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PubMed2004

Effects of class I antiarrhythmic drugs on the digitalis-induced triggered activity arrhythmia model: a rationale for the short-term use of class I drugs against triggered arrhythmias.

Delayed afterdepolarization (DAD)-induced triggered activity has been considered to be one of the generation mechanisms of ventricular arrhythmias in the presence of intracellular Ca2+ overload. In this study, we analyzed the antiarrhythmic effects of class I antiarrhythmic drugs, namely, disopyramide, procainamide, mexiletine, and flecainide, on a recently developed DAD-induced triggered arrhythmia model, which consists of a canine ventricular septum preparation cross-circulated with a blood-donor dog. After intravenous administration of ouabain to the donor dog, triggered arrhythmias were consistently induced in the cross-circulated preparation by train stimulation (cycle length: 300 ms; train number: 15). Intracoronary administration of disopyramide, procainamide, mexiletine, and flecainide as well as lidocaine suppressed the triggered arrhythmias at clinically relevant doses. Similar doses have been demonstrated to suppress intraventricular conduction in the same experimental model. These results suggest that the Na+ channel inhibition by class I drugs is an effective pharmacological intervention for suppressing Ca2+ overload, which may provide a rationale for the short-term use of class I drugs against the triggered arrhythmias in clinical practice.

Animals↗
PubMed2003

Advances in the acute pharmacologic management of cardiac arrhythmias.

Safe and effective control of rapid ventricular rates in acute-onset atrial fibrillation (AF) can be accomplished with intravenous calcium antagonists, beta-blockers or amiodarone; digoxin is less effective. If pharmacologic cardioversion of AF is desired, single oral doses of propafenone or flecainide are safe and effective in patients without structural heart disease. Intravenous ibulitide is moderately effective in the conversion of persistent AF or atrial flutter, with a small risk of proarrhythmia. In wide QRS complex tachycardia of uncertain origin, adenosine and lidocaine are no longer recommended. Procainamide or amiodarone are the treatment options, but attempts should be made to define the origin of tachycardia. In the treatment of monomorphic ventricular tachycardia, lidocaine is no longer recommended; procainamide or amiodarone are the recommended therapies. In polymorphic ventricular tachycardia with a normal QT interval, beta-blockers are recommended. In shock-refractory ventricular fibrillation, lidocaine, and magnesium are ineffective; intravenous amiodarone should be the treatment of choice.

Anti-Arrhythmia Agents↗
PubMed1989

Effect of cimetidine and ranitidine on cardiovascular drugs.

A compilation of drug interactions between H2 antagonists and cardiovascular drugs is found in Table I. Cimetidine's potency, lipophilicity, and affinity for binding to the P-450 cytochrome system can probably be attributed to the drug interactions that have been identified with the H2 antagonists. The mechanism for most cimetidine drug interactions is inhibition of hepatic metabolism. There is conflicting evidence regarding significance of altered liver blood flow for both cimetidine and ranitidine and their influence on other agents. Cimetidine may increase propranolol's blood concentrations and potentiate beta blocking effects through inhibition of hepatic microsomal enzymes and possibly through reduction of hepatic blood flow. Ranitidine has no effect on propranolol. Cimetidine, when administered concurrently with metoprolol, could possibly cause an increase in plasma metoprolol concentrations or bioavailability through inhibition of hepatic P-450 metabolizing enzymes. No effect of cimetidine on metoprolol pharmacodynamics was evident. Ranitidine has no effect on metoprolol pharmacokinetics or pharmacodynamics. Neither H2 antagonist altered the kinetics or physiologic effects of atenolol. Atenolol is the drug of choice in patients receiving H2 antagonists, since no interaction has been observed. Metoprolol could probably be used safely in most patients, as no change in pharmacodynamics has been evident. Concurrent administration of cimetidine and nifedipine may result in alterations in heart rate and blood pressure. The mechanism is inhibition of oxidative liver metabolism. Ranitidine has no effect on nifedipine. Studies are needed to investigate the interaction between the H2 antagonists and diltiazem or verapamil. Cimetidine, given concomitantly with lidocaine, may increase lidocaine concentrations and clinical symptoms of lidocaine toxicity. The mechanism involved is probably a reduction in oxidative drug metabolism or liver blood flow. Ranitidine has no significant effects on lidocaine pharmacokinetics. Cimetidine may increase quinidine levels and symptoms of quinidine toxicity. Additionally, enhanced arrhythmic effects may be observed. The interaction probably caused by an inhibition of hepatic drug metabolism of quinidine by cimetidine would be most significant in patients with liver disease and in the elderly. Ranitidine may enhance quinidine's arrhythmic effect. Cimetidine can possibly increase procainamide and NAPA serum concentrations, especially in the elderly and in patients with renal dysfunction, predisposing them to adverse side effects. The interaction is mediated by a reduction of tubular secretion of procainamide and NAPA.

