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At least 379 records · Page 21Linked to original sources
PubMed1994

[Persistent atrial flutter induced by propafenone (Rytmonorm)].

The case history of two patients with atrial fibrillation are presented. In order to prevent/terminate fibrillation propafenone (Rytmonorm, 450-600 mg/day) was started, however this therapy resulted in permanent atrial flutter of 230-270/min mainly with 2:1 antrioventricular conduction. Analyzing the cases the authors emphasize that although Class Ic antiarrhythmic drugs (flecainide, encainide, propafenone) are capable to prevent or terminate atrial fibrillation, they may also induce atrial flutter in approximately 3.5-5% of these patients. The mechanism and recognition of this atrial proarrhythmic action are discussed.

Aged↗
PubMed1994

Class I antiarrhythmic drugs: allosteric inhibitors of [3H] batrachotoxinin binding to rat cardiac sodium channels.

This study assessed whether class I antiarrhythmic drugs allosterically inhibit [3H]batrachotoxinin A 20-alpha-benzoate ([3H]BTXB) binding to sodium channels on freshly isolated rat cardiac myocytes. All class I drugs tested inhibited equilibrium [3H]BTXB binding in a concentration-dependent manner. Scatchard analysis showed that disopyramide, flecainide, transcainide, lidocaine and amiodarone reduced [3H]BTXB maximum binding (Bmax) whereas procainamide, mexiletine, quinidine, quinine, tocainide, propafenone, encainide and O-demethylencainide increased [3H]BTXB KD but had little effect on Bmax. Kinetic [3H]BTXB binding assays were used to assess the mechanism by which class I drugs inhibit [3H]BTXB binding. Drugs that increase the unidirectional dissociation rate constant (k-1) of [3H]BTXB probably bind to sodium channels to which [3H]BTXB is already bound. Although all class I drugs increased the k-1 of [3H]BTXB, they did so weakly and at concentrations above the IC50 values of the drugs. Thus, drug binding to [3H]BTXB-bound channels does not appear to be the predominant mechanism underlying their ability to inhibit [3H]BTXB binding. Conversely, drugs which allosterically decrease the unidirectional association rate constant (K+1) of [3H]BTXB probably bind to channels to which [3H]BTXB is not already bound. All class I drugs decreased the k+1 of [3H]BTXB, indicating drug binding to [3H]BTXB-free channels. The estimated affinities of drugs for [3H]BTXB-free channels correlated closely with the IC50 values of these drugs (r = 0.94, P < .001), suggesting that this effect is a common and major determinant in their ability to inhibit [3H]BTXB binding. The results are discussed in light of electrophysiologic theories of class I antiarrhythmic drug action.

Allosteric Regulation↗
PubMed1993

Pharmacologic therapy in patients with ventricular tachyarrhythmias.

Table 5 can be used as framework for a summary of the previous discussion on pharmacologic therapy for ventricular tachyarrhythmias. The system for grading the severity of symptoms of ventricular tachyarrhythmias, previously presented in Table 3, is arranged vertically along the left side of Table 5. Horizontally across the top, patients are grouped according to the presence or absence of structural heart disease, and those with structural heart disease are further dichotomized according to left ventricular ejection fraction. As can be seen, patients with class I symptoms should not be treated whenever possible, although in patients with reduced left ventricular function (especially coronary heart disease), an argument can be made for empirical treatment with beta-adrenoceptor blocking agents whenever possible. Patients with class II symptoms can be treated empirically with beta-adrenoceptor blocking agents. Other antiarrhythmic agents may be safer when there is no underlying structural heart disease, but this has not been proved. The use of antiarrhythmic agents other than beta-adrenoceptor blocking agents in patients with class II symptoms should probably be guided and monitored by ambulatory electrocardiographic recording and exercise tolerance testing. In the patient with hemodynamically stable ventricular tachycardia, electrophysiologic-guided therapy is probably preferable whenever possible. Encainide, flecainide, and similar drugs should be avoided when there is a possibility of residual ventricular premature depolarizations of three or more per hour. Some uncertainty remains concerning the treatment of patients with class III and class IV symptoms and no structural heart disease. Some patients may fall into a specific group that is very responsive to drug therapy. These patients should probably be treated like other patients with class III and class IV symptoms. Electrophysiologic testing may be helpful. When such patients have a reproducibly induced sustained ventricular tachyarrhythmia, it is likely that antiarrhythmic drug therapy will render the arrhythmia noninducible, and that they will do well while receiving long-term pharmacologic therapy. When such patients do not have a reproducibly induced sustained ventricular tachyarrhythmia, the main controversy is whether therapy is needed. If it is decided that such a patient needs therapy, the choice is usually between empiric amiodarone and an ICD, although catheter ablation may be helpful in selected instances. Patients with class III and class IV symptoms who have structural heart disease require therapy. Although this continues to be an evolving area of investigation, for many of these patients, the initial attempt at therapy should be pharmacologic.(ABSTRACT TRUNCATED AT 400 WORDS)

