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PubMed1981

Acetylation of procainamide and isoniazid by a rat liver-N-acetyl-transferase.

The genetic variation of the enzyme isoniazid-N-acetyltransferase has been studied in man and other species. Homogenates of liver samples of adult LEW rats also acetylate procainamide. The kinetic properties of isoniazid and procainamide acetylation are similar and are consistent with a ping-pong Bi-Bi mechanism. The experimental data support the hypothesis that one acetyltransferase catalyses both procainamide and isoniazid. Furthermore, a simple spectrophotometric assay to determine procainamide acetylation is presented.

Acetylation↗
PubMed1988

Epicardial mapping of polymorphous ventricular tachycardias induced in the canine heart with procainamide.

To elucidate the mechanisms of the arrhythmogenic and antifibrillatory action of procainamide, 24 episodes of polymorphous ventricular tachycardia were analyzed. They were induced electrically in 12 canine hearts before and after the administration of 40 mg/kg of procainamide. The isochronal maps of the epicardial activation sequence were successfully constructed by 40 simultaneously recorded bipolar electrograms in 14 of 17 episodes after procainamide. The isochronal maps showed a possible macroreentrant circuit in 12 episodes, and in four of them the functional block was noticed to have disappeared before the termination of tachycardia. This study suggests that procainamide predisposes the ventricle to reentrant tachyarrhythmias and that the dimension of the reentrant circuit induced is too large to be fragmented into multiple reentries, which results in the prevention of the development of ventricular fibrillation.

Animals↗
PubMed1989

Efficacy of procainamide on ventricular tachycardia: relation to prolongation of refractoriness and slowing of conduction.

The effect of procainamide on intraventricular conduction and refractoriness, and the prevention of induction of ventricular tachycardia (VT) were studied in 29 patients who had remote myocardial infarction and inducible sustained monomorphic VT. AFter intravenous administration of 15 mg/kg procainamide, induction of VT was suppressed in seven (24%) patients (responders), while in 22 (76%) VT was still inducible (nonresponders). The percent change in paced QRS duration at a cycle length (CL) of 400 msec produced by procainamide was significantly less in responders than in nonresponders: 29.8 +/- 3.9% versus 38.9 +/- 10.8% (p = 0.0020). The percent change in the right ventricular effective refractory period (ERP) at CLs of 600 and 400 msec was significantly greater in responders than in nonresponders: 14.6 +/- 6.9% versus 7.9 +/- 7.3% (p = 0.0414) for ERP at a CL of 600 msec and 15.1 +/- 7.0% versus 8.0 +/- 7.4% (p = 0.0386) for ERP at a CL of 400 msec. Stepwise discriminant analysis showed that greater percent increase in ERP at a CL of 400 msec and lesser percent increase in paced QRS duration at a CL of 400 msec were significantly independent markers for the responders. These findings suggest that lesser slowing of conduction and greater prolongation of refractoriness by procainamide tend to abolish reentry within the reentrant circuit. Greater slowing of conduction and lesser prolongation of refractoriness tend to stabilize a reentrant circuit, and promote the continued induction of VT.

Electrocardiography↗
PubMed1980

Strength-interval relation in the human ventricle: effect of procainamide.

The effects of procainamide on strength-interval relations were evaluated in 18 patients. At plasma concentrations of 4.3 to 13.6 micrograms/ml procainamide had minimal effects on threshold current in late diastole, but in early diastole it shifted the strength-interval curve to the right. The basic strength-interval relation (that is, decreasing refractory period as current is increased) was not altered. The control refractory period decreased by a mean of 44 ms as the current was increased from threshold to 10 mA, whereas a mean decrease of 42 ms was observed after procainamide. However, the steep portion of the strength-interval curve(absolute refractory period) was shifted to longer coupling intervals by a mean value of 24 ms. These findings suggest that procainamide may primarily affect active membrane properties, but exert little net effect on passive membrane properties late in diastole.

Action Potentials↗
PubMed1980

Simultaneous anterograde fast-slow atrioventricular nodal pathway conduction after procainamide.

