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PubMed1976

Simultaneous quantification of procainamide and N-acetylprocainamide with high-performance liquid chromatography.

A rapid, precise and specific method for the simultaneous determination of procainamide and N-acetylprocainamide (NAPA) in plasma using high-performance liquid chromatography is described. N-Formylprocainamide was utilized as internal standard. The coefficients of variation of the method for both procainamide and NAPA were 3.6% in the range of plasma levels to be expected clinically. The method is especially useful for rapid determination of acetylator phenotype in patients requiring procainamide for control of arrhythmias.

Arrhythmias, Cardiac↗
PubMed1986

Simultaneous appearance of endocardial late potentials and ability to induce sustained ventricular tachycardia after procainamide administration.

We describe a patient in whom procainamide induced the appearance of late potentials during intraoperative sinus rhythm electrogram mapping. Only nonsustained ventricular tachycardia (VT) could be induced while off all antiarrhythmic drugs. After administration of the procainamide, programmed stimulation induced sustained VT coincident with the appearance of late potentials during sinus rhythm. The late potential was recorded from the same site, during normal sinus rhythm, where mid to late diastolic activation during VT was recorded, and where cryotermination occurred during cryomapping. We hypothesize that procainamide slowed conduction, manifested as prolongation or appearance of late potentials in sinus rhythm, and facilitated induction of sustained reentrant ventricular tachycardia.

Adult↗
PubMed1995

Electrophysiologic effects of procainamide, mexiletine, and amiodarone on the transplanted heart. Experimental study.

The effects of procainamide, mexiletine, and amiodarone on automaticity, conduction, and refractoriness were studied in a model of heterotopic heart transplantation in dogs that combined an innervated heart (recipient) and a denervated transplanted heart (donor). After the surgical procedure, 500 mg procainamide (n = 13), 200 mg plus 0.1 mg/kg per minute mexiletine (n = 10), or 150 mg amiodarone (n = 10) was administered intravenously. During a baseline period and after drug administration, each heart was assessed for atrioventricular interval; cycle length; sinoatrial conduction time; atrioventricular node anterograde and retrograde block points; atrioventricular node and ventricular antegrade effective refractory periods; PR, QRS, and QT intervals on electrocardiogram; systemic arterial, pulmonary arterial, central venous, and pulmonary capillary wedge pressures; and cardiac output. In recipients, procainamide reduced cardiac output, depressed sinus automaticity, slowed conduction time without affecting the QRS interval, and prolonged the nodal and ventricular refractoriness; in donor hearts, it depressed automaticity and prolonged nodal refractoriness, but did not modify conduction or ventricular refractoriness. Mexiletine only moderately depressed sinus automaticity in recipient hearts; it did not affect the other parameters either in recipient or transplanted hearts, nor did it alter the hemodynamic situation. Amiodarone produced hypotension, reduced cardiac output, and prolonged all the electrophysiologic intervals except the QRS interval in recipient hearts. These changes were even more pronounced in the transplanted hearts and led to extreme sinus bradycardia in four cases. Of these three drugs, mexiletine appears to be the safest should treatment for arrhythmias be necessary in transplant recipients.

Amiodarone↗
PubMed1989

Severe retinal vaso-occlusive disease secondary to procainamide-induced lupus.

Systemic lupus erythematosus (SLE) is known to cause various forms of ocular problems, including severe retinal vaso-occlusive disease. Procainamide is one of many drugs that may cause a lupus-like syndrome which resembles SLE but can be distinguished through clinical features and laboratory studies. Presented is a patient with severe vaso-occlusive retinopathy on high-dose procainamide therapy. Associated clinical, laboratory, and pathologic findings suggest the diagnosis of drug-induced lupus and exclude other vasculitic or inflammatory etiologies. This represents the first documented case of retinal disease attributed to procainamide-induced lupus.

Aged↗
PubMed1985

Antinuclear antibodies as indicators for the procainamide-induced systemic lupus erythematosus-like syndrome and its clinical presentations.

