Nonsustained polymorphic ventricular tachycardia induced by electrical stimulation in 3 week old canine myocardial infarction

To study the electrophysiology of ventricular tachycardia 3 to 4 weeks after myocardial infarction in a canine model, an anteroapical transmural infarct was created in 40 dogs by ligation of the left anterior descending coronary artery. An average of 25 days after myocardial infarction 32 dogs that survived the infarction and 4 control dogs with a sham operation underwent open chest electrophysiologic study. No ventricular arrhythmias could be induced by any mode of ventricular stimulation in any of the four control animals. Twenty-seven of 32 dogs with myocardial infarction had reproducible ventricular arrhythmias in response to ventricular stimulation. In 17 animals sustained uniform ventricular tachycardia could be reproducibly initiated by programmed ventricular stimulation. In another 10 dogs with myocardial infarction, the same modes of ventricular stimulation reproducibly initiated ventricular fibrillation. Seven of these 10 dogs also manifested reproducible nonsustained polymorphic ventricular tachycardia, characterized by beat to beat variation in QRS complex configuration and cycle length, in response to programmed ventricular stimulation. Nonsustained polymorphic ventricular tachycardia and sustained uniform ventricular tachycardia were rarely observed in the same dog and appeared to have different underlying mechanisms.     

Day-to-day variations in inducibility of ventricular tachyarrhythmias during the late postmyocardial infarction phase in conscious dogs

The inducibility of ventricular tachyarrhythmias was studied daily on days 3 through 8 after experimental myocardial infarction in 15 conscious dogs. Although a sustained ventricular tachyarrhythmia was produced on one or more occasions in 11 of 15 dogs (73%), there was marked daily variation in the results of programmed stimulation. Ventricular fibrillation or sustained ventricular tachycardia was elicited in six dogs on day 3 after infarction. In two of these dogs, no sustained tachycardia could be induced by day 7. In nine dogs sustained ventricular arrhythmias were not inducible on day 3. By day 6 to 7, sustained ventricular tachycardia was inducible in five of these dogs. In clinical practice similar variation in the inducibility of sustained ventricular arrhythmias may conceivably complicate the use of results of programmed ventricular stimulation as determinants of risk of sudden death after myocardial infarction.     

Effect of flecainide acetate on prevention of electrical induction of ventricular tachycardia and occurrence of ischemic ventricular fibrillation during the early postmyocardial infarction period: evaluation in a conscious canine model of sudden death

The antiarrhythmic and antifibrillatory effects of flecainide acetate during the early postinfarction period were evaluated in a conscious canine model of sudden cardiac death. Ventricular tachycardia remained inducible early after infarction in eight of nine dogs receiving an intravenous loading dose of flecainide (2.0 mg/kg body weight) and seven of eight dogs receiving saline vehicle. In both the drug and vehicle groups, there was no significant change in the ventricular refractory period or in the cycle length of the induced ventricular tachycardia. With a maintenance intravenous infusion of flecainide, 1.0 mg/kg per h for 4 hours, the subsequent occurrence of acute posterolateral ischemia resulted in the development of ventricular fibrillation and sudden death in seven of eight flecainide-treated and eight of eight vehicle-treated dogs. Seven additional postinfarction dogs with noninducible tachycardia during pretreatment programmed stimulation, and thereby considered to be at "low risk" for the development of ischemic ventricular fibrillation, were also given flecainide in an intravenous loading and maintenance dosing regimen. The subsequent occurrence of posterolateral ischemia resulted in the development of ventricular fibrillation in three of these seven dogs. These findings suggest that flecainide acetate may not possess pharmacologic properties useful in managing ventricular tachycardia or in preventing ischemic ventricular fibrillation in the presence of recent myocardial damage.     

