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PubMed1976

Disopyramide: serum level and arrhythmia conversion.

The response of arrhythmias to oral disopyramide in relation to its serum levels has been documented. Disopyramide (100 mg.) was given orally, 6 or 8 hourly, to 16 patients with coronary or hypertensive heart disease who developed acute but stable cardiac arrhythmias (20 episodes) which persisted, despite bed rest and sedation with intravenous diazepam or diamorphine. Blood was taken when arrhythmia conversion was observed and the serum disopyramide levels were estimated by gas chromatography. Over-all control of arrhythmias was achieved in 13 (82 per cent) patients within 24 hours. Disopyramide-serum levels were as follows: effective for atrial arrhythmias, 2.80 to 3.18 mug per milliliter, and 3.27 to 7.48 mug per milliliter for ventricular; mean effective levels for all arrhythmias, 3.69 mug per milliliter; mean ineffective levels, 2.39 mug per milliliter (p less than 0.01). Side effects (prolongation of PR and QTc, fall of diastolic BP, urine retention) were observed with serum levels of 3.61 to 7.48 mug per milliliter (mean, 5.54 mug per milliliter) but they were not troublesome clinically. It is concluded that disopyramide is effective and safe with serum levels ranging from 2.39 to about 3.60 mug per milliliter, and this can be maintained with 100 mg., 8 hourly. The drug, however, should be given with caution to patients with severe myocardial disease or low arterial pressure and in the presence of an abnormal ECG.

Administration, Oral↗
PubMed1978

Disopyramide phosphate: is it just another quinidine.

We compared the effects of a therapeutic concentration of disopyramide with those of quinidine and lidocaine on the action potential characteristics and on the steady-state relationship between membrane potential and the maximum rate of rise of the action potential in the same normal Purkinje fiber in which constant impalement was maintained for more than 7 h. All the drugs depressed the steady-state upstroke velocity in the following order of magnitude: quinidine greater than disopyramide greater than lidocaine. Both lidocaine and disopyramide shifted the normalized steady-state curve to more negative membrane potentials indicating a greater depression of upstroke velocity at lower membrane potentials. Quinidine did not shift this curve. Lidocaine abbreviated all phases of repolarization while both disopyramide and quinidine shortened the plateau phase and lengthened the terminal phase of the action potential. The results suggest that the actions of disopyramide on upstroke velocity resemble those of lidocaine, while its effects on action potential duration resemble those of quinidine. The actions of this drug are therefore more complex than previously assumed.

Action Potentials↗
PubMed1977

The antiarrhythmic efficacy of intravenous therapy with disopyramide phosphate.

Disopyramide phosphate was administered intravenously to 57 patients with 60 episodes of arrhythmia (21 supraventricular and 39 ventricular) as a 2 mg/kg bolus. Conversion to sinus rhythm was achieved in three (38 percent) of eight patients with atrial flutter, two (20 percent) of ten patients with atrial fibrillation, one (33 percent) of three patients with paroxysmal atrial tachycardia, and two (50 percent) of four patients with sustained ventricular tachycardia. In nine (75 percent) of 12 patients with nonsustained ventricular tachycardia, suppression of the arrhythmia was accomplished following the intravenous bolus of disopyramide. In 18 (78 percent) of 23 patients with frequent ventricular premature contractions, greater than 50 percent suppression of the ventricular premature contractions was achieved. These effects were satisfactorily maintained in six (86 percent) of seven patients with nonsustained ventricular tachycardia and in 14 (88 percent) of 16 patients with frequent ventricular premature contractions in whom therapy with disopyramide phosphate was continued as a 20 mg/hour intravenous drip infusion for up to 24 hours. Side effects were observed in only eight patients (14 percent) and were primarily anticholinergic in nature. Transient hypotension, not necessitating treatment with pressor agents, was observed in three patients (5 percent), in two of whom discontinuance of therapy with disopyramide was deemed necessary. Intravenous therapy with disopyramide in the dosage regimen employed appears to be moderately effective against supraventricular arrhythmia and particularly effective against ventricular arrhythmia with minimal toxicity. It appears to be a suitable alternative to intravenous therapy with lidocaine and has the additional advantage of availability for oral administration.

