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PubMed2002

Pronounced effect of procainamide on clockwise right atrial isthmus conduction compared with counterclockwise conduction: possible mechanism of the greater incidence of common atrial flutter during antiarrhythmic therapy.

INTRODUCTION: It has been shown that the induction rates of common and reversed common atrial flutter are comparable during baseline control study, whereas the rate is significantly greater for common flutter than reversed common flutter during administration of antiarrhythmic agents. The mechanism of this discrepancy is not known. METHODS AND RESULTS: The study consisted of 15 patients (group 1) with clinically documented common atrial flutter either with (n = 10) or without (n = 5) Class I antiarrhythmic therapy, and 15 patients with paroxysmal supraventricular tachycardia (group 2). Bidirectional conduction velocity and minimal pacing cycle length of 1:1 conduction during incremental pacing from both the low lateral right atrium and coronary sinus were assessed. The response of these variables to procainamide was analyzed in correlation with the induction rate of each type of flutter during the pacing protocol. Conduction velocity in the clockwise (CW) direction was significantly slower for all pacing cycle lengths than conduction velocity in the counterclockwise (CCW) direction in group 1 but was similar in group 2. Minimal pacing cycle length of 1:1 conduction did not differ between CW and CCW conduction in either group. However, in group 1, minimal pacing cycle length of 1:1 conduction of CW conduction was prolonged to a greater degree after procainamide than that of CCW conduction. There also was a significant increase in the induction rate of common flutter. This preferential effect of procainamide on CW conduction was not observed in group 2. CONCLUSION: CW conduction over the isthmus is preferentially influenced by procainamide compared with CCW conduction, which may explain the greater incidence and induction probability of common flutter during antiarrhythmic therapy.

Adult↗
PubMed1978

Effect of acetylator phenotype on the rate at which procainamide induces antinuclear antibodies and the lupus syndrome.

To investigate the relation between acetvlator phenotype and the development of procainamide-induced lupus, we determined the rate of development of antinuclear antibodies in 20 patients of known acetylator phenotype receiving chronic procainamide therapy. The duration of therapy required to induce antibodies in 50 per cent of slow (11) and rapid (nine) acetylators was 2.9 and 7.3 months respectively. The median total dose that produced ant;bodies was 1.5 g per kilogram and 6.1 g per kilogram respectively. After one year antibodies had developed in 18 patients. Retrospective studies of patients in whom procainamide lupus had developed revealed that the duration of therapy required for induction in 14 slow and seven rapid acetylators was 12 +/- 5 and 48 +/- 22 months respectively (P less than 0.002). We conclude that acetylator phenotype influences the rate at which procainamide induces antinuclear antibodies and probably the lupus syndrome. Antibody production is probably related to the parent compound or a non-acetylated metabolite.

Acetylation↗
PubMed1998

Improved high-performance liquid chromatographic assay for the determination of procainamide and its N-acetylated metabolite in plasma: application to a single-dose pharmacokinetic study.

An improved high-performance liquid chromatographic assay for the determination of procainamide and N-acetylprocainamide (NAPA) at concentrations observed up to 32 h after a single oral dose administration of procainamide to human subjects is reported. Following liquid-liquid extraction of plasma samples, procainamide, NAPA, and the internal standard (N-propionylprocainamide) are separated on a reversed-phase C8 column with retention times of 4.0, 6.7, and 13.2 min, respectively. The ultraviolet detection limit (wavelength, 280 nm) of procainamide and NAPA is 2 ng/mL (signal-to-noise ratio, 3:1), and the quantitation limit is 4 ng/mL (signal-to-noise ratio, 5:1). Intra- and interday coefficients of variation are less than 8% in the range of 20-500 ng/mL.

Acecainide↗
PubMed1984

Acute effects of lignocaine, procainamide, metoprolol, digoxin and atropine on human myocardial refractoriness.

