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PubMed2004

[Treatment of atrial fibrillation in a Hungarian hospital department of cardiologic internal medicine at the turn of the millennium].

INTRODUCTION: The atrial fibrillation is a severe and frequent disease, which influences greatly the patients' quality of life. Only a few Hungarian studies exist which discuss the physicians' own experiences in its treatment. AIM: The description of the experiences acquired in an internal medicine department with cardiological profile during the treatment based on the actual guidelines and the review of the results of one year follow-up. METHOD: Retrospective analysis of the data of patients treated with atrial fibrillation between 1 january 1999 and 31 december 2001 and a one year follow-up was performed. The age, gender, success in cardioversion, the antiarrhythmic therapy at the discharge and the modification in it during the first year were evaluated. RESULTS: During the 3 years long period 1115 patients with atrial fibrillation were admitted (53.9% female, 46.1% male, the mean age was 72.0 +/- 10.4 years), 391 of whom were discharged with sinus rhythm. In 193 cases (49%) a spontaneous cardioversion was observed. 120 electrical (31%) and 78 pharmacological (20%) cardioversions were performed. The electrical form was carried out in 42 cases with acute atrial fibrillation (in 36 of them successfully) and in 100 cases as an elective procedure, in 84 successfully. Pharmacological cardioversion was made in 39 acute cases with the administration of propafenone (in 29 ones successfully) and in 57 elective cases with quinidine + beta-blocker + magnesium (in 49 ones successfully). For the maintenance of sinus rhythm in the 38.8% of cases amiodarone, 24.0% propafenone, 19.9% sotalol, 10.7% beta-blocker, 0.8% quinidine, 0.5% prajmaline was administered, and 5.1% of the patients didn't receive any special treatment. During the one year follow-up from the 391 patients 261 remained on sinus rhythm, in 81 cases (21%) the return of the atrial fibrillation was diagnosed (in 57 of them a successful cardioversion was performed again), 11 patients (3%) died and 38 (9%) were lost for observation. At the time of the one year control 57.8% of patients treated with amiodarone, 61.7% of those treated with propafenone, 67.9% with sotalol and 35.7% with beta-blocker remained on sinus rhythm. The amiodarone was omitted in 17 cases because of its side effects. CONCLUSIONS: The treatment of the atrial fibrillation has to be performed individually taking into account the guidelines, the comorbidity, the time of the beginning of rhythm disorder, the patients' present other drugs and the former antiarrhythmic therapy. A continuous and consistent follow-up of these patients is crucial.

Acute Disease↗

PubMed1990

Identification of antiarrhythmic drugs and their metabolites in urine.

Identification of the antiarrhythmic drugs ajmaline, aprindine, diltiazem, disopyramide, flecainide, gallopamil, lidocaine, lorcainide, mexiletine, phenytoin, prajmaline, propafenone, quinidine, sparteine, tocainide and verapamil and their metabolites in urine is described. After acid hydrolysis of the conjugates, extraction and acetylation, the urine samples were analysed by computerized gas chromatography-mass spectrometry. Using ion chromatography with the selective ions m/z 58, 72, 84, 86, 136, 224, 266, and 426, the possible presence of antiarrhythmic drugs and/or their metabolites was indicated. The identity of positive signals in the reconstructed ion chromatograms was confirmed by a visual or computerized comparison of the stored full mass spectra with the reference spectra. The ion chromatograms, reference mass spectra and gas chromatographic retention indices (OV-101) are documented. The method presented is integrated in a general screening procedure (general unknown analysis) for several groups of drugs.

Acetylation↗

PubMed2005

Differential effects of Na-K-ATPase pump inhibition, chemical anoxia, and glycolytic blockade on membrane potential of rat optic nerve.

