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PubMed1990

Is class III antiarrhythmic activity important?

The beginning of thought about a discrete Class III antiarrhythmic action stemmed from the observation that sotalol produced a very marked increase in the time course of repolarization with little or no change in conduction velocity in cardiac muscle. It is known that in patients with hypothyroidism or hypocalcemia, both of which are associated with a marked lengthening of the cardiac action potential, arrhythmias are exceedingly rare. The acetyl metabolite of procainamide also produces, as its sole action, a marked increase in the action-potential duration, and it has antiarrhythmic activity. It is clear that lengthening the action-potential duration is antiarrhythmic. Sotalol is a unique beta blocker in not only antagonizing sympathetic stimulation competitively, but also in exerting a potent antiarrhythmic effect by prolonging repolarization. Because of the augmented tension that is associated with the increase in action-potential duration, sotalol produces a less negative inotropic effect than that seen with other beta blockers. Sotalol is a potent broad-spectrum antiarrhythmic agent because of its Class III properties, resulting from an increase in the length of cardiac repolarization, a property that is modulated by its beta-adrenergic blocking actions.

Animals↗

PubMed1980

Metoclopramide: antipsychotic efficacy of a drug lacking potency in receptor models.

Metoclopramide is a substituted benzamide derivative, structurally similar to procainamide and sulpiride. In behavioral, biochemical, and neuroendocrine tests it displays classic neuroleptic dopamine (DA) antagonist properties; in contrast to other DA antagonists, it lacks potency in currently used DA receptor models. In clinical studies using low doses or dubious measures, it was considered not to be efficacious as an antipsychotic. We now find that it indeed has a clinical profile similar to known neuroleptics when used in a dose range predicted from animal models. The findings raise questions regarding the validity and universality of several predictive models, as well as hypotheses purporting to explain molecular mechanisms of action of neuroleptic agents. The drug's inactivity in receptor models suggests that an as yet unidentified DA receptor subpopulation may be important as the mediator of many DA dependent neurobiologic phenomena.

Antipsychotic Agents↗

PubMed1980

Prolactin response to exercise, metoclopramide and other provacative agents in children.

Metoclopramide (MCP), a derivative of procainamide was compared with exercise, arginine, insulin and thyrotropin releasing hormone (TRH) as a prolactin (PRL) releaser in children. The peak response of plasma PRL after oral administration of MCP was greater than that after strenuous exercise and after i.v. administration of pharmacodynamic agents. Normal PRL and TSH responses were observed after TRH administration in all subjects. Variable PRL responses were seen after exercise and after i.v. administration of arginine and insulin, despite significant growth hormone (GH) release following the administration of these agents. MCP produced no increase in plasma TSH. Metoclopramide may be useful for dynamic testing of PRL release in children. It can be taken orally and is free of side-effects.

Adolescent↗

PubMed1976

Relationship of antiarrhythmic to inotropic activity and antiarrhythmic qualities of the optical isomers of verapamil.

1. The relationship of antiarrhythmic to inotropic activity of the optical isomers of verapamil was studied by comparing their effects on functional refractory period and force of contraction in the isolated left atrium of the guinea pig and on maximum follow frequency and contractility in the dog heart. To evaluate the antiarrhythmic profile of the optical isomers of verapamil the relationship between threshold voltage and impulse duration in the left atrium of the guinea pig and the antagonistic action against ventricular arrhythmias in the rat were studied. 2. (-)Verapamil is nearly 10 times more effective than (+)verapamil in prolonging the functional refractory period in the isolated left atrium of the guinea pig. 3. In the dog heart (-)verapamil is about 8 times more active in reducing a maximum follow frequency at atrial pacing, as well as spontaneous heart rate and in prolonging PQ-duration. 4. In the guinea pig atrium (+)verapamil shows less negative inotropic activity than its enantiomorph. With (+)verapamil the concentration producing a 25% decrease in contractility is 3.7 times higher than that causing a 25% increase in refractory period. With (-)verapamil these concentrations are identical. 5. In the dog i.v. infusion of the isomers, at a dosage inducing identical reduction of maximum follow frequency, is accompanied by a decrease in left ventricular dp/dtmax with (-)verapamil, whereas with the (+)isomer a significant increase of dp/dtmax is observed at a certain dose level. 6. Because of the higher antiarrhythmic activity of (-)verapamil, the antiarrhythmic profile and the inotropic pattern of the racemic compound are mainly due to this isomer. 7. (+)Verapamil shifts the voltage duration curve of the isolated left atrium of the guinea pig to the right and leads to a significant increase in the chronaxie value. (-)Verapamil has no comparable effects on the excitability of the atrial myocardium. 8. In the intact animal (+)verapamil shows additional antiarrhythmic qualities. Like procainamide, but with higher activity, it antagonizes ventricular arrhythmias (ectopic beats, automaticity and flutter or fibrillation) which can be provoked in the rat by i.v. infusion of aconitine. (-)Verapamil and the racemic compound are ineffective against these ventricular rhythm disorders.