Administration, Oral↗
PubMed1978

Disopyramide in patients with the Wolff-Parkinson-White syndrome and atrial fibrillation.

The effect of administration of disopyramide on the ventricular response to atrial fibrillation was studied in six patients with the Wolff-Parkinson-White syndrome. The drug was given intravenously to five patients during intracardiac electrophysiologic studies and to a sixth patient during electrocardiographic monitoring in a coronary care unit. One patient with a very rapid ventricular response to atrial fibrillation underwent a second electrophysiologic study after oral treatment for four weeks with disopyramide. In all cases, administration of disopyramide reduced the mean ventricular rate and increased the shortest interval between consecutive preexcited ventricular complexes during atrial fibrillation. Therapy with disopyramide should therefore be useful in preventing ventricular fibrillation which can result from a rapid ventricular response to atrial fibrillation in patients with an accessory atrioventricular pathway. There has been no recurrence of paroxysmal tachycardia in the four patients who have been maintained on oral therapy with disopyramide.

Adult↗
PubMed1992

Disopyramide block of cardiac sodium current after removal of the fast inactivation process in guinea pig ventricular myocytes.

To determine the necessity of sodium channel fast inactivation for the block of sodium current (INa) by disopyramide, we studied the effects of disopyramide on INa in guinea pig ventricular myocytes treated with chloramine-T, which removes the fast component of INa inactivation. After exposure to chloramine-T (2 mM), INa amplitude was reduced at all voltages and INa decay was irreversibly prevented. Disopyramide (20 microM) produced both tonic block and use-dependent block of INa in chloramine-T-treated myocytes. Before treatment with chloramine-T, the time course of both the onset of and recovery from use-dependent block by disopyramide were best fit by the sum of double exponential functions, and the time constant of the slow phase of recovery increased as the membrane was hyperpolarized. After removal of the fast component of INa inactivation by chloramine-T, the fast phase of the onset block and the fast phase of recovery from block were abolished. However, the voltage dependency of the time course of recovery from block was unchanged. Thus, although the fast sodium inactivation process is not required for tonic and use-dependent block of INa by disopyramide, it contributes to the fast phase of block development and unbinding from use-dependent block.

Animals↗
PubMed1976

A study of the acute electrophysiological and cardiovascular action of disopyramide in man.

The acute electrophysiological and hemodynamic effects of intravenous disopyramide (1.5 mg/kg body weight) were studied in 12 patients with suspected coronary artery disease. Plasma levels of disopyramide were monitored. Disopyramide delayed conduction within the His-Purkinje system and increased the effective refractory period of the atrium. Conduction within the AV node and its refractory period, however, was not significantly altered by the drug. The corrected Q-T interval was significantly increased. Disopyramide increased systemic arterial pressure and slightly raised the left ventricular end diastolic pressure. Heart rate, cardiac and stroke index were unaltered. Peak mean levels of disopyramide were reached 5 minutes after the injection of the drug.

Adult↗
PubMed1979

Disopyramide kinetics in patients with acute myocardial infarction.

The kinetic behavior of disopyramide was studied in 20 patients with suspected myocardial infarction: in 13 of these, the diagnosis was subsequently confirmed. All received a 400-mg oral loading dose of disopyramide base followed by an oral maintenance regimen of either 100 or 200 mg 4 times daily. The elimination half-life (t1/2beta) was longer (p less than 0.05) in patients with confirmed infarction than in patients with unconfirmed infarction [38.0 +/- 3.7 hr (mean +/- SEM) compared to 24.3 +/- 0.8 hr, and 21.2 +/- 2.1 hr compared to 7.2 +/- 2.4 hr for the 100- and 200-mg maintenance dose regimens, respectively]. The t1/2beta was dose dependent for infarct and noninfarct patients. Two of the patients with confirmed infarction failed to reach trough plasma levels equal to or exceeding the lower end of the manufacturer's recommended therapeutic range (3.3 mug/ml) during the study. For the remaining 11 patients the time taken to achieve trough plasma levels of 3.3 mug/ml varied from 18 to 170 hr; hence plasma disopyramide concentration in these patients was suboptimal at a time when the risk of arrhythmias is high. Modification of existing oral loading dose regimens is therefore required for optimization of oral disopyramide therapy.

