Incidence of reentry with an excitable gap in ventricular tachycardia: a prospective evaluation utilizing transient entrainment.

The demonstration of transient entrainment has been proposed as evidence of reentry, with an excitable gap as the probable mechanism of tachycardia. A prospective series of 27 consecutive patients with sustained ventricular tachycardia induced by programmed electrical stimulation was studied to determine the frequency with which transient entrainment can be demonstrated and to define the optimal location of pacing and recording electrodes. In all patients, electrodes for pacing and recording were placed in both the left and right ventricles during electrophysiologic study. Among the 19 patients in whom the response to rapid pacing could be evaluated (25 episodes of ventricular tachycardia), transient entrainment was demonstrated in 79% (76% of episodes). Ten of 12 episodes of ventricular tachycardia with a left bundle branch block QRS configuration in lead V1 and 9 of 13 episodes with a right bundle branch block QRS configuration could be transiently entrained (p = NS). Transient entrainment was demonstrated for 8 of 11 episodes of ventricular tachycardia with a left bundle branch block configuration during pacing from the left ventricle, but for only 2 of 10 episodes during pacing from the right ventricular apex (p less than 0.05). Conversely, 9 of 13 episodes of ventricular tachycardia with a right bundle branch block configuration were transiently entrained during pacing from the right ventricular apex, but 0 of 10 episodes were transiently entrained by left ventricular pacing (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Region of slow conduction in sustained ventricular tachycardia: direct endocardial recordings and functional characterization in humans.

Direct endocardial recording from a discrete region of slow conduction in the left ventricle was performed in a patient during sustained ventricular tachycardia. The tachycardia had a right bundle branch block and superior axis configuration with the earliest site of endocardial activation in the posterolateral left ventricle. At this site, the left ventricular electrogram during the tachycardia displayed two deflections with distinctly different responses to rapid pacing. During rapid pacing from the right ventricular apex, one deflection was transiently entrained, representing activation of the ventricle distal to a region of slow conduction in the reentrant circuit. However, the other deflection was not entrained and arose from activation proximal to this region. At a critically rapid pacing rate, interruption of the tachycardia was associated with conduction block in the region of slow conduction, as demonstrated by dissociation of the two deflections on the posterolateral left ventricular electrogram. At pacing rates that transiently entrained but did not terminate the tachycardia, decremental properties of conduction were demonstrated in the region of slow conduction, but not in the rest of the reentrant circuit. These responses of the posterolateral left ventricular electrogram to pacing during ventricular tachycardia strongly suggest that the recordings bracketed a discrete region of slow conduction in the left ventricle that was critical for the maintenance of ventricular tachycardia. Furthermore, these data demonstrate that this region of slow conduction in the left ventricle had decremental conduction properties and was the site of block during rapid pacing at rates sufficient to interrupt the tachycardia.

Effect of pacing rate on the human atrial strength-duration curve.

The effect of rapid pacing on the atrial constant voltage stimulation threshold in humans has not been defined at rates applicable to those of antitachycardia pacing. The effect of pacing rate on the atrial strength-duration relation was determined in 10 patients at pacing rates between 125 and 300 beats/min to explore excitability over the range of rates used for permanent antitachycardia pacing systems. Two points that define the strength-duration curve were measured at each pacing rate: rheobase voltage--the lowest stimulus voltage that results in capture at a pulse duration of 2 ms; and chronaxie pulse duration--the threshold pulse duration at twice rheobase voltage. A permanent, tined, J-shaped pacing lead with a high current density and low polarization electrode was positioned in the right atrial appendage for cathodal stimulation. A constant voltage output, incorporating a fast recharge pulse designed to minimize electrode polarization, was used for stimulation. There was a significant increase in rheobase voltage (p = 0.009), chronaxie pulse duration (p = 0.001) and minimal threshold stimulus energy (p = 0.05) at pacing rates greater than 225 beats/min. A rheobase voltage greater than 5 V occurred in three patients at pacing rates greater than or equal to 275 beats/min. At a pacing rate of 300 beats/min, rheobase voltage had increased in 8 of 10 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Preferential effect of procainamide on the reentrant circuit of ventricular tachycardia.