Fifty patients on a regimen of procainamide were studied in regard to the association between antinuclear antibodies (ANA) and the development of drug-induced systemic lupus erythematosus (SLE)-like syndrome. Four groups were identified: Group 1 was ANA-positive, with clinical manifestations (serologic and clinical findings); Group 2 was ANA-positive, without clinical manifestations (serologic findings only); Group 3 was ANA negative (no patients with clinical manifestations); and Group 4 had SLE persisting after discontinuance of procainamide. The leukocyte-specific ANA (LSANA) patterns were predominant, with peripheral LSANA confined to Groups 1 and 4. Furthermore, the titer of the homogeneous LSANA, to which peripheral LSANA converts on dilution, was clinically significant. A homogeneous LSANA titer of 160 or greater was seen essentially only in patients with clinical manifestations of the SLE-like syndrome. Serial ANA determinations are therefore necessary to monitor patients receiving procainamide.

Antibodies, Antinuclear↗
PubMed1983

Thin-layer chromatographic determination of procainamide and N-acetylprocainamide in human serum and urine at single-dose levels.

Thin-layer chromatographic methods were applied for bioavailability studies of procainamide in serum and urine. Detection of the parent compound and the major metabolite was performed in the ultraviolet range at 275 nm. Using 100-microliter samples, detection limits were 60 ng of procainamide-HCl per ml serum and 7 micrograms/ml urine, and 60 ng of N-acetylprocainamide-HCl per ml serum and 5 micrograms/ml urine. Advantages over previous methods are discussed. From serum and urine data of five volunteers, the bioavailability of procainamide from a 250-mg dragee preparation compared with an intravenous dose was verified. Pharmacokinetic data were computed using one-compartment open models. Results corresponded well with values previously published.

Acecainide↗
PubMed1992

Relation between repolarization and refractoriness in the human ventricle: cycle length dependence and effect of procainamide.

The cycle length dependence of the action potential duration and the effective refractory period of the right ventricular endocardium were investigated in 24 patients undergoing electrophysiologic studies for suspected ventricular tachycardia. The action potential duration at 90% repolarization and the effective refractory period at twice diastolic threshold strength were measured at the same catheter site at steady state cycle lengths of 350 to 600 ms. Both measurements decreased linearly with decreasing cycle length, maintaining a parallel relation. When the relation between action potential duration and effective refractory period was expressed as the effective refractory period-action potential duration difference, nearly constant values (range -12 to -15 ms) were obtained at all cycle lengths. To determine whether sodium channel blocking drugs influence the effective refractory period-action potential duration relation in humans, measurements of these two variables were obtained in 15 patients before and during the infusion of procainamide. Procainamide prolonged the action potential duration at each cycle length by a near constant amount over baseline values (p less than 0.001). Procainamide also increased the effective refractory period at each cycle length but with a greater incremental increase at the shorter cycle lengths. The rate-dependent increase in the effective refractory period-action potential duration difference became significant at cycle lengths less than or equal to 400 ms; at these high rates, the effective refractory period-action potential duration difference became positive (1.6 ms, p less than 0.01 compared with baseline). Thus, in the human ventricle, the action potential duration and the effective refractory period have a close relation that remains fixed over a wide range of cycle lengths.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1986

Reduced acetylation of procainamide by para-aminobenzoic acid.

Acetylation is the major route of metabolism of many drugs including the antiarrhythmic agent procainamide. Coadministration of para-aminobenzoic acid was observed to decrease the biotransformation of procainamide to N-acetylprocainamide in a patient with rapid acetylation kinetics. In view of the distinct antiarrhythmic and toxic properties of procainamide and N-acetylprocainamide, the observed drug interference may have great clinical relevance in long-term oral antiarrhythmic therapy and in instances where other drugs converge for acetylation.

4-Aminobenzoic Acid↗
PubMed2001

Acoustic and optical transduction of BuChE binding to procainamide modified surfaces.

A novel polymer, poly(procainamide), PPA, containing numerous binding sites for cholinesterases was synthesized as a recognition layer for butyryl cholinesterase (BuChE) interaction with the ligand procainamide, utilizing TSM and SPR sensors. The polymer was synthesized by the reaction of methacryloyl chloride and procainamide followed by radical polymerization. Sensor surfaces (Au or SiO(2)) were spin-coated by the polymer solution to form thin layers. Binding of BuChE was found to be sensitive to the drying procedure of the polymer layer. The binding of BuChE to the polymer coated sensors was monitored on-line by following the response of thickness shear mode (TSM) and surface plasmon resonance (SPR) sensors. Binding of BuChE to PPA-coated TSM sensors were shown to follow a Langmuir isotherm giving association constant 3.4x10(6) M(-1).

