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Background: The implantable cardioverter-defibrillator (ICD) is highly effective in reducing mortality among patients at risk for fatal arrhythmias, but inappropriate ICD activations are frequent, with potential adverse effects., Methods: We randomly assigned 1500 patients with a primary-prevention indication to receive an ICD with one of three programming configurations. The primary objective was to determine whether programmed high-rate therapy (with a 2.5-second delay before the initiation of therapy at a heart rate of ≥200 beats per minute) or delayed therapy (with a 60-second delay at 170 to 199 beats per minute, a 12-second delay at 200 to 249 beats per minute, and a 2.5-second delay at ≥250 beats per minute) was associated with a decrease in the number of patients with a first occurrence of inappropriate antitachycardia pacing or shocks, as compared with conventional programming (with a 2.5-second delay at 170 to 199 beats per minute and a 1.0-second delay at ≥200 beats per minute)., Results: During an average follow-up of 1.4 years, high-rate therapy and delayed ICD therapy, as compared with conventional device programming, were associated with reductions in a first occurrence of inappropriate therapy (hazard ratio with high-rate therapy vs. conventional therapy, 0.21; 95% confidence interval [CI], 0.13 to 0.34; P<0.001; hazard ratio with delayed therapy vs. conventional therapy, 0.24; 95% CI, 0.15 to 0.40; P<0.001) and reductions in all-cause mortality (hazard ratio with high-rate therapy vs. conventional therapy, 0.45; 95% CI, 0.24 to 0.85; P=0.01; hazard ratio with delayed therapy vs. conventional therapy, 0.56; 95% CI, 0.30 to 1.02; P=0.06). There were no significant differences in procedure-related adverse events among the three treatment groups., Conclusions: Programming of ICD therapies for tachyarrhythmias of 200 beats per minute or higher or with a prolonged delay in therapy at 170 beats per minute or higher, as compared with conventional programming, was associated with reductions in inappropriate therapy and all-cause mortality during long-term follow-up. (Funded by Boston Scientific; MADIT-RIT ClinicalTrials.gov number, NCT00947310.).

Introduction: Bundle branch reentry is an uncommon mechanism for ventricular tachycardia. More infrequently, both fascicles of the left bundle may provide the substrate for such macroreentrant bundle branch circuits, so-called interfascicular reentry. The effect of adenosine on bundle branch reentrant mechanisms of tachycardia is unknown., Methods and Results: A 59-year-old man with no apparent structural heart disease and history of frequent symptomatic wide complex tachycardias was referred to our center for further electrophysiologic evaluation. During electrophysiologic study, a similar tachycardia was reproducibly initiated only during isoproterenol infusion, which had the characteristics of bundle branch reentry, possibly using a left interfascicular mechanism. Intravenous adenosine reproducibly terminated the tachycardia. Application of radiofrequency energy to the breakout site from the left posterior fascicle prevented subsequent tachycardia induction and rendered the patient free of spontaneous tachycardia during long-term follow-up., Conclusions: Patients with ventricular tachycardia involving a bundle branch reentrant circuit may be sensitive to adenosine. These results suggest that adenosine may not only inhibit catecholamine-mediated triggered activity but also some catecholamine-mediated reentrant ventricular arrhythmias.

Adenosine has been shown to reliably confirm the success of accessory pathway catheter ablation by producing transient atrioventricular (AV) block during atrial and ventricular pacing. This is due to the insensitivity of accessory pathway conduction to adenosine (with the rare exception of accessory pathways with decremental conduction properties). However, 4 of 204 consecutive patients who underwent successful accessory pathway ablation (as shown by adenosine-induced transient AV block) had recurrent AV reciprocating tachycardia involving a second, previously nonmanifest accessory pathway. In each case, the second accessory pathway was localized to a site disparate from the original pathway. No pathway showed decremental anterograde or retrograde conduction properties. In 2 patients, adenosine initially did not show the presence of the second concealed accessory pathway, because the refractory period of the accessory pathway was longer than the pacing cycle length used to assess ventriculoatrial conduction. Only when the refractory period of this second accessory pathway was shortened by infusion of isoproterenol did adenosine reveal the presence of the pathway during follow-up electrophysiologic study. In another patient, a non-decremental accessory pathway was shown to be sensitive to adenosine. In the remaining patient, the second accessory pathway may have been transiently injured during the initial study, thereby simulating adenosine sensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)

