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At least 1,423 records · Page 79Linked to original sources
PubMed1984

Shortening of ventriculoatrial conduction in patients with left-sided Kent bundles.

In six patients with electrophysiologic evidence of ventriculoatrial conduction through a left Kent bundle, we documented that programmed right ventricular stimuli falling within an interval of 60 to 160 msec from the end of the T wave propagated to the left atrium (distal coronary sinus unipolar lead) 10 to 20 msec earlier than the basic paced beats. This phenomenon could be reproduced 24 hours later in two patients, and it was abolished by procainamide and amiodarone in one instance. During this interval we were unable to induce reciprocating tachycardia. Our observations outline a new pattern in ventriculoatrial conduction in patients with left-sided Kent bundles. The findings suggest in addition, that (1) supernormal conduction may be responsible for the observed shortening in retrograde conduction and (2) this phenomenon does not facilitate induction of reciprocating tachycardia.

Adult↗
PubMed1987

Effects of intravenous N-acetylprocainamide on hemodynamics and left ventricular function in man.

N-acetylprocainamide (NAPA) is the active metabolite of procainamide currently undergoing evaluation for its antiarrhythmic properties. Its effects on hemodynamic variables and on ventricular function in man are poorly defined. The effects of intravenously administered NAPA (18 mg/kg over 30 minutes; mean plasma level 40.2 +/- 6.2 micrograms/ml) on hemodynamics and left ventricular ejection fraction (LVEF) assessed by radionuclide ventriculography were therefore determined in 14 patients undergoing diagnostic cardiac catheterization. The peak effects of the drug with respect to most measured variables were seen at 30 minutes and were still apparent at 60 minutes. NAPA increased heart rate (3% at 10 minutes; p less than 0.01), decreased mean pulmonary arterial pressure (14%; p less than 0.05) and capillary wedge pressure (27%; p less than 0.01), decreased mean arterial pressure (12%; p less than 0.01), cardiac index (8%; p less than 0.01), LV dp/dtmax (9%; p less than 0.05), and stroke work index (17%; p less than 0.01). The LVEF increased 5% (p less than 0.05). There was a trend for the systemic vascular resistance to decrease, but this did not reach statistical significance. The data show that NAPA exerts relatively weak peripheral arteriolar and venodilator effects associated with a mild reduction in contractility and cardiac output but an increase in LVEF in patients with preserved ventricular function.

Acecainide↗
PubMed1987

The antiarrhythmic effects of d-sotalol.

The antiarrhythmic properties of d-sotalol were studied in 38 patients undergoing electrophysiologic studies. Programmed electrical stimulation studies were performed in 28 men and in 10 women with a mean age of 67 years and a mean ejection fraction of 37 +/- 3%. All patients had inducible ventricular tachycardia while they were off all antiarrhythmic therapy. D-sotalol was given as a 2 mg/kg infusion over 15 minutes and did not significantly change the PR, QRS, or QTc intervals from baseline values in the group as a whole. In the group protected by d-sotalol, the percent change in the QTc interval as well as the percent change in refractoriness was significantly increased as compared to the group not protected. D-sotalol also significantly decreased heart rate. D-sotalol prevented the induction of ventricular tachycardia in 18 of the 38 patients, while significantly slowing the rate of the ventricular tachycardia in the group that could still have tachycardia provoked. Seventeen patients were tested on procainamide and only four were protected, while d-sotalol prevented the induction of ventricular tachycardia in 7 of these 17. Eleven patients were discharged on oral d-sotalol doses ranging from 100 to 400 mg twice daily. One patient died 1 month post discharge due to an acute myocardial infarction, and one patient had a cardiac arrest while on d-sotalol and survived and was switched to amiodarone therapy. The remaining nine patients are alive and well at 14 +/- 3 months. D-sotalol appears to be an effective antiarrhythmic drugs and appears to be well tolerated.

Administration, Oral↗
PubMed1989

QRS morphology-dependent, concordant frequency distribution of single and repetitive forms of ventricular ectopic activity.

We tested the relationship between the frequency of single premature ventricular complexes (PVCs) of specific QRS morphologies and repetitive forms (RF) of greater than or equal to 2 PVCs. Fourteen patients with multiform PVCs and RFs underwent 8-hour, two-channel continuous electrocardiographic monitoring. After a 2-hour baseline, procainamide was administered intravenously at 25 mg/min until PVC suppression or 1000 mg. Multiple regression analysis was used to relate the frequencies of repetitive forms initiated by PVCs of the most frequent QRS morphology (M1) and the second most frequent QRS morphology (M2) to the frequency of M1 and M2 single PVCs. Parallel changes in the frequency of M1 RFs and M1 PVCs occurred in 9 of 14 patients and parallel changes in the frequency of M2 RFs and M2 PVCs occurred in 7 of 14 patients (i.e., the relationships were concordant). In two patients, M1 RFs related to M2 PVC frequency; in three patients, M2 RFs related to M1 PVC frequency (i.e., the relationships were discordant). Thus concordant frequency distributions were present in 16 of 28 (57%) comparisons, while a discordant relationship occurred in only 5 of 28 (18%) comparisons (p less than 0.005). In conclusion, there is frequent concordance in the frequency distribution of single multiform PVCs and of RFs initiated by PVCs of the same QRS morphology during a pharmacologic intervention.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Complexes, Premature↗
PubMed1990

The role of beta-blockade therapy for ventricular tachycardia induced with isoproterenol: a prospective analysis.