Transient entrainment was used to test the hypotheses that 1) procainamide prolongs the cycle length of ventricular tachycardia in patients with coronary artery disease because it has a preferential effect on the reentrant tachycardia circuit, and 2) regions of slow conduction in the reentrant circuit are more susceptible to the effect of procainamide than are other areas of the ventricles. In five patients with prior myocardial infarction, sustained ventricular tachycardia with identical QRS configuration was inducible before and after intravenous infusion of procainamide. Transient entrainment of ventricular tachycardia was demonstrated at two or more cycle lengths by rapid pacing in the baseline state and after procainamide. Rapid pacing was performed from the same site during sinus rhythm at the cycle lengths that demonstrated transient entrainment of ventricular tachycardia. The conduction interval to the transiently entrained site during ventricular tachycardia (orthodromic interval) was compared with the conduction interval to the same site during pacing in sinus rhythm (antidromic interval). The mean tachycardia cycle length increased by 27% after procainamide administration (p = 0.002). The antidromic conduction intervals were prolonged by 9% (p = 0.06) compared with a 28% increase in the mean orthodromic conduction interval (p = 0.002). The difference between the orthodromic and antidromic conduction intervals increased by 40% (p = 0.003). Prolongation of the tachycardia cycle length after procainamide administration correlated positively with increases in the orthodromic conduction intervals (r = 0.94, p = 0.02) but not with changes in the antidromic intervals (r = -0.08, p = NS). The effect of procainamide on the difference between correlated strongly with changes in the cycle length of ventricular tachycardia (r = 0.97, p = 0.006).(ABSTRACT TRUNCATED AT 250 WORDS)

Rate-modulated cardiac pacing based on transthoracic impedance measurements of minute ventilation: correlation with exercise gas exchange.

The relation of pacing rate to physiologic variables of metabolic demand was examined in 10 consecutive patients with a minute ventilation-sensing, rate-modulating ventricular pacemaker implanted for complete heart block. All patients had paroxysmal (seven patients) or chronic (three patients) atrial fibrillation and were referred for catheter ablation of the atrioventricular junction. Treadmill exercise testing with measurement of expired gas exchange and respiratory flow was performed before ablation and 4 weeks after pacemaker implantation, with the pacemaker programmed to both the fixed-rate VVI and rate-modulating minute ventilation VVIR pacing modes in random sequence. The relation of pacing rate to oxygen consumption (VO2), expired carbon dioxide concentration (VCO2), respiratory quotient, tidal volume, respiratory rate and minute ventilation was determined during exercise in the rate-modulating minute ventilation pacing mode. Pacing rate was highly correlated with minute ventilation (r = 0.89), respiratory quotient (r = 0.89), VCO2 (r = 0.87), tidal volume (r = 0.87), VO2 (r = 0.84) and respiratory rate (r = 0.84). The mean exercise duration increased from 8.3 +/- 2.8 min in the fixed rate pacing mode to 10.2 +/- 3.4 min in the rate-modulating, minute ventilation mode (p = 0.0001). The maximal VO2 increased from 13.4 +/- 3.4 to 16.3 +/- 4.1 cc/kg per min (p = 0.0004). The maximal heart rate achieved in the minute ventilation pacing mode was 136 +/- 9.7 beats/min, similar to that observed in the patient's intrinsic cardiac rhythm before ablation (134.9 +/- 30.1 beats/min, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic effects of an irregular sequence of ventricular cycle lengths during atrial fibrillation.

