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PubMed1989

Hemodynamic effects of mexiletine and disopyramide after cardioplegic arrest.

To study the hemodynamic side effects of mexiletine and disopyramide when administered before cardioplegic arrest 15 dogs underwent sham cardiac surgery with a 90-min period of aortic cross-clamping. 5 dogs served as control, 5 were given 8 mg/kg/day mexiletine and another five 11 mg/kg/day disopyramide for 1 week before surgery. On the day of surgery a continuous infusion was started. After reperfusion treated animals exceeded their preischemic blood pressure and regained their preoperative cardiac output. Compared to control animals left ventricular work was higher in the treated animals after reperfusion. The two tested type I antiarrhythmics tend to add to myocardial protection when given before cardioplegic arrest and do not exhibit negative inotropic side effects.

Animals↗
PubMed1983

Disopyramide: six years' experience.

Since its approval by the FDA six years ago, oral disopyramide has earned a recognized role in the treatment of ventricular arrhythmias. During this time, clinical experience has refined our knowledge of this agent, allowing revision of dosing guidelines and better selection of patients. This review explores the recent therapeutic experience with disopyramide.

Arrhythmias, Cardiac↗
PubMed1983

A randomized, double-blind, parallel group comparison of disopyramide phosphate and quinidine in patients with cardiac arrhythmias.

This report summarizes the results of a randomized, double-blind, parallel group, multicenter study which compared the antiarrhythmic activity and safety of oral disopyramide phosphate and oral quinidine sulfate. A total of 124 outpatients, whose pretreatment rates of ventricular and/or supraventricular arrhythmias were documented by ambulatory ECG recordings, were randomly assigned to receive either oral disopyramide or oral quinidine for the eight-week course of the study. Every two weeks, ten-hour ambulatory ECG recordings were obtained from each patient and blood was drawn to determine serum concentrations of assigned drug.

Administration, Oral↗
PubMed1979

Disopyramide--an effective treatment for lignocaine resistant ventricular dysrhythmias.

Intravenous disopyramide was used in 13 patients who developed recurrent ventricular dysrhythmias despite initial treatment with intravenous lignocaine after admission to the Coronary Care Unit of a busy district hospital. This was effective in 8 of the 13 patients treated and there was no major side effects observed. Disopyramide has the advantage of being available both as an oral and an intravenous preparation and is a useful drug to be added to the list of more conventional anti-dysrhythmic agents.

Arrhythmias, Cardiac↗
PubMed1979

Disopyramide in pregnancy: a case report.

Disopyramide (200 mg 8-hourly) was given to a pregnant patient from the 26th week onwards for the treatment of bigeminy and paroxysmal ventricular tachycardia. Labour was spontaneous and normal. Although disopyramide was demonstrated in the foetal blood there was no evidence of congenital abnormality or growth retardation. The drug treated the mother satisfactorily with no apparent ill effects to the child.

Adult↗
PubMed1998

Disopyramide: a promising new approach to the medical treatment of the hypercyanotic spell complicating tetralogy of Fallot.

Under continuous ECG and oxygen saturation (SpO2) monitoring, the following measurements were taken by Doppler echocardiography in 6 consecutive patients with tetralogy of Fallot (TF) before and after intravenous administration of disopyramide (2mg/kg): left ventricular shortening fraction (LVSF); peak velocities in the right ventricular outflow tract (RVOT); diastolic and systolic internal diameters of the right ventricular outflow tract (dRVOT, sRVOT); and systolic blood pressure. SpO2 increased (p<0.01) from 78 to 98 (89 +/- 7, mean +/- standard deviation)% to 86-99 (94 +/- 5)%. LVSF decreased (p<0.05) from 0.34-0.56 (0.42 +/- 0.08) to 0.22-0.54 (0.33 +/- 0.13). The systolic blood pressure fell slightly (p<0.05) from 68-92 (79 +/- 8) to 64-92 (71 +/- 11)mmHg. The sRVOT increased (p<0.05) from 2.1-4.8 (2.7 +/- 1.5)mm to 3.0-8.1 (4.9 +/- 2.4)mm, while RVOT peak velocity decreased (p<0.05) from 2.20-4.88 (3.70 +/- 0.97)m/sec to 2.05-4.07 (2.92 +/- 0.72)m/sec. Disopyramide alleviates hypoxia in patients of TF through its negative inotropic action on right ventricular outflow obstruction.

