Ventricular Tachycardia Cycle Length Research Articles

Benefits of treatment with implantable cardioverter-defibrillators in patients with stable ventricular tachycardia without cardiac arrest.

The availability of implantable cardioverter-defibrillators (ICD) that are capable of antitachycardia pacing may lead to an increased use of ICDs in patients with haemodynamically tolerated ventricular tachycardia without a history of cardiac arrest. The frequency of potentially life-threatening fast ventricular tachycardias (cycle length < 250 ms) was investigated in patients who had a third generation ICD with endocardial leads implanted because they had haemodynamically tolerated ventricular tachycardia without a history of cardiac arrest. Between January 1990 and October 1993, 50 patients (age (mean (SD)) 60 (11); ejection fraction 39 (16)%; 82% with coronary artery disease and 8% with dilated cardiomyopathy) with haemodynamically tolerated ventricular tachycardia (cycle length (mean (SD)) 348 (60) ms; range 250-500 ms) and without a history of cardiac arrest were treated with third generation ICDs that were capable of antitachycardia pacing. Fast ventricular tachycardia had been induced in 14 (28%) during baseline electrophysiological study. The benefit of ICD treatment was estimated as the difference between total mortality and the occurrence of fast ventricular tachycardia that would have been fatal if it had not been terminated. During follow up of 17 (12) months, 33 patients (66%) had a total of 3861 episodes of ventricular tachycardia. 91% of these episodes were terminated by antitachycardia pacing. 11 patients (22%) had episodes of potentially life-threatening fast ventricular tachycardia and 3 of these also had inducible fast ventricular tachycardia. One patient died suddenly 27 months after implantation. The difference between survival without fast ventricular tachycardia and total mortality was 9%, 12%, 27%, and 27% at 6, 12, 18, and 24 months, respectively. About a fifth of patients who had been given an ICD to treat haemodynamically tolerated ventricular tachycardia and who had no history of cardiac arrest experienced fast ventricular tachycardia during follow up requiring immediate cardioversion. Prospective studies are needed to investigate whether the prognosis of patients with a history of haemodynamically tolerated ventricular tachycardia without cardiac arrest is improved by ICD therapy.

901-61 Localization of the Return Pathway in Ischemic Ventricular Tachycardia by Diastolic Potential Mapping

Successful treatment of ischemic VT, including by catheter ablation, requires accurate interpretation of the local electrograms. Diastolic potentials may be recorded over a wide area of the endocardium. This study investigated the relationship of the return pathway in VT to the area displaying diastolic activity. 78 VTs in 30 patients were mapped endocardially at time of surgery. Complete return pathways were seen in 17 VTs of 10 patients. The return pathway was defined by tracking diastolic potentials from the earliest diastolic signal towards the site of VT origin. Conduction time over the return pathway represented the diastolic interval. The area of diastolic activity was determined by calculating the area enclosed by electrodes showing diastolic potentials from an inflated endocardial balloon. The mean return pathway conduction time was 90 ± 31 ms (range 40-140 ms). Mean diastolic interval was 64 ± 23 ms Irange 30-115 ms). The mean area over which diastolic activity could be seen was 317 ± 255 mm 2 (range 28-920 mm 2 ). In all 17 VTs, diastolic activity was seen within 15 mm of site of origin, and this represented an area of 98 ± 65 mm 2 (range 28-170 mm 2 ). 62% local electrograms within 15 mm of site of origin showed a diastolic potential to QRS interval &lt; 70 ms. All patients with such a pattern were cured by surgery, but 2 of 4 patients with diastolic potential to QRS interval ≥ 70 ms had VT recurrence. VT cycle length correlated with the conduction time of return pathway (R = 0.765, p = 0.0002), but not with the area of the return pathway. 1) Region exhibiting diastolic potentials was far greater than the return pathway per se. 2) Characterization of the timing of diastolic potentials relative to the QRS complex helps to identify critical portions of the return pathway close to the VT site of origin. 3) Such analysis may differentiate critical areas of the return pathway from bystander regions. 4) These observations may help direct radio-frequency ablation in the catheter laboratory.

