A. Robert Denniss

Curative surgery for atrioventricular junctional (“AV Nodal”) reentrant tachycardia

A new surgical approach was studied prospectively in 10 consecutive patients with atrioventricular (AV) junctional reentrant tachycardia. The aim was to abolish tachycardia yet preserve normal AV conduction. On the basis of electrophysiologic study before operation, patients were classified as type A (ventriculoatrial [VA] intervals during tachycardia less than or equal to 40 ms) (seven patients) or type B (VA intervals greater than 40 ms) (three patients). Dual AV junctional pathways were demonstrable with single extrastimulus testing in seven patients before operation. Endocardial mapping during tachycardia at surgery revealed earliest atrial activation anteromedial to the AV node in type A patients and posterior to the node in the type B patients. The perinodal atrium in the region of earliest atrial activation during tachycardia was carefully disconnected from the AV node. After operation, AV junctional reentrant tachycardia was not inducible at comprehensive electrophysiologic study in any patient, and no clinical recurrences have occurred during a follow-up period of 2 to 14 months (mean 8 +/- 4). Normal AV conduction was preserved in all cases. Anterograde slow AV junctional pathway conduction was abolished in five of seven cases. Retrograde His to atrium conduction time was prolonged in type A patients but the capacity for retrograde VA conduction remained excellent. Retrograde His to atrium conduction was interrupted or severely compromised in the type B patients. These data show that there are at least two types of AV junctional reentry. Perinodal atrium appears to be part of the reentrant circuit in human AV junctional reentry. Although the most consistent effect of surgery was on the retrograde limb of the circuit, anterograde slow pathway conduction was also modified. AV junctional reentry is surgically curable with a high success rate.

Differences between patients with ventricular tachycardia and ventricular fibrillation as assessed by signal-averaged electrocardiogram, radionuclide ventriculography and cardiac mapping

This study examined 65 patients with ventricular tachycardia or fibrillation late after myocardial infarction to determine whether they differed with respect to duration of ventricular activation in sinus rhythm and left ventricular ejection fraction. Patients with spontaneous ventricular tachycardia had a longer ventricular activation time in sinus rhythm than did patients with spontaneous ventricular fibrillation. This difference was detected with the signal-averaged electrocardiogram (ECG) (tachycardia 181 +/- 33 ms, fibrillation 152 +/- 23 ms, p less than 0.001) and at epicardial mapping (tachycardia 210 +/- 17 ms, fibrillation 192 +/- 17 ms, p less than 0.02). Left ventricular ejection fraction was lower in patients with spontaneous ventricular tachycardia (0.22 +/- 0.09) than in patients with spontaneous ventricular fibrillation (0.27 +/- 0.09) (p less than 0.05). The patients with both spontaneous and inducible ventricular fibrillation had a shorter ventricular activation time on the signal-averaged ECG (129 +/- 17 ms) and a higher ejection fraction (0.36 +/- 0.05) than did either patients with spontaneous ventricular fibrillation and inducible ventricular tachycardia (158 +/- 21 ms and 0.25 +/- 0.08, respectively, each p less than 0.01) or patients with both spontaneous and inducible ventricular tachycardia (181 +/- 33 ms and 0.22 +/- 0.09, respectively, each p less than 0.001). Of the patients with inducible ventricular tachycardia, presentation with tachycardia rather than fibrillation was associated with a longer ventricular activation time on the signal-averaged ECG (181 +/- 33 versus 158 +/- 21 ms, p less than 0.02) and a longer cycle length of inducible ventricular tachycardia (290 +/- 61 versus 259 +/- 44 ms, p = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Value of programmed stimulation and exercise testing in predicting one-year mortality after acute myocardial infarction☆

The ability of programmed ventricular stimulation and exercise testing to predict 1-year mortality after acute myocardial infarction (AMI) was investigated in 228 clinically well survivors of AMI. Patients with inducible ventricular tachycardia (VT) or ventricular fibrillation (VF) had a higher mortality rate than those without inducible arrhythmias (26% vs 6%, p less than 0.001). Exercise-induced ST-segment change of 2 mm or more was associated with a higher mortality rate than ST change of less than 2 mm (11% vs 4%, 0.05 less p less than 0.10). Of patients who had both tests, 62% had no inducible ventricular tachycardia or ventricular fibrillation and ST change of less than 2 mm, and only 1% died during the first year. Thus, in clinically well survivors of AMI, programmed stimulation is a powerful predictor of first-year mortality; programmed stimulation and exercise testing together predict virtually all deaths within the first year, and they can identify a large group of patients with a very low mortality rate.

