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PubMed1996

Adherence and arrhythmic mortality in the cardiac arrhythmia suppression trial (CAST).

Patient adherence to therapy is essential to assess treatment efficacy, particularly in clinical trials. Active treatment usually is expected to benefit patients. The healthy adherer effect, the association or greater adherence to all health-promoting behaviors, including medication and overall concern for health, explains the improved survival of more adherent patients in both active and placebo medication groups of several clinical trials. The Cardiac Arrhythmia Suppression Trial (CAST), a placebo-controlled double-blind clinical trial of post-myocardial infarction (MI) patients with asymptomatic ventricular arrhythmias, in which active medication (encainide or flecainide) led to increased mortality, provided an opportunity to examine the relationship of adherence to survival from a different perspective. We consider whether adherence to active treatment was related to arrhythmic mortality and whether a healthy adherer effect might counteract the effect of treatment on mortality among patients taking active medication. Adherence (average pill count) at the first follow-up visit did not differ in the active treatment (92.2%, standard deviation (SD) = 11.97, n = 574) and placebo (90.8%, SD = 13.66, n = 579) groups. In a Cox proportional hazard regression model, medication adherence predicted arrhythmic mortality among the active (P < 0.0062) but not the placebo medication group. The effect of adherence on arrhythmic mortality was significant beyond the effects of ejection fraction, race, spouse, smoking status, diuretic medication, and history of MI. A 10% increase in adherence led to more than a threefold increase of risk of arrhythmic death. The design of the CAST, which included a titration phase, may have tended to select relatively adherent patients since only those whose arrhythmias were suppressed with active medication were randomized into the trial. The data do not support a strong healthy adherer effect in the CAST. There was no evidence in this study that a healthy adherer effect counterbalanced the effect of the active medication.

Anti-Arrhythmia Agents↗
PubMed1981

New drugs for treating cardiac arrhythmias.

The new and potent antiarrhythmic drugs herald an exciting era in the treatment of cardiac arrhythmias. Encainide, tocainide, and mexiletine are effective in treating acute and chronic ventricular arrhythmias. Verapamil promises to be the drug of choice for paroxysmal supraventricular tachycardia. Acetubolol provides the advantages of selective beta receptor blockade and has minimal influence on pulmonary function. Aprindine and amiodarone block conduction in accessory pathways and are very suitable for treating tachycardias associated with Wolff-Parkinson-White syndrome. Ethmozin is a phenothiazine derivative with potent antiarrhythmic effects. Many of these new agents are being used with striking success abroad and at specialized treatment centers for experimental research in the United States.

Acebutolol↗
PubMed1992

Effects of advancing age on the efficacy and side effects of antiarrhythmic drugs in post-myocardial infarction patients with ventricular arrhythmias. The CAST Investigators.

OBJECTIVE: To determine the effect of age on the response to anti-arrhythmic drugs. DESIGN: Randomized controlled trial comparing particular drugs. SETTING: Multi-institutional (The Cardiac Arrhythmia Suppression Trial, CAST). PARTICIPANTS: 2,371 patients, age less than 80, with ventricular arrhythmias after a recent myocardial infarction. Subjects classified by age as less than or equal to 55, 56-65, and 66-79 years. INTERVENTION: Upwardly titrated doses of encainide, flecainide or moricizine. After identification of a tolerated and effective dose of one of the drugs, participants were randomized to that drug and dose versus its placebo for up to 10 months. MAIN OUTCOME MEASURES: Efficacy of drug (suppression of ventricular premature depolarizations and/or non-sustained ventricular tachycardia), side effects and mortality. RESULTS: Older patients had more previous MIs, congestive heart failure (CHF), hypertension, NSVT, repolarization abnormalities, digitalis use, and diuretic use. They had less pathologic Q-waves or electrocardiographic injury pattern, and their left ventricular ejection fraction (LVEF) was lower. First dose VPD suppression with the first drug averaged 53% and is not associated with age (P = 0.29). Adverse events including death are more frequent in older patients taking study drugs (P less than 0.001). This trend is consistent in all three study drugs and at varying LVEFs. History of prior MI, low LVEF, VPD (in log scale), and digitalis therapy also correlates with adverse events (all P less than 0.05). Following adjustment for these factors, older age is an independent predictor of adverse events (relative risk 1.30 per decade of age, P less than 0.001). CONCLUSIONS: Older age increases the susceptibility to adverse cardiac events from a class of relatively toxic antiarrhythmic agents.