Objective: The aim was to determine the beat to beat variability in local activation time during sustained monomorphic ventricular tachycardia in a canine model of experimental myocardial infarction., Methods: A digital template matching algorithm was developed for detecting subtle beat to beat variability in local activation timing at each of multiple ventricular sites. Ten electrically induced sustained ventricular tachycardia episodes, mean cycle length 211 (SD 40) ms, were endocardially and epicardially mapped in mongrel dogs weighing 15-20 kg. Digitised data were analysed for beat to beat local activation time variability. Similar data recorded during ventricular pacing at comparable rates and during sinus rhythm served as controls., Results: The overall mean variability of local activation time for all 10 ventricular tachycardias was 3.2(1.6) ms, range 1.8(1.1) ms to 4.7(2.8) ms, in contrast to the overall mean variability of 0.2(0.4) ms (p = 0.0001) for ventricular pacing and 0.7(0.6) ms (p = 0.0001) for sinus rhythm. Oscillations in local activation time manifested alternans type periodicity during seven of 10 ventricular tachycardias independent of any alternans in local electrogram morphology., Conclusions: During sustained, monomorphic ventricular tachycardia, beat to beat variability and alternans type oscillations in local activation time are common and may be an intrinsic property of re-entry since they are negligibly small during ventricular pacing.

Background: The electrical current and energy required to terminate ventricular tachyarrhythmias are known to vary by arrhythmia: Ventricular tachycardia (VT) is generally considered to require less energy than ventricular fibrillation (VF). The hypothesis of our study was that current requirements for transthoracic termination of VT are further determined by VT rate and QRS complex morphology., Methods and Results: We prospectively studied 203 patients who received a total of 569 shocks for VT or VF by following a current-based protocol. This protocol recommended shocks for VT beginning at 18 A (70 +/- 22 J) and shocks for VF beginning at 25 or 30 A (137 +/- 52 J or 221 +/- 70 J). The ventricular tachyarrhythmias were subclassified as monomorphic VT (MVT): uniform QRS complex morphology on surface electrocardiogram and heart rate greater than 100 beats per minute; polymorphic VT (PVT): nonuniform QRS complex morphology and heart rate less than or equal to 300 beats per minute; or VF: nonuniform QRS complex morphology and heart rate greater than 300 beats per minute. We found that shocks of 18 A and 25 A for terminating MVT had success rates of 69% and 82%, respectively, whereas such low-current shocks were less successful for PVT (33% at 18 A) and for VF (19% at 18 A, 53% at 25 A). High-current shocks of 35 A and 40 A were equally successful for the three ventricular tachyarrhythmias. Subdividing MVT revealed that slower MVT (heart rate less than 200 beats per minute) had a significantly better success rate with low-current shocks of 18 A and 25 A than did faster MVT (greater than 200 beats per minute) (89% versus 72% success, p less than 0.01). Bundle branch block morphology, QRS axis, and duration of ventricular tachyarrhythmia did not alter current requirements., Conclusions: Heart rate and electrocardiographic degree of organization of ventricular tachycardia are important determinants of transthoracic energy and current requirements for cardioversion and defibrillation. Transthoracic termination of MVT requires relatively low current or energy, but PVT behaves more like VF and requires higher electrical current or energy.

A 65-year-old man developed incessant ventricular tachycardia following coronary artery bypass grafting while being weaned from cardiopulmonary bypass. The arrhythmia was refractory to procainamide, lidocaine, bretylium, and magnesium. Ventricular tachycardia subsided following reinitiation of cardiopulmonary bypass. Ultimately, the patient required ventricular assist devices to control his arrhythmia. This case is unique as the ventricular assist devices were used not for hemodynamic support, but for arrhythmia control. The mechanism of arrhythmia suppression may be related to contraction-excitation coupling.

