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PubMed1990

[Hemodynamic effects of disopyramide on postischemic and normal myocardium].

The acute effects of i.v. disopyramide (1.5 mg/kg) on the hemodynamics of postischemic hearts were investigated in comparison to normal ventricles. Infusion (7 min) was started in rats 20 min after 3 x 4 min of global ischemia during the period of stable postischemic dysfunction. 15 minutes after disopyramide i.v. (vs. NaCl control data) the cardiac output was reduced to 82 +/- 4% (vs. 101 +/- 5%; p less than 0.01) and dp/dtmax to 77 +/- 5% (vs. 83 +/- 3%). The maximum isovolumic pressure generating capacity as load-independent index of myocardial contractility was reduced to 89 +/- 2% (vs. 95 +/- 2%; p less than 0.05). In contrast to the results on postischemic myocardium no measureable change of the hemodynamics was detectable after the identical dose in normal animals without left ventricular dysfunction. Our results indicate an increased sensitivity of postischemic myocardium with modestly reduced contractile function to the hemodynamic effects of disopyramide, especially to the negative-inotropic effects.

Animals↗
PubMed1997

Disopyramide improves the balance between myocardial oxygen supply and demand in patients with hypertrophic obstructive cardiomyopathy.

We evaluated the effects of disopyramide in terms of the balance between myocardial oxygen supply and demand in patients with hypertrophic obstructive cardiomyopathy (HOCM). The myocardial oxygen supply was evaluated by measuring coronary flow velocity and the myocardial oxygen demand was assessed by the pressure-volume area (PVA). The time velocity integral of coronary flow did not change significantly (20 +/- 6 to 21 +/- 8 cm), but the peak left ventricular pressure and left ventricular external work decreased significantly (206 +/- 44 to 157 +/- 37 mmHg, P < 0.001; 1.09 +/- 0.33 to 0.80 +/- 0.23 J/beat, P < 0.001) after disopyramide administration. From theoretical analysis using these data, we concluded that disopyramide improves the myocardial oxygen supply-demand balance in patients with HOCM.

Adult↗
PubMed2000

The relationship between risk of hypoglycemia and use of cibenzoline and disopyramide.

OBJECTIVE: A case-control study was carried out to compare the risks of hypoglycemia caused by disopyramide and cibenzoline. METHODS: We selected 91 subjects with hypoglycemia from among 14,156 outpatients who consulted the National Cardiovascular Center (NCVC) and received drug therapy between September 1997 and February 1998. We used the fasting blood sugar (FBS) level of 75 mg/dl or less as the cut-off level to screen for hypoglycemia. For each case, five controls matched for gender and age were selected from the clinical division consulted by relevant subjects. RESULTS: Ninety-one cases and 455 controls were enrolled in this study. Of 91 cases with hypoglycemia, 8 (8.8%) were treated with cibenzoline and 3 (3.3%) with disopyramide. The percentage of cases treated with cibenzoline was greater than that in the controls (1.5%), and the prescription frequency of cibenzoline during the study period was 2%. With adjustment for potential confounding factors using conditional logistic regression, hypoglycemia was significantly correlated with the use of cibenzoline [OR 8.0 (95% CI 1.7-36.8)], insulin [OR 48.4 (95% CI 8.8-267.2)], and thyroid agents [OR 13.0 (95% CI 1.1-160.4)]. An increased risk of hypoglycemia associated with the use of sulfonylureas was not detected. In additional logistic regression analysis, including the variables with individual sulfonylureas, glibenclamide but not gliclazide significantly increased the risk of hypoglycemia. The use of disopyramide did not affect the risk of hypoglycemia. In separate analyses for diabetic and non-diabetic patients, the risks of hypoglycemia associated with the use of drugs other than beta-blocking agents in non-diabetic patients were estimated to be lower than those in diabetic patients. CONCLUSION: The use of cibenzoline was significantly correlated with an increased risk of hypoglycemia.

Adult↗
PubMed1980

Disopyramide (Norpace)-induced hypoglycemia.