Na(+)-K(+)-ATPase pump failure during either anoxia or ouabain perfusion induces rapid axonal depolarization by dissipating ionic gradients. In this study, we examined the interplay between cation and anion transporting pathways mediating axonal depolarization during anoxia or selective Na(+)-K(+)-ATPase inhibition. Compound resting membrane (V(m)) potential of rat optic nerve was measured in a grease gap at 37 degrees C. Chemical anoxia (2 mM NaCN or NaN(3)) or ouabain (1 mM) caused a loss of resting potential to 42 +/- 11% and 47 +/- 2% of control after 30 min, respectively. Voltage-gated Na(+)-channel blockade was partially effective in abolishing this depolarization. TTX (1 microM) reduced depolarization to 73 +/- 10% (chemical anoxia) and 68 +/- 4% (ouabain) of control. Quaternary amine Na(+) channel blockers QX-314 (1 mM) or prajmaline (100 microM) produced similar results. Residual ionic rundown largely representing co-efflux of K(+) and Cl(-) during chemical anoxia in the presence of Na(+)-channel blockade was further spared with DIDS (500 microM), a broad-spectrum anion transport inhibitor (95 +/- 8% of control after 30 min in anoxia + TTX vs. 73 +/- 10% in TTX alone). Addition of DIDS was slightly more effective than TTX alone in ouabain (74 +/- 5% DIDS + TTX vs. 68 +/- 4% in TTX alone, P < 0.05). Additional Na(+)-entry pathways such as the Na-K-Cl cotransporter were examined using bumetanide, which produced a modest albeit significant sparing of V(m) during ouabain-induced depolarization. Although cation-transporting pathways play the more important role in mediating pathological depolarization of central axons, anion-coupled transporters also contribute to a significant, albeit more minor, degree.

Animals↗

PubMed1995

Protective effects of antiarrhythmic agents against anoxic injury in CNS white matter.

Irreversible anoxic injury is dependent on extracellular Ca2+ in mammalian CNS white matter, with a large portion of the pathologic Ca2+ influx occurring through reverse Na(+)-Ca2+ exchange, stimulated by increased intracellular [Na+]. This Na+ leak likely occurs via incompletely inactivated voltage-gated Na+ channels. This study reports that clinically used antiarrhythmic compounds, likely by virtue of their Na+ channel-blocking properties, significantly protect CNS white matter from anoxia at concentrations that cause little suppression of the preanoxic response. Rat optic nerves were pretreated with various agents for 60 min, then subjected to 60 min of anoxia in vitro. Functional recovery was measured electrophysiologically as the area under the compound action potential (CAP). Without drug, the CAP areas recovered to a mean of 32 +/- 12% of control after 1 h of reoxygenation. Recoveries using prajmaline 10 microM were 82 +/- 15% (p < 0.0001), and using tocainide 1 mM, 78 +/- 8% (p < 0.0001), with little suppression (< or = 10%) of the preanoxic response. Ajmaline (10-100 microM), disopyramide (10-300 microM) and bupivacaine (10-100 microM) were somewhat less effective, whereas verapamil produced 52 +/- 11% recovery before reduction of the preanoxic CAP was observed at 30 microM. Procainamide (100-300 microM) was ineffective. These results suggest that Na+ channel blockers, including commonly used antiarrhythmic agents, may be effective in protecting central white matter, which is a target for anoxic/ischemic injury in diseases such as stroke and spinal cord injury.

Action Potentials↗

PubMed1989

Cardiodepressive effects of antiarrhythmic drugs.

Negative inotropic effects of antiarrhythmic drugs are ultimately mediated by alterations of intracellular Ca++. With class I antiarrhythmic drugs a strong correlation between the Na+ inward current and the Ca++ influx exists whereby Ca++ influx is changed by an exponent, n, of approximately 3. Generally, the longer the duration of Na+ -channel blockade the more pronounced is negative inotropy. Antiarrhythmic drugs of class I may be subdivided into those with a short recovery time of Na+ channels (lidocaine-type), those with an intermediate recovery time, such as quinidine and newer antiarrhythmics such as flecainide and propafenone, and those with a recovery time greatly exceeding 1 s, such as disopyramide and prajmaline. The degree of cardiodepression is modulated by peripheral circulatory effects such as vasoconstriction and vasodilation. In order to differentiate between general cardiodepressive effects and true negative inotropy, sophisticated methods, for example, volume-pressure relationship curves, have to be applied to determine the degree of pre- and afterload alterations, also accounting for cardiodepressive effects. The net effect of cardiodepression is due to several factors: true negative inotropy, additional influences on the peripheral circulation, the functional state of the myocardium, and the beneficial or detrimental effects on the prevailing arrhythmia. Based on these theoretical considerations, combined drug therapy of arrhythmias has to be installed under the aspect of cardiodepressive side-effects, especially in an already impaired heart.

