Idiopathic premature ventricular contractions arising from the intraventricular septum adjacent to the his bundle.

A 57-year-old woman with idiopathic premature ventricular contractions (PVCs) exhibiting a left bundle branch block and left inferior axis QRS morphology underwent electrophysiological testing. Mapping revealed that the earliest ventricular activation times during the PVCs recorded on either side of the interventricular septum were the same and no excellent pace maps were reproduced at these sites. Successful radiofrequency catheter ablation was achieved in the right ventricular septum adjacent to the recording site of the His bundle electrogram. These findings suggested that the origin of this PVC was located in the intraventricular septum rather than the endocardial surface.

Clinical outcomes after ablation and pacing therapy for atrial fibrillation : a meta-analysis.

BACKGROUND: Radiofrequency ablation of the atrioventricular node and permanent pacing are used for symptomatic relief in patients with medically refractory atrial fibrillation. In this study, meta-analysis was used to clarify clinical outcomes and survival after ablation and pacing therapy using data from the published literature. METHODS AND RESULTS: We used 21 studies with a total of 1181 patients in the meta-analysis. All patients had medically refractory atrial tachyarrhythmias, primarily atrial fibrillation (97%). Nineteen measures of clinical outcome, encompassing quality of life, ventricular function, exercise duration, and healthcare use, were derived from the studies. The meta-analysis demonstrated significant improvement after ablation and pacing therapy in all outcome measures except fractional shortening, which demonstrated a trend toward improvement (P=0.08). Ejection fraction did show significant improvement (P<0.001). The calculated 1-year total and sudden death mortality rates after ablation and pacing therapy were 6.3% and 2.0%, respectively. CONCLUSIONS: Ablation and pacing therapy improves a broad range of clinical outcomes for patients with medically refractory atrial fibrillation. The calculated 1-year mortality rates after this therapy are low and comparable with medical therapy.

Pathological effects of extensive radiofrequency energy applications in the pulmonary veins in dogs.

INTRODUCTION: The long-term complications of catheter ablation within the pulmonary veins are unknown. The development of pulmonary vein stenosis has recently been described after catheter ablation to treat either chronic or paroxysmal atrial fibrillation. The purpose of this study was to examine the pathological and hemodynamic effects of radiofrequency (RF) energy application within the pulmonary veins. METHODS AND RESULTS: Right heart and transseptal catheterization were performed in 9 anesthetized mongrel dogs. The pulmonary vein ostia were cannulated and pulmonary venous pressure was measured before RF energy application in up to 4 separate pulmonary veins. Animals were euthanized at intervals of 2 to 4 weeks (n=3), 6 to 8 weeks (n=3), or 10 to 14 weeks (n=3) after ablation. Repeat catheterization before euthanasia demonstrated statistically significant differences in pulmonary capillary wedge pressure, cardiac output, pulmonary vascular resistance, and systemic vascular resistance (P<0.05) compared with the baseline. Luminal narrowing was observed in 22 of 33 pulmonary veins to which RF energy was applied. Of these, 7 were totally occluded, 7 had severe stenosis, and 8 were only minimally narrowed. Histological examination revealed intimal proliferation with organizing thrombus, necrotic myocardium in various stages of collagen replacement, endovascular contraction, and a proliferation of elastic lamina. CONCLUSIONS: Applications of RF current within the pulmonary veins may result in pulmonary vein narrowing or complete occlusion. These observations should be considered in treatment of arrhythmias originating within the pulmonary veins.

Quantitation of chronotropic response: comparison of methods for rate-modulating permanent pacemakers.

OBJECTIVES: The aim of this study was to develop a technique for quantitating chronotropic response. BACKGROUND: Although the importance of chronotropic response for optimizing cardiac output during exercise is widely recognized, methods for quantitating the rate-modulating behavior of permanent pacemakers have not been developed. For a method of quantitating chronotropic response to be clinically useful, the rate-modulating characteristics of a pacing system should be defined at the onset of exertion, over a variety of exercise work loads and during recovery. METHODS: Three methods for quantitation of rate modulation were assessed in 10 patients during treadmill exercise testing using the chronotropic assessment exercise protocol with expired gas exchange analysis. To compare the observed chronotropic response with a standard, the "expected" heart rate throughout exercise was calculated by using the concept of heart rate reserve as described by Wilkoff. The pacing rate observed during exercise was analyzed with 1) standard linear regression analysis, 2) comparison of observed and expected pacing rates at the midpoint and end of each quartile of exercise, and 3) integration of the area under the rate-response curve with comparison with the area under the expected curve. RESULTS: With use of a normalized scale relating change in heart rate to change in metabolic work load, with values of heart rate and metabolic work load at rest set to 0 and those at maximal exertion set to a value of 1, the mean y intercept for the study group was 0.10 +/- 0.20 (range -0.14 to +0.45), with a mean slope of 0.81 +/- 0.25 (range 0.31 to 1.19). The correlation coefficient relating change in heart rate to change in exercise work load was a mean of 0.90 +/- 0.09 (range 0.63 to 0.98). Integration of the area under the rate-response curve observed during exercise yielded a mean area that was 101 +/- 36% of that expected. When the range of exercise work loads was divided into quartiles, the area under the observed rate-response curve was 151 +/- 114% of that expected during the first quartile of exercise, 113 +/- 70% during the second, 96 +/- 38% during the third and 92 +/- 20% during the fourth. The mean area under the curve during recovery was 93 +/- 29% of that expected. Although calculation of the observed heart rate as a percent of that expected at the midpoint and end of each quartile of exercise used fewer observations, it provided similar results. CONCLUSIONS: Quantitation of the rate-response curve with comparison with the expected heart rate curve provides accurate methods for quantitation of chronotropic response. Adoption of this method would facilitate comparisons of artificial sensors and provide a framework to address issues of optimal rate modulation.

