Abolition Of Ventricular Tachycardia Research Articles

Arrhythmogenic right ventricular dysplasia/cardiomyopathy assessed with 64-slice computed tomography

A 69-year-old man was admitted to hospital because of sustained ventricular tachycardia with right bundle branch block morphology. After abolition of ventricular tachycardia, an electrocardiogram showed atrial fibrillation, complete right bundle block, abnormal Q wave in III, and ST‐depression in V4–V6. Multislice computed tomography (CT) was performed with a 64-slice scanner (Aquilion 64, Toshiba Medical Systems) after an intravenous injection of contrast medium. …

Invasive and noninvasive methods to predict the long-term efficacy of amiodarone: a compilation of clinical observations using meta-analysis.

The method of choice to predict the long-term efficacy of amiodarone in the treatment of complex ventricular arrhythmias is unknown. Whether electrophysiological testing or Holter monitoring better predicts long-term outcome is controversial. We performed a meta-analysis of trials using electrophysiological testing or electrocardiographic monitoring to predict the efficacy of amiodarone in patients with sustained ventricular tachycardia. Arrhythmia recurrence data were combined after homogeneity testing across trials. Bayesian estimates and 95% credibility intervals were constructed to compare the arrhythmia-free probability among groups. Nine studies using electrophysiological testing (351 patients) and three using Holter monitoring (167 patients) met criteria for inclusion determined a priori. The combined arrhythmia-free probability estimate and credibility intervals were 0.86 (0.78-0.92) for patients rendered noninducible and 0.81 (0.73-0.87) for patients with abolition of ventricular tachycardia during Holter monitoring on amiodarone. With this primary analysis, there was no significant difference between the predictive value of noninducibility during electrophysiological testing and abolition of ventricular tachycardia with Holter. However, if only those electrophysiological studies using at least triple extrastimuli were included, arrhythmia-free probability for patients rendered noninducible increased to 0.96 (0.88-0.99), significantly better than noninvasive testing. Noninducible ventricular tachycardia during electrophysiological testing and abolition of ventricular tachycardia during electrocardiographic monitoring on amiodarone appear equally predictive of long-term amiodarone success, but this conclusion seems dependent on the stimulation protocol used. Although the yield is lower (compared to Holter monitoring), ventricular tachycardia rendered noninducible with a stimulation protocol using triple extrastimuli is the most highly predictive test of long-term amiodarone efficacy.

Sudden death during empiric amiodarone therapy in symptomatic hypertrophic cardiomyopathy

Amiodarone is reported to improve symptoms and to prevent sudden death in patients with hypertrophic cardiomyopathy (HC). Amiodarone treatment (loading dose 30 g given over 6 weeks; maintenance dose 400 mg/day) was prospectively evaluated in 50 patients with HC in whom the drug was initiated because of symptoms refractory to conventional drug therapy (calcium antagonists and β blockers). Twenty-one (42%) patients had ventricular tachycardia (VT) during Holter monitoring. Amiodarone significantly and often markedly improved the patients' New York Heart Association functional class status (from 3.3 to 2.7 at 2 months, p < 0.001) and treadmill exercise duration (p < 0.001). Eight patients, however, died (7 suddenly) during a mean follow-up period of 2.2 ± 1.8 years. Of the 7 sudden deaths, 6 occurred within 5 months of initiation of treatment. The 6-month and 1- and 2-year survival rates were 87, 85 and 80%, respectively. The survival rate of patients with VT was significantly worse than that of patients without VT (61 vs 97% at 2 years; p < 0.01). Sudden death occurred despite abolition of VT on Hotter monitoring. Amiodarone increased left ventricular peak filling rate by radionuclide angiography in 20 of 33 patients (61%) (p < 0.01). Decrease in peak left ventricular filling rate within 10 days of amiodarone therapy (8 of 33 patients) was associated with subsequent sudden death (p < 0.04). It is concluded that although amiodarone results in significant functional improvement in most symptomatic patients with HC and reduces VT on ambulatory monitoring, empiric therapy with this potent antiarrhythmic drug may result in a high early incidence of sudden death. Amiodarone may provoke malignant arrhythmias or conduction abnormalities in this subgroup of patients, particularly in patients in whom left ventricular diastolic filling is reduced by the drug.

