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PubMedDate not supplied

[Effect of intravenous disopyramide in supraventricular paroxysmal tachycardia refractory to vagal maneuvers].

The objective of this study was to prove the efficacy of intravenous disopyramide in the treatment of paroxysmal supraventricular tachycardia resistant to vagal maneuvers. Nine patients with this condition were admitted to the emergency service of the Instituto Nacional de Cardiología Ignacio Chávez. They were given an intravenous bolus of 2 mg/kg of the drug a maintenance dose of 0.4 mg/kg during 3 hours. The undesirable effects of the drug were arterial hypotension, dizziness, dry mouth, transient A-V dissociation and scape-capture rhythm. In conclussion, disopyramide is an excellent drug in the treatment of paroxysmal supra-ventricular tachycardia resistant to vagal maneuvers, but an strict monitorization of the arterial pressure and electrocardiogram should be kept during its administration.

Adult↗

PubMed1981

Enzyme immunoassay of disopyramide in serum.

Disopyramide, an antiarrhythmic drug, was quantitated in serum by a commercially supplied enzyme immunoassay procedure. Replicate analyses of serum controls resulted in a within-assay coefficient of variation of less than or equal to 5% and a between-assay coefficient of variation of less than or equal to 7%. Regression analysis of 105 serum samples analyzed by this technique (y) and by gas chromatography (x) gave the equation y = 0.99x + 0.04 (r = 0.97). Clinical evaluation of the results indicates the enzyme immunoassay technique to be highly specific and sensitive for disopyramide. The selectivity of the assay vs other drugs has been determined.

Chromatography, Gas↗

PubMedDate not supplied

Acute cardiac failure and hepatic ischemia induced by disopyramide phosphate.

Two patients abruptly developed congestive heart failure and elevation in serum transaminase levels when given disopyramide phosphate; enzyme abnormalities and hemodynamic status corrected upon withdrawal of the drug. Both patients had underlying ischemic cardiomyopathy. Myocardial infarction, pulmonary embolism, and viral hepatitis were ruled out in both patients. One patient had a liver biopsy documenting central hepatic necrosis with congestion, consistent with hepatic ischemia and not toxic hepatitis. In the other patient, cardiac decompensation and hepatocellular enzyme elevation were reproduced on rechallenge with the drug. Disopyramide should be used with caution in patients with heart failure.

Acute Disease↗

PubMed1981

Ventricular tachyarrhythmias induced by disopyramide and other similar anti-arrhythmic drugs.

Two patients with atrial arrhythmias are described who developed ventricular tachyarrhythmias shortly after starting disopyramide therapy. One patient had manifested ventricular tachycardia while on quinidine therapy earlier and the other patient, who died, had survived ventricular tachycardia and fibrillation complicating both quinidine and lidoflazine therapy 5 years earlier. We advise against the use of lidoflazine in patients with previously documented 'quinidine syncope' and caution that ventricular tachyarrhythmias appearing for the first time with the administration of disopyramide should be considered to be drug-induced until proved otherwise.

Aged↗

PubMed1981

Disopyramide-induced Torsade de Pointes.

Recurrent ventricular tachycardia (torsade de pointes) is a serious and sometimes fatal arrhythmia occurring usually with quinidine therapy. Four patients experienced ventricular tachycardia after receiving conventional doses of disopyramide phosphate (600 mg/day) for recurrent atrial fibrillation-two of them in combination with amiodarone hydrochloride. Isoproterenol hydrochloride infusion was effective in three patients, while ventricular pacing promptly abolished ventricular ectopic beats and the ventricular tachycardia in the fourth patient. Torsade de pointes is more likely to occur in patients with severe repolarization delay and sinus bradycardia or atrioventricular block, and its appearance in four patients within a period of nine months after the introduction of disopyramide treatment in our service raises the possibility that this is not a rare complication of this drug, especially if used in combination with other QT interval-prolonging agents.

Aged↗

PubMed1980

Gas-chromatographic determination of disopyramide and its mono-N-dealkylated metabolite in serum with use of a nitrogen-selective detector.

I describe a rapid, simple routine gas-liquid chromatographic method for simultaneous isothermal quantitation of disopyramide and its mono-N-dealkylated metabolite. The method involves one extraction step with dichloromethane, derivatization of the metabolite, and gas chromatography with an OV-17 liquid phase. Standard curves were linear over the concentration range tested (0.1-25 mg/L) and the maximum coefficient of variation was 9.2%. Quantitation of both disopyramide and its mono-N-dealkylated metabolite with the present method is less time-consuming than are gas-chromatographic methods previously described.

Chromatography, Gas↗

PubMed1980

Ventricular tachycardia with torsade de pointes morphology induced by oral disopyramide.