Cardiovascular Agents↗
PubMed1983

Idiopathic paroxysmal ventricular tachycardia with a QRS pattern of right bundle branch block and left axis deviation: a unique clinical entity with specific properties.

Electrophysiologic evaluation before and after the serial administration of verapamil, lidocaine, propranolol, and procainamide was undertaken in 4 young, asymptomatic patients with recurrent, sustained ventricular tachycardia (VT). No patient had obvious organic heart disease. The electrocardiogram during sinus rhythm showed S-T depression and T-wave inversion over the inferior and lateral precordial leads in 3 patients. QRS morphologic characteristics during episodes of VT showed a pattern of right bundle branch block and left axis deviation. In all 4 patients, VT could be both induced and terminated with electrical stimulation. Verapamil terminated VT and prevented the induction of sustained VT in 3 patients, and markedly slowed the rate of VT in 1 patient. Procainamide effectively prevented the induction of sustained VT in 2 patients, and although ineffective in preventing induction in 2 patients, it slowed the rate of tachycardia in both. Lidocaine and propranolol did not prevent the induction of VT in any patient. These findings suggest that slow-response tissues may be involved in the genesis of VT in these patients, and that VT in these patients may represent a unique clinical entity with distinct electrocardiographic, electrophysiologic, and electropharmacologic properties.

Adult↗
PubMed1984

Therapy of ventricular tachycardia.

Therapeutic modalities for ventricular tachycardia include antiarrhythmic drugs, direct current cardioversion, electrical pacing and surgical intervention. Lidocaine, procainamide and bretylium are all capable of controlling recurrent ventricular tachycardia; bretylium has the advantage of also being antifibrillatory and of raising the threshold for ventricular fibrillation. Lidocaine and bretylium are available only in i.v. form. Procainamide is available in i.v. as well as oral form. Other oral antiarrhythmic agents include quinidine, disopyramide, beta-blockers such as propranolol and verapamil. The latter may be useful in ventricular arrhythmias induced by ischemia; of these, only beta-blockers appear to significantly raise the threshold for ventricular fibrillation. Control of ventricular ectopy does not always preclude ventricular tachycardia and ventricular fibrillation. In treating ventricular tachycardia, bretylium tosylate is generally given 5 to 10 mg/kg i.v. over 10 to 20 minutes. Given too rapidly, it may cause nausea and vomiting. Orthostatic hypotension, a common side effect, generally abates with continued use and may be ameliorated with tricyclic antidepressants such as protriptyline. Significant supine hypotension may be encountered in patients with acute myocardial infarction and may be managed with pressor agents or fluids, or both. The antiarrhythmic efficacy of bretylium was analyzed in 40 patients. Five etiologic groups were defined by cardiac catheterization: 19 patients had atherosclerotic heart disease, 6 had primary myocardial disease, 4 had mitral valve prolapse, 4 had rheumatic heart disease and 7 had miscellaneous or no heart disease. All patients had recurrent ventricular tachycardia (VT); 23 had ventricular fibrillation (VF) as well. Other antiarrhythmic agents had failed in 38 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Antiarrhythmic drug efficacy for ventricular tachyarrhythmias associated with coronary artery disease as assessed by electrophysiologic studies.

The efficacy and proarrhythmic potential of antiarrhythmic agents were evaluated. Programmed ventricular stimulation was performed in 160 consecutive patients with coronary artery disease during a baseline study and 432 subsequent drug studies. The tachyarrhythmias induced during baseline studies were sustained ventricular tachycardia (121 patients), ventricular fibrillation (16 patients), and symptomatic nonsustained ventricular tachycardia (23 patients). Regimens were completely successful if fewer than 6 repetitive ventricular responses were inducible during therapy and partially successful if no more than 15 repetitive ventricular responses were inducible. Procainamide and quinidine were the most successful single agents, with overall success rates of 24% and 35%, respectively. Either procainamide or quinidine combined with mexiletine was the most successful combination (overall success of 23%). Each anti-arrhythmic regimen showed a proarrhythmic potential. The incidence of proarrhythmic effects ranged from 4 to 13%, with no significant difference between regimens. In 13% of patients at least 1 regimen produced a proarrhythmic effect. Patients treated with an antiarrhythmic regimen that prevented induction of arrhythmia had significantly fewer arrhythmia recurrences than patients treated with a regimen that failed to prevent it. In conclusion, identification of an effective drug regimen is possible in 38% of patients with lethal ventricular arrhythmias, proarrhythmic effects occur in a significant number of patients during electrophysiologic testing of antiarrhythmic regimens, and the clinical outcome in patients in whom ventricular arrhythmias are not inducible with ventricular stimulation have a better prognosis than those in whom arrhythmias continue to be inducible on therapy.