OBJECTIVES: The aim of this study was to determine the independent hemodynamic effects of an irregular sequence of ventricular cycle lengths in patients with atrial fibrillation (AF). BACKGROUND: Atrial fibrillation may reduce cardiac output by several possible mechanisms, including loss of the atrial contribution to left ventricular filling, valvular regurgitation, increased ventricular rate or irregular RR intervals. This study was designed to evaluate the effects of an irregular RR interval, independent of the average ventricular rate, on cardiac hemodynamic data during AF. METHODS: Sixteen patients with AF were studied invasively. During intrinsically conducted AF (mean rate 102 +/- 22 beats/ min), the right ventricular apex electrogram was recorded onto frequency-modulated (FM) tape. After atrioventricular node ablation, the right ventricular apex was stimulated in three pacing modes in randomized sequence: 1) VVI at 60 beats/min; 2) VVI at the same average rate as during intrinsically conducted AF (102 +/- 22 beats/min); and 3) during VVT pacing in which the pacemaker was triggered by playback of the FM tape recording of the right ventricular apex electrogram previously recorded during intrinsically conducted AF (VVT 102 +/- 22 beats/min). RESULTS: Compared with VVI pacing at the same average rate, an irregular sequence of RR intervals decreased cardiac output (4.4 +/- 1.6 vs. 5.2 +/- 2.4 liters/min, p < 0.01), increased pulmonary capillary wedge pressure (17 +/- 7 vs. 14 +/- 6 mm Hg, p < 0.002) and increased right atrial pressure (10 +/- 6 vs. 8 +/- 4 mm Hg, p < 0.05). CONCLUSIONS: An irregular sequence of RR intervals produces adverse hemodynamic consequences that are independent of heart rate.

Combined automatic implantable cardioverter-defibrillator and pacemaker systems: implantation techniques and follow-up.

The automatic implantable cardioverter-defibrillator (AICD) effectively prevents death due to ventricular tachycardia or ventricular fibrillation. Some patients who need an AICD also require cardiac pacing to treat symptomatic bradycardia, bradycardia after defibrillation, or to provide a rate floor to reduce the frequency of bradycardia-related ventricular arrhythmias. Some patients also can benefit from antitachycardia pacing. A mapping technique to implant a pacemaker and AICD sensing leads is presented. For patients with a pacemaker who later need an AICD, the left ventricle is mapped with use of the AICD rate-sensing electrodes to identify a site at which the minimal pacemaker stimulus and maximal ventricular electrogram amplitudes are recorded. An external cardioverter-defibrillator that has amplifiers similar to those in the AICD is used to monitor the rate-sensing electrogram. For patients with an implanted AICD, pacemaker implantation is undertaken by mapping the right ventricle with the pacemaker lead while the AICD is in standby mode; the AICD beep monitor is then used to determine a site where pacemaker stimulus detection by the AICD does not occur. Eight patients underwent implantation of a combined AICD-pacemaker system (four ventricular antitachycardia pacemakers, three ventricular demand pacemakers and one atrial demand pacemaker). Neither inhibition of AICD arrhythmia detection nor double counting occurred. Satisfactory AICD-pacemaker function was shown in all patients postoperatively, and no pacemaker malfunction was observed. Thus, with currently available technology, a combined AICD-pacemaker system can be implanted with satisfactory function of both devices and without adverse device-device interactions.

Intermediate septal accessory pathways: electrocardiographic characteristics, electrophysiologic observations and their surgical implications.