Blood Flow Velocity↗
PubMed1999

Dynamic outflow obstruction due to the transient extensive left ventricular wall motion abnormalities caused by acute myocarditis in a patient with hypertrophic cardiomyopathy: reduction in ventricular afterload by disopyramide.

A 65-year-old woman was admitted to the coronary care unit because of acute pulmonary edema. Immediate 2-dimensional and Doppler echocardiograms revealed extensive left ventricular wall motion abnormalities and left ventricular hypertrophy with extreme outflow obstruction. Although an ECG showed ST-segment elevation in the anterolateral leads, a coronary arteriogram revealed normal epicardial arteries. Heart failure was relieved after diminishing the dynamic outflow obstruction with disopyramide administration. An endomyocardial biopsy from the right ventricle on the 8th hospital day showed borderline myocarditis. Wall motion abnormalities gradually normalized within 2 weeks. It is speculated that her pulmonary edema would not have been relieved so readily without the immediate reduction in ventricular afterload by disopyramide. These clinical changes over time were observed with serial echo-Doppler examinations.

Acute Disease↗
PubMed1982

Effects of disopyramide on the maximum rate of rise of action potential (Vmax) in guinea-pig papillary muscles.

The correlation between the steady state and non-steady state depression of Vmax by 50 microM disopyramide was investigated in 2.7, 5.4 and 8.1 mM [K+]o using isolated guinea-pig papillary muscles. An elevation of [K+]o from 2.7 to 8.1 mM strengthened the depressant action of the drug on Vmax (steady state) at 1 to 5 Hz, but attenuated this action at 0.05 and 0.1 Hz. The Vmax-membrane potential (Vm) relationship (steady state) was examined at stimulation rates of 0.1 and 1 Hz by increasing [K+]o from 2.7 to 19 mM. The drug shifted the normalized Vmax-Vm curve at 1 Hz in a hyperpolarizing direction, but shifted the curve at 0.1 Hz upward at Vm between -90 and -65 mV without a shift along the Vm axis. The recovery process of Vmax (non-steady state) was examined by introducing premature stimuli or by interrupting the basic stimulus of 1 Hz for a certain period. The control recovery processes in three [K+]o were approximated by a triple exponential function (the earliest, intermediate and latest components). The drug slowed the intermediate component, but accelerated the latest one (the earliest component was situated within the refractory period) of [K+]o attenuated the depressant action of disopyramide on the Vmax at 0.05 and 0.1 Hz and accelerated the recovery process of Vmax at long diastolic intervals of more than 10 sec was quite unique.

Action Potentials↗
PubMed1994

Effects of NS-2, a new class 1 antiarrhythmic agent, and AFD-19, its active metabolite, on ventricular arrhythmias induced by coronary artery occlusion and reperfusion in anesthetized rats: comparison with disopyramide and mexiletine.

We studied the antiarrhythmic effects of NS-2 (4-diisobutylamino-1,1-diphenyl-1-butanol maleate) and AFD-19 (active metabolite of NS-2) on early stage ventricular arrhythmias induced by coronary artery occlusion and reperfusion in anesthetized male rats. These effects were compared with those of disopyramide and mexiletine. Drugs were intravenously administered either before or after coronary occlusion. When administered 5 min before occlusion, 3 mg/kg of NS-2 and AFD-19 exhibited equivalent anti-arrhythmic activity to that of 5 mg/kg of disopyramide and mexiletine, as assessed by reductions in the number of premature ventricular complexes and in the incidences of ventricular tachycardia and ventricular fibrillation. In a dose of 5 mg/kg, the antiarrhythmic effects of NS-2 and AFD-19 were more pronounced. When administered 5 min after coronary artery occlusion, only NS-2 and AFD-19 (in doses of 5 mg/kg) had significant antiarrhythmic effects. None of the drugs influenced the severe ventricular arrhythmias induced by reperfusion when administered 1 min before reperfusion. In conclusion, NS-2 might be effective in reducing the severity of the life-threatening ventricular arrhythmias that occur during acute myocardial infarction.