Background: The precision and limitations of ventricular pacemapping as a method to localize the site of earliest breakthrough of ventricular tachycardia (VT) were investigated in a canine model of experimental myocardial infarction., Methods and Results: Forty-one episodes of VT induced in 10 animals were mapped using a standard grid of 64 endocardial and epicardial bipolar electrodes to determine the site of earliest endocardial or epicardial breakthrough of activation during VT. Each of these 64 recording sites was also used for ventricular pacing during sinus rhythm at cycle lengths comparable to those of the VTs. Orthogonal X, Y, and Z Frank electrocardiographic (ECG) leads were recorded during all episodes of VT and ventricular pacing from all sites after the chest was closed in all animals. Surface ECG waveforms corresponding to each VT and each ventricular pacing were compared pairwise by measuring the Euclidean metric difference between the VT and ventricular pacing vectors with the orthogonal ECG leads as their X, Y, and Z components. The pacing site that generated the vector most similar to VT vector (smallest vectorial difference) was defined as the predicted breakthrough site. This predicted site of breakthrough was identical to the actual site of breakthrough determined by activation sequence mapping during VT for only nine VTs (22%). However, for an additional 27 VTs (66%), the observed and predicted breakthrough locations were at adjacent (1 cm or less apart) recording sites. For five VTs (12%), the two sites were remote, the distance between them exceeding 1 cm., Conclusions: In this model, locating the breakthrough site by pacemapping is exact in only a small minority of VTs. However, when orthogonal surface ECG leads are used for comparison, pacemapping can predict the site of earliest breakthrough during VT with a 1-cm resolution in the majority of VTs.

The immediate reproducibility of sustained ventricular tachycardia induction was evaluated prospectively during 106 studies performed in 53 patients with clinical sustained monomorphic ventricular tachycardia. Programmed electrical stimulation was performed twice, using the same protocol during 53 drug-free studies and 53 subsequent studies on antiarrhythmic therapy. Sustained monomorphic ventricular tachycardia was reproduced in 104 (98%) of the 106 studies. There was no significant difference in the incidence of reproducible tachycardia in the drug-free state compared with that observed during treatment with different classes of antiarrhythmic drugs. An increase in the number of extrastimuli was required to reinitiate the tachycardia in 9 (11%) of 83 studies in which single or double extrastimuli were initially required to induce the tachycardia. In 39 (37%) of 104 studies with reproducible tachycardia induction, the two tachycardias significantly differed in electrocardiographic (ECG) configuration and cycle length. These observations suggest that the overall reproducibility of ventricular tachycardia induction is sufficiently high to provide a reliable marker for evaluating the efficacy of therapeutic interventions. However, specific tachycardia characteristics such as cycle length and ECG configuration are more variable even within the same study and may be less useful in assessing the effects of subsequent interventions.

Electrophysiological testing was performed in 100 consecutive patients with spontaneous asymptomatic nonsustained ventricular tachycardia, chronic coronary artery disease, and ejection fraction of less than 40%. Fifty-seven patients without inducible sustained ventricular arrhythmias were discharged on no antiarrhythmic therapy. Sustained monomorphic ventricular tachycardia was induced in 37 patients, and polymorphic ventricular tachycardia or ventricular fibrillation was induced in six patients. Of the 43 patients with inducible sustained ventricular arrhythmias, three had spontaneous cardiac arrest during serial drug testing and were excluded from further analysis. Twenty patients were discharged on drug therapy, resulting in suppression of inducible sustained ventricular arrhythmias. The remaining 20 patients with persistently inducible sustained arrhythmias were discharged on drug therapy, resulting in maximal rate slowing of the induced tachycardia. During a mean follow-up of 16.7 months, there were 10 recurrent cardiac arrests or sudden deaths. The 1- and 2-year actuarial incidence of these events was 2% and 6%, respectively, in patients without inducible sustained ventricular arrhythmias; 0% and 11%, respectively, in patients in whom inducible arrhythmias were suppressed; and 34% and 50%, respectively, in patients with persistently inducible sustained ventricular arrhythmias. Multivariate Cox analysis identified only the persistence of inducible sustained ventricular arrhythmias as a significant independent predictor of sudden death or recurrent sustained arrhythmias (p less than 0.001; relative risk, 3.5; 95% confidence intervals, 2.1-4.9). In this population, therapeutic intervention to prevent sudden death is unnecessary in patients without inducible sustained ventricular arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

Nineteen patients with ventricular tachycardia were subjected to surgery using a normothermic map-guided approach. Surgical ablation was performed by endocardial resection and cryoablation. Eleven patients had multiple distinct morphologies, and eight patients needed concomitant coronary artery bypass surgery. Seventeen patients survived the perioperative period, and all but one patient had a successful surgical ablation of all documented morphologies. Ventricular tachycardia surgery can be accomplished with the sequential map-guided approach on the normothermic beating heart, and in this era of the implantable defibrillator should remain a mainstay of the surgical treatment for ventricular tachycardia.