Termination and Acceleration of Ventricular Tachycardia with Autodecremental Pacing, Burst Pacing, and Cardioversion in Patients with an Implantable Cardioverter Defibrillator

This multicenter study reports the outcome of ventricular tachycardia (VT) therapy (conversion or acceleration) and the relationship to initial tachycardia cycle length and other clinical variables using an implantable device with the capability of autodecremental or burst pacing, cardioversion, and defibrillation. The device was implanted in 444 patients (mean age 58 +/- 15 years) with 1,240 episodes of VT induced with noninvasive programming and reported in a multicenter database. Only the first sequence attempted for conversion by pacing or cardioversion was assessed, and cardioversion energies were 0.2-5 J. Autodecremental pacing was used to treat 700 induced episodes of VT during titration of pacing therapies (57% converted and 12% accelerated), burst pacing to treat 357 episodes (49% converted under 11% accelerated), and cardioversion to treat 183 episodes (82% converted and 4% accelerated). Cardioversion was the most effective treatment and had the lowest acceleration rate. Shorter VT cycle lengths were more likely to accelerate with burst pacing and longer VT cycle lengths to convert with both burst and autodecremental pacing. Patients with higher ejection fractions were more likely to convert with autodecremental and burst pacing. Use of cardioversion, higher ejection fraction, absence of unrepaired aneurysm, longer VT cycle lengths, coronary artery disease, and use of autodecremental pacing predicted conversion. Lower ejection fraction and VT cycle lengths < or = 300 msec predicted tachycardia acceleration.

Alternation of QRS Morphology and Effect of Radiofrequency Ablation in Idiopathic Ventricular Tachycardia

We performed electrophysiological studies in 13 patients with idiopathic VT and attempted radiofrequency (RF) catheter ablation in 4 of them. VT was induced by programmed stimulation in all patients and the mean cycle length was 363 +/- 58 msec. In 8 of 13 patients (62%), alternation of either the cycle length and/or morphology of VT was observed. Transient entrainment was achieved in all patients by rapid pacing from the right ventricular outflow tract so reentry was considered the underlying mechanism of VT. The site of earliest activation (EAS) during VT was located at the apicoposterior portion of the left ventricular septum and used as the target site for RF catheter ablation. Spikelike presystolic activity was detected 20-40 msec prior to the large deflection of the local electrogram in four patients. VT was terminated by a few seconds of RF current in all four patients, but subsequently new VTs with a slightly different morphology were induced in three of them and re-mapping showed a shift of the EAS. After additional RF ablation at the new EAS, VT was no longer induced. No complication was noted and VT did not recur during a follow-up period for a mean of 9.3 +/- 5.2 months. RF catheter ablation seems useful and safe for idiopathic VT. The alternation of QRS morphology and the findings at the time of catheter ablation suggest that an alternative pathway or multiple exists may be present in some patients with idiopathic VT, because the change in VT morphology was associated with a shift of the EAS.

Evaluation of intravenous lidocaine for the termination of sustained monomorphic ventricular tachycardia in patients with coronary artery disease with or without healed myocardial infarction

Prospective evaluations of intravenous lidocaine as therapy for sustained monomorphic ventricular tachycardia (VT) in the absence of acute myocardial infarction are lacking. Lidocaine has been promulgated as first-line therapy in patients with VT, but studies evaluating its efficacy in the electrophysiology laboratory suggest that it has poor effects in terminating or preventing induction of VT. Thus, this study sought to evaluate the clinical effectiveness of lidocaine in 3 cohorts with induced or spontaneous VT. One hundred twenty-eight patients with stable VT, occurring either spontaneously or induced at the time of electrophysiologic study either in the baseline state or at the time of pharmacologic testing, were evaluated. The response rate to lidocaine therapy as manifested by termination of VT was the primary goal of the study. Of these patients, 10 (8%) had termination of VT after lidocaine therapy. There were no significant differences in age, ejection fraction, VT cycle length, and mean dose of lidocaine between responders and 118 nonresponders. There were no serious side effects or adverse events (death, myocardial infarction, angina, or congestive heart failure). Lidocaine, although safe, is ineffective in terminating stable VT not associated with acute myocardial infarction.

Electrophysiologic effects of sotalol and amiodarone in patients with sustained monomorphic ventricular tachycardia

No prospective studies have compared sotalol and amiodarone during electropharmacologic testing. The purpose of this prospective, randomized study was to compare the electrophysiologic effects of sotalol and amiodarone in patients with coronary artery disease and sustained monomorphic ventricular tachycardia (VT). Patients with coronary artery disease and sustained monomorphic VT inducible by programmed stimulation were randomly assigned to receive either sotalol (n = 17) or amiodarone (n = 17). The sotalol dose was titrated to 240 mg twice daily over 7 days. Amiodarone dosing consisted of 600 mg 3 times daily for 10 days. An electrophysiologic test was performed in the baseline state and at the end of the loading regimen. An adequate response was defined as the inability to induce VT or the ability to induce only relatively slow hemodynamically stable VT. During the follow-up electrophysiologic test, 24% of patients taking sotalol and 41% of those taking amiodarone had an adequate response to therapy (p = 0.30). Amiodarone lengthened the mean VT cycle length to a greater degree than sotalol (28% vs 12%, p < 0.01). There were no significant differences in the effects of sotalol and amiodarone on the ventricular effective refractory period. In patients with coronary artery disease, amiodarone and sotalol are similar in efficacy in the treatment of VT as assessed by electropharmacologic testing. The effects of the 2 drugs on ventricular refractoriness are similar, but amiodarone slows VT to a greater extent than sotalol.