Aconitine↗

PubMed1979

Intracardiac electrophysiological effects of lorcainide in man.

The electrophysiological effects of lorcainide 1.25 or 2.5 mg/kg given iv over 2 or 4 min, were studied in 21 patients with normal and diseased impulse formation and conduction, by means of intracardiac recording and stimulation. Sinus rate and the effective atrial refractory period rose following both doses of lorcainide. The corrected sinus node recovery time rose only after lorcainide 2.5 mg/kg and then most markedly in patients with sinus node dysfunction. The P-A interval remained unchanged following the drug. The A-H interval during sinus rhythm, and the pooled A-H intervals during atrial pacing, increased slightly, and the functional and effective A-V nodal refactory period changed variably. Wenckebach periods above the bundle of His occurred at lower atrial pacing rates following both doses of lorcainide in 7 patients, at the same atrial pacing rate in 9 and at higher rates in 3. H-V intervals, pooled H-V intervals and QRS-width lengthened in all patients, most markedly in cases with a conduction delay below the His bundle, who had received lorcainide 2.5 mg/kg. Thus, lorcainide shares some electrophysiological properties with procainamide and aprindine. Higher doses should be used with caution in patients with pre-existing conduction delay below the bundle His.

Acetanilides↗

PubMed1987

Gallopamil binding to human serum proteins.

We have determined the extent and variability in the binding of gallopamil to human serum proteins. Binding was determined by equilibrium dialysis in healthy volunteer serum, human serum albumin (45 g.l-1), and alpha-1 acid glycoprotein (AAG) (600 mg.l-1) at a pH of 7.4. Nonlinear regression analysis of gallopamil binding over a wide range of concentrations (10(-9) to 10(-4) M) in healthy volunteer serum suggested two classes of binding sites (kass.1 = 4.7 x 10(5)M-1, kass.2 = 4.1 x 10(4)M-1). These values were in close agreement with those obtained from binding to AAG and human serum albumin. Gallopamil free fraction over the concentration range of 10 to 100 ng.ml-1 was independent of concentration. The free fraction in 20 volunteers was 0.075 at a concentration of 10 ng.ml-1. Gallopamil free fractions were also determined in human serum albumin, to which various concentrations of AAG were added. Bound/free ratios correlated with AAG. As we changed the pH of the serum from 7.0 to 8.0, the free fraction changed from 0.1 to 0.05. Verapamil, lignocaine, procainamide, propranolol, 40 H-propranolol, MEGX, and NAPA all caused an increase in the free fraction of gallopamil in serum. However, tocanide, quinidine, diltiazem, GX, norverapamil, D620, D617, and desacetyl diltiazem had no effect on gallopamil binding. Therefore, the data strongly suggest AAG as the high affinity, low capacity binding site and albumin as the low affinity, high capacity binding site for gallopamil, variability in gallopamil binding can be explained by alterations in AAG concentrations, pH, and the presence of other drugs and their metabolites.

Blood Proteins↗

PubMed1993

Clinical significance of genetic influences on cardiovascular drug metabolism.

Inherited differences in metabolism may be responsible for individual variability in the efficacy of drugs and the occurrence of adverse drug reactions. Among the cardiovascular drugs reported to exhibit genetic polymorphism are debrisoquine, sparteine, some beta-adrenoceptor antagonists, flecainide, encainide, propafenone, nifedipine, procainamide, and hydralazine. The implications of genetic differences in the metabolism of these drugs for cardiovascular therapeutics is the subject of this review.

