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At least 433 records · Page 24Linked to original sources
PubMed1984

Procainamide infusion and acute atrial fibrillation.

We report the use of intravenous procainamide infusion in the treatment of fifteen patients with acute atrial fibrillation. Procainamide was infused at 50 mg/min to a maximum of 20 mg/kg, with blood pressure and electrocardiographic monitoring. Ten patients responded, with a mean dose of 8.7 (standard deviation 4.3) mg/kg, four of these reverting to sinus rhythm after a low dose of less than 5.0 mg/kg. Hypotension was a common concomitant and was seen in four cases, but required termination of the infusion only in a patient with cardiomyopathy. An increase in ventricular rate or conversion to atrial flutter was not seen. Intravenous infusion of procainamide is a safe and moderately effective method of cardioversion in acute atrial fibrillation.

Acute Disease↗
PubMed1991

Procainamide-induced pseudo-obstruction in a diabetic patient.

We report the case of a 65-year-old black man who presented to our facility with pseudo-obstruction of the bowel within two weeks of the initiation of oral sustained-release procainamide hydrochloride therapy. The syndrome continued despite conversion to intravenous procainamide and only resolved after discontinuation of the medication. We believe that the anticholinergic properties of procainamide, coupled with the patient's diabetes, contributed to severe hypomotility of the gastrointestinal tract and, subsequently, a pseudo-obstructive state. The syndrome of drug-induced pseudo-obstruction is also reviewed.

Aged↗
PubMedDate not supplied

Comparison of acute hemodynamic effects of lidocaine and procainamide for postoperative ventricular arrhythmias in dogs.

Heart rate and systolic, diastolic, and mean pressures were measured in two groups of dogs during treatment of postoperative ventricular arrhythmias either with intravenous (IV) 2% lidocaine hydrochloride or procainamide hydrochloride. Hemodynamic parameters were not significantly changed after IV administration of either drug. Additionally, changes in hemodynamic parameters for dogs treated with 2% lidocaine were not significantly different from those of dogs treated with procainamide. When dosed appropriately in the clinical setting, one bolus of IV procainamide was safe for the treatment of postoperative ventricular arrhythmias.

Animals↗
PubMed1984

Severe neutropenia associated with sustained-release procainamide.

Neutropenia is a rare complication of procainamide therapy. However, over a period of 20 months, 8 patients developed severe neutropenia while taking a sustained-release preparation of the drug. Seven patients presented with fever and constitutional symptoms and one patient was asymptomatic. Bone marrow examinations showed myeloid aplasia or maturation arrest in 5 patients and myeloid hyperplasia in 1. Neutropenia resolved within 30 days of drug withdrawal, and all patients survived. A case-control study showed a significant association between sustained-release procainamide therapy and severe neutropenia in 5 of 114 patients (4.4%) recovering from open-heart surgery (Mantel-Haenszel chi square = 13.84; p less than 0.001). Thus, life-threatening neutropenia may be common with sustained-release procainamide preparations.

Aged↗
PubMed1976

Severe transient pancytopenia associated with procainamide ingestion.

A 73-year-old woman was found to have clinically significant pancytopenia in association with procainamide hydrochloride ingestion. The syndrome, resembling systemic lupus erythematosus, which has been reported to develop in patients treated with this agent, is characterized by mild to moderate anemia and mild to moderate granulocytopenia. Severe granulocytopenia in patients taking procainamide and unrelated to a lupus syndrome has not previously been reported in association with significant thrombocytopenia. The clinical severity of this patient's presentation, suggesting an aleukemic leukemia, and its complete remission after cessation of procainamide administration occasional this report.

Aged↗
PubMed2003

Reactivation of tumor suppressor genes by the cardiovascular drugs hydralazine and procainamide and their potential use in cancer therapy.

PURPOSE: The purpose of this study is to evaluate the demethylating and tumor suppressor-reactivating activity of hydralazine and procainamide. EXPERIMENTAL DESIGN: MDA-231, MCF-7, and T24 cell lines were treated for 5 days with 10 micro M hydralazine or 10 micro M procainamide. 5-aza-deoxycytidine at 0.75 micro M was used as positive control. BALB/c nu/nu mice xenografted with MDA-231 cells were treated with these drugs for 7 days by i.p. route. Methylation was assessed by PCR after digestion with methylation-sensitive enzymes for the ER gene and with methylation-specific PCR for retinoic acid receptor (RAR)beta and p16 genes. Gene expression was evaluated by reverse transcription-PCR and Western blot. The duration of the gene re-expressing effect of hydralazine was analyzed on T24 cells. Functionality of the re-expressed proteins was evaluated by the induction of the estrogen-responsive gene PS2 on MDA-231 cells and by the induction of G(1) arrest on T24 cells. The gene demethylating and re-expressing ability of hydralazine was tested in two patients with cervical and head and neck carcinomas, respectively. RESULTS: Hydralazine and procainamide induced de-methylation and re-expression of the ER, RARbeta, and p16 genes in cultured cells. Both drugs also demethylated and re-expressed the ER gene in mice. Hydralazine re-expressed the p16 gene longer as compared with 5-aza-deoxycytidine. The re-expressed genes were functional. In addition, the treatment with oral hydralazine demethylated and re-expressed the RARbeta and p16 genes in the cervical and head and cancer patients. CONCLUSIONS: These cardiovascular drugs have a promising tumor suppressor-reactivating action and could potentially be used in clinic as an anticancer treatment, most likely to increase the efficacy of current biological or chemotherapeutic treatments.

