potential representing an activation and electrotonic potentials that corresponded, respectively, to electrotonic and activation potentials on the other side of the arc of functional block.8 10
We analyzed epicardial activation patterns of spontaneous termination of 20 different episodes of SMVT from 8 dogs (Table⇓). SMVTs included in the study lasted from 30 seconds up to 10 minutes (mean±SD, 2.8±1.9 minutes). There were 6 more episodes of SMVT that lasted more than 10 minutes and were terminated by programmed stimulation or direct current shock (Table⇓) The VT cycle length of SMVTs that lasted ≤10 minutes ranged from 170 to 340 ms (mean±SD, 219±45 ms). This was not significantly different from SMVTs that lasted >10 minutes (mean±SD, 222±39 ms). There was no correlation between the cycle length, duration, or ventricular activation pattern of SMVT and spontaneous termination at ≤10 minutes. In all episodes of SMVT, the entire reentrant circuit could be mapped on the epicardial surface. During SMVT, the mean arterial blood pressure showed a moderate decrease from 99±18 to 86±16 mm Hg. All VTs showed a characteristic figure-8 pattern or a modification thereof.10 The figure-8 pattern consisted of clockwise and counterclockwise activation wave fronts around two separate arcs of functional conduction block that joined into a common central wave front. Termination of a figure-8 VT always occurred when the two circulating wave fronts blocked in the CCP. Four different patterns of spontaneous VT termination were observed.
Pattern 1: Acceleration of conduction in both the normal zone and the pivot points to the entrance to the CCP. This pattern of spontaneous termination was observed in 7 different episodes of SMVT and is shown in Figs 2⇓ and 3⇓. Fig 2⇓ illustrates the epicardial activation maps of the last 4 VT cycles, while Fig 3⇓ shows the ECG lead and selected electrograms along the clockwise circulating wave front of the reentrant circuit. Enlarged sections of the polar map as shown in Fig 1⇑ are illustrated. Activation isochrones are drawn at 10-ms intervals, and the arcs of functional conduction block are depicted as heavy solid lines. The activation maps show a modification of a figure-8 circuit. The cycle length of the SMVT was 240 ms. There was a stable clockwise wave front around a functional arc of block close to the anterolateral border of the epicardial ischemic zone. However, the counterclockwise wave front located in the lower anteroseptal and apical regions was not stable and varied from beat to beat as the result of changes in the location and configuration of the zone of functional conduction block. The two circulating wave fronts joined into a CCP where conduction was relatively slow, ie, crowded isochrones, compared with conduction at the outer borders of the arcs of block.
Fig 3⇑ illustrates the changes in cycle length of the VT at different sites along the reentrant circuit. The VT cycle length was stable at 240 ms but showed gradual shortening in the last 4 cycles that was more marked in the last 2 cycles. The last cycle length of VT at site N was 48 ms shorter compared with the stable VT cycle of 240 ms. Analysis of the activation maps reveal that approximately 20 ms of the shortening occurred between sites H and J along the outer border of the anterolateral arc of block, while the rest of the shortening occurred between sites J and N spanning the pivot point around the arc of block. The earlier arrival of the circulating wave front to the CCP resulted in conduction block and termination of circus movement. The site of block is represented in Fig 3⇑ between electrograms Q and A, where site A shows an electrotonic deflection. The last QRS complex of VT had a shorter duration that could be explained by failure of activation of a large part of the ventricles during the last cycle of VT. In summary, the spontaneous termination of the SMVT was due to acceleration of conduction in the last few cycles with earlier arrival of the circulating wave front to the CCP where conduction block occurred. The acceleration of conduction occurred both at the “normal zone” at the outer border of the arc of block and at the pivot points to the entrance to the CCP.
Pattern 2: Acceleration of conduction in parts of the reentrant circuit with compensatory slowing in the CCP prior to block. In 5 different episodes of SMVT, spontaneous termination was associated with gradual acceleration of conduction in parts of the reentrant circuit associated with a compensatory beat-to-beat slowing of conduction and eventual block in the CCP. In one episode, there was lengthening of the last VT cycle length. However, in 4 of the 5 episodes, no significant change in the cycle length of the VT was apparent in the surface ECG. This is illustrated in Figs 4⇓ and 5⇓. The bottom of Fig 4⇓ shows the surface ECG and selected electrograms of spontaneous termination of an episode of SMVT. The top of Fig 4⇓ illustrates the epicardial activation map of the last stable reentrant cycle (VT-5) and the next-to-last reentrant cycle (VT-1). During the stable figure-8 reentrant circuit, significant slowing of conduction occurred both at the pivot points to the entrance to the CCP and in the CCP itself. This is illustrated by the conduction delay between sites I and J and between sites K and A, respectively. During the last 5 reentrant cycles, there was a gradual acceleration of conduction around the pivot points of the entrance to the CCP associated with compensatory gradual slowing of conduction in the CCP. Finally, conduction block developed between sites K and A in the CCP, resulting in termination of reentry.