Adrenergic beta-Antagonists↗

PubMed1992

Isolation of a tripeptide (Ala-Gly-Ser) exhibiting weak acetylthiocholine hydrolyzing activity from a high-salt soluble form of monkey diaphragm acetylcholinesterase.

A high-salt soluble form of acetylcholinesterase (AChE) was purified from monkey (Macaca radiata) whole diaphragm by a two step affinity chromatographic procedure using m-aminophenyl trimethylammonium-chloride hydrochloride-Sepharose and procainamide-Sepharose columns. The purified enzyme showed three major protein bands at 80 kDa, 78 kDa and 60 kDa on SDS-gel electrophoresis. [3H]Diisopropyl fluorophosphate ([3H]DFP) labeled enzyme also gave three radioactive peaks corresponding to these three bands. The purified enzyme pretreated with dithiothreitol and subjected to limited trypsin digestion gave a peptide fragment of molecular weight approximately 300 Da showing weak acetylthiocholine hydrolyzing activity as identified by Sephadex G-25 gel filtration. Sequence analysis showed that the active peptide fragment was a tripeptide with the sequence Ala-Gly-Ser. When the purified AChE was labeled with [3H]DFP, digested with trypsin and subjected to Sephadex G-25 chromatography, a radioactive peak that would correspond to the tripeptide fragment was seen. The kinetics, inhibition characteristics and binding characteristics to lectins of the active peptide fragment was compared with the parent enzyme. A synthetic peptide of sequence Ala-Gly-Ser was also found to exhibit acetylthiocholine hydrolyzing activity. The kinetics and inhibition characteristics of the synthetic peptide was similar to those of the peptide derived from the purified enzyme, except that the synthetic peptide was more specific towards acetylthiocholine than butyrylthiocholine. The specific activity (units/mg) of the synthetic peptide was about 29480 times less than that of the purified AChE.

Acetylcholinesterase↗

PubMed1989

Oral N-acetylprocainamide compared to quinidine plus digoxin in the chronic suppression of atrial flutter in humans.

Antiarrhythmic therapy for the suppression of atrial flutter has conventionally entailed the use of a class Ia agent such as quinidine or procainamide. However, atrial flutter often recurs despite the use of these conventional antiarrhythmic regimens. Experimental and clinical evidence suggests that the pharmacologic suppression of atrial flutter may depend on the prolongation of the atrial action potential duration and consequently the voltage-dependent refractoriness. Therefore, the efficacy and tolerance of the class III antiarrhythmic agent N-acetylprocainamide was compared to that of the conventional regimen of the class Ia agent quinidine combined with digoxin (to control ventricular response) in patients with a history of symptomatic sustained atrial flutter. The study was randomized but nonblinded, with a crossover to the alternate regimen if the first failed. Eighteen patients entered the study and were followed for up to 18 months. Of the 12 receiving N-acetylprocainamide (eight randomized and four crossovers), one (8%) failed therapy due to side effects, but none had atrial flutter. Of the 11 receiving quinidine and digoxin (10 randomized and one crossover), three (28%) had a recurrence of atrial flutter, two of whom also had intolerable side effects, and two more (18%) had side effects alone requiring withdrawal of therapy (total 46% failed). The probability of therapeutic success over time was greater (p less than 0.04) for N-acetylprocainamide than for quinidine and digoxin. The data suggest that N-acetylprocainamide may be more effective and better tolerated than the conventional regimen of quinidine plus digoxin. Therefore, large-scale blinded studies of the efficacy of N-acetylprocainamide in the suppression of atrial flutter may be warranted.

Acecainide↗

PubMed1983

Do evacuated blood collection tubes interfere with therapeutic drug monitoring?