Administration, Oral↗
PubMed1975

Linear relationships between plasma binding and lipophilicity of disopyramide derivatives.

The extent of plasma binding and the partition coefficient of disopyramide and 20 disopyramide derivatives were determined. Structural variations on the four functional groups around the tetrahedral carbon in the disopyramide molecule was found to influence both parameters to varying degrees. Three linear equations were developed to correlate the observed effects, depending on the type of chemical modification. The linear correlation between drug-plasma interaction and lipophilic character was analyzed theoretically. A simple model was derived to relate quantitatively the variation in the extent of plasma binding to the change in lipophilicity of disopyramide derivatives.

Arrhythmias, Cardiac↗
PubMed1978

Electrophysiology of disopyramide in man.

The electrophysiological effects of an intravenous dose of disopyramide phosphate (2 mg per kg body weight) were studied in 17 patients. Studies were performed with the patients fasting, unpremedicated, and off all medication for three days. Blood samples for estimation of serum levels of disopyramide were collected in 15 of these patients. The effects of intravenous disopyramide were maximal at five minutes, less marked at 20 minutes, and largely gone by 30 minutes after administration of the drug. Sinus cycle length and corrected sinus node recovery time were shortened significantly. No index of atrioventricular nodal function was significantly changed. Both atrial and ventricular effective refractory periods were significantly prolonged. Further impairment of intraventricular conduction occurred in six patients with bundle branch block on electrocardiogram or prolonged HV interval. In one of two patients with Wolff-Parkinson-White syndrome, the bypass effective refractory period was prolonged. These electrophysiological changes are similar to quinidine and quinidine like drugs. It is recommended that disopyramide should be used cautiously in patients with evidence of His Purkinje system disease since it may lead to higher degrees of intraventricular block.

Adolescent↗
PubMed1979

Intravenous disopyramide phosphate and ventricular overdrive pacing in the termination of paroxysmal ventricular tachycardia.

Both antiarrhythmic drugs and bursts of rapid ventricular pacing provide alternatives to DC cardioversion for the treatment of paroxysmal ventricular tachycardia. This report considers the individual and combined success of burst ventricular pacing and intravenous disopyramide phosphate in the tretment of 11 examples of paroxysmal ventricular tachycardia. Rapid ventricular pacing, at a rate of up to 50 beats/min faster than the tachycardia rate terminated 7 of the tachycardias. Intravenous disopyramide resulted in increased tachycardiac cycle length (342 +/- 34 ms-385 +/- 56 ms), increased QRS complex width (147 +/- 42 ms-180 +/- 41 ms) and termination of 8 the tachycardias. The remaining 3 tachycardias could be terminated by bursts of ventricular pacing following the infusion of disopyramide. Of these, 2 could not be terminated prior to disopyramide. The use of both techniques allowed the extinction of all 11 tachycardias and prevented the need to proceed to DC conversion.

Adult↗
PubMed1977

The use of disopyramide in resistant cardiac arrhythmias due to acute ischaemic heart disease.

Disopyramide, a new anti-arrhythmic drug, has been assessed in twenty-one episodes of cardiac arrhythmia secondary to acute ischaemic heart disease which failed to respond to more conventional suppressive therapy with lignocaine and other standard drugs. The intravenous administration of 100 mg of disopyramide resulted in suppression of two out of seven episodes of supraventricular arrhythmia, and eleven out of fourteen episodes of ventricular arrhythmias. Successful suppression correlated with blood levels of disopyramide in most cases of ventricular arrhythmias but not in the supraventricular arrhythmias. There were no adverse effects on blood pressure or cardiac function. There were minimal effects on conduction in the electrocardiogram. It is concluded that disopyramide, which probably acts by direct depression of myocardial irritability, is a useful new anti-arrhythmic drug in acute myocardial infarction, especially in those patients with ventricular arrhythmias resistant to more conventional anti-arrhythmic therapy.

Acute Disease↗
PubMed1992

Mexiletine and disopyramide suppress ventricular premature contractions (VPC) irrespective of the relationship between the VPC and the underlying heart rate.