Anterior septal coronary artery infarction in the canine: a model of ventricular tachycardia with a subendocardial origin. Ablation and activation sequence mapping.

In humans, chronic ventricular tachycardia (VT) is usually associated with myocardial infarcts that involve the interventricular septum. In an effort to more closely mimic the anatomic substrate that gives rise to chronic VT in humans, we developed a canine model of VT in which the anterior septal coronary artery was ligated. The site of earliest activation, the subsequent activation sequence, and the mechanism of VT associated with the resultant ventricular septal infarct was then evaluated to determine if this model accurately reflected the characteristics of human VT. Seventeen dogs underwent occlusion-reperfusion ventricular septal infarcts. Four to 7 days later, electrophysiological studies were performed. VT was initiated by programmed electrical stimulation and terminated by pacing at a cycle length of 50% to 75% of the VT cycle length. Electrophysiological studies were performed using a 256-channel mapping system. A total of 15 VT morphologies were mapped in 9 animals. Fourteen of 15 morphologies had septal subendocardial sites of earliest activation and 1 had a septal midwall site of earliest activation. VT ablation was performed using a nitrous oxide cryoprobe and confirmed the site of earliest activation by subsequently rendering VT noninducible. Electrophysiological studies demonstrated four distinct VT activation sequences: (1) circular reentrant (n = 7), (2) concentric spread (n = 5), (3) figure-of-eight (n = 2), and (4) septal midwall (n = 1). This canine model of ventricular septal infarction produces VTs with sites of earliest activation and activation sequences similar to those in humans. A reentrant mechanism as the basis of these arrhythmias is supported by the following observations: (1) all VT was initiated and terminated with programmed electrical stimulation; (2) VT activation sequences were consistent with reentry; and (3) precise interruption of the sequence terminated the VT and rendered it noninducible.

The effects of beta-adrenergic stimulation on the frequency-dependent electrophysiologic actions of amiodarone and sematilide in humans.

The autonomic nervous system appears to play an important role in the development of clinical ventricular arrhythmias, and beta-adrenergic sympathetic stimulation may be important in modulating the electrophysiologic effects of class III antiarrhythmic agents. This study prospectively determined the effects of isoproterenol on the frequency-dependent actions of sematilide (a pure class III agent that selectively blocks the delayed rectifier potassium current) and amiodarone (a class III agent with a complex pharmacologic profile) on ventricular repolarization, refractoriness, and conduction. The frequency-dependent electrophysiologic effects of sematilide (n = 11) and amiodarone (n = 22) were determined at (1) drug-free baseline, (2) during steady-state (> 48 hours) dosing with sematilide (455 +/- 5 mg/d [mean +/- SEM]) or after 10.5 days of amiodarone loading (1618 +/- 32 mg/d), and (3) during isoproterenol administration (35 ng/kg per minute) to patients receiving sematilide or amiodarone. Electrophysiologic determinations were made at paced cycle lengths of 300 to 500 ms. The two groups were similar in all clinical characteristics. The ventricular action potential duration at 90% repolarization (APD90) was significantly prolonged by sematilide (mean increase, 7 +/- 1%, P < .01 by ANOVA) and amiodarone (mean increase, 12 +/- 1%, P < .001). However, while sematilide-induced APD90 prolongation was fully reversed to baseline values during isoproterenol infusion, the APD90 in patients receiving amiodarone remained significantly prolonged by a mean of 6 +/- 1% compared with baseline (P = .005). The reduction in the APD90 was frequency dependent for both agents, with a greater reduction at longer than shorter paced cycle lengths (P < .02). During isoproterenol infusion the right ventricular effective refractory period (RVERP) in patients receiving sematilide was significantly reduced to mean values of 8 +/- 2% below baseline (P < .05), whereas the RVERP in patients receiving amiodarone remained significantly prolonged by a mean of 7 +/- 1% above baseline values (P = .01). Sematilide and sematilide/isoproterenol had no effect on ventricular conduction. Amiodarone increased the QRS duration by 14 +/- 4% (paced cycle length, 500 ms) to 32 +/- 5% (paced cycle length, 300 ms) compared with baseline values. Isoproterenol attenuated amiodarone-induced QRS prolongation by a mean of 5 +/- 1% (P = .005), without frequency-dependent effects, consistent with isoproterenol-induced increases in the sodium current. During isoproterenol infusion there was a trend for the sustained VT cycle length to be reduced below baseline in patients receiving sematilide (275 +/- 16 versus 298 +/- 55 ms, P = .06), whereas it remained significantly prolonged compared with baseline in patients receiving amiodarone (327 +/- 17 versus 257 +/- 12 ms, P < .001). Isoproterenol fully reversed the effects of selective potassium channel block with sematilide on the APD90 and further reduced the RVERP to values significantly below baseline; it partially attenuated but did not fully reverse amiodarone-induced prolongation of the APD90 and RVERP, which remained significantly prolonged beyond baseline values. Isoproterenol exerted frequency-dependent effects in both patient groups on the APD90; it modestly attenuated amiodarone-induced conduction slowing without frequency-dependent actions; and the sustained VT cycle length remained significantly prolonged during isoproterenol administration to patients receiving amiodarone but not in those receiving sematilide. These findings may have important clinical implications regarding protection from arrhythmia development in patients receiving pure class III agents or amiodarone.