Anti-Arrhythmia Agents↗

PubMed1994

Electrophysiologic effects of detajmium on isolated dog cardiac ventricular and Purkinje fibers.

We studied the electrophysiologic effects of the antiarrhythmic compound detajmium (Tachmalcor) on isolated dog and rabbit cardiac preparations, applying the conventional intracellular microelectrode techniques. In dog ventricular muscle fibers (37 degrees C, stimulation frequency 1 Hz), 1 microM detajmium did not change resting potential (RP), action potential amplitude (APA), AP duration measured at 90% of repolarization (APD90), or effective refractory period (ERP) significantly, but reduced maximum rate of depolarization (Vmax) significantly from 236.7 +/- 28.9 to 177.3 +/- 22.5 V/s (n = 6, p < 0.01). In dog Purkinje fibers (37 degrees C, stimulation frequency 1 Hz), 1 microM detajmium significantly decreased APA from 111.1 +/- 12.3 to 100.0 +/- 2.5 mV (n = 8, p < 0.003), APD90 from 359.0 +/- 17.5 to 262.1 +/- 12.3 ms (n = 8, p < 0.001) and Vmax from 687.5 +/- 57.2 to 523.7 +/- 58.2 V/s (n = 8, p < 0.001) without changing maximal diastolic potential or ERP/APD ratio significantly. The effect of detajmium on Vmax in both dog ventricular muscle and Purkinje fibers was frequency dependent. Fractional Vmax block was 0.185 +/- 0.008 1/AP. The recovery kinetics of Vmax (offset kinetics) was extremely slow (time constant = 348.16 +/- 57.43 s) considerably slower than most of those of other antiarrhythmic drugs yet reported. Detajmium in concentration < 32 microM did not influence the beta-adrenoceptors or slow response APs in dog ventricular tissue significantly. On the basis of its electrophysiologic effects, detajmium, like prajmaline, encainide, or flecainide, can be best classified as a class I/C antiarrhythmic drug according to the Vaughan Williams' classification scheme.

Action Potentials↗

PubMed1988

Use of Holter functions of the implantable pacemaker to control antiarrhythmic therapy of supraventricular and ventricular recurrent tachycardias.

Holter functions of pacemakers were studied in a total of nine patients with paroxysmal atrial flutter (Group I--a Quintech DD 931 pacemaker, manufactured by Vitatron Medical, The Netherlands), and in 11 patients with recurrent postinfarction ventricular tachycardia (Group II--a DPG P 21 diagnostic pulse generator, Vitatron Medical. Seven patients (35%) were excluded from the study for myopotential interference. Group I patients were given six antiarrhythmic drugs for eight weeks each, with only prajmalin and amiodarone significantly shortening flutter duration. Group II patients were administered, according to the results of programmed extrastimulation, amiodarone alone or in combination with Class I antiarrhythmic drugs for a long period of time. While no recurrent tachycardias or sudden death were noted during treatment, pacemaker detected non-lethal ventricular tachycardia occurred in two, and sudden death without confirmed arrhythmia in one patient once the treatment had been discontinued for serious side effects (p less than 0.05). Diagnostic stimulation using bipelar sensing to eliminate myopotential interference might become a major method for long-term monitoring.

Anti-Arrhythmia Agents↗

PubMed1984

[Effect of anti-arrhythmia agents and nitroglycerin on enzyme activities of the liver].

In a prospective multicenter study the phenomenon of an anicteric reaction with increasing enzyme activities is tested with the antiarrhythmics prajmalin, propafenone, disopyramide and sparteine and additionally with nitroglycerine. Transaminases, alkaline phosphatase and gamma-GT increased with all five substances up to three times of the normal, concerning one, two or three and in a few cases four parameters. The bilirubin was always normal and no clinic symptoms were registered. Increased enzyme levels were found on the fourth day after exposition, the maximum on the 10th-16th day and normalisation on about the 25th day under continuing the same medication. No relation to age or sex was found. The results are discussed in comparison with the literature.

