Effect of isoproterenol on induction of ventricular tachyarrhythmias in the normal and infarcted canine heart

The influence of isoproterenol on induction of ventricular arrhythmias was evaluated in 10 normal dogs and 17 dogs with experimentally induced myocardial infarction. Programmed stimulation (using up to 6 extrastimuli) was performed before and then during infusion of isoproterenol (2 micrograms/minute followed by 4 micrograms/minute). Isoproterenol facilitated induction of sustained monomorphic ventricular tachycardia (cycle length 163 +/- 26 msec) in 5 of the 10 animals with no inducible baseline arrhythmia (P less than 0.05). Isoproterenol did not affect cycle length or the number of extrastimuli required in animals with baseline ventricular tachycardia (cycle length 158 +/- 15 msec before versus 163 +/- 17 msec during isoproterenol, P = 0.3; extrastimuli 3.8 +/- 0.6 before versus 3.8 +/- 0.4 during isoproterenol infusion, P = 0.3). Isoproterenol did not significantly facilitate induction of ventricular fibrillation in either normal dogs or those studied after production of myocardial infarction. We conclude that infusion of isoproterenol increases the incidence of inducible ventricular tachycardia in the infarcted heart, but does not facilitate the induction of ventricular fibrillation in infarcted or normal hearts, despite the use of an aggressive protocol for programmed stimulation. Isoproterenol is, therefore, a safe and useful adjunct to programmed stimulation in this setting.     

Comparison of effects of three anesthetic agents on induction of ventricular tachycardia in a canine model of myocardial infarction

The effects of three anesthetic agents on the inducibility of ventricular tachycardia by programmed stimulation were investigated in dogs with a surgically induced left ventricular infarct. Endocardial catheter electrodes were placed at the right ventricular apex under general anesthesia at least 2 weeks after infarction, and the dogs were allowed to recover for 24 hours before undergoing programmed stimulation in the conscious state on two occasions 2 hours apart. A protocol of programmed stimulation with up to seven ventricular extrastimuli was used. In 15 animals, ventricular tachycardia was inducible on both occasions with 3.4 +/- 0.4 (mean +/- SEM; range, 1-5) extrastimuli. Two hours after baseline conscious induction, the dogs were anesthetized with either halothane, pentobarbital, or a fixed combination of fentanyl-droperidol plus nitrous oxide. Halothane prolonged the PR interval from 99 +/- 4 to 117 +/- 6 msec (p = 0.001) and the ventricular effective refractory period from 140 +/- 4 to 157 +/- 6 msec (p = 0.008). The ability to induce ventricular tachycardia was abolished in five of 10 animals (p less than 0.05). In the animals that remained inducible, the cycle length of tachycardia increased from 153 +/- 10 to 168 +/- 10 msec (p = 0.015), while the number of extrastimuli required was unaltered. Pentobarbital prolonged the PR interval from 104 +/- 6 to 124 +/- 6 msec (p = 0.004) and the QTc interval from 270 +/- 10 to 310 +/- 6 msec (p = 0.006). Ventricular tachycardia remained inducible in only six of 10 dogs (p less than 0.05) with no change in cycle length or the number of extrastimuli required. Ventricular fibrillation was inducible in an additional three dogs with a number of extrastimuli similar to that required to induce ventricular tachycardia before anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiologic and anatomic characteristics of ventricular tachycardia induced at the right ventricular outflow tract but not at the apex.

