Effectiveness Of Amiodarone Research Articles

Supraventricular arrhythmia following lung resection for non-small cell lung cancer and its treatment with amiodarone.

From January 1998 to February 1999, 160 patients undergoing lung resection for non-small cell lung cancer were studied to define factors that increase the risk of postoperative supraventricular arrhythmia (SA) and to assess the effectiveness of amiodarone as an antiarrhythmic drug. All patients were monitored intraoperatively and postoperatively up to day 3. Onset of SA was documented with ECG. Amiodarone was administered to those who developed SA with a loading dose of 5 mg/kg in 30 min and a maintenance dose of 15 mg/kg in 24 h. Mean age was 64 years (range 27-83 years). There were nine wedge resections, six segmentectomies, 127 lobectomies and 18 pneumonectomies. Twenty-two patients (13%) had SA, all of which were atrial fibrillations. The incidence of supraventricular arrhythmia with pneumonectomy and lobectomy was 33 and 12%, respectively (P=0.02). None of the patients who had a minor resection developed SA. The peak incidence of onset of SA occurred on postoperative day 2 and lasted from 1 to 12 days (average 3.4 days). Sinus rhythm was achieved with amiodarone in 20 patients (90.9%) with no side effects. Two patients received electrical cardioversion because hemodynamically unstable. Mean preoperative pO(2) and pCO(2) were lower in patients with SA: pO(2) 80.8 vs. 85 mmHg (P=0.04); pCO(2) 35.5 vs. 38 mmHg (P=0.01). Patients with concomitant cardiopulmonary diseases presented an odds ratio for postoperative arrhythmia of 12.4 (confidence interval 4. 5-34.1) (P<0.0001). Concomitant cardiopulmonary diseases, lower pO(2), pCO(2) and extent of surgery increase the risk of postoperative SA after lung resection for non-small cell lung cancer. Cardiac monitoring in patients at risk is recommended. Amiodarone was both safe and effective in establishing and maintaining sinus rhythm.

Effectiveness of amiodarone as a single oral dose for recent-onset atrial fibrillation

The efficacy of amiodarone has been proved in long-term maintenance of sinus rhythm (SR) in patients with paroxysmal atrial fibrillation (AF). The present study evaluates the efficacy and safety of a single oral dose of amiodarone in patients with recent-onset AF (<48 hours). Seventy-two patients were randomized to receive 30 mg/kg of either amiodarone or placebo. Conversion to SR was verified by 24-hour Holter monitoring. Ten patients were excluded because of SR in the beginning of monitoring or technical failure during Holter monitoring. The remaining study groups were comparable (n = 31 for each), except that in the placebo group β blockers were more common. The patients receiving amiodarone converted to SR more effectively than those receiving placebo (p <0.0001). At 8 hours, approximately 50% of patients in the amiodarone group and 20% in the placebo group (Holter successful) had converted to SR, whereas after 24 hours the corresponding figures were 87% and 35%, respectively. The median time for conversion (8.7 hours for amiodarone and 7.9 hours for placebo) did not differ in the groups. Amiodarone was hemodynamically well tolerated, and the number of adverse events in the study groups was similar. Amiodarone as a single oral dose of 30 mg/kg appears to be effective and safe in patients with recent-onset AF.

Amiodarone versus propafenone for conversion of chronic atrial fibrillation: results of a randomized, controlled study