The acute intravenous effects of therapeutic doses of procainamide, lignocaine, metoprolol, digoxin and atropine on the monophasic action potentials (MAP) and effective refractory periods of the right ventricle (VERP) were studied in 48 healthy volunteers. Procainamide prolonged the VERP in the apex region. Lignocaine shortened the MAP duration at 90% repolarisation. Metoprolol did not affect any of the measured variables in spite of a significant decrease in heart rate. Digoxin produced a significant increase in the VERP at the outflow tract, but not in the apex region and the MAP variables did not change. Following atropine, the VERP at both recording sites decreased but the MAP signal was unaffected. In summary, the effects of procainamide, lignocaine, metoprolol and digoxin were in good agreement with previous studies in normal ventricular muscle cells in vitro. In addition, the findings following atropine, digoxin and procainamide are indicative of a parasympathetic innervation of the endocardial surface of the right ventricle.

Action Potentials↗
PubMed1993

Comparison of flecainide and procainamide in cardioversion of atrial fibrillation.

In this prospective, controlled and randomized cross-over study we tried to establish the efficiency and safety of flecainide vs procainamide for the treatment of acute atrial fibrillation. Eighty patients (30 females, 50 males, mean age: 55 +/- 14 years) were included. Patients entered into the study if they had atrial fibrillation of recent onset (< 24 h) with a ventricular rate > 100 beats.min-1 at rest and were < 75 years of age. Exclusion criteria were any sign of heart failure, conduction disturbances, sick sinus syndrome or acute ischaemic events. Randomly 40 patients received flecainide and 40 procainamide as the first treatment. There were no significant clinical difference between the two groups. Procainamide ws given at a dose of 1 g infused over 30 min, and followed by an infusion of 2 mg.min-1 over 1 h. Flecainide was given at a dose of 1.5 mg.kg-1 over 15 min followed by an infusion of 1.5 mg.kg-1 over 1 h. Drug infusion was continued until maximal dose, intolerance or reversion to sinus rhythm. After 1 h of wash out, patients remaining in atrial fibrillation were started on the second drug. Left atrial size was measured by echo. Serum levels of drug and atrial size did not differ between patients who returned to sinus rhythm and those who remained in atrial fibrillation. Conversion to sinus rhythm was achieved in 37 (92%) of the 40 patients treated with flecainide and 25 (65%) of those treated with procainamide (P < 0.001). The time required for reversion to sinus rhythm was similar between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Procainamide and quinidine inhibition of the human hepatic degradation of meperidine in vitro.

Procainamide and quinidine inhibition of the degradation of meperidine in human liver was investigated by incubation of two concentrations of either drug with meperidine in homogenates of human liver over 24 and 36 h. Meperidine concentrations declined by 26% after incubation for 24 h and by 42% after incubation for 36 h. In the presence of procainamide, however, they decreased by only 15% to 18% at 24 h and by only 26% to 28% at 36 h. In the presence of quinidine, they declined by only 18% to 19% at 24 h and by only 27% to 28% at 36 h. Procainamide and quinidine may inhibit human hepatic carboxylesterase hCE-1, which is responsible for catalyzing the hydrolysis of meperidine. This inhibition may prolong the biological half-life of meperidine in patients receiving the drug together with either procainamide or quinidine.

Chromatography, Gas↗
PubMedDate not supplied

Comparative vagolytic effects of procainamide and N-acetylprocainamide in the dog.

Procainamide exerts vagolytic effects which are deleterious in clinical therapy for supraventricular arrhythmias. The purpose of the present study was to determine if N-acetylprocainamide (NAPA), an active metabolite of procainamide which has been proposed as an effective and less toxic alternative, would exert an equivalent degree of vagal blockade. In anesthetized dogs, the right cervical vagus nerve was electrically stimulated at supramaximal voltage using frequencies from 0.5 to 20 Hz to slow the sinus rate. The ability of NAPA and procainamide to block this response was tested with infusion of equimolar doses (1.0 and 0.87 mg/kg/min i.v., respectively) continuously over a period of 40-78 min. Both drugs exerted statistically significant vagolytic effects at the higher frequencies of stimulation. Although the vagolytic effect appeared to be more pronounced with procainamide, this could not be demonstrated by statistical analysis of the data.

Acecainide↗
PubMed1976

The effect of food on procainamide absorption.

The effect of food on the absorption characteristics of procainamide was assessed after oral administration of the drug to eight male patients in the fasting and postprandial states. Serum concentration-time curves showed no significant difference in peak serum levels of procainamide, in the time the peak value was reached, or in the area under the serum concentration-time curves, indicating the total amount of procainamide present in the serum. The bioavailability of procainamide appears not to be significantly altered by taking an oral dose with food.