Adult↗
PubMed1987

Diseases and drugs causing prolongation of the QT interval.

The prolonged QT interval and its association with diseases and drugs was studied on the basis of computerized electrocardiograms recorded in the region of the Kuopio University Central Hospital, East Finland. Altogether, 33,655 persons in whom at least 1 electrocardiogram was recorded from 1975 to 1983 were found. The study population consisted of 183 persons with prolonged QT intervals (at least 470 ms) and 187 with normal QTc intervals (440 ms or less), aged 45 to 64 years. These subjects were selected from 14,990 persons eligible. No difference in the prevalence of diseases affecting the QTc interval was found between those with long QTc intervals and those with normal QTc intervals. No difference between the groups was found in use of quinidine, procainamide or disopyramide. When the comparison was made on the basis of all group 1A antiarrhythmic drugs (quinidine, procainamide and disopyramide combined), persons with prolonged QTc intervals used these drugs more often than did those with normal QTc intervals (p = 0.031). Use of sotalol was significantly more common (p less than 0.001) in subjects with long QTc intervals. The mortality rate was also higher in persons with prolonged QTc interval (p less than 0.001), and most deaths during follow-up were due to coronary artery disease.

Anti-Arrhythmia Agents↗
PubMed1988

Effects of basic drugs on the hepatic transport of cardiac glycosides in rats.

The effects of some basic and acidic drugs on the hepatic uptake of digoxin and ouabain were studied in isolated rat hepatocytes. Digoxin accumulated against a concentration gradient, and its initial uptake was energy- and temperature-dependent. Digoxin competitively inhibited the uptake of ouabain (Ki = 1.3 microM), which was reported to be transported by a carrier-mediated active transport system. All basic drugs tested (verapamil, dipyridamole, amiodarone, nifedipine, diltiazem, ajmaline, chlorpromazine, imipramine, disopyramide, quinidine, procainamide, propranolol and lidocaine: 50 microM) except for procainamide, propranolol and lidocaine significantly (P less than 0.05) reduced the uptake of digoxin, whereas acidic drugs (salicylic acid and phenytoin) had no effect. The same inhibitory effects were observed for ouabain uptake, whereas the uptake of alanine was not changed by these drugs. Quinidine inhibited the uptake of ouabain in a noncompetitive manner (Ki = 88 microM). These basic drugs had no effect on the permeability of the cells assessed by the trypan blue exclusion test and succinate-simulated oxygen consumption. But carbonylcyanide-m-chlorophenyl hydrazone-stimulated oxygen consumption decreased in the presence of some basic drugs and correlated with their inhibitory effects on digoxin uptake. Therefore, one of the mechanisms of the inhibitory effects of these drugs on digoxin uptake was the inhibition of oxidative phosphorylation. These basic drugs had no effect on the microtubular system, which was assessed by the measurement of tubulin polymerization and colchicine binding to tubulin. The results of our study suggested that many basic drugs have a potential to inhibit the hepatocellular uptake of cardiac glycosides.

Animals↗
PubMed1980

Effect of some antiarrhythmics on [3H]clonidine binding to alpha 2-adrenergic receptors.

The effects of the antiarrhythmics quinidine, propranolol, procainamide and lidocaine were determined on the specific binding of [3H]clonidine to the alpha 2-adrenergic receptor. Quinidine is effective in decreasing specific [3H]clonidine binding to the alpha 2 receptor within the range of therapeutic blood levels (Ki = 6 x 10 (-8) M). The effectiveness of all compounds tested, with the exception of quinidine and procainamide, correlate with the membrane/buffer partition coefficient, suggesting a relationship with the local anesthetic activity.

Animals↗
PubMed1995

Arylamine and arylalkylamine N-acetyltransferases in retina, pineal gland, brain and liver of chicks: a comparative study.

