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PubMed1980

The clinical pharmacology and antiarrhythmic efficacy of acetylprocainamide in patients with arrhythmias.

The actions of acetylprocainamide, the major metabolite of procainamide in man, were studied in a placebo-controlled oral-dose-ranging trial in 16 persons with arrhythmias. The occurrences of arrhythmias decreased in 15 patients receiving acetylprocainamide and increased subsequently in 10 of 13 patients given placebo. The frequency of arrhythmias was reduced by more than 75 percent in nine patients. Antiarrhythmic effects were dependent on dose and serum drug concentrations, with levels of 10 to 24 microgram/ml observed in patients with a reduction of more than 70 percent in premature ventricular complexes. The ratio of preejection period to left ventricular ejection time decreased during therapy. Side effects of light-headedness, insomnia, nausea and diarrhea occurred in six patients at serum levels ranging from 11 to 22 microgram/ml. The serum half-life of acetylprocainamide lengthened from 7 to 21 hours as the creatinine clearance decreased from 105 to 35 ml/min. Acetylprocainamide has antiarrhythmic efficacy, but causes side effects in human beings. This compound appears to contribute to the effects of procainamide therapy and may be useful as an antiarrhythmic drug.

Acecainide↗
PubMed1982

Method for evaluating the effects of antiarrhythmic drugs on ventricular tachycardias with different electrophysiologic characteristics and different mechanisms in the infarcted canine heart.

In a canine model of myocardial infarction caused by coronary occlusion and reperfusion, ventricular tachycardia occurs spontaneously at 24 hours and has many of the characteristics of an accelerated idioventricular rhythm. It cannot be induced by premature or rapid stimulation of the ventricles; overdrive pacing during this tachycardia usually causes some transient overdrive suppression but occasionally there is overdrive acceleration. We suggest that this arrhythmia is caused mainly by enhanced automaticity. Ventricular tachycardia also can be induced by premature or rapid ventricular pacing 3 to 5 days after infarction, but it does not occur spontaneously. It can be stopped by overdrive pacing, suggesting that it is caused by reentry. Electrocardiographic features are identical to chronic, recurrent sustained ventricular tachycardia in human patients. Because the arrhythmias occurring at different times probably result from different mechanisms this canine model is useful for comparing the actions of drugs on different kinds of arrhythmias. Lidocaine and procainamide generally abolished tachycardia 24 hours after infarction, but only procainamide abolished tachycardia 3 to 5 days after infarction. Isoproterenol accelerated tachycardia at both times. Verapamil did not abolish tachycardia 3 to 5 days after infarction.

Animals↗
PubMed1984

Lorcainide therapy for the high-risk patient post myocardial infarction.

Nonsustained ventricular tachycardia (VT) in the late period (7 to 21 days) after myocardial infarction (MI) is reported to be a predictor of sudden death. Patients with 3-beat VT on Holter monitoring in the late infarction period would be suspected to demonstrate electrical instability on electrophysiologic studies. Forty-seven patients were identified as having at least 3-beat VT on Holter monitoring. Eighteen patients refused electrophysiologic studies or were not referred. Eight patients died; 3 were sudden deaths in 13 +/- 5 months, a 17% incidence. Twenty-nine patients underwent invasive electrophysiologic studies and 28 had inducible VT, 18 sustained and 10 nonsustained. Lorcainide prevented VT induction in 21 of the 28 patients, whereas 12 of the 22 patients studied on procainamide were protected. Lidocaine, tested in 21 patients, prevented VT induction in only 5. Lorcainide and procainamide prolonged refractoriness in those patients protected at programmed electrical stimulation (PES), whereas the QT interval was prolonged in patients in whom VT could still be induced. Twenty-seven of the 28 patients were placed on drugs predicted to be effective by PES studies, 19 on lorcainide. After a mean follow-up of 12.5 +/- 4 months the patient with noninducible arrhythmia is alive and 26 of the 28 patients with inducible arrhythmia are alive and well. Two patients died, 1 of stroke and 1 of pump failure after a second MI. No sudden deaths were observed in this group. Two patients had breakthrough arrhythmias and were treated by alternative antiarrhythmic therapy that was also effective on initial electrophysiologic studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1984

Comparison of noninvasive arrhythmia induction techniques with electrophysiologic studies and evaluation of lorcainide in patients with symptomatic ventricular tachycardia.