Absorption↗
PubMed1988

Procainamide-induced lupus anticoagulants and thrombosis.

The specific factors predisposing to thrombosis in patients with LAs have not been resolved. With extensive cross-reactivity, and several proposed sites of action, LAs and their effects may be heterogeneous. While the risk of thrombosis with phenothiazine-induced LAs is probably low, the incidence of thrombosis in association with procainamide-induced LAs is uncertain. Procainamide is a commonly used antiarrhythmic drug associated with the induction of autoantibodies, and occasionally with a lupus-like syndrome. Serologic and coagulation profile monitoring may be required to detect patients in whom LAs develop since these individuals may be at increased risk for thrombosis. Monitoring may be especially important in patients who are receiving procainamide and who have atherosclerosis and cardiac disease, since they may be at increased risk for thrombosis of coronary and other arteries. Future prospective studies are needed to investigate whether the development of lupus anticoagulants during procainamide therapy increases the risk of thrombosis.

Aged↗
PubMed1986

Procainamide-induced incessant supraventricular tachycardia in the Wolff-Parkinson-White syndrome.

A patient with the Wolff-Parkinson-White syndrome presented with incessant orthodromic atrioventricular tachycardia following initiation of procainamide therapy. This finding was repeatedly documented both clinically as well as during electrophysiologic testing. Escape atrial complexes, which occurred following junctional premature complexes, failed to initiate tachycardia in the control state but tachycardia was always reinitiated by an identical escape sequence after procainamide. In addition, the tachycardia persisted and was repeatedly spontaneously reinitiated for prolonged periods after procainamide. The pro-arrhythmic effects of procainamide may be explained on the basis of both its vagolytic action on the atrioventricular node as well as by prolongation of refractoriness in the accessory pathway. These observations add to the literature on pro-arrhythmic effects of commonly used antiarrhythmic drugs.

Electrophysiology↗
PubMed1991

Effects of procainamide on refractoriness, conduction, and excitable gap in canine atrial reentrant tachycardia.

The effects of procainamide were studied in a model of atrial flutter around the tricuspid valve in seven open chest, chloralose-anesthetized dogs (31 +/- 3 kg). A Y-shaped incision in the intercaval area extending to the right atrial appendage was made and five bipolar electrodes were sutured on the atrial epicardium around the tricuspid valve. Reentry tachycardia was induced in the absence and presence of drug by burst pacing. Procainamide (15 mg/kg bolus followed by 0.075 mg/kg/min infusion) produced stable plasma levels (38 +/- 9 microM) during the study. At a pacing cycle length of 200 msec, mean (+/- SD) diastolic threshold at the five sites increased from 1.6 +/- 1.5 to 2.0 +/- 1.7 mA and mean atrial effective refractory period from 125 +/- 9 to 140 +/- 16 msec on drug (P less than 0.05). Procainamide prolonged the cycle length of atrial flutter from 144 +/- 10 to 160 +/- 13 msec and slowed conduction velocity during atrial flutter around the tricuspid valve from 73 +/- 6 to 66 +/- 6 cm/sec (P less than 0.05). A reset response curve was determined by introducing premature stimuli during atrial flutter. Procainamide prolonged effective refractory period during atrial flutter from 101 +/- 13 to 116 +/- 17 msec but did not change the duration of the excitable gap (38 +/- 9 vs 40 +/- 18 msec). Although the reset response curve was predominantly increasing, in six of seven experiments there was present a flat portion at long coupling intervals approaching the atrial flutter cycle length that comprised 23% +/- 10% of the excitable gap.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

Effects of procainamide and dl-sotalol on the changes of atrial electrophysiology induced by high current stimulation.