Effect of shock timing on efficasy and safety of internal cardioversion for ventricular tachycardia

Objectives. We examined the effect of shock timing within the QRS complex on cardioversion efficacy in a randomized crossover test of shocks delivered at two timing intervals relative to QRS onset.Background. The local ventricular electrogram is used in implantable cardioverter-defibrillators to synchronize cardioversion shocks to terminate ventricular tachycardia. However, the timing of the local electrogram relative to global ventricular depolarization is variable, depending on the site of ventricular tachycardia origin.Methods. Transvenous detibrillation leads were positioned in the right ventricular apex (cathode), coronary sinus and superior vena cava (anodes) of patients with sustained monomorphic ventricular tachycardia. After repeat ventricular tachycardia induction, sequential shocks with energy settings of 0.5 to 22 J were delivered simultaneously with QRS onset (QRS + 0 shock) or 100 ms after QRS onset (QRS + 100 shock). QRS onset was determined from the surface electrocardiogram. Cardioversion threshold, defined as the lowest shock energy for successful ventricular tachycardia termination, was measured for these two timings.Results. Fifteen patients (13 men, 2 women; mean [± SD] age 60.5 ± 7.7 years) completed testing. Cardioversion threshold was significantly lower with QRS + 100 shocks than QRS + 0 shocks (3.1 ± 3.5 vs. 10.5 ± 7.4 J, p < 0.01). Thirteen patients (87%) experienced ventricular tachycardia acceleration with QRS + 0 shocks, but only three patients (20%) had ventricular tachycardia acceleration using QRS + 100 shocks (p < 0.01). Of the 32 failed QRS + 0 shocks, 25 (78%) caused ventricular tachycardia acceleration, whereas only 5 (36%) of the 14 failed QRS + 100 shocks caused ventricular tachycardia acceleration (p < 0.05). Cardioversion threshold was not correlated with ventricular tachycardia cycle length, QRS duration, left ventricular ejection fraction or left ventricular diastolic volume (p = NS).Conclusions. Internal cardioversion shocks delivered late in the QRS complex during ventricular tachycardia are more effective and have a lower risk of ventricular tachycardia acceleration than those delivered near QRS onset.

Simultaneous 60-electrode mapping of ventricular tachycardia using percutaneous catheters

Objectives. We developed a new approach for mapping ventricular tachycardia at electrophysiologic study using simultaneous recordings from up to 60 catheter electrodes.Background. Good results for surgical or catheter ablation of ventricular tachycardia are limited by the ability to detect and completely map all of the underlying arrhythmogenic areas. Currently, catheter mapping of all configurations of ventricular tachycardia is impossible or unsatisfactory in at least 60% of patients because of poorly tolerated rapid rates, nonsustained ventricular tachycardia or multiple configurations.Methods. Twenty-four patients with recurrent ventricular tachycardia refractory to antiarrhythmic drugs were studied using up to six percutaneous decapolar catheters introduced into the ventricles. Left ventricular maps of ventricular tachycardia were achieved by two to three transseptal catheters, two to three transaortic catheters, a coronary sinus catheter and right ventricular catheters. Simultaneous endocardial maps of either right or left ventricles were possible with a resolution of ~1 to 2 cm. Up to 60 electrograms were digitized and recorded simultaneously using a custom-computerized mapping system.Results. Successful maps of 73 ventricular tachycardia configurations were obtained in 22 patients. The mapping procedure failed in two patients because of inability to catheterize the left ventricle in one and inability to induce monomorphic ventricular tachycardia in the other. The mean (±SD) ventricular tachycardia cycle length was 285 ± 53 ms (range 215 to 470). A total of 39 separate arrhythmogenic areas (median 1, interquartile [25% to 75%] range 1 to 3/patient) were detected, of which 21 (54%) were in the left ventricular free wall, 17 (44%) were in the ventricular septum, and 1 (2%) was in the right ventricular outflow tract. Ten patients (45%) had at least two arrhythmogenic areas. Thirteen patients subsequently underwent operation. All but one of the arrhythmogenic areas found at surgical mapping had been identified at preoperative catheter mapping. Complications of the preoperative mapping procedure occurred in four patients, with complete resolution in three and minor long-term sequelae in the other.Conclusions. This technique permits detailed catheter mapping of all types of monomorphic ventricular tachycardias, including those leading to hemodynamic collapse, and should enable better choice and direction of surgical or catheter ablation.