Amino Alcohols↗
PubMed2001

Electrophysiologic effects of an antiarrhythmic agent, bidisomide, on sodium current in isolated rat ventricular myocytes: comparison with mexiletine and disopyramide.

The effects of bidisomide, an antiarrhythmic agent, on sodium current (I(Na)) in isolated rat ventricular myocytes were investigated using a whole cell voltage clamp method. Bidisomide blocked I(Na) with a Ki of 214 microM at a holding potential of -140 mV. The blockade of I(Na) was enhanced at a less negative holding potential of -100 mV with a Ki of 21 microM. Bidisomide shifted the steady state inactivation curve to a negative potential direction by 20 mV without a significant change in the slope factor. Bidisomide slowed the time course of recovery of I(Na) at a holding potential of -140 mV with a slow recovery phase. The time constant of recovery phase for bidisomide, disopyramide and mexiletine were 2703, 1858 and 757 ms, respectively. The development of the block of I(Na) consisted of two phases in the presence of bidisomide. The fast and slow time constants were 11 and 648 ms. Bidisomide produced a use-dependent block of I(Na) when the depolarizing pulse was repeated at 1-3 Hz. Our results indicate that bidisomide binds to rat cardiac sodium channels and that the dissociation kinetics of bidisomide from the inactivated sodium channel is slower than that of disopyramide.

Animals↗
PubMed1981

Disopyramide-induced heart block.

A 57-year-old woman with right bundle branch block +LPH and ventricular premature contractions developed complete heart block (CHB) following administration of disopyramide phosphate (Norpace). The ECG at the onset of CHB suggested block to have occurred in the trifascicular conduction system. On rechallenging the patient with the drug following the implantation of a permanent pacemaker, intermittent complete heart block developed. This case suggests that disopyramide should be used with caution in patients with bifascicular block patterns on ECG.

Bundle-Branch Block↗
PubMed1982

Atypical ventricular tachycardia (torsade de pointes) induced by amiodarone: arrhythmia previously induced by quinidine and disopyramide.

A 44-year-old woman is described in whom amiodarone, disopyramide, and quinidine, administered alone separately, induced atypical ventricular tachycardia (AVT, torsade de pointes). Following a closed mitral valvotomy, she received quinidine, 1.2 g/day, without interruption for 17 years. Because of a recurrence of paroxysmal atrial fibrillation, the dose of the drug was increased to 1.4 g/day; 24 hours later AVT with syncope developed but responded promptly to atropine. Two years later, 24 hours following an increase in the dose of disopyramide from 300 to 600 mg/day, AVT with syncope occurred; isoproterenol abolished the arrhythmia instantly. Amiodarone was the third drug to induce AVT in this patient; she received 200 mg/day six days per week for six months. The dose was subsequently increased to 200 and 400 mg/day on alternate days, six days per week, and two months later AVT occurred. That time the only effective treatment was ventricular pacing.

Adult↗
PubMed1983

Effect of oral disopyramide therapy on left ventricular function.

To study the effect of oral disopyramide therapy on left ventricular function, a subject of some controversy, we obtained first-pass radionuclide ventriculograms with a multicrystal gamma camera in 19 patients with or without therapy. Our findings demonstrated that disopyramide causes deterioration in left ventricular function in patients with abnormal ejection fractions. This effect is rarely recognized clinically and occurs despite safe therapeutic serum levels.

Administration, Oral↗
PubMed1988

Danger of use of disopyramide in patients with hypertrophic obstructive cardiomyopathy. An electrophysiologic study.

A 61-year-old man with hypertrophic obstructive cardiomyopathy with asymptomatic ventricular tachycardia underwent electrophysiologic study. Double extrastimuli at the right ventricular outflow tract induced polymorphic ventricular tachycardia which degenerated into fibrillation. After intravenous administration of 50 mg of disopyramide, the pressure gradient in the outflow tract disappeared, but the tachycardia inducing zone appeared at the right ventricular apex. Although disopyramide may be used in patients with hypertrophic cardiomyopathy to relieve the intraventricular pressure gradient, it should be used only after evaluating its safety and efficacy electrophysiologically.