The relation between high current atrial stimulation and antiarrhythmic drugs was not clear. We evaluated the effects of procainamide and dl-sotalol on the electrophysiological changes induced by high current stimulation. Effects of high current atrial stimulation on effective refractory period, dispersion of refractoriness, conduction velocity, and wavelength of the earliest atrial premature beat were evaluated at baseline and after infusion of procainamide (10 patients) and dl-sotalol (10 patients). High current atrial stimulation shortened effective refractory period locally (-12% +/- 4.0%, -7.0% +/- 3.0%, -5.1 +/- 3.3%, and -3.0 +/- 2.0%, at 0, 7, 14, and 21 mm from the S1 stimulation site, respectively; P < 0.001); increased the dispersion of refractoriness (from 17.8 +/- 8.5 to 27.4 +/- 12.5 ms, P < 0.001); decreased conduction velocity of the earliest premature beat (from 0.58 +/- 0.10 to 0.52 +/- 0.09 ms, P = 0.01); and decreased wavelength of the earliest atrial premature beat (from 10.9 +/- 2.4 to 8.8 +/- 2.1 cm, P < 0.001). These effects of high current stimulation persisted after procainamide infusion. However, after dl-sotalol infusion, high current atrial stimuli did not change the dispersion of refractoriness (23.1 +/- 10 ms vs 26.4 +/- 10.4 ms; P > 0.05, twice diastolic threshold vs 10 mA); conduction velocity of the earliest premature beat (0.54 +/- 0.06 ms vs 0.50 +/- 0.06 ms, P > 0.05); or wavelength of the earliest premature atrial beat (11.5 +/- 1.6 m/s vs 10.1 +/- 1.7 cm; P > 0.05). Although high current atrial stimulation shortened effective refractory period locally, increased dispersion of refractoriness, and decreased the wavelength of the earliest premature atrial impulse, these effects were abolished by dl-sotalol but not procainamide.

Adult↗
PubMed1978

Serum levels and electrophysiological effects of N-acetlyprocainamide as compared with procainamide in the dog heart in situ.

The electrophysiological effects of procainamide and its major metabolite N-acetylprocainamide were tested and compared on the heart of the anaesthetized dog by means of His bundle electrography and programmed electrical stimulation. Both drugs exerted a negative chromotropic effect. They also increased intra-atrial and intraventricular conduction times; procainamide was, however, the more potent of the two drugs. In contrast to procainamide, N-caetylprocainamide did not increase His-Purkinje and atrioventricular nodal conduction times, and at the lowest dose employed, atrioventricular nodal conduction times were decreased during atrial pacing. Both drugs increased the functional and effective refractory period of the right atrium and ventricle. N-acetylprocainamide increased the functional refractory period of the atrioventricular node, but to a lesser extent than procainamide.

Animals↗
PubMed1993

Increase in antioxidant activity in procainamide-treated rats.

Recent studies suggest that in vivo procainamide oxidation underlies induction of autoimmunity by this drug. Since drug metabolism may be accompanied by generation of reactive oxygen species, plasma and liver thiobarbituric acid reacting substances (TBARS), activity of erythrocyte and liver superoxide dismutase, catalase, selenium-dependent glutathione peroxidase (Se-GPX), and plasma antioxidant activity in procainamide treated rats were evaluated. Procainamide administration increased liver lipid peroxide levels, intensified the activity of liver catalase and erythrocyte superoxide dismutase, as well as plasma antioxidant activity. The remaining biochemical parameters in the treated rats were within control values, except for the decreased erythrocyte catalase activity. We conclude, that the increased activity of free radicals observed in the treated rats could contribute to the development of procainamide induced side effects.

Animals↗
PubMed1976

Sustained release procainamide in patients with myocardial infarction.

Sustained release procainamide tablets were administered to 34 patients 48 hours after the onset of an acute myocardial infarct. Therapeutic blood levels of procainamide in the range of 4 to 8 mug/ml were consistently achieved using an 8-hourly maintenance dose of 1.5g after an initial loading dose of 2g. In contrast conventional procainamide capsules administered to 21 comparable patients repeatedly failed to produce plasma concentrations in the therapeutic range, despite the administration of a maintenance dose of 375 mg 3 hourly, after a loading dose of 1g. It is suggested that when the oral administration of procainamide is indicated for the management of ventricular arrhythmias after myocardial infarction, a sustained release preparation should be used.

Delayed-Action Preparations↗
PubMed1991

Transitions among atrial fibrillation, atrial flutter, and sinus rhythm during procainamide infusion and vagal stimulation in dogs with sterile pericarditis.