Effects of heptanol, class Ic, and class III drugs on reentrant ventricular tachycardia. Importance of the excitable gap for the inducibility of double-wave reentry.

Double-wave reentry (DWR) can be a mechanism for acceleration of ventricular tachycardia (VT) with a large excitable gap (EG). The purpose of this study was to determine the effects of heptanol, class Ic, and class III drugs on the inducibility of DWR. In 11 Langendorff-perfused rabbit hearts, a thin ring of anisotropic left ventricular epicardium was created by a cryoprocedure. VT with a revolution time of 180 +/- 26 milliseconds and an EG of 106 +/- 8 milliseconds was induced by incremental pacing. During control, entrainment with 10 stimuli at a 99 +/- 15-millisecond interval terminated VT in seven hearts. In four hearts VT was accelerated from 205 +/- 24 to 115 +/- 14 milliseconds by introduction of a second circulating wave in the ring. In the seven VTs that could not be accelerated, 0.5 mumol/L Org7797 (class Ic) and 1.0 mmol/L heptanol (uncoupling agent) prolonged the cycle length of VT by 32% and 37%, respectively. Because the refractory period (RP) only increased by 11%, the EG prolonged by 71% and the ratio between EG and RP was increased from 0.66 to 1.00. Under these conditions, DWR could be induced in all seven hearts. In the four VTs that could be accelerated during control, administration of the class III drug D-sotalol (35 mumol/L) only slightly slowed VT by 6%. Because the RP was prolonged by 15%, the ratio between the EG and the RP decreased from 0.76 to 0.63. Entrainment now failed to accelerate VT in two of four hearts, whereas in the two other hearts, double-wave reentry self-terminated within eight cycles. Drugs that increase the ratio of EG and RP enhance the susceptibility to acceleration of VT, whereas drugs that decrease this ratio prevent induction of sustained double-wave reentry.

Human ventricular tachycardia: Precise intraoperative localization with potential distribution mapping

Electrophysiologically guided operations for ventricular tachycardia (VT) have been directed exclusively by activation time maps. Even with computer-assisted mapping, extensive editing is required, which prolongs the duration of the operation and which may introduce significant error. In contrast, potential distribution maps can be constructed in less than 3 minutes and can be viewed as a movie of developing and receding potentials. In 4 patients undergoing operation for VT, endocardial mapping was performed using form-fitting electrodes containing 160 points. A computerized mapping system, capable of simultaneously recording 256 channels of data, was used to analyze data and to display potential distribution maps sequentially at 1-millisecond intervals as a color movie. A total of eight morphologies of sustained VT were mapped. The mean VT cycle length was 340 ± 40 milliseconds (range, 274 to 394 milliseconds). In 3 patients with ischemic heart disease, four VT morphologies originated from the subendocardium. All were successfully ablated with cryoablation alone or in conjunction with aneurysmectomy and endocardial resection. A fourth patient with VT secondary to cardiomyopathy had multiple morphologies and received an implantable cardioverter defibrillator. Potential distribution maps correlated well with the concomitant activation time maps. Thus, potential distribution mapping provides a rapid and accurate means of identifying the site of origin of VT facilitating intraoperative mapping in patients undergoing surgical ablation.

Effects of incremental doses of procainamide in patients with sustained uniform ventricular tachycardia.

