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PubMed1986

Antiguanosine antibodies: a new marker for procainamide-induced systemic lupus erythematosus.

Antinuclear antibodies are present in most patients receiving procainamide. To ascertain whether IgG antiguanosine antibodies are associated with the development of the symptoms of systemic lupus erythematosus, we compared the levels of these antibodies in the sera of 65 patients receiving procainamide: 18 with procainamide-induced symptoms and 47 asymptomatic patients. Antinuclear antibodies measured by immunofluorescence were present in the 18 patients with drug-induced symptoms but also in 24 asymptomatic patients. Similarly, elevated serum levels of antibodies to single-stranded DNA were found in 15 patients with symptoms and in 20 asymptomatic patients. In contrast, levels of IgG antiguanosine antibodies were elevated in 15 patients with drug-induced symptoms, but in only 3 asymptomatic patients. Antiguanosine antibodies binding to single-stranded DNA were found primarily in patients with arthritis, pleuritis, and pericarditis. These results suggest a strong association between IgG antiguanosine antibodies and major manifestations of procainamide-induced systemic lupus erythematosus.

Adult↗

PubMedDate not supplied

[Study of several electrophysiological effects of procainamide in man (author's transl)].

Several electrophysiological aspects of the effects of procainamide were analyzed, using a method which allows direct study in man. The following electrophysiological parameters were determined under normal conditions in pace-maker carriers: myocardial stimulation threshold (M.S.T.), above-normal excitability phase (A.N.P.), effective refractory period (E.R.P.), pre-automatic pause (P.A.P.) and frequency of spontaneous rhythm (S.R.). After i.v. somministration of 10 mg/kg of procainamide in six subjects, and of 20 mg/kg in one, the modifications resulting from the examined parameters were analyzed. They showed that procainamide determines the constant elevation of the M.S.T., the shortening of duration of the A.N.P., lengthening of the E.R.P. and depression of the ventricular, but the superventricular automatism. Hypotheses on the electrophysiological mechanism of the observed effects are analyzed, and some clinico-electrophysiopathological correlations are traced, which help in the understanding of the anti-arrhythmic activity of procainamide.

Aged↗

PubMed1975

The pharmacokinetics of procainamide in normal subjects using a specific gas chromatographic assay.

Previous procainamide pharmacokinetic studies have involved the use of colorimetric and fluorimetric methods for the determination of drug concentrations in plasma and urine. However, recent evidence shows that N-acetyl procainamide, the major metabolite in humans, is hydrolyzed during these assay procedures. As a result, a specific gas chromatographic method has been developed for the determination of procainamide in biological fluids. Using this assay procedure, the pharmacokinetics of procainamide were studied in 7 normal subjects following intravenous administration of the drug. The values of half-life (2.08 +/- 0.52 hr), volume of distribution (4.3 +/- 0.6 1/Kg) and total body clearance (1344 +/- 238 ml/min) found in this study differed from those previously reported. These discrepancies could be understood in terms of differences in assay specificity.

Blood Pressure↗

PubMed1992

Stability of procainamide hydrochloride in an extemporaneously compounded oral liquid.

The stability of procainamide hydrochloride 5, 50, and 100 mg/mL in an extemporaneous oral liquid formulation was studied. Oral liquids containing procainamide hydrochloride 5, 50, or 100 mg/mL were compounded from procainamide hydrochloride capsules, sterile water for irrigation, and cherry syrup or a 70:30 mixture of 1% methylcellulose and cherry syrup. The pH values of the liquids were 6 (unadjusted) and 5 (adjusted). The liquids were stored at 4-6 degrees C or 24-25 degrees C and tested for drug concentration by stability-indicating high-performance liquid chromatography at 0, 7, 14, 21, 28, 34, 147, and 180 days. The relationships among the variables drug concentration, type of vehicle, pH, and temperature and their effects on drug stability were analyzed by using repeated-measures analysis of variance. With respect to effects on stability across time, there was a significant three-way interaction among drug concentration, type of vehicle, and temperature. The effect of concentration on stability seemed to depend on the vehicle used, but this dependence was different for different temperatures and different pH values. When trends over time were considered, a significant interaction among time, vehicle type, and temperature was found. This reflected the stability of the concentration of procainamide hydrochloride over time under refrigeration for both vehicles, compared with the steady decline in drug concentration at room temperature. Overall, drug concentration was fairly stable over time in the 5- and 50-mg/mL oral liquids but declined steadily in the 100-mg/mL liquid.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed1989

[The effect of procainamide on the inducibility of ventricular tachycardia using programmed stimulation].

