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PubMed1985

Famotidine, a new H2-receptor antagonist, does not affect hepatic elimination of diazepam or tubular secretion of procainamide.

In 8 healthy male volunteers the pharmacodynamic responses to a single dose of diazepam and a single dose of procainamide were assessed before and after pre-treatment with the H2-receptor antagonist famotidine in a randomized crossover study. The pharmacokinetics of diazepam and procainamide were also studied, and the binding of famotidine to human liver microsomes was also measured. Cimetidine induced binding changes with a spectral dissociation constant (Ks) of 0.87 mM, whereas famotidine produced no measurable spectral alteration in concentrations up to 4 mM. The elimination half-life (t1/2: 45.6 h) and total plasma clearance (CL: 0.28 ml/min/kg) of diazepam were not significantly altered by famotidine (t1/2 = 39.0 +/- 11.4 h; CL = 0.31 +/- 0.08 ml/min/kg). Similarly, there was no enhancement of the sedative effect of diazepam by famotidine. The pharmacodynamics and pharmacokinetics of procainamide and N-acetylprocainamide (NAPA), too, were not significantly changed by famotidine: procainamide t1/2 2.9 vs 3.0 h under famotidine and renal clearance (CLR) 436 vs 443 ml/min; and NAPA CLR 195 vs 212 ml/min under famotidine. The data suggest that famotidine, in contrast to cimetidine, does not affect the pharmacokinetics of diazepam (hepatic elimination) or procainamide (tubular secretion). This new H2-receptor antagonist appears to be devoid of an interaction potential for either type of drug elimination.

Adult↗
PubMed1983

Cimetidine-procainamide pharmacokinetic interaction in man: evidence of competition for tubular secretion of basic drugs.

The hypothesis that basic drugs can compete for active tubular secretion by the kidney was tested in six healthy volunteers by comparing the single dose pharmacokinetics of oral procainamide before and during a daily dose of cimetidine. The area under the procainamide plasma concentration-time curve was increased by cimetidine by an average of 35% from 27.0 +/- 0.3 micrograms/ml X h to 36.5 +/- 3.4 micrograms/ml X h. The elimination half-life increased from an harmonic mean of 2.92 to 3.68 h. The renal clearance of procainamide was reduced by cimetidine from 347 +/- 46 ml/min to 196 +/- 11 ml/min. All these results were statistically significant (p less than 0.016). The area under the plasma concentration-time curve for n-acetylprocainamide was increased by a mean of 25% by cimetidine due to a significant (p less than 0.016) reduction in renal clearance from 258 +/- 60 ml/min to 197 +/- 59 ml/min. The data suggests that cimetidine inhibits the tubular secretion of both procainamide and n-acetylprocainamide, and, if so, represents the first documented evidence for this type of drug interaction in man. The clinical implications from this study necessitate dosage adjustments of procainamide in patients being concomitantly treated with cimetidine. The interaction is pertinent not only for basic drugs that are cleared by the kidney, but also for metabolites of basic drugs and endogenous substances which require active transport into the lumen of the proximal tubule of the kidney for their elimination.

Absorption↗
PubMed1988

The uptake and elution of lignocaine and procainamide in the hindquarters of the sheep described using mass balance principles.

Mass balance principles were used to describe the uptake and elution of lignocaine (lidocaine) and procainamide in the hindquarters of the sheep. Each of four sheep received a right atrial infusion of either lignocaine.HCl (2.7 mg/min) or procainamide.HCl (5.5 mg/min) for 180 min. Paired arterial and inferior vena cava (draining the hindquarters) blood samples were taken at 20-min intervals during the infusion and for 180 min after the infusion. Lignocaine and procainamide mean total body clearances were 2.9 L/min (SD 1.1) and 1.3 L/min (SD 0.2), respectively. An index of the uptake and elution of these drugs in the hindquarters was estimated from the net drug mass per unit hindquarter blood flow; indirect evidence suggested that hindquarter blood flow was constant. All the net mass/flow of procainamide that was taken into the hindquarters during the infusion also eluted after the infusion, demonstrating reversible distribution into the tissues. However, uptake of procainamide was still occurring when blood concentrations were constant, indicating that the concentrations of procainamide in the hindquarters were not in equilibrium with the inferior vena cava concentrations. Lignocaine did not reach constant blood concentrations during the infusion and showed no tendency to reach arterio-venous equilibration; an arterio-venous difference of 22% (SD 5%) across the hindquarters was measured during the last 60 min of the infusion. By 180 min after the lignocaine infusions, 79% (SD 8%) of the lignocaine net mass/flow had not eluted from the hindquarters when arterial and venous lignocaine concentrations were not significantly different. This drug could remain uneluted due to metabolism and/or avid tissue binding, and presents difficulties in the interpretation of pharmacokinetic data whether based on arterial or venous blood sampling.