The effects of mexiletine (300 mg/day, 24 patients) and disopyramide (300 mg/day, 20 patients) on ventricular premature contractions (VPCs) were studied using a 24-hour ambulatory electrocardiogram. The VPC frequency was evaluated as a function of the underlying heart rate (HR). The VPC-HR correlation was classified into 2 major types, depending on whether the frequency of the VPC increased with the increased HR (positive type) or not (nonpositive type). The effects of the drugs were assessed based on the VPC-HR correlation and on the percent reduction of the VPC frequency. Mexiletine and disopyramide significantly decreased the frequency of the VPCs of both the positive and nonpositive types. Each drug was assumed to be effective when the percent reduction of the VPC frequency exceeded 70%. Mexiletine (300 mg/day) was 58.5% effective in positive type patients and 33.3% effective in nonpositive type patients, with a total efficacy of 45.8%. Disopyramide was effective in 50% of total cases with 44.4% in positive type patients and 54.5% in nonpositive type patients. However, the efficacy of these drugs on the 2 different types of VPCs was the same statistically. The findings strikingly contrasted those obtained with diltiazem and atenolol, which predominantly suppressed VPCs of the positive type which share similar characteristics with a triggered activity in vitro. We conclude that the mode of action of class I antiarrhythmics on the VPCs differs from that of class II or IV antiarrhythmics, as viewed from the VPC-HR relationship, and that the difference probably comes from the different arrhythmogenesis for positive and nonpositive types of VPCs, in addition to the different electrophysiological actions of mexiletine and disopyramide.

Cardiac Complexes, Premature↗
PubMed1992

[Effects of disopyramide on normal and pathological atrioventricular conduction].

Disopyramide is a Vaughan-Williams class Ia antiarrhythmic, which is distinguished by its anticholinergic activity, which is due to its active metabolite: mono-N-alkyl disopyramide. In cells with a rapid response, such as those in the His-Purkinje tissue, it depresses conduction. In slow-responding cells (sinus node and Tawara's node) direct depression of conduction and automatism, and anticholinergic stimulation have opposing effects. In terms of clinical electrophysiology, this is a Touboul class IIa compound: and action mainly on the His-Purkinje system involving extension of the conduction time and of the refractory time. Nodal conduction is improved according to measurement of the alternate Wenckebach; according to studies of the denervated heart in transplanted patients, there is a depressant effect on automatism and conduction at all levels, but the vagolytic effect corrects this activity at Tawara's node. Clinical trials have demonstrated the absence of any deterioration, and in some cases and actual improvement of nodal conduction disorders in response to disopyramide and good safety in the presence of non-major intraventricular conduction problems (such as bundle branch block). In practice, these properties mean that moderate nodal conductive disorders and simple bundle branch block do not constitute an obstacle to the use of disopyramide. In junctional tachycardia, it is particularly indicated for use in tachycardia involving an accessory pathway, but is also effective in intranodal tachycardia due to its twofold action.

Arrhythmias, Cardiac↗
PubMed1977

Effects of disopyramide and aprindine on arrhythmias after acute myocardial infarction.

The incidence of ventricular arrhythmias after myocardial infarction was compared in a double blind study of disopyramide (33 patients), aprindine (34 patients) and placebo (31 patients). Total ventricular arrhythmias were less frequent in the aprindine group than in the disopyramide group (P less than 0.05) or than in the combined disopyramide and placebo groups (P less than 0.05). The incidence of life-threatening arrhythmias and of ventricular arrhythmias in high risk patients was also reduced by aprindine compared to disopyramide (P less than 0.001) or placebo (P less than 0.001). It is concluded that aprindine is effective in reducing ventricular arrhythmias and that further investigations on its preventive use after the onset of myocardial infarction are justified.

Acute Disease↗
PubMed1976

[Antiarrhythmic effect of disopyramide in ventricular extrasystole and auricular fibrillation].