Animals↗
PubMed1991

[Electrophysiological properties of atrial fibrillation with WPW syndrome and the role of procainamide in conversion].

Fifty one patients with recurrent episodes of atrial fibrillation associated with WPW syndrome were studied by pre-operative clinical electrophysiogical testing. The results showed that: these patients had an markedly prolonged intra-atrial conduction time (PA intervals: 42.22 +/- 10.93 ms) than the patients only with attack of atrioventricular reentry tachycardia (AVRT) (PA intervals: 17.21 +/- 9.68ms, P less than 0.001). The attack of atrial fibrillation related to an markedly prolonged atrial vulnerable phase and the retrograde conduction of accessory pathway (AP). The clinical results of atrial fibrillation were decided by the antegrade effective refractory period (AERP) of AP. When the shortest R-R (V-V) intervals during attack of atrial fibrillation was shorter than 180ms, the atrial fibrillation spontaneously turned to the ventricular fibrillation. The conversion of atrial fibrillation to sinus rhythm showed that procainamide not only prolonged AERP of AP, which were 248.57 +/- 15.74ms and 388.57 +/- 63.9 ms (P less than 0.001) respectively before and after intravenous procainamide infusion, but also prolonged intra-atrial conduction time significantly, the PA interval before and after intravenous procainamide infusion were 42.22 +/- 10.93 ms and 57.14 +/- 11.12 ms (P less than 0.025) respectively.

Adolescent↗
PubMed1991

Procainamide inhibits DNA methyltransferase in a human T cell line.

Procainamide, a widely used antiarrythmic, causes DNA hypomethylation in the human T cell line Jurkat, but the mechanism is unknown. We report that procainamide inhibits the DNA methyltransferase catalyzed transfer of methyl groups from S-adenosylmethionine to DNA, but has no effect on other known regulators of DNA methylation. Our results suggest that procainamide could inhibit cellular DNA methylation by inhibiting DNA methyltransferase activity.

Animals↗
PubMed1990

Intrahepatic cholestasis due to hypersensitivity reaction to procainamide.

Hypersensitivity reactions to procainamide involving liver dysfunction are rare. We describe a patient who developed liver dysfunction after procainamide administration, manifested by fever, jaundice, elevated bilirubin concentration, and alkaline phosphatase concentration. Hepatobiliary scintigraphy demonstrated good hepatic uptake of the radionuclide without movement from hepatic parenchyma. To our knowledge, this is the first reported case of procainamide-induced intrahepatic cholestasis as demonstrated by radionuclide hepatobiliary scintigraphy.

Aged↗
PubMed1990

Stability of esmolol hydrochloride in the presence of aminophylline, bretylium tosylate, heparin sodium, and procainamide hydrochloride.

The visual and chemical compatibility of esmolol hydrochloride mixed with aminophylline, heparin sodium, bretylium tosylate, or procainamide hydrochloride in 5% dextrose injection was studied. Esmolol hydrochloride 600 mg was injected into polyvinyl chloride bags containing 100 mL of 5% dextrose injection with aminophylline 100 mg, heparin sodium 5000 units, bretylium tosylate 100 mg, or procainamide hydrochloride 400 mg. All admixtures were prepared in triplicate and stored at room temperature under fluorescent light. Esmolol concentrations were measured with high-performance liquid chromatography at 0, 2, 4, 8, and 24 hours. Samples were also examined for precipitate formation and pH and color changes by using visual, microscopic, and spectrophotometric methods. No detectable changes in color or pH and no particulate formation were observed in any of the sample bags. Esmolol concentrations varied by less than 5% throughout the 24-hour study period. Esmolol hydrochloride was visually compatible and chemically stable for at least 24 hours when mixed with aminophylline, heparin sodium, bretylium tosylate, or procainamide hydrochloride in polyvinyl chloride bags containing 5% dextrose injection.

Aminophylline↗
PubMedDate not supplied

Disposition of procainamide and N-acetylprocainamide in protein-calorie malnutrition.