OBJECTIVESThe purpose of this study was to investigate the efficacy and safety of amiodarone and propafenone in the conversion of chronic atrial fibrillation in a prospective, randomized, placebo-controlled study.BACKGROUNDThe effectiveness of amiodarone and propafenone in the treatment of patients with chronic atrial fibrillation has not been adequately studied.METHODSOne hundred one patients (48 men, mean age 64 ± 9 years) with atrial fibrillation lasting >3 weeks participated in the study. Thirty-four patients received amiodarone (300 mg intravenously over 1 h, followed by 20 mg/kg over the next 24 h plus 600 mg orally, in three doses, for 1 week, then 400 mg/day orally, for three weeks), 32 received propafenone (2 mg/kg intravenously over 15 min, followed by 10 mg/kg over 24 h and then 450 mg/day orally, for one month) and the remaining 35 served as control subjects. All patients received digoxin and anticoagulant treatment as indicated (International Normalized Ratio 2 to 3).RESULTSConversion to sinus rhythm was achieved in 16 (47.05%) patients who received amiodarone, in 13 (40.62%) who received propafenone and in none of the control subjects (p < 0.001 for both groups vs. control subjects). Those who converted had smaller atria than those who did not and atrial fibrillation of shorter duration in both the amiodarone and propafenone groups. Treatment was discontinued in one patient of the propafenone group because of significant QRS widening.CONCLUSIONSAmiodarone and propafenone appear to be safe and equally effective in the termination of chronic atrial fibrillation. Left atrial diameter and arrhythmia duration are independent predictors of conversion.

Effectiveness and safety of intravenous amiodarone in drug-resistant tachyarrhythmias of children.

Experience with pediatric use of intravenous amiodarone is limited. In this study, our experiences with intravenous amiodarone in children with acute life-threatening or chronic tachyarrhythmias are reviewed. Twelve patients, with a mean age of 3.4 +/- 3.1 years, range 9 months-10 years (two with incessant ventricular tachycardia, one with ectopic atrial tachycardia, two with atrioventricular re-entrant tachycardia (three episodes), four with postoperative or congenital junctional ectopic tachycardia, two with bradycardia-tachycardia syndrome, one with atrial tachycardia) were treated with intravenous amiodarone during 13 tachycardia episodes. Left ventricular systolic functions were depressed in six patients. In 11 patients, a median of two drugs (range one-four), including adenosine infusion and in five cases direct current cardioversion were tried without success prior to intravenous amiodarone. The loading dose of amiodarone was 5 mg/kg in all episodes, infused over 1 h. Maintenance infusion was required in 12 episodes. In 10 episodes (77%), amiodarone was considered effective, in one (7.6%) partially effective (junctional ectopic tachycardia) and in two (15.4%) ineffective (sick sinus syndrome, atrial tachycardia). Therapeutic effect was obtained in a median period of 30 h (range 1-103 h). The mean effective maintenance dose was 10 +/- 4.7 micrograms/kg per min (range 5-15 micrograms/kg per min). In one patient, mild hypotension, and in three patients cellulitis occurred, but none of them necessitated termination of treatment. Intravenous amiodarone is found to be an effective and safe antiarrhythmic agent for children with acute life-threatening and chronic tachyarrhythmias and depressed left ventricular systolic functions.

Recommandations pour le traitement des tachycardies supraventriculaires réciproques du nourrisson

The effectiveness and safety of antiarrhythmic agents, mostly digoxin and amiodarone given to prevent recurrences, were compared in 141 infants of less than 1 year (77% < 1 month) with re-entrant supraventricular tachycardia. Digoxin was the drug of first choice in 114 patients at a dose of 10-20 micrograms/kg/d and was effective in 74 cases (65%). Amiodarone was used as first line therapy or after failure of digoxin. It was given at a maintenance dose of 250 mg/m2/d, alone in 22 infants and together with digoxin in another 36; it was effective in 56 cases (96.5%). Early adverse events occurred in six patients receiving digoxin: ventricular fibrillation requiring cardioversion in three, two of whom had Wolff-Parkinson-White syndrome, significant sinus bradycardia in two, accidental overload in one. At further follow-up, one child treated with digoxin but having also gastroesophageal reflux, died suddenly at 3 months of age; autopsy was normal and the digoxin blood level was 3 ng/mL. Among the 58 infants who received amiodarone, there were no proarrhythmia, a slight and transient increase in TSH in six infants and only one required a short-term treatment for hypothyroidism. Prophylactic therapy was maintained for 6 to 12 months and only ten patients had recurrences in the year following withdrawal. Amiodarone was found to be safer and more effective than digoxin. No significant side-effect was demonstrated in infants receiving a short-term treatment. Amiodarone may be proposed as first line therapy for prophylaxis of re-entrant supraventricular tachycardia in infancy, especially for those patients with reentry and Wolff-Parkinson-White syndrome.