The site of ventricular stimulation is an important variable in the initiation of ventricular tachycardia (VT) by programmed ventricular stimulation. Among 169 patients studied consecutively, 17 (10%) had ventricular tachycardia induced by programmed electrical stimulation from the right ventricular outflow tract but not from the apex. Fourteen of these 17 patients had had prior myocardial infarction (12 had inferior, and two had both inferior and anterior myocardial infarction), two had a dilated cardiomyopathy, and one had a localized cardiomyopathy. Fourteen patients had echocardiograms suitable for analysis. Of these, 12 had posterior/inferior ventricular wall motion abnormalities located at the base of the heart. The ventricular effective refractory periods from the right ventricular outflow tract and right ventricular apex were 237 +/- 4 and 244 +/- 5 msec, respectively (p less than 0.05, mean +/- SEM). Induced VT had a cycle length of 229 +/- 4 msec and had the morphology of right bundle branch block in 12 patients, of left bundle branch block in three patients, and had both morphologies in two patients. In 14 patients the axis was superior. VT was initiated with two extrastimuli in 15 patients and with burst right ventricular pacing in two patients. Similar pacing techniques with identical pacing intervals did not induce VT at the right ventricular apex in 14 of these 17 patients. Further, among the 15 patients whose VT was induced at the right ventricular outflow tract with two extrastimuli, neither burst pacing (n = 13) nor two extrastimuli introduced at faster paced rates (n = 12) induced VT at the right ventricular apex.(ABSTRACT TRUNCATED AT 250 WORDS)     

Induced ventricular arrhythmias in regionally denervated porcine heart with healed myocardial infarction

STUDY OBJECTIVE--The aim was to test the hypothesis that chronic sympathetic denervation of the boundaries of a healed myocardial infarction may modify the arrhythmogenic response to programmed electrical stimulation. DESIGN--Electrical induction of ventricular arrhythmias and infarct size were evaluated in a control group of pigs with a one month old myocardial infarction induced by ligature of the left anterior descending coronary artery below the first diagonal branch. These were compared with a group of similarly infarcted pigs subjected to regional denervation of the peri-infarction area induced by topical pericoronary application of phenol. Denervation was verified by the absence of adrenergic histofluorescent reaction to glyoxylic acid in myocardial samples. EXPERIMENTAL MATERIAL--24 pigs (weight 15-20 kg) with myocardial infarction were studied, 13 of which were subjected to regional peri-infarction denervation, and 11 acted as controls. MEASUREMENTS AND MAIN RESULTS--Programmed ventricular stimulation with one to four extrastimuli at 500 and 400 ms basic cycle length at the left and right ventricles induced fewer episodes of ventricular fibrillation in the denervated than in the non-denervated group (five episodes in three pigs v 14 in nine pigs, p less than 0.005), but more episodes of sustained ventricular tachycardia (79 in eight pigs v 23 in two, p less than 0.001). Unlike fibrillation, induction of ventricular tachycardia increased with multiple extrastimuli and with short basic cycle length. The denervated preparations tended to develop smaller infarcts but this difference was not statistically significant: infarct weight (g) relative to total ventricular mass (g) = 7.2 (SD 2.4)% v 10.5(4.5)%. CONCLUSIONS--Neural integrity of the non-ischaemic myocardium bordering a healed infarction modulates inducibility of ventricular tachycardia and fibrillation during programmed ventricular stimulation.     

Prospective comparison of right and left ventricular stimulation for induction of sustained ventricular tachycardia

Thirty-eight patients who had sustained monomorphic ventricular tachycardia (VT) or sudden cardiac death underwent programmed ventricular stimulation. To assess the relative efficacy of right and left ventricular (RV and LV) stimulation, a tandem protocol with 1 to 4 extrastimuli and burst pacing was used. Each step of the protocol was performed in a rotating sequence at the RV apex, basal RV septum and LV apex. Sustained VT was induced from the RV apex in 26 patients, right ventricle (either site) in 27, and LV apex in 24, and spontaneous VT was reproduced from those sites in 11, 14 and 12 patients, respectively. In the 23 patients who had sustained VT induced from both ventricles, RV stimulation always required fewer or the same number of extrastimuli for induction. At every stage of the protocol, the cumulative yield of sustained VT was consistently greater from the right ventricle than from the left ventricle. After delivering 4 extrastimuli and burst pacing, LV stimulation only increased the yield of sustained VT by 1 patient, and spontaneous VT by 3 patients. Inducibility or noninducibility in the right ventricle generally predicted the same outcome in the left ventricle. Previously undocumented VT or ventricular fibrillation was induced from the right ventricle in 19 patients and from the left ventricle in 13. Thus, LV stimulation was less efficacious than RV stimulation. LV stimulation increased the yield over RV stimulation only minimally and did not reduce the number of extrastimuli required to induce sustained VT.     