The effect of intravenously administered procainamide (0.5-1 g, mean 0.966 g) on the inducibility of sustained ventricular tachycardia by programmed ventricular stimulation was tested in 15 patients (12 men and 3 women, mean age 57.2 +/- 16.6 years) with confirmed sustained ventricular tachycardia. Eleven patients had a previous myocardial infarction and two had congestive heart failure. The programmed ventricular stimulation (1-3 premature stimuli following after ventricular stimulation at a rate of 100/120 and 140/min. and a number of quick stimuli with a rising frequency from the apex of the right ventricle at an intensity equal to twice the diastolic threshold) was administered before and after procainamide administration. Sustained ventricular tachycardia was induced during the controlled examination in all 15 patients (100% sensitivity). Induced ventricular tachycardia had a haemodynamically important course with a rapid onset of unconsciousness in three patients whose index of risk of ventricular tachycardia (ratio of its frequency and the ejection fraction at rest) was significantly higher than in the remaining 12 patients (9.0 +/- 2.2 as compared with 4.9 +/- 1.2). Procainamide prevented the induction of sustained ventricular tachycardia in six patients (group I), i. e. in 40%. In the remaining nine patients (group II) ventricular tachycardia induced after procainamide had a significantly lower frequency (192 +/- 34/min.), as compared with controls (214 +/- 42/min.), but its haemodynamic impact was not affected. Patients of group I had, as compared with group II, a significantly higher ejection fraction (47 +/- 14% as compared with 35 +/- 10%) and a significantly lower index of the risk of tachycardia (4.5 +/- 1.3 as compared with 6.5 +/- 2.4).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗

PubMed1988

B cell activation in patients with active procainamide induced lupus.

Cellular immune abnormalities have been described in asymptomatic patients receiving procainamide therapy, but not in patients with active procainamide induced lupus. We tested patients with active procainamide lupus for evidence of T or B cell activation similar to that observed in idiopathic lupus. Symptomatic patients had a significant increase in spontaneous IgG synthesis, but T cells bearing activation markers were not significantly different from age matched controls. Our results demonstrate that patients with active procainamide lupus have evidence for B cell activation, similar to idiopathic lupus.

Aged↗

PubMed1986

Procainamide elicits a selective autoantibody immune response.

The specificity of the in vivo humoral immune response elicited by procainamide was examined by solid-phase assays, immunofluorescence, immunoprecipitation and a cytotoxicity assay. Serial samples obtained from patients during their procainamide therapy showed a progressive increase in antibodies to histones and denatured DNA, and both activities decreased after discontinuation of therapy. In contrast antibodies to tetanus, human IgG (rheumatoid factor) and heterologous lymphocytes were unaffected by procainamide treatment, indicating that they were not drug-induced. Of 29 sera examined by protein-A-facilitated immunoprecipitation, four sera had antibody to ribosomal RNA and three sera immunoprecipitated a 40kD protein. Antinuclear antibodies were invariably present but absorption studies showed that these activities were due to anti-histone antibodies. These results indicate that procainamide-induced autoimmunity is characterized predominantly by an anti-histone and anti-denatured DNA immune response.

Antibodies, Antinuclear↗

PubMed1977

Agranulocytosis associated with procainamide therapy--report of a case.

The case of a 69-year-old woman with procainamide-induced agranulocytosis is reported, and literature reports of 14 other such cases are reviewed. The patients was exposed to procainamide, prescribed for atrial fibrillation, for 26 days, with a daily dose of 1.5 to 4 g and a total dose of 57.5 g. She recovered from agranulocytosis after discontinuation of the drug and hospital treatment for 16 days. Among the reported cases of procainamide-induced agranulocytosis, the daily dosage ranged from 750 mg to 4.5 g; the total ingested dose before agranulocytosis was observed ranged from 36.5 to 316.3 g. Patients treated with procainamide should be instructed to report any soreness of the mouth, throat or gums; unexplained fever; or any symptoms of upper respiratory tract infection. If white blood cell counts indicate bone marrow depression, the drug should be withdrawn and appropriate evaluation begun at once.

Aged↗

PubMed1984

Fluoroimmunoassays for procainamide and N-acetylprocainamide compared with a liquid-chromatographic method.