Biosensing Techniques↗
PubMed1989

Effect of the immunomodulator tilorone on the in vivo acetylation of procainamide in the rat.

Interferon and interferon inducers have been found to inhibit cytochrome P-450-dependent metabolism in animals and man. The effect of these agents on the acetylation of drugs has not been previously reported. Since these agents stimulate the reticuloendothelial system, together with the abundance of N-acetyltransferase in the reticuloendothelial system, it was hypothesized that these immunomodulators may affect drug acetylation. To test this hypothesis, the effect of tilorone (a synthetic interferon inducer) on the in vivo acetylation of procainamide was examined in the rat. Pretreatment with tilorone hydrochloride (50 mg/kg) 48 hr prior to the administration of procainamide hydrochloride (50 mg/kg) resulted in a 32% increase in the urinary recovery of N-acetylprocainamide and a 35% increase in the metabolic clearance of procainamide to N-acetylprocainamide. These data indicate that interferon inducers increase the N-acetylation of drugs in vivo.

Acecainide↗
PubMed1983

Reticulocytopenic, coombs' positive anemia induced by procainamide.

A case of Coombs' positive anemia in a man who had procainamide-induced lupus erythematosus syndrome is reported. The patient had a hemoglobin of 4.3 gm/dl and reticulocytopenia (3.1% corrected). Serum lactate dehydrogenase and haptoglobin levels were normal, and total bilirubin was only slightly elevated. Two other reported cases of procainamide-induced hemolytic anemia have demonstrated similar findings. Apparently, procainamide occasionally may induce a reversible, reticulocytopenic, Coombs' positive anemia that is not associated with laboratory evidence of acute hemolysis.

Anemia, Hemolytic↗
PubMed1996

Stability of ketoconazole, metolazone, metronidazole, procainamide hydrochloride, and spironolactone in extemporaneously compounded oral liquids.

The stability of drugs commonly prescribed for use in oral liquid dosage forms but not commercially available as such was studied. Ketoconazole 20 mg/mL, metolazone 1 mg/mL, metronidazole 50 mg/mL, procainamide hydrochloride 50 mg/ mL, and spironolactone 25 mg/mL were prepared in a 1:1 mixture of Ora-Sweet and Ora-Plus (Paddock Laboratories), a 1:1 mixture of Ora-Sweet SF and Ora-Plus (Paddock Laboratories), and cherry syrup and placed in 120-mL polyethylene terephthalate bottles. The sources of the drugs were powder, capsules, and tablets. Six bottles were prepared per liquid; three were stored at 5 degrees C and three at 25 degrees C, all in the dark. A sample was removed from each bottle immediately after preparation and at intervals up to 60 days and analyzed for drug concentration by stability-indicating high-performance liquid chromatography. At least 93% of the initial drug concentration was retained in all the oral liquids for up to 60 days. There were no substantial changes in the appearance or odor of the liquids, or in the pH. Ketoconazole 20 mg/mL, metolazone 1 mg/mL, metronidazole 50 mg/mL, procainamide hydrochloride 50 mg/ mL, and spironolactone 25 mg/mL were stable for up to 60 days at 5 and 25 degrees C in three extemporaneously compounded oral liquids. INDEX TERMS: Anti-infective agents; Antifungals; Capsules; Cardiac drugs; Cherry syrup; Compounding; Containers; Diuretics; Incompatibilities; Ketoconazole; Liquids; Metolazone; Metronidazole; Polyethylene terephthalate; Powders; Procainamide hydrochloride; Spironolactone; Stability; Storage; Suspending agents; Tablets; Temperature; Vehicles.

Administration, Oral↗
PubMed1976

Influence of procainamide on sodium and potassium exchange and permeabilities in cultured human cells.

