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PubMed1988

Effect of class I antiarrhythmic agents on slow Ca2+ channels of myocardial cells.

The effects of several class I antiarrhythmic drugs (aprindine, cibenzoline, disopyramide, mexiletine, lidocaine, tocainide and 711389-S) were studied on slow Ca2+ channels of rabbit sinus node cells using a double microelectrode voltage clamp technique. All these drugs decreased the heart rate, the maximum rate of rise (Vmax), the action potential amplitude and the slope of the phase 4 depolarization in spontaneously beating sinus node preparations. The order of inhibitory potency on the heart rate was: aprindine greater than 711389-S greater than cibenzoline greater than or equal to disopyramide greater than mexiletine greater than or equal to lidocaine greater than tocainide. On the current systems, these drugs decreased the slow inward current (Isi) and the time-dependent potassium current (Ik). However, the major effect was a reduction of Isi. These agents also exerted a frequency-dependent block of Isi. Furthermore, comparing the effects of class I antiarrhythmic agents on slow Ca2+ channels, the order of inhibitory effect on Vmax of sinus node cells was: aprindine greater than 711389-S greater than cibenzoline greater than or equal to disopyramide greater than mexiletine greater than lidocaine greater than tocainide. These electrophysiological observations suggest that class I antiarrhythmic drugs have a depressant effect on slow Ca2+ channels as well as fast Na+ channels of myocardial cells, and that so-called "slow" kinetic drugs may depress slow Ca2+ channels more strongly than "fast" kinetic drugs.

Animals↗
PubMed2000

Efficacy of agents for pharmacologic conversion of atrial fibrillation and subsequent maintenance of sinus rhythm: a meta-analysis of clinical trials.

CONTEXT: Physicians have little evidentiary guidance for pharmacologic agent selection for atrial fibrillation (AF). OBJECTIVE: To assess antiarrhythmic agent efficacy for AF conversion and subsequent maintenance of sinus rhythm (MSR). DATA SOURCE: We searched the clinical trial database of the Cochrane Collaboration and MEDLINE encompassing literature from 1948 to May 1998. STUDY SELECTION: We selected 36 (28%) articles eligible as randomized trials of nonpostoperative AF conversion or MSR in adults. DATA EXTRACTION: Study quality; rates of conversion, MSR, and adverse events were extracted. DATA SYNTHESIS: Compared with control treatment (placebo, verapamil, diltiazem, or digoxin), the odds ratio (OR) for conversion was greatest for ibutilide/dofetilide (OR=29.1; 95% confidence interval [CI], 9.8-86.1) and flecainide (OR=24.7; 95% CI, 9.0-68.3). Less strong but conclusive evidence existed for propafenone (OR=4.6; 95% CI, 2.6-8.2). Quinidine (OR=2.9; 95% CI, 1.2-7.0) had moderate evidence of efficacy for conversion. Disopyramide (OR=7.0; 95% CI, 0.3-153.0) and amiodarone (OR=5.7; 95% CI, 1.0-33.4) had suggestive evidence of efficacy. Sotalol (OR=0.4; 95% CI, 0.0-3.0) had suggestive evidence of negative efficacy. For MSR, strong evidence of efficacy existed for quinidine (OR=4.1; 95% CI, 2.5-6.7), disopyramide (OR=3.4; CI, 1.6-7.1), flecainide (OR=3.1; 95% CI, 1.5-6.2), propafenone (OR=3.7; 95% CI, 2.4-5.7), and sotalol (OR=7.1; 95% CI, 3.8-13.4). The only amiodarone data, from comparison with disopyramide, provided moderate evidence of efficacy for MSR. No trial evaluated procainamide. Direct agent comparisons and adverse event data were limited. CONCLUSIONS: Although multiple antiarrhythmic agents had strong evidence of efficacy compared with control treatment for MSR, ibutilide/dofetilide and flecainide had particularly strong evidence of efficacy compared with control treatment for AF conversion. There is sparse and inconclusive evidence on direct agent comparisons and adverse event rates. Obtaining information regarding these relative efficacies should be a research priority.

Aged↗
PubMed1979

[Medical management of tachycardias (author's transl)].