Electrophysiologic studies in patients with unexplained syncope

This study examined the role of electrophysiologic study in the evaluation of patients with unexplained syncope. The incidence of abnormalities (conduction disease, supraventricular tachycardia, ventricular tachycardia) was compared in patient groups with and without heart disease, and the effect of treatment of these abnormalities on recurrence of syncope was examined. Electrophysiologic study was performed in 111 consecutive patients with syncope, with antiarrhythmic medications being discontinued 1 week prior to study. There was no mortality associated with the procedure and only 9 patients (8%) had complications (groin haematoma, atrial fibrillation or brady-arrhythmias persisting after the procedure). Abnormalities were detected in 31 of 73 patients with heart disease (42%) but in only 6 of 38 patients with no heart disease (16%, P less than 0.01). During follow-up, syncope recurred in 2 of 37 patients (5%) treated because of abnormal findings, compared with a recurrence rate of 24% (18 of 74 patients) in the untreated group (P less than 0.05). Probability of remaining free from syncope at 2 years was 0.94 in the treated group and 0.72 in the untreated group (P less than 0.05). Mortality during follow-up was confined to the heart disease group with 5 of 30 treated patients in this group dying (17%) compared with 3 of 43 untreated patients (7%, P = not significant). Syncope patients with heart disease were thus more likely to have a diagnostically useful study than patients with normal hearts. Treatment directed at correction of abnormalities detected at electrophysiologic study reduced recurrence of syncope but did not significantly affect mortality. Syncope did not appear to be a prelude for sudden death in patients with normal hearts. Electrophysiologic study had no mortality and low morbidity.

Effect of antiarrhythmic therapy on delayed potentials detected by the signal-averaged electrocardiogram in patients with ventricular tachycardia after acute myocardial infarction

The ability of class I and class II antiarrhythmic drugs to either abolish delayed potentials or modify their timing was investigated in 39 patients with spontaneous ventricular tachycardia (VT) after myocardial infarction. Before the study all patients had delayed potentials on the signal-averaged electrocardiogram and inducible VT with programmed stimulation. These investigations were repeated during 67 trials of oral antiarrhythmic therapy (mexiletine 25, quinidine 24, metoprolol 13, disopyramide 2, procainamide 1, drug combinations 2). Delayed potentials were abolished in only 5 trails (7%), which was within the baseline variability of 8.5% for detection of delayed potentials. In the 7 trials in which VT inducibility was suppressed, delayed potentials persisted in 6 and mean ventricular activation time was virtually unchanged (151 ms before drug therapy, 152 ms after). Quinidine, mexiletine and metoprolol caused no consistent change in ventricular activation time. There was also no change in mean ventricular activation time (164 ms before and 163 ms after drug treatment) in patients in whom spontaneous VT did not recur with drug therapy during follow-up. Thus, the tested antiarrhythmic drugs had no consistent effects on presence or timing of delayed potentials on the signal-averaged electrocardiogram, even when VT inducibility was suppressed or recurrence of spontaneous VT was prevented.

Effect of excision of ventricular myocardium on delayed potentials detected by the signal-averaged electrocardiogram in patients with ventricular tachycardia

The ability of surgical excision of electrically abnormal ventricular myocardium to either abolish delayed potentials or modify their timing was investigated in 21 patients with spontaneous ventricular tachycardia (VT) late after myocardial infarction. This study also examined whether modification of delayed potentials after surgery was associated with loss of ability to induce VT or improvement in left ventricular function. Signal averaging of the electrocardiogram (ECG), programmed stimulation and radionuclide ventriculography were performed preoperatively and were repeated 10 to 14 days postoperatively. At preoperative investigation, all patients had delayed potentials on the signal-averaged ECG and inducible VT at programmed stimulation. In 7 patients (33%), delayed potentials were abolished by surgery, exceeding the baseline variability of 8.5% for detection of delayed potentials. VT was no longer inducible postoperatively in 16 patients (76%), including the 7 in whom delayed potentials were no longer detectable. In the patients in whom VT was no longer inducible, mean ventricular activation time decreased from 178 ms preoperatively to 151 ms postoperatively (standard error of the mean difference = 6 ms, p less than 0.001). In the 5 patients with inducible VT postoperatively, no significant change in mean ventricular activation time was seen, 181 vs 171 ms (standard error of mean difference = 9 ms). Reductions in ventricular activation time were not associated with an improvement in left ventricular ejection fraction unless aneurysmectomy was performed in addition to excision of electrically abnormal myocardium. Thus, the signal-averaged ECG may have a role in assessing the efficacy of antiarrhythmic surgery.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of repetition of extrastimuli on sensitivity and reproducibility of mode of induction of ventricular tachycardia by programmed stimulation