Twenty-six patients (19 men and 7 women) with symptomatic ventricular tachycardia (VT) were studied using invasive and noninvasive techniques to induce VT. Of the study population, 12% had syncope and VT on Holter monitoring, 30% had cardiac arrest and 58% had symptomatic VT. All patients had antiarrhythmic agents stopped 5 half-lives before evaluation and then had autonomic profile (upright tilt, cold pressor test, exercise testing and hand grip) as well as programmed electrical stimulation studies performed. Autonomic profile testing induced VT in 5 of 26 patients (19%) and in only 1 patient was the arrhythmia reproducibly induced. All 26 patients had VT induced on electrophysiologic testing; 9 patients had nonsustained and 17 had sustained VT. Lorcainide administered intravenously prevented VT induction in 20 of 26 patients tested, whereas procainamide was effective in 11 of 24 patients. Ten of the 13 not protected by procainamide were protected by lorcainide. Twenty patients were started on long-term lorcainide therapy and followed up for 29 +/- 3.4 months. Five patients have discontinued therapy, 2 because of breakthrough arrhythmias, 2 because of severe sleep-wake disturbances and 1 because of private physician preference. An additional 3 patients died during therapy because of myocardial infarction in 1, progressive myopathy in 1 and sudden death in 1. Sixty percent of patients started on lorcainide therapy have continued. In this patient population, noninvasive induction of VT is not a sensitive or reproducible technique in assessing antiarrhythmic therapy. Furthermore, when selected on the basis of electrophysiologic testing, lorcainide is a well-tolerated and effective antiarrhythmic agent.

Aged↗
PubMed1987

Beta blockers in combination with class I antiarrhythmic agents.

The hemodynamic and antiarrhythmic interactions between nadolol and a commonly used class I antiarrhythmic agent, quinidine or procainamide, were evaluated in 18 patients with ventricular arrhythmias in a double-blind, parallel study. Patients qualified for entry into the study if their ventricular arrhythmias remained poorly controlled (greater than or equal to 10 ventricular premature complexes/hr) with the class I agent alone and they had a left ventricular ejection fraction greater than 30%. Patients received their usual therapeutic doses of quinidine or procainamide throughout the study, which consisted of 3 treatment periods; a 2-week placebo treatment period, a 2-week open-label oral nadolol dose titration period, during which the dosages of nadolol were gradually increased from 40 mg daily to a maximum tolerated dose up to 120 mg daily, and a 4-week randomized, parallel comparison period during which patients were treated with either a class I agent alone or a combination of a class I agent and nadolol. Left ventricular ejection fractions by radionuclide ventriculography and 24-hour ambulatory electrocardiographic (Holter) recordings were obtained at the end of each treatment period. A positive treatment response was defined as greater than or equal to 75% reduction in ventricular premature complex frequency. During the dose titration phase, combination therapy with nadolol (mean dose 94 mg daily) and class I agents produced a mean decrease in ventricular premature complexes of 79% (p less than 0.01), and a mean decrease in ventricular couplets of 95% (p less than 0.01). A positive response was observed in 57% of patients treated with nadolol plus a class I agent.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1988

Strength-interval relation for ventricular functional refractoriness.

Successful initiation and termination of presumed reentrant ventricular tachycardia frequently depends on the ability to deliver closely coupled impulses to the region of the tachycardia origin. To evaluate systematically the relative influence of local latency and large-scale conduction delay in limiting the delivery of closely coupled impulses, the strength-interval relation of the effective refractory period (RP), and the local and remote functional RP in 35 patients at paced cycle length of 500 ms were measured. The pacing threshold was less than or equal to 0.25 mA in all patients. The drive-train (S1) and the extrastimulus (S2) were applied from the same site, the right ventricular (RV) apex, in 25 patients, and from separate sites (RV apex and RV outflow tract) in 10 patients. The effect of procainamide (plasma concentration 10.1 +/- 2.3 micrograms/ml) on the strength-interval relations in 10 patients was also assessed. Although effective RP decreased significantly with each successive increase in current strength (p less than 0.001), local functional RP decreased only up to current strength of 4 mA, and remote functional RP decreased only up to 2 mA. Procainamide shifted the effective RP and local and remote functional RP strength-interval curves uniformly to the right without altering their relation. These data indicate that large-scale conduction delay provides the principal limitation for using increasing current strengths of a single extrastimulus to initiate or terminate ventricular tachycardia.