Sustained therapeutic efficacy and safety of oral propafenone for treatment of chronic ventricular arrhythmias: A 2-year experience

Thirty-two men with chronic ventricular arrhythmias responded to propafenone, a new potent antiarrhythmic agent, in short-term trials with 85% or greater reduction of total ventricular premature complexes (VPCs) per hour, 95% or greater reduction of ventricular couplets (VCs) per hour, and 100% abolition of ventricular tachycardia (VT) beats per 24 hours. These patients were continued on long-term propafenone therapy to assess sustained therapeutic efficacy and safety. Thirty patients completed 1 year and 26 patients completed 2 years of testing with this agent; one patient died of sudden death and another died of a noncardiac cause. Although there were significantly fewer patient responders at 1 and 2 years, the majority of patients (>79%) continued to respond optimally to propafenone. Side effects were minor and included bitter taste, dizziness, congestive heart failure, fatigue, and significant prolongation of the PR and QRS intervals. Propafenone has sustained antiarrhythmic efficacy after 2 years without serious toxicity.

Propafenone. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic use in the treatment of arrhythmias.

Propafenone is a Class I antiarrhythmic agent with weak beta-adrenoceptor antagonist activity which can be given both intravenously and orally. Dosage must be individualised because of dose-dependent pharmacokinetics, a wide range of clinically effective plasma concentrations (64 to 3271 micrograms/L) after comparable doses, the presence of an active metabolite (5-hydroxy-propafenone) and genetically determined metabolic oxidation. In non-comparative studies propafenone 450 and 900 mg/day orally significantly suppressed premature ventricular complexes and couplets in 96% and 75% of patients, respectively, and abolished ventricular tachycardia in 75% of patients. Efficacy was confirmed in placebo-controlled studies in which propafenone 300 to 900mg daily suppressed premature ventricular complexes (greater than 80%) in 77% of patients; 87% of patients had significant reductions in couplets and abolition of ventricular tachycardia. In patients with ventricular arrhythmias refractory to other antiarrhythmic agents, propafenone 450 to 1200 mg/day suppressed arrhythmias in 63% of patients (in long term therapy 66%). Electrically induced arrhythmias were prevented by intravenously administered propafenone in 12 to 23% of patients. However, long term oral therapy was effective in 77% of patients selected using programmed electrical stimulation. Propafenone was also effective in suppressing atrial and AV nodal/junctional re-entrant tachycardias and Wolff-Parkinson-White tachycardias involving accessory pathways. A limited number of comparisons with other antiarrhythmic drugs indicate that the antiarrhythmic efficacy of propafenone is superior or similar to that of quinidine, disopyramide and tocainide, and comparable to that of lignocaine (lidocaine), flecainide and metoprolol against ventricular arrhythmias and a smaller number of atrial arrhythmias. Cardiovascular side effects indicate a proarrhythmic effect similar to that with other Class I drugs, occasional precipitation of congestive heart failure and conduction abnormalities; the latter two occur more often in patients with underlying ventricular dysfunction. Non-cardiovascular side effects (neurological, gastrointestinal) are well tolerated and generally resolve with continued therapy or dosage reduction. Thus, propafenone is an effective antiarrhythmic agent, and is a useful addition to currently available drugs, although further studies will be required to determine clearly its place in therapy compared with more established antiarrhythmic drugs.