Guidelines for a step-wise plan of treatment of tachycardias have been compiled based on clinical empirical experience and with the aid of surface electrocardiograms, intracardial electrograms and stimulation techniques. The plan is primarily with the aid of surface electrocardiograms, intracardial electrograms and stimulation techniques. The plan is primarily oriented with respect to the antiarrhythmic efficacy, the adverse reactions and the practicability of the respective agents. Any type of tachycardia, including premature atrial or ventricular contractions, may be regarded as indication for treatment. Treatment is not indicated only in those asymptomatic patients with rare and evanescent tachycardias and in those with less than 300 premature contractions per hour. Beta-adrenergic blockers are the drugs of choice for the persistent sinus tachycardia. Should the latter agents be contraindicated, propafenon, amiodarone or aprindine may be administered. Verapamil and/or digitalis are indicated only for suppression of paroxysmal sinus tachycardias. Atrial premature contractions are best managed with guinidine or disopyramid. An acute reduction of rapid ventricular rates associated with atrial tachycardias, atrial flutter or fibrillation can best be attained through the administration of verapamil prior to digitalis or beta-adrenergic blockers. Re-establishment of sinus rhythm and prophylactic suppression of the latter should be undertaken with quinidine or disopyramid in combination with digitalis and/or either a beta-adrenergic blocker or intravenously-administered verapamil. Verapamil is the drug of choice for initial management of AV-junctional tachycardia for which a combination with digitalis may be considered. An alternative combination is that of a beta-adrenergic blocker and digitalis. For the acute treatment of ventricular tachycardias, lidocain has proved most effective. Although ajmaline and/or propafenon may be given should no response be obtained, electrical cardioversion would be more appropriate. To prevent ventricular tachycardia or when treatment is indicated for ventricular premature beats, ajmaline, propafenon, quinidine, disopyramid or mexiletine, occasionally in combination with a beta-adrenergic blocker should be employed. Verapamil and/or ajmaline, are usually very effective for termination of reciprocal tachycardias. Ajmaline or propafenon in combination with a beta-adrenergic blocker is recommended for the prophylactic treatment of reciprocal tachycardia. In patients who additionally have bradycardia, prolonged QT-intervals or pre-excitation syndromes, the guidelines should be modified accordingly.

Anti-Arrhythmia Agents↗
PubMed1993

Female gender as a risk factor for torsades de pointes associated with cardiovascular drugs.

OBJECTIVE: To test the hypothesis that female prevalence is greater than expected among reported cases of torsades de pointes associated with cardiovascular drugs that prolong cardiac repolarization. DATA SOURCES: A MEDLINE search of the English-language literature for the period of 1980 through 1992, using the terms torsade de pointes, polymorphic ventricular tachycardia, atypical ventricular tachycardia, proarrhythmia, and drug-induced ventricular tachycardia, supplemented by pertinent references (dating back to 1964) from the reviewed articles and by personal communications with researchers involved in this field. STUDY SELECTION: Ninety-three articles were identified describing at least one case of polymorphic ventricular tachycardia (with gender specified) associated with quinidine, procainamide hydrochloride, disopyramide, amiodarone, sotalol hydrochloride, bepridil hydrochloride, or prenylamine. A total of 332 patients were included in the analysis following application of prospectively defined criteria (eg, corrected QT [QTc] interval of 0.45 second or greater while receiving drug). DATA EXTRACTION: Clinical and electrocardiographic descriptors were extracted for analysis. Expected female prevalence for torsades de pointes associated with quinidine, procainamide, disopyramide, and aminodarone was conservatively estimated from gender-specific data reported for antiarrhythmic drug prescriptions in 1986, as derived from the National Disease and Therapeutic Index, a large pharmaceutical database; expected female prevalence for torsades de pointes associated with sotalol, bepridil, and prenylamine was assumed to be 50% or less since these agents are prescribed for male-predominant cardiovascular conditions. RESULTS: Women made up 70% (95% confidence interval, 64% to 75%) of the 332 reported cases of cardiovascular-drug-related torsades de pointes, and a female prevalence exceeding 50% was observed in 20 (83%) of 24 studies having at least four included cases. When analyzed according to various descriptors, women still constituted the majority (range, 51% to 94% of torsades de pointes cases), irrespective of the presence or absence of underlying coronary artery or rheumatic heart disease, left ventricular dysfunction, type of underlying arrhythmia, hypokalemia, hypomagnesemia, bradycardia, concomitant digoxin treatment, or level of QTc at baseline or while receiving drug. When cases of torsades de pointes were analyzed by individual drug, observed female prevalence was always greater than expected, representing a statistically significant difference (P < .05) for all agents except procainamide. CONCLUSIONS: These findings strongly suggest that women are more prone than men to develop torsades de pointes during administration of cardiovascular drugs that prolong cardiac repolarization. The pathophysiological basis for, and therapeutic implications of, this gender disparity should be further investigated.