Anti-Arrhythmia Agents↗
PubMed1996

What have clinical trials taught us about proarrhythmia?

Proarrhythmia is defined as the developmental of a new arrhythmia, or the worsening of a preexisting arrhythmia, following the institution of anti-arrhythmic therapy. The most important manifestation of proarrhythmia is sudden arrhythmic death. Possible mechanisms of proarrhythmia include early afterdepolarizations, dispersion of repolarization, a conduction-slowing effect that promotes reentry, and the interaction of arrhythmic drugs with ischemia. Recent trials of arrhythmic drugs have focused attention on the increase in mortality due to some of these drugs. In many studies, the effect of placebo has been compared with that of antiarrhythmic drugs on mortality in high-risk patients following myocardial infarction (MI). In most of these trials, anti-arrhythmic drugs were associated with an increase in mortality has been most clearly shown with encainide, flecainide, moricizine and d-sotalol. In addition, increased mortality has been suggested in patients treated with antiarrhythmics for atrial fibrillation especially in the presence of structural heart disease. In contrast, several post-MI benefit. This suggests that amiodarone may be safe for the treatment of arrhythmias in the post-MI patient. Further evidence will come from two majors studies (CAMIAT and EMIAT) which should be available by early 1996.

Amiodarone↗
PubMed1996

[Class-I antiarrhythmic drugs].

Classification, mechanism of action, pharmacokinetic properties and clinical applications of class-I antiarrhythmic agents were summarized. Class-I drugs were subdivided into three groups, Ia, Ib, Ic. This subclassification is based on their action to modify the action potential duration. In the Cardiac Arrhythmia Suppression Trial (CAST), flecainide and encainide were associated with greater mortality than placebo in patients with non-life threatening arrhythmias. Results of CAST and other megatrials suggested that antiarrhythmic agents were unsafe in some groups of patients and the limitation of antiarrhythmic therapy. Proarrhythmia and combination therapy of antiarrhythmic agents were mentioned.

Anti-Arrhythmia Agents↗
PubMed1998

Toward improved antihypertensive therapy with calcium channel blockers.

Outcome trials are the scientific method of determining if an antihypertensive agent really works; and for a therapy to work well, it should reduce mortality. The FDA requires only that blood pressure be controlled safely, but current evidence-based medicine demands answers to the mortality/morbidity question. We need this outcome trial information on all the classes of antihypertensives, including calcium channel blockers. For example, we often rely on surrogate endpoints such as control of blood pressure or control of PVCs. If we treat hypertensives with PVCs using beta-blockers or calcium channel blockers, we may see both control of blood pressure and suppression of PVCs. However, as we learned from the CAST trial with flecainide and encainide, PVCs can be controlled, but mortality may increase. On the other hand, the Lewis trial demonstrated that captopril, an ACE inhibitor, reduced proteinuria, which is another surrogate endpoint in diabetic hypertensives with nephropathy, although blood pressure was controlled with diuretic and conventional therapy. Importantly, captopril also reduced morbidity and mortality without influencing blood pressure. Unfortunately, there are no outcome trials measuring mortality endpoints for most of the antihypertensive agents in use today, especially in patients with uncomplicated hypertension.

Black People↗
PubMed1992

Classifying antiarrhythmic actions: by facts or speculation.