The oral administration of disopyramide for the maintenance of sinus rhythm after cardioversion from atrial fibrillation resulted in prolongation of the Q-T interval and three episodes of ventricular tachycardia with the torsade de pointes morphology. This morphology is characteristic of the arrhythmias of quinidine 'syncope'. Its appearance with disopyramide is not unexpected in view of the quinidine-like effects of the latter and suggests that it should be prescribed with the same caution as quinidine.

Administration, Oral↗

PubMed1977

Antiarrhythmic effect of disopyramide injected into the sinus nodal artery.

In a anaesthetized dogs, the antiarrhythmic drug disopyramide was injected directly into the sinus nodal artery in doses that ranged from 10 to 200 microgram/ml. Lower concentrations of the drug induced a non-significant increase in sinus rate of atropinic origin and were incapable of blocking atrial fibrillation induced by 10 microgram/ml of acetylcholine injected into the sinus modal artery. Only concentrations higher than 100 microgram/ml of the drug, which caused bradycardia, proved to be effective in preventing the arrhythmia. It is concluded that the antidyshythmic effect of disopyramide in sinus arrhythmia is a consequence of a direct negative chronotropic effect opposite to its known atropinic effect.

Acetylcholine↗

PubMed1978

[Clinical studies of the antiarrhythmic efficacy of disopyramide phosphate (Norpace) (author's transl)].

The antiarrhythmic action of Norpace was investigated in three clinical studies. 1. A single blind placebo controlled study in 10 centers confirmed the antiarrhythmic action of Norpace in 120 patients with ventricular or supraventricular cardiac arrhythmias. It was shown by means of continuous ECG recordings that Norpace produced a statistically significant reduction in the frequency of both ventricular and supraventricular extrasystoles. Paroxysmal ventricular tachycardia was prevented in 70% of the patients. 2. In a double blind comparative study of Norpace and quinidine sulphate a similar antiarrhythmic action against ventricular and supraventricular extrasystoles was shown in both patient groups. In contrast, the tolerance of Norpace was markedly superior to quinidne sulphate. 3. An acute study of the action of Norpace was also conducted. Therapeutic plasma levels were attained within 2 1/2 hours following an initial single dose and within 60 to 120 minutes when this dose was doubled. Orally administered disopyramide phosphate has therefore proved effective in both the short and longer term treatment of various types of supraventricular and ventricular arrhythmias. Its antiarrhythmic properties are very similar to those of quinidine sulphate. The dosage of disopyramide phosphate should be sufficiently high and must be individualized. The dosage generally lies between 400 and 800 mg daily and should be given in 4 divided doses at intervals of 6 hours. To achieve rapid therapeutic effects an initial dose of 2 x 150 mg is recommended. This method of administration will produce effective therapeutic plasma levels within 1 to 2 hours. Due to possible negative inotropic effects it is necessary to digitalize patients with congestive heart failure and caution should be exercised in poorly compensated patients. Observed side effects were mainly of the anticholinergic type.

Administration, Oral↗

PubMed1998

Percutaneous absorption of disopyramide, lidocaine and trimecaine.

Promoting effect of cyclic monoterpenes on percutaneous absorption of antiarrythmics drugs disopyramide, lidocaine and trimecaine was investigated in the rats. Laurocapram (Azone) was used as a standard comparator of penetration enhancement. The absorption of trimecaine was significantly enhanced by addition of limonene, trans-p-menthane and Azone in 1% concentration. Lidocaine and disopyramide penetrated across the skin only when 1% of limonene was used. Other cyclic monoterpenes showed no effect on percutaneous absorption of examined drugs.

Animals↗

PubMed2000

Enantioselective binding of propranolol, disopyramide, and verapamil to human alpha(1)-acid glycoprotein.

We investigated the binding of propranolol (PL), disopyramide (DP), and verapamil (VP) enantiomers by human alpha(1)-acid glycoprotein (AGP; also called orosomucoid) and the relationships between the extent of drug binding and lipophilicity, desialylation, and genetic variants of AGP. Desialylation had little effect on the affinity of AGP for the drugs tested. The percentage binding correlated significantly with the partition coefficients for the drugs tested. Each enantiomer was competitively displaced from AGP by another enantiomer of the same drug, suggesting that they bind to the same site. However, the enantiomers bound to AGP with stereospecific affinities; the (-)-isomers of DP and VP had higher Kd values (4.27 and 4.97 microM, respectively) than the (+)-isomers (1.51 and 2.48 microM, respectively). When enantiomers of the different drugs were used in competitive binding experiments, VP binding was only partially inhibited by DP. This result suggested that drug binding is specific to different variants of AGP (A, F1, S). DP was found to specifically bind to variant A, whereas PL and VP bind to both A and F1/S variants.

