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At least 19 recordsLinked to original sources
PubMed1985

Effects of oral prajmaline bitartrate on exercise test responses in patients with coronary artery disease.

The safety, tolerability and haemodynamic effects of oral prajmaline bitartrate were assessed in a double-blind, randomized, placebo-controlled, crossover trial in 21 patients with stable angina pectoris and coronary artery disease. No serious side-effects occurred. Prajmaline bitartrate produced no statistically significant changes in resting heart rate or systolic blood pressure or in work capacity on the treadmill, or in heart rate or systolic blood pressure at maximum exercise compared to placebo values. No new arrhythmias or conduction abnormalities were produced in any patient. We conclude that oral prajmaline bitartrate is well tolerated and can be given safely to patients with coronary artery disease without producing deleterious haemodynamic effects or changes in exercise capacity.

Administration, Oral↗
PubMed1984

Acute haemodynamic effects of ajmaline and prajmaline in patients with coronary heart disease.

Thirty patients undergoing cardiac catheterisation for coronary artery disease received parenteral ajmaline (15 patients) or prajmaline (15 patients). There were no statistically significant induced changes in left ventricular systolic or end diastolic pressures, indirect left atrial pressure, pulmonary artery mean pressure, cardiac output or left ventricular ejection fraction compared to control values. Intravenous prajmaline bitartrate in 15 patients with angina did not significantly alter work capacity, maximum exercise heart rate or systolic blood pressure compared to control values. Five patients developed transient minor conduction defects ( 2LBBB , 1 RBBB, 2 prolonged PR interval): all five were also receiving long-term treatment with beta blockers and nifedipine.

Adult↗
PubMed1990

Comparative analysis of the action of class I antiarrhythmic drugs (lidocaine, quinidine, and prajmaline) in rabbit atrial and ventricular myocardium.

Effects of three class I antiarrhythmic drugs (quinidine, lidocaine, and prajmaline) on transmembrane resting (RMP) and action potentials (AP) of isolated rabbit atrial and ventricular myocardium were studied at different stimulation rates. The frequency-dependent depression of the maximal upstroke velocity (Vmax) of the AP (sodium channel block) was analyzed according to the "guarded receptor" hypothesis. The resting block (Vmax depression after a resting period) induced by prajmaline (10(-6) M), quinidine (2.2 x 10(-5) M), and lidocaine (4.3 x 10(-5) M) was more expressed in the atrium (44, 28, and 19%, respectively) than in the ventricle (32, 9, and 0%, respectively). There were also significant (p less than 0.05) atrioventricular differences in the frequency-dependent extra block (Vmax reduction on stimulation at 3.3 Hz) for quinidine (39 vs. 26%) and lidocaine (4 vs. 25%). From the analysis, according to the guarded receptor hypothesis, it follows that the three compounds bind preferentially to inactivated sodium channels with about the same affinity to the atrium and ventricle, except for quinidine which shows a significantly smaller dissociation constant in the atrium (5 x 10(-6) M vs. 2.7 x 10(-5) M; p less than 0.001). We conclude that the atrioventricular differences in the resting block are mainly due to atrioventricular differences in the RMP, whereas the differences in the frequency-dependent extra block are based on the shorter atrial AP duration (lidocaine) or are due to higher affinity to atrial sodium channels (quinidine).

Action Potentials↗
PubMed1995

[Antiarrhythmic effects of prajmaline (Neo-Gilurythmal) in stable angina pectoris in light of Holter electrocardiographic monitoring].

40 patients with various type of arrhytmia with stable angina were treated with 3 x 20mg Prajmalin (Neo-Gilurytmal) over 6-day period. A positive antyarhytmic response was observed in 30 patients (75%). In the remaining 10 patients considering the lack of adequate response after 6 days on 60 mg the trial was continued at a dose of 100 mg/day (5 x 20mg). With this dose bringing on the desired results. In 32 patients with VE'e and SVE's Neo-Gilurytmal was used in mono therapy. While in other types of arthymia it was used as previously as a first treatment and also in cases where other antiarhytmic drugs (e.g. Propahenone, Mexitil or Beta-blockers) were unsuccessful. Antiarhytmic effects were verified using 24-hour Holter monitoring before introduction of Neo-Gilurytmal, during the first fourth and seventh day of administration and also the eleventh day of observation (in 30 patients three days after cessation of treatment and in 10 cases three days after commencing on 100 mg daily). The results, as mean of the 24-hour observation was statistically analysed using the Wilcoxon test. We analysed the mean from the first day (H1), fourth day (H2), seventh day (H3) i.e. 6 days after administration and in 10 patients three day after increasing the dose to 100 mg/day (H4). We compared this to a base value (Ho) obtained before drug administration. The results obtained showed the Neo-Gilurythmal is an effective drug significantly reducing meanly VE's and SVE's and also gigemini, trigemini, coupled, runs. It was concluded that Neo-Gilurythmal did not significantly effect the heart rate and QT intervals and also QT adjusted to the heart rate. It was also noticed that these was a lack of therapeutic effect 3 days after cessation of treatment, which was suggested that constant therapy is required. Neo-Gilurythmal was find to be effective even in the case where other previously used antiarhymics were ineffective. We also observe a positive result in treatment of paroxismal tachycardia, in treatment of WPW Syndrome and also in prophylactic againts its recurrence. In our study no adverse effects (e.g. cardiac muscle depression, hypotensive episodes or noted in other studies gepatotoxicity or cholestatic episodes) were observed.

