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PubMed1987

Procainamide, disopyramide and quinidine: discordant antiarrhythmic effects during crossover comparison in patients with inducible ventricular tachycardia.

A crossover comparison of intravenous procainamide, disopyramide and quinidine was made in 32 patients. All three drugs had dosage-related effects on electrocardiographic intervals, refractory periods and cycle length of ventricular tachycardia. Significant linear relations between serum drug levels and changes in refractory periods and ventricular tachycardia cycle length were also observed. Ventricular tachycardia was no longer inducible on at least one drug in 11 patients but concordance of this effect on both of the others was 36% and on either of the others it was 45%. Ventricular tachycardia remained inducible on at least one drug in 28 patients and concordance of this effect on both of the others was 75% and on either of the others was 79%. Continued inducibility on quinidine, the drug producing the greatest electrophysiologic effects, was the best individual predictor of continued inducibility on the others. Subdivision of continued inducibility into easier to induce, inducibility unchanged, or harder to induce dramatically decreased concordance of this effect. Thus the antiarrhythmic effects of these drugs are discordant in individual patients despite electrophysiologic similarities. Nevertheless, continued inducibility after high dosages of any one of these drugs is clinically useful for screening for continued inducibility on the others and this is dose-related rather than drug specific.

Adult↗
PubMedDate not supplied

Resolution of caffeine-induced complex dysrhythmia with procainamide therapy.

A case report of a 38-year-old male who ingested 20 gm of caffeine is presented. The patient exhibited clinical and laboratory evidence of caffeine toxicity. Cardiac monitoring revealed a chaotic rhythm with variable supraventricular and ventricular dysrhythmias without hemodynamic compromise. Procainamide was used effectively to convert this complex dysrhythmia. The mechanisms, manifestations, and therapy of caffeine toxicity are reviewed.

Adult↗
PubMed2003

Solution and solid state properties of a set of procaine and procainamide derivatives.

A set of potential Class III antiarrhythmic agents of structure p-HOOC-R-CO-NH-C(6)H(4)-CO-X-C(2)H(5)-N(C(2)H(5))(2) were isolated as crystalline solids of the amide and ester derivatives, I: succinylprocainamide (X=-NH-, R=-C(2)H(4)-); II: succinylprocaine (X=-O-, R=-C(2)H(4)-); III: maleylprocainamide (X=-NH-, R=-C(2)H(2)-) and IV: maleylprocaine (X=-O-, R=-C(2)H(2)-). Although compounds I-IV exhibit similar solution properties (i.e. acid-base speciation, with zwitterionic (+-) to neutral (00) form ratios higher than 10(4)), aqueous solubility of -NH- derivatives is significantly higher than that of -O- derivatives and also, solvent effects on solubility (i.e. the change of water by ethanol) is clearly different in both series. Solution and solid-state properties of I-IV were characterized to account for the observed differences. Results indicate that procainamide derivatives I and III crystallizes as (+-)(s) but procaine derivatives II and IV as (00)(s). Besides, I is anhydrous but II-IV are hydrates. Aqueous solubility and solvent effect on solubility are controlled by the intrinsic solubility of the species (+-) in I and III and (00) in II and IV. The rise of hydrophilicity of species (00) due to the structural change from -O- to -NH- would determine the change in the structure of the precipitating crystals from (00)(s) to (+-)(s). Solid structure (zwitterionic or neutral), as well as composition (anhydrous or hydrated) may be recognized as the main factors in determining the rank of aqueous solubility of the set: (+-)>(+-.H(2)O)>(00.H(2)O).

Anti-Arrhythmia Agents↗
PubMedDate not supplied

Solid-phase synthesis of lidocaine and procainamide analogues using backbone amide linker (BAL) anchoring.