The influence of dietary protein deficiency on the disposition of procainamide (PA) and its major metabolite, N-acetylprocainamide (NAPA) was investigated in male Sprague-Dawley rats fed for 4 weeks on a 23 (control) or a 5% (low) protein diet ad libitum. Procainamide and N-acetylprocainamide in plasma and urine were determined by a sensitive and specific HPLC assay using a cation-exchange column. After an iv dose of 50 mg/kg procainamide hydrochloride, the average mean residence time (MRT) was approximately 82% higher, while the total plasma clearance (CI) per kg of body weight and terminal elimination rate constant (k) were significantly decreased by 46 and 49%, respectively, in the protein-deficient animals. No significant differences were found in the two groups of animals with respect to the apparent steady state volume of distribution (Vss). Although the percentage of PA recovered unchanged in the urine over 48 hr was not significantly different between control and protein-deficient animals, rats on a low protein diet excreted a smaller percentage of the administered PA dose (mean +/- SE, 19.0 +/- 4.0 vs. 30.8 +/- 1.4%) as NAPA. In addition to the apparent decrease in metabolic clearance (CIm) to NAPA (6.8 +/- 1.4 vs. 19.9 +/- 2.3 ml/min/kg) in the protein-deficient rats, there was a 55% decrease in the renal clearance of PA. There appeared to be no significant difference in the disposition characteristics of NAPA (i.e. MRT, Vss, CI, and k) between the two groups of animals after a 25 mg/kg dose of N-acetylprocainamide hydrochloride.(ABSTRACT TRUNCATED AT 250 WORDS)

Acecainide↗
PubMed1988

Quantitative structure activity studies of antiarrhythmic properties in a series of lidocaine and procainamide derivatives.

The use- and voltage-dependent depression of the maximum upstroke velocity of the cardiac action potential by a series of lidocaine and procainamide derivatives was studied in guinea pig papillary muscles. The derivatives were chosen to test the effects of the structural and physicochemical differences between lidocaine and procainamide on the kinetics of sodium channel block. Three derivatives were similar to lidocaine with a rapid onset of use-dependent block at fast stimulation rates and short time constants of recovery at normal resting potentials. Seven derivatives were similar to procainamide having slower rates of block development and longer recovery time constants. In order to quantify the differences in sodium channel block the data were analyzed by a model based on the modulated receptor hypothesis. This hypothesis proposes that each of the sodium channel states (rested, open and inactivated) has characteristic association and dissociation rate constants for each sodium channel blocker, drug bound channels do not conduct sodium and have altered inactivation kinetics. This model was solved for the dissociation constants of the drug for the rested and open states, the association and dissociation rate constants for the inactivated channels and the voltage shift of the inactivation kinetics for drug-bound channels. Quantitative structure-activity analysis on the derived parameters revealed that the affinity of the drugs for the open channel state is related to the compounds lipid solubility, the degree of voltage shift was proportional to molecular weight and the dissociation from the inactivated channels was correlated with both the molecular weight and charge.

Action Potentials↗
PubMed1985

Thrombocytopenia following sustained-release procainamide.

Procainamide hydrochloride-induced thrombocytopenia has infrequently been reported in the past. We report six cases of thrombocytopenia following the administration of the sustained-release form of procainamide. Three of these cases had platelet counts of less than 15,000/microL. The mean time to onset of thrombocytopenia from drug administration was 40 days (range, nine to 71 days). The mean time until normalization of the platelet counts after the drug therapy was stopped was 7.8 +/- 3.1 days (range, four to nine days). Oral prednisone therapy had little apparent benefit. The thrombocytopenia was not part of a systemic lupus erythematosus syndrome. We believe that thrombocytopenia is an important side effect of sustained-release procainamide therapy.

Acecainide↗
PubMed1988

Lichen planus following procainamide-induced lupus erythematosus.

A case of procainamide-induced lupus erythematosus with prominent cutaneous features is presented. The patient subsequently showed typical lesions of lichen planus, which has been associated with spontaneously occurring lupus erythematosus, but not previously reported with drug-induced lupus or as a result of procainamide therapy. A review of the immunologic alterations induced by procainamide raises questions about possible mechanisms causing the lupus and lichen planus.

Humans↗
PubMed1988

Comparative bioavailability of two oral sustained-release procainamide products.