Adult↗
PubMed1988

[Intrahepatic cholestasis and aplastic anemia following administration of prajmaline].

Intrahepatic cholestasis and aplastic anemia after N-propylajmaline. A 43 year old female patient taking oral contraceptives for more than five years received the antiarrhythmic drug N-propylajmaline for treatment of ventricular arrhythmia. After twelve days (total dosage 510 mg N-propyl-ajmaline) acute severe intrahepatic cholestasis and aplastic anemia developed. The erythropoeisis improved after three weeks of treatment with corticosteroids. However, despite treatment with phenobarbital the jaundice receded very slowly. Even after nine years of follow-up cholestatic enzymes are still significantly elevated although serum bilirubin levels are in the normal range. This case report demonstrates that antiarrhythmic drugs may induce nearly irreversible intrahepatic cholestasis and severe hematological disturbances.

Adult↗
PubMedDate not supplied

[Diagnostic difficulties in prajmaline-induced intrahepatic cholestasis].

A case of prajmalium-induced intrahepatic cholestasis is presented. A proper diagnosis was delayed because differential diagnosis did not include toxic liver damage. Pathogenetic considerations included immunological background of the disease which improved completely within one year. No clinical and biochemical complications were seen.

Arrhythmias, Cardiac↗
PubMed1996

[Cardiogenic shock and ventricular fibrillation induced by prajmalium and metoprolol poisoning].

Prajmaline is not a relatively well known and frequently used antiarrhythmic belonging to Class IA group of antiarrhythmics, which was administered to a young male with metoprolol for the treatment of parasystole. The patient took in 120 mgs prajmaline and 600 mgs metoprolol during the day of the case, which leads to cardiogenic shock, ventricular tachycardia and ventricular fibrillation. The patient's parameters were normalized after successful resuscitation, temporary pacemaker and two days long Dopamin therapy. Therapy was not regarded to be necessary for a few ventricular premature beats detected during a week observation period. The patient is without complaints now, and significant ventricular arrhythmias, or malignant ventricular ectopy hasn't been proved with ECG tests and Holter monitoring for more than three months. Due to adverse effect profile of prajmaline, even at commonly used doses it should be administered carefully and other agents should probably be considered first before beginning long term treatment with prajmaline.

Adult↗
PubMed1997

[A case of fatal poisoning with the anti-arrhythmia agents Katen and Neo-Gilurytmal].

The case is presented on 17-year-old student who ingested larger doses of tablets and capsules in privacy. She ingested antiarrhythmics Katen and Neo-Gilurytmal without clinical therapy by these drugs and without history of suicidal attempt. The imminent case of death was asphyxiation by aspiration of vomits from gastric contents after ingestion of excessive doses of drugs. The secondary findings as brain edema, petechiae under the serous membranes and congestion of the abdominal cavity, were relieved at autopsy. Noxae was identified by the postmortem toxicological analysis of blood, liver, kidney, gastric contents and intestinal contents. Mexiletine and prajmaline were analysed by the capillary gas chromatography with FID detection. Retention time of mexiletine was 6.66 minutes, prajmaline 15.15 minutes, respectively. Blood alcohol concentration was 0.21 mg.g-1. Concentration of prajmaline in gastric contents was 3.03 mg.g-1, mexiletine 0.11 mg.g-1, respectively.

Adolescent↗
PubMed1992

Reverse use dependence of antiarrhythmic class Ia, Ib, and Ic: effects of drugs on the action potential duration?

UNLABELLED: The prolongation of the action potential duration (APD) induced by sotalol has been shown to be diminished with increasing heart rate. This phenomenon is called "reverse use dependence." We examined the Ia, Ib, and Ic effects of different Class I drugs on the APD under normal and fast stimulation rates (1.0 and 2.5 Hz) in isolated rabbit atrial and ventricular muscles by means of intracellular microelectrodes. Results (n = 98): With 1.0 Hz lidocaine (Ib, 4.3 x 10(-5) M) shortened the APD at 90% repolarization (APD90) in the atrium by 9% and in the ventricle by 8% (NS), whereas quinidine (Ia, 2.2 x 10(-5) M) and prajmaline (Ia, 10(-6) M) prolonged the APD90 in the atrium (quinidine +45%; prajmaline +10%, P < 0.001) and in the ventricle (+42%, P < 0.001; +17%, P < 0.05). Propafenone (Ic, 2.6 x 10(-6) M) showed this effect only in the atrium (APD90 +33%; P < 0.01). With the faster stimulation rate of 2.5 Hz we could not find a significant influence of any drug on the APD90 in the ventricle and only quinidine prolonged the APD90 in the atrium by 16% (P < 0.05). CONCLUSIONS: The subclassification of Class I antiarrhythmic drugs that is based on APD modifying influences is only valid under normal heart rates (1.0 Hz). During tachycardia these actions are absent and the phenomenon of "reverse use dependence" is found in Class I drugs. Therefore, an additional antiarrhythmic effect due to APD modification by the examined drugs should not be expected at rapid heart rates.

