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Query: CAS:41708-72-9 (Tocainide)
 93 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tocainide is a derivative of lidocaine with anti-arrhythmic action and, unlike lidocaine, can be used for oral treatment. Tocainide was alternatively with carbamazepine given to 12 patients with trigeminal neuralgia in a double-blind cross-over study for 2 weeks. The analgesic effect was estimated each day by the patients using a 0-10-point scale summarizing the frequency and severity of the attacks. The similarity in analgesic effect of the two drugs was striking. A possible analgesic mechanism could be that tocainide blocks the sodium channels in the hyperexcitable nerve membranes in the pain-producing foci in trigeminal neuralgia.
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PMID:The analgesic effect of tocainide in trigeminal neuralgia. 310 44

Tocainide is an effective oral antiarrhythmic agent. We report a 77-year-old man who developed agranulocytosis and anemia while receiving tocainide therapy. These hematologic abnormalities were detected on routine evaluation six weeks after beginning tocainide therapy. The absolute granulocyte count decreased to 50/mm3 (0.05 X 10(9)/L). The anemia was mild; hemoglobin count, 10.9 g/dL (109 g/L). These abnormalities were associated with local and stromal adipocytic bone marrow damage, and decreased production of red blood cells and granulocytes. The platelet count was not affected. The patient had no evidence of infection. Hematologic values were restored to normal two weeks after discontinuation of tocainide therapy, indicating that bone marrow toxicity of tocainide is reversible.
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PMID:Tocainide-induced reversible agranulocytosis and anemia. 310 62

A case is reported in which tocainide, a relatively new cardiac antiarrhythmic for oral use, is believed to have caused a delirium. The patient had been admitted to a coronary intensive care unit for the treatment of ventricular arrhythmia and had developed confusion, impairment in concentration and severe anxiety. Her EEG was compatible with metabolic encephalopathy. The clinical picture varied with the use of tocainide so closely that it appeared to be the most likely cause of the delirium. Other factors were taken into consideration but did not seem to adequately disprove this impression. Tocainide has been known to cause minor, transient and treatable side effects in the form of gastrointestinal and central nervous symptoms--mainly nausea, tremor and dizziness. There have also been three case reports of paranoid psychoses. It is suggested that psychiatrists be aware of the above complications as they may have occasion to see patients taking tocainide, especially in consultation-liaison work. A table with the more common side effects and their frequencies is included.
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PMID:Mental changes associated with tocainide, a new antiarrhythmic. 310 61

The effects of lidocaine, tocainide and mexiletine were examined in 17 patients with coronary artery disease and chronic, recurrent, sustained ventricular tachycardia (VT) or ventricular fibrillation and inducible VT. Eleven patients presented with sustained VT; 6 patients had had an episode of sudden death from which they had been resuscitated. All patients were refractory to conventional antiarrhythmic agents. Lidocaine prevented induction of VT in only 3 patients (18%). Tocainide prevented induction of VT in only 1 lidocaine-responsive patient. Mexiletine prevented VT induction in 1 patient who had responded to lidocaine but not tocainide. Neither tocainide nor mexiletine was effective in preventing induction of VT in any patient who did not respond to lidocaine. Lidocaine terminated VT in 3 patients, but this did not predict noninducibility with lidocaine, tocainide or mexiletine. Cycle length of VT was prolonged slightly by lidocaine (control 311 +/- 14 ms, lidocaine 361 +/- 26 ms, p less than 0.05), tocainide (344 +/- 16 ms, p less than 0.05) and mexiletine (371 +/- 27 ms, mean +/- standard error of the mean, p less than 0.05). Thus, class lb agents are infrequently effective in preventing induction of VT in this group of patients, electrophysiologic inefficacy of lidocaine is highly predictive of continued inducibility with tocainide and mexiletine, and termination of VT with lidocaine does not correlate with its ability to prevent VT induction.
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PMID:Efficacy of class Ib (lidocaine-like) antiarrhythmic agents for prevention of sustained ventricular tachycardia secondary to coronary artery disease. 310 28

A 26-year-old woman committed suicide by ingestion of a large quantity of tocainide, a recently developed oral antiarrhythmic agent with chemical similarities to lidocaine. Blood and bodily fluid analysis by thin-layer chromatography, high pressure liquid chromatography, and mass spectroscopy confirmed the presence of tocainide, with a serum level of 68 mg/L, nearly 7 times the upper recommended therapeutic level for this drug. Tocainide was also detected at significant levels in vitreous fluid and bile. Although the mechanism of death from tocainide intoxication in animal studies is related to central nervous system toxicity, the presentation of ventricular tachyarrhythmias with coma in this patient suggests that tocainide at high levels may have primary myocardiotoxicity in humans.
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PMID:Fatal intoxication by tocainide. 311 60