Fig 5⇑ illustrates the gradual acceleration of conduction between sites I and J associated with gradual slowing of conduction between sites K and A. Note the gradual shortening of the interval between the electrotonic and activation potentials in electrogram J. Also note the gradual widening of the duration of electrogram K associated with gradual increase of the conduction time between K and A and the shortening of the duration of the last K potential associated with the development of conduction block between K and A. The conduction time between sites I and A showed minor oscillations; however, the duration between surface QRS complexes was almost constant. The changes of conduction in the central part of the reentrant circuit could not have been detected by analysis of the intervals between electrograms outside this zone.
Pattern 3: Acceleration of conduction of the last one or few cycles with termination of the original VT and initiation of a different short-lived slower circuit. This pattern of spontaneous termination was observed in 3 different episodes of VT and is illustrated in Figs 6 through 10⇓⇓⇓⇓⇓. Fig 6⇓ illustrates the isochronal activation map of the original stable VT circuit. The circuit consisted of a counterclockwise wave front around an arc of functional conduction block at the anterolateral border of the epicardial ischemic zone and a clockwise wave front around a separate arc of block at the apical region of the ischemic zone. The two wave fronts joined into a broad, common wave front. Note that the arcs of functional conduction block are long and that most of the slowed conduction took place at the pivot points around the end of the arcs of block rather than in the broad CCP.
Fig 7⇑ shows the surface ECG lead and selected electrograms of the counterclockwise wave front of the last 6 VT cycles prior to termination. The stable VT cycle length of 185 ms is represented by VT-5. There was a 10-ms progressive shortening of the cycle lengths of VT-3 and VT-2 (see electrogram Q) that resulted in termination of the original reentrant circuit (see block between electrograms R and S). This was followed by the development of different slower reentrant wave fronts that lasted for two complete cycles (VT-2 and VT-1) before it terminated (VT).
Fig 8⇑ illustrates the epicardial activation maps of the last 6 reentrant cycles (VT-5 to VT). The VT-5 map represents the last stable VT cycle. The maps of VT-3 and VT-2 illustrate the acceleration of conduction of the circulating wave fronts, with an earlier arrival of the wave front to the entrance of the CCP resulting in conduction block and termination of the original reentrant circuit as shown in VT-2. However, reentrant excitation continued in the form of a very slow and circuitous wave front at the apical region that circulated for two cycles before it blocked with termination of VT.
Fig 9⇑ illustrates in more detail the acceleration of conduction of the counterclockwise wave front during VT-3 and VT-2. The acceleration of conduction occurred primarily in the “normal zone” along the outer border of the arc of block between electrode sites K and g. Fig 10⇑ illustrates in more detail the complex activation pattern of the last 3 reentrant cycles, VT-2, VT-1, and VT, as well as selected electrograms along the reentrant pathway. The electrograms show bridging of the diastolic intervals. However, the resolution of recording sites was inadequate to accurately map the details of the slow and circuitous reentrant pathway.
Pattern 4: Breakthrough of the reentrant wave front across a stable arc of functional conduction block resulting in premature activation and conduction block in the CCP. This mechanism of spontaneous termination of SMVT was observed in 5 different episodes and is illustrated in Figs 11 through 13⇓⇓⇓. Fig 11⇓ illustrates the activation map of the stable VT represented by VT-2. The circuit had a figure-8 pattern in the form of clockwise and counterclockwise wave fronts that joined into a long CCP. The CCP narrowed significantly in the middle portion as the result of extension of the arcs of functional conduction block. Fig 12⇓ shows the surface ECG lead and selected electrograms of spontaneous termination of the SMVT. The last QRS of the VT is inscribed prematurely and has a different configuration. Electrogram X represents a site in the middle of the CCP very close to the lateral arc of functional block, while electrogram C represents a contiguous site on the other side of the arc of block. Electrogram X has two deflections, one of which is marked by an asterisk and represents activation, while the second deflection represents the electrotonus of the activation potential at the contiguous site C across the arc. Also note the presence of a low-amplitude electrotonic potential in electrogram C corresponding to the activation potential of X. Fig 13⇓ illustrates the activation maps of the last two VT cycles. During the VT-1 cycle, the activation wave front at site X suddenly reactivated site C across the arc of functional block. This is represented in electrogram C in Fig 12⇓ by a series of slow deflections that started at the electrotonic potential and ended by a sharper activation potential. The slow conduction between sites X and C was approximately 40 ms (see the enlarged section in Fig 13⇓). Once site C was reactivated, the wave front circulated in both clockwise and counterclockwise directions around the lateral arc of block. The clockwise wave front then prematurely conducted to the narrow isthmus of the CCP, resulting in conduction block and termination of reentry (the VT map). Fig 12⇓ shows the site of block between electrograms M and N.
