Effect of ventricular premature beats on idioventricular pacemaker activity

The effect of ventricular premature beats on idioventricular pacemaker activity was studied in open-chest dog hearts with a surgically induced block in the His bundle. While the ventricle was paced by basic stimuli at a given rate, the pacing was interrupted for about 2.5 seconds following every twelfth basic beat (V₁) in order to obtain the interval between V₁ and the first escape beat (V_e) or the basic escape interval (V₁V_e). Ventricular premature beats (V₂) were then introduced at various coupling intervals (V₁V₂) and the effect of these premature beats on the postextrasystolic escape interval (V₁V_e) was observed. The plot of V₂V_e against V₁V₂ intervals showed that the V₂V_e interval was shortest at shorter V₁V₂ intervals, and it increased gradually with the increase in V₁V₂ intervals. The V₂V_e intervals at shorter coupling intervals were much shorter than the basic escape interval (V₁V_e), indicating enhanced automaticity after early premature beats. The V₂V_e at longer coupling intervals were much longer than the basic escape intervals, indicating suppressed automaticity after late premature beats. The similar response to ventricular premature beats was noted during spontaneous idioventricular rhythm. The suppression was more pronounced at faster pacing rates and following two successive premature beats, probably due to the phenomenon of overdrive suppression. The same phenomena of altered automaticity after premature beats could be observed under the influence of ouabain, epinephrine, lidocaine, and propranolol, although these agents either decreased or increased the average escape intervals. The results may explain the clinically observed alteration of the idioventricular pacemaker rate following ventricular premature beats.     

Ventricular arrhythmias following one-stage and two-stage coronary reperfusion: evidence for both reentry and enhanced automaticity

We studied the effects of reperfusion in 60 dogs following a 30-45 minute period of left anterior descending coronary artery occlusion using electrocardiograms and composite electrogram recordings. One-stage reperfusion in 14 of 15 dogs produced ventricular arrhythmias which degenerated into ventricular fibrillation within 60 seconds. The onset of ventricular arrhythmias was associated with continuous electrical activity in epicardial and intramural electrograms recorded from the reperfused zone. Vagal slowing during reperfusion (64 +/- 8/min) did not prevent ventricular fibrillation (eight of eight dogs) and escape beats were often followed by one or more coupled ectopic beats associated with continuous electrical activity. Rapid atrial pacing (270/min) also did not prevent the appearance of ventricular arrhythmia with associated continuous electrical activity and ventricular fibrillation (six of six dogs) nor did 4 mg/kg lidocaine (15 of 16 dogs). In another group of 15 dogs reperfusion was performed in two stages resulting in no ventricular fibrillation but in 8 of 15 dogs ventricular arrhythmias were observed beginning within two minutes after reperfusion and lasting 20-30 minutes. These ventricular arrhythmias were not associated with continuous electrical activity in any of the recorded leads. Atrial pacing suppressed ventricular arrhythmias and idioventricular rate averaged 157 +/- 10/min versus 55 +/- 10/min pre-reperfusion control. The earliest site of activation indicated automatic foci arising in the subendocardium of the reperfused zone. Lidocaine (2-4 mg/kg) rapidly (less than 90 sec) restored normal sinus rhythm and suppressed automaticity (72 +/- 11/min) as did left anterior descending artery reocclusion (52 +/- 6/min). We conclude that both reentry and enhanced automaticity play a role in ventricular arrhythmias due to reperfusion. Lidocaine (2-4 mg/kg) suppresses automatic but not reentrant ventricular arrhythmias in this experimental setting.     

Effects of verapamil on ventricular rhythm during acute coronary occlusion

The effects of verapamil on electrophysiologic parameters of the ventricle were studied during acute coronary occlusion in anesthetized open-chest dogs. Those parameters measured in the study were idioventricular automaticity, ventricular conduction, and fibrillation threshold. The incidence of rapidly repetitive beats and fibrillation induced by two successive premature beats was also studied. Verapamil significantly decreased idioventricular automaticity (in five dogs), improved conduction through the ischemic area (in six dogs), and increased fibrillation threshold of the ischemic ventricular (in eight dogs). The drug was effective in abolishing rapidly repetitive beats and fibrillation induced by closely coupled premature beats during acute coronary occlusion. Rapidly repetitive beats occurred in nine out of 15 dogs and these repetitive beats were degenerated into fibrillation in seven dogs before verapamil. Following pretreatment with the drug, rapidly repetitive beats and fibrillation occurred in none of the 15 dogs. The results indicate that verapamil can be very effective against ventricular arrhythmias occurring in association with myocardial infarction.     