Tocainide, mexiletine, flecainide, encainide, and amiodarone are antiarrhythmic agents that have recently been approved by the Food and Drug Administration for general use in the treatment of ventricular arrhythmias. All five agents are effective in the treatment of patients with ventricular arrhythmias, whereas encainide, flecainide, and amiodarone are also useful in patients with supraventricular arrhythmias and the Wolff-Parkinson-White syndrome (although not yet approved for these indications). Tocainide and mexiletine are similar to lidocaine and are as effective as quinidine in patients with ventricular arrhythmias. Encainide and flecainide are superior to quinidine for the control of ventricular ectopic beats and as effective as quinidine for patients with ventricular tachycardia. Amiodarone is the most effective agent available for treating patients with ventricular tachycardia, but it is also the most toxic antiarrhythmic agent and should be used only when other antiarrhythmic drugs have not been effective or tolerated.
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PMID:New antiarrhythmic drugs: tocainide, mexiletine, flecainide, encainide, and amiodarone. 311 16

Eighty-two patients with drug-resistant ventricular tachycardia or fibrillation were treated with oral tocainide. Treatment in 54 patients, all with inducible ventricular tachycardia or fibrillation at baseline electrophysiologic testing, was based on the results of invasive electrophysiologic testing. Twenty-eight additional patients with frequent spontaneous ventricular tachycardia or no inducible arrhythmia during electrophysiologic testing were treated on the basis of the findings of electrocardiographic (ECG) Holter monitoring. Tocainide was effective in 7 (13%) and partially effective in 5 (8%) of the 54 patients in the electrophysiologic study group and was effective in 17 (61%) of the 28 patients in the ECG monitoring group. History of previous myocardial infarction and failure of response to lidocaine correlated with failure to respond to tocainide. Side effects were common both during initial therapy and during long-term treatment and necessitated discontinuation of tocainide therapy in 17% of the patients. At a mean follow-up period of 14 months, 13 patients are still receiving tocainide and are arrhythmia-free. In conclusion, the usefulness of oral tocainide in the management of drug-refractory sustained ventricular tachycardia or fibrillation is limited because of its low effectiveness and frequent side effects.
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PMID:Tocainide for drug-resistant sustained ventricular tachyarrhythmias. 312 11

Tocainide and quinidine were administered both as single agents and in combination to 14 patients with chronic ventricular arrhythmias. Therapy with tocainide was limited by the occurrence of dose-related adverse reactions in 8 patients, but could be titrated to a dose that was well-tolerated in 13 of 14 and effective in 2 of 13. The addition of quinidine gluconate to the tolerated dose of tocainide increased the number of patients with arrhythmia suppression from 2 to 6. After tocainide washout, quinidine alone suppressed arrhythmias in only 3 patients. Analysis of electrocardiogram intervals showed that the drugs had additive effects on the coupling interval of the sinus beat to the predominant ectopic beat, but exerted antagonistic effects on the corrected QT interval. These findings suggest that the combination may be clinically useful, exerting pharmacologic effects unlike either agent alone.
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PMID:Tocainide plus quinidine for treatment of ventricular arrhythmias. 312 37

The isometric force of arm and leg muscles was studied in five unrelated patients with recessive generalized myotonia (Becker). The symptom of myotonia was present mainly in the legs, whereas transient weakness was the prominent symptom in the arms. Tocainide improved both symptoms, although it improved the stiffness more than the weakness. A specimen of intact muscle fibers was excised from the external intercostal muscle of one of the patients. The resting potential of the fibers was normal, but on injection of depolarizing current the fibers responded with repetitive action potentials. In normal interstitial fluid the current-voltage relationship was N-shaped, with a region of negative slope between -70 and -55 mV. Replacement of chloride by an impermeant anion changed this relationship very little, suggesting an abnormally small chloride conductance. The potassium current through the inward-going rectifier was larger than normal. The force of tetanic contractions of a rested bundle was not sustained but fell quickly to a plateau that increased with repeated stimulation. The relaxation of a rested tetanus was slow and accompanied by spontaneous electrical activity. In subsequent contractions the relaxation became faster and electrical after-activity decreased. However at 23 degrees C the speed of relaxation was always high despite a large amount of electrical after-activity. The electrical instability of the membrane and the transient weakness can be explained on the basis of the N-shaped membrane characteristic.
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PMID:Transient weakness and altered membrane characteristic in recessive generalized myotonia (Becker). 335 55

The haemodynamic effects and regional clearances of tocainide were investigated in sheep with chronic intravascular cannulae to measure blood flow through, and drug extraction by, lungs, kidneys, liver and gut. 2. Tocainide, at arterial blood concentrations in the therapeutic range, caused no haemodynamic effects and was significantly extracted only by the liver. 3. In the presence of general anaesthesia with halothane, the mean hepatic blood flow and tocainide extraction ratio were each reduced by approximately 25% so that the mean hepatic clearance and intrinsic clearance of tocainide each were reduced by approximately 50%. Thus arterial blood tocainide concentrations were increased by 50%. 4. While the clinical implications of this interaction are unclear because of insufficient information about the margin of safety of tocainide, the pharmacological implications are plain. Because general anaesthesia may alter the relationship between dose and blood drug concentrations, pharmacokinetic and pharmacodynamic data should not be interchanged between awake and anaesthetized subjects.
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PMID:The effects of general anaesthesia on tocainide clearance in the sheep. 366 Aug 50


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