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At least 19 recordsLinked to original sources

PubMed1981

Ventricular tachycardia: prediction of response to oral aprindine with intravenous aprindine.

Aprindine was administered both intravenously and orally to 25 patients with ventricular tachycardia refractory to conventional antiarrhythmic agents to test the hypothesis that the response to intravenous aprindine predicts the response to oral aprindine. Ten patients had incessant ventricular tachycardia and 15 had paroxysmal sustained inducible ventricular tachycardia. Eleven patients (43 percent) had conversion to sinus rhythm with intravenous aprindine (nine with incessant and two with paroxysmal sustained ventricular tachycardia). Thirteen patients (all with paroxysmal sustained ventricular tachycardia) manifested slowing of the tachycardia without conversion, whereas in one patient with incessant ventricular tachycardia, the tachycardia became less frequent and nonsustained after intravenous aprindine. All 11 patients who had conversion to sinus rhythm with intravenous aprindine remained free of ventricular tachycardia during oral treatment with aprindine (at 2 weeks) and for a follow-up period of 2 to 38 months (mean 16 +/- 13). Of the 14 patients who did not have conversion to sinus rhythm with intravenous aprindine, 12 had spontaneous or inducible ventricular tachycardia, or both, at evaluation 1 to 2 weeks after initiation of oral aprindine. In conclusion, administration of intravenous aprindine to patients with ventricular tachycardia is helpful in predicting the subsequent response to oral aprindine. In addition, the pattern of ventricular tachycardia predicted the response to aprindine; patients with incessant ventricular tachycardia tended to respond, and those with paroxysmal sustained ventricular tachycardia tended not to respond.

Administration, Oral↗

PubMed1986

Effect of sotalol, aprindine and the combination aprindine-sotalol on monophasic action potential duration.

The effects of sotalol, aprindine and the combination aprindine-sotalol in the intact dog heart were evaluated during constant atrial pacing with the use of monophasic action potential (MAP) recording. A first group of five dogs was given 1.5 mg kg-1 body weight of sotalol, followed by a second infusion of 1.5 mg kg-1 30 min later. Both doses of sotalol produced a statistically significant increase in right atrial MAP duration at 50% of repolarization (RAMAP50) and right ventricular MAP duration at 90% of repolarization (RVMAP90). To a second group of six dogs aprindine 1 mg kg-1 and aprindine 2 mg kg-1 were administered intravenously. The infusion of aprindine did not alter right atrial and right ventricular MAP duration. The addition of 1.5 mg kg-1 of sotalol to the dogs pretreated with aprindine 2 mg kg-1 resulted in a 25% increase in RAMAP50 and a 21% prolongation of RVMAP90. In summary, sotalol lengthens atrial and ventricular monophasic action potential duration and still prolongs repolarization of monophasic action potentials after previous administration of aprindine. A combination of sotalol, a beta-adrenergic blocker possessing class III efficacy, with a class I antiarrhythmic agent may be useful with respect to their electro-physiological action.

Animals↗

PubMed1987

Effects of intravenous sotalol, aprindine and the combination of sotalol and aprindine on chronic high frequency ventricular arrhythmias in man.

The comparative antiarrhythmic efficacy of three different intravenous drug regimens was evaluated in 12 symptomatic patients (mean age: 72 years) with chronic high frequency ventricular arrhythmias (mean: 834 PVCs h-1). In a cross-over study with latin square distribution the following drug regimens were administered intravenously to all patients aprindine 2 mg kg-1, sotalol 1.5 mg kg-1, aprindine 1 mg kg-1 & sotalol 0.75 mg kg-1. The mean percentage of PVC reduction was 41% (P less than 0.05) for aprindine 2 mg kg-1; 51% (P less than 0.05) for sotalol 1.5 mg kg-1 and 72% (P less than 0.01) for the combined drug therapy (aprindine 1 mg kg-1 and sotalol 0.75 mg kg-1). The mean plasma concentration was 1371 ng ml-1 after administration of aprindine 2 mg kg-1 and 1730 ng ml-1 after infusion of sotalol 1.5 mg kg-1. After combined drug therapy, mean plasma levels were 942 ng ml-1 for aprindine and 992 ng ml-1 for sotalol. The different drug regimens were well tolerated in all patients and no side-effects occurred. Combination therapy consisting of a drug that prolongs action potential duration with an antiarrhythmic agent that has a high affinity for the inactivated channels may thus achieve an antiarrhythmic efficacy comparable to single agent therapy, permitting the use of lower dosages.