Cardiac Pacing, Artificial↗
PubMed2001

Disopyramide-induced pneumonitis, diagnosed by lymphocyte stimulation test using bronchoalveolar lavage fluid.

A 72-year-old man was admitted to our hospital with fever and cough. He had been on disopyramide treatment for nine days to control cardiac arrhythmia. On admission, chest X-ray examination revealed reticulonodular opacities in both lungs, and impending respiratory failure was evident. A differential cell count of the bronchoalveolar lavage fluid (BALF) showed a marked increase of lymphocytes. A lymphocyte stimulation test (LST) for disopyramide using BALF was positive, although the test using peripheral blood was negative. This case suggests that LST using BALF is useful for the diagnosis of drug-induced pneumonitis.

Aged↗
PubMed1986

A HPLC method for the simultaneous determination of disopyramide, lidocaine and their monodealkylated metabolites.

This paper describes a simple high-performance liquid chromatographic method for the determination of disopyramide and lidocaine simultaneously with their dealkylated metabolites. After basic tert-butyl methyl ether extraction and back-extraction with phosphoric acid, the drugs and their metabolites were injected into a Supelcosil CN column and the absorbance of the eluate was measured at 215 nm. The sensitivity was 0.3 mumol/l and the obtained precision, selectivity and stability during storage were adequate for the performed clinical studies in patients therapeutically treated with disopyramide and/or lidocaine. Some results from the clinical studies are briefly presented.

Chromatography, High Pressure Liquid↗
PubMed1999

[A comparison of alpha 1-acid glycoprotein (AAG) concentration and disopyramide binding in Chinese and Japanese].

The mean concentration of alpha 1-acid glycoprotein (AAG) in plasma and disopyramine binding capacity to AAG (bound disopyramine/AAG) were compared between fourteen Chinese and sixteen Japanese subjects. As a results, the author observed that the mean AAG-concentrations in Chinese and in Japanese were 0.55 +/- 0.11 mg/ml and 0.64 +/- 0.13 mg/ml, respectively. When disopyramine concentration was at 5.0 micrograms/ml, the bound disopyramine/AAG was 7.3 +/- 1.3 micrograms/mg in Chinese and 6.5 +/- 1.3 micrograms/mg in Japanese. Unbound fractions of disopyramine in Chinese and Japanese were 0.23 +/- 0.05% and 0.19 +/- 0.07%, respectively. These results indicated that there was no significant difference in the AAG-concentration and the bound disopyramine/AAG between Chinese and Japanese subjects. In male subjects, however, the AAG-concentration and the bound disopyramine/AAG in Chinese (0.57 +/- 0.14 mg/ml and 7.47 +/- 1.78 micrograms/mg) were significantly different from those in Japanese (0.72 +/- 0.11 mg/ml and 5.84 +/- 0.76 micrograms/mg, p < 0.05), though unbound fraction of disopyramide was not found different between Chinese and Japanese subjects. In female, the AAG-concentration, the bound disopyramine/AAG and unbound fraction of disopyramide did not significantly differ between Chinese and Japanese subjects. These findings suggest a possible structural difference of monosaccharides in plasma-AAG between Chinese and Japanese male subjects.

Adult↗
PubMed1975

[Electrophysiological effects of the antiarrhythmia agents disopyramide and propafenone on human heart conduction system].

The effect of Disopyramide and Propafenone on intracardiac conduction and refractory periods was tested by means of His bundle electrography and atrial stimulation. Disopyramide (1,7 mg/kg) was administered in 10 patients. There was no significant change of heart rate and conduction time within the atrium and the AV-node. The conduction velocity within the His-Purkinje system was significantly slowed by 13% of the control value. The ERP of the atrium as well as the ERP and FRP of the AV node were prolonged. Propafenone (1,7 mg/kg) was tested in 18 patients. The heart rate was significantly slowed by 13% of the control value. The conduction velocity within all compartments of the heart was depressed uniformly. The all-over-all prolongation of the HBE-intervals was 15%. Furthermore the results are in favour of a prolongation of the ERP of the atrium and the ERP of the AV node. The results can only partially explain the antiarrhythmic effect of the drugs. However, the data are important for assessing the possible side effects during antiarrhythmic treatment especially in patients with disease of the conduction system.

Adult↗