Adult↗
PubMed1989

Stress and pharmacologic tests as methods to identify patients with Wolff-Parkinson-White syndrome at risk of sudden death.

Noninvasive stress and pharmacologic tests with procainamide and propafenone were studied as methods to identify patients with Wolff-Parkinson-White syndrome (WPW) who would otherwise be judged at risk of sudden death on the basis of electrophysiologic criteria: the shortest RR interval during induced atrial fibrillation less than or equal to 250 ms or accessory pathway anterograde effective refractory period less than or equal to 250 ms. Sixty-five patients were studied. Twenty-four patients fulfilled the electrophysiologic risk criteria (group A) and 41 patients fulfilled none of these criteria (group B). Persistence of preexcitation during stress test showed a sensitivity of 96% and a specificity of 17% to identify group A patients; its positive predictive value was 40% and negative predictive value 88%. With both procainamide and propafenone tests persistence of preexcitation identified group A patients with a sensitivity of 96% and a specificity of 51%; their positive and negative predictive value were, respectively, 53 and 95%. Stress and pharmacologic tests have good sensitivity and negative predictive value, but low specificity and positive predictive value.

Adolescent↗
PubMed1990

Effectiveness of sotalol for therapy of complex ventricular arrhythmias and comparisons with placebo and class I antiarrhythmic drugs.

In new antiarrhythmic drug development, key comparisons include those with placebo, standard (class I) agents and other beta blockers. This review will cover the first 2 comparisons. The effectiveness of 2 doses of sotalol for complex ventricular arrhythmias has been compared with placebo in a 6-week, multicenter study (parallel, double-blind design) in 102 patients. The frequency of ventricular premature complexes (VPCs) was reduced only 10% with placebo, 75% with low-dose sotalol (160 mg administered twice daily) and 88% with high-dose sotalol (320 mg administered twice daily) (both p less than 0.05 vs placebo). The defined efficacy criterion (greater than or equal to 75% VPC suppression) was achieved by 6% of patients taking placebo, 34% of patients taking low- and 71% of patients taking high-dose sotalol. Sotalol was generally well tolerated, especially with the lower dose. Heart rate decreased, and PR and QTc intervals increased modestly. An open, randomized, crossover study compared sotalol with procainamide in 33 patients. A reduction in VPCs of greater than or equal to 75% was achieved in 22 patients (67%) with sotalol and in 13 patients (39%) with procainamide. Quinidine and sotalol have also been compared in a multicenter study in patients with chronic, complex VPCs, with results to be presented in the near future. Thus, sotalol's antiarrhythmic efficacy is well demonstrated by comparisons with placebo, and its effectiveness and tolerance are likely to compare favorably with standard class I drugs, suggesting its potential as a first-line antiarrhythmic agent.

Anti-Arrhythmia Agents↗
PubMed1990

Effects of sotalol on ventricular tachycardia and fibrillation produced by programmed electrical stimulation: comparison with other antiarrhythmic agents.