Disopyramide↗

PubMed1991

In vitro assessment of stereoselective hepatic metabolism of disopyramide in humans: comparison with in vivo data.

Metabolism of disopyramide (DP) enantiomers has been investigated in primary cultures of adult human hepatocytes. Results were compared with in vivo data obtained from a previous pharmacokinetic study (Le Corre et al. Drug Metab. Dispos. 16:858-864 1988). Metabolism of DP enantiomers as a function of incubation time showed constant velocity over time. The intracellular/extracellular distribution of both DP and mono-N-desisopropyldisopyramide did not appear to be stereoselective. Metabolism of DP enantiomers as a function of substrate concentration followed a first order kinetics. The average fractions of (-)-(R)-DP and (+)-(S)-DP metabolized in vitro (4.7 +/- 2.7 and 7.1 +/- 4.2%, respectively, n = 4) were about 5-fold lower than the fractions metabolized in vivo (26.0 +/- 6.0 and 40.2 +/- 8.8%, respectively, n = 6). The stereoselective index [(+)-(S)/(-)-(R)] of the N-dealkylation pathway obtained in vitro (1.51 +/- 0.11, n = 4) was very close to the one obtained in vivo (1.55 +/- 0.10, n = 6). These results highlight the interest of hepatocyte cultures in the evaluation of drug metabolism and especially in the assessment of stereoselectivity.

Adult↗

PubMed1992

Stereoselective biliary elimination of disopyramide and mono-N-desisopropyldisopyramide in humans.

The results of a previous pharmacokinetic study of disopyramide (DP) enantiomers in humans suggested that DP and/or mono-N-desisopropyldisopyramide (MND) may show stereoselective extrarenal elimination. Thus, the present study investigates the biliary elimination of DP and MND enantiomers in three patients who had undergone cholecystectomy for cholelithiasis. DP and MND enantiomers displayed biliary elimination. In both subjects, this elimination pathway showed the same characteristics: (1) biliary elimination of DP and MND was stereoselective, (2) the stereoselectivity was opposite to that observed for the metabolic and renal elimination pathways, i.e., the elimination of the (-)-(R)-enantiomer was higher than that of the (+)-(S)-enantiomer, and (3) biliary elimination of MND was higher than that of DP, for both enantiomers. Estimates of the relative contribution of the biliary clearance in the total clearance of DP and MND indicated that this elimination pathway was secondary, especially for DP. The biliary clearance (expressed as % of total clearance) was 1.9 to 4.0% for (-)-(R)-DP, 1.2 to 1.7% for (+)-(S)-DP, 7.8 to 22.9% for (-)-(R)-MND, and 5.2 to 10.5% for (+)-(S)-MND.

Bile↗

PubMed1979

A double-blind trial of disopyramide, procaineamide and digoxin in paroxysmal suptraventricular tachycardia.

A double-blind cross-over study has been performed in 10 patients with an established diagnosis of paroxysmal suptraventricular tachycardia to compare the effectiveness of three active agents with placebo. The drugs were administered in random sequence for two-week periods with three-day washout intervals and in standard dose regimes as recommended for prophylaxis by authoritative works on the subject. The results suggest that digoxin is ineffective at the recommended dosage. Procaineamide was effective in controlling some arrhythmias, but disopyramide was the most effective agent studied. All these patients showed a mixture of arrhythmias, and also had a lot of ectopic activity. Arrhythmic activity is erratic and unpredictable, and a larger number of patients would need to be studied for long periods of time to obtain enough data for valid statistical assessment.

Adult↗

PubMed1984

Dihydroquinidine versus disopyramide: efficacy in patients with chronic stable ventricular ectopy.

Dihydroquinidine (DQ) is contained in substantial amounts in quinidine salts, but its direct antiarrhythmic action has not been studied. The efficacy of oral DQ (300 mg t. i. d.) compared to disopyramide (D) (200 mg t.i.d.) was thus investigated using a double-blind crossover placebo-controlled protocol in 12 patients, aged 13 to 67 years, with chronic stable high frequency premature ventricular beats (PVB), defined as greater than 100 PVB/h during 48-72-h control Holter monitoring. The protocol included three 72-h treatment periods: DQ, D, and placebo at random. On days 2 and 3 of each period a 24-h Holter recording was carried out; drug blood levels were determined at peak (days 2 and 3) and trough time (day 3). No significant difference in the mean PVB/h was found between control (735 +/- 400) and placebo periods (564 +/- 388), or between the two Holter recordings of each period. Compared to placebo both DQ (106 +/- 113, p less than 0.005) and D (240 +/- 263, p less than 0.05) reduced the mean PVB/h, but the decrease was significantly higher with DQ (78 versus 53%, p less than 0.02). Nine patients (75%) on DQ and 5 (42%) on D had a greater than 70% decrease in mean PVB/h; complex PVBs were abolished in 3 of 6 patients on both treatments. On day 3, DQ plasma levels were 1.31 +/- 0.44 (peak) and 0.92 +/- 0.45 (trough) mg/l; D plasma levels were 2.88 +/- 0.64 (peak) and 2.02 +/- 0.31 (trough) mg/l; no significant difference was found between day 2 and day 3 samples.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed2001

