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PubMed1983

Electropharmacology of antiarrhythmic drugs.

Cardiac arrhythmias may be caused by abnormalities of impulse initiation, impulse propagation, or a combination of the two. The specific mechanisms that may induce arrhythmias are reviewed, as are the means whereby antiarrhythmic drugs might be expected to modify arrhythmias. The cellular electrophysiologic effects of the following antiarrhythmic drugs are discussed: quinidine, procainamide, disopyramide, lidocaine, tocainide, mexiletine, phenytoin, beta-blocking and slow-channel-blocking drugs, aprindine, bretylium, ethmozin, and amiodarone. A knowledge of the similarities and differences of their actions on the determinants of conduction, on repolarization and refractoriness, on automatic mechanisms, and on afterdepolarizations, when considered in the context of the mechanism of clinically occurring tachyarrhythmias, may provide the correct framework for the choice of an appropriate agent for the control of an individual disorder of rhythm. However, it is emphasized that neither the precise mechanism of various dysrhythmias nor the fundamental basis for the salutary action of antiarrhythmic compounds is completely understood.

Action Potentials↗
PubMed1977

Influence of excitability on the ventricular fibrillation threshold in dogs.

The influence of the excitability threshold on the ventricular fibrillation threshold was studied in dogs during myocardial ischemia and potassium and aprindine infusion. Interventions that influenced excitability threshold were associated with similar changes in ventricular fibrillation threshold although the percent change in both values differed. Although it is possible that the interventions studied caused parallel but independent changes in excitability threshold and ventricular fibrillation threshold, it is likely that the excitability threshold influences the ventricular fibrillation threshold. An increase in excitability threshold could result in an increase in ventricular fibrillation threshold in spite of an increase in the actual tendency of the heart to fibrillate spontaneously. Such discordance between the "electrical stability of the heart" and the ventricular fibrillation threshold was found during myocardial ischemia.

Animals↗
PubMed1990

Molecular pharmacological aspects of antiarrhythmic activity. I. Class I and class III compounds and lipid peroxidation.

The effect of nineteen antiarrhythmic agents on nonenzymatic lipid peroxidation, using rat hepatic microsomes, was studied. Lipid peroxidation was induced by Fe2(+)-ascorbic acid and assayed spectrophotometrically by measuring the 2-thiobarbituric acid reactive material. The compounds tested have various structural characteristics and represent class I and III of antiarrhythmics as classified by Vaughan Williams. The RM values, derived from reversed-phase thin-layer chromatography, were determined, and sigma f values calculated in order to correlate lipophilicity and antioxidant activity. The antiarrhythmics studied inhibited lipid peroxidation to various degrees. No apparent structural factor could definitely be attributed to this effect and antioxidants are found among both class I and class III compounds. There is a trend toward a parabolic relationship between antioxidant potency and lipophilicity. Three of the tested antiarrhythmics, namely the lipophilic amiodarone, aprindine and asocainol, were very potent antioxidants, and a further investigation of concentration and time dependency of lipid peroxidation was performed. It is suggested that, at least for some antiarrhythmic drugs, antioxidant activity may be part of their mode of action, and that it may form an additional beneficial feature for the treatment of cardiac failure.

Amiodarone↗
PubMed2003

Usefulness and safety of bepridil in converting persistent atrial fibrillation to sinus rhythm.

The aim of this study was to investigate the efficacy and safety of bepridil (a multichannel blocker including several potassium channels) for conversion of long-lasting atrial fibrillation (AF). Bepridil restored sinus rhythm alone or in combination with aprindine in 69% of 32 patients with persistent AF lasting > or = 3 months. The time to conversion after starting bepridil was 30 +/- 12 days. An increase in fibrillation cycle length with bepridil was greater in responders (31 +/- 10%), but an increase in QTc did not differ between responders and nonresponders. Bepridil is effective and safe for terminating long-lasting persistent AF.

Anti-Arrhythmia Agents↗
PubMed2002

Atrial fibrillation threshold predicted long-term efficacy of pharmacological treatment of patients without structural heart disease.