The mechanism of atrial flutter and fibrillation induced by rapid pacing in 22 dogs with 3-day-old sterile pericarditis was investigated by computerized epicardial mapping of atrial activation before and after administration of agents known to modify atrial electrophysiologic properties: procainamide, isoproterenol, and electrical stimulation of the vagosympathetic trunks. Before the administration of any of these agents, a total of 30 episodes of sustained atrial flutter (greater than 1 min duration, monomorphic; regular cycle length, 127 +/- 12 ms, mean +/- SD) was induced in 15 out of 22 dogs and 9 episodes of unstable atrial flutter (duration, less than 1 min; cycle length, 129 +/- 34 ms; monomorphic, alternating with fibrillation) were induced in the remaining 7 preparations. In the latter, administration of procainamide transformed unstable atrial flutter and atrial fibrillation to sustained atrial flutter (cycle length, 142 +/- 33 ms; n = 9 episodes). During control atrial flutter, atrial maps displayed circus movement of excitation in the right atrial free wall with faster conduction parallel to the orientation of intra-atrial myocardial bundles. Vagal stimulation changed atrial flutter to atrial fibrillation in 32 of 73 trials; this was associated with acceleration of conduction in the lower right atrium, leading to fragmentation of the major wave front. Isoproterenol produced a 6-25% increase of the atrial rate in 6 out of 14 trials of atrial flutter and induced atrial fibrillation in 4. After procainamide, the reentrant pathway was lengthened and conduction was slowed further in the right atrium. Maps obtained during unstable atrial flutter showed incomplete circuits involving the right atrium. Following procainamide infusion, the area of functional dissociation or block was enlarged and a stable circus movement pattern, which was similar to the pattern seen in control atrial flutter, was established in the right atrium. We conclude that (1) the transitions among atrial fibrillation, atrial flutter, and sinus rhythm occur between different functional states of the same circus movement substratum primarily located in the lower right atrial free wall, and (2) the anisotropic conduction properties of the right atrium may contribute to these reentrant arrhythmias and may be potentiated by acute pericarditis.

Animals↗
PubMed1985

Effects of infarction, procainamide, coupling interval, and cycle length on refractoriness of extrastimuli.

The effects of prematurity, cycle length, site of stimulation, and procainamide on ventricular refractoriness following an extrastimulus (S2) were assessed in 10 dogs with and 10 dogs without infarction. Extrastimuli were introduced at preselected coupling intervals (S1-S2) from normal right and left ventricular sites and from left ventricular sites of infarction during drive cycle lengths (S1-S1) of 350 and 250 ms. At each S1-S2 interval, the effective refractory period of S2 was determined by introducing a second extrastimulus (S3). At all stimulation sites, cycle lengths, and before and during infusion of procainamide (mean concn 18.6 +/- 3.5 micrograms/ml), shortening (greater than 10 ms change) in refractoriness was most marked over a narrow range of closely coupled S1-S2 intervals. Regardless of stimulation site, the effective refractory period of S2 was less during a cycle length of 250 ms compared with a cycle length of 350 ms. In dogs without infarction, the effective refractory periods of S2 from left ventricular sites tended to be longer than from right ventricular sites, particularly during procainamide administration. The refractory period of S2 at sites of infarction did not differ consistently from those at normal sites. Finally, at all stimulation sites and cycle lengths, procainamide prolonged refractoriness of S2 at each S1-S2 interval and blunted the total shortening in refractoriness in response to S2.

Animals↗
PubMed1986

Lethal accumulation of procainamide metabolite in severe renal insufficiency.

Four patients, 64-80 years of age, with severe renal dysfunction and heart disease received conventional doses of procainamide as treatment for cardiac arrhythmias. Serum procainamide concentrations at these times ranged from 6.2 to 13.3 micrograms/ml and were within the recently expanded therapeutic range for resistant ventricular arrhythmias. All 4 patients demonstrated marked and delayed accumulation of the active metabolite N-acetylprocainamide, with highest observed serum concentrations ranging from 42.0 to 59.4 micrograms/ml. Cardiotoxicity associated with these levels included progressive widening of the QRS and corrected Q-T intervals, induction of polymorphic non-sustained ventricular tachycardia (torsades de pointes), and severe depression of left ventricular function which appeared to be important factors in the deaths of these patients. The use of lower procainamide doses and careful anticipatory monitoring of serum concentrations of procainamide and N-acetylprocainamide are essential in this high-risk group.

Acecainide↗