A 33-year-old man with a right-bundle branch, left-axis deviation ventricular tachycardia was medically treated unsuccessfully. Surgical mapping and ablation was performed with a successful surgical result. A discussion of surgical results for this problem is provided.

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.

Concomitant coronary revascularization and implantation of the automatic cardioverter/defibrillator is an increasingly common procedure. To determine whether cardioversion/defibrillation thresholds measured after weaning patients from cardiopulmonary bypass are sufficient to justify immediate implantation of the pulse generator, we prospectively compared postpump values to those obtained 1 week later in five patients. R-wave amplitudes during both sinus rhythm and ventricular tachycardia, lead impedance, defibrillation thresholds and cardioversion thresholds remained stable or improved from the postpump to the 1 week values. Five other patients had the generator implanted at the time of revascularization. Immediate postbypass cardioversion thresholds (mean 10 +/- 8 joules) in these ten patients did not significantly differ from those of 20 nonpump implantations (VT mean 7 +/- joules; VF 15 +/- 4 joules and defibrillation thresholds mean 17 +/- 6 joules). These findings suggest that the residual effects of cardioplegia, core-cooling and operative ischemia have no significant effects on intraoperative testing of implanted defibrillators. This clinical experience supports the practice of immediate implantation of the pulse generator at the time of revascularization.

A patient with catecholamine-sensitive right ventricular outflow tract tachycardia refractory to pharmacological therapy underwent intraoperative mapping and cryoablation. Epicardial and endocardial mapping demonstrated earliest ventricular activation in the free-wall of the outflow tract, and cryoablation of the area resulted in surgical cure. No histologic abnormalities at the site of tachycardia origin were detected. Catecholamine sensitivity does not appear to result from a diffuse myocardial process, and permanent ablation of the tachycardia in this group of patients with a regional procedure is feasible.

The automatic implantable cardioverter/defibrillator is an accepted mode of therapy for medically refractory sustained ventricular tachycardia or fibrillation. At the Loyola University Medical Center, Maywood, Ill, 39 implantations were performed in a 14-month period. The method of implantation was the median sternotomy. Our population included 9 patients in whom sternotomies had to be redone and 17 patients with concomitant revascularization. Two patients died due to pump failure, and one major complication (infection) occurred that was directly related to the automatic implantable cardioverter/defibrillator. The median sternotomy, because of good results, continues to be our method of choice for insertion of the automatic implantable cardioverter/defibrillator.

The incidence and determinants of multiple morphologically distinct ventricular tachycardias were examined prospectively in 71 consecutive patients with at least one documented spontaneous episode of sustained monomorphic ventricular tachycardia. Mean frontal and horizontal QRS axes were determined from the 12 lead electrocardiograms (ECGs) of 190 spontaneous and 352 induced tachycardias. Two or more morphologically distinct spontaneous tachycardias were observed in 19 (43%) of 44 patients who had at least two documented spontaneous episodes. In 43 (61%) of the 71 patients, multiple morphologically distinct tachycardias were induced by programmed ventricular stimulation. Overall, 57 (80%) of the 71 patients had at least two morphologically distinct tachycardias. Predictors of multiple tachycardia configurations were selected by multivariate analysis from clinical and angiographic variables and were similar for both spontaneous and induced ventricular tachycardia: presence of multiple previous myocardial infarctions (p = 0.032 spontaneous, p = 0.005 induced) and number of different antiarrhythmic drug treatments during which ventricular tachycardia was documented (p = 0.0089 spontaneous, p less than 0.0001 induced). These data demonstrate that a large majority of patients with sustained monomorphic ventricular tachycardia exhibit more than one distinct QRS configuration when adequate ECG documentation of multiple episodes is obtained during different antiarrhythmic drug treatments. In individual patients, caution should be used in attributing clinical significance to a single unique QRS configuration.