Chronic amiodarone reduces transmural dispersion of repolarization in the canine heart.

Amiodarone is a potent antiarrhythmic agent used in the management of both atrial and ventricular arrhythmias. In addition to its beta-blocking properties, amiodarone is known to block the sodium, potassium, and calcium channels in the heart. Its complex electropharmacology notwithstanding, the reasons for the high efficacy of the drug remain unclear. Also not well understood is the basis for the low incidence of proarrhythmia seen with amiodarone relative to other agents with Class III actions. The present study was designed to examine the effects of chronic amiodarone in epicardial, endocardial, and M cells of the canine left ventricle. We used standard microelectrode techniques to record transmembrane activity from endocardial, epicardial, mid-myocardial, and transmural strips isolated from the canine left ventricle. Tissues were obtained from mongrel dogs receiving amiodarone orally (30 to 40 mg/kg per day) for 30 to 45 days or from untreated controls. Chronic amiodarone produced a greater prolongation of action potential duration in epicardium and endocardium, but less of an increase, or even a decrease at slow rates, in the M region, thereby reducing transmural dispersion of repolarization. In addition, chronic amiodarone therapy suppressed the ability of the IKr blocker, d-sotalol, to induce a marked dispersion of repolarization or early afterdepolarization activity. Our data demonstrate for the first time a direct effect of chronic amiodarone treatment to differentially alter the cellular electrophysiology of ventricular myocardium so as to produce an important decrease in transmural dispersion of repolarization, especially under conditions in which dispersion is exaggerated. These results may contribute to our understanding of the effectiveness of amiodarone in the treatment of life-threatening arrhythmias as well as to our understanding of the low incidence of proarrhythmia attending therapy with chronic amiodarone in comparison with other Class III agents.

The role of intravenous amiodarone in the management of cardiac arrhythmias.

To review the electropharmacology, clinical applications, side effects, and hemodynamic profile of intravenous amiodarone. The MEDLINE database was searched for English-language material, including reports of clinical trials and in vivo studies, review articles, and abstracts presented at national symposia, that was published between 1985 and 1996. Bibliographies of textbooks and articles were also examined. Studies that reported on the efficacy, toxicity, and hemodynamic profile of intravenous amiodarone and studies that examined the pharmacologic behavior of intravenous amiodarone in laboratory models were reviewed. Study design and quality and relevant data on efficacy of suppression and treatment of arrhythmias with oral and intravenous amiodarone therapy, the reported mechanisms of antiarrhythmic effect, and hemodynamic changes seen with therapy were analyzed. Amiodarone is a unique antiarrhythmic agent that is now available in oral and intravenous forms in the United States. The use of intravenous amiodarone in the short-term treatment of life-threatening or hemodynamically unstable rhythm disturbances has generated much interest. Amiodarone has many electropharmacologic actions, some of which differ between the oral and intravenous forms. The wide clinical application of amiodarone includes treatment and prevention of supraventricular and ventricular arrhythmias and arrhythmias related to myocardial infarction. Intravenous amiodarone is effective for supraventricular and ventricular arrhythmias that are resistant to other antiarrhythmic agents. The effectiveness of intravenous amiodarone as short-term treatment also suggests that the drug has an important role in protocols of advanced cardiac life support. Intravenous amiodarone seems to have an overall favorable hemodynamic profile and does not produce many of the unwanted long-term side effects associated with oral therapy. Intravenous amiodarone shows much promise for the short-term treatment of unstable arrhythmias. Its favorable hemodynamic effects and minimal short-term side effects make it an attractive option in the management of cardiac arrhythmias.

An Evaluation of Possible Mechanisms Underlying Amiodarone-Induced Pulmonary Toxicity

The effectiveness of amiodarone in the treatment of cardiac arrhythmias is limited due to the development of pulmonary toxicity. Although the biochemical and morphologic characteristics associated with amiodarone-induced pulmonary toxicity (AIPT) are well-defined, the mechanisms underlying this disorder remain unknown. This review focuses on proposed mechanisms of AIPT, in particular (i) direct cellular damage; (ii) the role of phospholipidosis; (iii) the correlation between drug burden and toxicity; (iv) the role of the immune system; (v) the generation of oxidants; (vi) changes in membrane properties; and (vii) miscellaneous biochemical considerations. Additional discussion of the role of amiodarone's primary metabolite, desethylamiodarone, in AIPT and the involvement of preexisting lung dysfunction in the susceptibility to AIPT is included. With a clearer understanding of the possible contributions of these mechanisms to AIPT, it may be possible to develop strategies to alleviate toxicity and prolong the usefulness of amiodarone in the treatment of cardiac arrhythmias.

