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PubMed1979

Quantitative high-performance liquid-chromatographic method for determining disopyramide (Norpace) in serum.

We report a high-performance liquid-chromatographic method for measuring disopyramide (Norpace, Searle) in serum. The drug is extracted from 0.5 ml of serum into chloroform containing the internal standard p-chlorodisopyramide, separated on a reversed-phase octadecylsilyl column at room temperature, and detected at 254 nm. The method is sensitive to 0.2 mg of disopyramide per liter, with a linear response to at least 10 mg/liter. Within-day precision (CV) for frozen serum pools is 8.3 (n = 21) and (n = 22) at mean concentrations of 2.6 and 5.9 mg/liter, respectively. Day-to-day precision (CV) is 9.4 (n = 80) and 9.3 (n = 29) at mean concentrations of 2.8 and 6.7 mg/liter, respectively. Recoveries for disopyramide in serum averaged 98% over the linear range when compared against an aqueous standard taken through the entire analytical procedure. The method is relatively specific, as evidenced by interference studies with over 85 drugs.

Chromatography, High Pressure Liquid↗
PubMed1982

Disopyramide.

Since disopyramide was introduced 5 years ago, the therapeutic spectrum of this drug in treating patients with ventricular and atrial arrhythmias has been found to be similar to that of the other type I antiarrhythmic drugs, quinidine and procainamide. Disopyramide has the potential to suppress sinus node function and, therefore, must be used cautiously in patients with the sick sinus syndrome. The available data indicate that it can be used safely in patients with bundle branch block and first-degree or type I second-degree atrioventricular block. Disopyramide has been found at times to precipitate ventricular tachycardia or ventricular fibrillation. Because this drug often causes decompensation in patients with congestive heart failure, it must be used very cautiously, if at all, in such patients.

Arrhythmias, Cardiac↗
PubMed1999

Preterm labor and accidental hemorrhage after disopyramide therapy in pregnancy. A case report.

BACKGROUND: Treatment of arrhythmias during pregnancy is complicated by concerns about the safety of antiarrhythmic therapy. This is the first case report of preterm labor and abruptio placentae following the administration of disopyramide during pregnancy. CASE: A 26-year-old woman, gravida 2, para 1, was diagnosed as having Wolff-Parkinson-White syndrome during the third trimester of pregnancy. Recurrent episodes of supra-ventricular tachycardia were refractory to medical therapy and required repeated direct current cardioversion. Administration of disopyramide led to the initiation of painful uterine contractions and accidental hemorrhage. CONCLUSION: Caution must be exercised during the use of disopyramide during pregnancy, and intensive monitoring should be instituted to avoid adverse maternal and fetal effects.

Abruptio Placentae↗
PubMed2000

[Efficacy of continuous intravenous drip infusion of disopyramide in hypertrophic obstructive cardiomyopathy during cardiogenic shock: a case report].

A 54-year-old woman was admitted to our hospital complaining of dyspnea due to hypertrophic obstructive cardiomyopathy. On admission, she was treated with 4 antiarrhythmic drugs and 2 beta-blockers. After 4 of these 6 drugs were withdrawn, the left ventricular outflow pressure gradient markedly increased and then she fell into cardiogenic shock. Therefore, disopyramide(600 mg/day) was administered by continuous intravenous drip infusion to reduce the left ventricular outflow pressure gradient. After intravenous administration of disopyramide, the left ventricular outflow pressure gradient markedly decreased from 100 to 16 mmHg and the cardiogenic shock could be improved. Continuous intravenous drip infusion of disopyramide is effective for the treatment of cardiogenic shock due to severe left ventricular outflow obstruction in patients with hypertrophic obstructive cardiomyopathy.

Anti-Arrhythmia Agents↗
PubMed2003

[Comparison of the efficacies of disopyramide, cibenzoline and aprindine for the termination of paroxysmal and persistent atrial fibrillation in elderly and non-elderly patients].

OBJECTIVES: The relationship between the efficacy of the anticholinergic action of disopyramide, cibenzoline and aprindine and age was examined in patients with paroxysmal and persistent atrial fibrillation. METHODS: This prospective, randomized study included 278 patients (200 men, 78 women, mean age 61 +/- 11 years) divided into two groups; the non-elderly group (age below 60 years) and the elderly group (age over 60 years). Successful termination was defined as conversion of sinus rhythm within 30 min of intravenous administration of 50 mg disopyramide (n = 91), 70 mg cibenzoline (n = 93) or 100 mg aprindine (n = 94) in this prospective and randomized study. RESULTS: No statistically significant difference was found in patient characteristics between the three agents. 1) The rate of conversion to sinus rhythm after disopyramide administration in the non-elderly group(37.8%) was significantly higher than that in the elderly group (17.4%, p = 0.0361). 2) The rate of conversion to sinus rhythm after cibenzoline administration in the non-elderly group (62.2%) tended to be greater than that in the elderly group (43.8%, p = 0.0972). 3) The rate of conversion to sinus rhythm after aprindine administration in the non-elderly group (25.6%) was not significantly higher than that in the elderly group (18.2%, p = 0.4474). CONCLUSIONS: The anticholinergic action of antiarrhythmic agents has an effect on successful termination in non-elderly patients with paroxysmal and persistent atrial fibrillation.