Aged↗

PubMed1981

Alterations in regional myocardial distribution and arrhythmogenic effects of aprindine produced by coronary artery occlusion in the dog.

Little information exists regarding the effects of coronary artery occlusion on the distribution and actions of antiarrhythmic agents. We administered aprindine to dogs before, 5 min after, and 24 h after one-stage left anterior descending coronary artery (LAD) occlusion. Coronary artery occlusion performed after aprindine administration slowed the rate of disappearance of aprindine from the ischaemic zone compared with the normal zone, so that ischaemic zone aprindine concentrations averaged more than twice normal zone aprindine concentrations 1 h after LAD occlusion. When LAD occlusion was performed before aprindine administration, ischaemic zone aprindine concentrations were initially less than 15% of normal zone aprindine concentrations and increased with time to approach half of normal zone aprindine concentrations 70 min after LAD occlusion. Seventeen of 35 dogs (49%) receiving aprindine before LAD occlusion experienced sustained ventricular tachycardia or ventricular fibrillation, compared with 5/34 (14%) receiving aprindine immediately after LAD occlusion (P less than 0.01), 1/10 (10%) undergoing LAD occlusion without receiving aprindine (P less than 0.05) and 0/16 receiving aprindine without LAD occlusion (P less than 0.01). Aprindine administered 24 h after CO reduced premature ventricular complexes from a mean of 35 to 12 per 100 beats (P less than 0.01) occlusion importantly modifies the regional myocardial distribution of aprindine and its effects on ventricular arrhythmias after coronary artery occlusion.

Animals↗

PubMed1991

Combination therapy with aprindine and verapamil for paroxysmal supraventricular tachycardia as assessed by transesophageal atrial pacing.

UNLABELLED: To assess the efficacy of combination therapy of aprindine (40 mg/day) and verapamil (160 mg/day), transesophageal programmed atrial stimulation was performed on 21 patients with paroxysmal supraventricular tachycardia (including 12 patients with atrioventricular nodal reentrant tachycardia and nine patients with atrioventricular reentrant tachycardia) under four conditions: a) control, b) aprindine alone, c) verapamil alone, and d) aprindine + verapamil. RESULTS: a) Aprindine, verapamil, and aprindine + verapamil prevented paroxysmal supraventricular tachycardia induction in 2/21, 3/21, and 9/21 patients, respectively; b) aprindine + verapamil prolonged the cycle length of paroxysmal supraventricular tachycardia more than aprindine or verapamil alone; c) aprindine, verapamil, and aprindine + verapamil decreased the AV blocking rate by 15, 23, and 35 beats/min, respectively, in comparison with the control state; d) aprindine, verapamil, and aprindine + verapamil prolonged the effective refractory period of atrioventricular conduction system by 20, 34, and 76 msec, respectively, compared with the control state. In conclusion, aprindine + verapamil appear to be more effective than aprindine or verapamil alone in preventing paroxysmal supraventricular tachycardia with nodal reentry, but there was less benefit in those without nodal reentry (Wolff-Parkinson-White group).

Administration, Oral↗

PubMed1991

Aprindine blocks the sodium current in guinea-pig ventricular myocytes.