Animals↗
PubMed1983

Conversion of atrial fibrillation to sinus rhythm by acute intravenous procainamide infusion.

We evaluated the efficacy of an intravenous infusion of procainamide in 26 consecutive candidates for cardioversion of atrial fibrillation. Procainamide was administered at a rate of 15 to 20 mg/min up to a maximum of 1000 mg. The treatment was considered effective only if cardioversion occurred during the procainamide infusion. Conversion to sinus rhythm occurred in 15 patients. Converters had a significantly shorter mean duration of atrial fibrillation (6 +/- 7 days, mean +/- S.D.) compared to nonconverters (79 +/- 88 days) (p less than 0.01). The mean left atrial size of converters (4.3 +/- 0.6 cm) did not differ significantly from that of nonconverters (4.7 +/- 0.9 cm). The dose of procainamide required for cardioversion ranged from 3.6 to 16.4 mg/kg. Two patients developed nonsustained ventricular tachycardia, and there was one episode of bifascicular block during the infusion. Intravenous procainamide is an effective form of therapy for conversion of atrial fibrillation of new onset.

Adult↗
PubMed1986

The efficacy of cibenzoline and propafenone against inducible sustained and nonsustained ventricular tachycardias in conscious dogs with isolated chronic right ventricular infarction: a comparative study with procainamide.

The efficacy of intravenous cibenzoline (3 mg/kg), propafenone (4 mg/kg), and procainamide (20 mg/kg) against inducible sustained and nonsustained ventricular tachycardias (VT) was evaluated in 12 conscious dogs with chronic isolated right ventricular (RV) infarction. RV infarct was caused by permanent occlusion of the right coronary artery in the closed-chest dog by intracoronary balloon inflation. Three to 10 days following the occlusion period, programmed electrical stimulation reproducibly induced sustained and/or nonsustained VT, allowing evaluation of antiarrhythmic drug efficacy. Propafenone was effective in preventing the induction of sustained VT in only one out of six dogs tested, but caused a significant (p less than 0.05) slowing of VT rate (269 +/- 13 to 230 +/- 10 bpm). Procainamide had effects similar to those seen with propafenone. Propafenone and procainamide were ineffective against nonsustained VT, and on established sustained VT once induced. Cibenzoline was effective in preventing the induction of sustained VT in two out of seven dogs, an effect which was not significantly different from either propafenone or procainamide. However, cibenzoline was significantly (p less than 0.05) more effective than either procainamide or propafenone in terminating an established induced sustained VT (four out of six dogs). Furthermore, cibenzoline converted nonsustained to sustained VT in four out of seven dogs tested. Histopathologic studies have shown infarction of the basal two thirds of the RV (38.5 +/- 7.8% of the RV) with no left ventricular involvement. It is concluded that the isolated RV infarction model is highly suitable for serial drug testing against inducible VT in conscious dogs, and this model of VT appears to be fairly resistant to standard and newer antiarrhythmic drug therapy.

Animals↗
PubMed1987

Enhanced antiarrhythmic efficacy of propafenone when used in combination with procainamide or quinidine.

