Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Disopyramide”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,333 records · Page 74Linked to original sources
PubMed1991

Antiarrhythmic and cardiovascular profiles of the fused indole compound (3aR,12R,12aR,12bS)-12-amino-2,3,3a,4,11,12,12a,12b-octahydro-10-hydrox yisoquino [2,1,8-lma]carbazol-5(1H)-one hydrochloride 1.5 hydrate.

Antiarrhythmic and cardiovascular profiles of a fused indole compound, (3aR,12R,12aR,12bS)-12-amino-2,3,3a,4,11,12,12a,12b -octahydro- 10-hydroxyisoquino [2,1,8-lma]carbazol-5(1H)-one hydrochloride 1.5 hydrate (RS-2135, CAS 133775-36-7), were investigated in anesthetized dogs. Class I antiarrhythmic agents such as disopyramide, lidocaine, mexiletine and flecainide were used as reference compounds. RS-2135 exerted more potent antiarrhythmic activity than reference compounds against ouabain-induced arrhythmias in dogs. The onset of action was slow, but the duration of action was longer than with the other compounds tested. The agent suppressed the conduction in the atrium, A-V node and ventricle more markedly than the reference compounds. RS-2135, however, did not change blood pressure and heart rate at a dose 5 times the dose for antiarrhythmic activity and decreased cardiac contractility to a lesser extent than the reference compounds.

Animals↗
PubMedDate not supplied

Drug-induced torsade de pointes.

Three patients who developed torsade de pointes associated with antiarrhythmic or psychotropic drugs are described, and the electrocardiographic characteristics, clinical presentation, predisposing factors, and management of this form of ventricular tachycardia are reviewed. The first patient was a 56-year-old schizophrenic man receiving thioridazine hydrochloride, trifluoperazine hydrochloride, and benztropine mesylate who was admitted to a hospital after a syncopal episode. Subsequently, the patient experienced several episodes of ventricular tachycardia combined with multifocal premature ventricular contractions (PVCs) and torsade de pointes; the arrhythmias were attributed to antipsychotic therapy. The second patient was a 69-year-old man who experienced ventricular tachycardia that progressed to ventricular fibrillation 41 days after surgery. Quinidine sulfate probably induced the ventricular tachycardia, which was identified as torsade de pointes. The third patient was a 71-year-old man admitted to the hospital for treatment of refractory ventricular arrhythmias. Previous drug therapy with quinidine sulfate and procainamide hydrochloride had been associated with torsade de pointes. Despite unsuccessful treatment of ventricular ectopy, the patient was discharged on maintenance therapy with pindolol, topical nitrates, and phenytoin. No additional episodes of torsade de pointes have been observed. Torsade de pointes is characterized by polymorphous electrocardiographic appearance and delayed repolarization (prolonged QT interval). It may occur in association with a number of disease states and also as a complication of treatment with therapeutic doses of drugs that affect repolarization (quinidine, disopyramide, procainamide, and phenothiazines). Clinical outcomes range from asymptomatic, self-terminating arrhythmias to ventricular fibrillation resulting in cardiac arrest. The definitive emergency therapy for torsade de pointes is overdrive pacing; cautious isoproterenol administration can also be used. Lidocaine and bretylium are often ineffective in treating this form of ventricular tachycardia. Potassium and magnesium repletion appear to be essential in abolishing drug-induced torsade de pointes. Drug-induced torsade de pointes is best prevented by avoiding agents known to induce arrhythmias in patients with a pre-existing prolonged QT interval. Periodic serum electrolyte assessment is warranted, and new drugs that prolong the QT interval should be considered potential causative agents of torsade de pointes.

Acecainide↗
PubMed1987

Antiarrhythmic agents for chronic ventricular arrhythmias.

A vast array of new antiarrhythmic agents have joined the old agents among the clinician's available resources. While treatment of ventricular arrhythmias is completely justifiable for patients with symptoms, their use to prevent sudden cardiac death has not yet been established. Because of their potential risks, the benefit/risk ratio must always be kept in mind. If we elect to treat patients who have benign or potentially lethal ventricular arrhythmias (usually to eliminate refractory symptoms) we typically begin with either a beta blocker or one of the new potent class IC antiarrhythmic agents such as flecainide or encainide. These drugs cause few side effects, no organ toxicity, and in the case of encainide or flecainide, have marked potency. Few important proarrhythmic effects are seen with these potent drugs in this group of patients. If these fail, one can try either a class IA or IB agent or a combination of a IA and IB agent. We always avoid amiodarone. In patients with lethal ventricular arrhythmias, one should choose a drug without negative inotropic potential such as quinidine or encainide as initial therapy. The combination of IA and IB agents should also be considered early in therapy. In patients with overt congestive heart failure with markedly depressed left ventricular function in the setting of lethal arrhythmias, disopyramide, beta blockers, and flecainide should be avoided. Amiodarone is used in this population only when the other available agents have proven to be ineffective or badly tolerated.