Adolescent↗
PubMed1991

Effects of combined use of class I antiarrhythmic agents on Vmax of guinea-pig ventricular muscles.

The effects of the combined use of class-I antiarrhythmic drugs on the resting potentials (RP), amplitude of action potential (AMP), and Vmax of the action potential were investigated in guinea-pig ventricular papillary muscles that were superfused with oxygenated Krebs-Ringer solution at 35 degrees C. Disopyramide (40 microM) reduced Vmax to 68.6 +/- 3.1% (mean +/- SE, n = 5) of the control with minimal changes in RP and AMP when preparations were stimulated at 1 Hz. The addition of mexiletine (20 microM) to the solution containing disopyramide (40 microM) caused a minimal reduction of Vmax (less than 5%) for the stimulation of 1 Hz, but a significant reduction of Vmax (13% p less than 0.05) when stimulation was increased to 2 Hz. This amount of the reduction is compatible with that obtained by mexiletine alone, suggesting a simple additive Na+ channel inhibition by this drug combination. This additive effect was also observed in the recovery process of Vmax from the use-dependent block induced by train stimuli at 1 Hz. Flecainide (5 microM) reduced Vmax to 58.6 +/- 13.3% (n = 5). The addition of mexiletine to the superfusate with flecainide produced a further depression of 14 +/- 2.6% of Vmax, even at 1 Hz. This depression was larger than that produced by mexiletine, suggesting a synergistic action of the two drugs on the Na+ channel. Such information about the interaction of the class I drug combinations with the Na+ channel may be clinically important.

Action Potentials↗
PubMed1983

Influence of volume shifts on drug binding during equilibrium dialysis: correction and attenuation.

A time-dependent volume shift from buffer to plasma, which occurs during equilibrium dialysis, decreased the protein binding of disopyramide and its capacity constant, and had no effect on the binding association constant. The volume-dependent decrease in disopyramidine binding may be corrected for by use of a derived equation. Inclusion of dextran, 2.5% (w/v), and use of a thick, low molecular weight cutoff membrane was the most effective technique in attenuating the volume shift. The plasma (serum) protein binding of the basic drugs lidocaine, disopyramide, propranolol, and diazepam was decreased when protein was diluted to 88% or less of its undiluted concentration as a consequence of the volume shift. The protein binding of clofibrate, a highly bound acid drug, was more sensitive to volume shifts than the four basic drugs. Correction of drug binding for volume shifts was reasonably successful for most drugs. The highest binding measured for all drugs was associated with the lowest volume shift.

Blood Proteins↗
PubMed1998

Effects of antiarrhythmic drugs on the monophasic action potential of the canine isolated, blood-perfused ventricular septum preparation.

The present study was designed to combine the monophasic action potential (MAP) recording technique with a well-established canine isolated, blood-perfused ventricular septum preparation for examining, simultaneously, electrical and mechanical drug-induced changes. A MAP catheter was positioned onto the base of a papillary muscle for recording the local MAP, using a manual micromanipulator together with a commercially available catheter sheath to keep the optimal contact pressure against the ventricular wall. The catheter sheath was filled with saline to eliminate the background electrical noise. Tetrodotoxin, disopyramide, lidocaine, and verapamil were used to clarify the potential utility of the preparation. Tetrodotoxin and lidocaine shortened the MAP duration, while disopyramide prolonged it. Verapamil slightly shortened the MAP duration but not significantly. Each drug showed negative inotropic and coronary vasodilator effects. Sodium channel blockers slowed intraventricular conduction and decreased the maximum upstroke velocity of MAP, while verapamil showed no effects. These results suggest that utilization of the blood-perfused ventricular septum preparation together with MAP recording will become a valuable model for evaluating drugs with multiple sites of action on cardiac muscles.

Action Potentials↗
PubMed1982

Electrophysiologic drug testing in prophylaxis of sporadic paroxysmal atrial fibrillation: technique, application, and efficacy in severely symptomatic preexcitation patients.