Adult↗
PubMed1993

Efficacy of type 1C antiarrhythmic agents for treatment of resistant atrial fibrillation.

In order to determine the efficacy of type 1C agents (flecainide, encainide, propafenone) in patients with atrial fibrillation who have failed to maintain sinus rhythm with type 1A agents (quinidine, procainamide, disopyramide), 147 patients, that were admitted into the John Dempsey Hospital with new or recurrent atrial fibrillation between 1987-1991, were studied retrospectively. Out of the total, 29 patients converted spontaneously to sinus rhythm, 14 patients were left in atrial fibrillation, and 104 patients were given a type 1A antiarrhythmic. Sixty-five of these patients remained in sinus rhythm (54% converted on drug alone, 46% required electrical cardioversion) for at least 6 months. Of the remaining 39 patients, 28 were given a type 1C antiarrhythmic; 13 were successfully converted (61% chemical, 39% electrical) to and remained in sinus rhythm for at least 6 months; the remaining 15 either failed to convert or reverted to atrial fibrillation. New onset atrial fibrillation had a significantly lower incidence of congestive heart failure (10%) than recurrent atrial fibrillation (33%; P < 0.01). No differences in digoxin, beta blocker use, or other clinical characteristics were seen either between type 1A or type 1C successes or failures. Similarly, echocardiographic dimensions did not predict success or failure with either class of agent. In conclusion, type 1C antiarrhythmics for suppression of recurrent atrial fibrillation represent a reasonable therapeutic alternative for suppression of atrial fibrillation in patients who have failed type 1A agents. Prognostic factors predicting success or failure remain undetermined.

Aged↗
PubMed1995

Association between ease of suppression of ventricular arrhythmia and survival.

BACKGROUND: We tested the hypothesis that patients whose ventricular arrhythmias are easy to suppress have a lower rate of arrhythmic death, defined as arrhythmic death and nonfatal cardiac arrest, the primary end point in the Cardiac Arrhythmia Suppression Trials (CAST-I and CAST-II), than patients whose ventricular arrhythmias are hard to suppress. In addition, we evaluated the association between ease of suppression of ventricular arrhythmias and mortality of all causes. METHODS AND RESULTS: CAST-I investigated the effect on arrhythmic death of ventricular premature depolarization (VPD) suppression achieved by three drugs, encainide, flecainide, and moricizine, at two different dose levels; CAST-II investigated the same effect, using moricizine alone at three dose levels. If suppression was achieved, patients were randomized to the effective active drug or corresponding placebo. To examine the independence of easily suppressed ventricular arrhythmias as a predictor of arrhythmic death, we adjusted statistically for other variables that were related both to ease of suppression and arrhythmic death. Patients with ventricular arrhythmias (n = 1778) that were easy to suppress had fewer arrhythmic deaths during follow-up than those with ventricular arrhythmias that were hard to suppress (n = 1173) (relative risk, .59; P = .003). Patients whose VPDs were easily suppressed were older and had a lower frequency of prior history of heart failure and myocardial infarction. They also had a higher incidence of anterior myocardial infarction, VPD frequency, and average ejection fraction. After adjusting for these variables, we found that easily suppressed ventricular arrhythmias were still significant predictors of arrhythmic death (relative risk, .66; P = .013). CONCLUSIONS: This study shows that the ease of VPD suppression identifies a subgroup of postmyocardial infarction patients who have low risk of arrhythmic death.

Aged↗
PubMed1991

[What is the latest in anti-arrhythmia therapy?].

Ventricular premature beats are an independent risk factor for sudden cardiac death. Class Ic antiarrhythmic drugs suppress these premature contractions. The Cardiac Arrhythmia Suppression Trial (CAST-Trial) tested the hypothesis that the suppression of ventricular premature beats after myocardial infarction reduces the incidence of cardiac death. The results of treatment in this low risk group were, however, disappointing. Cardiac mortality (mortality related to arrhythmia and myocardial infarction) was higher in the group treated with flecainide or encainide than in the placebo group. After a treatment period of 10 months, 89 of 1498 patients had died, 63 (8.3%) of them in the flecainide/encainide and only 26 (3.5%) in the placebo-treated group. Drugs that increase the refractory period of a myocardial substrate are obviously more effective in suppressing cardiac death than drugs that delay conduction. In the Basel Antiarrhythmic Study of Infarct Survival (BASIS study) patients with complex ventricular arrhythmias after infarction were treated with low dose amiodarone (200 mg/day). After a follow-up period of 12 months, mortality was lower in the amiodarone treated group (5/98 patients, 5%) than in the group that received no antiarrhythmic treatment (15/114 patients, 13%). Amiodarone was also more beneficial than individual antiarrhythmic therapy (mortality 10/100 patients, 10%). In the past few years no new antiarrhythmic drugs have been registered in Switzerland. Our pathophysiological and clinical knowledge has, however, increased and we know that the asymptomatic patient with low grade ventricular ectopies after myocardial infarction need not be treated. However, if we decide to use antiarrhythmic drugs, strict quality control of the effects of the treatment is mandatory.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiodarone↗
PubMed1989