Aged↗
PubMed1992

Selectivity of class I antiarrhythmic agents, disopyramide, pirmenol, and pentisomide for peripheral muscarinic M2 and M3 receptors.

The interactions of the class I antiarrhythmic agents, disopyramide, pirmenol, and pentisomide with peripheral muscarinic receptors were investigated by binding assay with [3H]N-methylscopolamine ([3H]NMS) as a ligand. All the agents inhibited the specific [3H]NMS binding to membrane preparations obtained from guinea pig submandibular gland (SG) and urinary bladder (UB) smooth muscle. The competition curves of these agents for [3H]NMS binding to SG membranes were monophasic, indicating competition with [3H]NMS at a single site. Comparison of results with those of our previous binding experiments using guinea pig left atrial (LA) membranes, showed that pirmenol had sevenfold lower affinity for glandular-type muscarinic receptors (M3) than for cardiac-type muscarinic receptors (M2). On the other hand, the dissociation constants (Ki) for disopyramide and pentisomide in SG were comparable to the high-affinity Ki values for these agents at M2 receptors. The competition curves of the three agents for [3H]NMS binding to UB membranes were biphasic and showed high- and low-affinity states of binding. The high- and low-affinity Ki values for pirmenol in UB were similar to its Ki values at M2 and M3 receptors obtained in LA and SG, respectively. The high-affinity Ki values for disopyramide and pentisomide were consistent with the respective Ki values determined in SG, whereas the low-affinity binding sites for these agents were presumably the result of their allosteric interactions with the receptors. All agents at higher concentrations slowed the dissociation of [3H]NMS elicited by an excess of atropine in both UB and SG, thus indicating allosteric interactions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

[Torsades de pointes ventricular tachycardia induced by disopyramide at therapeutic serum concentration].

We describe a patient who developed torsades de pointes ventricular tachycardia after several years of treatment with disopyramide. The case demonstrates that measuring disopyramide serum concentration provides limited information about correct dosages. Life-threatening arrhythmias may arise even at recommended doses and therapeutic serum concentration. Clinical trials have shown that class Ic antiarrhythmic drugs, and perhaps all class I antiarrhythmics, may increase the risk of serious arrhythmias and sudden death in certain groups of patients. Aspects of the pharmacology of disopyramide are discussed, with particular emphasis on the variable plasma protein binding and the narrow therapeutic specter. This complexity seems to be the most important reason for the limited reliability of serum concentration measurements for predicting the best dosage for the individual patient.

Aged↗
PubMed2003

[Relationship between duration of arrhythmia and subsequent preventive effect of disopyramide after cardioversion in patients with symptomatic paroxysmal and persistent atrial fibrillation].

OBJECTIVES: The relationship between the duration of arrhythmia and the subsequent long-term efficacy of disopyramide in preventing atrial fibrillation was investigated in patients with symptomatic paroxysmal and persistent atrial fibrillation. METHODS: A total of 60 patients (39 men, 21 women, mean age 65 +/- 11 years) were given disopyramide (300 mg/day) after electrical and pharmacological cardioversion based on American Heart Association Task Force on Practice Guidelines. The patients were divided into two types based on the duration of atrial fibrillation: conversion within 48 hr (group A, n = 35) and more than 48 hr (group B, n = 25) after the episode. Mean follow-up period was 47.1 +/- 28.7 months. RESULTS: Patient characteristics showed no statistically significant difference between groups A and B. The actuarial rates of maintenance of sinus rhythm at 1, 3, 6, 12, 18 and 24 months were 88.6%, 77.1%, 57.1%, 48.6%, 42.9% and 37.1%, respectively, in group A, and 72.0%, 44.0%, 28.0%, 16.0%, 12.0% and 8.0%, respectively, in group B. There was a significant difference in the rate at 24 months between groups A and B (p < 0.05). The periods for maintenance of sinus rhythm in groups A and B were 20.9 +/- 3.9 and 6.7 +/- 2.1 months, respectively, with a significant difference between groups A and B (p < 0.01). CONCLUSIONS: The efficacy of disopyramide in preventing the recurrence of atrial fibrillation varies with the duration of the previous episode. These results demonstrate that it is important to convert to normal sinus rhythm earlier to prevent the recurrence of atrial fibrillation in the long term.