Facilitation of A-V nodal reciprocation by procainamide.

Procainamide is known to depress conduction through the A-V node, and this property may facilitate the development of ventricular reciprocal beats or echoes. The occurrence of ventricular reciprocal beats was studied in 20 open-chest dogs before and after the administration of procainamide. While the ventricle was paced by basic stimuli, early ventricular premature beats were introduced at various coupling intervals to induce ventricular echoes. When ventricular echoes could be induced in a given heart, there was a continuous range of coupling intervals (or echo zone) within which ventricular echoes occurred. In the control state, no echo occurred in eight dogs and the echoes developed in 12 dogs with the mean echo zone of 38.3 msec. The effect of procainamide was studied at its therapeutic blood levels about 25 minutes after an intravenous injection of the drug in a dose of 10 mg. per kilogram. Of the first group of eight dogs, in which no echo occurred in the control state, four dogs developed ventricular echoes after the administration of procainamide with the mean echo zone of 29.3 msec. for the group. Of the second group of 12 dogs, in which ventricular echoes were induced in the control state, the administration of procainamide increased the echo zone in 10 dogs with the mean echo zone of 67.8 msec. for the group. Ventricular reciprocal beats were often sustained to produce short runs of supraventricular tachycardia in five dogs after the administration of procainamide. The results demonstrated a potentially deleterious effect of procainamide in facilitating the inducation of A-V nodal reciprocation by closely coupled ventricular premature beats.     

Reflections on reentry and focal activity

Initiation and maintenance of reentrant arrhythmias, such as ventricular tachycardia and fibrillation in the acute phase of myocardial ischemia, may be due to different mechanisms. The characteristics of circus movement reentry, both with and without involvement of an anatomic obstacle, are discussed. The concept of wavelength of a reentrant circuit as calculated by the product of refractory period and conduction velocity is emphasized. To maintain circus movement tachycardia in an acutely ischemic myocardium, the ischemic tissue mass must be larger than the wavelength. For maintenance of fibrillation, several independent reentrant wavelets must be simultaneously present. Agents that prolong wavelength (by lengthening refractory period, increasing conduction velocity or both) may prevent reentry. Experiments are described that show the effectiveness of lidocaine, which depresses action potentials of ischemic myocardial cells, in preventing ventricular fibrillation when administered before coronary artery occlusion in isolated pig hearts. Ventricular premature depolarizations or beats are usually necessary to initiate reentrant rhythms. They may be caused by reflection, a type of reentrant excitation involving slow conduction, or by electronic transmission over short segments of depressed or unexcitable tissue. An example of microreentry in a 4 mm segment of papillary muscle exposed to elevated extracellular K+ concentrations, resulting in a ventricular premature beat, is shown. Focal mechanisms, such as abnormal automaticity or triggered activity, may also be responsible for premature impulses. Agents that suppress premature depolarizations may be effective against reentrant arrhythmias, even when they do not affect the reentrant mechanism itself. Experiments are described, showing that moricizine HCl suppresses abnormal automaticity in isolated papillary muscle, partially depolarized by application of electric current.     