The clinical use of class IC antiarrhythmic drugs.

Flecainide, encainide, and propafenone belong to class IC antiarrhythmic drugs. They are new and potent drugs which markedly depress Phase 0 of the action potential without affecting repolarization. Class IC drugs are very potent suppressors of premature ventricular complexes but their efficacy in the treatment of ventricular tachycardia is only comparable to that of class IA agents. Although noncardiac side effects are minimal, myocardial depression and serious proarrhythmic effects are not infrequently noted. A thorough understanding of the pharmacodynamics and toxicity potential of these drugs is therefore essential for their safe usage.

Anilides↗
PubMed1984

New drugs in the management of ventricular arrhythmias.

New antiarrhythmic drugs are chiefly assigned to Class 1C and 1B: "procainamide analogues" (acecainide, lorcainide, flecainide, encainide) and propafenone for the former, and mexiletine, tocainide and aprindine for the latter. Pharmacokinetics vary widely among the different antiarrhythmic agents. These and other problems which regulate therapeutic interventions, such as patient compliance, drug interactions, efficacy/toxicity ratio, drug combinations, and drug monitoring with plasma concentrations of antiarrhythmic agents are briefly considered.

Acecainide↗
PubMedDate not supplied

[New anti-arrhythmia drugs].

In this paper some of the new antiarrhythmic drugs are reviewed. The origin, electrophysiologic effects, mechanisms of action, pharmacokinetic properties, hemodynamic changes, clinical utilization with indications and contraindications as well as the collateral effects of: Verapamil Amiodarone, Aprindine, Encainide, Mexiletine and Tocainide are analyzed. A conclusion is drawn for each one of these drugs in accordance with the available information in the literature and the author's criteria and experience.

Amiodarone↗
PubMed1993

Interaction between selected sodium and potassium channel blockers in guinea pig papillary muscle.

Previous studies have reported that enhanced antiarrhythmic effects occur when agents that prolong repolarization are combined with agents that block the sodium channels. The mechanism(s) of this interaction have not been elucidated. In this study, the interactions between the prolongation of action potential duration (APD) by a potassium channel blocker and the reduction in the maximal upstroke velocity of phase 0 of action potential (Vmax) by sodium channel blockers were investigated in guinea pig papillary muscle using conventional microelectrode techniques. Agents that produce selective electrophysiologic effects were chosen, including low concentrations of barium chloride (BaCl2), which selectively blocks the inwardly rectifying potassium current without effects on other repolarizing or depolarizing currents, O-demethyl-encainide (ODME), which blocks the activated sodium channel with slow onset/offset kinetics, and mexiletine, which preferentially blocks the inactivated sodium channel with rapid onset/offset kinetics. Mexiletine (4 x 10(-6) M) decreased Vmax from 195 +/- 29 V/sec at baseline to 180 +/- 26 V/sec (P < .05). Whereas BaCl2 (10(-5) M) prolonged action potential duration, it had no effect on Vmax. However, the addition of BaCl2 to mexiletine synergistically decreased Vmax from 180 +/- 26 V/sec with mexiletine to 166 +/- 18 V/sec (P < .05). ODME (3 x 10(-7) M) decreased Vmax from 179 +/- 17 V/sec at baseline to 133 +/- 15 V/sec (P < .01). However, the addition of BaCl2 to ODME did not produce a further decrease in Vmax as compared with ODME alone. In summary, a synergistic effect on Vmax was observed when BaCl2 and mexiletine were combined.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1990

Clinical approach to paroxysmal atrial fibrillation.