Influence of infarct age on reproducibility of ventricular tachycardia induction in a canine model

The inducibility and reproducibility of ventricular tachycardia were evaluated in 97 dogs after myocardial infarction produced by single stage coronary artery ligation. Arrhythmia induction was performed with use of an endocardial electrode catheter positioned at the right ventricular apex before each study. An aggressive protocol of programmed stimulation was used, employing up to seven extrastimuli and three attempts at arrhythmia induction in each study. Electrophysiologic study was performed in individual dogs at the following times after infarction: 1) 7.7 +/- 0.3 and 15 +/- 0.2 days (34 consecutive dogs); 2) 14 +/- 0.6 and 26 +/- 1.7 days (24 selected dogs); 19 +/- 2 and 43 +/- 3 days (12 selected dogs); 4) 36 +/- 2 and 60 +/- 6 days (8 selected dogs); and 5) 59 +/- 12 and 130 +/- 10 days (3 selected dogs). Inducibility of ventricular tachycardia decreased significantly from 74% 1 week after infarction to 41% 2 weeks after infarction. Thus, early reproducibility was low (48%). Reproducibility increased thereafter, with 88% of the dogs having reproducible ventricular tachycardia between 2 and 4 weeks (p less than 0.025) and 100% having reproducibly inducible ventricular tachycardia between 4 weeks and 4 months after infarction. Dogs with no inducible arrhythmia early after infarction did not develop inducible ventricular tachycardia or fibrillation at later studies. Twelve dogs developed spontaneous ventricular tachycardia or sudden arrhythmic death late after infarction. Overall, 22% of dogs with inducible ventricular tachycardia with a cycle length greater than 140 ms developed spontaneous ventricular tachycardia or sudden death. Arrhythmia induction decreases significantly during the 1st 2 weeks after myocardial infarction, but long-term reproducibility of ventricular tachycardia induced greater than or equal to 2 weeks after infarction is very high. This canine model of long-term, reliably inducible ventricular tachycardia is suitable for investigation of antiarrhythmic drugs, surgery and other interventions.     

Role of triple extrastimuli during electrophysiologic study of patients with documented sustained ventricular tachyarrhythmias

Electrophysiologic studies were performed in 172 consecutive patients for evaluation of documented sustained ventricular tachyarrhythmias. One hundred thirteen patients presented with sustained ventricular tachycardia that was hemodynamically stable, and 59 patients presented with cardiac arrest. Seventy-one patients without previously documented or suspected ventricular arrhythmias were also studied to determine the specificity of our electrophysiologic study protocol. The stimulation protocol included single, double, and triple right ventricular extrastimuli and rapid ventricular pacing at multiple cycle lengths performed at one or more right ventricular sites. Stimulation was performed at one or more left ventricular sites in patients with documented spontaneous arrhythmias when right ventricular programmed stimulation failed to induce sustained ventricular tachycardia. Ventricular tachyarrhythmias were induced in 110 (97%) of the patients who presented with sustained ventricular tachycardia, in 48 (81%) of the patients who presented with cardiac arrest, and in 28 (40%) of the patients without documented spontaneous arrhythmias. Right ventricular triple extrastimuli induced tachycardia in 22% of patients who presented with sustained ventricular tachycardia vs 46% of those who presented with cardiac arrest (p less than .001). Left ventricular stimulation was required for tachycardia induction in 3% of patients with stable tachycardia vs 19% of those with cardiac arrest (p less than .01). Triple extrastimuli induced 57% of tachycardias in the 28 patients without spontaneous arrhythmias, and virtually all of these tachycardias were polymorphic and nonsustained. The cycle lengths of tachycardias induced in each group by double and triple extrastimuli were similar, but the tachycardias induced in patients with cardiac arrest were significantly faster than those induced in the ventricular tachycardia group (mean cycle length 218 vs 291 msec, p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of transmural versus nontransmural myocardial infarction on inducibility of ventricular arrhythmias during sympathetic stimulation in dogs