The influence of various brands of evacuated blood collection systems (the old type, red stoppered Vacutainer; the new type, blue stoppered Vacutainer; Monoject and Venoject) on therapeutic drug monitoring was investigated. No interferences were found in the assay of ethosuximide, phenobarbital, phenytoin, valproic acid, digitoxin, digoxin, procainamide, gentamicin and theophylline. Using Monoject and old type Vacutainer tubes, lower levels were found in the disopyramide assay: 91.3 +/- 4.6% (p less than 0.05) and 91.7 +/- 7.0% (not significant) respectively, and in the quinidine assay: 82.8 +/- 6.7% (p less than 0.02) and 83.9 +/- 4.4% (p less than 0.001) respectively as compared with glass tubes. In the carbamazepine assay a decrease was found in the Monoject tubes only: 93.7 +/- 1.7% (p less than 0.01). The stoppers of Monoject tubes and the old type Vacutainer tubes contained the plasticizer tris-(2-butoxyethyl)phosphate (TBEP), which has been shown to be a potent inhibitor of the binding of several drugs to alpha 1-acid glycoprotein. Using the new type Vacutainer and the Venoject, no interferences were found.

Blood Specimen Collection↗

PubMed1985

Determination of some anticonvulsants, antiarrhythmics, benzodiazepines, xanthines, paracetamol and chloramphenicol by reversed phase HPLC.

In this article assays are described for caffeine, theophylline, procainamide, N-acetylprocainamide, quinidine, dihydroquinidine, paracetamol, phenobarbital, phenytoin, carbamazepine, chloramphenicol, oxazepam, temazepam, diazepam, desmethyldiazepam, chlordiazepoxide, desmethylchlordiazepoxide and demoxepam using a uniform working procedure, five (slightly) different mobile phases and one HPLC system. Changing from one eluent to another is simple and a stable base-line is achieved within half an hour. Three of the five eluents are interchangeable and recycling of eluent causes no problems. Sample pretreatment is a single step extraction. Interferences can be overcome by changing the selectivity of the eluent by adjusting the tetrahydrofuran or triethylamine content. Furthermore it is shown how triethylamine can improve peak shapes of basic components and shorten their retention times.

Acetaminophen↗

PubMedDate not supplied

The effect of selected antiarrhythmic drugs on neutrophil free oxygen radicals production measured by chemiluminescence.

The evidence that free oxygen radicals produced by polymorphonuclear neutrophils (PMN) participate in generation of reperfusion arrhythmias is well documented. The in vitro effect of selected antiarrhythmic drugs on PMN free radicals production was evaluated by luminol- (LuCL) and lucigenin- (LgCL) amplified chemiluminescence stimulated with opsonized zymosan (o.z.) and phorbol myristate acetate (PMA). Fast sodium channel inhibitors varied in the influence on PMN chemiluminescence: from an inhibition in all models studied by procainamide, to lack of an effect by mexiletine. Propafenone, similarly to ajmaline and verapamil, inhibited LuCL stimulated with PMA, as well as LgCL after stimulation with both PMA and o.z. Bretylium tosylate decreased LuCL stimulated with both inducers, with no effect on LgCL. Amiodarone in high concentrations inhibited both LuCL and LgCL. beta-blockers propranolol and practolol impaired LuCL stimulated with o.z., as well as LgCL induced with PMA, whereas alpha-blocker phentolamine inhibited LuCL and LgCL stimulated with both inducers. The drugs' effect on PMN free oxygen radicals production may constitute an additional mechanism of their activity.

Acridines↗

PubMed2003

Atrial fibrillation after ondansetron for the prevention and treatment of postoperative nausea and vomiting: a case report.

PURPOSE: Even though clinical safety has been established in large studies, ondansetron has been reported to cause adverse cardiovascular events. We present a case of atrial fibrillation in association with ondansetron in the postoperative period. CLINICAL FEATURES: A 47-yr-old, 81 kg female presented with a benign lump in her left breast for lumpectomy. Her past medical history was unremarkable. Physically she was very active, non-smoker and had no allergies. She underwent the procedure under general anesthesia. She received 4 mg of ondansetron intravenously for postoperative nausea and vomiting prophylaxis at the end of the procedure and an additional 4 mg in the recovery room for nausea. Within 15 min after the second dose she was noted to be in atrial fibrillation that required admission to the hospital and procainamide infusion for conversion to normal sinus rhythm. She did not have any evidence of myocardial ischemia, valvular abnormality or pulmonary embolism. CONCLUSION: The 5-hydroxytryptamine 3 receptor (5-HT(3)) antagonist ondansetron has been reported to cause myocardial ischemia, supraventricular and ventricular tachycardia. Postulated mechanism includes inhibition of Bezold-Zarisch cardiac reflex and coronary vasoconstriction. Inhibition of 5-HT(3) receptors in the heart could lead to unopposed action of other serotonin receptors leading to atrial fibrillation or other tachyarrhythmias described in the literature.