New solid-phase strategies have been developed for the synthesis of lidocaine (1) and procainamide (2) analogues, using backbone amide linker (BAL) anchoring. Both sets were prepared starting from a common resin-bound intermediate, followed by four general steps: (i) attachment of a primary aliphatic or aromatic amine to the solid support via reductive amination (as monitored by a novel test involving reaction of 2,4-dinitrophenylhydrazine with residual aldehyde groups); (ii) acylation of the resultant secondary amine; (iii) displacement of halide with an amine; and (iv) trifluoroacetic acid-mediated release from the support. A manual parallel strategy was followed to provide 60 novel compounds, of which two dozen have not been previously described. In most cases, initial crude purities were >80%, and overall isolated yields were in the 40-88% range.

Lidocaine↗
PubMed1999

Procainamide, a drug causing lupus, induces prostaglandin H synthase-2 and formation of T cell-sensitizing drug metabolites in mouse macrophages.

Procainamide (PA) may cause drug-induced lupus, and its reactive metabolites, hydroxylamine-PA (HAPA) and nitroso-PA, are held responsible for this. Here, we show that N-oxidation of PA to these metabolites can take place in macrophages and lead to formation of neoantigens that sensitize T cells. Murine peritoneal macrophages (PMvarphi), exposed to PA in vitro, generated neoantigens related to HAPA as indicated by (1) their capacity to elicit a specific recall response of HAPA-primed T cells in the adoptive transfer popliteal lymph node (PLN) assay and (2) the appearance of metabolite-bound protein in PA-pulsed PMvarphi, as determined by Western blot. Analysis of five phase I enzymes that might be responsible for HAPA formation by PMvarphi pointed to prostaglandin H synthase-2 (PGHS-2) as a likely candidate. Experimental evidence that PA can be oxidized to HAPA by PGHS was obtained by exposing PA to PGHS in vitro. The resulting metabolites were identified by mass spectral analysis and covalent protein binding in ELISA. In vitro, PA exposure of PMvarphi of slow acetylator A/J and fast acetylator C57BL/6 mice failed to show significant strain differences in enzyme mRNA expression, enzyme activities, or formation of HAPA-related neoantigens. By contrast, after long-term PA treatment in vivo only in slow acetylators the PMvarphi harbored HAPA-related neoantigens and T cells were sensitized to them. PMvarphi of fast acetylator C57BL/6 mice only contained HAPA-related neoantigens, and their T cells were only sensitized to them if, in addition to long-term PA treatment, their donors had received injections of phorbol myristate acetate (PMA), a known enhancer of oxidative enzymes in phagocytes. In conclusion, PA treatment leads to N-oxidation of PA by enzymes, in particular PGHS-2, present in antigen-presenting cells (APC) and, hence, to generation of neoantigens which sensitize T cells. The enhanced neoantigen formation and T cell sensitization seen in slow acetylators might be explained by their higher concentration of PA substrate that is available for extrahepatic N-oxidation in APC.

Animals↗
PubMed1981

N-Acetyl-procainamide kinetics in the elderly.

Plasma and saliva N-acetyl-procainamide (NAPA) concentrations were measured by high-power liquid chromatography (HPLC) after intravenous infusion of 750 mg to 14 elderly patients (x age = 69 yr). The plasma NAPA disappearance curve can best be described by a two-compartment body model. Mean total body clearance was 10.6 1/hr, Vdss 125.8 1, and terminal half-life (t 1/2) 8.8 hr. A nonrenal clearance of 2.72 1/hr was calculated, that is, 19% of the expected total body clearance with normal kidney function. Saliva concentrations show huge inter- and intraindividual variability and are probably not usable for NAPA monitoring in older patients.

Acecainide↗
PubMedDate not supplied

Amitriptyline and procainamide inhibition of cocaine and cocaethylene degradation in human serum in vitro.

Amitriptyline (AMI) and procainamide (PA) have been reported to inhibit the activity of human plasma butyrylcholinesterase, an enzyme important in the metabolic degradation of cocaine (COC) and its ethyl analogue cocaethylene (CE). Because both AMI and PA may be used in the treatment of COC intoxication and abuse, the effect of high pharmacological concentrations of these compounds on the degradation of COC and CE in pooled human serum was studied. AMI (1.8 micromol/L) modestly inhibited the degradation of COC by 4.2% and of CE by 4.0%. PA (42.5 micromol/L) profoundly inhibited degradation of COC by 42.7% and of CE by 47.2%. In contrast, lithium carbonate (1 mmol/L, control) showed no inhibition of degradation of either COC or CE. These results suggest that AMI and PA may prolong the half-life of COC and CE in human serum.