This study evaluated the efficacy and safety of combining propafenone with procainamide or quinidine for treating ventricular arrhythmias in patients in whom procainamide or quinidine therapy alone failed to suppress arrhythmias. In 30 patients, the addition of propafenone resulted in a significant reduction of premature ventricular contraction (PVC) frequency compared to drug-free baseline (406 PVC/hr vs 33, p less than 0.001) and to procainamide or quinidine monotherapy (211 PVC/hr vs 27, p less than 0.01). Propafenone alone was also more effective than either procainamide or quinidine and resulted in significant suppression of PVC compared to the drug-free state (406 PVC/hr vs 38, p less than 0.001). However, higher propafenone doses were necessary during monotherapy as compared to propafenone therapy combined with procainamide or quinidine (730 mg/day vs 480 mg/day, p less than 0.001). Of the 30 patients, 22 required an increase in propafenone dose during monotherapy as compared to combination therapy. Thus, propafenone is an effective antiarrhythmic agent when used in combination with type IA antiarrhythmic drugs. With these combinations, lower doses of propafenone can be utilized effectively than with propafenone alone.

Adult↗
PubMed1995

Role of intracellular calcium in the antiarrhythmic effect of procainamide during ventricular fibrillation in rat hearts.

Increased intracellular calcium (calcium overload) is considered one of the factors that can initiate ventricular fibrillation. In addition, ventricular fibrillation itself can cause and possibly maintain calcium overload. The goal of this study was to determine whether the class IA antiarrhythmic agent procainamide can reduce calcium overload during ventricular fibrillation and, if so, whether this reduction could be responsible for the recovery of the left ventricular function after defibrillation. For this purpose, the effects of 0.1 mmol/L of procainamide perfusion on left ventricular developed pressure, cardiac rate, and intracellular calcium during pacing-induced ventricular fibrillation were measured in isolated perfused rat hearts. Intracellular calcium was assessed by surface fluorometry after indo 1 loading. The concentration of procainamide was selected such that approximately half of the hearts would functionally recover from fibrillation. Cardiac rate and intracellular calcium were compared among four groups, depending on both the perfusate used and the recovery of left ventricular developed pressure at the end of the experiment. We found that procainamide reduced intracellular calcium to steady-state levels in hearts in which left ventricular function completely recovered (developed pressure > 67% of the steady-state value). However, intracellular calcium remained elevated in partially recovered hearts (33% < or = pressure < or = 67%) and in nonrecovered hearts (pressure < 33%). Thus procainamide can reduce calcium overload during ventricular fibrillation, and this reduction could be responsible for the recovery of left ventricular function after defibrillation. This reduction was use dependent, that is, dependent on high cardiac rates during fibrillation rather than on the decrease of cardiac rates before or during defibrillation.

Analysis of Variance↗
PubMed1980

Antiarrhythmic efficacy, pharmacokinetics and safety of N-acetylprocainamide in human subjects: comparison with procainamide.

The antiarrhythmic efficacy and pharmacokinetics of N-acetylprocainamide (NAPA), the major metabolite of procainamide, were investigated in 23 patients with chronic, high frequency ventricular ectopic depolarizations. An extensive trial design incorporated the approaches of (1) generation of dose-response relations, (2) randomized crossover, and (3) prolonged electrocardiographic monitoring. Seven patients with reproducible suppression of arrhythmias (70 percent or greater reduction in frequency) were thus identified. The mean plasma concentration of acecainide associated with efficacy was 14.3 micrograms/ml (range 9.4 to 19.5) and with side effects (primarily gastrointestinal) was 22.5 micrograms/ml (10.6 to 37.9). The antiarrhythmic response to procainamide did not predict response to acecainide; this finding implies that estimates of the antiarrhythmic contribution of acecainide concentrations achieved during long-term procainamide therapy are unlikely to be meaningful in a given person. The mean half-life of elimination after a single 500 mg dose of acecainide was 7.5 hours; this had prolonged significantly (p < 0.05) to 10.3 hours after higher dosages. No variable examined (including acetylator phenotype) was found to be a predictor of responsiveness to acecainide. Outpatient therapy (2 to 20 months) was not associated with the development of antinculear antibodies or the lupus syndrome; one patient's procainamide-induced arthritis resolved during therapy. Acecainide, unlike procainamide, is an agent whose pharmacokinetics allow long-term therapy on a practical schedule. It is effective in a subset of patients with ventricular arrhythmias yet appears much less likely to induce the lupus syndrome seen with the parent compound.