Inhibition of HERG potassium channel current by the class 1a antiarrhythmic agent disopyramide.

The Class 1a antiarrhythmic drug disopyramide (DISO) is associated with 'acquired' prolongation of the QT interval of the electrocardiogram (ECG). This potentially proarrhythmic effect is likely to reflect drug actions on ion channels involved in ventricular action potential repolarisation. In this study, we examined the effects of DISO on potassium channels encoded by HERG, as this K channel type has been implicated in both congenital and acquired long-QT syndromes (LQTS). Chinese hamster ovary cells were transiently transfected with HERG cDNA for subsequent whole cell patch clamp recording. HERG tail currents recorded at -40 mV following test pulses to +30 mV were inhibited in a dose-dependent fashion by DISO concentrations within the clinical range (IC50 = 7.23 +/- 0.72 microM; mean +/- SEM). Experiments with 10 microM DISO indicated that the degree of HERG blockade showed some voltage dependence. Further data obtained using an 'envelope of tails' protocol (pulse potential +40 mV) were consistent with a significant role for open-channel blockade at lower drug concentrations. At higher concentrations it is possible that blockade may have involved drug binding to both resting and open channels. Inhibition of the inactivation-deficient mutant HERG-S631A was comparable to that seen for wild-type HERG. Therefore, channel inactivation was not obligatory for DISO to exert its effect. Native delayed rectifier tail currents from rabbit isolated ventricular myocytes were also inhibited by DISO. We conclude (a) that DISO inhibits HERG encoded potassium channels at clinically relevant concentrations and (b) that this action may constitute the molecular basis for acquired LQTS associated with this drug.

Animals↗

PubMed1981

Pharmacokinetics of disopyramide in patients with imminent to moderate cardiac failure.

The parmacokinetics of disopyramide (DP) in 10 patients with imminent to moderate cardiac failure has been studied and compared with the results in normal volunteers. The biological half life of rapid distribution (T1/2 alpha) and of elimination (T1/2 beta) were increased (11.1 +/- 4.4 min and 9.7 +/- 4.2 h, respectively). Total body clearance (Clt) was decreased (0.467 +/- 0.215 ml . min-1 . kg-1), and the volume of distribution (Vd) was slightly reduced (0.610 +/- 0.1361 . kg-1), probably due to the lower cardiac index. After oral administration, the time of peak serum concentration was increased (139 +/- 89 min), and the mean peak serum concentration (2.4 +/- 0.8% dose . 1-1) was also higher than reported in normal subjects. Comparison of the areas under the concentration versus time curves after intravenous and oral administration (AUC i. v. and AUC oral) showed that DP was almost completely absorbed, its bioavailability being 97.5 +/- 15.0%.

Administration, Oral↗

PubMed1977

Antiarrhythmic and electrocardiographic effects of single oral doses of disopyramide.

Ten patients with various heart diseases and ventricular arrhythmia received a single oral dose of disopyramide (DE) 200 mg. The ECG was recorded continuously for about 50 h from 2-4 h before drug administration. A statistically significant reduction in the number of ventricular ectopic beats (VEBs) was seen 1.0-3.5 h after drug intake; the average number of VEBs per 30 min decreased from 317 during the control period to 92 by 1.0-3.5 h after treatment and if one patient who did not respond is excluded, the corresponding figures were 272 and 14, respectively. Consecutive VEBs were seen in seven patients before DE was given and decreased significantly (p less than 0.05) 1.5-5.5 h after drug administration. There was no change in the PQ interval, the QRS interval showed a slight increase, whereas the QT interval was prolonged 0.5-4 h after administration of DE. A specific gas chromatographic method was used for DE assay in plasma and urine. Absorption was rapid in all patients. Urinary excretion during the first 48 h after drug intake varied between 35 and 75%. The lowest effective antiarrhythmic concentration estimated in six patients ranged from 1.4 to 7.0 mug/ml. beta-Phase half-life in five patients was between 10.3 and 22.1 h.

Aged↗