AIMS: To ascertain if an electrophysiological study could predict long-term efficacy of anti-arrhythmic drugs in the treatment of lone atrial fibrillation. METHODS AND RESULTS: Forty-four patients (36 males, 8 females, age 55.5 +/- 10.6) with paroxysmal atrial fibrillation were enrolled to undergo serial electrophysiological studies at the bedside. Two quadripolar catheters were inserted via the subclavian vein. Disopyramide (D: 2 mg/kg iv), cibenzoline (C: 1.4 mg/kg iv), aprindine (A: 2 mg/kg iv), pilsicainide (P: 2 mg/kg po) and flecainide (F: 3 mg/kg po) were tested. Atrial fibrillation threshold (AFT) was measured as the lowest current amplitude of rapid pacing (50 Hz for 1 s) to induce atrial fibrillation lasting more than 30 s. Before drug treatment, AFT was 3.9 +/- 0.3 mA. Pharmacological treatment raised AFT as follows: D 5.9 +/- 0.9 mA, C 7.6 +/- 1.2 mA, A 8.1 +/-1.1 mA, P 6.0 +/- 0.8 mA, F 7.3 +/- 1.1 mA. Recurrence of atrial fibrillation was observed during 1-year follow-up in 12% of cases when they were treated with a drug that raised AFT by 5 mA or more. On the other hand, the recurrence rate was 87% when patients were treated with a drug that raised AFT by less than 5 mA (P = 0.001). CONCLUSION: AFT was a good predictor of long-term efficacy of pharmacological treatment against atrial fibrillation.

Aged↗
PubMed1983

[Long-term drug therapy in ventricular cardiac arrhythmias. Is an improvement of the prognosis possible?].

Oral long-term treatment with various antiarrhythmic drugs (aprindine, mexiletine, disopyramide, amiodarone) was assessed in 82 patients with recurrent tachycardias demonstrated in the ECG using programmed ventricular stimulation. It was shown that sudden cardiac death and recurrence of tachycardia were clearly reduced in the group of patients (n = 29) in whom drug treatment prevented ventricular tachycardia following electric stimulation. Amiodarone was demonstrated to be the most effective substance in this respect, notwithstanding some side effects.

Adult↗
PubMed1981

New drugs for treating cardiac arrhythmias.

The new and potent antiarrhythmic drugs herald an exciting era in the treatment of cardiac arrhythmias. Encainide, tocainide, and mexiletine are effective in treating acute and chronic ventricular arrhythmias. Verapamil promises to be the drug of choice for paroxysmal supraventricular tachycardia. Acetubolol provides the advantages of selective beta receptor blockade and has minimal influence on pulmonary function. Aprindine and amiodarone block conduction in accessory pathways and are very suitable for treating tachycardias associated with Wolff-Parkinson-White syndrome. Ethmozin is a phenothiazine derivative with potent antiarrhythmic effects. Many of these new agents are being used with striking success abroad and at specialized treatment centers for experimental research in the United States.

Acebutolol↗
PubMed1987

Clinical trials of antiarrhythmic therapy--an improper answer to a proper question?

Pharmacologic prevention of ventricular fibrillation (VF) and sudden cardiac death (SCD) is based on the assumption that the abnormal impulse that causes premature ventricular complexes (PVCs) may trigger VF and that antiarrhythmic drug therapy will thus inactivate the trigger. However, results available from secondary preventive trials of antiarrhythmic agents, including the Ghent-Rotterdam Aprindine (GRAP) study, have not established conclusively the value of antiarrhythmic therapy. A number of factors could explain this failure, e.g., PVCs and VF might not be causally related, thus, antiarrhythmic drugs might not prevent VF; the number of patients enrolled in investigations might have been too small to accommodate statistical proof of benefit; or the subjects might have been poorly selected. A serious design defect that could interfere with demonstrating a benefit for treatment might arise from the fact that all patients in the GRAP and similarly designed studies had to show complex ventricular arrhythmias at randomization and that antiarrhythmic treatment was usually continued regardless of its effect on the underlying arrhythmias. Given the variability of arrhythmias, it would be expected that arrhythmias would persist in only a fraction of patients randomized to placebo. However, arrhythmias also persisted, although to a lesser extent, in treated patients. If one considers that SCD risk may be reduced in the face of arrhythmia suppression but that it may be increased if the arrhythmia persists due to a toxic or proarrhythmic drug effect, any advantageous effects of successful antiarrhythmic drug therapy would be offset by the negative effects of unsuccessful arrhythmia suppression, which would distort the comparison with placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1983

Quantitative analysis of the antiarrhythmic effect of drugs on canine ventricular arrhythmias by the determination of minimum effective plasma concentrations.