Effects of amiodarone on the circadian rhythm and power spectral changes of heart rate and QT interval: Significance for the control of sudden cardiac death

Effects of chronic amiodarone therapy on the circadian rhythmicity and power spectral changes of heart rate and QT intervals from Holter recordings were evaluated in three groups of patients: group 1 baseline ( n = 10); group 2, treated for 3 to 6 months ( n = 11); and group 3, treated for >1 year ( n = 13). Amiodarone reduced heart rate, which reached steady state at 3 to 6 months; bradycardia was evident during the entire 24 hours. The corrected QT (QT c) interval increased as a function of treatment duration. It was 457 ± 39, 530 ± 28 ( p < 0.001), and 581 ± 36 ( p < 0.0002) msec for groups 1, 2, and 3, after 6 months, respectively. The circadian rhythmicity of QT c was abolished in group 3. Power spectral analysis showed a tendency for amiodarone to reduce both R-R and QT interval variabilities, suggesting inhibition of autonomic control on the heart by the drug. The effectiveness of amiodarone against ventricular arrhythmias may result in part from the sustained bradycardia in concert with continuous uniform prolongation of myocardial repolarization.

A comparison of propafenone and amiodarone in reversion of recent-onset atrial fibrillation to sinus rhythm

In a single-blind, randomized study, the effectiveness of propafenone and amiodarone for reversion of recent-onset (≤1 week) atrial fibrillation was compared in 61 consecutive patients (New York Heart Association functional class I and II). Thirty-one patients were treated with propafenone (2 mg/kg intravenously over 10 minutes followed by a continuous infusion of 0.007 mg/kg per minute) and 30 patients with amiodarone (5 mg/kg intravenously over 10 minutes followed by an infusion of 15 mg/kg per day). Drug efficacy was measured by rate of reversion to sinus rhythm within 1 hour after the start of drug infusion. At 1 hour, 13 patients reverted with propafenone treatment and 3 with amiodarone treatment (42% vs 10%, P < 0.02). Restoration of sinus rhythm within 24 hours was achieved in 27 patients receiving propafenone and in 24 receiving amiodarone (87% vs 80%, P = NS). The median time to conversion was shorter for propafenone than for amiodarone (90 minutes vs 450 minutes, P < 0.005). No major adverse effects occurred in either treatment group. In conclusion, propafenone, administered intravenously as a loading dose followed by a maintenance infusion, is effective in reverting recent-onset atrial fibrillation to sinus rhythm and works faster than intravenous amiodarone. Both treatments were safe in patients without clinical evidence of heart failure.

Amiodarone management of junctional ectopic tachycardia after cardiac surgery in children.

To assess the effectiveness and safety of amiodarone in the treatment of junctional ectopic tachycardia (JET) after open heart surgery in children. Between January 1990 and December 1991, 16 consecutive patients aged 6 days to 14 years with JET associated with significant haemodynamic impairment after cardiopulmonary bypass were treated with amiodarone as the principal antiarrhythmic drug. Amiodarone 5 mg/kg was administered intravenously over one hour and the same dose was subsequently infused over 12 hours. This was reviewed every 12 hours and repeated as necessary until a satisfactory heart rate and stable haemodynamics were achieved. Atrial pacing was used whenever possible to provide atrioventricular synchrony. Except for one patient with a JET rate of 160/min, the maximum JET rate ranged from 180/min to 245/min with a mean(SD) of 200 (20)/min. After amiodarone, the heart rates reduced to a mean(SD) of 170 (20), 164 (27), 158 (27), 157 (24), and 153 (19)/min at two, four, eight, 12, and 24 hours respectively. A reduction in tachycardia rate allowing atrial pacing was achieved in 10 patients by two hours. Haemodynamic variables improved in most patients with an increase in mean systolic blood pressure by an average of 15 mm Hg and a decrease in atrial filling pressures by an average of 3.5 mm Hg at four hours after amiodarone administration. There were three deaths: one was a moribund patient who died soon after the onset of JET and the other two deaths were not directly related to JET. Late bradycardia with hypotension was recorded in one patient. Asymptomatic late sinus bradycardia was seen in several others. Amiodarone can be used safely and effectively to control JET with haemodynamic improvement in most patients. The addition of atrial pacing confers the advantage of atrioventricular synchrony.