Transmural myocardial infarction interrupts sympathetic nerves and denervates viable muscle distal to myocardial infarction. The effect of sympathetic stimulation on responses to programmed ventricular stimulation was studied in dogs without myocardial infarction (Group I: n = 5), with transmural anterior wall myocardial infarction (Group II: n = 6) and with nontransmural anterior wall myocardial infarction (Group III: n = 9). Ventricular effective refractory period during sympathetic stimulation decreased by 16 +/- 18, 1 +/- 2 and 12 +/- 8 ms (mean +/- SD) in viable muscle of the inferoapical left ventricle in Groups I, II and III, respectively, suggesting efferent sympathetic denervation by transmural myocardial infarction only. Sustained ventricular tachycardia or fibrillation was induced more easily during sympathetic stimulation in six of the six dogs with transmural infarction, but in only two of the nine dogs with nontransmural infarction (p less than 0.01). It is concluded that the partial sympathetic denervation produced by transmural myocardial infarction enhances the ease of induction of ventricular tachycardia and fibrillation during sympathetic stimulation. A similar mechanism may lead to increased risk for lethal arrhythmias during periods of high sympathetic tone in patients with transmural myocardial infarction.     

Frequency and significance of induced sustained ventricular tachycardia or fibrillation two weeks after acute myocardial infarction

Electrophysiologic study, 24-hour ambulatory electrocardiographic monitoring, treadmill exercise test and angiographic evaluations were performed in 45 patients 14 +/- 3 days (mean +/- standard deviation) after acute myocardial infarction. Electrophysiologic study protocol included burst ventricular pacing and 1 to 3 ventricular extrastimuli at 2 cycle lengths from right ventricular apex, right ventricular outflow and left ventricle. Sustained monomorphic ventricular tachycardia (VT) (13 patients) or ventricular fibrillation (VF) (7 patients) was induced in 20 patients (44%) (group I). In these 20 patients, VT/VF was inducible with 2 extrastimuli in 10 patients, 3 extrastimuli in 9 patients and burst pacing in 1 patient. In the remaining 25 patients (56%), induction of no fewer than 7 ventricular beats were noted (group II). Severe left ventricular (LV) wall motion abnormalities occurred in 70% of group I patients and 22% of group II patients (p less than 0.005). There was no difference in the site of infarction, frequency and grade of ventricular ectopic rhythm on ambulatory electrocardiographic monitoring, double product on submaximal exercise, LV ejection fraction, and number of obstructed coronary arteries (70% or greater) (p greater than 0.1) between group I and group II patients. During a mean follow-up of 10 +/- 3 months, 1 patient in each group died suddenly, and in 1 group I patient spontaneous sustained VT developed which was identical in morphologic configuration to that induced during electrophysiologic study. In conclusion, electrical induction of sustained VT or VF during electrophysiologic study is common in patients 2 weeks after acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Can potentially significant polymorphic ventricular arrhythmias initiated by programmed stimulation be distinguished from those that are nonspecific?