Acecainide↗
PubMed1981

Procainamide-induced polymorphous ventricular tachycardia.

Seven cases of procainamide-induced polymorphous ventricular tachycardia are presented. In four patients, polymorphous ventricular tachycardia appeared after intravenous administration of 200 to 400 mg of procainamide for the treatment of sustained ventricular tachycardia. In the remaining three patients, procainamide was administered orally for treatment of chronic premature ventricular contractions or atrial flutter. These patients had Q-T prolongation and recurrent syncope due to polymorphous ventricular tachycardia. In four patients, the arrhythmia was rapidly diagnosed and treated with disappearance of further episodes of the arrhythmia. In two patients, the arrhythmia degenerated into irreversible ventricular fibrillation and both patients died. In the seventh patient, a permanent ventricular pacemaker was inserted and, despite continuation of procainamide therapy, polymorphous ventricular tachycardia did not reoccur. These seven cases demonstrate that procainamide can produce an acquired prolonged Q-T syndrome with polymorphous ventricular tachycardia.

Administration, Oral↗
PubMed1982

Use of procainamide in patients with the Wolff-Parkinson-White syndrome to disclose a short refractory period of the accessory pathway.

Like ajmaline, procainamide can be used to identify patients with the Wolff-Parkinson-White syndrome who have a short refractory period of the accessory pathway in an anterograde direction. Procainamide given intravenously in a maximal dose of 10 mg/kg body weight over a 5 minute period during sinus rhythm produced complete anterograde block in the accessory pathway in 20 of 39 patients. An electrophysiologic investigation performed 24 to 48 hours later revealed that in 19 of the 20 patients the effective refractory period of the accessory pathway was 270 ms or greater. In 18 of the 19 patients not exhibiting anterograde block in the accessory pathway, the refractory period was less than 270 ms. When ajmaline was compared with procainamide in the same patients, 100 mg of procainamide had approximately the same effect as 10 mg of ajmaline. The use of intravenous procainamide is a reliable and rapid method of identifying patients with the Wolff-Parkinson-White syndrome who may be at risk for circulatory insufficiency or sudden death in case of atrial fibrillation.

Adolescent↗
PubMed1984

Effect of amiodarone on serum quinidine and procainamide levels.

Serum levels of quinidine or procainamide were measured in patients who had amiodarone added to their antiarrhythmic regimen. Dosages of quinidine or procainamide were held constant. Eleven of 11 patients had an increase in the serum quinidine level, and 11 of 12 other patients had an increase in the serum procainamide level. The dose requirement to maintain a stable plasma level of quinidine or procainamide decreased by 37% and 20%, respectively. Clinical toxicity occasionally occurred with the increase in serum levels of quinidine and procainamide, and the dose of these drugs should be decreased when amiodarone is administered concurrently.

Adult↗
PubMed1984

Effects on ventricular function of disopyramide, procainamide and quinidine as determined by radionuclide angiography.

To evaluate the effects of the 3 commonly used antiarrhythmic agents--disopyramide, procainamide and quinidine--on left ventricular (LV) function, these 3 agents were administered in random sequence after control radionuclide angiography performed at rest and during exercise in 17 patients. Drug dosages were tailored to achieve therapeutic blood levels 5 minutes before and 2 to 3 hours after drug administration. The mean dose of disopyramide was 141 +/- 26 mg every 6 hours, procainamide, 441 +/- 100 mg every 4 hours, and quinidine, 401 +/- 101 mg of the gluconate preparation every 6 hours. The patients received the appropriate dosage for 7 or more days before repeat radionuclide angiography was performed. The ejection fraction at rest was: control 60 +/- 13%, disopyramide 55 +/- 11%, procainamide 58 +/- 11%, and quinidine 59 +/- 12%. The exercise ejection fraction was: control 61 +/- 14%, disopyramide 58 +/- 13%, procainamide 58 +/- 12% and quinidine 61 +/- 13%. In neither case, at rest nor during exercise was there any significant difference observed between any of the agents or between any individual agent and control. However, at rest 8 subjects had a 5% or more decrease from the control value with disopyramide, 5 had a 5% or more decrease with procainamide and 6 had a 5% or more decrease with quinidine, whereas during exercise the decreases were 8, 6 and 5%, respectively. These values were not statistically different but suggest that caution should be taken in administering all 3 agents, particularly to patients with impaired LV function, because individual sensitivity to a given agent may precipitate a significant decline in LV function.