Aprindine is a class Ib antiarrhythmic agent. We studied effects of aprindine (3 mumol/l) on the Na+ current using whole cell voltage clamp (tip resistance = 0.5 M omega, [Na]i ando = 10 mmol/l at 18 degrees C). Aprindine revealed tonic block (Kdrest = 37.7 mumol/l, Kdi = 0.74 mumol/l; n = 4). Aprindine, shifted inactivation curve to hyperpolarizing direction by 11.4 +/- 3.5 mV (n = 4) without changes in slope factor. In the presence of 3 mumol/l aprindine, aprindine showed phasic block, i.e., duration-dependent block at 2 Hz (64% +/- 3% at 1.5 ms, 82% +/- 6% at 20 ms, 93% +/- 7% at 200 ms; n = 4). Short single prepulse also produced aprindine-induced phasic block (12% at 1.5 ms, 22% at 100 ms; n = 2). After removal of fast inactivation of Na+ current by 3 mmol/l tosylchloramide sodium, aprindine revealed phasic block, independent of holding potential. The recovery time constant from aprindine-induced phasic block was 4.8 s at holding potential = -100 mV and 5.0 s at holding potential = -140 mV. This use-dependent block of aprindine had pH dependency. Under acidic condition (pH 6.0), 3 mumol/l aprindine showed smaller use-dependent block (14% +/- 7% at 2 Hz; n = 4) comparing with either at pH 7.4 (68% +/- 13%; n = 4) or at pH 8.0 (90% +/- 12%; n = 4). The results suggest that aprindine could bind to the receptor via activation process through channel pore, resulting in decrease of Na+ current, and egress from the receptor through the lipid bilayer. These effects might be attenuated under acidic condition due to changes in intracellular ratio of charged to neutralized form of drug molecule.

Action Potentials↗

PubMed1990

Electrophysiologic actions of aprindine in rabbit atrioventricular node.

Aprindine hydrochloride is a potent antiarrhythmic agent against various atrial and ventricular tachyarrhythmias. To elucidate its pharmacological actions in the atrioventricular node, electrophysiologic experiments were conducted by applying microelectrode and voltage clamp methods to small preparations of the rabbit atrioventricular node. At a concentration 1 mumol/l, aprindine decreased the spontaneous firing frequency, maximal rate of depolarization, action potential amplitude, and take-off potential (P less than 0.05, n = 7). The spontaneous and rate-controlled action potential durations at 50 and 100% repolarization were prolonged by aprindine. Voltage-clamp experiments using the double microelectrode method revealed that aprindine blocked the slow inward current (Isi) in a voltage-dependent manner with a dissociation constant of 10 mumol/l and Hill coefficient of 0.8. The steady-state inactivation curve for Isi was shifted toward more negative potentials by 2.5 +/- 0.9 mV (P less than 0.05, n = 5) without a significant change in the slope factor. This finding suggests that aprindine has a higher affinity for inactivated slow inward (or Ca2+) channels than for resting channels. Aprindine caused use-dependent block of Isi, a result consistent with the drug's slow dissociation from inactivated Ca2+ channels. The delayed rectifying K+ current (IK) tail obtained on repolarization from +10 mV to -60 mV was significantly decreased from 15.4 +/- 2.4 to 6.8 +/- 1.4 nA (P less than 0.01, n = 6) and the deactivation time constant significantly increased by 20.7% (P less than 0.01, n = 6). The steady-state activation curve for IK was shifted in the hyperpolarized direction by 6.9 +/- 2.9 mV, suggesting a potent voltage-dependent block of this current by aprindine. The hyperpolarization-activated inward current (Ih) was decreased from 14.4 +/- 5.4 to 12.0 +/- 5.5 nA (P less than 0.05, n = 5). The transient outward and inward currents induced by 1 mumol/l acetylstrophanthidin were almost completely suppressed after the addition of 1 mumol/l aprindine. These results suggest that aprindine exerts a negative chronotropic action both by slowing deactivation of IK and by reducing Isi and Ih, and delays atrioventricular nodal conduction by reducing Isi and IK. These blocking actions of aprindine together with its inhibition of the transient outward and inward currents may explain its antiarrhythmic effects on the atrioventricular node.

Action Potentials↗

PubMed1981

[Comparison of the efficacy of aprindine and quinidine in chronic ventricular rhythm disorders].