Inducible sustained ventricular tachycardia and ventricular fibrillation in conscious dogs with isolated right ventricular infarction: relation to infarct structure

The susceptibility of infarcted right ventricular myocardium to inducible ventricular tachyarrhythmias was serially evaluated in 18 conscious dogs during the first 2 weeks after permanent right coronary artery occlusion. Properly timed double premature stimuli applied to the right ventricular outflow tract induced sustained (longer than 1 minute) ventricular tachycardia at rates of 190 to 400 beats/min in nine dogs, and ventricular fibrillation in six dogs. No ventricular arrhythmias could be induced in the remaining three dogs. The zone of premature coupling intervals within which ventricular tachyarrhythmias could be induced decreased in each dog as the infarct aged, and by day 12 after occlusion, no ventricular arrhythmias could be induced in any of the dogs studied. Both the size and the degree of patchiness (graded from 0 for no patchiness to +4 for patchiness throughout the infarct) of the infarct appear to be related to the nature of the induced rhythm. Infarcts with greater heterogeneity and those that were larger than 8% of the right ventricular volume were associated with a higher incidence of ventricular fibrillation, and infarcts with a lesser degree of patchiness were more suitable for sustained ventricular tachycardia (3.4 +/- 1.2 versus 1.4 +/- 0.4, p less than 0.05). These findings indicate that the infarcted right ventricular myocardium, independent of left ventricular involvement, can be associated with malignant ventricular tachyarrhythmias, ventricular tachyarrhythmias can be induced only during a well defined postinfarction period; and both the size and geometry of the right ventricular infarct determine the nature of the induced ventricular rhythm.     

Effects of timolol and propranolol on inducible sustained ventricular tachyarrhythmias in dogs with subacute myocardial infarction

Timolol and propranolol reduce the incidence of cardiac death after myocardial infarction (MI). To explore possible mechanisms of this reduction in mortality, the antiarrhythmic effects of these 2β blockers were compared in a dog model of inducible sustained ventricular tachycardia (VT) or fibrillation (VF) 4 to 6 days after experimental closed-chest MI. Dogs with inducible VT or VF underwent drug studies with timolol and propranolol; the sequence of drug administration was randomized. Timolol doses were 0.1, 0.3, and 1.0 mg/kg; propranolol doses were 1.0, 3.0 and 10.0 mg/kg. Timolol and propranolol were equally effective in abolishing inducible VT or VF: 77 % of instances of inducible VT or VF responded to 1 or bothβ blockers. The VF threshold was significantly elevated by both timolol and propranolol; the elevation in the VF threshold was significantly greater in “responders,” i.e., dogs in whom VT was prevented by p blockade (15±9vs8±9 mA, p < 0.05). The ventricular effective refractory period was prolonged by both drugs; again, more so in the responders than in the nonresponders (16 ± 9 vs 8 ± 14 mA, p < 0.05). The QTc interval was not significantly affected by eitherβ blocker. Among the responders, no difference was detected between timolol and propranolol in the extent to which the effective refractory period was prolonged or the VF threshold elevated. However, the highest dose of propranolol decreased the mean blood pressure significantly more than the comparable dose of timolol.In conclusion, timolol and propranolol are equally effective in abolishing inducible VT or VF in the dog after subacute MI. Both drugs tend to elevate the VF threshold and to prolong the ventricular effective refractory period without significantly altering the QTc interval, suggesting a possible direct membrane depressant effect for both drugs. At a high dose, propranolol tends to lower mean blood pressure more than the comparable dose of timolol.     

Day to day reproducibility of electrically inducible ventricular arrhythmias in survivors of acute myocardial infarction

Day to day reproducibility of the response to programmed ventricular stimulation has not been evaluated in survivors of acute myocardial infarction. Programmed ventricular stimulation was performed prospectively on 2 consecutive days in 56 patients on an average of 12 +/- 5 days (range 7 to 29) after an acute myocardial infarction. No patient had a history of documented or suspected sustained ventricular tachycardia or fibrillation occurring greater than 48 h after infarction. During initial programmed ventricular stimulation, 21 patients had induction of sustained ventricular tachycardia or fibrillation (Group I), and 35 patients had induction of either nonsustained ventricular tachycardia or no ventricular tachycardia (Group II). Repeat programmed ventricular stimulation in Group I patients induced sustained ventricular tachycardia or fibrillation in 16 of 21 patients (reproducibility 76%); the maximal induced response in the other 5 patients was nonsustained ventricular tachycardia in 2 patients and fewer than six repetitive ventricular responses in 3 patients. The day to day reproducibility was significantly higher for inducible sustained ventricular tachycardia of cycle length greater than or equal to 240 ms compared with rapid sustained ventricular tachycardia of cycle length less than 240 ms (100% versus 44%, p less than 0.009) or ventricular fibrillation (100% versus 43%, p less than 0.009). Repeat programmed ventricular stimulation in Group II patients did not induce sustained ventricular arrhythmias in 31 of 35 patients (reproducibility 89%). Thus, in survivors of acute myocardial infarction, inducible slow sustained ventricular tachycardia was a highly reproducible finding, whereas inducibility of rapid sustained ventricular tachycardia and ventricular fibrillation showed a significant day to day variability.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prevalence,characteristics and significance of ventricular tachycardia (three or more complexes) detected with ambulatory electrocardiographic recording in the late hospital phase of acute myocardial infarction