Antiemetics↗

PubMed1979

[A case of malignant hyperthermia occuring in a dental clinic].

Malignant hyperthermia, a life-threatening complication of anaesthesia, occurred in a 5 1/2-year-old girl undergoing dental surgery in a dental clinic. During induction, after 20 mg of succinylcholine, the anaesthetist noted a moderate rigidity of the mandible that did not interfere with the tracheal intubation. However, after 45 minutes, the temperature rose to 38.8 degrees C, pulse was rapid at 160 per minute and the child was slightly cyanosed. The diagnosis of malignant hyperthermia was made (the temperature eventually reached 40.8 degrees C). The child was immediately treated with refrigeration, procainamide and sodium bicarbonate. She was then moved to a hospital centre where the treatment was continued and she recovered completely. After extensive investigation, we found that the paternal grandfather of the child died at age 58, several hours after a bilateral lumbar sympathectomy under general anaesthesia. The cause of the death, as confirmed by hospital records, was malignant hyperthermia. No genetic counselling was given at that time; this omission has since been corrected. Early diagnosis and the availability on the premises of the necessary drugs and equipment to treat such a complication probably saved this child's life. In 1975, "La Corporation Professionnelle des Médecins du Québec" published standards for practice of anaesthesia outside a hospital setting. The compliance of the dental clinic with such standards has contributed to the avoidance of a catastrophe.

Anesthesia, Dental↗

PubMedDate not supplied

Adverse reactions and interactions with H2-receptor antagonists.

Histamine H2-receptor antagonists have been used in the treatment of gastrointestinal diseases for more than a decade and during this period have become one of the most commonly prescribed groups of drugs in the world. The deserved popularity of the H2-receptor antagonists reflects, in part, their therapeutic efficacy, which has revolutionised the treatment of peptic ulcer disease. An equally, or more, important reason for the widespread use of H2-receptor antagonists is their remarkably low toxicity. We have attempted, in this review, to present a detailed account of the minor and more serious adverse reactions, while emphasising the low incidence of the former and the rarity of the latter. The toxicology of the H2-receptor antagonists is discussed under two main headings: adverse effects; and drug interactions. The latter category is potentially the more significant, since the frequent use of therapy with multiple drugs may give rise to drug interactions, some of which are serious and may even be lethal. These drug interactions occur especially in the gastrointestinal tract, the liver and the kidneys. Thus, the absorption of other drugs may be altered because the H2-receptor antagonists inhibit gastric secretion--an effect illustrated by ketoconazole, the absorption of which is reduced when given in combination with cimetidine. Very important drug interactions are caused by inhibition of the hepatic microsomal enzyme cytochrome P450 by some of the H2-receptor antagonists. This effect appears to be related to the chemical structure of the individual H2-receptor antagonists and is not attributable to histamine H2-receptor blockade. For example, cimetidine is a powerful inhibitor of cytochrome P450, while the interaction of ranitidine with this system is weaker. Consequently, cimetidine reduces the metabolism of many drugs which are normally degraded by phase I reactions, leading to potentially toxic plasma concentrations of therapeutic agents such as some oral anticoagulants, beta-blockers, anticonvulsants, benzodiazepines and xanthines. Some of the H2-receptor antagonists are actively secreted by the renal tubules and may thus compete with other drugs for cationic tubular transport mechanisms, resulting in reduced urinary excretion and hence potentially toxic plasma concentrations. This type of drug interaction has been reported after administration of both cimetidine and ranitidine with procainamide or quinidine.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2003

[Cardiac arrhythmias during pregnancy--what to do?].