Regulation of arylamine N-acetyltransferase (A-NAT) and arylalkylamine N-acetyltransferase (AA-NAT) was examined in retina, pineal gland, brain and liver of chicks. Enzyme activities were determined using as substrates p-phenetidine and procainamide for A-NAT, tryptamine and phenethylamine for AA-NAT. The activity of A-NAT in all tissues studied does not appear to be regulated by a light-dark cycle. On the other hand, AA-NAT showed distinct light-dark dependent changes (with high values at night) in the retina and pineal gland, but not in brain and liver. The nocturnal increase of retinal and pineal AA-NAT activity was prevented by cycloheximide; the drug did not affect A-NAT activity in these tissues. Treatment of light-adapted chicks with aminophylline significantly increased AA-NAT activity of the retina and pineal gland, without altering the enzyme activity in brain and liver. In these animals, the activity of A-NAT (procainamide) did not change in any tissue studied, whereas the enzyme activity measured using p-phenetidine as a substrate did decrease but only in the retina. A similar pattern of changes in retinal A-NAT and AA-NAT activities was observed after intraocular injection of d,b-cAMP. The rate of inactivation at 4 degrees C was significantly slower for AA-NAT than A-NAT. NATs from brain and liver displayed the highest and lowest, respectively, liability in the cold. The results indicate that the chick retina contains both A-NAT and AA-NAT. The two enzymes have distinct characteristics and the regulation of their activities is different. The retinal A-NAT is similar to A-NAT present in other tested tissues; however, AA-NAT can be induced at night only in the retina and pineal gland. It is suggested that there are two forms of retinal A-NAT, and that, under specified conditions, the activity of one form (A-NAT; p-phenetidine) may be regulated in an opposite manner to AA-NAT activity.

Analysis of Variance↗
PubMed1992

Propafenone-mexiletine combination for the treatment of sustained ventricular tachycardia.

OBJECTIVES: The purpose of this study was to explore the efficacy of combined therapy with propafenone and mexiletine for control of sustained ventricular tachycardia. BACKGROUND: Combination antiarrhythmic drug therapy may enhance efficacy and lead to control of ventricular arrhythmias in some patients. Few reports have studied the combination of class IB and class IC drugs. Thus, this study was designed to investigate a combination of mexiletine and propafenone in patients with refractory ventricular tachycardia. METHODS: Sixteen patients with sustained ventricular tachycardia had their clinical arrhythmia induced by programmed stimulation. Procainamide and propafenone alone failed to prevent reinduction of tachycardia in all. Mexiletine was subsequently added to propafenone and programmed stimulation was repeated. RESULTS: With combination therapy ventricular tachycardia was noninducible in three patients (19%). A fourth who had presented with polymorphic ventricular tachycardia had slow bundle branch reentry (cycle length 500 ms) induced. In the other 12, tachycardia cycle length increased from 262 +/- 60 ms at baseline to 350 +/- 82 ms with propafenone and to 390 +/- 80 ms with propafenone plus mexiletine (p less than 0.0001 compared with baseline). Hemodynamic deterioration requiring defibrillation occurred in six patients at baseline study, in five taking propafenone and in two taking both drugs. CONCLUSIONS: The combination of propafenone and mexiletine is effective in suppressing the induction of ventricular tachycardia in some patients refractory to procainamide and propafenone alone. In those in whom ventricular tachycardia could still be induced, the rate was slower and hemodynamically tolerated.

Adult↗
PubMed1982

Simultaneous analysis of antiarrhythmic drugs and metabolites by high performance liquid chromatography: interference studies and comparisons with other methods.

Our previously described HPLC method for the simultaneous analysis of several antiarrhythmic drugs and metabolites in serum [Clin. Biochem. 14. 113-118 (1981)] was correlated with an enzyme immunoassay technique (EMIT) for quinidine, procainamide, N-acetyl procainamide, and disopyramide. Correlation coefficients in each case was greater than 0.95. Our method compared favorably with a fluorescent procedure for the quantitation of propranolol in plasma. Interference studies with 34 drugs indicated that the measurements of quinidine and monodealkyldisopyramide were affected by quinine and lidocaine, respectively. Carbamazepine and glutethimide interfered with propranolol, but additional clean-up extractions removed these interferences.

Anti-Arrhythmia Agents↗
PubMed2000

Taste effects of lingual application of cardiovascular medications.