A 24 hour electrocardiographic recording was performed before hospital discharge in 430 patients who survived the cardiac care unit phase of acute myocardial infarction. Fifty patients (11.6 percent) had ventricular tachycardia, that is, three or more consecutive ventricular complexes. In 25 (50 percent) of these 50 patients, there was only one episode of ventricular tachycardia and, in 15 patients (30 percent), the longest run of ventricular tachycardia was only three consecutive ventricular premature depolarizations. The average rate of tachycardia was 119/min. Tachycardia rarely started with R on T ventricular premature complexes (4 of 1,370 episodes in 50 patients).There was no difference between the groups with and without ventricular tachycardia with respect to age and sex, but the patients with tachycardia had a significantly greater prevalence of previous myocardial infarction, left ventricular failure in the cardiac care unit, atrial fibrillation, ventricular tachycardia or ventricular fibrillation in the cardiac care unit and significantly more frequent use of digitalis and diuretic and antiarrhythmic drugs at the time of hospital discharge.The group with tachycardia had a 38.0 percent 1 year mortality rate compared with the rate of 11.6 percent in the group without tachycardia. Ventricular tachycardia had a strong association with 1 year mortality (odds ratio = 4.7). Although ventricular tachycardia had a significant association with many other postinfarction risk factors, it was still significantly associated with the 1 year mortality (p < 0.05) when other important risk variables were controlled statistically using a multiple logistic regression model. The 36 month cumulative mortality rate was 54.0 percent in the group with ventricular tachycardia compared with 19.4 percent in the group without tachycardia.     

Quantitative measurement of electrical instability as a function of myocardial infarct size in the dog

To investigate the relation between electrical instability and myocardial infarct size, 20 foxhounds were studied in the awake state 3 to 5 days after closed chest coronary occlusion. Programmed right ventricular stimulation was performed with use of an epicardial electrode. After six paced beats at 10 percent greater than control rate, single and then double extrastimuli were introduced, scanning from late diastole to ventricular refractoriness in steps of 10 to 20 ms. Abnormal responses observed after this provocation were repetitive ventricular response, unsustained ventricular tachycardia, sustained ventricular tachycardia and ventricular fibrillation. Scores for electrical instability were determined for each dog, with higher scores assigned for more hazardous tachyarrhythmias (ventricular fibrillation greater than sustained ventricular tachycardia greater than unsustained ventricular tachycardia greater than repetitive ventricular response) and for those provokable later in diastole. An electrical instability index derived from these scores correlated well with infarct size measured with tetrazolium staining (r = 0.94). When scores were given only for the type of abnormal response elicited, excluding the effect of diastolic timing and the number of extrastimuli or vice versa, there was no significant difference in correlation with infarct size (r = 0.85 versus 0.92). Thus the results demonstrate that inducible electrical instability early after infarction is directly related to infarct size. Further, these data demonstrate the usefulness of an electrical instability index derived from the results of programmed right ventricular stimulation in assessing the severity of ischemic damage to the heart.     

Serial analysis of electrically induced ventricular arrhythmias in a canine model of myocardial infarction