Clinical efficacy and safety of intravenous amiodarone in infants and children

The effectiveness and safety of intravenous amiodarone in children are not well established. This study reviewed its use in 30 infants and children for life-threatening tachyarrhythmias: 18 patients (19 episodes) with supraventricular tachycardia, and 12 with ventricular tachycardia. Eighteen patients had structural heart defects with arrhythmias that occurred after surgery. The mean loading dose was 5 mg/kg infused over 1 hour, with a starting maintenance dose of 5 μg/kg/min. In 18 treatment episodes, amiodarone was used alone or in combination with digoxin. Thirteen patients received amiodarone combined with other antiarrhythmic agents. Intravenous amiodarone was effective or partially effective in 94% of patients, achieving a therapeutic effect in a median time of 1 day (range 1 hour to 5 days). The mean effective maintenance dose was 9.5 μg/kg/min (13.7 mg/kg/day), and median treatment duration was 5 days (range 1 to 30). Adverse effects occurred in 18 patients (58%), however none necessitated termination of amiodarone therapy. Potentially significant electrocardiographic abnormalities occurred in 5 patients during combination antiarrhythmic therapy with propafenone. Sinus bradycardia requiring temporary postoperative pacing occurred in 3 patients treated with amiodarone alone. Intravenous amiodarone used alone or in combination therapy is an effective treatment for resistant, life-threatening arrhythmias in infants and children. Combination drug therapy with propafenone must be used cautiously. Potential bradycardia pacing may be necessary during administration of amiodarone after surgery.

Indications and limitations of class II and III antiarrhythmic drugs in atrial fibrillation.

In summary, the Class III antiarrhythmic agents amiodarone and sotalol are effective in restoring sinus rhythm in patients with chronic atrial fibrillation with a higher effectiveness of amiodarone. Both agents successfully prevent recurrent episodes of atrial fibrillation after electrical cardioversion and both can control heart rate in persistent atrial fibrillation. Amiodarone appears to be particularly suitable in patients with atrial fibrillation and concomitant congestive heart failure because it lacks clinically relevant negative inotropic activity. Both substances are also effective in controlling ventricular arrhythmias that are frequently present in patients with atrial fibrillation. Finally, both drugs possess antiadrenergic activity, which makes the substances particularly attractive in patients with coronary heart disease as the underlying cause of atrial fibrillation.

Effectiveness of Amiodarone and electrical cardioversion for chronic rheumatic atrial fibrillation after mitral valve surgery

Thirty consecutive patients with chronic rheumatic atrial fibrillation (AF) ≥3 months after successful mitral valve surgery and left atrial diameter ≤60 mm were treated with oral amiodarone. Protocol included high loading dosages of amiodarone for 4 weeks, and if conversion to sinus rhythm (SR) was not achieved then electrical cardioversion was performed. Patients converted to SR were maintained on low-dose amiodarone for another 4 weeks when treatment was discontinued. Overall, 23 patients (77%) converted to SR after 4 weeks of therapy: 12 (40%) taking amiodarone alone and 11 (37%) with the addition of electrical cardioversion. The duration of AF >48 months was an adverse factor in the ability to restore SR. Sixteen patients (70%) remained in SR at a mean follow-up of 17 months. The duration of AF ≤48 months alone or in combination with left atrial diameter ≤48 mm were the best predictors for long term maintenance of SR. Thus, short-term amiodarone with or without electrical cardioversion is effective and safe in the treatment of chronic rheumatic AF after mitral valve surgery. The duration of AF and left atrial size can be used to identify patients with successful outcome.