Amiodarone↗
PubMed1988

Chronic atrial fibrillation. Long-term results of direct current conversion.

One hundred consecutive patients admitted in 1980-82 for direct current conversion of chronic atrial fibrillation (AF) were followed. The first attempt to convert was made without the institution of class I antiarrhythmics. If AF relapsed, patients were selected for further conversions, in connection with which quinidine or disopyramide treatment was instituted. The proportion of patients maintaining sinus rhythm (SR) one and two years after the first conversion was 23% and 16%, after the second conversion 40% and 33% and after any number of conversions [1-12] 54% and 41%. Fifty-three per cent of the patients were symptomless before at least one conversion. Of the patients maintaining SR two years after conversion, 46% did not receive antiarrhythmic therapy. More than two conversions should be exceptional since symptoms of AF are often absent and the additional effect of further conversions is minor. A first attempt to convert without antiarrhythmics identifies a substantial proportion of patients maintaining SR without any prophylactic antiarrhythmic therapy.

Adult↗
PubMed1985

N-(2,6-Dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate (SUN 1165): a new potent and long-acting antiarrhythmic agent.

N-(2,6-Dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate (SUN 1165) at the doses of 2.5 mg/kg i.v. and 3-10 mg/kg i.d. or p.o. restored sinus rhythm from ventricular multifocal arrhythmias induced by two-stage ligation of the coronary artery in the conscious dogs, Harris model, without causing gastrointestinal and central nervous system side effects. The onset of antiarrhythmic action was 1-2 min after i.v. injection and 15-30 min after an oral administration, and this action lasted longer than 1 h after i.v. and 6 h after oral administration, respectively. SUN 1165 was also effective in suppressing ouabain-and halothane-epinephrine-induced ventricular arrhythmias at the doses of 1.7 and 1.2 mg/kg i.v. and 1-10 mg/kg i.d. It did not impair parasympathetic nerve activity. SUN 1165 showed a local anesthetic or membrane stabilizing activity comparable to lidocaine and disopyramide. In conscious dogs without arrhythmia, SUN 1165 had no deleterious cardiohemodynamic effect and no gross behavioral effect at the oral doses of 3 and 10 mg/kg. Thus, it is concluded that SUN 1165 is an orally effective, potent and long-acting class I type antiarrhythmic agent without serious side effects common to other antiarrhythmic drugs.

Anesthetics, Local↗
PubMed1979

Feedback control in the management of cardiac arrhythmias.

We have devised a computer technique for the control of drug therapy in the management of cardiac arrhythmias. In our system the computer monitors the electrocardiogram in real time, determines the percent of premature ventricular beats (PVBs) using a correlation coefficient technique, and compares it to a desired rhythm. If the measured rhythm departs from the setpoint, an antiarrhythmic drug is infused by the computer. Based upon the pharmacokinetics of the drug, the infusion is delivered so as to attain an immediate change in the blood drug concentration utilizing an exponential infusion technique. The control algorithm is a modified proportional controller. Closed-loop control experiments have been performed in canines with an induced myocardial infarction. The antiarrhythmic agent disopyramide phosphate was used to correct the resulting arrhythmias. Our results suggest that computer control of drug therapy can profitably be applied to the management of cardiac arrhythmias in the coronary care unit.

Animals↗
PubMedDate not supplied

Electrophysiological effects of 711389-S, a new antiarrhythmic agent, on guinea-pig isolated cardiac muscle.