Although intravenously administered procainamide has been used extensively during electropharmacologic testing for more than 10 years, there is little information available on the effects of incremental dosing of procainamide in patients with inducible, monomorphic ventricular tachycardia (VT). Twenty-nine patients with coronary artery disease had sustained monomorphic VT reproducibly induced in the baseline, drug-free state. Programmed stimulation was repeated 5 minutes after loading infusion (50 mg/min) of 7.5 and 15 mg/kg (all patients) and 22.5 mg/kg of procainamide (15 patients), while maintaining continuous infusion of 0.055, 0.11, and 0.165 mg/kg per minute after each increment in dose, respectively. Corresponding procainamide plasma concentrations were 5.6 +/- 2, 10.5 +/- 3, and 14.5 +/- 3 mg/L before, and 4.7 +/- 2, 9.6 +/- 3, and 14.6 +/- 4 mg/L after electrophysiologic study at each increment in dose of procainamide, respectively. Each incremental dose of procainamide resulted in significant prolongation of tachycardia cycle length and QRS duration during sinus rhythm and right ventricular pacing. Five (17%), 7 (24%), and 1 (7%) patients, respectively, had no inducible sustained VT following the incremental dosing of procainamide. Three of five patients who had no inducible VT at 7.5 mg/kg had VT induced again at a higher dose of procainamide. Four of 24 patients whose VT remained inducible at 7.5 mg/kg of procainamide had no VT induced at 15 mg/kg of procainamide. Twelve (41%), 15 (52%), and 6 (40%) patients, respectively, no longer had VT with baseline morphology induced following the incremental dosing of procainamide. VT with new morphology compared to baseline was induced in more than 40% of patients at one or more of the three different procainamide dosing regimens. The mean cycle length of VTs with new morphology was significantly shorter than the cycle length of tachycardias with baseline morphology at each particular dose of procainamide. Similar serum procainamide concentrations before and after programmed stimulation can be achieved at the described dosing regimen. Although 7.5 and 15 mg/kg of procainamide are both effective in suppressing induction of all VT in 20% to 25% of patients, non-inducibility at a particular dose of procainamide does not predict noninducibility at a respectively higher or lower dose. New morphologies of VT that are frequently faster than VTs with baseline morphology at a particular dose of procainamide can be induced in approximately half of the patients, and the clinical significance of these arrhythmias remains to be determined.

Ventricular fibrillation induced by low-energy shocks from programmable implantable cardioverter-defibrillators in patients with coronary artery disease

Many of the newest implantable cardioverter-defibrillators (ICDs) provide the option of programmable low-energy cardioversion for monomorphic ventricular tachycardia (VT). Whereas these devices may provide less myocardial damage and increased comfort in patients receiving frequent shocks for VT, the proarrhythmic effects of low-energy cardioversion from ICDs in patients with structural heart disease are not clear. The purpose of this study was to determine prospectively the per-patient incidence of ventricular fibrillation (VF) induction after low-energy cardioversion of VT by ICDs in patients with coronary artery disease. The estimated cardioversion energy requirement was determined during the course of routine predischarge ICD testing in 40 patients with newly implanted ICDs. Two groups of patients were identified during determination of the cardioversion energy requirement: (1) a non-VF group consisting of 26 of 40 patients (65%) without VF induced by low-energy shock and, (2) a VF group consisting of 14 of 40 patients (35%) who developed VF during low-energy cardioversion. There was no difference between the 2 groups in terms of patient age, sex, concurrent antiarrhythmic drug therapy, VT cycle length, or type of ICD system implanted. Compared with the non-VF group, the VF group was more likely to have both a lower ejection fraction (25 ± 5% vs 33 ± 8%; p = 0.005) and a cardioversion energy requirement >2 J (79 vs 27%; p = 0.005). Our results suggest that low-energy cardioversion is associated with a high per-patient risk of VF induction, and the risk is higher in patients with poorer left ventricular function and, possibly, higher cardioversion energy requirement. These results suggest that caution should be exercised in programming low-energy cardioversion for VT in patients with high-cardioversion energy requirement and poor ventricular function.

Mapping of reset of anatomic and functional reentry in anisotropic rabbit ventricular myocardium.

Premature stimulation is used to characterize the reentrant circuit during ventricular tachycardia (VT) in patients. The goal of this study was to compare the effects of premature stimulation on functional and anatomic reentrant VT. In 18 Langendorff-perfused rabbit hearts, thin layers of anisotropic left ventricular subepicardium were created by a cryoprocedure. In 8 hearts, rapid pacing induced reentry around a line of functional conduction block; in 10 hearts, reentry occurred around a fixed epicardial obstacle created by a cryoprobe. The cycle lengths (CL) of functional and anatomic VT were 110 +/- 10 and 167 +/- 17 milliseconds, respectively. During anatomic VT, the excitable gap measured 43% of the CL and premature stimuli could always reset VT (44 +/- 12 milliseconds). During early premature beats, conduction of the orthodromic wave was slightly depressed, but anatomic VT was never terminated. Reset curves at different sites in the ventricle revealed three different response types, both determined by and characterizing the spatial and temporal relation between pacing and recording sites. Premature stimulation during functional VT revealed a local excitable gap at the pacing site measuring 27% of the cycle length of VT. However, in only 3 of 8 hearts, premature stimuli could reset functional VT by 8%. In 5 VTs, advancement of the paced activation was fully compensated by prolongation of the return cycle, and VT was not reset. Due to slow conduction both toward and inside the circuit, the paced orthodromic wave lost its prematurity already within a distance of 6 to 10 mm from the pacing site. Both during anatomic and functional reentry, an excitable gap is present in the reentrant circuit. Three different response curves reveal the localization of the pacing and recording sites in the circuit. Anatomic VT can always be reset by premature stimuli, whereas in 5 of 8 hearts, functional VT could not be reset. In the other 3 hearts, VT could only be reset for less than 7% to 11% of the VT interval. Therefore, it seems very unlikely that clinical VT based on functional reentry can be reset.