Aged↗
PubMed1991

[Efficacy and tolerance of disopyramide in arrhythmia associated with sinus node dysfunction].

The aim of this study was to assess the effect of delayed release Disopyramide 500 mg daily on sinus node function in 12 subjects with sinus node dysfunction and supraventricular and/or ventricular excitability. An ECG, Holter monitoring and electrophysiological studies of sinus node function with an oesophageal electrode were performed before and after 5 days treatment. The drug had to be discontinued in 1 patient because of urinary retention. The Disopyramide suppressed the clinical tachyarrhythmias in 8 out of the 11 subjects. The maximal sinus pause observed on Holter monitoring did not change significantly. It only increased in one subject. The mean sinus cycle length during electrophysiological study slightly decreased but there was a global increase in sinoatrial conduction time from 309 +/- 164 to 413 +/- 125 msec and of the corrected sinus mode recovery time from 470 +/- 168 to 605 +/- 303 msec. However, these changes were not significant. This study of delayed released Disopyramide shows a discordance between the tendency for sinus node function to deteriorate when assessed by electrophysiological studies and good clinical tolerance as assessed by Holter monitoring in the bradycardia-tachycardia syndrome.

Aged↗
PubMedDate not supplied

Ventricular tachycardia-flutter associated with disopyramide therapy: a report of three cases.

Three patients developed episodes of ventricular tachycardia and/or flutter-fibrillation while receiving disopyramide (Norpace). Syncope was the presenting complaint in all of them. The arrhythmias did not recur after disopyramide was discontinued. The Q-T interval was markedly prolonged in all three patients. One patient developed syncope associated with both quinidine and Norpace therapy. It is postulated that disopyramide, like quinidine, may provoke ventricular flutter-fibrillation in sensitive patients by similar mechanisms.

Aged↗
PubMed1989

Beneficial effects of lidocaine and disopyramide on oxygen-deficiency-induced contractile failure and metabolic disturbance in isolated rabbit hearts.

The purpose of the present study was to determine whether antiarrhythmic agents, lidocaine and disopyramide, which reveal a membrane stabilizing action, may exert a beneficial effect on posthypoxic recovery of cardiac function and metabolism. Rabbit hearts were perfused for 20 min under hypoxic conditions, followed by 45-min reoxygenation. Hypoxic insults induced cessation of cardiac contractile force, rise in resting tension, depletion of myocardial high-energy phosphates, accumulation of tissue calcium and release of creatine kinase and ATP metabolites such as adenosine, inosine and hypoxanthine. These alterations were not returned to the initial levels upon reoxygenation. Administration of either 69 microM lidocaine or 55 microM disopyramide after the onset of oxygen deficiency (between 8th and 20th min of the hypoxia) resulted in a significant suppression of hypoxia-induced rise in resting tension, tissue calcium accumulation and release of creatine kinase and ATP metabolites, whereas hypoxia-induced decline in cardiac contractile force and depletion of myocardial high-energy phosphates were not affected by the treatment. The latter two variables were improved markedly during 45-min reoxygenation when the heart had been treated with the agents. The improvement was accompanied by a suppression of the release of creatine kinase and ATP metabolites and the tissue calcium accumulation. The results suggest that lidocaine and disopyramide are beneficial for posthypoxic recovery of cardiac function and metabolism.

Adenosine Triphosphate↗
PubMedDate not supplied

Combination of disopyramide and propranolol in hypertrophic cardiomyopathy.

Fifteen patients were studied by echocardiography, apexcardiogram and carotid pulse tracings in four ways: basally; on propranolol 40 mg, three times daily; on disopyramide 200 mg single dose, three days after propranolol discontinuation; and on both drugs. The following data were measured: systolic anterior mitral motion slope, systolic anterior mitral distance from the septum, outflow tract diameter, the A wave to the total apexcardiographic excursion ratio, carotid pulse contour and left ventricular ejection time index. Propranolol did not produce any significant changes while disopyramide was much more effective in changing the data in a direction suggesting diminution of left ventricular outflow gradient. The combination of propranolol and disopyramide had the greatest influence. Fourteen patients received the two drugs for 12.3 +/- 4.3 months with improvement of NYHA class.

Adult↗
PubMed1982

[Antiarrhythmic effect of disopyramid retard versus propranolol retard in ventricular extrasystole].