Method for evaluating the effects of antiarrhythmic drugs on ventricular tachycardias with different electrophysiologic characteristics and different mechanisms in the infarcted canine heart

In a canine model of myocardial infarction caused by coronary occlusion and reperfusion, ventricular tachycardia occurs spontaneously at 24 hours and has many of the characteristics of an accelerated idioventricular rhythm. It cannot be induced by premature or rapid stimulation of the ventricles; overdrive pacing during this tachycardia usually causes some transient overdrive suppression but occasionally there is overdrive acceleration. We suggest that this arrhythmia is caused mainly by enhanced automaticity. Ventricular tachycardia also can be induced by premature or rapid ventricular pacing 3 to 5 days after infarction, but it does not occur spontaneously. It can be stopped by overdrive pacing, suggesting that it is caused by reentry. Electrocardiographic features are identical to chronic, recurrent sustained ventricular tachycardia in human patients. Because the arrhythmias occurring at different times probably result from different mechanisms this canine model is useful for comparing the actions of drugs on different kinds of arrhythmias. Lidocaine and procainamide generally abolished tachycardia 24 hours after infarction, but only procainamide abolished tachycardia 3 to 5 days after infarction. Isoproterenol accelerated tachycardia at both times. Verapamil did not abolish tachycardia 3 to 5 days after infarction.     

Reentrant ventricular arrhythmias in the late myocardial infarction period. II. Burst pacing versus multiple premature stimulation in the induction of reentry

Isochronal maps of ventricular activation were analyzed in dogs 1 to 5 days after infarction utilizing a 64 channel multiplexer. Only dogs in which circus movement reentry could not be induced by a single premature stimulus were analyzed. Reentrant rhythms could be successfully induced equally by multiple (double or triple) premature stimuli and by burst pacing. Successive premature stimuli as well as successive beats during burst pacing resulted in progressively longer arcs of functional conduction block or slower circulating wave fronts, or both, that succeeded in reexciting myocardial zones on the proximal side of the arc of block to initiate reentry. However, for manifest reentry to be induced by burst pacing, the paced run had to be terminated after the beat that resulted in a critical degree of conduction delay. Otherwise, reentrant activation could be confined (concealed) by the subsequent paced wave front, which could also arrive earlier to the reentrant circuit zone of slow conduction resulting in block and interruption of reentry. Termination of a paced run after this beat would not result in reentry. If the paced run was extended past this beat, a new sequence of ventricular activation patterns characterized by progressively longer arcs of block or slower conduction, or both, developed again. The number of beats in a paced run that could initiate reentry varied with the cycle length of pacing, as well as in different experiments, and was difficult to standardize. It is therefore concluded that random burst pacing as a technique for induction of reentrant rhythms should probably be abandoned in favor of multiple premature stimulation.     

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.     

Effects of thioridazine (Mellaril) on ventricular electrophysiologic properties

The effects of therapeutic and toxic doses of thioridazine (Mellaril) (10 and 50 mg/kg body weight, respectively) on ventricular electrophysiologic properties were studied In 12 anesthetized dogs. Threshold pacing currents (diastolic threshold), effective refractory period and conduction time were significantly increased, and idioventricular automaticity was suppressed after administration of 10 mg/kg of thioridazine; the effects were much more pronounced after administration of 50 mg/kg. Rapidly repetitive responses or tachycardia could be induced in the ventricle by two early premature beats in 9 of the 12 dogs after the 50 mg/kg dose, but they did not occur before drug administration or after the 10 mg/kg dose. These results indicate that the antiarrhythmic and arrhythmogenic effects of thioridazine are dose-dependent and that careful monitoring with frequent electrocardiograms is needed for patients receiving large doses of this drug.     

Failure of idioventricular suppression in man by overdrive pacing as well as lidocaine: the role of abnormal automaticity

Five patients with third-degree atrioventricular block and an idioventricular escape rhythm who showed unusual responses to overdrive ventricular pacing and lidocaine are presented. In four cases, the idioventricular rhythm was not suppressed by overdrive; in one, the recovery time of the escape rhythm was shorter than the escape cycle length. Lidocaine did not affect the cycle lengths and recovery times of the idioventricular rhythms. These responses are characteristic of abnormal automaticity. The role of abnormal automaticity in human idioventricular escape rhythms has not been previously supported by these characteristic responses to overdrive pacing and lidocaine.     