The effects of 711389-S, a newly developed antiarrhythmic agent, on transmembrane action potentials were examined in isolated papillary muscles of guinea pigs. 711389-S above 10(-6) M caused a dose-dependent decrease in the maximum upstroke velocity (Vmax) and a slight prolongation of the action potential duration (APD) at a late repolarization phase. The resting potential, the amplitude, and APD at an early repolarization phase were not affected even at 10(-5) M. In the presence of 711389-S, trains of stimuli higher than 0.1 Hz led to an exponential decline in Vmax to a new plateau level. This use-dependent block was augmented at the higher stimulation frequency. The time constant for the recovery from the use-dependent block was 47 s at 3 X 10(-6) M. At 1.0 Hz, 711389-S caused an appreciable shift (6.8 mV) of the curve relating the membrane potential and Vmax along the voltage axis in the hyperpolarizing direction, but no shift at 0.1 Hz. The antagonistic effect of 711389-S against acetylcholine in guinea-pig isolated atria was much less than that of disopyramide. These findings suggest that 711389-S has similar electrophysiological effects to those of other Class Ia antiarrhythmic drugs but has much less anticholinergic activity.

Acetylcholine↗
PubMed1983

Antiarrhythmic, hemodynamic and cardiac electrophysiological evaluation of N-(2,6-dimethylphenyl)-N'-[3-(1-methylethylamino)propyl]urea (Wy-42,362).

The antiarrhythmic, hemodynamic and cardiac electrophysiological effects of (Wy-42,362, in the following briefly called Wy) N-(2,6-dimethylphenyl)-N'-[3-(1-methylethylamino)propyl]urea were examined in several experimental preparations. Wy is an effective antiarrhythmic agent when administered i.v. or p.o. in various models of canine cardiac arrhythmia. Wy elevated ventricular fibrillatory threshold voltage and reverted ouabain-induced, 24- and 48-h post coronary artery ligation-induced Ventricular arrhythmias,, and aconitine-induced atrial arrhythmias at i.v. doses of 4-15 mg/kg. Wy lacked anticholinergic or CNS-stimulant activity. In closed-chest anesthetized dogs, Wy at 15 or 25 mg/kg i.v. decreased cardiac output (CO). Unlike disopyramide, i.v. Wy did not produce greater reductions in CO in anesthetized dogs subjected to previous infarction (72-96 h) as compared to normal intact dogs. Wy at 10 or 15 mg/kg i.v. produced slight to moderate decreases in contractile force and showed a tendency to reduce heart rate and blood pressure. Wy produced a generalized depression of cardiac impulse conduction in open-chest, pentobarbital anesthetized dogs but conscious dogs exhibited relatively little ECG evidence of such depression following double the therapeutic i.v. dose. In isolated canine cardiac Purkinje fibers bathed in normal K+-containing physiological solutions. Wy (1-2 X 10(-5) mol/l) produced significant reductions in action potential duration while 2 X 10(-5) mol/l also reduced Vmax and shifted membrane responsiveness curves to the right suggesting depressant action on fast Na+ channel conductance. The data indicate that Wy is an effective antiarrhythmic agent presumably with a class I mechanism of action.

Aconitine↗
PubMed1980

[Pharmacokinetics of anti-arrhythmics. 2. Clinical applications].

The clinical usage of antiarrhythmic drugs may pose problems which could be solved by the direct application of the basic principles of pharmacokinetics. These problems involve the calculation of intravenous infusion rates and or oral dosages. Examples are provided by the rate of initial infusion of lignocaine in order to obtain a concentration within the therapeutic range, the eventual adjustment of this rate of infusion and the calculation of a loading dose. As regards the oral route, the calculation of the doses of procainamide is taken as an example. The estimation of the serum procainamide is a method for determining whether the dose should be increased or whether the drug is ineffective when no clinical result is observed. The pharmacokinetics of the main antiarrhythmic drugs are reviewed; procainamide, quinidine, propanolol, phenytoin, disopyramide. The therapeutic dose, clearance, extraction coefficient, bioavailability and half-life are the object of particular study. The fractioning of the dose and the total dose in a 24 hour period depend on these factors. The effects of cardiac, renal and hepatic failure on the clearance of each drug are recalled. These pharmacokinetic principles help the clinician not only in the prescription of an antiarrhythmic drug but also in deciding on the indications for drug serum concentration, estimations which are particularly useful in some difficult clinical situations, and in interpreting the results.

Administration, Oral↗
PubMed1981

[Determination of plasma concentrations of anti-arrhythmia agents].

The measurements of the plasma concentrations of antiarrhythmic drugs is useful both for studying the pharmacokinetics and bio-availability of a drug, and for assessing the relationship between pharmacological activity and plasma levels in clinical practice so that dosages may be adapted to obtain optimal efficacity in each individual patient and to avoid side-effects caused by drugs with low therapeutic indices. Many methods are available, including spectrophotometry, spectrofluorometry, gas chromatography, liquid chromatography and immuno-enzymology. The practicability, sensitivity and specificity of these techniques are compared with respect to their objectives. Particular attention is paid to the principal antiarrhythmic agents with fairly well defined zones of efficacity: procainamide, quinidine, disopyramide, propranolol, lignocaine and mexiletine.