The object of this study was to compare the efficacity and the side effects of Aprindine and Quinidine in patients with stable ventricular arrhythmias. A series of 33 patients with chronic stable ventricular arrhythmias were given successively Aprindine and Quinidine on the principle of extrasystoles (VES) determined by computer analysis of Holter recordings. The VES were counted every hour and the statistical study used analysis of variance followed by linear contrast and also the sign test. The stability of the arrhythmia was verified by several control Holter recordings without therapy (average : 3,3 per patient). Low dose regimes were used in 17 patients (an average of 50 to 60mg/day Aprindine, and 481 mg Quinidine base), and Quinidine was shown to be the more active (p less than 0.05 to 0.003 according to the test used), reducing the number of VES by 39% compared to an average of 21% for Aprindine. In the other 16 patients with a higher dosage regime, 109 mg Aprindine and 707 mg Quinidine base, there was no significant difference between Quinidine and Aprindine (p less than 0.08 to 0.12), Quinidine reducing the number of VES by an average of 54%, and Aprindine by 36%. Quinidine caused diarrhoea in I patient on the low dose and 4 patients in the high dose regime. Aprindine caused neurological side effects in 2 patients on the low dose, and 7 patients on the high dose regime. Aprindine at 100 mg/day may therefore be used in the same manner as Quinidine at usual dosages as regards the incidence of side effects of the two drugs. However, the ratio of effective dose/toxic dose is lower with Aprindine than with Quinidine.

Aprindine↗

PubMed1999

Effect of aprindine on heart rate variability indices in patients with ischemic heart disease.

BACKGROUND: Decreased heart rate variability indices (HRV) are associated with untoward outcome of patients with ischemic heart disease (IHD). Most class I antiarrhythmic agents decrease HRV, but aprindine (a new class I antiarrhythmic agent) is reported to increase HRV in patients without ischemia. HYPOTHESIS: The study was undertaken to determine whether apridine might increase HRV in patients with IHD. METHODS: To investigate the effect of aprindine on HRV in patients with IHD, we performed 24-h ambulatory electrocardiogram (ECG) at the end of placebo and aprindine (60 mg daily) treatment phases on 38 patients with IHD and at least isolated premature ventricular contractions (PVC). The study protocol utilized a single blind, 4-week, placebo-controlled design. Heart rate variability from ambulatory ECG included SDNN (ms), SDANN (ms), SD (ms), rMSSD (ms), pNN50 (%); frequency analysis of HRV consisting of total (ms, 0.01-1.00 Hz), low (ms, 0.04-0.15 Hz), and high (ms, 0.15-0.40 Hz) components. RESULTS: Study patients were divided into three groups according to the severity of IHD and antiarrhythmic efficacy of aprindine. Group 1 consisted of 15 patients with angina with single-vessel disease, and Group 2 was composed of 10 patients with either multivessel disease or post myocardial infarction; PVCs decreased in both groups as result of aprindine treatment. Group 3 consisted of 13 patients who showed no decreased PVC after aprindine treatment. RMSSD increased, and pNN50 and high-frequency spectra tended to increase in Group 1, while SD, rMSSD, pNN50, and total and low-frequency spectra decreased in Group 3; no significant changes were observed in Group 2. Aprindine significantly augments vagal activity, as reflected by the increase of rMSSD, pNN50, and high-frequency spectra in mild IHD. CONCLUSION: These salutary effects are less in more severe IHD, but aprindine does not aggravate HRV. Thus, if there are salutary effects on arrhythmias and no proarrhythmic effects, aprindine could be prescribed to patients with IHD without concern about decreasing HRV.

Adult↗

PubMed2002

Inhibitory effect of aprindine on Na+/Ca2+ exchange current in guinea-pig cardiac ventricular myocytes.