Polymorphic ventricular arrhythmias (PVAs) initiated by programmed electrical stimulation may be a nonspecific response or evidence of ventricular electrical instability. To determine if PVAs initiated in patients with spontaneous sustained ventricular tachycardia or fibrillation differ from those which are clearly a nonspecific response in structurally normal hearts, the initiation, characteristics, and relationship to ventricular repolarization of PVAs greater than five beats in duration were evaluated in 32 patients without structural heart disease and in 36 patients with spontaneous sustained ventricular arrhythmias more than 9 days after myocardial infarction. Patients received one to four extrastimuli during sinus rhythm and right ventricular pacing. In a comparison with patients who completed the same steps (defined by the basic drive cycle length and number of extrastimuli) in the stimulation protocol, there was no difference in the cumulative risk of initiation of a PVA between the patients with and those without heart disease at any step. This risk was 51% vs 38% for patients who received two or fewer extrastimuli at four basic cycle lengths (p = NS). PVAs were initiated by the same mean number of extrastimuli (2.3 +/- 0.5 vs 2.6 +/- 0.9 p NS) with the same degree of prematurity in both groups. Forty-four percent of the PVAs in the myocardial infarction group had a cycle length greater than 250 msec or a coupling interval of the first tachycardia beat to its initiating stimulus greater than 320 msec as opposed to only one (6%) in the group without heart disease (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

Dispersion of Refractoriness in Ventricular Tachycardia Induction from the Right Ventricle

To determine whether dispersion of ventricular refractoriness plays a role in ventricular tachycardia induction from the right ventricle, we measured effective and functional refractory period at the apex and outflow tract. Induction was attempted at both sites using two train cycle lengths and up to two extrastimuli. Twenty-two patients with remote myocardial infarction and documented ventricular tachycardia or sudden death were studied. Fourteen (group IA) had tachycardia inducible using this protocol; eight (group IB) did not. Dispersion defined as the absolute difference between the two sites was significantly greater in group IA than in group IB for functional refractoriness (e.g., 22 ± 21 msec vs 9 ± 11 msec at a cycle length of 600 msec), whereas dispersion of ventricular effective refractory period was not. A dispersion of 20 msec or greater had a positive predictive value of 90% for tachycardia induction. These results were compared to two control groups: group II (13 patients) with remote infarction but neither documented nor inducible ventricular tachycardia and group III (19 patients) without infarction or ventricular tachycardia. Dispersion of refractoriness in these two groups was similar to that in group IB.
With the study protocol, ventricular tachycardia was inducible at the apex only in eight cases and at the outflow tract only in five. Functional refractory period was 17 ± 30 msec shorter at the site of induction. The site of shortest functional refractory period and the site of induction were, however, identical in only 8/13 cases (62%), but in these eight, the coupling intervals necessary for induction were attainable only at the induction site. This indicates at least a moderate role for local properties of refractoriness in determining the site of successful induction.     

Determinants of induced sustained arrhythmias in survivors of out-of-hospital ventricular fibrillation

We prospectively studied 196 consecutive survivors of out-of-hospital ventricular fibrillation (VF) not associated with acute myocardial infarction and 46 consecutive, control patients without prior ventricular arrhythmias. Programmed stimulation included two extrastimuli (S3 protocol) in all patients and three extrastimuli (S4 protocol) in the last 140 study patients and in all control patients. Sustained ventricular tachycardia (VT) or VF was not induced in any control patient. In study patients, logistic regression identified two independent predictors of induced, sustained VT for both S3 and S4 protocols: prior spontaneous, sustained VT (37 patients; p less than or equal to .001) and prior myocardial infarction (113 patients; p = .005). With the S3 protocol, sustained VT was induced in 54% of patients with both prior myocardial infarction and prior sustained VT vs 4% without either; with the S4 protocol, sustained VT was induced in 91% vs 13%, respectively. Eighty-three percent of induced VT episodes had a cycle length less than 300 msec, and all required termination by cardioversion or pacing. VF was induced only in survivors of out-of-hospital VF without prior, spontaneous, sustained VT (S3 protocol, 9%; S4 protocol, 24%) but not in study patients with prior sustained VT (S3, p = .10; S4, p = .05) or control patients (S3, p = .06; S4, p = .01). The mean coupling intervals of extrastimuli that induced VF were not significantly different from the intervals that induced sustained VT.(ABSTRACT TRUNCATED AT 250 WORDS)     

Bepridil versus nifedipine for ventricular tachycardia induced in the late postinfarction phase in conscious dogs