Fast and slow idioventricular rhythms in the canine heart: A study of their mechanism using antiarrhythmic drugs and electrophysiologic testing

Complete heart block in dogs was induced by injecting the His bundle with formalin. For the 1st few days after surgery, a fast idioventricular rhythm (cycle length 471 ± 37 ms, mean ± standard error of the mean) occurred either as the only ventricular rhythm or interspersed with a slow idioventricular rhythm (cycle length 1,307 ± 17 ms). The response to cardiac pacing, lidocaine, ethmozin and verapamil in conscious dogs was studied 1 day and 1 to 2 weeks after surgery. The fast idioventricular rhythm could not be suppressed by overdrive pacing, and at times its rate actually increased after pacing. The basic cycle length of the fast idioventricular rhythm was prolonged by ethmozin but not by verapamil or lidocaine. The recovery cycle length (that is, that of the first beat after cessation of overdrive pacing) was prolonged by ethmozin and verapamil, but not lidocaine. The slow rhythm was suppressed by overdrive pacing and its rate was decreased by lidocaine, unaltered by ethmozin and increased by verapamil. The recovery cycle length of the slow rhythm also was prolonged by lidocaine, unaltered by ethmozin and decreased by verapamil.

The results are consistent with the slow rhythm resulting from normal automaticity (that is, that which occurs at high levels of membrane potential and is overdrive-suppressed) and the fast rhythm resulting from an abnormal automatic mechanism (that which occurs at low membrane potentials and is not overdrive-suppressed). The results obtained with verapamil are consistent with drug-induced catecholamine release.     

Premature escape beats induced by overdrive pacing in canine Purkinje fibers. Evidence for the role of normal automaticity as an underlying cellular mechanism.

Premature escape beats induced in conscious dogs with chronic complete atrioventricular block have been defined as escape beats occurring on cessation of overdrive pacing and having a coupling interval to the last paced beat shorter than the coupling interval between the premature escape beat and the second postpacing beat. Triggered activity has been proposed as the primary underlying mechanism. We used standard microelectrode techniques to study the effects of overdrive pacing on normal automatic canine Purkinje fibers to determine if premature escape beats could be induced and if so, to define the underlying cellular mechanism(s). For this purpose, we overdrive-paced Purkinje fibers for 10 and 50 seconds and for 10 and 50 beats at a pacing cycle length (PCL) of 1,000-200 msec. In addition, to help distinguish among major arrhythmogenic mechanisms, we used a matrix of drugs consisting of propranolol, nadolol, lidocaine, ethmozin, and doxorubicin. Fifty-second stimulation trains induced "classic" overdrive suppression of the first three postpacing impulses, whereas 10-second overdrive pacing induced significant overdrive suppression only at a PCL of 200 msec. With 50-beat overdrive pacing and a PCL of 1,000-600 msec, there was overdrive suppression of postpacing impulses, whereas reduced overdrive suppression was observed at a PCL of 400-200 msec. Ten-beat stimulation trains induced a "flat response" of postpacing impulses. Ten- and 50-beat overdrive pacing provoked premature escape beats in 66% of the fibers, with the higher incidence at a PCL of 200 msec for 50-beat stimulation trains. No shortening of the coupling interval of premature escape beats was observed at faster pacing rates. Only lidocaine (which suppresses normal automaticity) abolished premature escape beats. We conclude that normal automaticity is the most likely mechanism underlying premature escape beats in Purkinje fibers with high levels of membrane potential.     

Effect of procainamide on reentry within the His-Purkinje system in man

The effects of a single intravenous infusion of 500 mg of procainamide on macro-reentry within the His-Purkinje system were assessed, in 10 patients using bundle of His electrograms and the ventricular extrastimulus method. Procainamide did not abolish reentry in any of the 10 patients and produced repetitive reentry (two or more consecutive reentrant beats) in 8 of 10 patients. On the average, procainamide caused reentry to be initiated at longer S₁-S₂ intervals, widening the zone of reentry. In all but one patient reentry was manifest at significantly longer S₂-H₂ intervals than control values. The H-V intervals of reentrant beats (H₂-V₃ intervals) after procainamide were longer than control values at comparable S₂-H₂ intervals. Procainamide shortened or abolished the retrograde gap zones thereby causing reentry to be present more frequently within the zone of reentry. No significant change was seen in effective refractory period of ventricular muscle.