Disopyramide (Norpace) is a recently released antiarrhythmic agent with quinidine-like actions, but structurally unique. We describe a patient in whom impressive hypoglycemia developed following treatment with this agent. Blood glucose levels returned to normal after cessation of therapy, but dropped again following rechallenge with the drug. The pathogenesis of the hypoglycemia was investigated by assessment of serum insulin, plasma glucagon and serum alanine levels during disopyramide rechallenge. Clinicians should be aware of fasting hypoglycemia as an unusual but potentially serious complication of disopyramide therapy.

Aged↗
PubMed1990

The effect of disopyramide on uterine contractions during pregnancy.

To evaluate the effect of disopyramide on uterine contractions during pregnancy, the drug was given for 48 hours to 10 women with indications for labor induction. Placebo was given to 10 other women with the same indications for induction. During the study period, regular uterine contractions occurred in 10 women in the study group, as compared with none in the control group (p less than 0.0001). Eight women in the study group were delivered of infants within 48 hours, as compared with none in the control group (p less than 0.0001). The mean time until the appearance of regular uterine contractions in the study group (4.15 +/- 1.76 hours) was significantly shorter (p less than 0.001) than that in the control group (56.13 +/- 5.28 hours). Patients who were not delivered of infants within 48 hours received other medications (prostaglandin E2, oxytocin). The mean maternal blood level of disopyramide at the time of appearance of uterine contractions was 1.52 +/- 0.9 mg/ml. The mean maternal level at delivery was 0.93 +/- 0.43 mg/ml and the cord blood level at the time of delivery was 0.33 mg/ml (cord blood/maternal level ratio = 0.36, r = 0.73, p less than 0.05). These results indicate that disopyramide should not be used in pregnancy for antiarrhythmic purposes because it may induce uterine contractions and delivery.

Adult↗
PubMed1989

Effects of verapamil, diltiazem and disopyramide on sinus function: a comparison with bepridil.

Cardiac drugs known to affect sinus function mostly exhibit negative chronotropic activity. However, impulse conduction within the sinus node can also be influenced. Recently we studied the direct effects of bepridil on rabbit sinus function. It appeared that sinoatrial impulse conduction was depressed markedly with drug concentrations that did not affect sinus automaticity. In the present study the direct effects of verapamil, diltiazem and disopyramide on rabbit sinus function and atrial conduction properties were studied. Verapamil (8.8 x 10(-8) M) reduced the sinoatrial impulse conduction velocity by 35% and prolonged sinoatrial refractoriness by 36%. On the other hand, the sinus rate and atrial conduction parameters were hardly affected. Diltiazem (5 x 10(-6) M) exerted similar actions on the sinoatrial impulse conduction velocity and caused a simultaneous reduction in the sinus rate of 48%. Atrial conduction remained unaffected. Disopyramide (5 x 10(-5) M) depressed both the atrial and nodal conduction properties markedly, whereas the sinus rate was reduced moderately, by almost 20%. Thus, verapamil, diltiazem and disopyramide act differently on sinus function and atrial conduction, whereby the predominant effect of verapamil and diltiazem on sinoatrial conduction properties favours the occurrence of a sinus exit block.

Animals↗
PubMed1993

Propafenone and disopyramide enhance post-ischemic contractile and metabolic recovery of perfused hearts.

The effects of sodium channel blockers, propafenone and disopyramide, on post-ischemic contractile dysfunction of perfused rat hearts were examined. Isolated hearts were subjected to 35 min ischemia, followed by 60 min reperfusion with and without administration of either drug during 3 min of pre-ischemia. Ischemia/reperfusion induced complete cardiac dysfunction, rise in left ventricular end-diastolic pressure, increase in perfusion pressure, accumulation of Na+ and Ca2+ and loss of K+ and Mg2+, and release of creatine kinase and purine nucleosides and bases from the heart. These observations suggest that ischemia/reperfusion in the current study induces cardiac cell necrosis or an increase in cell membrane permeability to ions, substrates and macromolecules. Treatment of perfused hearts with either propafenone at concentrations ranging from 5 to 70 microM, or disopyramide at concentrations of 100 microM or higher resulted in a pronounced contractile recovery of the heart, associated with suppression of reperfusion-induced tissue ion alteration and inhibition of reperfusion-induced release of creatine kinase and purine nucleosides and bases. Ischemic insult itself caused tissue Na+ accumulation and K+ loss without any change in tissue Ca2+ and Mg2+. The alterations in the electrolytes were attenuated by treatment with either agent. The results suggest that prevention of ischemia- and reperfusion-induced ionic disturbance of cardiac cells by propafenone and disopyramide plays a role in the improvement of post-ischemic contractile dysfunction.