The effects of the two calcium antagonists bepridil and nifedipine on induced ventricular tachyarrhythmias were studied by programmed electrical stimulation in 15 dogs, 4-8 days after myocardial infarction. Recordings from the infarcted and normal anterior wall of the left ventricle were obtained with an epicardial implanted 'composite' electrode. Bepridil (5 mg/kg) or nifedipine (0.025 mg/kg) were administered i.v. on different days and testing was repeated. Sustained ventricular tachycardia was prevented or significantly slowed by bepridil in 11/12 experiments compared with none of 9 experiments with nifedipine. Paradoxically, in 10/15 dogs nifedipine accelerated arrhythmias or even provoked ventricular fibrillation. Bepridil prolonged refractoriness of infarcted myocardium by 15 +/- 4% (mean +/- SD, p less than 0.01), which was greater than the increase it produced in the effective refractory period of normal tissue (9.0 +/- 3.8%) or QTc interval (11 +/- 5.5%). In contrast, nifedipine significantly shortened these parameters. Both drugs did not influence conduction in infarcted and normal zones as indicated by unchanged late potentials, QRS duration and normal-zone electrograms, respectively. The data indicate that the antiarrhythmic action of bepridil was predominantly related to the prolongation of ventricular refractoriness and repolarization (class III effects).     

Programmed electric stimulation following acute myocardial infarct. Significance of stimulation timing

To assess the influence of time on the inducibility by programmed electrical stimulation of ventricular arrhythmias after acute myocardial infarction, we studied 18 patients on the 5th and 24th day after infarction with a stimulation protocol employing a maximum of 3 right ventricular extrastimuli during sinus rhythm and at 3 paced cycle lengths. All patients were without documented sustained ventricular arrhythmias (sustained ventricular tachycardia or ventricular fibrillation) prior to the investigation. Sustained ventricular arrhythmias were induced in 2 patients on day 5, but in 9 on day 24 after infarction. This difference in incidence was statistically significant (p less than 0.05), as was the change in the distribution ratio of induced sustained ventricular arrhythmias from day 5 to day 24 (p less than 0.05). The types of arrhythmia induced on day 24 were sustained ventricular tachycardia with a mean cycle length of 207 ms in 6 cases (5 monomorphic, 1 polymorphic), and ventricular fibrillation in 3 cases. These 9 patients did not differ from the remaining 9 patients in maximal CPK, infarct site, number of stenosed coronary arteries, global left ventricular ejection fraction, and in the results of 24-hour Holter monitoring, but they had a significantly shorter right ventricular effective refractory period (223 +/- 10 ms versus 259 +/- 28 ms; p less than 0.05). During the follow-up period of 24 +/- 5 months no patient died, had syncopal attacks, or developed spontaneous episodes of sustained ventricular arrhythmia. The timing of programmed electrical stimulation with a maximum of 3 right ventricular extrastimuli strongly influences the inducibility of sustained ventricular arrhythmias after acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prospective evaluation of a protocol for induction of sustained ventricular tachycardia in patients referred to a tertiary centre.

All eight stages of a stimulation protocol that used one then two extrastimuli from the right ventricular apex in sinus rhythm and three ventricular drive rates (100, 120, and 140 beats/min) were performed in 24 patients with recurrent spontaneous sustained ventricular tachycardia despite drug treatment. Twenty two of the patients had sustained a previous myocardial infarct and 18 were on long term treatment with amiodarone. Sustained (greater than 30 s) ventricular tachycardia was induced in all patients. Two extrastimuli were significantly more likely to induce sustained ventricular tachycardia than one extrastimulus, both overall and individually for the three ventricular drive rates. A ventricular drive rate of 140 beats/min was significantly more likely to induce ventricular tachycardia than ventricular drive rates of 100 and 120 beats/min which were significantly more effective than sinus rhythm. A ventricular drive rate of 140 beats/min with one or two extrastimuli induced ventricular tachycardia in 23/24 (95%) of the patients in this study. The full eight stage protocol was progressive separately for both extrastimuli and ventricular drive rate but the last two stages (ventricular drive rate of 140 beats/min with one or two extrastimuli) were as effective as the entire protocol in inducing ventricular tachycardia.     