Electrophysiologic drug testing was performed in nine patients with severely symptomatic sporadic (2 to 13 [mean 4.2] attacks/24 months) paroxysmal atrial fibrillation (PAF). All patients had control inductions of sustained (greater than 30 seconds) AF by high right atrial stimulation, and attempted inductions following serial administration of drugs. Drugs tested were intravenous procainamide (1.0 to 1.5 gm) (five patients), intravenous propranolol (0.1 mg/kg) (three patients), oral quinidine (1.6 to 2.4 gm/day) six patients), oral disopyramide (1.2 to 1.6 gm/day) (four patients), and oral aprindine (100 to 250 mg/day) (four patients). In all patients, one or more drugs prevented induction of sustained AF: procainamide (one patient), quinidine (five patients), disopyramide (four patients), and aprindine (four patients). All patients were treated with drugs which prevented induction of sustained AF and followed for 8 to 40 (mean 24) months. Seven patients tolerated their drugs: six had no AF and one had several short nonsustained attacks. Two patients did not tolerate their drugs: one had paroxysmal palpitation (on decreased aprindine dosage), and one had AF (while off of aprindine). In conclusion, electrophysiologic drug testing is feasible in patients with sporadic PAF. Inability to induce sustained AF following drug administration suggests successful prophylaxis of spontaneous PAF with the same drug.

Administration, Oral↗
PubMed1995

Antiarrhythmic and bradycardic drugs inhibit currents of cloned K+ channels, KV1.2 and KV1.4.

We investigated the effects of the antiarrhythmic drugs, quinidine, disopyramide, flecainide, clofilium, verapamil, and the bradycardic drug, bertosamil, on the currents of the cloned K+ channels, KV1.2 (IK(V1.2)) and KV1.4 (IK(V1.4)), using the Xenopus oocyte expression system. Both IK(V1.2) and IK(V1.4) were inhibited in a concentration-dependent manner by quinidine (10 microM to 1 mM), flecainide (10 microM to 1 mM), clofilium (10-300 microM), verapamil (10 microM to 1 mM) and bertosamil (10 microM to 1 mM) but not by disopyramide (10 microM to 1 mM). The inhibitory effects of clofilium, verapamil and bertosamil on IK(V1.2) were time-dependent. The decay time course of IK(V1.4) was accelerated by clofilium, verapamil and bertosamil, but decelerated by quinidine and flecainide. These results indicate that IK(V1.2) and IK(V1.4) are targets for the four antiarrhythmic drugs and the bradycardic drug.

Animals↗
PubMed1990

Effect of class Ia antiarrhythmic agents on fasciculoventricular fibers.

In four patients with fasciculoventricular (FV) fibers, the electrocardiographic and electrophysiologic characteristics were studied based on their response to class Ia antiarrhythmic agents. Three patients had paroxysmal atrial fibrillation, and one showed atrioventricular nodal Wenckebach-type block with dual pathways. Three of the four patients showed complete block of FV fibers after administration of disopyramide 0.28-0.60 mg/kg, procainamide 1.7-2.6 mg/kg, and ajmaline 0.18-0.26 mg/kg, respectively. Normalization in the remaining patient was not seen after disopyramide 2 mg/kg or procainamide 10 mg/kg, but was achieved by ajmaline 0.86 mg/kg. Ventricular preexcitation beats showed initial q waves (3 patients) or a decrease in the height of the r wave (1 patient) in V1, no initial q wave in V6 (4 patients), and ST-T changes (1 patient). Since these findings resemble ischemic change or intraventricular conduction disturbance, drug testing is necessary for precise diagnosis and proper clinical management.

Adult↗
PubMed1987

High maintenance rate of sinus rhythm after cardioversion in post-thyrotoxic chronic atrial fibrillation.

We performed rhythm conversion on 33 euthyroid patients with post-thyrotoxic atrial fibrillation who do not revert spontaneously to sinus rhythm from atrial fibrillation. The duration of atrial fibrillation ranged from 9 to 59 months (mean 25 +/- 14). The protocol of rhythm conversion was to first attempt pharmacological conversion with disopyramide and then to perform electrical cardioversion on the non-converters. Of 33 patients, 25 were converted to sinus rhythm (6 by disopyramide and 19 by electrical cardioversion), resulting in 8 non-converters. However, it was later discovered that cardioversion had been applied to 4 of the 8 non-converters when these patients had had a recurrence of thyrotoxicosis. These 4 patients were subjected to a second electrical cardioversion after attaining the euthyroid state. Sinus rhythm was restored in all 4 patients, giving a cardioversion rate of 88%. The sinus rhythm was maintained in 25 of the total 29 converters (86%) at the time of follow-up (10-68 months, mean 35 +/- 19 months). Our studies suggest that cardioversion should be encouraged for thyrotoxic atrial fibrillation, even if the duration of atrial fibrillation is long-standing, since there is excellent maintenance of sinus rhythm and even delayed application of cardioversion may improve its success rate.