Adenosine Triphosphate↗
PubMed1984

Stereoselective binding of disopyramide to human plasma protein.

The binding of racemic disopyramide and its two enantiomers to protein were compared in two samples of human plasma, two samples of freshly drawn serum and in a solution of alpha 1-acid glycoprotein. The binding of S(+)-disopyramide was higher at all concentrations as compared to to R(-)-disopyramide, and the binding of the racemate was intermediate. Differences in binding were due to differences in the association constant.

Binding Sites↗
PubMed1989

Evidence that the Na+-Ca2+ exchange system is related to the antiarrhythmic action of disopyramide.

1. Disopyramide induced a concentration-dependent decrease in action potential amplitude and Vmax, and prolonged action potential durations (APD50 and APD90) in ventricular muscle. 2. Na+-loaded membrane vesicles isolated from canine ventricular muscle rapidly accumulated Ca2+. 3. Monensin (10(-5) M) abolished Na+-dependent Ca2+ uptake, and Na+ enhanced Ca2+ efflux. 4. Na+-Ca2+ exchange by membrane vesicles was more active in preparations pretreated with disopyramide (10(-5) M) than in control membranes. 5. The results suggest that disopyramide changes Na+ influx from Na+ channel mediated to Na+-Ca2+ exchange mediated. This is verified in part by increased Ca2+ efflux.

Animals↗
PubMed1988

Distribution of lidocaine and disopyramide in human blood and tissue, a case report of death caused by spinal anesthesia.

An 11-year-old girl was anesthetized with hyper-baric solution of lidocaine as spinal anesthesia for an appendectomy in a surgical clinic. Respiratory arrest which occurred soon after the injection, was not discovered for a period of time. Since spontaneous respiration recovered within 2 h of intensive resuscitation, the patient was transferred to a community hospital for intensive care. Ten hours after the spinal anesthesia, she died of cardiac failure. The concentration of lidocaine in the brain was 5-10 times more than that in other tissues. The relationship between the possibility of malpractice of spinal anesthesia and tissue distribution of the drug was discussed. In addition to lidocaine, a toxic amount of disopyramide, an antiarrhythmic drug, was detected in the body. The distribution of disopyramide was also estimated, and the pharmacokinetics of disopyramide in plasma and tissues were studied experimentally in rats.

Anesthesia, Spinal↗
PubMed2006

Extractive-spectrophotometric determination of disopyramide and irbesartan in their pharmaceutical formulation.

Picric acid, bromocresol green, bromothymol blue, cobalt thiocyanate and molybdenum(V) thiocyanate have been tested as spectrophotometric reagents for the determination of disopyramide and irbesartan. Reaction conditions have been optimized to obtain coloured comoplexes of higher sensitivity and longer stability. The absorbance of ion-pair complexes formed were found to increases linearity with increases in concentrations of disopyramide and irbesartan which were corroborated by correction coefficient values. The developed methods have been successfully applied for the determination of disopyramide and irbesartan in bulk drugs and pharmaceutical formulations. The common excipients and additives did not interfere in their determination. The results obtained by the proposed methods have been statistically compared by means of student t-test and by the variance ratio F-test. The validity was assessed by applying the standard addition technique. The results were compared statistically with the official or reference methods showing a good agreement with high precision and accuracy.

Biphenyl Compounds↗
PubMed2006

Disopyramide is an effective inhibitor of mutant HERG K+ channels involved in variant 1 short QT syndrome.