In addition to the role of the electrophysiological substrate, paroxysmal atrial fibrillation depends on the modulation of the atrial tissues by the autonomic nervous system. Experimentally, models of atrial fibrillation can be based on either adrenergic or vagal stimulations that provoke the arrhythmia by disturbing in a different way conduction and refractory periods of the atrium. Clinically, the role of the autonomic nervous system can be suspected from the clinical history, and paroxysmal attacks can typically be observed either at daytime or at night, at exercise or at rest. Careful attention should be paid to the changes of heart rate that occur in the minutes or tens of minutes prior to the attacks, and the trend of acceleration or slowing of cardiac frequency observed in Holter tracings provides reliable indications of the state of the vago-sympathetic balance in these patients. During the attacks, the electrocardiographic aspect of atrial flutter alternating with a pattern of atrial fibrillation is typical of vagally dependent arrhythmias, whereas atrial tachycardia is more frequently observed at the onset of adrenergic atrial fibrillation. When the paroxysmal forms of arrhythmia are resistant to usual pure antiarrhythmic therapy including type IA agents and flecainide or encainide, one should take into account the role of the autonomic nervous system. Propafenone, or beta-blockers combined with type I drugs, are very effective every time an adrenergic factor is involved, but prevent the beneficial role of other agents if a vagal mechanism is predominant.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Fibrillation↗
PubMed1991

Operations for atrial fibrillation.

Atrial fibrillation is the most common of all sustained cardiac arrhythmias, yet it has no effective medical or surgical therapy. During the past decade, multipoint computerized electrophysiological mapping systems were used to map both experimental and human atrial fibrillation. On the basis of these studies, a new surgical procedure was developed for atrial fibrillation. Between September 25, 1987, and May 1, 1991, this procedure was applied in 22 patients with either paroxysmal atrial flutter (n = 2), paroxysmal atrial fibrillation (n = 11), or chronic atrial fibrillation (n = 9) of 2 to 21 years' duration. All patients were refractory to all antiarrhythmic medications and each patient failed an average of 5.2 drugs preoperatively. There were no operative deaths and all perioperative morbidity resolved. All 22 patients have been cured of atrial fibrillation with surgery alone. One late isolated episode of atrial flutter occurred in a patient who is now receiving encainide. Preservation of atrial transport function has been documented in all of the patients postoperatively and all have experienced marked clinical improvement.

Adult↗
PubMed1994

A consensus report on antiarrhythmic drug use.

During the past few years, a number of new antiarrhythmic agents have become available for use in the United States, encainide has been withdrawn from use, and others have had indications for use modified. Therefore, a meeting of arrhythmia specialists was convened in an attempt to develop guidelines for antiarrhythmic therapy. The resultant discussions and guidelines presented in this article address general issues such as the most important antiarrhythmic drug attributes, as well as therapy for particular arrhythmias such as premature ventricular contractions, ventricular tachycardia, ventricular fibrillation, ventricular ectopy, and supraventricular tachyarrhythmias.

Anti-Arrhythmia Agents↗
PubMed1990

Antiarrhythmic drug therapy for suppression of ventricular arrhythmia: experience with 122 patients treated for two years.

Although there are many reports of the short-term effectiveness of antiarrhythmic drugs for suppression of ventricular ectopic depolarizations, there are less data available on the long-term use of these drugs. We treated 122 patients for up to 2 years with antiarrhythmic drugs for suppression of frequent ventricular ectopic depolarizations. The percent suppression of ventricular ectopic depolarizations and nonsustained ventricular tachycardia for each drug was determined at 1, 3, 6, 12, 18, and 24 months of therapy. Among 33 patients treated with flecainide, the mean suppression of ventricular ectopic depolarizations (average of all data during 24 months) was 93 +/- 17% and of nonsustained ventricular tachycardia was 97 +/- 7%. In 27 patients treated with encainide, the mean suppression of ventricular ectopic depolarizations was 88 +/- 18% and of ventricular tachycardia was 95 +/- 16%. Among 26 patients treated with propafenone, the mean suppression of ventricular ectopic depolarizations was 77 +/- 32% and of ventricular tachycardia was 93 +/- 15%. For the 20 patients treated with moricizine, the mean suppression of ventricular ectopic depolarizations was 62 +/- 35% and of ventricular tachycardia was 90 +/- 14%. Among 16 patients treated with amiodarone, the mean suppression of ventricular ectopic depolarizations was 92 +/- 14% and of nonsustained ventricular tachycardia was 99 +/- 3%. In 54 of the 122 patients (44%), the study drug was stopped during 2 years of therapy because of death (2 sudden, 2 unwitnessed and 6 noncardiac), side effects (21 patients), lack or of loss of efficacy (13 patients), and noncompliance (10 patients).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Early and late proarrhythmia from antiarrhythmic drug therapy.