Medications used to treat cardiovascular diseases such as congestive heart failure, high blood pressure, and arrhythmia, are prescribed extensively in Western countries. However, taste complaints are common side effects of many of these cardiovascular medications. Although clinical observations are helpful in determining potential taste problems from a medication, experimental studies are necessary to obtain quantitative data on taste. In the studies performed here, nine cardiovascular medications (labetalol HCl, captopril, diltiazem HCl, enalapril maleate, hydrochlorothiazide, propranolol HCl, mexiletine HCl, procainamide HCl, and propafenone HCl) were applied to the tongue in human volunteers to measure the direct effect of these drugs on taste receptors. The medications were applied topically to the tongue surface of both young and elderly subjects to mimic the situation in which the drug is secreted into the saliva. Detection thresholds ranged from 0.048 mM (propafenone) to 0.438 mM (procainamide). The detection thresholds of healthy elderly subjects did not significantly differ from young controls. The compounds tested had a predominantly bitter taste with other qualities as well. In addition, topical application of the medications to the tongue affected the taste of one or more taste stimuli, with medications differing in the pattern of taste effects exhibited. The mechanism of taste effects is not fully known, but the results of this study suggest one route may be due to medications' effect on peripheral taste receptors.

Administration, Sublingual↗
PubMed1997

Large-scale purification and long-term stability of human butyrylcholinesterase: a potential bioscavenger drug.

Butyrylcholinesterase from human plasma (HuBChE) is a potential drug candidate for detoxification of certain harmful chemicals that contain carboxylic or phosphoric acid ester bonds. Large quantities of purified HuBChE, displaying a high stability upon long-term storage, are required for the evaluation of its therapeutic capacity and its pharmaceutical properties. Several modifications of a previously reported procedure enabled us to purify the enzyme > 15,000-fold from pools of up to 100 1 of human plasma. The three-step procedure is based on precipitation of plasma proteins by ammonium sulfate (step I) and batch adsorption of HuBChE on procainamide-Sepharose 4B gel (step II). Ammonium sulfate was also employed in the third stage to fractionate the final product from procainamide-containing HuBChE solution. The overall yield (63%) of electrophoretically pure enzyme was significantly higher than that previously reported (34%) for the purification of HuBChE from 12.5 1 of plasma or from 5 kg of Cohn fraction IV-4. Purified HuBChE was stored at 5 degrees C in 10 mM phosphate buffer (pH 7.4) containing 1 mM EDTA and 0.02% NaN3. The specific activity, protein migration on gel electrophoresis, thermostability at 54 degrees C and the mean residence time in the circulation of mice remained essentially constant for at least 46 months. The modifications introduced can provide large quantities of purified enzyme that maintains its activity and bioavailability properties for several years.

Animals↗
PubMed1998

Idiopathic ventricular fibrillation: clinical, electrophysiologic characteristics and long-term outcomes.

The long-term prognosis, including risks of arrhythmic recurrence of idiopathic ventricular fibrillation (VF), is uncertain; moreover, the role of electrophysiologic study in the diagnosis and guiding of antiarrhythmic drugs therapy for idiopathic VF remains controversial. The purpose of this study was to study the clinical features, electrophysiologic characteristics and long-term clinical outcomes of six consecutive patients (five males) who had at least one episode of aborted cardiac arrest (5 patients) or syncope (1 patients) with documentation of ventricular fibrillation (VF) in the absence of apparent heart disease. Idiopathic VF was diagnosed by exclusion. All patients underwent the electrophysiologic study including intravenous antiarrhythmic drug testing. Recurrences of VF after therapy and the long-term outcomes were assessed. The mean age at the first episode was 43+/-19 years (range from 16 to 63 years). All patients had sustained VF induced by double (3 patients) or triple (3 patients) ventricular extrastimuli at a paced cycle length of 400 or 500 ms from the right ventricular apex. Intravenous procainamide and/or mexiletine could suppress the reinduction of sustained VF in 4 (67%) of 6 patients. Recurrence of VF (documented VF attack, sudden cardiac arrest or syncope) was observed in 3 (100%) of 3 patients who received procainamide or mexiletine alone. Four patients (including 3 patients who experienced recurrence) received amiodarone alone or in combination with mexiletine, and these drugs could effectively prevent recurrence of VF. One patient with exercise-induced VF remained asymptomatic without any treatment during a follow-up period of 95 months. Another patient received an implantable cardioverter-defibrillator without concomitant antiarrhythmic drug therapy and had no discharge of electrical shock during 28 months of follow-up. During a mean follow-up period of 64+/-40 months (range from 28 to 128 months), all the patients were alive except patient No. 2 who died of acute hepatic failure. In conclusion, electrophysiologic study is a reliable diagnostic method, but it was of limited value in guiding antiarrhythmic drug therapy for preventing recurrence of idiopathic VF. Class I drug alone was associated with a high recurrence rate (100%) despite predictions that it would be effective by the electrophysiologic study. Amiodarone alone or in combination with mexiletine effectively prevented the recurrence of VF during the long-term follow-up along with a favourable outcome.