To determine the rate of induction, specificity and evolution of electrically induced postmyocardial infarction ventricular arrhythmias, 10 dogs that underwent a sham operation and 20 dogs with experimental transmural apical myocardial infarction underwent serial closed chest electrophysiologic studies with programmed ventricular stimulation under light anesthesia 1, 2, 4 and 6 weeks after the operation. The reproducibility of the electrically induced ventricular arrhythmias was at a maximum when three extrastimuli were used during ventricular pacing for induction. The reproducibility of the arrhythmias was also a function of the age of the infarct. Electrically induced sustained monomorphic ventricular tachycardia, observed in 45 to 50% of the animals, was a highly specific postinfarction finding (0% specificity in control animals, regardless of the mode or timing of programmed cardiac stimulation), whereas nonsustained polymorphic ventricular tachycardia was not. The specificity of induced ventricular fibrillation was a function of the mode and timing of programmed stimulation. The rate of induction of the electrically induced ventricular arrhythmias did not change significantly during the 6 week period after myocardial infarction. A large infarct size (determined by postmortem examination) and a low left ventricular ejection fraction (determined during premortem cardiac catheterization) were the only variables identified that predisposed the animals to electrically induced sustained monomorphic ventricular tachycardia. These factors, however, did not correlate with the presence of electrically induced ventricular fibrillation or nonsustained ventricular tachycardia.     

Reduction in incidence of inducible ventricular tachycardia after myocardial infarction by treatment with streptokinase during infarct evolution

The aim of this study was to determine whether intravenous streptokinase administered with or without oral aspirin to patients with evolving myocardial infarction reduces the inducibility of ventricular tachycardia at electrophysiologic study and thus the risk of sudden death in infarct survivors. Of 159 patients randomized at Westmead Hospital to the multicenter Second International Study of Infarct Survival (ISIS-2) after streptokinase and aspirin in acute myocardial infarction, 87 underwent electrophysiologic testing 6 to 28 days after infarction to determine their risk of subsequent ventricular arrhythmias (streptokinase 20 patients; aspirin 25 patients; streptokinase and aspirin 21 patients; both placebos 21 patients). Patients who underwent electrophysiologic testing had similar clinical characteristics to those of patients who did not. The stimulation protocol comprised up to and including four extrastimuli applied to the right ventricular apex at twice diastolic threshold. An abnormal result was defined as ventricular tachycardia with a cycle length greater than or equal to 230 ms lasting greater than or equal to 10 s. Ventricular tachycardia was inducible at electrophysiologic study in 8 patients who received placebo streptokinase, but in no patient who received active streptokinase (8 of 46 versus 0 of 41; p = 0.005, Fischer's exact test). Ventricular tachycardia was inducible in 4 patients who received aspirin therapy and 4 who did not (4 of 41 versus 4 of 46; p = NS). During a mean follow-up period of 39 +/- 9 months, there were no spontaneous episodes of ventricular tachycardia, ventricular fibrillation or witnessed sudden death in the streptokinase-treated group compared with three such events in the placebo-treated group (p = 0.13). When compared with placebo therapy, intravenous streptokinase substantially reduced the incidence of inducible ventricular tachycardia in infarct survivors. No similar benefit was attributable to aspirin therapy.     

The effects of premature stimulation of the His bundle on epicardial activation and body surface late potentials in dogs susceptible to sustained ventricular tachyarrhythmias

Experiments were performed on 20 anesthetized dogs to determine the effects of premature stimulation of the His bundle on epicardial conduction and late potentials recorded on the body surface. Fifteen dogs underwent occlusion of the left anterior descending coronary for 2 hr followed by reperfusion, and five that did not undergo operation served as controls. Animals were studied 2 to 52 weeks after the induction of infarction, and four animals with infarction and four control animals exhibited no sustained arrhythmias in response to programmed ventricular extrastimulation. Five dogs with infarction and one control dog had ventricular fibrillation while the six remaining dogs had inducible sustained ventricular tachycardia. All animals with ventricular tachycardia had late potentials in the terminal portion of the signal-averaged body surface QRS complexes during sinus rhythm and QRS durations in the animals were 64 msec or greater. The voltage in the last 20 msec of the QRS complex was 13.5 microV or less and the duration of late activity below 30 microV was 18.2 msec or more. These values did not overlap values in animals with no inducible arrhythmias. Ventricular fibrillation was a nonspecific end point in these experiments and values overlapped those in animals with no arrhythmias and those with ventricular tachycardia. All animals with infarction and late potentials associated with their QRS complexes also had delayed and prolonged epicardial electrograms that extended into the time of the late potentials recorded from 45 standard sites in the infarcted regions. A single premature beat evoked by His bundle pacing (coupling interval of 192 to 270 msec) had no significant effect on late potentials or their relationship to epicardial activation in the area of infarct. However, changes in the durations of electrograms in response to premature beats were different in animals with infarction and ventricular tachycardia than in those with ventricular fibrillation. In animals with ventricular tachycardia, electrograms at 15 of 210 sites increased in duration by more than 10 msec while those at 61 of 210 sites decreased in duration. In animals with ventricular fibrillation, electrograms at 40 of 207 sites were of increased duration while those at 26 of 207 decreased. The decreases in duration were usually due to components of fractionated electrograms "dropping out" and likely represent local conduction block near the recording electrode.(ABSTRACT TRUNCATED AT 400 WORDS)     