Anti-Arrhythmia Agents↗
PubMed1980

Evaluation of the antiarrhythmic efficacy of mexiletine in patients with chronic ventricular arrhythmias.

For the evaluation of arrhythmias and the assessment of antiarrhythmic therapy prolonged periods of recording, as provided by the Holter system, are needed. The 12 lead electrocardiogram and rhythm strips are unsuitable for these purposes. However an exercise test may provide useful additional information. In two trials mexiletine was compared with other antiarrhythmic drugs (atenolol, disopyramide, lorcainide) and placebo. In both trials mexiletine was shown to have a good antiarrhythmic efficacy on chronic ventricular premature beats. The high incidence of side-effects was probably due to the high dosage used.

Arrhythmias, Cardiac↗
PubMed1995

The relationship between neurally mediated hypotension and the chronic fatigue syndrome.

OBJECTIVE: To compare the clinical symptoms and response evoked by upright tilt-table testing in healthy individuals and in a sample of those satisfying strict criteria for chronic fatigue syndrome. DESIGN: Case-comparison study with mean (SD) follow-up of 24 (5) weeks. SETTING: Tertiary care hospital. PATIENTS AND OTHER PARTICIPANTS: A sample of 23 patients with chronic fatigue syndrome (five men and 18 women; mean age, 34 years), each of whom fulfilled the strict diagnostic criteria of the Centers for Disease Control and Prevention, was recruited from regional chronic fatigue support groups and from the investigators' clinical practices. There were 14 healthy controls (four men and 10 women; mean age, 36 years). INTERVENTIONS: Each subject completed a symptom questionnaire and underwent a three-stage upright tilt-table test (stage 1, 45 minutes at 70 degrees tilt; stage 2, 15 minutes at 70 degrees tilt with 1 to 2 micrograms/min of isoproterenol; and stage 3, 10 minutes at 70 degrees with 3 to 4 micrograms/min of isoproterenol). Patients were offered therapy with fludrocortisone, beta-adrenergic blocking agents, and disopyramide, alone or in combination, directed at neurally mediated hypotension. MAIN OUTCOME MEASURES: Response to upright tilt and scores on symptom questionnaires prior to and during follow-up. RESULTS: An abnormal response to upright tilt was observed in 22 of 23 patients with chronic fatigue syndrome vs four of 14 controls (P < .001). Seventy percent of chronic fatigue syndrome patients, but no controls, had an abnormal response during stage 1 (P < .001). Nine patients reported complete or nearly complete resolution of chronic fatigue syndrome symptoms after therapy directed at neurally mediated hypotension. CONCLUSIONS: We conclude that chronic fatigue syndrome is associated with neurally mediated hypotension and that its symptoms may be improved in a subset of patients by therapy directed at this abnormal cardiovascular reflex.

Adolescent↗
PubMedDate not supplied

[Demonstration of the fibrillatory effect of class I anti-arrhythmia agents based on the time of fibrillation onset and electrical threshold in myocardial ischemia].

In recent clinical studies, certain class I antiarrhythmic drugs (flecaïnide, lidocaïne) appeared to be responsible for an increase in mortality, when used to treat ventricular arrhythmias occurring after or during infarction. Experimentally, in pigs whose rate of ventricular beats was kept constant by pacing, all the studied class I antiarrhythmic drugs, disopyramide, lidocaïne and flecaïnide, proved to be to a variable degree capable of shortening time to onset of fibrillation (TOF) elicited by controlled myocardial ischemia. Fibrillation occurred at the end of the decline, under the influence of ischemia, of electrical fibrillation threshold (EFT) down to near 0 mA. The fall of EFT to this level was checked by ischemias of increasing duration to be hastened by the cited antiarrhythmic drugs. In other words, these drugs exert a profibrillatory effect in the ischemic heart.

Animals↗
PubMed1993

[Antiarrhythmic treatment after reduction of atrial fibrillation by external shock].