Action Potentials↗
PubMed1990

[Dissection of the accessory conduction pathways with simultaneous mitral valve surgery].

The case of surgical treatment of a 44-years old female with a double atrio-ventricular accessory pathway and mitral stenosis was described. Fast ventricular rates due to conduction through the accessory pathways during atrial fibrillation in course of mitral stenosis caused severe heart failure, occasionally with deep hypotonia. Combined treatment with prajmaline and propafenone blocked conduction through accessory pathways. The ventricular rate slowed from approx. 200/min to 150/min. Addition of digoxin slowed the ventricular rate down to approx 80-100/min. There were no signs of preexcitation. Treatment with diuretics and vasodilators was continued. The state of patient improved. Echocardiographic and hemodynamic evaluation revealed: mitral stenosis (orifice - 75 mm2) with moderate regurgitation, small aortic and tricuspid regurgitation. The coronary arteries were normal. On the base of the ECG recordings during atrial fibrillation both accessory pathways were localized on lateral and posterior parts of the left free wall. The patient was operated on. Both atrio-ventricular by-pass tracts were dissected using Sealy's method in Cox modification and then mitral valve prosthesis Medtronic-Hall 27 mm was implanted. Prajmaline and propafenone were discontinued and preexcitation did not recovered. The sinus rhythm was restored by electroversion. The patient had no overt heart failure on discharge from the Institute.

Adult↗
PubMed1990

Differential analysis of the frequency-dependent effects of class 1 antiarrhythmic drugs according to periodical ligand binding: implications for antiarrhythmic and proarrhythmic efficacy.

The frequency-dependent block of cardiac sodium channels by class 1 antiarrhythmic drugs can be described by a periodical ligand binding process between drug molecules and channel binding sites. This predicts a linear relation between onset-rate constant of frequency-dependent block and diastolic interval as well as saturation of block with high stimulation rates. From both relationships, the binding kinetics (time constant, tau on) and saturation level of block (bdinf) can be estimated. This is exemplified for the frequency-dependent block (reduction of the maximal upstroke velocity of action potentials) induced by prajmaline (10(-6) M). In the same way, the frequency-dependent effects of 11 other class 1 drugs reported in the literature were analyzed and compared with each other. When the drugs are ranked with respect to their binding kinetics (tau on), there is a close relationship to the subclasses (1a, 1b, 1c), with 1b drugs exhibiting the fastest and 1c drugs the slowest kinetics. However, differences also exist in the saturation behavior of frequency-dependent block even within the same subclasses (1a and 1c). Thus, the class 1 drugs can also be subdivided in three other groups exhibiting clearly separated bands of block-frequency relations, with half-maximal saturation occurring at different stimulation rates. Our findings may have differential implications for the antiarrhythmic and proarrhythmic efficacy of class 1 drugs.

Animals↗
PubMed1990

Clinical course and outcome in class IC antiarrhythmic overdose.

120 cases of class IC antiarrhythmic overdose, including propafenone, flecainide, ajmaline and prajmaline overdose, were evaluated with respect to clinical course, therapy and outcome. Whereas drug overdose in general has an overall mortality of less than 1%, intoxication with antiarrhythmic drugs of class IC was associated with a mean mortality of 22.5%. Nausea, which occurred within the first 30 minutes after ingestion, was the earliest symptom. Spontaneous vomiting probably led to self-detoxication in about half the patients. Cardiac symptoms including bradycardia and, less frequently, tachyrhythmia occurred after about 30 minutes to 2 hours. Therapeutic measures included administration of activated charcoal, gastric lavage and a saline laxative, catecholamines, and in some patients, hypertonic sodium bicarbonate, insertion of a transvenous pacemaker and hemoperfusion. Fatal outcome was mainly due to cardiac conduction disturbances progressing to electromechanical dissociation or asystolia. Resuscitation, which had to be performed in 29 patients, was successful in only two of them. No correlation was found between fatal outcome, the type of antiarrhythmic, and ingested dose. Since a specific treatment is not available and resuscitive procedures including sodium bicarbonate and insertion of a pacemaker are of limited therapeutic value, early diagnosis and primary detoxification are most important for prevention of fatal outcome.

Ajmaline↗
PubMed2000

The structure of the ring-opened N beta-propyl-ajmaline (Neo-Gilurytmal) at physiological pH is obviously responsible for its better absorption and bioavailability when compared with ajmaline (Gilurytmal).

Prajmaline, the semisynthetic propyl derivative of ajmaline, shows a much better bioavailability when compared with the Rauvolfia alkaloid ajmaline. Early NMR and IR-studies, fluorescence spectroscopic investigations and extraction experiments combined with ion-pair chromatography proved the thesis of a tautomeric equilibrium between an aldehyde-amine and a quaternary carbinol-ammonium component. The aim of this study was to confirm this thesis by HPLC-separation and by structure-determination of both tautomeric compounds.

Ajmaline↗