Adult↗
PubMed1990

Effect of quinidine or procainamide versus no antiarrhythmic drug on sudden cardiac death, total cardiac death, and total death in elderly patients with heart disease and complex ventricular arrhythmias.

A prospective study correlated the effect of quinidine or procainamide versus no antiarrhythmic drug on sudden cardiac death, total cardiac death and total death in 406 elderly patients with heart disease and asymptomatic complex ventricular arrhythmias detected by 24-hour ambulatory electrocardiograms. Of 397 patients treated with quinidine, 184 (46%) developed adverse effects during the first 2 weeks of therapy and were given no further antiarrhythmic therapy. Of 9 patients treated with procainamide, 2 (22%) developed adverse effects during the first 2 weeks of therapy and were given no further antiarrhythmic therapy. Adverse effects developed during long-term therapy in 6 patients (2%) receiving quinidine and in 3 patients (33%) receiving procainamide. Mean follow-up was 24 +/- 15 months in both groups. Sudden cardiac death, total cardiac death and total death occurred in 21, 43 and 65% of patients receiving quinidine or procainamide, respectively, and in 23, 44 and 63% of patients receiving no antiarrhythmic drug, respectively (difference not significant). Survival by Kaplan-Meier analysis showed no significant difference between the 2 groups for sudden cardiac death, total cardiac death or total death through 4 years. Patients with abnormal left ventricular ejection fraction had a 3.4 times higher incidence of sudden cardiac death, a 2.4 times higher incidence of total cardiac death and a 1.4 times higher incidence of total death than patients with normal left ventricular ejection fraction. These data showed no significant difference in sudden cardiac death, total cardiac death or total death between patients treated with quinidine or procainamide or with no antiarrhythmic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Antiarrhythmic and hemodynamic evaluation of indecainide and procainamide in nonsustained ventricular tachycardia.

The present trial was a placebo-controlled, randomized, parallel study comparing indecainide to procainamide. A 24-hour intravenous phase measured and compared invasive hemodynamics, followed by oral administration for assessment of arrhythmia suppression. Thirty-two patients (mean age 61 years) with asymptomatic or mildly symptomatic nonsustained ventricular tachycardia (VT) were evaluated, 15 while receiving indecainide and 17 while receiving procainamide. A total of 8 patients had serious toxicity during the intravenous phase; 6 receiving indecainide experienced increased left ventricular dysfunction or worsening arrhythmia (sustained VT, arrhythmic death) while 2 receiving procainamide developed serious hypotension. Proarrhythmia developed in 3 of 15 (20%) of the indecainide patients, but in no procainamide patient. In those tolerating indecainide, long-term suppression of ventricular premature complexes (VPCs) and of runs of VT was more consistent than with procainamide. While indecainide was a potent suppressor of spontaneous VPCs and VT, patients with significant left ventricular dysfunction could not tolerate it. The indecainide patients developing serious toxicity had a common hemodynamic profile: ejection fraction less than 25%, elevated left ventricular filling pressures, low cardiac and stroke volume index and minimal cardiac reserve. Indecainide has a poor risk-benefit ratio in patients similar to the current population, who have potentially lethal ventricular arrhythmias and severe left ventricular dysfunction.

Administration, Oral↗
PubMed1990

Cycle-length response of ventricular tachycardia associated with coronary artery disease to procainamide and amiodarone.

We undertook this study to determine if the cycle-length response of ventricular tachycardia (VT) to procainamide and amiodarone is similar in the individual patient. We enrolled 40 patients with uniform, monomorphic VT at a baseline, drug-free electrophysiologic study, after procainamide infusion and during oral amiodarone therapy. We found a significant correlation (p less than 0.01) between VT cycle-lengths on the 2 agents as well as the percent change in cycle length from baseline. Only 60% of the patients exhibited VT rates within 10% between the 2 agents. Importantly, less than 20% of patients had further slowing of the VT rate (greater than 10% slowing) during amiodarone therapy as compared to procainamide. Thus, although the cycle-length response of VT to procainamide correlates with the cycle-length response to amiodarone, 40% of patients have a disparate response (greater than 10% difference in cycle length) to the 2 agents; additional slowing of VT rates in response to amiodarone beyond that seen with procainamide is unlikely. These results have important implications regarding the institution of amiodarone therapy and the need for repeat electrophysiologic testing during amiodarone therapy.