Intermediate septal accessory pathways are located in close proximity to the atrioventricular (AV) node and His bundle, have unique features that distinguish them from typical anterior and posterior accessory pathways and have been associated with a high risk for unsuccessful pathway division and the production of complete AV block after surgery. Between July 1986 and May 1990, 4 of 70 patients (3 men and 1 woman; mean age 33 +/- 13 years) undergoing surgery for accessory pathway division were found to have an intermediate septal accessory pathway. The presenting arrhythmia was atrial fibrillation with rapid anterograde conduction over the accessory pathway in two patients and recurrent orthodromic reciprocating tachycardia in two patients. In all patients, the delta wave on the electrocardiogram (ECG) was inverted in lead V1, but two patterns of delta wave configuration were observed. In three patients (type 1 intermediate septal accessory pathway), the delta wave was upright in lead II, inverted in lead III and isoelectric in lead a VF; the transition from a negative to an upright delta wave occurred in lead V2. The fourth patient exhibited a different delta wave pattern (type 2 intermediate septal accessory pathway). The delta wave was upright in each of leads II, III and aVF; the transition from a negative to an upright delta wave occurred at lead V3. Intraoperative electrophysiologic study localized the atrial insertion of type 1 pathways to the midpoint of Koch's triangle close to the AV node.(ABSTRACT TRUNCATED AT 250 WORDS)

A prospective evaluation of intracoronary ethanol ablation of the atrioventricular conduction system.

The clinical efficacy and complications associated with ablation of the atrioventricular (AV) conduction system by the selective infusion of ethanol into the AV node artery were prospectively assessed in 12 consecutive patients with medically refractory atrial arrhythmias. Six of the patients had previously failed to have permanent complete AV block created with direct current or radiofrequency catheter ablation. The AV node artery was cannulated with a 0.016 in. (0.041 cm) guide wire in all 12 patients. It was also possible to advance a 2.7F infusion catheter into the AV node artery in all patients. Transient AV block was induced by selective injections into the AV node artery of iced saline solution (8 patients) and of radiographic contrast agent (ioxaglate) (10 patients). The infusion of 2 ml of ethanol (96%) induced immediate complete AV block in all 10 patients who demonstrated AV block with ioxaglate. The escape rhythm exhibited a narrow QRS complex preceded by a His bundle deflection in nine patients and left bundle branch block in one patient. The immediate mean rate of the escape rhythm was 45.3 +/- 13.4 beats/min. In two patients who demonstrated reflux of contrast agent into the distal right coronary artery with selective injections into the AV node artery, transient ST segment elevation developed in the inferior electrocardiographic leads with the infusion of ethanol. There was no change in the left ventricular ejection fraction from the baseline value (0.53 +/- 0.12) to that measured after ablation (0.55 +/- 0.11) and no patient developed wall motion abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)

Classification of death in antiarrhythmia trials.

OBJECTIVES: We sought to develop and apply a new scheme for the classification of death to be used in trials of antiarrhythmia treatments. BACKGROUND: Because presently accepted classifications of death do not fully describe or tabulate all significant aspects of terminal events, nor do they consider unique aspects of arrhythmia investigations, a new classification scheme that addresses these issues is desirable. METHODS: A classification scheme of deaths that occur in antiarrhythmia trials was developed using the following categories: 1) primary organ cause (cardiac [arrhythmic, nonarrhythmic or unknown], noncardiac or unknown); 2) temporal course (sudden, nonsudden or unknown); 3) documentation (witnessed, monitored [yes, no or unknown]); 4) operative relation (preoperative, perioperative or postoperative); and 5) system relation (procedure related, pulse generator related and lead related [yes, no or unknown]). RESULTS: The classification scheme was used in a clinical trial of a new implantable cardioverter-defibrillator (1,250 patients, of whom 79 died) and used in an application for device market approval. Application of the classification to data reported using an older classification scheme is demonstrated. CONCLUSIONS: We propose a descriptive classification scheme that 1) fully describes and tabulates all significant aspects of terminal events; 2) incorporates previously used categorizations of death and new categorizations that address unique aspects of arrhythmia investigations; and 3) tabulates sufficient data to allow comparison with other studies. Events in a clinical trial of implantable defibrillator therapy were classified using the new classification scheme.

Radiofrequency ablation for treatment of primary atrial tachycardias.