UNLABELLED: Three patients with paroxysmal supraventricular tachycardia underwent electrophysiologic studies that included His bundle recordings, incremental atrial and ventricular pacing and extrastimulation before and after intravenous infusion of 500 mg of procainamide. In all three patients the tachycardia was induced during atrial pacing or premature atrial stimulation, or both. Two of the three patients had discontinuous atrioventricular (A-V) nodal curves with induction of a slow-fast tachycardia during failure in anterograde fast pathway conduction and one patient had a smooth A-V nodal curve with induction of a slow-fast tachycardia at critical A-H interval delays. After procainamide: (1) in all three patients atrial pacing induced A-V nodal Wenckebach periodicity (cycle length 300 to 400 ms) resulting in simultaneous anterograde fast and slow pathway conduction (one atrial beat resulting in two QRS complexes) and retrograde fast pathway conduction initiating an echo response or a slow-fast tachycardia, or both; (2) in all three patients there was enhanced conduction and shortening of refractoriness of the anteriograde fast pathway and depressed conduction and lengthening of refractoriness of the retrograde fast pathway; and (3) in two patients there was inability to sustain tachycardia because of selective block within the retrograde fast pathway. IN CONCLUSION: (1) procainamide altered conduction and refractoriness of the anterograde fast and slow pathways so that simultaneous conduction could occur during atrial pacing, resulting in a double ventricular response and a slow-fast echo or tachycardia, or both; and (2) the differential effects of procainamide on anterograde fast and retrograde fast pathways suggests two functional A-V nodal fast pathways, oine for anterograde and the other for retrograde conduction.

Aged↗
PubMed1975

Effects of N-acetylprocainamide as compared with procainamide in isolated rat atria.

The actions of procainamide and its major metabolite N-acetylprocainamide were tested and compared on isolated rat atria. While procainamide exerted a negative chronotropic and iontropic effect, N-acetylprocainamide had the opposite effect. It is suggested that a N-acetylprocainamide-induced increase in myocardial work can counteract the negative inotropic action of procainamide and thus to some extent explain the variable results with the latter compound on myocardial performance reported from in vivo experiments. Procainamide increased the refractory period and reduced the excitability of isolated rat atria. N-acetylprocainamide, on the other hand, caused negligible effects on these parameters.

Animals↗
PubMed1990

A dual electrophysiologic test for atrial antireentry and ventricular antifibrillatory studies. Effects of bethanidine, procainamide, and WY-48986.

We have developed a dual electrophysiologic test that allows measurement of both antireentry and antifibrillatory activities of potential antiarrhythmics in the same anesthetized dog. The reentry portion of the model was created surgically by a Y-shaped crushing around the tissue between the superior and inferior vena cava and tissue parallel to the AV groove. The pacing-induced tachycardia that results from circus movements around the tricuspid ring is very persistent in duration and regular in cycle length. The antifibrillatory activities were assessed by determination of the ventricular fibrillation threshold (VFT) using train-stimuli method. Control VFT was measured every 15-20 min in duplicate and followed by induction of atrial reentry. A drug was infused to intervene the atrial tachycardia. After the conversion of the arrhythmia (either by drug regimens or pacing), postdrug VFT was measured, again in duplicate. Bethanidine (20 mg/kg), procainamide (30 mg/kg), and WY-48986 (10 mg/kg), a Class III antiarrhythmic, were evaluated in this dual test. Bethanidine and procainamide prolonged the cycle length of atrial reentry to a greater extent than WY-48986. The atrial arrhythmias were consistently terminated by procainamide and WY-48986 whereas bethanidine converted the tachycardias in one of the five dogs studied. All three agents elevated VFT with bethanidine producing higher values than procainamide and WY-48986. In conclusion, the dual electrophysiologic testing system offers both economic and scientific advantages for the study of modes of action of antiarrhythmic agents.

Animals↗
PubMed1991

Comparative effects of procainamide, tocainide and lorcainide on Na(+)-K(+)-ATPase in guinea pig heart preparations.