We measured procainamide and its active metabolite, N-acetylprocainamide (NAPA), in 80 sera from 37 patients by a new fluorimmunoassay procedure and an established "high-performance" liquid-chromatographic method. Additive and proportional differences between the methods were 0.07 mg/L and 9%, respectively, for procainamide and 0.62 mg/L and 16% for NAPA. Between-day CVs by the chromatographic and immunoassay methods, respectively, were 3.9% and 2.2% for procainamide at a concentration of 6 mg/L, and 5.1% and 1.2% for NAPA (14 mg/L). We applied a modification of the fluoroimmunoassay for determination of procainamide concentrations, using sera obtained during a pharmacokinetic study, and demonstrated excellent agreement with the chromatographic method.

Acecainide↗

PubMedDate not supplied

[Electrophysiological effects of subtherapeutic levels of procainamide on hypoxic myocardial cells (author's transl)].

1. The electrophysiological effects of hypoxia alone or combined with subtherapeutic concentrations of procainamide superfusion were investigated in guinea-pig ventricular muscle fibres in order to elucidate the procainamide activity on suffering myocardial cells. 2. A first 30 minute-long hypoxia depressed action potential characteristics but never induced cellular inexcitability. These alterations were entirely reversible. A second consecutive hypoxia period similarly affected cellular activity. 3. After a control hypoxia period, procainamide 0.15 microM and 1.5 microM further depressed or abolished the hypoxia-altered transmembrane potentials. 4. In procainamide 0.15 microM and 1.5 microM pretreated cells, hypoxia more extensively depressed or abolished the myocardial cell activity than in unpretreated cells. 5. It has been demonstrated that antiarrhythmic drugs only slowly and incompletely reached the ischaemic myocardium. The present results suggest that in clinical situations, such weak concentrations may be efficient for inducing pronounced modifications in ischaemic areas and rapid antiarrhythmic effects.

Action Potentials↗

PubMed1982

The electrophysiologic effects of procainamide in the immature heart.

The electrophysiologic effects of procainamide in young animals have not been established. To test the effects of this drug on the immature heart, we studied eight nonsedated, chronically instrumented puppies (age range 12-28 days, median 16 days; weight range 0.7-1.1 kg, median 0.8 kg). The electrophysiologic study was performed before and 30 minutes after procainamide was given intravenously (20 mg/kg infusion). At the time of the study, the serum concentrations of procainamide (8.2 +/- 1.7 micrograms/ml to 6.2 +/- 1.6 micrograms/ml; mean +/- SEM) were in the usual adult human therapeutic range (4-10 microgram/ml). Procainamide in puppies caused a significant lengthening of the atrial and ventricular refractory periods, a significant decrease of the sinus node recovery time and the sinus of atrial echo zone, a significant decrease in the heart rate, and a significant increase in the sinoatrial conduction time.

Electrocardiography↗

PubMed1980

Myocardial depression associated with effective refractory period prolongation after pentobarbital and procainamide but not after dantrolene.

Effective refractory period (ERP) and contractile force (CF) of isolated rabbit left atria were monitored before and during cumulative concentration-response curves to procainamide, pentobarbital and dantrolene. CF reductions and ERP increases were observed after addition of pentobarbital or procainamide. Dantrolene, however, atypically reduced CF without affecting ERP. The prolonged ERP correlated with simultaneous CF reductions during pentobarbital and procainamide activity. These results suggest that the sarcolemmal stabilizing effects of pentobarbital and procainamide could be related to CF reductions while the cardiac depression of dantrolene is unrelated to this action and, as in skeletal muscle, may result from intracellular activity.

Action Potentials↗

PubMed1994

Effects of procainamide and propafenone on the composition of the excitable gap in canine atrial reentry tachycardia.

The effects of procainamide and propafenone on the composition of the excitable gap (EG) were studied in a canine model of atrial flutter (AFI) around the tricuspid valve. In 14 open-chest, chloralose-anesthetized dogs, a Y-shaped incision was made in the intercaval area extending to the right atrial appendage. Atrial effective refractory period (ERP) was measured at constant stimulation cycle lengths (CLs) (200 and 300 msec) at each of five recording sites around the tricuspid valve. The EG as defined by the reset-response curve was determined by introducing premature stimuli during AFI induced by burstpacing. Seven dogs each received procainamide or propafenone as a bolus followed by infusion. At constant plasma levels, both drugs increased ERP at constant paced CL and prolonged the reentry CL. In the absence of drug, reset-response curves were mixed, demonstrating an EG composed of both partially (increasing portion) and fully (flat portion) excitable tissue. Procainamide and propafenone shifted the curve upward and to the right and prolonged ERP during AFI, but did not change the duration of the EG. On procainamide, fully excitable tissue was preserved, but on propafenone, in some cases, the fully excitable part of the gap was reduced markedly or even eliminated. In conclusion, both drugs can prolong AFI CL by a direct effect on conduction velocity in fully excitable tissue. In addition, propafenone's effect on refractoriness can contribute significantly in some cases to slowing of AFI.