Encainide for ventricular arrhythmias: Placebo-controlled and standard comparison trials

Efficacy data obtained from the use of encainide in the treatment of patients with benign or potentially lethal ventricular arrhythmias are reviewed. These include an oral dose multicenter titration study involving 111 patients in whom encainide was given from 25 to 75 mg, 4 times/day, which was followed by a 3-center, reduced dose study in which 35 patients received a forced escalation of encainide from 10 to 30 mg, 4 times/day. Frequent Holter monitoring was used to judge efficacy. An 8-center, double-blind, parallel, placebo-controlled outpatient trial was conducted using encainide from 10 to 50 mg, 3 times/day, in 125 patients. This trial defined the lower end of the dose response curve for encainide to be 25 mg, 3 times/day. The data from all these trials show that when properly titrated, encainide is effective in decreasing ventricular premature complex frequency by at least 75% in about 80% of patients. A similar percentage will have abolition of ventricular tachycardia. When encainide was compared with quinidine in a 9-center placebo-controlled crossover study, encainide demonstrated more efficacy at 25 mg, 4 times/day, compared with quinidine at 200 mg, 4 times/day, in all arrhythmia parameters. Encainide was also better tolerated than quinidine and there was no statistically significant difference in the prevalence of asymptomatic proarrhythmia as detected by Holter monitoring between these 2 drugs. Long-term data in 220 patients over 36-month follow-up show continued encainide efficacy. Thus, encainide is a potent, effective class 1C antiarrhythmic agent and it has minimal negative inotropic effects and is well tolerated. It may be an ideal agent to determine whether or not the treatment of patients with potentially lethal ventricular arrhythmias will, in fact, prevent sudden cardiac death.

The role of beta blocking agents as adjunct therapy to membrane stabilizing drugs in malignant ventricular arrhythmia

Antiarrhythmic drugs are often either partially or totally ineffective for the suppression of ventricular arrhythmias in a given patient. Drug combinations afford an additional therapeutic option. We report the role of beta-blocking agents as adjunct therapy to membrane stabilizing drugs in the management of patients with malignant ventricular arrhythmias. The study group included 54 patients who were evaluated by 24-hour ambulatory monitoring and symptom-limited exercise testing. Patients underwent control studies without antiarrhythmic drugs, were evaluated on membrane stabilizing drugs and beta blocking agents separately, and were then tested on combination therapy. The combination of a beta-blocking agent and a membrane stabilizing drug abolished ventricular tachycardia and couplets in 83% and 86% of exercise tests in patients with this arrhythmia present during therapy with membrane drugs alone (p < 0.01). The addition of a beta blocker to a membrane drug, as evaluated by ambulatory monitoring, resulted in an abolition of ventricular tachycardia and couplets in 43% and 20% of studies (p < 0.05). Ventricular premature beat frequency was reduced by more than 50% in 65% of exercise tests and in 52% of monitoring studies (p < 0.05). In this population, beta-blocking agents failed to reduce ventricular arrhythmias when used alone. Thus the addition of a beta blocker to a membrane stabilizing drug significantly enhances the suppression of ventricular arrhythmia, especially when assessed by exercise testing. This results from synergistic drug effects of the combination rather than from the effect of the individual drugs.

Relation of serum reverse T3 to amiodarone antiarrhythmic efficacy and toxicity

The relation of serum reverse T3 (rT3) to amiodarone efficacy and toxicity was studied in 31 patients with frequent and complex ventricular arrhythmias. Baseline studies included 48-hour Holter recordings and rT3 levels (normal 33 ng/dl or less). Amiodarone therapy was initiated with a 5 mg/kg infusion followed by 600 to 800 mg/day for 7 to 10 days, then 200 to 400 mg/day. Holters and rT3 levels were repeated every 1 to 3 months and amiodarone was titrated to achieve at least a 70% reduction in total ventricular premature complexes, at least a 90% reduction in couplets and abolition of ventricular tachycardia. The baseline rT3 level was 18 ± 7 ng/dl (range 10 to 30) and patients were followed 12 ± 9 months. Arrhythia control was achieved in 25 patients (81%), including 21 patients with elevated rT3 levels (36 to 105 ng/dl) and 4 patients with normal rT3 (15 to 33 ng/dl). Six patients were uncontrolled with rT3 (27 to 90 ng/dl) and 14 patients had minor side effects with rT3 (27 to 123 ng/dl). Three of 4 patients in whom rT3 levels exceeded 130 ng/dl died suddenly (137 to 174 ng/dl before the event). Thus, amiodarone efficacy and minor toxicity occurs at rT3 levels less than 105 ng/dl and sudden death may be associated with levels greater than 130 ng/dl.