Sotalol, a beta blocker, is now recognized as an important class III agent. The drug lengthens the action potential in most cardiac tissues without affecting conduction. Several studies have shown that sotalol is very effective in treating life-threatening arrhythmias. One hundred thirty-eight patients with inducible and clinically sustained tachycardia were retrospectively analyzed. With the use of the S1S2S3 stimulation protocol for ventricular tachycardia (VT) induction, sotalol prevented VT/ventricular fibrillation (VF) induction in 45% of the patients; other class I agents prevented VT/VF induction in only 15 to 22%. Data were also analyzed from a prospective multicenter study comparing sotalol with procainamide in suppressing sustained VT in 153 patients with symptomatic sustained VT/VF. With the use of the S1S2S3S4 stimulation protocol, sotalol prevented VT/VF induction in 35% of the patients, whereas procainamide prevented VT/VF induction in only 22% (difference not significant). When patients whose VT induced by the triple-stimuli protocol were excluded, sotalol prevented VT induction in 53%. These findings indicate that the antiarrhythmic effects of sotalol are comparable to those of class I agents in treating malignant arrhythmias. Although more data are needed on the comparative effects of sotalol, available data establish sotalol as an important addition to available antiarrhythmic agents.

Anti-Arrhythmia Agents↗
PubMed1993

Usefulness of sotalol for life-threatening ventricular arrhythmias.

Two trial designs have been used in evaluating sotalol in patients with sustained tachyarrhythmias: open-label dose escalation and randomized comparison with reference agents. At least 7 open-label studies (n = 16-65) have been reported from single centers in patients in whom trials of numerous other antiarrhythmic agents were unsuccessful. At the doses used, usually 320-640 mg/day, plasma concentrations were in the range associated with both beta blockade and class III antiarrhythmic activity (2-3 micrograms/mL). These concentrations produced electrophysiologic changes that were consistent across studies: 10-16% increase in right ventricular effective refractory period (ERP), 4-8% increase in corrected QT interval (QTc), and 17-30% increase in sinus cycle length (corresponding to a 15-23% decrease in heart rate). In these open-label trials, sotalol suppressed inducible ventricular tachyarrhythmias in 20-72% of patients; the higher degrees of efficacy were reported when induction protocols were confined to double extrastimuli. Side effects leading to discontinuation of sotalol in patients with sustained ventricular tachycardia or fibrillation include fatigue (4.0%), marked bradycardia (3.0%), torsades de pointes (3.0%), and heart failure or pulmonary edema (1.0%). A multicenter randomized trial compared intravenous sotalol with intravenous procainamide in a double-blind prospective fashion. Sotalol suppressed ventricular tachyarrhythmias inducible with triple extrastimuli in 15 (30%) of 50 patients, whereas procainamide was effective in 10 (20%) of 50. In this and other series, responsiveness to sotalol was prospectively identified by a particularly fast tachycardia at baseline (e.g., cycle length of < 270 msec), but not by the extent of changes in global indices of repolarization (QTc, ERP).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Suppression of ventricular automaticity by antidysrhythmic agents.

In view of the potentially important role of automaticity in the genesis of ventricular dysrhythmias, the effects of four widely used antidysrhythmic agents on ventricular automaticity were examined in anesthetized dogs at doses previously shown to antagonize experiments induced rhythm disturbances. Quinidine, and particularly procainamide, lidocaine and propranolol slowed ventricular rate in A-V blocked dogs. Quinidine and procainamide but particularly the last two agents also markedly prolonged overdrive suppression. Thus, all four substances depressed automaticity. However, propranolol was effective at doses substantially lower than those required to antagonize several experimental dysrhythmias.

Animals↗
PubMed1979

Effects of disopyramide on SA nodal pacemaker activity and contractility in the isolated blood-perfused atrium of the dog.

The isolated blood-perfused preparations of canine atrium were suspended in a bath and perfused with arterial blood led from the carotid artery of the heparinized donor dog. Disopyramide caused dose-related negative chronotropic and inotropic effects in a dose range of 30-1000 microgram when injected directly into the cannulated sinus node artery of the isolated atrium. The order of potencies for inducing the negative chronotropic effect in isolated atrium preparations was verapamil greater than propranolol greater than lidocaine = quinidine greater than phenytoin greater than or equal to disopyramide greater than procainamide. On the other hand, the order of potencies for inducing the negative inotropic effect was verapamil = propranolol greater than lidocaine greater than or equal to phenytoin greater than disopyramide greater than procainamide greater than or equal to quinidine. When disopyramide (1 mg/kg or 3 mg/kg) was administered i.v. into the jugular vein of the donor dog, the systemic blood pressure of the donor dog was markedly decreased. However, the tension developed and sinus rate of the isolated atrium were only slightly decreased. Disopyramide produced greater suppression at higher frequencies and slightly depressed the calcium chloride-induced positive inotropic effects.