Amitriptyline↗
PubMedDate not supplied

Procainamide inhibition of human hepatic degradation of cocaine and cocaethylene in vitro.

Procainamide (PA), a cardioactive drug, inhibited the degradation of both cocaine (COC) and cocaethylene (CE) when either was incubated in human liver homogenates for 3 h at 37 degrees C. PA appeared to enhance the formation of CE when COC and ethanol (ETOH) were incubated together in liver homogenate. These observations are clinically significant because cardiotoxicity is common after COC abuse and because PA may be administered to individuals who use COC alone and with ETOH.

Aged↗
PubMedDate not supplied

An HPLC method for the simultaneous quantitation of quinidine, procainamide, N-acetylprocainamide, and disopyramide.

A high performance liquid chromatographic method is reported, which incorporates three internal standards (I-cinchonidine, N-propylprocainamide, and para-chlorodisopyramide) for the simultaneous quantitation of four commonly prescribed antiarrhythmic drugs: quinidine, procainamide, N-acetylprocainamide, and disopyramide. Compounds were separated using combined ion-pairing and adsorption chromatography on a silica column. Inter-run variation was 5.9 CV% for all drugs.

Acecainide↗
PubMed1976

Porcine malignant hyperthermia induced by halothane and succinylcholine: failure of treatment with procaine or procainamide.

Metabolic, hemodynamic and neuroendocrine responses to the combined use of halothane and succinylcholine (SCh) were measured in five normal swine and five swine susceptible to malignant hyperthermia (MH). Constant-volume ventilation was used, and no therapy was instituted. The overall response in susceptible swine was fulminant, in that it involved the rapid onset of SCh-induced MH combined with the more severe metabolic, endocrine, and cardiovascular effects of halothane-induced MH. Maximal changes in VO2 were equivalent with either drug or both combined, while changes in lactate, potassium (K+), pH, and catecholamines were perhaps synergistic. Utilizing similar measurements, procaine or procainamide was used in 20 susceptible swine in attempts to prevent MH initiated by halothane, SCh, or both. Recommended therapeutic doses of either drug did not prevent characteristic MH changes in oxygen consumption, cardiac output, lactate, K+, pH, catecholamines, or temperature.

Animals↗
PubMed1992

Electrophysiologic interactions of procainamide and N-acetylprocainamide in isolated canine cardiac Purkinje fibers.

The study objective was to characterize the electrophysiologic interactions of procainamide (PA) and its metabolite, N-acetylprocainamide (NAPA), in canine Purkinje fibers. Cell (N = 43) action potentials were measured in Tyrode's solution (K+ = 4.0 mM, 36 degrees C) at a basic cycle length of 1,000 ms using standard microelectrode techniques. Six PA concentrations (0.020-0.32 mM) and six NAPA concentrations (0.010-0.24 mM) were studied alone and in combination. PA caused concentration-dependent decreases in Vmax and APD50 but did not alter APD90, ERP, or RMP. NAPA caused a small but not significant concentration-dependent decrease in Vmax, no change in RMP, and significant concentration-dependent increases in APD50, APD90, and ERP. Low NAPA concentrations increased, intermediate concentrations did not affect, and high NAPA concentrations again increased PA's effect on Vmax. PA-NAPA combinations resulted in concentration-dependent changes in APD50 that were intermediate between the effects of PA or NAPA alone. PA did not significantly alter NAPA's effects on APD90 at NAPA concentrations less than or equal to 0.040 mM, while it antagonized NAPA's effect at higher concentrations. The effects of PA-NAPA combinations on ERP were generally similar to their effects on APD90. The electrophysiologic effects of PA-NAPA combinations in normal canine Purkinje fibers are complex functions of the relative and absolute concentrations of the two compounds.

Acecainide↗
PubMed1979

Agranulocytosis during combined procainamide and phenytoin therapy.