1. The effects of three class 1 antiarrhythmic drugs procainamide (class 1A) tocainide (class 1B) and lorcainide (class 1C) on microsomal Na(+)-K(+)-ATPase activity were compared with those of ouabain in guinea pig heart preparations. 2. All three antiarrhythmic drugs exhibited concentration-dependent inhibitory actions on the enzyme activity in a fashion similar to that of ouabain. 3. The rank order of their potencies showed the following tendency: lorcainide much greater than tocainide greater than procainamide. However, while the actions of lorcainide were comparable to those of cardiotonic steroids, those of procainamide became significant only at concentrations above 80 microM. 4. The IC50 values were 1.8 +/- 0.5 microM for ouabain, 14.6 +/- 3.4 microM for lorcainide, 2.8 +/- 0.7 mM for tocainide and 6.7 +/- 1.1 mM for procainamide. 5. The results demonstrate that these antiarrhythmic agents inhibit the ouabain-sensitive myocardial Na(+)-K(+)-ATPase activity in vitro with comparatively varying potencies. 6. These interactions may be pertinent to the proarrhythmic or arrhythmogenic effects of the class 1 type of antiarrhythmic drugs.

Animals↗
PubMed1993

Popliteal lymph node response to procainamide and isoniazid. Role of beta-naphthoflavone, phenobarbitone and S9-mix pretreatment.

The popliteal lymph node assay (PLNA) was proposed for the preclinical prediction of xenobiotics-induced autoimmune reactions in humans. Among the substances so far tested in this model, procainamide and isoniazid gave negative PLNA responses despite reports of lupus syndromes in man. To confirm the hypothesis that a metabolite instead of the parent molecule is involved, rats were pretreated with phenobarbital or beta-naphthoflavone, then injected with procainamide or isoniazid. In additional groups of animals, procainamide or isoniazid were injected together with S9-mix following various incubation times. Pretreated rats had a positive PLNA response when injected with procainamide, whereas preincubation with S9-mix resulted in a positive response to isoniazid. These results further support the validity of the PLNA.

Animals↗
PubMed2004

DNA methylation inhibitor, procainamide, may decrease the tamoxifen resistance by inducing overexpression of the estrogen receptor beta in breast cancer patients.

Estrogen is the main stimulant in the development and growth of breast cancer. The estrogen receptor antagonist tamoxifen has been mainstay of hormonal therapy. Although tamoxifen has been an effective adjuvant therapy, approximately 30% of patients treated with this agent still die within 10 years of follow-up treatment, and relapses can occur for > or = 20 years following therapy. However, the underlying cause of treatment failure in many breast cancer patients receiving tamoxifen is resistance to tamoxifen. ERbeta may influence estrogen action through the ERalpha pathway and the hormone refractoriness of breast cancer. ERbetacx, the carboxy terminal splicing variant of ERbeta, has been considered a dominant repressor of ERalpha function, because ERbetacx inhibits transcriptional activity of ERalpha rather than ERbeta wild type (wt). Tamoxifen responders tended to exhibit a lower ratio of ERbetacx to ERbetawt than non-responders. Induction of ERbeta reduces growth of exponentially proliferating cells. Since the promoter region of ERbeta is rich in CpG dinucleotides, loss of expression of ERbeta observed in some tumours could be due to aberrant methylation of CpG islands. Treatment of ERbeta-negative cell lines with DNA methyl transferase inhibitors restored ERbeta expression, providing experimental evidence that silencing of ERbeta in breast carcinomas could be due to promoter hypermethylation. Procainamide, used for cardiac arrhythmias, has been proposed as being a non-nucleoside inhibitor of DNA methylation and also demthylates and reactivate tumor suppressor genes in breast cancer cell lines. Therefore, concomitant use of procainamide with tamoxifen in ERalpha-positive and ERbeta-negative breast cancers may increase the tamoxifen response. Procainamide, given orally may also be used in breast cancer patients who developed resistance during the tamoxifen treatment. In vivo and in vitro studies evaluating effectiveness of concomitant use of procainamide and tamoxifen in tamoxifen resistant and ERbeta-negative breast cancer may further support our hypothesis.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1999

Procainamide-induced postoperative pyrexia.