Animals↗
PubMed1990

Effect of class Ia antiarrhythmic agents on fasciculoventricular fibers.

In four patients with fasciculoventricular (FV) fibers, the electrocardiographic and electrophysiologic characteristics were studied based on their response to class Ia antiarrhythmic agents. Three patients had paroxysmal atrial fibrillation, and one showed atrioventricular nodal Wenckebach-type block with dual pathways. Three of the four patients showed complete block of FV fibers after administration of disopyramide 0.28-0.60 mg/kg, procainamide 1.7-2.6 mg/kg, and ajmaline 0.18-0.26 mg/kg, respectively. Normalization in the remaining patient was not seen after disopyramide 2 mg/kg or procainamide 10 mg/kg, but was achieved by ajmaline 0.86 mg/kg. Ventricular preexcitation beats showed initial q waves (3 patients) or a decrease in the height of the r wave (1 patient) in V1, no initial q wave in V6 (4 patients), and ST-T changes (1 patient). Since these findings resemble ischemic change or intraventricular conduction disturbance, drug testing is necessary for precise diagnosis and proper clinical management.

Adult↗
PubMed1986

A simplified procedure for the purification of large quantities of fetal bovine serum acetylcholinesterase.

A simple procedure has been developed for the large scale purification of fetal bovine serum acetylcholinesterase (AChE) (EC 3.1.1.7). The procedure involves two steps: batch adsorption of the AChE from 250 L of serum onto a procainamide affinity Sepharose 4B gel; and analytical procainamide affinity chromatography of the step-1 product. Over 100 mg of AChE was purified in 10 days to apparent homogeneity with this procedure.

Acetylcholinesterase↗
PubMed1989

Ligand stabilization of cholinesterases.

Stabilization of fetal bovine serum (FBS) acetylcholinesterase (acetylcholine acetylhydrolase, EC 3.1.1.7) (AChE) and human butyrylcholinesterase (acylcholine acylhydrolase, EC 3.1.1.8) (BuChE) by ligands and inhibitors was studied as a function of physical and chemical perturbation. Denaturation of AChE occurred as a binary exponential function in the temperature range studied (50-56 degrees C); the slower fraction progressively diminished as the temperature was increased. Inclusion of ligands or inhibitors stabilized AChE as a function of temperature, ligand concentration and time. The rank order in which ligands stabilized AChE was: edrophonium greater than decamethonium greater than pralidoxime chloride much greater than procainamide. BuChE denaturation was retarded by ligands in the order: decamethonium greater than procainamide greater than edrophonium greater than pralidoxime. A plot of the quotient of the fast/slow ratio against the log of the 50% inhibitory concentration (I50) for ligands providing substantial protection yielded a linear relation, suggesting that these compounds stabilized AChE by a common mechanism involving the anionic site of the active center. Urea-induced cholinesterase denaturation was also retarded by these ligands.

Acetylcholinesterase↗
PubMed1987

High-performance liquid chromatographic drug analysis by direct injection of whole blood samples. II. Determination of hydrophilic drugs.

The determination of hydrophilic drugs in whole blood by direct injection high-performance liquid chromatography was investigated. A pre-column equipped with an inlet filter of pore size 40 microns and an outlet filter of pore size 2 microns was packed with Butyl Toyopearl 650-M. A whole blood sample was injected directly into the pre-column to trap proteins, hydrophobic compounds and blood cytomembranes, and hydrophilic compounds emerged into an analytical column (Nucleosil 5SA, particle size 5 microns) and were determined after column switching. Proteins in 40 microliters of rabbit whole blood were adsorbed in the pre-column (0.63 ml of wet gel) in 0.4% perchloric acid solution. The recovery of procainamide and N-acetylprocainamide from whole blood was quantitative with good reproducibility (coefficient of variation less than 4%). It was shown that procainamide added to rabbit whole blood was subjected to N-acetylation by N-acetyltransferase in blood cells.