1. Using the whole-cell voltage clamp technique, the effect of aprindine on Na+/Ca2+ exchange current (I(NCX)) was examined in guinea-pig single cardiac ventricular myocytes and CCL39 fibroblasts expressing a dog cardiac Na+/Ca2+ exchanger (NCX1). 2. I(NCX) was recorded by ramp pulses from the holding potential of -60 mV with the external solution containing 140 mM Na+ and 1 mM Ca2+, and the pipette solution containing 20 mM Na+, 20 mM BAPTA and 13 mM Ca2+ (433 nM free Ca2+). 3. External application of aprindine suppressed I(NCX) in a concentration-dependent manner. The IC50 values of outward (measured at 50 mV) and inward (measured at -100 mV) I(NCX) components were 48.8 and 51.8 microM with Hill coefficients of 1.3 and 1, respectively. 4. Intracellular application of trypsin via the pipette solution did not change the blocking effect of aprindine, suggesting that aprindine does not affect the exchanger from the cytoplasmic side. 5. Aprindine inhibited I(NCX) of a mutant NCX1 with a deletion of amino acids 247 - 671 in the large intracellular domain between the transmembrane segments 5 and 6 in a similar manner to that of the wild-type, suggesting that the site of aprindine inhibition is not in the large intracellular domain of NCX1. 6. A kinetic study indicated that aprindine was cooperatively competitive with KB-R7943, another inhibitor of NCX and that aprindine was a competitive inhibitor with respect to external Ca2+. 7. We conclude that aprindine may modestly inhibit I(NCX) in a therapeutic range of concentrations (around 2.5 approximately 6.9 microM) possibly at an external or intra-membranous site of the exchanger.

Animals↗

PubMed1977

Treatment of recurrent ventricular tachycardia and fibrillation with aprindine.

Twenty-three patients with recurrent ventricular tachycardia or ventricular fibrillation, or both, were treated with aprindine, a new antiarrhythmic agent. It was found that: (1) no patient had a recurrence of ventricular fibrillation after aprindine therapy was begun, except as a terminal event subsequent to the development of acute myocardial infarction and cardiogenic shock or refractory congestive heart failure; (2) 6 patients experienced ventricular tachycardia after the loading dose, but with continued aprindine therapy the ventricular tachycardia was suppressed in 3 of these 6 patients, and a fourth patient was asymptomatic during brief paroxysms of ventricular tachycardia; (3) in 2 patients, aprindine was ineffective and was discontinued; (4) electrical cardioversion was not required in any patient receiving aprindine; (5) premature ventricular extrasystoles were decreased in 18 of the 23 patients treated with aprindine; (6) aprindine was discontinued in 1 patient because of intolerable side effects, although ventricular arrhythmias were suppressed in this patient; and (7) 5 patients died from acute myocardial infarction or severe heart failure while receiving aprindine.

Administration, Oral↗

PubMed1999

Inhibitory effects of aprindine on the delayed rectifier K+ current and the muscarinic acetylcholine receptor-operated K+ current in guinea-pig atrial cells.

In order to clarify the mechanisms by which the class Ib antiarrhythmic drug aprindine shows efficacy against atrial fibrillation (AF), we examined the effects of the drug on the repolarizing K+ currents in guinea-pig atrial cells by use of patch-clamp techniques. We also evaluated the effects of aprindine on experimental AF in isolated guinea-pig hearts. Aprindine (3 microM) inhibited the delayed rectifier K+ current (IK) with little influence on the inward rectifier K+ current (IK1) or the Ca2+ current. Electrophysiological analyses including the envelope of tails test revealed that aprindine preferentially inhibits IKr (rapidly activating component) but not IKs (slowly activating component). The muscarinic acetylcholine receptor-operated K+ current (IK.ACh) was activated by the extracellular application of carbachol (1 microM) or by the intracellular loading of GTPgammaS. Aprindine inhibited the carbachol- and GTPgammaS-induced IK.ACh with the IC50 values of 0.4 and 2.5 microM, respectively. In atrial cells stimulated at 0.2 Hz, aprindine (3 microM) per se prolonged the action potential duration (APD) by 50+/-4%. The drug also reversed the carbachol-induced action potential shortening in a concentration-dependent manner. In isolated hearts, perfusion of carbachol (1 microM) shortened monophasic action potential (MAP) and effective refractory period (ERP), and lowered atrial fibrillation threshold. Addition of aprindine (3 microM) inhibited the induction of AF by prolonging MAP and ERP. We conclude the efficacy of aprindine against AF may be at least in part explained by its inhibitory effects on IKr and IK.ACh.