Action Potentials↗

PubMed1993

Procainamide-induced psychosis.

The occurrence of procainamide-induced psychosis has not been mentioned previously in the nursing literature and is rarely reported in the medical literature. With the increasing use of procainamide in patients with both atrial and ventricular dysrhythmias, it is quite possible that nurses may encounter the phenomenon more frequently. It is also possible that it has been mistaken previously for ICU or psychologically-induced psychosis. Nurses routinely monitoring patients for physiologic effects of procainamide should also be alert for psychological effects as well. The onset of acute psychological sequelae such as procainamide-induced psychosis further complicates care of physiologically compromised patients. Rapid identification and intervention is important. It is especially important to listen to patient and family cues.

Aged↗

PubMed1998

[Procainamide-induced lupus in a patient with bilateral pleural effusion].

A 70-year-old physician was admitted to our hospital because of bilateral pleural effusion and left-sided chest pain on deep inspiration. On admission, the APTT was prolonged and was not corrected with a 1:1 mixture of normal plasma. Results of serological examinations included a positive lupus-anticoagulant test and a positive ANA test at a titer of 1:1,280 in a homogeneous pattern. The patient's age, sex, symptoms, signs, and laboratory results all argued against the diagnosis of SLE except for ANA and lupus anticoagulant test. Because procainamide had been prescribed (250 mg every 6 h) for premature ventricular contractions for eight years before admission, procainamide-induced lupus was suspected. Procainamide was discontinued. Chest pain persisted and tests for c-reactive protein were positive. Prednisolone was administered. Procainamide induced lupus was diagnosed, because anti-histone H 2 A-H 2 B complex antibodies were high by enzyme-linked immunosorbent assay, and IgM-class anti-histone antibodies were found in response to H1, H 2 B and H 2 A-H 2 B complex (immunoblotting), which suggested the drug induced lupus. There are only a few reports of drug induced lupus in which the lupus-anticoagulant test was positive and prednisolone was indicated. The measurements of anti-histone antibodies and of expression of anti-histone antibodies were useful in distinguishing drug-induced lupus from SLE.

Aged↗

PubMed1981

Procainamide-induced myasthenia-like weakness in a patient with peripheral neuropathy.

Because procainamide hydrochloride (Pronestyl) may block neuromuscular transmission (NMT), this drug is contraindicated in cases of myasthenia gravis. Reduction of the safety factor of NMT is also seen in other conditions, including peripheral neuropathies. A patient with uremic peripheral neuropathy in whom myasthenia-like weakness developed during procainamide therapy is described. Procainamide should be given with caution in cases of peripheral neuropathies in which there may be a reduction of the safety factor of NMT.

Adult↗

PubMed1978

Circulating inhibitors of blood coagulation associated with procainamide-induced lupus erythematosus.

We studied a patient being treated with procainamide in whom we observed a high antinuclear antibody titer and prolonged activated partial thromboplastin (PTT), prothrombin (PT), and Stypven times (ST). Serum antibody concentrations against single-stranded DNA were elevated while those aginst native DNA were not elevated, suggesting the procainamide-induced lupus syndrome. Dilution of the patient's plasma with normal plasma failed to correct the PTT and PT, indicating the presence of an inhibitor(s) to blood coagulation. The anticoagulant activity was associated with the IgG fraction of the patient's serum. Addition of purified or partially purified human factors IX, X, VIII, VII, XIa, prekallikrein, high molecular weight kininogen, or phospholipids to the patient's plasma failed to correct the PTT, PT, or ST; however, purified human factor XII and prothrombin corrected the PTT and ST, respectively. These results indicate that production of antibodies directed against antigenic determinants on coagulation proteins can be a manifestation of procainamide-induced lupus erythematosus.

Blood Coagulation↗

PubMed1984

Procainamide-induced agranulocytosis with reversible myeloid sensitivity.

A 56-year-old man developed procainamide-induced agranulocytosis. Bone marrow aspiration showed the absence of myeloid elements beyond the promyelocyte stage. Procainamide at therapeutic concentrations in vitro depressed bone marrow granulocyte-macrophage colonies (CFUc) while CFUc growth was normal in the absence of drug. Following the patient's recovery, CFUc growth was no longer suppressed by procainamide in vitro. The observations in this patient showing reversible sensitivity to drug contrast with those on other patients with drug-induced agranulocytosis that show persistent marrow injury or drug sensitivity despite clinical recovery.

Agranulocytosis↗