Procainamide-induced changes in reentrant ventricular tachycardia with special reference to the tachycardia-interrupting critical paced cycle length during transient entrainment with rapid pacing.

With rapid ventricular pacing, sustained ventricular tachycardia (VT) is often entrained and interrupted at a critical paced cycle length. In this paper, the possible mechanism and determinant of the critical cycle length interrupting VT are addressed. Sixteen consecutive patients underwent rapid ventricular pacing in 18 morphologically distinct sustained VTs before and after procainamide. The VT morphology was identical before and after the drug. The VT origin was determined by endocardial mapping as the earliest site of activation of VT and an electrode catheter was located at the site. Rapid pacing was performed to entrain VT and repeated in 10 msec decrements of cycle length until VT was interrupted at a critical paced cycle length which was defined as the block cycle length. The effective refractory period was measured at the pacing site. The paced QRS duration and the local conduction time were measured and used as indices of conduction time in the normal myocardium. VT was entrained and interrupted in all patients. At the block cycle length, initial constant fusion was replaced abruptly by the fully paced QRS complex. At the same time, the local electrogram at the site of VT origin showed changes in the morphology and the timing of activation which were identical to those of the fully paced beat. This loss of fusion and the changes in the local electrogram were considered to be a result of orthodromic block and the block cycle length was assumed to represent the cycle length at which 1:1 conduction fails in the area of slow conduction. After procainamide, both the VT cycle length and the block cycle length were prolonged to a similar degree (p < 0.001) but the relative degree of change varied from patient to patient. The paced QRS duration and the conduction time were prolonged by procainamide but in smaller degrees than the cycle length of VT or the block cycle length (p < 0.02-01). The effective refractory period at the pacing site and the QT interval showed small changes after procainamide. The postrepolarization refractoriness rather than the duration of action potential can be responsible for the procainamide-induced prolongation of the block cycle length, and the block cycle length might be used as a new index to characterize the electrophysiologic property of the VT circuit and also the action of antiarrhythmic drugs.

Interaction of acute ventricular dilatation and d-sotalol during sustained reentrant ventricular tachycardia around a fixed obstacle.

Antiarrhythmic therapy of ventricular tachycardia is associated with decreased efficacy and increased proarrhythmia in patients with congestive heart failure, but the explanation for these observations is not known. This study examined the interaction of ventricular dilatation and d-sotalol in a model of reentry ventricular tachycardia. Thin epicardial layers of anisotropic myocardium were created in Langendorff-perfused rabbit left ventricles by a cryo procedure. A fluid-filled, latex balloon was secured within the left ventricle to change ventricular volume. Sustained reentrant ventricular tachycardia, around a central cryolesion, was induced by rapid pacing in all preparations (n = 7). Epicardial mapping was performed through 248 electrodes. Single premature beats introduced within the reentry circuit were used to define the excitable gap. Dilatation did not influence ventricular tachycardia cycle length or conduction velocity. A 1.25-mL increase in left ventricular volume widened the excitable gap by 12% (range, 5% to 29%) (P < .001) because of a decrease in myocardial refractoriness. d-Sotalol (final concentration, 10 mg/L) narrowed the excitable gap 18% (range, 7% to 29%) (P = .002) in the undilated left ventricle. d-Sotalol was less effective in the dilated left ventricle, narrowing the excitable gap only 9%, a difference that was not statistically significant. During pacing to induce or terminate tachycardia, tachycardia acceleration was observed significantly more frequently in the dilated than in the undilated ventricle. Ventricular tachycardia acceleration was due to the development of double-wave reentry (two successive waves traveling in the same circuit in the same direction). d-Sotalol, which narrowed the excitable gap, prevented tachycardia acceleration and double-wave reentry. Antiarrhythmic efficacy may be decreased by dilatation because of widening of the initial excitable gap and a decrease in the gap-narrowing effect of these agents. Double-wave reentry, more likely with a widening of excitable gap, may partially explain tachycardia acceleration in the dilated ventricle.