The recently identified idiopathic short QT syndrome (SQTS) is associated with an increased risk of arrhythmia and sudden death. The use of implantable cardioverter defibrillators helps to protect SQTS patients from ventricular fibrillation; however, pharmacological treatments to normalise the QT interval are limited: thus far only quinidine has been found to be effective in a subset of patients, with the SQT1 variant. SQT1 is associated with an amino acid substitution (N588K) in the KCNH2-encoded HERG K(+) channel that reduces HERG current (I(HERG)) inactivation and sensitivity to drug block. We demonstrate here that the N588K-HERG mutation only slightly attenuates I(HERG) blockade by the Class Ia antiarrhythmic drug disopyramide (1.5-fold elevation of IC(50)), compared to quinidine (3.5-fold elevation of IC(50)) and the Class III antiarrhythmic drug E-4031 (11.5-fold elevation of IC(50)). Thus, of the drugs studied to date, disopyramide is the one least affected by the SQT1 HERG mutation. Disopyramide is associated with QT prolongation in normal use and our findings provide a rational basis for its evaluation as a treatment for SQT1.

Animals↗
PubMed1981

Torsade de pointes ventricular tachycardia. A complication of disopyramide shared with quinidine.

Two cases of documented torsade de pointes ventricular tachycardia in association with the use of disopyramide are described. One patient had previously experienced an episode suggestive of quinidine induced ventricular tachycardia while the other developed ventricular tachycardia during quinidine treatment which was later exacerbated and sustained by the administration of disopyramide. Both patients exhibited a prolonged QTc or QUc interval at the time of the arrhythmia. These cases suggest that a propensity of ventricular arrhythmias induced by quinidine may identify individuals who are likely to develop similar arrhythmias disopyramide treatment as well.

Aged↗
PubMed1997

Discrepant drug action of disopyramide on ECG abnormalities and induction of ventricular arrhythmias in a patient with Brugada syndrome.

An electrophysiologic study was attempted in a patient who experienced cardiac arrest. Programmed electrical stimulation from the right ventricle, without the use of any drugs, induced ventricular fibrillation (VF) twice. Disopyramide prevented the induction of ventricular arrhythmia by rendering VF to a nonsustained polymorphic ventricular tachycardia when administered at 300 mg/day, and noninducible at 400 mg/day. However, ST-segment elevation and the rSr' pattern in leads V(1-3) characteristic of Brugada syndrome became exaggerated by disopyramide. Disopyramide exerted discrepant action on the electrocardiographic (ECG) abnormalities and induction of VF in this patient, suggesting the efficacy of antiarrhythmic drugs assessed by an electrophysiologic study may be unrelated to ECG abnormalities in cases of Brugada syndrome.

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↗
PubMed1980

Randomised placebo-controlled trial comparing oxprenolol with disopyramide phosphate in immediate treatment of suspected myocardial infarction.

473 patients with suspected acute myocardial infarction were entered into a randomised, double-blind, placebo-controlled comparison of disopyramide phosphate, 150 mg three times a day, and oxprenolol, 40 mg three times a day. When analysed on an intension-to-treat basis there was no significant difference in 6-week mortality between the groups, but patients who were able to continue on the active medications fared better than the patients who had to be withdrawn. The withdrawal rate because of heart failure in patients randomised to receive disopyramide was significantly increased. Patients receiving this agent also showed a reduced number of arrhythmic episodes on 24-h tape recordings but this trend did not achieve statistical significance. The results show that the early use of either oxprenolol or disopyramide phosphate in patients with suspected acute myocardial infarction is unlikely to improve mortality.

Acute Disease↗
PubMed1989

Concentration-response relationships of disopyramide in patients with ventricular tachycardia.

The protein binding of disopyramide is altered when concentration is increased within the therapeutic range. A wide range of free concentrations may be produced at a given total concentration. The present study assessed whether intracardiac electrophysiologic responses to disopyramide related better to free or to total concentration. Intravenous infusions of disopyramide were evaluated in 17 patients with inducible sustained ventricular tachycardia. The first maintenance infusion produced total serum concentrations of 11.7 +/- 2 mumols/L, and no significant increase occurred at higher-dose infusions. However, free concentrations during the first and second maintenance infusions were significantly different at 5.3 +/- 1 mumols/L and 6.8 +/- 1 mumols/L, respectively. Free fraction also increased significantly, from 45% +/- 8% to 50% +/- 7%. Overall change in QTc interval and ventricular tachycardia cycle length correlated with free concentration but not with total concentration. This study showed that some intracardiac measurements correlate with free concentration but that none correlate with total concentration.

Disopyramide↗