Discordance between ambulatory monitoring and programmed stimulation in assessing efficacy of class IA antiarrhythmic agents in patients with ventricular tachycardia

Concordance between programmed stimulation and 24 hour ambulatory electrocardiographic (Holter) monitoring was studied in 54 patients with sustained ventricular tachycardia during 84 therapeutic trials with class IA antiarrhythmic agents. During baseline studies before treatment, all patients had frequent (greater than or equal to 30/h) ventricular premature complexes on Holter recordings and sustained ventricular tachycardia inducible by one to three extrastimuli. During treatment, programmed stimulation and Holter monitoring were repeated. Efficacy of treatment determined by programmed stimulation (ventricular tachycardia no longer inducible or nonsustained) was compared with three Holter criteria of efficacy: I = 83% or more reduction of ventricular premature complexes and abolition of ventricular tachycardia; II = 50% or more reduction of ventricular premature complexes and 90% or more reduction of couplets and abolition of ventricular tachycardia; III = abolition of ventricular tachycardia in patients with ventricular tachycardia during a baseline Holter recording. Treatments were judged effective by programmed stimulation criteria in only 25% of cases but in 51, 63 and 75% of cases by Holter criterion I, II and III, respectively. Results of programmed stimulation and Holter monitor were discordant (effective by one criterion but ineffective by the other) in 50% of cases using Holter criterion I, in 54% using Holter criterion II and in 61% using Holter criterion III. In the majority of discordant results, treatments appeared efficacious by Holter criteria but ineffective by programmed stimulation criteria, suggesting insensitivity of efficacy by Holter criteria or nonspecificity of induced ventricular tachycardia during treatment, or both.

Combination of procainamide and quinidine for better tolerance and additive effects for ventricular arrhythmias

The efficacy and tolerance of quinidine and procainamide used individually and in combination were studied in 19 patients with frequent ventricular premature complexes (VPCs). During single-drug treatment, the maximum tolerated dose of quinidine without extracardiac dose-related side effects was 1.6 ± 0.21 g/day and that of procainamide was 4.1 ± 1.05 g/day. During combination therapy with smaller doses (p < 0.05) of quinidine (1.16 ± 0.26 g/day) and procainamide (2.80 ± 0.98 g/day), no patient had side effects. Before treatment, all patients had frequent (more than 60 per hour) VPCs and 17 had ventricular tachycardia on Holter monitoring. The frequency of VPCs was reduced to 22 ± 19% with quinidine, 47 ± 40% with procainamide and 9 ± 11% with combination therapy (p < 0.05, combination vs procainamide or quinidine alone). Individually, an effective regimen (more than 83% reduction of VPCs and abolition of ventricular tachycardia) was found in 5 patients (26%) receiving quinidine alone at maximal tolerated dose, in 4 (21%) receiving procainamide alone at maximal tolerated dose, and in 14 (74%) receiving combination therapy (p < 0.01 vs quinidine or procainamide). Thus, the antiarrhythmic effects of quinidine and procainamide are additive. When quinidine or procainamide is ineffective because dose-related extracardiac side effects limit the maximal tolerated dose, combination therapy in smaller and tolerable doses avoids side effects and is more effective than either drug alone at the maximal tolerated dose.