Antiarrhythmic effects and minimum antiarrhythmic plasma concentrations (min PC) were examined using three canine ventricular arrhythmia models, i.e., two-stage coronary ligation arrhythmia (Cor), halothane-adrenaline arrhythmia (Adr) and digitalis arrhythmia (Dig). Disopyramide suppressed these three arrhythmias and its min PCs were 5.3 +/- 1.8 (Cor), 4.2 +/- 1.1 (Adr) and 1.7 +/- 0.4 micrograms/ml (Dig). Procainamide suppressed coronary ligation arrhythmia and its min PC was 27.1 +/- 4.0 micrograms/ml, but was not effective on adrenaline arrhythmia. Aprindine was effective on three arrhythmias and its min PCs were 1.6 +/- 0.3 (Cor), 1.0 +/- 0.4 (Adr) and 0.8 +/- 0.4 micrograms/ml (Dig). Lidocaine was not effective on coronary ligation arrhythmia, but was effective on adrenaline arrhythmia and its min PC was 15 micrograms/ml. Phenytoin was effective on three arrhythmias and its min PCs were 9.8 +/- 2.0 (Cor), 12.1 +/- 3.1 (Adr) and 11.3 +/- 3.0 micrograms/ml (Dig). It was not specifically effective on canine digitalis arrhythmia. Propranolol and other beta-blockers were effective on adrenaline arrhythmia, but very high doses were necessary for suppressing coronary ligation and digitalis arrhythmias. Verapamil was only effective on adrenaline arrhythmia and its min PC was 0.03 +/- 0.01 microgram/ml. Canine min PCs of drugs were almost the same as those reported in man except for procainamide and lidocaine. Membrane stabilizing effects seem to be important for suppressing canine ventricular arrhythmias.

Animals↗
PubMed1988

Therapeutic effectiveness and plasma levels of single or combination use of class I antiarrhythmic agents for ventricular arrhythmias.

The efficacy of disopyramide (DP), mexiletine (MX), aprindine (AP) and cibenzoline (CZ) on ventricular arrhythmias was compared (single drug therapy). In addition, the efficacy of the combination therapy of DP with MX was also studied (combination therapy). One hundred of the 106 patients completed the protocol of the single drug therapy. Fifty percent or more reduction in the frequency of ventricular premature contractions (VPCs) was obtained in 24 of 43 patients (56%) with DP, in 24 of 44 (55%) with MX, in 18 of 29 (62%) with AP and 10 of 18 (56%) with CZ. AP was comparatively more effective than the other drugs tested. DP was significantly effective on VPCs with organic heart disease as compared to idiopathic VPCs (p less than 0.05), while the other 3 drugs did not have such a tendency. With MX therapy, 10 of the 12 patients with fast VT rate (greater than or equal to 150 beats/min) showed a significant effect while only 4 of the 12 patients with non-fast VT rate (greater than or equal to 100 and 150 beats/min) had a significant one (p less than 0.05). On the other hand, DP, AP and CZ showed almost the same efficacy at any cycle length of VT. Six patients withdrew from the study, 4 because of digestive troubles with MX therapy, 1 because of micturition disturbances with DP and 1 because of skin rash with AP. The average therapeutic plasma levels of DP, MX, AP and CZ were 1.76 +/- 0.54 microgram/ml, 1.08 +/- 0.41 microgram/ml, 0.85 +/- 0.43 microgram/ml and 268.2 +/- 123.3 ng/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2006

[Strategy for cardiac arrhythmias in acute coronary syndrome].

Acute coronary syndrome causes several types of arrhythmia because of its electrical instability and ischemia. The most important arrhythmia is ventricular tachycardia which degenerates to ventricular fibrillation. Prompt direct current cardioversion will be needed and prevention of ventricular tachyarrhythmia by potassium channel blocker became more popular in Japan. Nifekalant or amiodarone should be selected. Atrial fibrillation also occurred in the patients with acute coronary syndrome, and it may deteriorate hemodynamics condition. Therefore, termination and prevention of atrial fibrillation is another important issue in acute coronary syndrome. Aprindine, amiodarone, or bepridil will be the choice to prevent recurrent atrial fibrillation after direct current cardioversion.

Amiodarone↗
PubMed1989

[Drug-induced major anomalies of ventricular repolarization masked by a left branch block].