OBJECTIVES: The purpose of this study was to determine the safety and efficacy of radiofrequency ablation as definitive therapy for primary atrial tachycardias. BACKGROUND: Primary atrial tachycardias are often difficult to control with antiarrhythmic medications and frequently require nonpharmacologic interventions for definitive therapy. Despite isolated reports of successful treatment of primary atrial tachycardias with radiofrequency ablation, the safety and efficacy of this technique have not been established in a larger series with long-term follow-up. METHODS: The immediate procedural success rate, associated complications and follow-up data of radiofrequency ablation were evaluated in 15 consecutive patients (11 adults and 4 children) with primary atrial arrhythmias that were refractory to medical management. RESULTS: The clinical arrhythmia was ectopic atrial tachycardia in 11 patients and sinus node reentry in 4. The site of origin of the tachycardia was in the right atrium in 14 patients and in the left atrium in 1 patient (with two distinct foci) where the local atrial electrogram preceded the onset of the P wave by 10 to 30 ms. Radiofrequency energy successfully terminated the primary atrial tachycardia in each of the patients, and all were discharged from the electrophysiology laboratory in sinus rhythm without inducible atrial tachycardia. A mean of 10.8 +/- 9.9 radiofrequency applications were delivered using 30 W of power for 30 s. The local intracardiac activation time (relative to the P wave in the surface electrocardiogram) was a mean of -21 +/- 5 ms at the successful ablation site and -15 +/- 6 ms at unsuccessful sites (p < 0.001). No complications were observed, although one patient with incessant ectopic atrial tachycardia had sinus pauses after ablation. During a mean follow-up period of 277 +/- 133 days, the clinical arrhythmia recurred in three patients (20%, 95% confidence intervals 3% to 37%) including two patients with ectopic atrial tachycardia and one patient with sinus node reentry. One of these patients was successfully treated in a second ablation session. CONCLUSIONS: Thus, radiofrequency catheter ablation appears to be a safe and effective technique for the treatment of primary atrial arrhythmias that are refractory to antiarrhythmic medications.

The influence of ventricular fibrillation duration on defibrillation efficacy using biphasic waveforms in humans.

OBJECTIVES: The purpose of this study was to prospectively investigate the influence of ventricular fibrillation (VF) durations of 5, 10 and 20 s on the defibrillation threshold (DFT) during implantable cardioverter-defibrillator (ICD) implantation. BACKGROUND: Although the DFT using monophasic waveforms has been shown to increase with VF duration in humans, the effect of VF duration on defibrillation efficacy using biphasic waveforms in humans is not known. METHODS: Thirty patients undergoing primary ICD implantation or pulse generator replacement were randomly assigned to have the DFT determined using biphasic shocks at two durations of VF each (5 and 10 s, 10 and 20 s or 5 and 20 s). RESULTS: There was no statistically significant difference in the mean DFT comparing VF durations of 5 s (9.5+/-6.0 J) and 10 s (10.8+/-7.0 J) (p=0.4). The mean DFT significantly increased from 10.9+/-6.1 J at 10 s of VF to 12.6+/-5.6 J (p=0.03) at 20 s of VF, and from 7.0+/-3.5 J at 5 s of VF to 10.5+/-6.3 J (p=0.04) at 20 s of VF. An increase in the DFT was observed in 14 patients as VF duration increased. There were no clinical characteristics that differentiated patients with and without an increase in the DFT. CONCLUSIONS: Defibrillation efficacy decreases with increasing VF duration using biphasic waveforms in humans. Ventricular fibrillation durations greater than 10 s may negatively affect the effectiveness of ICD therapy.

Evidence for a central site of action to explain the negative chronotropic effect of atropine: studies on the human transplanted heart.