Nature of inducible ventricular tachyarrhythmias in a canine chronic myocardial infarction model

A canine model suitable for serial conscious studies was developed to evaluate the nature of sustained ventricular tachyarrhythmias in chronic experimental myocardial infarction. Thirteen dogs underwent left anterior descending coronary artery ligation followed by complete reperfusion; 11 sham-operated dogs served as controls. In this model, ventricular tachyarrhythmias are inducible in most dogs with experimental infarction and in several dogs without this condition. The morphologic features, rate and drug response of the induced arrhythmias are unlike those of human ventricular tachycardia. Tachyarrhythmia induction is facilitated by anesthesia and thoracotomy. This canine infarct model does not adequately imitate human recurrent ventricular tachycardia, but may simulate human sudden cardiac death.     

Sinus rhythm mapping in healed experimental myocardial infarction: contrasting activation patterns for inducing ventricular tachycardia versus fibrillation

The inducibility of ventricular tachycardia (VT) and fibrillation (VF) is variable in healed myocardial infarction (MI) in the dog. To better understand the electrophysiologic basis for these arrhythmias, MI was produced in dogs by ligating the left anterior descending artery. One week later, epicardial mapping was performed with the dog in sinus rhythm using a hand-held bipolar electrode. Transmural mapping was performed with the dog in sinus rhythm with 4 pairs of bipolar electrodes mounted on a #14 needle. Ventricular arrhythmias were induced by the S₁S₂S₃ technique or 3- to 5-beat burst pacing at twice diastolic threshold. Only VF could be induced in 11 dogs, while sustained VT was induced in 6 dogs. Significantly more marked and more extensive delay in activation was seen both in the epicardium and transmurally in dogs with VT than in dogs with VF. In addition, dogs with VT had morphologic evidence of a large transmural MI, whereas dogs with VF had only a subendocardial MI. It is concluded that inducible sustained VT in the dog is usually associated with a large transmural MI and an activation sequence in sinus rhythm characterized by an extensive area of marked delay in activation. This activation pattern in sinus rhythm presumably is necessary to provide the underlying electrophysiologic milieu for sustained reentry.     

Histopathologic correlates of inducible ventricular tachycardia in two experimental canine models of myocardial infarction

Ventricular tachyarrhythmias are the leading cause of sudden cardiac death. Determination of the substrates conducive to the initiation of ventricular tachyarrhythmias remains an important clinical goal. The purpose of this study was to correlate electrophysiologic and histopathologic parameters conducive to the initiation of sustained ventricular tachycardia using programmed electrical stimulation in two canine models of myocardial infarction. Histopathologic correlates included: infarct pattern (heterogeneous vs. homogeneous morphology), distribution (viable epicardial or endocardial rim), and size. Twenty-one adult dogs were randomly divided into two groups: (1) 12 dogs underwent two-stage, 2-hour occlusion of the proximal left anterior descending coronary artery (LAD); and (2) nine animals had permanent, complete occlusion of the LAD with latex embolization. Using programmed ventricular pacing with two premature ventricular extrastimuli, initiation of ventricular tachycardia was attempted at both 1 and 2 weeks after infarction with the chest closed and opened each time. Electrophysiologic evaluation of the infarct type correlated significantly with the histologic morphology of the infarction (p less than 0.001), the presence of a viable epicardial rim was an extremely important discriminating variable for ability to induce sustained ventricular tachycardia (p = 0.04). The presence of an endocardial rim was not significant (p = 1.0). Infarct size alone was only marginally related to ventricular tachycardia inducibility (p = 0.08). Non-uniform infarcts were more conducive to the initiation of sustained ventricular tachycardia than homogeneous infarcts (p = 0.025). The presence of a large, non-uniform infarct was the best overall discrimination variable for inducibility (p = 0.0002). Thus, in these experimental models, specific infarct morphologies correlate significantly with susceptibility to inducible sustained ventricular tachyarrhythmias.     