Classification of antiarrhythmic actions is reviewed in the context of the results of the Cardiac Arrhythmia Suppression Trials, CAST 1 and 2. Six criticisms of the classification recently published (The Sicilian Gambit) are discussed in detail. The alternative classification, when stripped of speculative elements, is shown to be similar to the original classification. Claims that the classification failed to predict the efficacy of antiarrhythmic drugs for the selection of appropriate therapy have been tested by an example. The antiarrhythmic actions of cibenzoline were classified in 1980. A detailed review of confirmatory experiments and clinical trials during the past decade shows that predictions made at the time agree with subsequent results. Classification of the effects drugs actually have on functioning cardiac tissues provides a rational basis for finding the preferred treatment for a particular arrhythmia in accordance with the diagnosis.

Animals↗
PubMed1993

Efficacy of class 1C antiarrhythmic agents in patients with inducible ventricular tachycardia refractory to therapy with class 1A antiarrhythmic drugs.

The efficacy of class 1C antiarrhythmic agents was determined in 36 patients with inducible sustained monomorphic ventricular tachycardia during baseline electrophysiology study (EPS), who continued to have inducible monomorphic ventricular tachycardia during EPS on class 1A antiarrhythmic therapy. Of 12 patients who partially responded to class 1A drugs, 11 (91.7%) continued to have a partial response during EPS on class 1C therapy, whereas one patient did not respond. Of 24 nonresponders to class 1A therapy, 2 (8.3%) responded during EPS on class 1C therapy, 7 (29.2%) partially responded, and 15 (62.5%) did not respond. In the 24 nonresponders to class 1A therapy, 9 of 17 patients (53%) with left ventricular ejection fraction (EF) > or = 30% responded or partially responded to class 1C therapy, compared with none of 7 patients with EF < 30% (P < .05). The EPS on class 1C agents in patients who fail to respond to class 1A therapy may be warranted only in those with EF > or = 30%.

Adult↗
PubMed1990

Clinical aspects of trial design: what can we expect from the cardiac arrhythmia suppression trial?

The controlled clinical trial, i.e., a prospective study that compares the effect of one or more interventions against a control in human subjects, is the most definitive method to determine the benefit/risk ratio for a treatment. Some of the elements are a clear statement of the primary and secondary hypothesis, carefully defined end points, randomization, double blinding, and concomitant controls for the experimental treatment using either placebo or standard treatment. Randomization tends to produce study groups that are comparable with respect to both known and unknown factors that influence the outcome, and also removes bias in the assignment of subjects to treatments to ensure that statistical hypothesis testing will have valid significance levels. An adequate sample size is critically important for a successful trial. The Cardiac Arrhythmia Suppression Trial (CAST) is a randomized, placebo-controlled, double-blind, international, multicenter clinical trial to determine whether suppression of ventricular arrhythmias after myocardial infarction with long-term antiarrhythmic drug treatment will reduce arrhythmic death. Survivors of myocardial infarction who are less than 80 years of age and have greater than or equal to six ventricular premature depolarizations (VPD) per hour on a 24-hour continuous ECG recording obtained between 6 days and 2 years after myocardial infarction are eligible for CAST.(ABSTRACT TRUNCATED AT 250 WORDS)

Anilides↗
PubMed1982

Selection of an antiarrhythmic drug for a sudden-death-prevention trial.

Several therapeutic approaches have sought to prevent the occurrence of sudden cardiac death. Many sudden deaths are presumed to be due to an arrhythmia, but the drugs best known for antiarrhythmic activity, the local anesthetic agents, have not been suitable prophylactic agents because of their toxicities and other undesirable pharmacologic characteristics. Several new drugs in this class have been synthesized and are currently being tested for antiarrhythmic activity in clinical trials. One of them may prove to be worthy of a large-scale clinical trial to determine whether chronic arrhythmia suppression reduces the risk of sudden death. The characteristics of the "ideal" antiarrhythmic agent are discussed, and a brief summary of the drugs currently being tested in the United States is presented. The discussion of each drug emphasizes the characteristics that might make it suitable--or unsuitable--for use in a sudden-death trial. Many agents being tested are clearly not satisfactory for such a trial. However, they may be prototypes for an ideal drug or combination of drugs that might yet be developed.

Acecainide↗