Adult↗
PubMed1994

Inhibitors of ATP-sensitive potassium channels stimulate intestinal cholecystokinin secretion.

Recently, a role for adenosine 5'-triphosphate(ATP)-sensitive potassium channels in the regulation of cholecystokinin (CCK) secretion has been described in STC-1 cells, an intestinal CCK-secreting cell line. To examine whether a similar mechanism might participate in the regulation of hormone secretion from native CCK cells, the effects of two established inhibitors of ATP-sensitive potassium channels (e.g. glucose, disopyramide) were examined on CCK release from dispersed murine intestinal cells. Both glucose and disopyramide were found to stimulate CCK secretion. Furthermore, CCK release induced by glucose was inhibited by the calcium channel blocker diltiazem. It is concluded that, ATP-sensitive potassium channels may play a role in the regulation of intestinal CCK secretion.

Adenosine Triphosphate↗
PubMed1993

Clinical evaluation of the use-dependent QRS prolongation and the reverse use-dependent QT prolongation of class I and class III antiarrhythmic agents and their value in predicting efficacy.

We measured the QRS duration during a treadmill exercise test and the QT interval using a 24-hour Holter electrocardiogram at various heart rates to identify use-dependent QRS prolongation and reverse use-dependent QT prolongation of class I and III antiarrhythmic drugs. Use-dependent QRS prolongation was detected in 61%, 53%, and 64% of patients receiving disopyramide, mexiletine, and pilsicainide, respectively. Reverse use-dependent QT prolongation was found in 40% and 70% of patients receiving disopyramide and E4031. Drugs suppressed > or = 75% of the total premature ventricular contractions in all patients who had both use-dependent QRS prolongation and reverse use-dependent QT prolongation, in 79% of patients with use-dependent QRS prolongation alone, in 70% with reverse use-dependent QT prolongation alone, and in 11% with neither use-dependent QRS prolongation nor reverse use-dependent QT prolongation. Use-dependent QRS prolongation and reverse use-dependent QT prolongation were identified noninvasively and were useful in evaluating antiarrhythmic efficacy.

Adult↗
PubMed2000

Block of wild-type and inactivation-deficient cardiac sodium channels IFM/QQQ stably expressed in mammalian cells.

The role of inactivation as a central mechanism in blockade of the cardiac Na(+) channel by antiarrhythmic drugs remains uncertain. We have used whole-cell and single channel recordings to examine the block of wild-type and inactivation-deficient mutant cardiac Na(+) channels, IFM/QQQ, stably expressed in HEK-293 cells. We studied the open-channel blockers disopyramide and flecainide, and the lidocaine derivative RAD-243. All three drugs blocked the wild-type Na(+) channel in a use-dependent manner. There was no use-dependent block of IFM/QQQ mutant channels with trains of 20 40-ms pulses at 150-ms interpulse intervals during disopyramide exposure. Flecainide and RAD-243 retained their use-dependent blocking action and accelerated macroscopic current relaxation. All three drugs reduced the mean open time of single channels and increased the probability of their failure to open. From the abbreviation of the mean open times, we estimated association rates of approximately 10(6)/M/s for the three drugs. Reducing the burst duration contributed to the acceleration of macroscopic current relaxation during exposure to flecainide and RAD-243. The qualitative differences in use-dependent block appear to be the result of differences in drug dissociation rate. The inactivation gate may play a trapping role during exposure to some sodium channel blocking drugs.

Amino Acid Substitution↗
PubMed1997

Pirmenol inhibits muscarinic acetylcholine receptor-operated K+ current in the guinea pig heart.

We examined the effects of pirmenol and disopyramide on the muscarinic acetylcholine receptor-operated K+ current (I[K.ACh]) in atrial cells and on experimental atrial fibrillation in isolated guinea-pig hearts. In isolated atrial myocytes, both pirmenol and disopyramide concentration-dependently inhibited the I(K.ACh) induced by carbachol or intracellular loading of GTPgammaS. Their inhibitory effects on the carbachol-induced current were more potent than those on GTPgammaS-induced current, suggesting that these drugs inhibit I(K.ACh) mainly by blocking muscarinic receptors. In Langendorff-perfused hearts these drugs reversed the carbachol-induced decreases in effective refractory periods and atrial fibrillation threshold. These drugs may be useful for the prevention of vagally induced atrial fibrillation.