Antiarrhythmic drug therapy is used with the hope of suppressing arrhythmias and therefore decreasing their associated symptoms or prolonging life. Unfortunately, many antiarrhythmic drugs have the opposite effect of exacerbating or provoking arrhythmias, a phenomenon that is termed proarrhythmia when such an event is specifically due to the drug in use. Early proarrhythmic events (within 30 days of initiation of drug use) have been reasonably well characterized and are predicted by either type of drug employed or the nature of the patient's cardiac disease and arrhythmia type. Late proarrhythmic events, as defined by placebo-controlled trials, have now been recognized as an increased risk of arrhythmic death in patients on antiarrhythmic drugs after many months of therapy. Initially, this late proarrhythmic event was identified with encainide and flecainide, but now several new studies have demonstrated that the risk of late proarrhythmia of comparable magnitude may be present in patients subjected to commonly used drugs, such as quinidine, mexelitine, etc. At present, only moricizine and the class II drugs (beta-adrenergic blockers) appear not to have this potential late proarrhythmic response. Therefore, before instituting antiarrhythmic drug therapy, the physician must be able to quantitate the degree of proarrhythmia and other risks of such therapy, as compared to their potential benefit, to define the proper indications for these agents.

Anti-Arrhythmia Agents↗
PubMed1990

Comparative hemodynamics of antiarrhythmic drugs.

It is important to consider the hemodynamic effects of antiarrhythmic drugs, because the majority of patients who require these drugs already have compromised cardiac function. The presently available antiarrhythmic agents vary in their potential for producing negative inotropic effects on the myocardium; they vary, as well, as to the mechanisms by which these effects are produced. The drugs in each of the Vaughan-Williams' classes are discussed in terms of the extent to which they affect cardiac output and the mechanisms by which they may depress cardiac function. Practically all antiarrhythmic agents can decrease cardiac output when administered intravenously. However, when given orally to patients with congestive heart failure, amongst Class I agents, encainide and mexilitine appear to have a reasonably good safety record with respect to the worsening of congestive heart failure. Class III antiarrhythmics also appear to be well tolerated in patients with severe LV dysfunction.

Administration, Oral↗
PubMed1993

Use-dependent block of the delayed K+ current in rabbit ventricular myocytes.

Block of the delayed K+ current, iK, and the concomitant increase in refractoriness is considered an alternative to a decrease of conduction in the treatment of reentry arrhythmias. Ideally an agent should selectively prolong the action potential at high frequencies. A minimum requirement is use-dependent block. A number of drugs were tested for the existence of use dependence by applying a train of depolarizing clamps to single cardiac myocytes of the rabbit ventricle. Development of block during a long depolarizing clamp and recovery from block were also measured. Five of the nine drugs tested, i.e., disopyramide, encainide, quinidine, sotalol, and tedisamil, did not show use dependence. When a train of depolarizing clamps was applied, block was already present for the first depolarization and did not increase with repetition of the pulse. This result suggests block of the channel in the rested state or a very fast block of the open channel. Almokalant and amiodarone, and to a lesser extent dofetilide and E4031, showed use-dependent block, i.e., block increased during the train of depolarizing clamps. The time constant for the open channel block was 1.07 seconds for almokalant and 0.67 seconds for amiodarone. Recovery from block for almokalant and amiodarone was very slow: time constants measured at -50 mV were 13.9 and 12.7 seconds, respectively. For dofetilide it was in the order of minutes. The existence of this slow recovery explains why frequency-dependent changes in block were negligible or absent for frequencies above 0.5 Hz. Future research should be aimed to select drugs with a slower onset of active state block and faster recovery from block.

Action Potentials↗
PubMed1993

Clinical significance of genetic influences on cardiovascular drug metabolism.

Inherited differences in metabolism may be responsible for individual variability in the efficacy of drugs and the occurrence of adverse drug reactions. Among the cardiovascular drugs reported to exhibit genetic polymorphism are debrisoquine, sparteine, some beta-adrenoceptor antagonists, flecainide, encainide, propafenone, nifedipine, procainamide, and hydralazine. The implications of genetic differences in the metabolism of these drugs for cardiovascular therapeutics is the subject of this review.

Adrenergic beta-Antagonists↗