The chronotropic response to atropine is biphasic; low doses cause slowing of the sinus rate and high doses cause acceleration. Although it is accepted that atropine functions as a competitive antagonist at high doses, the mechanism of the negative chronotropic response at low doses is controversial. Specifically, it is unclear whether the effect is mediated centrally or peripherally. Since at the time of cardiac replacement all central nervous system connections to the heart are severed, the transplanted heart is a unique model for separating these effects. Graded doses of atropine sulfate (0.5, 1.0, 2.0, 4.0, 8.0 and 40.0 micrograms/kg body weight) were administered to 12 human heart transplant recipients to test the hypothesis that the bradycardiac effect of low dose atropine is centrally mediated. The baseline sinus cycle lengths of the decentralized donor and innervated native sinus nodes were 694 +/- 20 and 733 +/- 27 ms, respectively. At the 0.5 and 1.0 microgram/kg doses, the cycle lengths of the native sinus node increased by 29.1 +/- 13.5 and 23.1 +/- 14.2 ms, respectively. At the 2.0 micrograms/kg dose the sinus cycle length again shortened to control. At the maximal dose of atropine the sinus cycle length shortened by 138.3 +/- 29.7 ms compared with control. In contrast, the decentralized donor sinus node exhibited a flat dose response to atropine. High dose atropine (40 micrograms/kg) caused no change in the donor heart's atrial effective refractory period, corrected sinus node recovery time, or sinoatrial conduction time measured by either the Strauss or the Narula method.(ABSTRACT TRUNCATED AT 250 WORDS)

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)

New insights into the definition and meaning of proarrhythmia during initiation of antiarrhythmic drug therapy from the Cardiac Arrhythmia Suppression Trial and its pilot study. The CAST and CAPS Investigators.

OBJECTIVES: This study was undertaken to determine the characteristics of worsening ventricular arrhythmia during antiarrhythmic drug titration. BACKGROUND: Proarrhythmia is an evolving concept in cardiology. Its definition, incidence and clinical significance in various patient settings require refinement. METHODS: The impact of early proarrhythmia was analyzed in 3,840 patients in the Cardiac Arrhythmia Suppression Trial (CAST). RESULTS: Drug therapy did not affect the incidence of new, sustained but nonfatal ventricular tachycardia (placebo 0.5%, active drug 0.4%). Nevertheless, there was a threefold increase in arrhythmic death (placebo 0.5% vs. active drug 1.6%). The incidence of increased ventricular premature depolarizations was equivalent (3% to 5%) for the three study drugs and indistinguishable from that seen with placebo. Patients with increased ventricular premature depolarizations on the first drug tested had fewer at baseline (65 +/- 94 vs. 137 +/- 260 per hour; mean +/- SD) (p < 0.01). When increased ventricular premature depolarizations occurred with the first drug, they were much more likely also to be present with the second drug (for example, 42% vs. 5%, p < 0.001). Increased ventricular premature depolarizations during initiation of therapy independently predicted increased risk of subsequent arrhythmic death (independent relative risk 2.34, p = 0.0053) in the absence of continued antiarrhythmic drug therapy. CONCLUSIONS: The overall incidence of early worsening of arrhythmia in the present study was low. In the absence of placebo control, the incidence of proarrhythmia will be overestimated. Increased ventricular premature depolarizations had characteristics that suggest they often represent spontaneous variability rather than proarrhythmia. The main finding is that markedly increased ventricular premature depolarizations during drug titration predict long-term increased risk of arrhythmic death in this patient population despite absence of long-term antiarrhythmic drug therapy.

Intracoronary ethanol ablation for the treatment of recurrent sustained ventricular tachycardia.