This study examined the effect of repeating the delivery of a programmed extrastimulus that previously failed to induce ventricular tachycardia, without the usual practice of concurrently altering other stimulation variables such as pacing site or basic cycle length. The impact of such repetition on both sensitivity and day to day variability in mode of arrhythmia induction was assessed in 24 patients with documented sustained ventricular tachycardia or fibrillation. Programmed stimulation in the absence of drugs was performed in each patient on 3 separate days. In the first 12 patients, each extrastimulus was scanned through diastole to refractoriness four times if no ventricular tachyarrhythmia was induced (longitudinal repetition); in the second 12 patients, each extrastimulus was delivered four times at a particular coupling interval before the interval was decreased in 10 ms steps to a closer coupling interval (lateral repetition). Day to day reproducibility of the mode of arrhythmia induction was compared with reproducibility in a control group of 18 similar patients studied previously on 3 separate days without repetition. A sustained ventricular tachyarrhythmia was inducible in all studies with four or fewer extrastimuli. In the group studied with longitudinal repetition, there was a 25% increased yield of induced ventricular tachycardia due solely to repetition of each extrastimulus scan, and the 95% confidence limit for tachycardia induction with any extrastimulus was achieved by delivering that extrastimulus three times. In the group studied with lateral repetition, there was also an increased yield of induced ventricular tachycardia at any extrastimulus coupling interval achieved by repetitive delivery of that coupling interval.(ABSTRACT TRUNCATED AT 250 WORDS)

Reproducibility of measurements of ventricular activation time using the signal-averaged Frank vectorcardiogram

Interobserver and day-to-day variability in detecting delayed potentials and in measuring duration of ventricular depolarization using the signal-averaged Frank vectorcardiogram were investigated in 20 patients, 12 with and 8 without ventricular tachycardia (VT). No patients were taking antiarrhythmic medications, digoxin or beta blockers at the time of study. The presence of delayed potentials and duration of ventricular activation were measured 2 times a mean of 5 days apart by 2 observers. Analysis of variance showed no significant interobserver variability in ventricular activation time. Day-to-day differences in ventricular activation times were small in patients without VT, none of whom had delayed potentials at either study. Delayed potentials were present in all 12 patients with VT at the first recording and in 11 at the repeat recording. However, significant (p less than 0.01) day-to-day variability was found in ventricular activation times, and 3 of the 12 patients had marked (more than 20 ms) day-to-day changes. It is concluded that in the absence of medical or surgical intervention, delayed potentials detected on 1 day have a high chance of being present at a repeat recording. However, the exact timing of these delayed potentials shows marked day-to-day variation in some patients. Interobserver variability is not significant with this method of detecting delayed potentials.

Quantitation of day to day variability in mode of induction of ventricular tachyarrhythmias by programmed stimulation

Spontaneous day to day variability in the mode of induction of ventricular tachycardia at programmed stimulation in the drug-free state has been described but not quantitated. To quantitate this variability, this study employed a new protocol of programmed stimulation in which the number of extrastimuli required for tachycardia induction was the only major stimulation variable. This protocol was applied to 18 consecutive patients with previously documented sustained ventricular tachyarrhythmia due to coronary artery disease. One to seven extrastimuli were available for arrhythmia induction if required. Each patient underwent programmed stimulation in the absence of antiarrhythmic drugs on 3 separate days with a mean interval of 5 +/- 2.7 days between studies. A sustained ventricular tachyarrhythmia was inducible in all studies with less than or equal to 4 extrastimuli; the mean number of extrastimuli required was 2.4 +/- 0.8. Day to day variability in the number of extrastimuli required for tachycardia induction was observed in the majority of patients (72%). Eleven patients (61%) varied by one extrastimulus over the three control studies, and two patients (11%) varied by two extrastimuli. At analysis of variance, the 95% confidence interval for the degree of day to day variability was +/- 1 extrastimulus from the mean number required in the three studies. Multiple configurations of induced ventricular tachycardia were frequently observed at repeat studies and occurred in 15 patients (83%). In conclusion, spontaneous day to day variability in mode of induction of ventricular tachycardia in the absence of drugs is common.(ABSTRACT TRUNCATED AT 250 WORDS)

Correlation between signal-averaged electrocardiogram and programmed stimulation in patients with and without spontaneous ventricular tachyarrhythmias☆

This study examined the incidence of delayed ventricular activation on signal-averaged electrocardiograms and the incidence of inducible sustained ventricular tachycardia (VT) at programmed stimulation (1 or 2 extrastimuli) in patients with and patients without spontaneous ventricular tachyarrhythmias. The correlation between delayed ventricular activation and inducible VT was investigated in 371 patients with acute myocardial infarction (AMI). In 32 patients with no ventricular disease and no spontaneous arrhythmias (group I), ventricular activation time averaged 115 +/- 2 ms, compared with 166 +/- 3 ms (p less than 0.001) for 65 patients with spontaneous ventricular tachyarrhythmias late after AMI (group II). In AMI patients with no spontaneous arrhythmias, ventricular activation time averaged 133 +/- 2 ms for 306 patients studied 1 to 4 weeks after AMI (group III) and 130 +/- 2 ms for 67 patients studied 3 to 12 months after AMI (group IV). The values for group III and group IV patients were each significantly higher than for group I (p less than 0.001), but lower than that for group II (p less than 0.001). The incidence of delayed ventricular activation was 89% for group II, 26% for group III and 18% for group IV. Sustained VT was not inducible in group I patients, but was inducible in 78% of group II (p less than 0.001 vs group I) and 20% of group III (p less than 0.05 vs group I; p less than 0.001 vs group II) (group IV was not studied).(ABSTRACT TRUNCATED AT 250 WORDS)