Intravenous amiodarone for the rapid treatment of life-threatening ventricular arrhythmias in critically ill patients with coronary artery disease

This study examined the effectiveness of intravenous amiodarone for rapid control and prevention of recurrent life-threatening ventricular tachyarrhythmias associated with cardiovascular collapse. In 22 critically ill patients with coronary artery disease (mean ejection fraction 27 ± 13%), recurrent ventricular tachyarrhythmias proved refractory to 3.7 ± 1.1 (mean ± standard deviation) conventional antiarrhythmic drugs. In the 24-hour period before intravenous amiodarone treatment, patients experienced 2.4 ± 2.3 (range 1 to 9) episodes of lifethreatening ventricular tachycardia, ventricular fibrillation or both, requiring 4.0 ± 3.9 direct current cardioversions. Within the 24 hours after initiation of intravenous amiodarone therapy (900 to 1,600 mg/day), 20 of 22 patients remained alive and had 1.1 ± 1.6 episodes of life-threatening ventricular arrhythmias, requiring 1.9 ± 3.1 direct current cardioversions. In the second 24-hour period, there were 19 survivors and life-threatening arrhythmias were reduced to 0.4 ± 0.7 episode/ patient requiring 0.4 ± 0.9 direct current cardioversion. Overall, arrhythmias were controlled in 11 of 22 (50%) patients within the first 24 hours, and in 14 of 22 (64%) in the second 24 hours. Intravenous amiodarone therapy was well tolerated. Twelve patients were discharged from the hospital and 8 remained alive at a mean follow-up of 22 ± 14 months. Thus, in critically ill patients, intravenous amiodarone may be useful for rapid control of spontaneous, refractory, life-threatening ventricular tachyarrhythmias.

Effectiveness of amiodarone on ventricular arrhythmias during and after acute myocardial infarction

A randomized, placebo-controlled study examined the effect of amiodarone on the incidence of ventricular arrhythmias after acute myocardial infarction (AMI). Two hundred patients with AMI were randomized to receive amiodarone, 200 mg every 8 hours for 1 month, followed by 200 mg/day, or placebo, starting 48 hours after the onset of chest pain. Twenty-four-hour Holter monitoring was performed on day 1, repeated after 8 days and subsequently at 3-month intervals. One hundred seventy-two patients were followed for 6 to 42 months and monitor data were available at 6 to 9 months in 129 patients. Amiodarone was well tolerated, with no serious side effects; 12 patients were withdrawn from therapy. At 6 to 9 months more than 1 ventricular premature complex per hour was present in 3 of the 59 amiodarone-treated patients (5%) and 24 of the 70 placebo-treated patients (34%) (p < 0.02). Complex arrhythmias (multifocal, early cycle, repetitive, bigeminy, trigeminy or ventricular tachycardia) were present in 5 of 59 of the amiodarone-treated patients (8%) and 20 of 70 placebo-treated patients (28%) (p < 0.005). Sixteen patients in the amiodarone group and 11 in the placebo group died (difference not significant). Thus, amiodarone can reduce the frequency and complexity of ventricular arrhythmias after AMI, but it is unlikely that this will result in a substantial beneficial effect on post-AMI mortality risk.

Electrophysiologic basis for the suppression by amiodarone of orthodromic supraventricular tachycardias complicating pre-excitation syndromes