Efficacy and electrophysiologic effects of oral sotalol in patients with sustained ventricular tachycardia caused by coronary artery disease.

The efficacy of oral sotalol in preventing sustained ventricular tachycardia induction by invasive electrophysiological testing was assessed in 22 patients (60 +/- 9 years) with prior myocardial infarction. Programmed stimulation consisted of two basic drives followed by up to three extrastimuli at two right ventricular sites. At baseline, sustained monomorphic ventricular tachycardia was inducible in all patients. With sotalol (360 +/- 172 mg/day), it was no longer inducible in 10 patients; in 12 others, it remained inducible and its cycle length was only minimally prolonged (322 +/- 42 to 345 +/- 44 msec, p less than 0.05). Sotalol markedly prolonged sinus cycle length, uncorrected QT interval, and right ventricular effective and functional refractory periods, but had little effect on ventricular conduction time either in sinus rhythm or with right ventricular pacing. There was no significant difference in drug dose or in electrophysiologic effect of drug that related to efficacy, nor was there any correlation between drug-induced prolongation of ventricular tachycardia cycle length and its effects. Six patients received oral sotalol over the long term without spontaneous recurrence of ventricular tachycardia (follow-up: 23 +/- 18 months). These results demonstrate that sotalol is effective (45%) against sustained ventricular tachycardia induction at moderate doses and is well tolerated over a long term in the setting of remote myocardial infarction. However, its electrophysiologic effects as measured at invasive testing are not predictive of efficacy against ventricular tachycardia induction.     

Influence of tachycardia cycle length and antiarrhythmic drugs on pacing termination and acceleration of ventricular tachycardia

We examined the influence of ventricular tachycardia (VT) cycle length and antiarrhythmic drugs on the frequency of VT termination and acceleration by single and double extrastimuli and right ventricular burst pacing. In 57 patients, 89 episodes of sustained VT (32 control, 57 drug) were induced by programmed electrical stimulation. Overall, 60 of 89 (67%) episodes of ventricular tachycardia were terminated by means of programmed electrical stimulation. In patients with relatively slow ventricular tachycardia (VT cycle length greater than or equal to 350 msec) pacing terminated 37 of 44 (84%) episodes but terminated only 24 of 45 (51%) episodes of more rapid VT (VT cycle length less than or equal to 349 msec, p less than 0.005). Pacing successfully terminated VT in nine of 49 (18%) episodes using a single extrastimulus, 22 of 52 (42%) episodes using double extrastimuli, and 40 of 66 (61%) episodes using burst right ventricular pacing. VT acceleration occurred in none of 49 attempts with a single extrastimulus, in eight of 52 (15%) attempts with double extrastimuli, and in 12 of 66 (18%) attempts using burst right ventricular pacing. During therapy, the frequency of either ventricular tachycardia termination or acceleration did not change regardless of the pacing termination method used. However, by prolonging the mean VT cycle length from 311.1 +/- 82.2 msec to 401.9 +/- 103.5 msec (p less than 0.01), drugs increased the overall frequency of VT termination. We conclude that: (1) pacing terminates VT more frequently if the VT cycle length is long and if right ventricular bursts are used, (2) burst right ventricular pacing increases the risk of VT acceleration, and (3) drugs increase the frequency of ventricular tachycardia termination by prolonging VT cycle length but do not affect frequency of VT acceleration.     