On the assumption that many clinically encountered ventricular arrhythmias that respond to procainamide result from micro-reentry, the observed differences between the effects of procainamide on macro- and micro-reentry may be explained on the basis of the relation between drug effect and size of the reentrant circuit. Procainamide may produce a greater increase in refractoriness in a micro-reentrant circuit than in macro-reentry, thereby producing bilateral block and abolishing reentry in the former; or if the degree of electrophysiologic changes produced by procainamide were the same in both types of circuits, then for a given change, the pathway in a micro-reentrant circuit may be too small to sustain reentry.     

Concept of reentry versus automaticity

Arrhythmias can result from abnormal impulse initiation or conduction. Abnormal initiation results from either automatlcity or triggered activity. Enhanced automaticity may be due to a normal automatic mechanism (a normal property of the sinus node and specialized conducting fibers) or to an abnormal mechanism such as automaticity in depolarized fibers. Triggered activity is caused by afterdepolarizations that occur either during repolarization (early afterdepolarization) or after repolarization is complete (delayed afterdepolarization). Triggered activity due to delayed afterdepolarizations is dependent on critical heart rates. Overdrive pacing may distinguish between normal and abnormal automaticity. Antiarrhythmic drugs can alter arrhythmias that result from abnormal impulse initiation. To suppress an arrhythmia resulting from abnormal impulse generation, a drug may (1) suppress the abnormal automatic mechanism, i.e., specific effect on ionic current; (2) suppress afterdepolarizations; (3) depress conduction in tissue surrounding automatic focus; or (4) modify refractory period of tissue in and around automatic focus.Abnormal impulse conduction results in reentrant excitation. Conditions necessary for reentry include a combination of unidirectional block and slowed conduction. A reentrant mechanism can be determined by an anatomically defined circuit or solely by the functional properties of the tissue (leading circle mechanism). Circus movement reentry around an anatomic obstacle may respond to antiarrhythmic drugs differently from reentry caused by a leading circle mechanism. Initiation and perpetuation of a reentry mechanism depends on a delicate interplay between conduction velocity and duration of the functional refractory period in the reentry circuit. Drugs can prevent a reentry mechanism by (1) eliminating premature beats that initiate the mechanism; (2) reducing the disparity in effective refractory periods; (3) improving conduction, thereby preventing unidirectional block; (4) further depressing conduction in a part of the circuit producing a bidirectional block; and (5) lengthening the functional refractory period in the tachycardia circuit more than the total circuit time. The effectiveness of drugs on reentry depends on the electrophysiologic substrate contributing to the reentrant mechanism.All of these mechanisms cause arrhythmias in the in situ canine heart and probably occur in humans. However, clinical pacing techniques are not sufficiently discriminating to distinguish between arrhythmic mechanisms. Ability to inltiate ventricular tachycardia with 1 or more premature beats is suggestive of reentry but does not rule out triggered automaticity. Demonstration of continuous fragmented electrical activity before the first beat of tachycardia and perpetuation of such activity during tachycardia provides more definitive evidence for a reentry mechanism.     

Effects of antiarrhythmic drugs on the repetitive extrasystole threshold and the ventricular fibrillation threshold

The effects of class 1 antiarrhythmic drugs on the repetitive extrasystole threshold (RET) and the ventricular fibrillation threshold (VFT) were studied in 32 anesthetized dogs with localized transmural necrosis. All four drugs significantly increased VFT. Although lidocaine and mexiletine increased RET, procainamide and disopyramide did not. We conclude that class 1b antiarrhythmic agents prevent ventricular fibrillation by suppressing the initiation of reentry, and that class 1a drugs decrease the vulnerability by preventing the reentrant repetitive excitation from degenerating into chaotic multiple reentries.     

Ventricular reentry and automaticity in myocardial infarction. Effect of size of injury

The effects of the size of acute myocardial infarction on ventricular reentry and automaticity were studied in 36 mongrel dogs. Large transmural myocardial infarctions were produced by ligation of the left anterior descending coronary artery (major ligation; diameter of infarction above 4.0 cm), and small subendocardial or intramural infarctions were produced by ligating a small diagonal branch of the left anterior descending coronary artery (minor ligation; diameter of infarction less than 1.5 cm). Reentrant arrhythmias were induced by rapid ventricular stimulation, and ventricular automaticity was determined during vagal stimulation. Ventricular automaticity became enhanced only 30 to 45 minutes after both major and minor coronary arterial ligations; however, the animals with major ligations attained a higher level of increased automaticity. While automaticity became enhanced in both groups reentrant arrhythmias could never be produced artificially (or observed spontaneously) in the animals with myocardial infarctions. The dependence of the so-called reentrant arrhythmias on the size of the infarction is a major support for the theory of reentry as the basis for these arrhythmias.     