The selective infusion of ethanol into the coronary circulation supplying the site of origin of incessant ventricular tachycardia has been demonstrated to abolish this arrhythmia in selected patients. The present study was designed to evaluate the efficacy and safety of the intracoronary ethanol ablation technique in patients with paroxysmal ventricular tachycardia related to prior myocardial infarction. Twenty-three patients with sustained monomorphic ventricular tachycardia that was refractory to conventional antiarrhythmic drug therapy were prospectively studied. After induction of ventricular tachycardia by programmed electrical stimulation, the response of the arrhythmia to the infusion of radiographic contrast medium or saline solution into the ostia of the native coronary arteries and coronary artery bypass grafts was assessed. If ventricular tachycardia was reliably interrupted by injections into the proximal coronary artery or bypass graft, the vessel was cannulated with a steerable guide wire and 2.7F infusion catheter to determine the smallest arterial branch that would result in termination of the arrhythmia with selective injections. If reliable interruption of ventricular tachycardia was observed with saline or contrast injections, ethanol (2 ml) was then delivered through the infusion catheter. Ventricular tachycardia could be terminated by injections of saline solution or contrast medium in 11 of 21 patients in whom the protocol could be completed. Ethanol was infused in 10 of these patients. Ventricular tachycardia was inducible in only 1 of 10 patients immediately after ethanol infusion. At a follow-up electrophysiologic study performed 5 to 7 days after ablation, ventricular tachycardia became inducible in two other patients, in one of whom the arrhythmia substrate was successfully ablated after three sessions. The mean left ventricular ejection fraction was 0.33 +/- 0.1 before and 0.35 +/- 0.11 after ablation. Complications of the procedure included complete atrioventricular block in four patients and pericarditis in one patient. Thus, intracoronary ethanol ablation is associated with a moderate degree of efficacy but the potential for important complications. Despite these limitations, this technique may provide effective long-term control of ventricular tachycardia for some patients.

Events in the Cardiac Arrhythmia Suppression Trial (CAST): mortality in the entire population enrolled.

To test the hypothesis that suppression of ventricular arrhythmias by antiarrhythmic drugs after myocardial infarction improves survival, the Cardiac Arrhythmia Suppression Trial (CAST) was initiated. Suppression was evaluated before randomization during an open label titration period. Patients whose arrhythmias were suppressed were randomized in the main study and those whose arrhythmias were partially suppressed were randomized in a substudy. Overall survival and survival free of arrhythmic death or cardiac arrest were lower [corrected] in patients treated with encainide or flecainide than in patients treated with placebo. However, the death rate in patients randomized to placebo therapy was lower than expected. This report describes the survival experience of all patients enrolled in CAST and compares it with mortality in other studies of patients with ventricular arrhythmias after myocardial infarction. As of April 18, 1989, 2,371 patients had enrolled in CAST and entered prerandomization, open label titration: 1,913 (81%) were randomized to double-blind, placebo-controlled therapy (1,775 patients whose arrhythmias were suppressed and 138 patients whose arrhythmias were partially suppressed during open label titration); and 458 patients (19%) were not randomized because they were still in titration, had died during titration or had withdrawn. Including all patients who enrolled in CAST, the actuarial (Kaplan-Meier) estimate of 1-year mortality was 10.3%. To estimate the "natural" mortality rate of patients enrolled in CAST, an analysis was done that adjusted for deaths that might be attributable to encainide or flecainide treatment either during prerandomization, open label drug titration or after randomization. Because the censoring procedure excluded patients treated with encainide or flecainide after randomization, the mortality estimate will be less than the unadjusted mortality estimate of 10.3%.(ABSTRACT TRUNCATED AT 250 WORDS)

Relative effectiveness of the implantable cardioverter-defibrillator and antiarrhythmic drugs in patients with varying degrees of left ventricular dysfunction who have survived malignant ventricular arrhythmias. AVID Investigators. Antiarrhythmics Versus Implantable Defibrillators.