Efficacy of propafenone compared with quinidine in chronic ventricular arrhythmias

A double-blind, randomized study was designed to evaluate the efficacy of oral propafenone and oral quinidine in suppressing premature ventricular complexes (Ms). Twenty-five men were studied for 3 weeks. Twelve were randomized to the quinidine group and 13 to the propafenone group. Small doses of the drugs were administered for 1 week (200 mg of quinidine every 6 hours or 300 mg of propafenone every 12 hours) and large doses were administered for another week (400 mg of quinidine every 6 hours or 300 mg of propafenone every 8 hours). Strict criteria were used to define responders to antiarrhythmic therapy. For more than 85% reduction in total PVCs per hour: During the low-dose week, 36 % in the quinidine group and 50 % in the propafenone group were responders (difference not significant [NS]), while during the high-dose week 33% and 64% were responders (NS). For more than 95 % reduction of ventricular couplets per hour: During the low-dose week, 45% in each group were responders, while during the high-dose week, 56% and 60% were responders (NS). For 100% abolition of ventricular tachycardia (VT) beats per 24 hours: During the low-dose week, 60% in the quinidine group and 56 % in the propafenone group were responders (NS); during the high-dose week 80% and 67% were responders (NS). There was no significant difference in the 2 groups in incidence of side effects. This study shows comparable efficacy and tolerance of propafenone and quinidine for the control of ventricular arrhythmias in ambulatory patients with diverse forms of heart diseases.

Intravenous and oral loading versus oral loading alone with amiodarone for chronic refractory ventricular arrhythmias

To determine whether combined intravenous (i.v.) and oral loading with amiodarone can shorten its onset of action, a comparative study was conducted. Twenty patients with refractory ventricular arrhythmias were treated with amiodarone. All patients had frequent (≥30/hour) and complex (repetitive) ventricular premature beats on a 48-hour baseline Holter recording. Ten patients (group A) received oral loading alone: 800 mg/day for 7 days, 600 mg/day for 3 days, then a maintenance dose 200 to 400 mg/day. Ten patients (group B) received i.v. and oral loading: 5 mg/kg i.v., and then the same regimen as for group A. Follow-up 24-hour Holter recordings were obtained daily for 7 days, weekly for 1 month, and then monthly. Arrhythmia control was defined as at least a 70% reduction in ventricular premature beats, a 90% or greater reduction in couplets and abolition of ventricular tachycardia. The time to optimal ventricular arrhythmia control was shorter for group B (20 ± 18 vs 105 ± 83 days, p < 0.05) and the cumulative amiodarone dose at the time of control was smaller for group B (10 ± 8 vs 48 ± 39 g, p < 0.05). No complications were encountered with i.v. amiodarone. Thus, initial loading with i.v. amiodarone can shorten the time to optimal ventricular arrhythmia control and lower the cumulative dose required.

Efficacy and safety of intravenous tocainide compared with intravenous lidocaine for acute ventricular arrhythmias immediately after cardiac surgery

In this double-blind parallel study, 99 patients with acute ventricular tachyarrhythmias after open-heart surgery were given either tocainide (50 patients) or lidocaine (49 patients) intravenously as 2 bolus injections 15 minutes apart, plus a fixed-rate infusion that started at the first bolus. If needed, a third bolus was administered and simultaneously the infusion rate was doubled. The boluses and initial infusion rate for tocainide treatment were, respectively, 250, 250 and 125 mg and 1.04 mg/min, and for lidocaine treatment, 100, 50 and 50 mg and 2.08 mg/min. When efficacy was defined as 80% or greater reduction in single ventricular premature complexes (VPCs) or complete abolition of ventricular couplets or ventricular tachycardia, no difference in efficacy between the 2 treatments was found by bedside electrocardiographic monitoring. By computer analysis of 24-hour taped electrocardiograms and a regression analysis of the proportion of patients responding favorably to treatment, it was estimated that an 80% or greater reduction of single VPCs occurred in 55% of patients during tocainide treatment and in 48% of patients during lidocaine treatment; abolition of couplets occurred in 74% and 68% of patients, respectively; and abolition of ventricular tachycardia in 87% and 73% of patients, respectively. These treatment-related differences were different (p less than 0.004). Adverse reactions occurred in 5 patients (10%) given tocainide (hypotension in 4; junctional rhythm in 1 patient; and nausea-vomiting in 1) and led to discontinuation of treatment in 3 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Efficacy of a new oral agent (tocainide) in the acute treatment of refractory ventricular arrhythmias