Amiodarone↗
PubMed1986

Serologic changes during induction of lupus-like disease by procainamide.

Procainamide-induced lupus is a well-recognized syndrome, but the events leading up to clinical symptoms are obscure. In the present study, serologic changes in a 69-year-old man were monitored during his treatment with procainamide and after discontinuation of procainamide because of symptoms of drug-induced lupus. Antihistone antibodies of unique specificity and in vivo complement activation were detected after one year of procainamide therapy during a period prior to development of significant clinical symptoms. Antihistone antibodies and complement activation substantially increased during a full-blown episode of lupus-like symptoms. Progressive return to normal laboratory findings occurred after procainamide was discontinued. The antihistone/complement profile may be useful in the diagnosis of drug-induced lupus and warn of impending clinical deterioration in patients with minimal symptoms.

Aged↗
PubMed1989

Effect of procainamide on renal tubular transport of cimetidine in the isolated perfused rat kidney.

The effect of procainamide on renal tubular transport of cimetidine was studied in isolated perfused rat kidney based on the multiple indicator dilution (MID) technique. T-1824-labeled albumin (a vascular reference), [14C]creatine (an extracellular reference), and [3H]cimetidine were rapidly injected into the renal artery of isolated perfused rat kidney in the presence or absence of procainamide (100 microM) in the perfusate, and normalized outflow-time patterns were secured from rapidly sampled renal perfusate. A distributed two-compartmental model was fitted to the dilution data by non-linear least-squares regression, and the influx, efflux and sequestration rate constants were estimated. Net transport and influx processes of cimetidine were competitively inhibited by procainamide (PA), while the efflux and sequestration processes were increased. The increase in the values of the efflux and sequestration rate constants by addition of procainamide may be explained by the increase in the tissue binding of cimetidine. However, these three processes were not significantly affected by p-aminohippurate (PAH). These results suggest that both cimetidine and procainamide are secreted into the lumen by an organic base transport mechanism in the perfused kidney, in which the spatial organization and cell polarity of the kidney are maintained.

Albumins↗
PubMed1987

The action of procainamide and quinidine on the alpha 1-receptor-operated channels in smooth muscle cells of guinea-pig taenia caeci.

The effect of procainamide (2.0-5.0 mM) and quinidine (0.2-1.0 mM) on the alpha 1 response evoked by adrenaline (3 X 10(-6) M) in smooth muscle cells of guinea-pig taenia caeci (22 degrees C) was studied in the presence of yohimbine (3 X 10(-6) M), propranolol (3 X 10(-6) M) or atropine (10(-6) M). The electrotonic potential elicited by the application of a constant current to the preparation was slightly increased (about 10%) by procainamide (5.0 mM) but not by quinidine (1.0 mM). The double-sucrose gap method was used for measurements. The alpha 1 response evoked by adrenaline in the absence of extracellular calcium (15 min) was represented by a transient hyperpolarization of the muscle cells, while the hyperpolarization elicited in the presence of calcium was sustained. The hyperpolarization is caused by enhancement of the potassium efflux assumed to be linked with mobilization of calcium form a cellular structure. Superfusion of the preparation with calcium-containing solution to replenish the calcium store in the presence of procainamide (10 min) before the alpha 1 response evoked in the absence of calcium and procainamide did not affect the transient hyperpolarization. Quinidine, however, suppressed the alpha 1 response when the same procedure was followed. Both the transient and the sustained hyperpolarization evoked in smooth muscle cells in the presence of procainamide (15 min) or quinidine in calcium-containing or in calcium-free solution, respectively, were inhibited. The alpha 1 response was reflected by a depolarization of the muscle cells after the potassium channels had been blocked with apamin (3 X 10(-7) M, 20 min).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