The bioavailability characteristics of two sustained-release oral procainamide preparations, Procan SR and Pronestyl-SR, were compared in 10 patients with arrhythmias. Each patient was randomly assigned to receive either Procan SR 1 g or Pronestyl-SR 1 g, both administered orally every six hours. The initial drug was continued for 48 hours (eight doses), at which time the second drug, given at the same dosage and dosing interval, was substituted for a 48-hour period. Serum samples for procainamide determination were obtained hourly between 42 and 48 and between 90 and 96 hours after initiation of procainamide therapy. Values for area under the serum concentration-time curve (AUC) during the steady-state dosing interval, maximum serum drug concentration (Cmax), minimum serum drug concentration (Cmin), Cmax:Cmin ratio (representing fluctuations in serum drug concentrations within the dosing interval), and the time to maximum serum drug concentration (tmax) were determined. Mean ( +/- S.D.) tmax values for Procan SR and Pronestyl-SR were 2.2 +/- 0.8 hours and 3.8 +/- 1.1 hours, respectively. Only the differences between tmax values were statistically significant. The study had an 83% chance of detecting a 20% difference in AUC values. The chances of detecting a 20% difference in values for Cmax and Cmin were 62% and 71%, respectively. These two preparations would probably possess similar therapeutic properties when given at the same dosage and dosing schedule; however, studies with larger subject populations are needed to project bioavailability data to the general population.

Aged↗
PubMed1985

Sustained-release procainamide: use of serum concentrations to determine dosage.

The utility of the antiarrhythmic drug procainamide (PA) is limited by the required dosage schedule (every three to four hours). A commercially available, slow release procainamide (P-SR) is recommended to be given every six hours. We compared procainamide capsules (P-Caps) given every four hours with P-SR given every six hours in a crossover study of 12 patients. Doses of P-Caps were chosen to produce a therapeutic result and serum drug concentrations within the therapeutic range. Doses of P-SR were adjusted until serum PA concentrations were similar to those when P-Caps were used. The dosage for P-Caps was 58 mg/kg/day +/- 24.6; P-SR dosage was 53 mg/kg/day +/- 15.18 (mean +/- SD) (P not statistically significant). The PA peak to trough variation for P-Caps was 2.2 micrograms/ml +/- 2.3 and for P-SR 1.5 micrograms/ml +/- 1.4 (P not significant). We conclude that P-SR given every six hours in the same daily dose as PA capsules given every four hours will provide similar therapeutic concentrations with no greater peak to trough variation.

Aged↗
PubMed1982

Simultaneous quantitation of quinidine, procainamide, and N-acetylprocainamide in serum by gas-liquid chromatography with a nitrogen-phosphorus selective detector.

We describe a single-run method for quantitating quinidine, procainamide, and N-acetylprocainamide, involving gas-liquid chromatography with a nitrogen-phosphorus selective detector. Within-run precision (CV) was 3% (x = 2 mg/L, n = 20), 6.9% (x = 4 mg/L, n = 10), and 1.5% (x = 8 mg/L, n = 8) for quinidine; 7.7% (x = 4 mg/L, n = 14), 1.6% (x = 8 mg/L, n = 16), and 2.3% (x = 12 mg/L, n = 12) for procainamide; and 6.3% (x = 5 mg/L, n = 6), 3.6% (x = 10 mg/L, n = 20), and 4.0% (x = 20 mg/L, n = 10) for N-acetylprocainamide.l Between-run precision was 3.0%(x = 2 mg/L, n = 20), 7.0% (x = 4 mg/L, n = 9), and 2.8% (x = 8 mg/L, n = 9) for quinidine; 4.7% (x = 4 mg/L, n = 10). 3.3% (x = 8 mg/L, n = 20), and 1.9% (x = 12 mg/L, n = 10) for procainamide; and 9.3% (x = 5 mg/L, n = 6), 4.3% (x = 10 mg/L, n = 20), and 3.8% (x = 20 mg/L, n = 10) for N-acetylprocainamide. Tube stoppers that contain a rubber plasticizer interfere with the technique. Clinical application and correlation with drug concentrations by this technique are discussed.

Acecainide↗
PubMed1983

Interaction of antacids with antiarrhythmics. V. Effect of aluminium hydroxide and magnesium oxide on the bioavailability of quinidine, procainamide and propranolol in dogs.

The influence of aluminium hydroxide and magnesium oxide on the oral bioavailability of quinidine, procainamide and propranolol in the dog was investigated. The administration of aluminium hydroxide with a quinidine sulfate capsule causes a significant decrease of maximal plasma concentration (Cpmax) and a shift in tmax (time to reach Cpmax). The area under the curve is not significantly decreased. Administration of magnesium oxide together with a quinidine sulfate capsule or a sustained-release preparation of quinidine bisulfate causes a significant decrease of both Cpmax and the area under the curve. A shift of tmax was observed for the conventional preparation only. The administration of aluminium hydroxide with procainamide hydrochloride diminishes only Cpmax in a significant way. Administration of magnesium oxide together with procainamide hydrochloride has no influence on the different parameters. Administration of aluminium hydroxide or magnesium oxide with propranolol hydrochloride has a significant negative influence on both the Cpmax and the area under the curve.

Aluminum Hydroxide↗