Characterization and incidence of inducible monomorphic ventricular tachycardia in a postinfarction rabbit model

Objective

Ventricular tachycardia (VT), occurring late after myocardial infarction, is an important cause of sudden death. Animal models are useful for the investigation of this arrhythmia. The aim of this study is to develop and characterize a model of late postinfarction monomorphic VT in the rabbit.

Methods and Results

Myocardial infarction was created by ligation of the left circumflex artery. Cardiac electrophysiologic studies were performed 10 to 17 days postinfarction in 39 rabbits, in 10 sham-operated rabbits, and 6 control rabbits. Ventricular tachycardia was defined as a broad-complex tachycardia with a cycle length of more than 100 milliseconds, a duration of more than 10 seconds, and monomorphic QRS complexes. Using programmed stimulation, we induced VT in 9 rabbits (23%) in the infarct group but in none of the sham or control animals. The mean infarct size was 23% ± 9% (mean ± SD) of the left ventricle.

Conclusion

Coronary ligation in the rabbit creates a substrate, which allows the induction of sustained monomorphic VT with programmed stimulation. Monomorphic VT is not inducible in rabbits without myocardial infarction. This model might allow the testing of interventions that reduce the incidence of VT late after myocardial infarction.     

Antiarrhythmic Efficacy of Oral Sotalol in Patients with Sustained Ventricular Tachycardia or Ventricular Fibrillation Postmyocardial Infarction

In order to assess the antiarrhythmic efficacy of oral sotalol we studied 46 patients with sustained monomorphic ventricular tachycardia (n = 40) or ventricular fibrillation (n = 6) by programmed ventricular stimulation. All patients had coronary artery disease with a history of myocardial infarction. Prior to sotalol, patients were treated with a mean of 3.4 ± 1.4 antiarrhythmic Class I drugs. None of these drugs prevented sustained monomorphic ventricular tachycardia or ventricular fibrillation. During control programmed ventricular stimulation (PVS 1) ventricular fibrillation was induced in 7 patients (15%), sustained monomorphic ventricular tachycardia in 30 patients (65%), and nonsustained ventricular tachycardia in 9 patients (20%). After loading with oral sotalol (320 mg/day) programmed ventricular stimulation (PVS 2) was repeated 4.2 ± 3.3 weeks after PVS 1. Ventricular fibrillation was not inducible in any of the patients; in 10 patients (22%) sustained monomorphic ventricular tachycardia was induced, and nonsustained ventricular tachycardia was induced in 10 patients (22%). In 26 patients (57%) either no response or a short ventricular response was inducible. Our data show that oral sotalol is an effective antiarrhythmic agent in patients with sustained monomorphic ventricular tachycardia or ventricular fibrillation following myocardial infarction.     

Halothane anesthesia reduces inducibility of ventricular tachyarrhythmias in chronic canine myocardial infarction

Summary This study examined the effects of 2% halothane general anesthesia on ventricular electrophysiological properties and inducibility of sustained ventricular tachycardia (VT) and ventricular fibrillation (VF). Dogs with chronic anterior infarction and control dogs (no infarction) were studied before and after anesthesia using chronically implanted ventricular epicardial electrodes. PQ interval was increased by 15% with halothane, but QRS duration, QT interval, QTc, and sinus rhythm cycle length were unaffected by anesthesia. Diastolic threshold was unchanged by halothane. Halothane caused significant increases of 10–30% in ventricular effective refractory period (ERP) both in control and in infarct animals. VT and VF were not inducible in any of the nine control animals either before or after anesthesia. In infarct animals 34 of 75 (45%) had inducible VT or VF prior to halothane, but the incidence of inducible arrhythmias was significantly lower at 29% (22 of 75 animals) after halothane (p<0.01). In 75% of animals in which halothane suppressed inducibility of tachyarrhythmias, halothane-induced increases in ERP prevented achievement of the short extrastimulus coupling intervals at which the arrhythmias were induced before anesthesia. In conclusion: halothane anesthesia reduces the incidence of inducible sustained ventricular tachyarrhythmias in chronic canine myocardial infarction.A preliminary report of this study was given to the American Heart Association, Dallas, Texas, USA, November 1986.     