To assess the efficacy of tocainide, a new oral analog of lidocaine, 30 patients with ventricular arrhythmias refractory to quinidine, procainamide and propranolol were treated with this agent. The dose of tocainide ranged from 400 to 800 mg every 8 hours. Peak tocainide blood levels 1 to 4 hours after administration ranged from 5.0 to 15.0 microgram/ml (mean 10.3). The suppression of ventricular premature beats by 75 percent or more was arbitrarily used as a measure of drug efficacy. In 13 patients who met this criterion, ventricular premature complexes, assessed with 24 hour ambulatory tape monitoring, decreased by an average of 88 percent. In 8 of 11 patients, repeated symptomatic bouts of ventricular tachycardia were completely suppressed. Considering both the response of ventricular premature complexes and the abolition of ventricular tachycardia, 18 patients (60 percent) responded to tocainide. Twenty-one patients (70 percent) had initial gastrointestinal and central nervous system side effects; most of these were transient or responded to a reduction in dose. In two patients disorientation and a skin rash required withdrawal of tocainide. These adverse effects did not appear to be due to the interaction of tocainide with other antiarrhythmic agents. It is concluded that tocainide is an effective oral agent for the therapy of potentially lethal ventricular arrhythmias refractory to other medication.

The effectiveness of magnesium chloride in the treatment of ventricular tachyarrhythmias due to digitalis intoxication

Efficacy of magnesium chloride in treatment and prevention of digitalis toxicity was studied in 39 dogs. A persistent ventricular tachycardia, lasting more than five minutes was induced in 29 dogs by deslanoside, 0.18 mg. per kilogram intravenously. In 19 animals, administration of magnesium chloride (5 to 10 ml. of a 20 per cent solution) administered intravenously converted the ventricular tachycardia into a sinus rhythm. The cardiac output was found to be increased following this treatment (P < 0.01). The serum electrolytes and digoxin levels remained unchanged. With larger doses of magnesium chloride, significant bradycardia occurred in two instances following abolition of ventricular tachycardia. When pretreatment with magnesium chloride (10 ml. intravenously and 20 ml. intramuscularly of a 20 per cent solution) was employed in a group of five dogs prior to administration of deslanoside, ventricular tachycardia from the usual or greater doses of the glycoside was invariably prevented. Deslanoside dosage larger by 83.3 per cent was then required to produce cardiotoxicity; however, VT appeared in only one out of five dogs, whereas serious A-V conduction impairment was seen in other dogs. None of the magnesium-pretreated animals developed ventricular fibrillation in spite of marked bradycardia. In 10 dogs used as control animals, the ventricular tachycardia either persisted or deteriorated into ventricular fibrillation. In conclusion, the experimental data demonstrate that magnesium chloride is effective in treatment of digitalis-induced ventricular arrhythmias.

A clinical trial of antazoline in the treatment of arrhythmias

Antazoline is a comparatively safe and effective antiarrhythmic drug in many situations, for both the conversion and prevention of arrhythmias. It appeared to be most effective in the abolition of ventricular tachycardia, possibly helpful in 2 cases of cardiac arrest due to ventricular fibrillation and beneficial in the prevention of atrial and ventricular premature beats. It was useful and deserves further trial in the prevention of paroxysmal ventricular tachycardia. It was almost ineffective in the conversion and prophylaxis of atrial flutter and atrial fibrillation but appeared to be of value in the prevention of paroxysmal atrial tachycardia. There was a high incidence of mild side effects, mostly of the gastrointestinal type, some of which were prevented by taking the drug with meals or with an antacid preparation. No irreversible or serious side actions were encountered, but diarrhea, central nervous system symptoms and chills and fever necessitated stopping the drug in a small percentage of patients.