Procainamide is an effective antiarrhythmic that is often used to convert atrial fibrillation to normal sinus rhythm. A side effect of procainamide, rarely reported in the surgical literature, is pyrexia. The pyrexia is a manifestation of an allergic response to this medication. If unrecognized, procainamide-induced pyrexia can lead to unnecessary testing, hospitalization, and treatment. We present a case of a post-coronary artery bypass surgery patient who repeatedly displayed pyrexia when reexposed to procainamide indicating an allergic response to this drug.

Anti-Arrhythmia Agents↗
PubMed1975

Comparison of procainamide and mexiletine in prevention of ventricular arrhythmias after acute myocardial infarction.

The incidence of ventricular arrhythmias after myocardial infarction has been compared in a controlled study of procainamide, mexiletine, and placebo. Sixty male patients who has sustained a myocardial infarction and had received lignocaine for ventricular tachycardia or ventricular ectopic beats which were R-on-T, multiform, or close-coupled took part. The efficacy of the drugs was evaluated by continuous 24-hour recordings of the electrocardiogram on the 4th and 10th days after admission to the study. Procainamide was given as 500 mg. 4-hourly and mexiletine as 250 mg. 8-hourly with corresponding placebo regimens for 12 days. 77% of patients receiving placebo showed serious ventricular rhythm disorders compared with 33% receiving antiarrhythmic therapy (p smaller than 0.05). Although only 35% of patients receiving procainamide achieved accepted therapeutic plasma concentrations compared with 95% of those receiving mexiletine, both drugs were equally effective antiarrhythmically. The only major adverse effect of therapy noted was development of a positive antinuclear factor in a procainamide-treated patient. These results demonstrate the efficacy of oral antiarrhythmic agents in the management of ventricular arrhythmias after acute myocardial infarction. Mexiletine has the advantage of less frequent administration and lower toxicity.

Administration, Oral↗
PubMed1984

Use of procainamide in chronic ambulatory peritoneal dialysis: report of a case.

A patient on chronic ambulatory peritoneal dialysis (CAPD) was treated with procainamide for control of ventricular arrhythmias. A procainamide half-life of 11.5 hours was observed, with a dialysis clearance of 6.5 mL/min. The N-acetylprocainamide (NAPA) dialysis clearance was 5.3 mL/min. The CAPD clearance of procainamide and its active metabolite, NAPA, is much lower than that reported for hemodialysis. Procainamide therapy should be initiated with reduced dosages in patients with renal failure.

Acecainide↗
PubMed2005

Effect of antiarrhythmic agents on heart rate variability indices after myocardial infarction: comparative experimental study of aprindine and procainamide.

The cardiac arrhythmic suppression trial (CAST) reported that antiarrhythmic treatments in post-myocardial infarction (MI) patients resulted in poor outcome and decreased in heart rate variability indices (HRV). The goal of the present study was to determine whether aprindine and procainamide, antiarrhythmic agents that increase HRV, result in beneficial effects in post-MI rabbits. Four weeks before experiment, MI was induced in four rabbits by ligating the major branch of left coronary artery. A total of eight rabbits (four post-MI and four normal rabbits) were randomly assigned to treatment with either intravenous aprindine (1 mg/kg) or intravenous procainamide (15 mg/kg). Frequency domain HRV (low frequency spectra, LF, 0.04-0.15 Hz; high frequency spectra, HF, 0.15-0.40 Hz) were assessed by MemCalc software. Aprindine significantly increased HF and LF in both MI and normal rabbits, whereas procainamide tended to decrease HF and LF in MI and normal rabbits (in total rabbits; aprindine, LF, from 6.3 +/- 7.9 to 16.5 +/- 15.0 ms(2)/Hz, P < 0.05; HF, from 8.0 +/- 11.7 to 17.5 +/- 15.0 ms(2)/Hz, P < 0.05; procainamide, LF, from 4.9 +/- 7.4 to 4.8 +/- 8.5 ms(2)/Hz, NS; HF, from 11.1 +/- 23.0 to 5.1 +/- 10.6 ms(2)/Hz, NS). Under pharmacological denervation with propranolol (0.1 mg/kg) and atropine (0.04 mg/kg), aprindine increased LF and HF (LF, from 0.2 +/- 0.2 to 0.8 +/- 0.7 ms(2)/Hz, P < 0.05; HF, from 0.1 +/- 0.0 to 0.2 +/- 0.0 ms(2)/Hz, P < 0.05). These data suggest that aprindine can increase HRV in post-MI rabbits. Further experiments in human subjects would be of benefit.