Adult↗

PubMed1993

[Difficulties with pharmacologic treatment of a patient with atrioventricular nodal reentrant tachycardia].

A case history of a 38 year old teacher with AVNRT is described. She had been treated for 11 years with 11 antiarrhythmic drugs in various combinations. No treatment prevented recurrence of arrhythmia. During long term treatment with class IA, IC, II, III and IV antiarrhythmic drugs, various side effects occurred. There was also suspicion of proarrhythmic effect, especially of prajmaline. Some of the drugs terminated tachycardia while administered intravenously. But often deep hypotonia, heart automatism disturbances and even asystole occurred, MAS syndrome occurred 5 times. The patient was referred to our laboratory to perform percutaneous radiofrequency ablation of the slow pathway. The procedure was performed without any complications. Efficacy of the ablation was proved by electrophysiologic study before and after intravenous atropine administration. During the 11 months follow-up the patient had no tachycardia. She is on no antiarrhythmic medication and continues her normal activity.

Adult↗

PubMed1981

Evaluation of prajmalium-induced cholestasis by immunologic tests.

Cholestatic jaundice developed in four patients after the administration of prajmalium bitartrate. The clinical, histologic, ultrastructural, and immunologic findings were determined. In all patients, the clinical and morphologic features indicated idiosyncrasy. Two antibodies distributed in a granular pattern along the bile canaliculi were detected by immunofluorescence in all patients. In one patient, autoimmune markers were found in the serum, and in two instances, the migration-inhibition factor assay against the offending drug was found to be positive. The data support the concept that immunologic processes may participate in the production of the cholestatic syndrome.

Aged↗

PubMed1994

Chemically modified cardiac Na+ channels and their sensitivity to antiarrhythmics: is there a hidden drug receptor?

Elementary Na+ currents were recorded at 19 degrees C in inside-out patches from cultured neonatal rat cardiocytes. In analyzing the sensitivity of chemically modified Na+ channels to several class 1 antiarrhythmic drugs, the hypothesis was tested that removal of Na+ inactivation may be accompanied by a distinct responsiveness to these drugs, open channel blockade. Iodate-modified and trypsin-modified cardiac Na+ channels are noninactivating but strikingly differ from each other by their open state kinetics, a O1-O2 reaction (tau open(1) 1.4 +/- 0.3 msec; tau open(2) 5.4 +/- 1.1 msec; at -40 mV) in the former and a single open state (tau open 3.0 +/- 0.5 msec; at -40 mV) in the latter. Lidocaine (150 mumol/liter) like propafenone (10 mumol/liter), diprafenone (10 mumol/liter) and quinidine (20 mumol/liter) in cytoplasmic concentrations effective to depress NPo significantly can interact with both types of noninactivating Na+ channels to reduce the dwell time in the conducting configuration. Iodate-modified Na+ channels became drug sensitive during the O2 state. At -40 mV, for example, lidocaine reduced tau open(2) to 62 +/- 5% of the control without detectable changes in tau open(1). No evidence could be obtained that these inhibitory molecules would flicker-block the open Na+ pore. Drug-induced shortening of the open state, thus, is indicative for a distinct mode of drug action, namely interference with the gating process. Lidocaine proved less effective to reduce tau open(2) when compared with the action of diprafenone. Both drugs apparently interacted with individual association rate constants, a(lidocaine) was 0.64 x 10(6) mol-1 sec-1 and a(diprafenone) 13.6 x 10(6) mol-1 sec-1. Trypsin-modified Na+ channels also appear capable of discriminating among these antiarrhythmics, the ratio a(diprafenone)/a(lidocaine) even exceeded the value in iodate-modified Na+ channels. Obviously, this antiarrhythmic drug interaction with chemically modified Na+ channels is receptor mediated: drug occupation of such a hypothetical hidden receptor that is not available in normal Na+ channels may facilitate the exit from the open state.