The antiarrhythmic effect of disopyramide retard (DR) in a dose of 2 X 300 mg/day, propranolol retard (PR) in one of 1 X 160 mg/day and placebo was compared in a randomized crossover study in patients with ventricular premature beats (VPB). 10 patients with VPB (Lown classes II-V) were given the drugs as follows: placebo I for 3 days. DR or PR for 7 days, placebo II for 5 days and PR or DR for 7 days. During every phase Holter ECG was registered over a period of 24 hours. Under DR 6 patients showed a favourable qualitative effect improving by at least one Lown class, while under PR only one patient did so. Under DR an over 80% reduction of VPB occurred in 6 patients and under PR in one patient. In all patients with any reduction of VPB this reduction was 79% under DR and 57% under PR. These results suggest that the antiarrhythmic effect of disopyramide in slow release preparations is comparable with that of disopyramide in standard capsule formulation given in the usual and more complicated regime with four divided doses. In the above mentioned (and still recommended) dose PR has no antiarrhythmic effect.

Adult↗
PubMed1984

[Beneficial effects of disopyramide on left ventricular outflow obstruction in a case of hypertrophic obstructive cardiomyopathy].

The Authors describe a patient with hypertrophic cardiomyopathy (HCM), severe left ventricular outflow tract obstruction and lack of response to beta-blockers or verapamil. Intravenous infusion of disopyramide resulted in a virtual disappearance of the LV pressure gradient, reduction of the systolic anterior motion of the mitral valve and slowing of the LV isovolumetric relaxation. One month after maintenance therapy with oral disopyramide a decrease of the anginal episodes and an improvement of the exercise tolerance were noted. Thus disopyramide, probably because of its negative inotropic action, is useful in the management of patients with HCM when LV outflow obstruction is the main cause of the clinical-hemodynamic findings.

Angina Pectoris↗
PubMed1983

Disopyramide-associated liver dysfunction.

A case of disopyramide-associated cholestatic jaundice is presented, and all reported cases of disopyramide-associated liver dysfunction are reviewed. Manifestations of liver dysfunction usually appear during the first week of treatment. Discontinuing administration of the drug often results in prompt clinical resolution, although in rare instances, laboratory abnormalities persist up to 18 months. Physicians should be aware of this rare but serious complication of disopyramide therapy.

Adult↗
PubMed1980

Disopyramide and mexiletine: which is the agent of choice in the long term-oral treatment of lidocaine-responsive arrhythmias? Efficacy comparison in a randomized trial.

Forty patients with serious lidocaine-responsive ventricular arrhythmias were randomly assigned to treatment with either oral disopyramide (100 mg 4 times daily) or mexiletine (200 mg 4 times daily) for 3 weeks. A satisfactory arrhythmias control (greater than 75 % reduction of premature ventricular complexes per minute as compared to the control period prior to lidocaine administration) was achieved in 19 patients in the mexiletine group and in 16 in the disopyramide treated patients. Furthermore, disopyramide failed to maintain the reduction of the number of ventricular extrasystoles per minute obtained with lidocaine, while mexiletine succeeded. Finally, the number of ventricular extrasystoles per minute in the mexiletine treated group was significantly lower than in the other group. Gastrointestinal disturbances were more frequent during mexiletine administration.

Arrhythmias, Cardiac↗
PubMed1981

Liquid-chromatographic determination of antidysrhythmic drugs: procainamide, lidocaine, quinidine, disopyramide, and propranolol.

We present a method for the analysis of antidysrhythmic drugs [procainamide, acecainide (NAPA), lidocaine, quinidine, disopyramide, N-desisopropyl disopyramide, and propranolol] in serum. The drugs, together with an internal standard, are extracted from 0.2-1.0 ml of serum, separated on an octyl-bonded reversed-phase column using a mobile phase consisting of acetonitrile/phosphate buffer, and monitored by either ultraviolet or fluorescence spectrophotometry. The proposed method offers good reproducibility, sensitivity, linearity, and accuracy. Of more than 50 drugs and metabolites, tested for possible interference, only diazepam, flurazepam, and the N-oxide metabolite of quinidine interfere with quinidine analysis, while meperidine coelutes with disopyramide. However, diazepam and flurazepam do not interfere with quinidine analysis with fluorescence detection.

Anti-Arrhythmia Agents↗
PubMed1978

[Hemodynamic effects of disopyramide and procainamide in open-chest animals].

Hemodynamic effects of two antiarrhythmic agents, disopyramide and procainamide, have been evaluated in anesthetized open-chest healthy pigs after random administration. At therapeutic plasma concentrations none of these agents proved to have deleterious hemodynamic effects. The most important action was observed after disopyramide infusion and consisted in significant bradycardia which confirmed the known effect on sinus node automaticity of the drug. Left ventricular dp/dt, an index of cardiac contractility, was unchanged after infusion of both drugs. On the ECG intervals, only procainamide provoked a significant prolongation of QTc. It is concluded that at therapeutic dosage disopyramide does not present deleterious hemodynamic effects in animals and proves to be a valid alternative to other traditional antiarrhythmic agents.

Animals↗