Disopyramide (B 712) was tested in 39 patients with chronic arrhythmias of different kind: 23 cases with atrial fibrillation, 16 cases with ventricular ectopic beats, two cases with supraventricular tachycardias. The effect of disopyramide was compared to a pretreatment with one or several antiarrhythmic drugs (quinidine, beta-blocking agents, verapamil, ajmalin-bitartrat, aprindine, propafenone, diphenylhydantoin) which had been discontinued either due to ineffectiveness or the occurrence of intolerable side effects. Therapeutical effectiveness was controlled by on-line arrhythmia computers in the CCU or Holter monitoring. 15 patients were treated longer than 4 weeks up to 16 months (mean 35+/-22,6 weeks). The following results were achieved: 1 atrial fibrillation, abolition or significant reduction of the rate of recurrence in 10 out of 23 patients; slight reduction or no effect in 13 patients; 2. ventricular ectopic beats: abolition or significant reduction in 6 out of 16 patients, slight reduction or no effect in the remaining 10 patients. Patients who were treated successfully received the same dosis as those without therapeutical success. In cases with atrial fibrillation, the success was dependent on the duration of this arrhythmia prior to treatment. In comparison to the pretreatment with one or several of the above-mentioned anti-arrhythmic drugs, disopyramide was as effective as the drug given before. The analysis of the Ecg revealed a slight but insignificant prolongation of the time intervals. In 22 patients reversible dosage-dependent side effects were observed which are due to the vagolytic action of the drug: dry mouth, blurred vision, urinary hesitancy, nausea, headache. These side effects occurred at daily dosages between 400 to 800 mg increasing markedly in patients on 800 mg a day. The drug had to be discontinued in 4 cases because of side effects. During long-term treatment no severe side effects were observed. Thus, disopyramide may serve as an alternative to quinidine, especially if the latter has to be stopped because of side effects.

Adolescent↗
PubMed1975

Haemodynamic effects of intravenous disopyramide in heart failure.

The haemodynamic effects of disopyramide have been studied in 11 patients with manifest or imminent heart failure. Disopyramide, 2 mg per kg body weight, was given intravenously during right and left heart catheterisation. The cardiac index decreased by an average of 28% (p less than 0.01); mean maximal left and right ventricular end-diastolic pressures were increased by 5.0+/-0.9 mm Hg (p less than 0.01) and 5.0+/-0.6 mm Hg (p less than 0.05), respectively; and left ventricular systolic pressure fell slightly but significantly (p less than 0.05). No significant change in right ventricular systolic pressure was seen. Pulmonary wedge pressure rose on average by 2.7 mm Hg (p less than 0.05). No significant change in heart rate was observed in 5 patients with sinus rhythm. In 6 patients with atrial fibrillation, there was a significant (p less than 0.01) increase in heart rate; the average increase in heart rate for the entire group was 19.6 beats per minute. The maximum effect on all the parameters occurred 7-11 minutes after the injection, and it gradually subsided during the following 10 minutes. It was concluded that disopyramide had a potentially serious myocardial depressant effect.

Adult↗
PubMed1976

Oral disopyramide in prophylaxis of arrhythmias following myocardial infarction.

Oral disopyramide given prophylactically following myocardial infarction has been compared with placebo in a double-blind trial using continuous-tape monoriting of the electocardiogram. It caused a significant reduction in the incidence of ventricular arrhythmias and of the various degrees of heart-block. There was a significant reduction of reinfarction during hospital stay in patients who had received disopyramide. Disopyramide appears to be a safe and effective oral therapy in the prevention of potentially serious arrhythmias following myocardial infarction.

Administration, Oral↗
PubMed1977

Oral disopyramide for the prevention of arrhythmias in patients with acute myocardial infarction admitted to open wards.

Patients with acute myocardial infarction admitted to open wards of three hospitals were given either oral disopyramide (100 mg four times daily) or matching placebo, prophylactically, for seven days. The drug was associated with a significant reduction in mortality (p = 0-0025) and in incidence of extension of infarction (p = 0-01), ventricular fibrillation (p = 0-05), and ventricular tachycardia (p = 0-01). Disopyramide was not associated with any particular complication or side-effect. Unitl information is available to the contrary, oral disopyramide should be given for the first seven days after myocardial infarction to all patients not managed in an intensive-care unit.

Acute Disease↗