Action Potentials↗

PubMedDate not supplied

Aprindine inhibits calmodulin-stimulated phosphodiesterase and Ca-ATPase activities.

Aprindine, an antiarrhythmic agent with structural similarities to lidocaine and procainamide, has proved effective in treatment of patients with ventricular premature depolarizations, ventricular tachycardia, and supraventricular arrhythmias. While its effects at an electrophysiologic level have been elucidated, its mechanism of action at a biochemical level has remained largely undefined. The data in this communication demonstrate that aprindine inhibits the activation of bovine brain cyclic 3':5'-nucleotide phosphodiesterase (EC 3.1.4.17) by calmodulin. This inhibition is specific for the calmodulin-stimulated enzyme, as no effect of aprindine is seen when phosphodiesterase is assayed in the absence of calmodulin. The inhibition is competitive with respect to substrate (cyclic AMP) and calmodulin concentrations. In the presence of 10 nM calmodulin, the ID50 for aprindine is 18 microM. This inhibition is not the result of aprindine acting as a calcium chelator because increasing the calcium concentration does not reverse the inhibitory effect. Aprindine also inhibits calmodulin-stimulated Ca-ATPase (ATP phosphohydrolase EC 3.6.1.3) activity, but again has no effect on the enzyme in the absence of calmodulin. Aprindine has hydrophobic properties which may be responsible for the inhibitory effect. Sufficient concentrations of aprindine are achieved in myocardial tissues to interfere with the ability of calmodulin to stimulate a number of enzymes present in the heart.

Animals↗

PubMed1975

Antiarrhythmic and antifibrillatory properties of aprindine.

The effectiveness of aprindine, N-[3-(diethyl amino)propyl]-N-phenyl-2-indanamine, was examined against experimentally induced arrhythmias. Ouabain-induced ventricular tachycardia was reversed in six of six dogs by aprindine, 5 mg/kg i.v. The threshold for extrasytoles induced by a 250-msec train of 60 Hz 2-msec pulses starting 75 msec after the pacing pulse was elevated from a control value of 0.18 +/- mA to a peak of 0.29 +/- 0.03 mA 5 minutes after aprindine, 5 mg/kg (P less than .005). The similarly determined ventricular fibrillation threshold was increased from a control value of 2.45 +/- 0.78 mA to a maximum of 5.68 +/- 1.47 mA 30 minutes after aprindine, 5 mg/kg i.v. (P less than .025). Aprindine failed to protect against fibrillation associated with one-stage occlusion and release of the left anterior descending coronary artery. Conscious dogs 24 hours after two-stage ligation of the left anterior descending coronary artery showed ectopic beats averaging 107 +/- 5 beats/min. Aprindine, 5 mg/kg i.v., caused an initial reduction of the ectopic rate to 1 +/- 1 beats/min (P less than .001) returning to 57 +/- 19 beats/min (P less than .05) 30 minutes postdrug. An additional 5 mg/kg dose reduced the ectopic rate to 1 +/- 1 beats/min (P less than .001) returning to 15 +/- 8 beats/min (P less than .005) 60 minutes after drug. Evaluation of these animals at 48 hours showed a similar pattern, although one animal fibrillated after 5 mg/kg of aprindine. Aprindine is an effective antiarrhythmic agent in some experimental cardiac arrhythmias, but the appearance of central nervous system toxicity at therapeutic drug concentrations in conscious animals indicates that it may have a narrow margin of safety.

Animals↗

PubMedDate not supplied

Effective plasma concentrations of aprindine in canine ventricular arrhythmias.

Antiarrhythmic effects of aprindine were examined using three canine ventricular arrhythmia models (induced by digitalis, adrenaline, and two-stage coronary ligation), and the minimum effective plasma concentration of aprindine was determined for each arrhythmia model. Aprindine suppressed all three arrhythmias, and the minimum effective plasma concentrations for arrhythmias induced by digitalis, adrenaline, and 24-h and 48-h coronary ligation were 0.8 +/- 0.4, 1.0 +/- 0.4, 1.6 +/- 0.3, and 3.1 +/- 0.5 micrograms/ml, respectively (mean +/- SD, n = 6-7). The minimum effective plasma concentrations of aprindine for digitalis- and adrenaline-induced arrhythmias were significantly lower than those for coronary ligation-induced arrhythmias. Oral aprindine was also effective in suppressing both the 24- and 48-h coronary ligation-induced arrhythmias. Aprindine had a hypotensive effect when it was given intravenously, but this effect was not observed when it was given orally. The correlations between the aprindine plasma concentrations and the antiarrhythmic effects were not very strong and indicated individual variations in sensitivity to aprindine.