Age-related effects of ischemia, lidocaine and verapamil on overdrive-induced suppression of ventricular pacemakers in isolated rat heart.

The effect of age on ventricular automaticity in the isolated perfused rat heart was determined under different conditions. When the ventricle is electrically stimulated at a faster rate, drive cessation is followed by a temporary suppression of ventricular automaticity (overdrive suppression). The effects of ischemia, lidocaine and verapamil on overdrive suppression were studied in isolated perfused adult and senescent rat hearts with complete atrio-ventricular block, by monitoring ventricular escape rate and escape rhythm recovery time after 1 minute of overdrive at a constant multiple (x3) of the spontaneous rate. The results demonstrated that: 1) lidocaine decreases ventricular automaticity especially in senescent hearts; 2) verapamil does not modify ventricular automaticity in basal conditions in either adult or senescent hearts; 3) myocardial ischemia causes a reduction in ventricular automaticity and more markedly in senescent hearts; and 4) lidocaine exaggerates the effect of ischemia, while verapamil seems to antagonize its depressant effect more in adult than in senescent hearts.     

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 greater than 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 less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)     

The concepts of reentrant activity responsible for ectopic rhythms

Many ectopic rhythms are, no doubt, due to enhanced automaticity of the specialized fibers in the heart. Some features of clinical and experimental ectopic rhythms indicate that reentrant activity also plays an important part in the genesis of some ectopic rhythms. There are 2 basic types of reentrant activity: (1) focal reexcitation due to the flow of current between adjacent myocardial fibers that are repolarized at grossly disparate times; and (2) the circus movement of an impulse or circus reentry resulting from local impairment of excitability and conductivity in the cardiac tissues. Reentrant activity may occur intermittently or repetitively at various sites within the same tissue or between different tissues in the heart, producing occasional premature beats or sustained tachyarrhythmias. Premature beats have the potential of initiating episodes of tachyarrhythmias with serious physiologic consequences. Whatever is the mechanism for the genesis of premature beats, the same mechanism may not be responsible for causing sustained tachyarrhythmias. The continuous circus reentry appears to play a major role in the maintenance of tachyarrhythmias. The efficacy of appropriately timed premature beats or vagal stimulation in terminating some episodes of tachyarrhythmias may be related to their ability to occlude the reentry pathway.     

Reentrant ventricular arrhythmias in the late myocardial infarction period. 12. Spontaneous versus induced reentry and intramural versus epicardial circuits

One to 5 days after one-stage ligation of the left anterior descending coronary artery in dogs, reentrant excitation can be induced by programmed premature stimulation in the surviving electrophysiologically abnormal, thin epicardial layer overlying the infarct. In experiments in four dogs, reentrant excitation occurred "spontaneously" during a regular sinus or atrial rhythm. A tachycardia-dependent Wenckebach conduction sequence in a potentially reentrant pathway was the initiating mechanism for spontaneous reentrant tachycardias and was the basis for both manifest and concealed reentrant extrasystolic rhythms. In all dogs showing spontaneous reentry, reentrant excitation could also be induced by premature stimulation at cycle lengths much shorter than those associated with spontaneous reentry, and induced reentrant circuits were always different from those during spontaneous reentry. In two dogs, the reentrant circuit was located intramurally in close proximity to a patchy septal infarction. The study illustrates that irrespective of the anatomic localization of reentrant circuits (epicardial or intramural), their dimension (large or small) or their mechanism of initiation (programmed premature stimulation or "spontaneous"), reentrant excitation always occurred in a figure 8 configuration (or a modification thereof). The figure 8 model, rather than the ring model or the leading circle model, may be the common model of reentry in the mammalian heart.