Among the drugs recommended to prevent recurrences of atrial fibrillation after external electric shock, antiarrhythmic agents of classes Ia (quinidine, disopyramide), Ic (cibenzoline, flecainide, propafenone) and III (sotalol) seem to have the same effectiveness in maintaining the sinus rhythm in about 50 percent of the cases after 6 months and one year. Amiodarone, seldom used as first-line treatment, appears to be the most effective drug. The percentage of side-effects requiring discontinuation of treatment is the same for all drugs (about 10 percent). All these drugs have potential proarrhythmic effects. In case of recurrence electric shocks can be repeated in some special cases. The therapeutic strategy according to the clinical context (atrial fibrillation of vagal nerve or catecholergic origin, normal or altered left ventricular function) is discussed.

Amiodarone↗
PubMed1993

[Two cases of idiopathic ventricular fibrillation with interesting electrocardiographic findings].

We encountered two cases of ventricular fibrillation (VF) without overt heart disease. The first case we report is that of a 47-year-old man, and the second case is a 39-year-old man. VF occurred in the night unrelated to myocardial ischemia or myocarditis. Their basic ECGs showed normal sinus rhythm, but neither QT prolongation nor abnormal Q wave was seen. But we could see IRBBB and ST segment elevation in the V1-2 lead not only in the acute phase, but also in the chronic phase. Abnormal findings were not found in noninvasive cardiac examinations, nor in cardiac catheterization and histological examinations. In the second case, VF was induced by electrical stimulation, and Disopyramide was found to be effective for the prevention of VF. The patient in the first case died suddenly two years after his first attack. Both cases have interesting ECG findings, and it may be that they play on important role in discovering the etiology of sudden cardiac death.

Adult↗
PubMedDate not supplied

Chromatographic (TLC) analysis of diltiazem in pharmaceutical form in presence of other antiarrhythmics.

Diltiazem was identified by TLC method on silica gel by ascending technique, in presence of five another antiarrhythmic drugs (disopyramide, flecainide, lidocaine, lorcainide, procainamide). Suitable conditions for separation of diltiazem were established using ethanol-benzene-dioxane-ammonia (2:20:16:3) as the mobile phase. When using acidified iodoplatinate solution or Dragendorff reagent as indicators, the amount of diltiazem as small as 100 ng can be identified. The TLC method is simple and sensitive and it was used to identify diltiazem in tablets.

Ammonia↗
PubMed1997

[Iatrogenic collapse; can this be prevented?].

In four patients, two men aged 65 and 35 years, and two women aged 87 and 83 years, who presented with collapse, administration of Q-T time prolonging drugs (sotalol, erythromycin, disopyramide) appeared to be the cause. These patients had so-called 'concealed long Q-T syndrome'. The proarrhythmogenic properties of antiarrhythmic and other drugs and of several clinical conditions such as cardiac diseases should be kept in mind when treating patients with antiarrhythmic substances.

Adult↗
PubMed2006

Antiarrhythmic drugs for maintaining sinus rhythm after cardioversion of atrial fibrillation: a systematic review of randomized controlled trials.

BACKGROUND: A variety of antiarrhythmic drugs have been used to prevent recurrence of atrial fibrillation after conversion to sinus rhythm. We performed a systematic review to determine the effect of long-term treatment with those drugs on death, embolisms, adverse effects, and atrial fibrillation recurrence. METHODS: We searched MEDLINE, EMBASE, the Cochrane Library (all up to May 2005), and the reference lists of retrieved articles. We included randomized controlled trials that compared any antiarrhythmic against control (placebo or no treatment) or another antiarrhythmic, for more than 6 months. Postoperative atrial fibrillation was excluded. Two evaluators independently reviewed the retrieved studies and extracted all data. Disagreements were resolved by discussion. All results were calculated at 1 year of follow-up. RESULTS: Forty-four trials were included, with a total of 11 322 patients. Several class IA (disopyramide phosphate, quinidine sulfate), class IC (flecainide acetate, propafenone hydrochloride), and class III (amiodarone, dofetilide, sotalol hydrochloride) drugs significantly reduced recurrence of atrial fibrillation (number needed to treat, 2-9), but all increased withdrawals due to adverse effects (number needed to harm [NNH], 9-27) and all but amiodarone and propafenone increased proarrhythmia (NNH, 17-119). Class IA drugs, pooled, were associated with increased mortality compared with controls (Peto odds ratio, 2.39; 95% confidence interval, 1.03-5.59; P = .04; NNH, 109). No other antiarrhythmic showed a significant effect on mortality compared with controls. We could not analyze other outcomes because data were lacking. CONCLUSION: Class IA, IC, and III drugs are effective in maintaining sinus rhythm but increase adverse effects, and class IA drugs may increase mortality.

Anti-Arrhythmia Agents↗