Late potentials on the signal-averaged electrocardiogram after canine myocardial infarction: correlation with induced ventricular arrhythmias during the healing phase

Signal-averaged electrocardiograms (ECGs) and programmed ventricular stimulation were serially performed in 12 dogs (3 weeks of age) after experimental anteroapical myocardial infarction. At electrophysiologic study, sustained ventricular tachyarrhythmia was induced in seven dogs on at least one occasion. Of a total of 39 electrophysiologic studies, sustained monomorphic ventricular tachycardia was induced in seven studies and ventricular fibrillation in eight studies. In the remaining studies, no ventricular arrhythmia could be induced with triple ventricular extrastimuli. There was considerable day to day variability in the response to programmed stimulation and the results of the signal-averaged ECG. The signal-averaged QRS complex was significantly longer in dogs with inducible ventricular tachycardia or fibrillation (61 +/- 5 versus 57 +/- 3 ms, p = 0.02), had a lower terminal QRS amplitude (24 +/- 20 versus 46 +/- 33 microV, p = 0.04) and a longer late potential duration (19 +/- 4 versus 15 +/- 3 ms, p = 0.003) compared with that in animals with no inducible ventricular arrhythmia. Late potentials were defined as a total QRS duration greater than 58 ms, a terminal QRS amplitude less than 20 microV and a late potential duration greater than 18 ms. Using this definition, late potentials were seen in two distinct phases--immediately after coronary ligation and then beyond the first 72 h after infarction. The appearance of late potentials coincided with a change in arrhythmia inducibility from no ventricular arrhythmia to initiation of sustained monomorphic ventricular tachycardia. There is a close relation between inducibility of ventricular tachycardia in experimental canine myocardial infarction and the appearance of late potentials on the surface ECG.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of collateral flow reduction on electrophysiologic properties of preexisting ischemic area and inducibility of ventricular arrhythmias in the dog

Electrophysiologic properties of the left ventricle, vulnerability to ventricular arrhythmias and regional myocardial blood flow (RMBF) of the left ventricle were examined during superposition of acute ischemia on a healed myocardial infarction. The left circumflex coronary artery (LCX) was ligated in 13 dogs with a 28-day-old anteroapical infarction. Six (46%) of 13 dogs had reproducible ventricular tachycardia in response to programmed ventricular stimulation before LCX ligation. Ventricular fibrillation could be induced in 2 of these 6 dogs. After LCX ligation, 11 (85%) of 13 dogs had ventricular arrhythmias induced by ventricular stimulation. Nine of 13 dogs had ventricular tachycardia and 7 of 13 dogs had ventricular fibrillation. The heterogeneity of the effective refractory period (delta ERP) and the local intraventricular conduction time (LIVCT) in the border and the infarct zones of the left ventricle increased significantly after LCX ligation. RMBF in the border and the infarct zones were markedly decreased by LCX ligation. The magnitude of reduction of RMBF was correlated significantly with the prolongation of LIVCT. In conclusion, acute critical reduction of the collateral blood supply causes a more heterogeneous refractory period and conduction delay in the preexisting ischemic area of the heart, increasing the vulnerability to lethal ventricular arrhythmias.     

Postinfarction sudden death: significance of inducible ventricular tachycardia and infarct size in a conscious canine model

The relationship between inducible ventricular tachycardia in the convalescent phase of myocardial infarction and subsequent spontaneous ventricular fibrillation is uncertain. Thirty conscious instrumented dogs underwent programmed ventricular stimulation 5 days after anterior infarction; 15 had inducible ventricular tachycardia and 15 were noninducible. Following programmed ventricular stimulation, the application of a 150 uA current to the intima of the proximal circumflex artery initiated intimal damage, thrombosis, and acute ischemia of the posterolateral wall. After 20 minutes of ischemia, 73% inducible and 15% noninducible animals developed ventricular fibrillation (p less than 0.005) without previous hypotension. At 24 hours, 7% inducible and 85% noninducible animals survived (p less than 0.001). Anterior infarct size (percentage of left ventricular mass) was much larger in inducible (24.7 +/- 1.7%) than in noninducible (5.3 +/- 1.1%) (p less than 0.001) animals. Inducible ventricular tachycardia following infarction was highly predictive of spontaneous ventricular fibrillation during a later ischemic episode in this model. The mass of previously injured myocardium was a critical determinant of both.