Administration, Oral↗
PubMed1997

Acetylcholinesterase in Spirographis spallanzanii (Polychaeta: Sedentaria): presence of two dimeric membrane-bound forms.

In the annelid polychaete Spirographis spallanzanii two acetylcholinesterases, named DS and HSDS, were detected. They differ in relative amount, membrane anchoring and pharmacological properties. Studies with inhibitors evidenced complete inhibition of both acetylcholinesterases by 10(-3) M eserine and different sensitivities for edrophonium or procainamide. Both enzymes, sensitive to BW284c51, were unaffected by iso-OMPA; at variance, only the HSDS form underwent excess-substrate inhibition. DS and HSDS enzymes were solubilized by homogenization in a low-salt or high-salt-Triton X-100 buffer and then purified by affinity chromatography on edrophonium- or procainamide-Sepharose column respectively. According to gel-filtration chromatography, sedimentation analysis and SDS-PAGE, the least represented (30%) DS form is a G2 amphiphilic globular dimer (124-130 kDa, 6.0-7.0S) with S-S linked monomers (66 kDa). Phosphatidylinositol anchors give cell membrane insertion, self-aggregation and detergent (Triton X-100, Brij 97) interaction. The prevailing (70%) HSDS acetylcholinesterase is once again a G2 form similar to DS enzyme in its molecular size (117-125 kDa), sedimentation coefficient (6.0S) of the native form and presence of S-S linked subunits (66 kDa). However, it is likely attached to the cell membrane by involvement of strong electrostatic interactions. DS acetylcholinesterase displays moderate active site specificity with differently sized substrates. The HSDS form is inactive on butyrylthiocholine. DS and HSDS forms show a comparable catalytic efficiency (kcat/K(m)) approaching that of other invertebrate enzymes. The results suggest that DS and HSDS enzymes, likely encoded by distinct genes, are both functional in cholinergic synapses.

Acetylcholinesterase↗
PubMed2002

Syncope with ST-segment abnormalities resembling Brugada syndrome due to reversible myocardial ischemia.

This report describes a case of syncope with an initial ECG that showed ST-segment elevation in the right precordial leads suggestive of Brugada syndrome. Procainamide infusion induced a significant increase in the ST-segment abnormalities, further increasing the suspicion for this syndrome. Cardiac catheterization showed lesions in the proximal left anterior descending artery and distal right coronary artery. Following percutaneous coronary intervention at these sites, the ST-segment abnormalities resolved and a repeat procainamide challenge was negative. Electrophysiological study did not provoke any ventricular arrhythmias. Silent myocardial ischemia may result in ECG changes that resemble those seen in patients with Brugada syndrome.

Aged↗
PubMed1992

Effect of antiarrhythmic drugs on choline uptake in cardiac cells in culture.

OBJECTIVE: The aim was to examine the effect on choline uptake of various antiarrhythmic drugs: lignocaine, tocainide, encainide, flecainide, propafenone, procainamide, N-acetylprocainamide, bretylium, and amiodarone. METHODS: Cardiac ventricular myocytes from 7 d old chick embryos were exposed in culture to these drugs, at concentrations ranging from 10(-6) to 10(-4) M, for 24 h. Myocyte choline uptake was assessed by the addition of methyl [3H] choline to media. After 120 min, media were removed, the cells were harvested, and intracellular [3H] actively was counted. RESULTS: Lignocaine and tocainide produced a significant (p less than 0.05) dose dependent increase in intracellular [methyl 3H] choline. Encainide produced a small increase and flecainide a small decrease in choline, neither of which was dose dependent. Propafenone significantly (p less than 0.05) altered choline uptake: at 10(-6) M and 10(-5) M choline uptake was increased and at 10(-4) M it was decreased. Amiodarone produced a marked and significant (p less than 0.05) dose dependent reduction in choline uptake. Bretylium, procainamide, and N-acetylprocainamide did not alter myocyte choline. CONCLUSIONS: Choline incorporation into cardiac myocyte is altered by some antiarrhythmic drugs, suggesting this may be part of their antiarrhythmic properties.

Amiodarone↗