Animals↗

PubMed1983

Prajmalium bitartrate in chronic ventricular arrhythmias: comparison with disopyramide.

24-h ECG recordings were used to assess the efficacy of prajmalium bitartrate (PB) in reducing the incidence and the severity of premature ventricular complexes (PVCs), and to compare its antiarrhythmic action with that of Disopyramide. 13 patients with frequent PVCs were distributed randomly into 2 groups. The first group of 7 patients received PB 80 mg/day for 4 days as their first treatment, and disopyramide 400 mg/day for a further 4 days as the second therapy. The succession of the drugs was reversed in the other group of 6 patients. Analysis of the Holter recordings showed that PB and disopyramide reduced PVC frequency to a similar extent as compared to the corresponding wash-out period, viz. by 56.7% (p less than 0.05) and 62.1% (p less than 0.01), respectively. Thus, PB appears to be an effective antiarrhythmic drug and comparable to disopyramide. It may be used to prevent premature ventricular complexes and runs of ventricular tachycardia.

Adult↗

PubMed1984

Prajmaliumbitartrate-associated liver damage. Report on seven further cases with follow-up for two to five years.

Seven further cases with n-propyl-ajmaliumbitartrate (NPAB)-associated liver damage observed between 1976 and 1980 in two collaborating institutions are reported. The cause/effect relationship could be classified as probable in three cases and as potential in the remaining four patients. No drug rechallenge was carried out. In the clinical management, definite exclusion of biliary tract obstruction had a clear priority over histologic documentation of the degree of the transient liver damage. Follow-up data after 2 years 8 months to 5 years 9 months by personal reinvestigation of three patients and by questionnaire to family physicians and patients in the remaining four cases gave no clinical or serologic indication of persisting or relapsing liver damage. Liver biopsies were not considered to be warranted in the follow-up of these asymptomatic patients with normal liver function tests.

Adult↗

PubMed1985

Pharmacokinetics of N-propylajmaline in relation to polymorphic sparteine oxidation.

In order to determine whether the metabolism of the antiarrhythmic drug N-propylajmaline is under the same genetic control as sparteine metabolism, the pharmacokinetics of this antiarrhythmic drug were studied in a groups of six extensive and four poor metabolizers of sparteine. Pronounced differences in terminal half-life, total plasma clearance, metabolic clearance and urinary excretion of N-propylajmaline were observed between extensive and poor metabolizers. A close relationship between the total clearance and metabolic clearance of N-propylajmaline and sparteine could be demonstrated. Clinically available N-propylajmaline is a 55% to 45% mixture of the i- and n-diastereomers. The extensive metabolizers exhibited stereoselective metabolism; the i-diastereomer was preferentially metabolized. Poor metabolizers were characterized by a loss of this stereoselective metabolism. Five subjects were treated for 7 days with a daily N-propylajmaline dosage of either 60 mg or 20 mg. Since a close relationship between the clearance of N-propylajmaline and the metabolic ratio of sparteine had been observed after single dosing the metabolic ratio of sparteine was used to predict N-propylajmaline steady-state plasma concentrations during multiple dosing. Only in two extensive metabolizers with a metabolic ratio less than 0.4 predicted and observed, steady-state plasma concentrations were in good agreement. In the other three subjects observed steady-state plasma concentrations were appreciably higher than predicted. In these three subjects metabolic N-propylajmaline clearance decreased indicating saturation N-propylajmaline metabolism during multiple dosing. The data indicate that N-propylajmaline metabolism is subject to a genetic polymorphism controlled by the sparteine/debrisoquine gene locus.

Adult↗

PubMedDate not supplied

[Pharmacokinetics and biotransformation of N-propylajmaline hydrogen tartrate in man].