The effect of procainamide on membrane cation exchange was investigated using monolayer cultures of Girardi heart cells. The initial effect of procainamide (10(-6) to 10(-3) mol/litre) was to produce a prompt reduction of the passive Na influx, dose-dependent along a sigmoid log dose-response curve. This effect was complete within 3 min and thereafter showed no further time-dependent increase. Mean passive Na influx (pmol-cm-2/s) decreased from 19.1 to 17.7 (P less than 0.05) and 10.4 (P less than 0.001) in 10(-5) and 10(-3) mol/litre procainamide, respectively. No effect on active Na extrusion was noted before 3 min following exposure to the drug, after which time it progressively declined reaching a minimum value for each concentration by 6 min and remaining at this level throughout a further 60 min exposure. For each concetnration this minimum value was similar to the Na influx measured under identical conditions. Na-coupled active K influx showed a parallel pattern of inhibition. K efflux was not decreased until approximately 20 min following exposure to the drug, but once present the reduction was similar in magnitude to that in the correspondingly measured K influx. Kinetic flux analysis revealed a decrease in both PNa and PK but indicated a greater effect on PNa. The results suggest that all of the above effects could be explained on the basis of one direct action of the drug, namely, the prompt initial decrease in PNa and Na influx. All other effects noted, both active and passive, could then be secondary to this phenomenon.

Cell Membrane Permeability↗
PubMed1978

Responses of cultured heart cells to procainamide and lignocaine.

The effects of procainamide and lignocaine, in concentrations from 10(-6) to 10(-2) mol.litre(-1), on the Na influx and contraction frequency of cultured heart cells were studied. Both drugs produced a prompt, dose-dependent reduction in Na influx which was significant (P less than 0.01) for all concentrations tested. Lignocaine affected only that portion of the Na influx which was also verapamil-sensitive, whereas procainamide suppressed in addition, the verapamil-insensitive influx. In addition both drugs produced a concomitant decrease in the spontaneous contraction frequency of the cells. A close linear correlation (r = 0.99) between verapamil-sensitive Na influx and contraction frequency, in the presence of both procainamide and lignocaine was found. From this, and previous studies indicating a dependency of contraction frequency on the inward verapamil-sensitive Na influx, it is suggested that the drugs modify the automaticity of this preparation by a primary influence on membrane Na exchange.

Animals↗
PubMed1985

Effects of lidocaine, procainamide, metoprolol, digoxin and atropine on the conduction of premature ventricular beats in man.

The acute electrophysiologic effects of clinical doses of procainamide, lidocaine, metoprolol, digoxin and atropine upon the conduction of ventricular premature beats, were studied in 48 healthy volunteers. The conduction time of the first premature beat, induced 1 ms after the ventricular effective refractory period (VERP) was longer than that of the basic paced beats in 41 of the 48 subjects (85%); in 31 (65%) the delay was greater than 5 ms, indicating subnormal conduction. Digoxin decreased the delay so that it became insignificant, while, after procainamide, the delay increased significantly. The other agents did not significantly affect the subnormal conduction. The mean conduction times of premature beats, induced 30-50 ms after the VERP, were shorter than the basic conduction time in 43 of the 48 subjects (90%), and in 25 (52%) the decrease was greater than 5 ms, showing supernormal conduction. Lidocaine abolished the supernormal conduction. The other agents did not significantly alter the supernormal conduction. In the healthy heart, sub- and supernormal conduction of premature beats seem to be common phenomena, and seem, with few exceptions, to be largely unaffected by clinical doses of procainamide, lidocaine, metoprolol, digoxin and atropine.

Action Potentials↗
PubMed1981

Procainamide and peripheral neuropathy.

I have described a case of procainamide-induced peripheral neuropathy with a complete resolution after withdrawal of the drug. Extremely close observation is suggested, and if paresthesia and/or polyarthralgias develop, this agent must be withdrawn. The SLE-like syndrome inducted by procainamide completely resolves on withdrawal of the drug. N-acetylprocainamide (NAPA) should probably be prescribed in preference to procainamide.

Aged↗
PubMed1984

Procainamide-induced agranulocytosis.

We have described six new patients accounting for seven episodes of agranulocytosis due to procainamide. Six episodes involved the slow-release oral preparation. With continued use of this convenient antiarrhythmic agent, it is important that physicians be alert to the possibility of agranulocytosis in febrile patients receiving procainamide. If agranulocytosis occurs, procainamide should be discontinued promptly and the fever should be treated aggressively with combination broad spectrum antibiotics.

Administration, Oral↗
PubMed1990

Procainamide-induced myasthenic crisis.

We describe a case of procainamide-induced respiratory failure in a myasthenic patient with no prior history of respiratory weakness. Respiratory failure was induced secondary to procainamide alone since no N-acetyl-procainamide level was detectable. The patient's strength rapidly improved and he was successfully extubated 12 h after the offending dose.

Aged↗