We have presented two cases of agranulocytosis occurring in patients receiving a combination antiarrhythmic regimen. As multiple drug therapy for ventricular arrhythmias becomes more commonplace, increased scrutiny should be given to agents chosen, in an effort to prevent any possible adverse interactions. When future cases are encountered, the acetylator pheontype should be determined. This information would aid in assessing the predicative value of the acetylator phenotype in the development of agranulocytosis. Due to the inherent danger, neither patient was rechallenged with procainamide nor phenytoin.

Acetylation↗
PubMed1981

Plasma concentrations of desethyl N-acetylprocainamide in patients treated with procainamide and N-acetylprocainamide.

We describe a method for routinely measuring plasma concentrations of procainamide (PA), N-acetylprocainamide (NAPA) and desethyl N-acetylprocainamide (NAPADE) by high-performance liquid chromatography (HPLC). The method has been used together with mass spectrometry of the appropriate chromatographic fraction to demonstrate that NAPADE is a metabolite of NAPA. In addition, comparison of NAPADE concentrations in the plasma of patients receiving PA and NAPA indicates that NAPA is not an intermediate for most of the NAPADE formed from PA. We propose that the principal route of NAPADE formation from PA occurs by initial dealkylation to form rho-amino-N-[2-(ethylamino)ethyl]benzamide (PADE), a hypothetical PA metabolite that has yet to be identified.U

Acecainide↗
PubMed1983

Improved liquid chromatographic determination of procainamide and N-acetylprocainamide in serum.

A liquid chromatographic method for the determination of procainamide (PA) and N-acetylprocainamide (NAPA) in serum has been developed. This method utilizes isocratic conditions, ambient temperature, and a conventional fixed-wavelength 280-nm detector. Sample pretreatment involves extraction of PA and NAPA, along with p-amino-N-(2-dipropylaminoethyl)-benzamide hydrochloride as internal standard, into an organic phase and reextraction into an aqueous acidic phase. Using this sample pretreatment, interferences due to commonly used drugs are eliminated. The method accurately measures PA and NAPA to levels as low as 1 mg/L.

Acecainide↗
PubMed1993

Procainamide-induced myasthenia-like weakness and dysphagia.

A 64-year-old man with chronic renal insufficiency was hospitalized with dysphagia and inability to keep his head erect 11 months after beginning procainamide hydrochloride (PA) for control of atrial flutter. Evaluation revealed esophageal dysmotility, worsening renal function, and elevated serum PA and N-acetylprocainamide (NAPA) concentrations. No evidence of autoimmune myasthenia gravis was found. PA was discontinued and normalization of PA and NAPA concentrations was associated with a decrease in muscle weakness and resolution of dysphagia. The correlation between clinical findings and serum concentrations of PA and NAPA suggests that drug excess due to impaired clearance was the basis for this unusual adverse drug reaction.

Acecainide↗
PubMed1996

Comparison of fluorescence polarization immunoassay with liquid chromatography for quantification of procainamide and N-acetylprocainamide in urine.

The objective of this study was to compare the precision and accuracy of fluorescence polarization immunoassay (FPIA) with high-performance liquid chromatography (HPLC) for measurement of procainamide (PA) and N-acetylprocainamide (NAPA) concentrations in urine. To determine the correlation between FPIA and HPLC, urine PA and NAPA concentrations were assayed using both techniques in samples obtained from study patients receiving PA and in spiked samples. In samples from patients, FPIA-determined PA and NAPA concentrations were 19 +/- 9% lower and 28 +/- 31% higher, respectively, than those determined by HPLC. The slope of the FPIA-HPLC regression lines for PA and NAPA differed significantly from that of the line of unity (the slope that would result if FPIA and HPLC yielded identical concentrations). In spiked samples, FPIA-determined PA and NAPA concentrations were 15 +/- 2% and 11 +/- 2% lower than HPLC-determined concentrations, respectively, and the slopes of the FPIA-HPLC regression lines differed significantly from the line of unity. Therefore, FPIA cannot be recommended as a urine assay method when quantitative assessment of urine PA or NAPA excretion is needed for pharmacokinetic studies.

Acecainide↗