Ten patients with refractory recurrent supraventricular tachycardia were found by electrophysiologic study to have bypass tracts and orthodromic atrioventricular reentrant tachycardia. All had failed to respond to conventional antiarrhythmic therapy and were therefore treated with oral amiodarone (1,600 to 2,000 mg/day for 2 weeks, then 800 to 1,200 mg/day for another 2 weeks with subsequent 200 to 600 mg/day maintenance doses). During or after the fourth week of therapy, electrophysiologic study was repeated. In 9 of 10 patients, supraventricular tachycardia could not be reinduced by programmed stimulation. In the remaining patient, nonsustained supraventricular tachycardia (greater than 10 beats, lasting less than 30 seconds) with a slower basic cycle length than that during the control period was provoked. Significant increases in the effective refractory period of the accessory pathway in both the anterograde (+26%, p less than 0.05) and retrograde (+40%, p less than 0.02) directions were noted, the magnitude of change being independent of the control effective refractory period. There were also significant increases in the effective refractory period of the right atrium (+24%, p less than 0.01) and the right ventricle (+15%, p less than 0.01) during long-term therapy with amiodarone. Over a mean follow-up period of 20 months, symptomatic control of the arrhythmia occurred in all patients; in only one patient treatment with amiodarone could not be continued because of side effects. These data establish the electrophysiologic basis for the effectiveness of amiodarone in the prophylactic control of refractory paroxysmal supraventricular tachycardia complicating the bypass tract syndromes.

Control of sudden recurrent arrhythmic deaths: Role of amiodarone

Patients resuscitated after out-of-hospital cardiac arrest have electrical instability of the myocardium, with 30% to 40% propensity for recurrent arrest in the first year. About 85% to 90% of such patients have complex ventricular ectopy and runs of ventricular tachycardia; in 70% to 80%, ventricular tachycardia or fibrillation are inducible by programmed electrical stimulation. The attempt to control recurrent cardiac arrest using these parameters and conventional antiarrhythmic drugs has yielded conflicting or variable results. Amiodarone was therefore studied in 40 consecutive patients (with previous cardiac arrests) in whom conventional antiarrhythmic therapy had proved ineffective or was not tolerated. The mean ejection fraction of the group was 0.29 ± 0.12. At a mean follow-up of 16 months (range 5 to 40 months) six patients had died, three from heart failure, one from liver failure (not drug induced), and two from sudden (presumably arrhythmic) death. Late occurrences of arrhythmia were found in two patients (complicated by digitalis intoxication in one). Ambulatory ECG recordings showed that amiodarone had a potent suppressant effect on ventricular ectopy and runs of VT, but electrophysiologic studies demonstrated that it did not inhibit inducible VT VF in 65% despite an excellent clinical outcome. Limiting adverse reaction was seen in only one patient; other relatively minor side effects occurred in 10% to 15% of patients receiving maintenance therapy. Our data provide further evidence for the effectiveness of amiodarone in life-threatening ventricular arrhythmias, with a potential for the prolongation of survival in patients resuscitated after out-of-hospital cardiac arrests.

Amiodarone for control of sustained ventricular tachyarrhythmia: Clinical and electrophysiologic effects in 51 patients

We evaluated the electrophysiologic effects of amiodarone and its ability to control ventricular arrhythmia in a selected group of 51 patients with refractory sustained ventricular arrhythmia. Amiodarone in doses of 400 to 800 mg/day prolonged refractoriness in the atria, atrioventricular (AV) node, and ventricle as well as conduction through the AV node and His-Purkinje system. Although It had no effect on measurements of sinus nodal function (sinus nodal recovery time and sinoatrlal conduction time), it prolonged the sinus cycle length and 2 patients required a permanent pacemaker for symptomatic sinus bradycardia. Amiodarone did not alter the ease of Inducibllity in any consistent manner, and only 5 of 43 patients (12%) who had Inducible ventricular tachycardia before amiodarone therapy had none induced during amiodarone treatment. The clinical effectiveness of amiodarone could be evaluated in 46 patients followed up for 8.6 ± 6 months (range 0.5 to 22). It provided effective therapy in 23 patients (50%), partly effective therapy in 13 (28%), and was ineffective in 10 (22%). Adverse effects were noted in 28 of 51 patients (55%), and in 11 of these (22%) the drug had to be discontinued because of adverse effects. We conclude that amiodarone Is a useful agent for the treatment of refractory sustained ventricular arrhythmia. Its use should be reserved for patients with life-threatening sustained arrhythmia because of the significant Incidence of adverse effects. Furthermore, good clinical response can be observed in patients receiving amiodarone In spite of continued Inducibllity.

Effectiveness of Amiodarone in Resistant Arrhythmias

Effectiveness of Amiodarone in Resistant Arrhythmias