Action Potentials↗
PubMed1978

Liquid chromatography in the monitoring of plasma levels of antiarrhythmic drugs.

High-performance liquid chromatography has been employed in the development of assay methods for six antiarrhythmic drugs, disopyramide, lidocain, tocainide, procainamide, aprinidine and quinidine. Liquid-solid chromatography has been used and separation times of about 5 min have usually been sufficient. Owing to the capacity of the liquid chromatographic system, sample preparation has been minimized to a single extraction and direct injection of a considerable part of the extract. The overall time of analysis is very short and the methods are well suited for monitoring of plasma levels of the antirrhythmic drugs and in some instances (procainamide and disopyramide) also for their main metabolites. UV detection at the optimal wavelength has permitted determinations down to 50 pmole (20 ng) in 1 ml of plasma for the amines with high absorbance.

Anilides↗
PubMed1986

Periodic changes in cycle length of ventricular tachycardia: a Wenckebach type exit block?

A 55-year-old female developed ventricular tachycardia (VT) which showed a Wenckebach periodicity in cycle length. She had had a myocardial infarction about ten years previous and, at age 51, felt fatigability and palpitations. The ECG showed VT. Thereafter, she had had palpitations of short duration two to three times a year. On the last admission she developed fatigability; the ECG showed VT. Lidocaine (100 mg i.v.) did not terminate VT. Procainamide (600 mg) could not terminate the VT, but the rate became slower. Programmed stimulation was given at bedside which effectively terminated VT. Electrophysiologic study induced VT in a reproducible manner. Ventricular tachycardia showed initial fluctuation in cycle length which stabilized at 270 msec. Disopyramide therapy (400 mg/day p.o.) was begun and electrophysiologic study was repeated one week later. VT was again induced but the cycle length was a little longer. A periodic change in cycle length from 328 to 442 msec was repeated. The change in cycle length was uniformly found in surface leads (I, II, V1) and intracardiac electrograms from the right ventricular apex and the His bundle region. No change in QRS complex was found and the periodicity was unrelated to atrial activity. A Wenckebach type exit block was therefore suggested; disopyramide might be responsible for the development of the block. We could not find another such case in the literature.

Bundle of His↗
PubMed1987

Proarrhythmic effects of antiarrhythmic drugs during programmed ventricular stimulation in patients without ventricular tachycardia.

The proarrhythmic effects of class IA antiarrhythmic drugs were prospectively evaluated during programmed ventricular stimulation in 24 consecutive patients with frequent ventricular premature beats whose baseline study, performed while no antiarrhythmic drugs were being taken, showed no inducible sustained ventricular arrhythmias. No patient had nonsustained (greater than 5 beats) or sustained ventricular tachycardia by history or baseline 24 hour ambulatory electrocardiographic monitoring. Sequential stimulation studies using up to three extra-stimuli were performed after administration of procainamide, quinidine and disopyramide on different days. Proarrhythmic response was defined as induction of one or more of the following: sustained monomorphic ventricular tachycardia; sustained polymorphic ventricular tachycardia; ventricular fibrillation; reproducibly inducible nonsustained monomorphic ventricular tachycardia. During 55 antiarrhythmic drug trials (24 of procainamide, 21 of quinidine, 10 of disopyramide) in the 24 patients, 6 patients had a proarrhythmic response: sustained monomorphic ventricular tachycardia in 3, ventricular fibrillation in 2, nonsustained monomorphic ventricular tachycardia in 1. Thus, 11% of drug trials resulted in a proarrhythmic response and 25% of patients had a proarrhythmic response to one of the drugs tested. A proarrhythmic response to one drug did not predict a similar response to another drug of the same class. The 6 patients with a proarrhythmic response did not differ significantly from the other 18 patients with regard to underlying heart disease, electrocardiographic or baseline 24 hour ambulatory electrocardiographic characteristics; however, they did have a higher incidence of digoxin usage (p less than 0.02), a shorter baseline right ventricular effective refractory period (p less than 0.01) and a smaller increment in effective refractory period during antiarrhythmic drug testing (p = 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