10 and 20 mg of N-Propyl-ajmalin-hydrogentartrate (N-PAB, Neo-Gilurytmal) were administered i.v. and orally respectively to healthy volunteers. In the study 14C-labelled N-PAB was used. The pharmacokinetics and the metabolic behaviour was examined. A fast and complete absorption of the compound could be observed. The bioavailability was 78%. The terminal plasma elimination half-life (beta-phase) was in the range of 4 to 6 hours. A total of 33% of the administered radioactivity was excreted via the kidney. 35 to 48% of the radioactivity found in urine was unchanged N-PAB. The excretion-kinetics of the three main metabolites as well as of the parent compound were determined. The possible presence of non-metabolizers is suggested.

Adult↗

PubMedDate not supplied

Pharmacokinetics of n-propyl-ajmaline-bitartrate in elderly patients with ventricular ectopic activity.

11 patients (9m, 2f, median age 59 years) with ventricular ectopic activity of at least Lown grade III received 20 mg N-Propyl-ajmaline-bitartrate (N-PAB) p.o. Plasma concentrations of N-PAB were determined with HPLC from blood samples within 26 hours after administration. An open two-compartment model was used. In 8 patients with normal function of the liver and the kidneys, the median clearance of N-PAB was 6.86 ml/min/kg and the median volume of distribution was 1.56 l/kg. Two patients had a clearly diminished clearance of 1.58 ml/min/kg without obvious impairment of liver or renal function. One patient with chronic glomerulonephritis (plasma creatinine 3.4 mg/dl) had a N-PAB clearance of 2.79 ml/min/kg. None of the Spearman rank correlation coefficients between the pharmacokinetic parameters of N-PAB with age, plasma albumin/globulin-quotient, plasma creatinine and cholin-esterase were significant. All calculated parameters were in the range determined in young subjects. It is concluded that physiological changes with age do not lead to significant changes of the pharmacokinetics of N-PAB. On the other hand in patients with increased levels of plasma creatinine a diminished clearance of N-PAB can be expected. It is also possible that patients without an obvious impairment of liver or renal function may have diminished N-PAB clearance.

Aged↗

PubMed2001

[Brugada syndrome].

BACKGROUND: A high take-off descending ST segment associated with right bundle branch block is the typical ECG criterion of the Brugada-Brugada syndrome. It leads to ventricular fibrillation or syncopes in case of a familiar disposition. CASE REPORT: We describe a 56-year-old man in whom oral prajmalium bitartrate therapy previously prescribed for symptomatic ventricular extrasystoles unmasked an electrographic pattern characteristic of a Brugada syndrome. After the ongoing invasive diagnostic a right ventricular dysplasia in the same case is possible. The patient was treated with an ICD pacemaker.

Anti-Arrhythmia Agents↗

PubMed1980

Comparison of antiarrhythmic effects of oral prajmalium bitartrate and intravenous lidocaine in acute myocardial infarction.

In 35 patients with acute myocardial infarction premature ventricular complexes were quantified from stored continuous electrocardiographic tape recordings using a semiautomated arrhythmia detection system. Seventeen patients, separated at random, received no antiarrhythmic drug and formed the control group. In nine patients prajmalium bitartrate was given orally at a dose of 60 mg. (20 mg. every 4 hours). Nine patients had permanent infusions of 2.1 mg./minute lidocaine (corresponding to a daily dose of 3 g.). In both treated groups premature ventricular complexes decreased significantly as compared to the spontaneous frequency in the control group. Six hours after the onset of therapy premature ventricular complexes were reduced to 37% of the initial value in the prajmalium bitartrate group and to 51% in the lidocaine group, whereas in the control group frequency increased (169%). The peak effect was reached after ten hours when premature ventricular complexes were reduced to 5% under prajmalium bitartrate and to 20% under lidocaine administration. Runs of premature ventricular complexes were nearly completely suppressed after administration of prajmalium bitartrate. Under lidocaine administration runs were moderately and not significantly reduced. Eight hours after the onset of therapy, runs were reduced to 8% of the initial value under prajmalium bitartrate and to only 79% under lidocaine. The effect of prajmalium bitartrate on runs of premature ventricular complexes was significantly more pronounced than the effect of lidocaine. The present study documents that orally administered prajmalium bitartrate is an alternative to intravenous administration of lidocaine in the treatment of ventricular arrhythmias after acute myocardial infarction.

Administration, Oral↗