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.

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.

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)

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)

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)

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.

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)

Torsade de pointes: the long-short initiating sequence and other clinical features: observations in 32 patients.

The clinical setting, precipitating factors, electrocardiographic features and response to treatment of 32 patients with torsade de pointes were reviewed. Thirty-one patients had underlying cardiac disease and 30 patients had a previous underlying cardiac arrhythmia. Antiarrhythmic medications, often in association with electrolyte abnormalities (such as hypokalemia and hypomagnesemia) were the most common precipitating factors. In 22 of 26 patients, the serum drug levels of the antiarrhythmic agents were found to be within the therapeutic range. However, before the administration of agents known to prolong the QT interval, 20 of the 32 patients had, either alone or in combination, baseline prolongation of the QT interval, hypokalemia or hypomagnesemia. All patients had QTc interval prolongation (mean 0.59 second) immediately before the development of torsade de pointes. Marked lability of T wave morphology was frequently noted. Cardiac pacing was the only consistently effective mode of therapy. A characteristic long-short ventricular cycle length as the initiating sequence was found in 41 of 44 episodes of torsade de pointes. Reported data support the high frequency of this electrocardiographic feature of torsade de pointes in which its onset could be analyzed. It is suggested that this electrocardiographic characteristic will aid in both establishing the diagnosis of torsade de pointes and distinguishing it from other polymorphic forms of ventricular tachycardia.

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.

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.

Comparison of survival of amiodarone-treated patients with coronary artery disease and malignant ventricular arrhythmias with that of a control group with coronary artery disease.

Although amiodarone is effective in the treatment of ventricular arrhythmias, it is associated with serious toxic effects. In addition, the prognosis of patients with malignant ventricular arrhythmias and coronary artery disease treated with amiodarone remains poor. The survival of 54 consecutive patients with angiographically documented coronary artery disease and symptomatic ventricular tachycardia or ventricular fibrillation treated with amiodarone was compared with that of 5,125 medically treated patients with coronary artery disease. The amiodarone group was older, with worse left ventricular function and more peripheral and cerebrovascular disease. The 1 year survival probability was 0.73 for the amiodarone group and 0.94 for the control coronary artery disease group. At 2 years of follow-up, the survival probabilities were 0.60 and 0.90 for the amiodarone and the control group, respectively. When the survival curves were adjusted for group differences in baseline prognostic characteristics (integrated as a previously published hazard score), there was no difference in the prognosis of the two groups. These findings suggest that treatment with amiodarone of malignant ventricular arrhythmias associated with coronary artery disease maintains patients on an underlying survival curve determined by the degree of myocardial dysfunction, clinical characteristics and coronary anatomy, and that amiodarone does not have a deleterious effect on survival.

Characterization of retrograde conduction by direct endocardial recording from an accessory atrioventricular pathway.

Accessory pathway electrograms are rarely recorded in patients with Wolff-Parkinson-White syndrome. In one patient, during electrophysiologic study, simultaneous local ventricular (V) accessory pathway (AP) and atrial (A) deflections were recorded during bipolar catheter endocardial mapping over the pathway. Analysis of changes in electrographic intervals during performance of the ventricular extrastimulus technique allowed characterization of the retrograde conduction properties of the pathway. As coupling intervals were decreased, an initial increase was seen in the AP2A2 interval with subsequent ventriculoatrial block between the accessory pathway and atrium. When coupling intervals were further decreased, the V2AP2 interval lengthened with ultimate block between the ventricle and accessory pathway. These findings support the concept of impedance mismatch as the cause of conduction block in accessory pathways with the distal junction of the accessory pathway being the most vulnerable.

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.

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)