METHODS: Atrial premature beats are frequently diagnosed during pregnancy, supraventricular tachycardia (atrial tachycardia, AV nodal reentrant tachycardia, circus movement tachycardia) less frequently. For acute therapy, electrical cardioversion with 50-100 J is indicated in all unstable patients. In stable supraventricular tachycardia, initial therapy includes vagal maneuvers to terminate breakthrough tachycardias. For short-term management, when vagal maneuvers fail, intravenous adenosine is the drug of first choice and may safely terminate the arrhythmia. For long-term therapy, beta-blocking agents with beta(1) selectivity are first-line drugs; class Ic agents or the class III drug sotalol represent effective and therapeutic alternatives. Ventricular premature beats are also frequently present during pregnancy and benign in most of the unstable patients; however, malignant ventricular tachyarrhythmias (sustained ventricular tachycardia, ventricular flutter, ventricular fibrillation) are less frequently observed. Electrical cardioversion is necessary in all patients with hemodynamically unstable situation and life-threatening ventricular tachyarrhythmias; in hemodynamically stable patients, initial therapy with ajmaline, procainamide or lidocaine is indicated. If prophylactic therapy is needed, beta-blocking agents with beta(1) selectivity are regarded as drugs of first choice. If this therapy proves ineffective, class Ic agents or sotalol can be considered. In patients with syncopal ventricular tachycardia, ventricular fibrillation, ventricular flutter or aborted sudden death, an implantable cardioverter-defibrillator is indicated. In patients with symptomatic bradycardia, a pacemaker can be implanted using echocardiography at any stage of pregnancy. CONCLUSIONS: The treatment of the pregnant patient with cardiac arrhythmias requires important modifications of the standard practice of arrhythmia management. The goal of therapy is to protect the patient and fetus through delivery, after which chronic or definitive therapy can be administered.

Anti-Arrhythmia Agents↗

PubMed2000

Effects of antiarrhythmic drugs on cloned cardiac voltage-gated potassium channels expressed in Xenopus oocytes.

The effects of 17 commonly used antiarrhythmic drugs on the rapidly activating cardiac voltage-gated potassium channels (Kv1.1, Kv1.2, Kv1.4, Kv1.5, Kv2.1 and Kv4.2) were studied in the expression system of the Xenopus oocyte. A systematic overview on basic properties was obtained using a simple and restricted experimental protocol (command potentials 10 mV and 50 mV positive to the threshold potential; concentration of 100 micromol/l each). The study revealed that 8 of 17 drugs yielded significant effects (changes >10% of control) on at least one type of potassium channel in the oocyte expression system. These drugs were ajmaline, diltiazem, flecainide, phenytoin, propafenone, propranolol, quinidine and verapamil, whereas the effects of adenosine, amiodarone, bretylium, disopyramide, lidocaine, mexiletine, procainamide, sotalol and tocainide were negligible. The drug effects were characterized by reductions of the potassium currents (except for quinidine and ajmaline). A voltage-dependence of drug effect was found for quinidine, verapamil and diltiazem. The different effect of the drugs was not related to the fast or slow current inactivation of the potassium channels (except for verapamil). Profiles of the individual drug effects at the different potassium channel types were identical for propafenone and flecainide and differed for all other substances. The study demonstrates marked differences in sensitivity to antiarrhythmic drugs within the group of voltage-operated cardiac potassium channel types. Taking the restrictions of the oocyte system into consideration, the findings suggest that several antiarrhythmic drugs exert significant effects at rapidly activating cardiac potassium channels.

Animals↗

PubMedDate not supplied

Role of amiodarone in the treatment of fetal supraventricular tachyarrhythmias and hydrops fetalis.

We report three consecutive hydropic fetuses with fetal tachyarrhythmias treated with amiodarone-two in combination with digoxin and one with digoxin, procainamide, and propranolol. Sinus rhythm was achieved in one case and ventricular rate control was achieved in two cases. All fetuses treated with amiodarone gradually improved. Observed side effects of amiodarone were a maternal rash in one mother and transient neonatal hypothyroidism in one infant. We conclude that amiodarone might be effective and safe for fetal tachyarrhythmias and impending hydrops. The small number of patients suggests that a multicenter cooperative approach is required in order to determine if this is correct.

Amiodarone↗