The presence of a left bundle branch block (LBBB) may hamper the electrocardiographic diagnosis of diseases that involve the QRS complexes. That it may conceal, or even completely erase, major abnormalities of ventricular repolarization induced by certain drugs is not so well known. In this paper, two highly demonstrative examples of such abnormalities observed with bepridil (case 1) or with the amiodarone-aprindine combination (case 2) are reported. In both cases, the intermittent character of the LBBB revealed the phenomenon which deserves to be known as it is not without practical consequences: in patients under treatments likely to modify repolarization and induce severe dysrhythmias (notably torsades de pointes) the presence of a LBBB indicates that the QT and/or QU intervals must be very carefully measured. In case of phase 3 LBBB compression of the carotid sinus or intravenous ATP injection helps the diagnosis since in the presence of even moderately prolonged ventricular cycles such manoeuvres create a refinement of QRS complexes which then demonstrate the major alteration of the underlying repolarization.

Aged↗
PubMed1979

Influence of moxaprindine treatment on ventricular arrhythmias occurring during maximal exercise stress testing.

Moxaprindine, a new anti-arrhythmic drug, with characteristics similar to aprindine, has been demonstrated to be highly effective in suppressing ventricular arrhythmias occurring before, during and after maximal exercise stress testing. This effect was obtained both in subjects with clinically normal hearts and in a limited number of patients with ischemic heart disease. These findings demonstrate the efficacy and safety of anti-arrhythmic treatment by drugs prolonging ventricular depolarization for ventricular arrhythmias occurring during exercise.

Adult↗
PubMed1984

New drugs in the management of ventricular arrhythmias.

New antiarrhythmic drugs are chiefly assigned to Class 1C and 1B: "procainamide analogues" (acecainide, lorcainide, flecainide, encainide) and propafenone for the former, and mexiletine, tocainide and aprindine for the latter. Pharmacokinetics vary widely among the different antiarrhythmic agents. These and other problems which regulate therapeutic interventions, such as patient compliance, drug interactions, efficacy/toxicity ratio, drug combinations, and drug monitoring with plasma concentrations of antiarrhythmic agents are briefly considered.

Acecainide↗
PubMedDate not supplied

[New anti-arrhythmia drugs].

In this paper some of the new antiarrhythmic drugs are reviewed. The origin, electrophysiologic effects, mechanisms of action, pharmacokinetic properties, hemodynamic changes, clinical utilization with indications and contraindications as well as the collateral effects of: Verapamil Amiodarone, Aprindine, Encainide, Mexiletine and Tocainide are analyzed. A conclusion is drawn for each one of these drugs in accordance with the available information in the literature and the author's criteria and experience.

Amiodarone↗
PubMed1981

[Effects of antiarrhythmic agents on ventricular arrhythmias following myocardial infarct induced with glass beads in dogs (author's transl)].

Ventricular arrhythmias due to myocardial infarct were produced in 14 dogs, and the antiarrhytmic effects of quinidine (Qd), lidocaine (Lid), aprindine (Apr), and dl-propranolol (dl-Prop) were investigated. While recording the blood pressure and lead II ECG, a coronary cannula was inserted into a coronary orifice via the left carotid artery and a glass bead (diameter, 1.5 mm) was flushed into the left coronary artery. Beads were found at the descending branches in 12 and circumflex branches in 2 out of 14 gods, at autopsy. Using a telemetry system to record the lead II ECG of conscious, non-restricted dogs, the antiarrhythmic effects of Qd, Lid, Apr, and dl-Prop on ventricular arrhythmias 24 hours after coronary occlusion were compared. Apr and dl-Prop were about three times more potent than Qd and Lid. Although the durations of the antiarrhythmic effects of Apr, Lid, and dl-Prop were 20 to 30 min, that of Qd lasted longer. Since stable ventricular arrhythmias can be obtained by surgical intervention and the antiarrhythmic effects of standard compounds with glass beads can be used to study antiarrhythmic effects.

Animals↗
PubMed1993

[Recent progress in Holter electrocardiography, focussed on heart rate variability].

Heart rate variability has attracted attention as an index of the effects of the autonomic nerve system on the heart rhythm. Heart rate variability (HRV) is low in patients at risk for sudden death. We evaluated the effects of caffeine, whole-day work without sleep and drugs on HRV. Caffeine had no effects on HRV or ventricular extrasystoles in young adults but aggravated those in obese middle-aged subjects. Whole-day work without sleep increased blood catecholamines and decreased HRV. These findings also suggest the usefulness of HRV as an index in health management. Tofisopam, enalapril and aprindine significantly improved HRV. These drug may be useful for maintaining normal autonomic nerve activity and preventing autonomic nerve diseases or sudden cardiac death in this stressful society.

Adult↗