Animals↗

PubMed1976

GLC determination of aprindine: quantitation and stability measurement.

A GLC method of analysis of a new antiarrhythmic agent, aprindine, is described. The raw material of the new drug substance, supplied as the hydrochloride salt, is dissolved in deionized water, and the base is liberated by a 10% aqueous solution of sodium carbonate. aprindine is extracted with chloroform and mixed with the internal standard, 5alpha-cholestane. GLC is perfomed on a glass column packed with 3.8% W-98 on Chromosorb W-HP. Quantitation is achieved by computer calculation of the peak area ratios. GLC-mass spectral analysis indicates that the observed peak is that of aprindine, with a molecular ion at m/e 322. The retention times of aprindine and the internal standard are 2.0 and 5.8 min, respectively. All synthetic precursors show a shorter retention time than aprindine. This GLC method is applied to the quantitative determination of aprindine as raw material and in capsule and ampul formulations. The method is also used to measure the stability of aprindine to acid, base, dry, heat, refluxing, and UV light and to pH variations.

Aprindine↗

PubMed1978

Suppression of the repetitive ventricular response: an index of long-term antiarrhythmic effectiveness of aprindine for ventricular tachycardia in man.

The repetitive ventricular response, defined as the production of two or more ventricular premature complexes in response to a single ventricular pacing stimulus, is common in patients with serious ventricular arrhythmias. Twenty-seven patients with refractory ventricular tachycardia were studied to determine whether acute suppression of the repetitive ventricular response by aprindine predicts long-term effectiveness of this agent. Twenty-three of the 27 patients had the repetitive ventricular response before intravenous administration of aprindine, whereas only 6 had the response after aprindine. All patients were maintained on a regimen of oral aprindine and evaluated repeatedly for a mean of 12 months. Twenty of the 21 patients who had no repetitive ventricular response after intravenous aprindine manifested clinical improvement compared with only 1 of the 6 in whom the repetitive response was present after aprindine (P less than 0.0005). Aprindine is a useful agent in refractory ventricular tachycardia, and the absence of the repetitive ventricular response after its intravenous administration predicts long-term clinical responsiveness to the oral form.

Administration, Oral↗

PubMed2002

Double-blind placebo-controlled trial of aprindine and digoxin for the prevention of symptomatic atrial fibrillation.

A multicenter, placebo-controlled, randomized, double-blind trial compared the preventive effect of aprindine and digoxin on the recurrence of atrial fibrillation (AF) with placebo, and also compare the effectiveness of these 2 drugs in the prevention of AF. Patients with symptomatic paroxysmal or persistent AF who had converted to sinus rhythm (SR) were randomly assigned aprindine (40 mg/day), digoxin (0.25 mg/day) or placebo and followed up on an outpatient basis every 2 weeks for 6 months. Of the 141 patients from 36 participating centers, 47 were given aprindine, 47 digoxin, and 47 were on placebo. After the 6-month follow-up, the Kaplan-Meier estimates of the percentage of patients remaining free of recurrent symptomatic AF on aprindine, digoxin and placebo were 33.3%, 29.2% and 21.5%, respectively. In patients remaining in SR for 15 days after from the start of follow-up, freedom from recurrence was significantly more prevalent in the aprindine group than in the placebo group (p=0.0414), but there was no significant difference between the digoxin and placebo groups. The rate of adverse events was similar in the 3 groups. In conclusion, neither aprindine nor digoxin had a significant effect on preventing relapse of symptomatic AF; however, recurrence of AF occurred later with aprindine than with placebo or digoxin.

Aged↗