Acecainide↗
PubMed1995

Insights into the Electrophysiology Study Versus Electrocardiographic Monitoring Trial: its programmed stimulation protocol may introduce bias when assessing long-term antiarrhythmic drug therapy.

OBJECTIVES: We hypothesized that if the Electrophysiology Study Versus Electrocardiographic Monitoring (ESVEM) trial programmed stimulation protocol misclassified some drug trials as effective, then the misclassification rate would be proportionally greater for drugs other than sotalol. BACKGROUND: In the ESVEM trial, patients treated with sotalol had fewer arrhythmic recurrences than those treated with other antiarrhythmic drugs despite similar efficacy predictions during electrophysiologic testing. METHODS: We retrospectively compared the standard programmed stimulation protocol used at Case Western Reserve University, which used three extrastimuli during all follow-up studies, with the ESVEM protocol in 176 antiarrhythmic drug trials: sotalol (n = 54), procainamide (n = 73) and quinidine/mexiletine (n = 49). RESULTS: Predictions of efficacy were higher in the sotalol trials (14 of 54 standard, 20 of 54 ESVEM) than in procainamide trials (7 of 73 standard, 14 of 73 ESVEM) or quinidine/mexiletine trials (1 of 49 standard, 7 of 49 ESVEM). Thus, the two protocols classified 19 of 176 trials differently: not effective by the standard protocol but effective by the ESVEM trial. Discordant predictions of drug efficacy constituted a smaller proportion of ESVEM protocol efficacy predictions for sotalol (6 [30%] of 20) than for the other drugs (13 [62%] of 21, p < or = 0.05). CONCLUSIONS: In the present study, the ESVEM programmed stimulation protocol predicted efficacy more often than the standard protocol. Discordant predictions represented a smaller portion of efficacy predictions for sotalol than for the other drugs. Thus, in the ESVEM trial, the superior long-term follow-up observed in patients assigned to sotalol may have been an artifact of the stimulation protocol utilized by the ESVEM investigators.

Anti-Arrhythmia Agents↗
PubMed1996

Electrophysiologic characteristics, electropharmacologic responses and radiofrequency ablation in patients with decremental accessory pathway.

OBJECTIVES: This study sought to characterize the functional properties of decremental accessory atrioventricular (AV) pathways and to investigate their pharmacologic responses. BACKGROUND: Although decremental AV pathways associated with incessant reciprocating tachycardia have been studied extensively, information about the electrophysiologic characteristics and pharmacologic responses of anterograde and retrograde decremental AV pathways is limited. METHODS: Of 759 consecutive patients with accessory pathway-mediated tachyarrhythmia, 74 with decremental AV pathways were investigated (mean age 43 +/- 18 years). After baseline electrophysiologic study, the serial drugs adenosine, verapamil and procainamide were tested during atrial and ventricular pacing. Finally, radiofrequency catheter ablation was performed. RESULTS: Five patients had anterograde decremental conduction over the accessory pathway but had no retrograde conduction. Of the 64 patients with retrograde decremental conduction over the accessory pathway, anterograde conduction over the pathway was absent in 41 (64%), intermittent in 5 (8%) and nondecremental in 18 (28%). In the remaining five patients, anterograde and retrograde decremental conduction over the same pathway was found. The anterograde and retrograde conduction properties and extent of decrement did not differ between anterograde and retrograde decremental pathways. Posteroseptal pathways had the highest incidences of anterograde and retrograde decremental conduction. Intravenous adenosine, procainamide and verapamil caused conduction delay or block, or both, in 10 of 10, 10 of 10 and 4 of 10 of the anterograde and 20 of 20, 20 of 20 and 8 of 20 of the retrograde decremental pathways, respectively. All patients had successful ablation of the decremental pathways without complications. During the follow-up period of 31 +/- 19 months, only one patient experienced recurrence. CONCLUSIONS: Decremental accessory pathways usually had functionally distinct conduction characteristics in the anterograde and retrograde directions. Their pharmacologic responses suggested the heterogeneous mechanisms of decremental conduction.

Adenosine↗