Comparison of SMVT that spontaneously terminated within 10 minutes with SMVT that lasted >10 minutes. The Table⇑ shows that the cycle length of the 6 episodes of SMVT that lasted >10 minutes was not significantly different from SMVT that spontaneously terminated within 10 minutes. The cycle length of the nonterminating SMVT remained constant until the arrhythmia was terminated by programmed stimulation or direct current shock. In one experiment (No. 3), an SMVT with a similar activation pattern was induced twice, and both times it terminated spontaneously as the result of acceleration of conduction in the last few cycles. In two other experiments (Nos. 1 and 6), an SMVT with similar activation pattern was induced twice in the same experiment, and only one of the episodes terminated spontaneously. The spontaneous termination was due to abrupt acceleration of conduction in the last few cycles. By contrast, the similar episode that failed to terminate within 10 minutes maintained a constant cycle length.
The present study illustrates some of the topological variations of the classic figure-8 reentrant circuit. Although the typical topology is in the form of two circulating wave fronts that join into a CCP, in some instances a single, stable, circulating wave front could sustain the reentrant process as shown in Fig 2⇑. We have shown previously that a single reentrant loop also could develop in a syncytium if the functional block extends to an anatomic barrier, as in the case of circus movement atrial flutter.11 The topology and degree of slow conduction in the CCP can also vary. A relatively short and narrow CCP is usually associated with markedly slow conduction, as shown in Fig 4⇑, while conduction velocity may or may not be significantly slowed in a circuit with a long and broad CCP as shown in Figs 2⇑ and 6⇑. In both types of figure-8 circuits, however, a major component of conduction delay takes place at the pivot points around the two arcs of functional conduction block and especially at the entrance to the CCP. The slowing of conduction at the pivot points of the reentrant circuit could be related primarily to alterations in current loading resulting from the pivoting process that depresses excitability and slows local conduction.12 13 Although there was no attempt in the present study to correlate precisely the location of the arcs of functional conduction block in relation to epicardial fiber orientation, in many instances the arcs appeared to occur both along and across fiber orientation.8
The present study showed essentially two basic mechanisms for spontaneous termination of SMVT. The first mechanism is an acceleration of conduction in some parts of the reentrant circuit leading to premature activation and block in the CCP. The acceleration of conduction could be associated with slowing of conduction prior to conduction block in the CCP. The acceleration of conduction occurred in the last few cycles of VT and was either gradual in nature (Figs 5⇑ and 9⇑) or irregular (Figs 2⇑ and 3⇑). The acceleration of conduction occurred both at the outer border of the arcs of functional conduction block, ostensibly in “normal” myocardial zones, and at the pivot points to the entrance to the CCP where conduction is usually slowed. The acceleration of conduction around the pivot points was not associated with any discernible shortening of the length of the arc. Although in most instances the acceleration of conduction represented the primary event that was followed by slowing of conduction in the CCP, in one instance it was difficult to exclude as a primary event the slowing of conduction in the CCP with compensatory acceleration in other parts of the reentrant circuit. When the 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 VT prior to termination, as seen in the surface ECG or in electrograms outside the reentrant circuit (Figs 4⇑ and 5⇑). In three different episodes of SMVT, the termination of the original reentrant circuit was followed by the development of different slower circulating wave fronts that lasted for one or few cycles prior to termination (Figs 6⇑, 8⇑, and 10⇑). In these episodes, marked variations in the last few VT cycle lengths in the surface ECG were observed in the form of shortening, followed by lengthening of one or more cycles.
The second mechanism of spontaneous termination of SMVT was more intriguing. During SMVT, the activation wave front in the CCP abruptly broke across a stable arc of functional conduction block, resulting in premature activation of the CCP leading to conduction block. This process was associated with slowed conduction at the site of reactivation across the arc (see Figs 12⇑ and 13⇑). Premature activation across the arc suggests that the intensity of the local electrotonic current provided to that site by the activating current on the other side of the arc has reached the threshold voltage for a propagated activation. This could be due to changes of passive or active membrane properties at the current source, ie, the activating wave front or the current sink, ie, the reactivated site. These changes are usually rate dependent.14 However, we were not able to discern any changes in the cycle length of VT, the amplitude, or the configuration of the local electrograms prior to the abrupt reactivation across the arc.