Late induction of tachycardia in patients with ventricular fibrillation associated with acute myocardial infarction

A prospective study was made of 57 asymptomatic patients, 1 to 24 months after acute myocardial infarction, 17 with (Group I) and 40 without (Group II) ventricular fibrillation during the acute event. None of the 57 patients had symptomatic arrhythmias, uncontrolled heart failure or unstable angina. There was no significant difference between the two patient groups in time from acute myocardial infarction, medication used or left ventricular ejection fraction. Repetitive forms of arrhythmia (Lown grade 4) were more prevalent (29 versus 16%, not significant) during 24 hour ambulatory monitoring in patients in Group I (ventricular fibrillation group). Programmed extrastimulation was performed using 1 to 3 twice-threshold, 2 ms decremental extrastimuli delivered during right ventricular drive. Of the 17 patients in Group I, 8 had no induced arrhythmia (less than or equal to 4 extra responses), 4 had nonsustained ventricular tachycardia and 5 had sustained ventricular tachycardia (degenerating into ventricular fibrillation requiring electrical reversion in 4). None of the 40 patients in Group II had induced sustained ventricular tachycardia (p less than 0.005), although 9 had nonsustained ventricular tachycardia. Patients with ventricular fibrillation during acute myocardial infarction may have an increased risk for ventricular tachycardia or ventricular fibrillation that may be exposed by programmed electrical stimulation even when not yet clinically manifest.     

Electrophysiological effects of acute ischaemia on electrically stable myocardial infarction

The purpose of this study was to examine the effects of acute ischaemia superimposed on an electrophysiologically stable, small myocardial infarction, and to determine the mechanisms of induced ventricular arrhythmias, using a canine infarction model. Ten dogs without inducible ventricular tachycardia or fibrillation on the 7th day post-myocardial infarction (Group 1) and 14 control dogs (Group 2) were subjected to 30 min acute ischaemia by occlusion of the proximal left anterior descending artery. The areas of infarcted myocardium ranged from 1.0 to 20.4% (mean 8.9, SD 7.7) of total left ventricular weight. Ventricular arrhythmias were inducible by programmed electrical stimulation in eight of 10 dogs (80%) after acute ischaemia, but in only one of 14 control dogs (7%) (p less than 0.005). In seven of eight Group 1 dogs, epicardial mapping showed that ventricular arrhythmias did not originate from the epicardial region. In one dog, in which there was simultaneous epicardial and endocardial mapping, an endocardial electrogram from the boundary area between infarcted and acutely ischaemic zones recorded continuous fragmented activity. It was thus suggested that re-entry in a relatively isolated endocardial site could be attributed to the induction of ventricular tachyarrhythmias, and that the electrical instability could be significantly enhanced during acute ischaemia when underlying myocardial infarction was present.     

Comparison of endocardial and epicardial programmed stimulation for the induction of ventricular tachycardia

Twenty-seven patients who had pairs of stainless steel wire electrodes placed on the right and the left ventricle during cardiac surgery underwent both epicardial and endocardial programmed ventricular stimulation to assess the inducibility of ventricular tachycardia. Twenty-six of the patients had coronary artery disease and were studied to evaluate map-guided surgery for treatment of ventricular arrhythmias. Burst ventricular pacing and up to three ventricular extrastimuli coupled to two drive train cycle lengths were delivered from the right and left ventricular epicardial wire electrodes and from endocardial catheter electrodes placed at the apex and outflow tract of the right ventricle. Ventricular tachycardia was reproducibly induced in three patients by both endocardial and epicardial stimulation. In one patient ventricular tachycardia was reproducibly induced by epicardial stimulation, but nonreproducible, nonsustained ventricular tachycardia was induced by endocardial stimulation. Ventricular tachycardia remained inducible by both endocardial and epicardial stimulation in three instances (two patients) during drug therapy. A negative study (less than 10 consecutive ventricular beats induced) was obtained in 23 patients by both endocardial and epicardial stimulation. The patients were followed up for 12 to 43 months (average 31). Sudden death or documented ventricular tachycardia occurred in two of the three patients with a positive study by both endocardial and epicardial stimulation. Nineteen (83%) of the 23 patients with concordantly negative studies remained free of arrhythmias. On the basis of concordant results of endocardial and epicardial stimulation (p = 0.001) these results suggest that epicardial stimulation of the right and the left ventricle is an acceptable method to assess the postoperative inducibility of ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)