Adrenergic beta-Antagonists↗
PubMed2002

Effects of procainamide on transmural ventricular repolarisation.

To investigate the pharmacological effect of procainamide on transmural ventricular repolarisation in normal heart, the transmural activation-recovery intervals (ARI) and their responses to procainamide (20 mg/min i.v. for 20 min) were studied in 6 open-chest, pentobarbitone-anaesthetised sheep. ARI was measured from the unipolar ECGs acquired with 4 plunge needles inserted into the basal and apical parts of the left ventricular wall. During sinus rhythm (cycle length 500-700 ms), there was no significant difference in the pooled ARI between the epicardium (266.0 +/- 30.5 ms), midmyocardium (265.0 +/- 28.9 ms) and endocardium (265.7 +/- 28.1 ms) (p > 0.05). Procainamide prolonged ARI in all myocardial layers. The pooled ARI prolongation from the epicardium, midmyocardium and endocardium of the 6 animals was 66.8 +/- 18.3, 70.3 +/- 14.7 and 65.3 +/- 15.7 ms (p > 0.05), respectively. In conclusion, sodium channel blocker procainamide results in a similar repolarisation prolongation in the left ventricular epicardium, midmyocardium and endocardium of a healthy heart.

Animals↗
PubMed1982

Procainamide elimination kinetics in pediatric patients.

Procainamide kinetics were studied in six children after a single intravenous dose. Two-compartment kinetic analysis of serum concentration-time curves of five children, who received a dose of 5.5 +/- 0.9 mg/kg (mean +/- SD), revealed the following values for kinetic parameters: distribution half-life, 10.3 +/- 3.4 min; elimination half-life, 1.7 +/- 0.1 hr; elimination constant, 1.2 +/- 0.3 hr-1; plasma clearance 19.4 +/- 2.0 ml/min/kg, and steady-state volume of distribution, 2.2 +/- 0.3 l/kg. A sixth patient, who received an accidental overdose of 28 mg/kg, had altered elimination kinetics due to drug-induced hypotension. N-acetylprocainamide (NAPA) was detected in serum samples obtained soon after procainamide dosing and peak concentrations were attained at 1 to 2 hr. NAPA levels were lower than corresponding procainamide concentrations at most sampling periods. The findings of short elimination half-life and rapid plasma clearance of procainamide in children suggest that continuous intravenous infusion may be necessary to maintain therapeutically effective plasma concentrations in these patients.

Arrhythmias, Cardiac↗
PubMed1984

Cimetidine inhibits renal procainamide clearance.

Procainamide and cimetidine are eliminated in large part by the kidneys. Both are secreted by an active transport mechanism in the proximal tubule and each inhibits secretion of the other in the isolated, perfused rabbit tubule. In this study in man, cimetidine inhibited renal clearance of oral procainamide by 36%. This was associated with a 28% decrease in the ratio of systemic clearance of procainamide to bioavailability, an 18% decrease in the elimination rate constant, and a 24% prolongation of elimination t1/2. These results suggest that cimetidine increases plasma t1/2 and decreases systemic clearance of procainamide in part by inhibiting its active secretion by the kidneys.

Acecainide↗
PubMedDate not supplied

Procainamide-induced hemolytic anemia.

The paper reports a case of hemolytic anemia induced by procainamide hydrochloride treatment. Decreases in hemoglobin concentration are correlated with 11 months of procainamide treatment along with a marked increase in hemoglobin following cessation of the drug. The patient exhibited no symptoms suggestive of drug-induced Lupus Erythematosus that has been frequently reported as a sequela of procainamide therapy. Direct antiglobulin tests were consistently positive throughout the clinical course, and an ether-eluate prepared from the patient's red blood cells showed panagglutinability. The antibody in the eluate reacted with Rhnull, D--, LW negative, and U negative red blood cells without addition of procainamide or pretreatment of red blood cells with the drug. It is noted that this antibody reacts similarly to the antibody produced as a consequence of alpha-methyl-dopa therapy.

ABO Blood-Group System↗