OBJECTIVES: We sought to assess the effect of baseline ejection fraction on survival difference between patients with life-threatening ventricular arrhythmias who were treated with an antiarrhythmic drug (AAD) or implantable cardioverter-defibrillator (ICD). BACKGROUND: The Antiarrhythmics Versus Implantable Defibrillators (AVID) study demonstrated improved survival in patients with ventricular fibrillation or ventricular tachycardia with a left ventricular ejection fraction (LVEF) < or =0.40 or hemodynamic compromise. METHODS: Survival differences between AAD-treated and ICD-treated patients entered into the AVID study (patients presenting with sustained ventricular arrhythmia associated with an LVEF < or =0.40 or hemodynamic compromise) were compared at different levels of ejection fraction. RESULTS: In patients with an LVEF > or =0.35, there was no difference in survival between AAD-treated and ICD-treated patients. A test for interaction was not significant, but had low power to detect an interaction. For patients with an LVEF 0.20 to 0.34, there was a significantly improved survival with ICD as compared with AAD therapy. In the smaller subgroup with an LVEF <0.20, the same magnitude of survival difference was seen as that in the 0.20 to 0.34 LVEF subgroup, but the difference did not reach statistical significance. CONCLUSIONS: These data suggest that patients with relatively well-preserved LVEF (> or =0.35) may not have better survival when treated with the ICD as compared with AADs. At a lower LVEF, the ICD appears to offer improved survival as compared with AADs. Prospective studies with larger patient numbers are needed to assess the effect of relatively well-preserved ejection fraction (> or =0.35) on the relative treatment effect of AADs and the ICDs.

In-hospital versus out-of-hospital presentation of life-threatening ventricular arrhythmias predicts survival: results from the AVID Registry. Antiarrhythmics Versus Implantable Defibrillators.

OBJECTIVES: This study describes the outcomes of patients from the Antiarrhythmics Versus Implantable Defibrillators (AVID) Study Registry to determine how the location of ventricular arrhythmia presentation influences survival. BACKGROUND: Most studies of cardiac arrest report outcome following out-of-hospital resuscitation. In contrast, there are minimal data on long-term outcome following in-hospital cardiac arrest. METHODS: The AVID Study was a multicenter, randomized comparison of drug and defibrillator strategies to treat life-threatening ventricular arrhythmias. A Registry was maintained of all patients with sustained ventricular arrhythmias at each study site. The present study includes patients who had AVID-eligible arrhythmias, both randomized and not randomized. Patients with in-hospital and out-of-hospital presentations are compared. Data on long-term mortality were obtained through the National Death Index. RESULTS: The unadjusted mortality rates at one- and two-year follow-ups were 23% and 31.1% for patients with in-hospital presentations, and 10.5% and 16.8% for those with out-of-hospital presentations (p < 0.001), respectively. The adjusted mortality rates at one- and two-year follow-ups were 14.8% and 20.9% for patients with in-hospital presentations, and 8.4% and 14.1% for those with out-of-hospital presentations (p < 0.001), respectively. The adjusted long-term relative risk for in-hospital versus out-of-hospital presentation was 1.6 (95% confidence interval [CI] 1.3-1.9). CONCLUSIONS: Compared with patients with out-of-hospital presentations of life-threatening ventricular arrhythmias not due to a reversible cause, patients with in-hospital presentations have a worse long-term prognosis. Because location of ventricular arrhythmia presentation is an independent predictor of long-term outcome, it should be considered as an element of risk stratification and when planning clinical trials.

Clinical investigation of antiarrhythmic devices. A statement for healthcare professionals from a joint task force of the North American Society of Pacing and Electrophysiology, the American College of Cardiology, the American Heart Association, and the Working Groups on Arrhythmias and Cardiac Pacing of the European Society of Cardiology.

The goal of radiofrequency catheter ablation and the criterion for efficacy is the elimination of arrhythmogenic myocardium. The application of radiofrequency current in the heart clearly results in lower morbidity and mortality rates than thoracic and cardiac surgical procedures in general, and comparisons of therapy with radiofrequency catheter ablation and therapy with thoracic and cardiac surgical procedures in randomized clinical trials is unwarranted. Trials of radiofrequency catheter ablation versus medical or implantable cardioverter-defibrillator therapy may be indicated in certain conditions, such as ventricular tachycardia associated with coronary artery disease. Randomized trials are recommended for new and radical departures in technology that aim to accomplish the same goals as radiofrequency catheter ablation. Surveillance using registries and/or databases is necessary in the assessment of long-term safety and efficacy.