The episodes of SMVT that failed to terminate within 10 minutes maintained a constant cycle length. The number of observations was too small to answer the question of whether acceleration of conduction in parts of the circuit can occur without spontaneous termination. However, in the two experiments in which an SMVT with a similar activation pattern was induced twice, the one episode that terminated spontaneously showed acceleration of conduction in the last few cycles as contrasted with the constant cycle length of the nonterminating episode.
Several clinical studies analyzed the ECG correlates of spontaneous termination of SMVT in patients with coronary artery disease. Some studies showed no specific patterns of cycle length variability characteristic of VT termination, although cycle length variability increased immediately before spontaneous termination.1 A change in QRS morphology occurred before termination in only a small percentage of VT episodes.1 Transient shortening of QRS just before termination and paradoxical prolongation of the QRS to the peak of T-wave interval after abrupt shortening of VT cycle length were also described.2 It is difficult to relate any of these ECG changes to a particular electrophysiological mechanism.
On the other hand, there are few basic studies of the mechanism of spontaneous termination of sustained reentry. Simson et al15 demonstrated in a computer model of atrioventricular reentrant tachycardia that for a reentrant circuit to continue, it must be able to dampen spontaneous oscillations in conduction and refractoriness. Frame and Simson3 later investigated the mechanism of cycle length oscillation and its role in spontaneous termination of reentry in an in vitro preparation of canine atrial tissue surrounding the tricuspid orifice. Oscillations caused most spontaneous terminations in this model. Two dynamic tissue properties, interval-dependent conduction and interval-dependent changes in action potential duration, ie, electrical restitution, were sufficient to explain the local changes in conduction that contribute to the oscillations and the mechanism by which oscillations caused termination. Cycle length oscillations were not observed in the present study and were not reported in clinical ECG studies of spontaneous VT termination.1 2
Brugada et al4 have shown in a reentry model in rings of anisotropic left ventricular epicardium of the rabbit that termination of VT could occur 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. Such a mechanism was not observed in the present study.
In a preliminary report by Waldecker et al,16 the mechanisms of spontaneous termination of SMVT in the canine postinfarction heart were investigated. Conduction slowing in the CCP prior to block and abrupt activation across the arc of block were observed. However, acceleration of conduction in parts of the reentrant circuit as a primary event prior to slowing of conduction in the CCP was not observed. Further, in 9 of 21 episodes of VT, no changes in conduction or cycle length were observed, and the mechanism of termination was not discernible. This is in sharp contrast to the present study, in which distinct electrophysiological changes always preceded spontaneous termination of SMVT.
Limitations of the Study
As in many studies on mapping of cardiac activation, the resolution of the activation map is directly related to the number and density of recording sites. Although the present study used relatively high-resolution recordings in the ischemic zone, some fine details of activation could not be analyzed adequately. These include but are not limited to details of the changes of conduction at the pivot points to the CCP prior to block (Fig 3⇑), the circuitous conduction in some of the reentrant circuits (Fig 10⇑), and the nature of the very slowed conduction in some CCP, as in Fig 4⇑ (possibly a markedly circuitous wave front).
The most significant limitation of the present study, however, is that it provides no explanation of the apparently sudden acceleration of conduction in parts of the reentrant circuit prior to termination. We can only speculate that this may be related to a local change in the autonomic tone and/or circulating catecholamines. In a previous study we have shown differential effects of these changes on refractoriness and conduction of the normal and ischemic zones of the postinfarction canine heart.17 The trigger for such changes, however, remains unclear. In this regard we were not able to discern any changes in the arterial blood pressure immediately prior to termination. An alternative mechanism for acceleration of conduction is suggested by the work of Davidenko et al,18 who showed that the excitability of normal myocardium may increase during activity, ie, active facilitation. Primary slowing of conduction in the CCP, possibly a “fatigue” phenomenon, with secondary acceleration of conduction in other parts of the circuit may be operational in some episodes of VT termination but was not observed in the present study. More intriguing is the mechanism by which a passive electrotonus can suddenly reach threshold and trigger active propagation. These basic hypotheses require further investigation.
Selected Abbreviations and Acronyms
|CCP||=||central common pathway|
|LAD||=||left anterior descending|
|SMVT||=||sustained monomorphic ventricular tachycardia|
This work was supported by Veterans Administration Medical Research Funds (Merit Grants) to Dr El-Sherif and Dr Restivo. The authors would like to thank Antoinette Wells and her staff in the animal facility, Mohammed Piracha, and Richard Levin for their technical assistance and Valerie Sussman for typing the manuscript.
- Received August 23, 1995.
- Revision received October 18, 1995.
- Accepted October 20, 1995.
- Copyright © 1996 by American Heart Association
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