Comparison of electrophysiologic effects of quinidine and amiodarone in sustained ventricular tachyarrhythmias associated with coronary artery disease

Fifteen patients with spontaneous ventricular tachyarrhythmias underwent electrophysiologic studies at baseline and during therapy with quinidine and amiodarone. In 9, ventricular tachycardia (VT) with a similar QRS morphology was induced with quinidine, amiodarone and under the control state. Both quinidine and amiodarone significantly increased QRS duration and the VT cycle length. Amiodarone increased the VT cycle length more than quinidine (85 vs 121 ms, p < 0.05). Amiodarone increased the percent QRS duration (during sinus rhythm, ventricular pacing and VT) significantly less than percent VT cycle length, whereas quinidine did so only at stow rates (at faster rates the percent increase in QRS duration is not different from the percent increase in VT cycle length). The percent increase in QRS duration produced by quinidine correlated significantly with the percent increase in VT cycle length (the best correlation was observed during pacing, r = 0.78). In contrast, no such significant correlations were obtained for amiodarone. Thus, amiodarone prolongs VT cycle length more than quinidine (at the doses used). The effects of quinidine on conduction in tissue mostly unrelated to tachycardia origin predict effects in the tachycardia cycle length. In contrast, the effects of amiodarone on the latter are more intense but not predicted by those on tissue unrelated to the tachycardia origin.

Cardioversion, defibrillation, and overdrive pacing of ventricular arrhythmias: the effect of moricizine in dogs with sustained monomorphic ventricular tachycardia.

The purpose of this investigation is to define whether the antiarrhythmic drug moricizine has beneficial or adverse effects on currently used antitachycardia and antifibrillatory devices. These studies were performed in a dog model of sustained monomorphic ventricular tachycardia (VT). In 11 dogs, the left anterior descending artery and all surrounding epicardial collateral feeder vessels were ligated. Defibrillator patches were implanted and the dogs were allowed to recover. After a 7-day recovery period, effective refractory period (ERP), end diastolic threshold (EDT), VT induction, and VT and ventricular fibrillation (VF) termination data were collected before and after moricizine infusion (2 mg/kg). In this experimental model, moricizine caused the following electrophysiological changes: a prolongation of the ERP from 173 +/- 14 to 182 +/- 15 (P < 0.02) with no significant effect on the EDT for pacing; a prolongation of the VT cycle length from 175 +/- 18 to 201 +/- 23 msec (P < 0.003); an increased cycle length required for overdrive pacing from 136 +/- 20 to 157 +/- 22 msec (P < 0.01); no effect on the energy required to cardiovert VT; an increase in the defibrillation threshold from 7.5 +/- 4 to 9.4 +/- 4 joules (P < 0.006) and; in 5 of the 8 dogs with VT, the VT could be initiated with somewhat less aggressive stimulation. Significant beneficial electrophysiological physiological effects were noted on the VT cycle length, including a proportionately prolonged overdrive pacing cycle length for VT termination.(ABSTRACT TRUNCATED AT 250 WORDS)

Prospective, randomized comparison of conventional and high dose loading regimens of amiodarone in the treatment of ventricular tachycardia

Objectives. The purpose of this prospective randomized study was to compare the electrophysiologic effects of conventional and high dose loading regimens of amiodarone in patients with sustained ventricular tachycardia.Background. Uncontrolled studies in which patients have been treated with an oral loading dose of 2 to 4 g/day of amiodarone have suggested that, compared with a conventional loading dose, this dosing regimen results in more rapid control of spontaneous ventricular tachycardia and ventricular tachycardia induced by programmed stimulation.Methods. Patients in whom sustained monomorphic ventricular tachycardia was inducible by programmed stimulation and who were refractory to class I antiarrhythmic medications were randomly assigned to receive either a conventional (n = 15) or a high (n = 17) loading dose of amiodarone. The conventional dose consisted of 600 mg twice a day for 10 days. The high dose regimen consisted of 50 mg/kg body weight per day on days 1 to 3, 30 mg/kg per day on days 4 and 5 and 600 mg twice a day on days 6 to 10. An electrophysiologic test was performed in the baseline state and after 3 and 10 days of therapy. An adequate response to amiodarone was defined as the inability to induce ventricular tachycardia or the ability to induce only relatively slow (cycle length 5 ≥ 350 ms) hemodynamically stable ventricular tachycardia.Results. After 3 days of therapy, 2 of 14 patients who received the conventional loading dose and 6 of 15 patients who received the high dose loading regimen had an adequate response to amiodarone (p = 0.08). After 10 days of therapy, four patients in each group had an adequate response to amiodarone (p = NS). Three patients who received the high dose and one patient who received the conventional dose of amiodarone had an adequate response after 3 days of therapy but not after 10 days of therapy. There were significant increases in the sinus cycle length, atrioventricular block cycle length, ventricular effective refractory period and ventricular tachycardia cycle length after 3 and 10 days of therapy compared with baseline values regardless of the dosing regimen. The extent of the effects of amiodarone on these variables after 3 and 10 days of therapy was similar with both dosing regimens.Conclusions. The therapeutic and electrophysiologic effects of conventional and high dose loading regimens of amiodarone do not differ significantly after 3 or 10 days of therapy. High oral loading doses of amiodarone do not offer any significant clinical advantage over a conventional loading dose of amiodarone for controlling ventricular tachycardia induced by programmed stimulation.