Isoproterenol is sometimes required for ventricular tachycardia (VT) induction. However, the role of beta-blockade for treatment of such VT has not been critically assessed. The use of beta-blockade was evaluated prospectively in 14 consecutive patients who required isoproterenol 2.4 +/- 1.3 (+/- S.D.) micrograms/min to induce sustained monomorphic VT (greater than 30 seconds, or requiring termination due to hemodynamic collapse) after a negative baseline study. The VT mechanisms were enhanced automaticity (group A, six patients), triggered automaticity (group B, three patients), and reentry (group C, five patients). Groups A and B had serial intravenous electropharmacologic tests with propranolol alone (0.2 mg/kg), verapamil alone (0.15 mg/kg), and propranolol plus verapamil, and group C had serial tests with propranolol alone, procainamide or quinidine (class Ia drug) alone, and propranolol plus a class Ia drug until VT could no longer be induced. All six patients in group A responded to propranolol alone. In group B, one patient responded to verapamil alone, and two patients responded to propranolol plus verapamil. In group C, three patients responded to propranolol alone, one patient responded to a class Ia drug alone, and one patient responded to propranolol plus a class Ia drug. During a follow-up of 7 to 37 (17.9 +/- 10.7) (+/- S.D.) months, VT has not recurred in any patient. Three patients treated initially with propranolol alone have required substitution of amiodarone due to refractory congestive heart failure. In patients requiring isoproterenol for VT induction, beta-blockade alone appears to be effective in preventing reinduction of VT caused by enhanced automaticity. A heterogeneous response occurs when the VT mechanisms are triggered automaticity or reentry.

Adolescent↗
PubMed1993

Evidence for a reexcitability gap in man after treatment with type I antiarrhythmic drugs.

The intention of this study was to determine whether type IA antiarrhythmic drugs cause a disparity between refractoriness and repolarization, and if so, its magnitude. We simultaneously measured monophasic action potential duration (MAPD) and effective refractory period (ERP) at a right ventricular site in 11 patients without overt right ventricular disease. The pacing protocol, which included sinus rhythm and a 600 and 400 msec cycle length of ventricular drive, was performed at baseline and after the intravenous administration of 15 mg/kg of procainamide in nine patients, and of 10 mg/kg of quinidine in two patients. Despite trivial changes in sinus rates, drug therapy caused a 10% to 17% increase in MAPD and ERP that shortened with decreasing drive cycle lengths. At baseline there was a small gap (10 to 13 msec) between MAPD and ERP in sinus rhythm and with a 600 or 400 msec drive. However, the type IA drug caused a significant widening of this gap that was most profound in sinus rhythm (45 msec) and that shortened but was not abolished with a 600 and 400 msec drive (28 and 29 msec, respectively). The disparity was caused in one third of cases by postrepolarization refractoriness. Type I drugs increase the difference between repolarization and refractoriness, and this effect is partially reversed with increases in heart rate. The clinical implications of these findings are discussed.

Action Potentials↗
PubMed1975

Pharmacologic therapy of ventricular arrhythmias.

To treat patients with ventricular arrhythmias properly, one must characterize the arrhythmia, define the underlying heart disease and look for and treat reversible causes. When arrhythmias are suitable for pharmacologic suppression, it is necessary to predefine therapeutic goals, then carefully document that the drug accomplishes these goals. Knowledge of a drug's metabolism, excretion, active metabolites and plasma protein binding is often required for full understanding of its clinical effect. Pharmacokinetic principles require that antiarrhythmic drugs be given on a rigid schedule and that plasma drug levels be frequently determined. Use of compartment models and the principle of superposition can enable one to achieve and maintain therapeutic drug concentrations while avoiding toxic side effects. The drugs commonly used to treat arrhythmias, lidocaine, propranolol, procainamide, diphenylhydantoin and quinidine, as well as some newer agents, have specific pharmacokinetics and toxic effects that must be understood.

Anti-Arrhythmia Agents↗
PubMed1978

Pharmacokinetics of antiarrhythmic drugs.

A knowledge of the determinants of the plasma concentrations of antiarrhythmic drugs is important because variation in plasma levels is often greater than the desired therapeutic range. The basic principles of pharmacokinetics are outlined and their application to the design of dosage regimens described. These principles are illustrated in a review of the pharmacokinetics of lidocaine and its congeners, procainamide and its active metabolite (N-acetylprocainamide), quindine, disopyramide, phenytoin and propranolol, with particular emphasis of the factors that contribute to altered disposition.

Administration, Oral↗
PubMed1980

Effect of drugs in the Wolff-Parkinson-White syndrome. Importance of initial length of effective refractory period of the accessory pathway.

The effect of procainamide, quinidine, ajmaline and amiodarone on the effective refractory period of the accessory pathway in the (A-V) anterograde and retrograde directions was studied in relation to the length of this period before drug administration. All patients had the Wolff-Parkinson-White syndrome and were studied with intracavitary recordings and programmed electrical stimulation of the heart using identical basic cycle lengths and test stimulus intervals before and after drug administration. The patients were separated into two groups, those in whom the effective refractory period of the accessory pathway was 270 ms or greater (Group 1) and those in whom it was less than 270 (Group 2). In the anterograde direction the magnitude of increase in the length of the effective refractory period of the accessory pathway after drug administration was related to its initial length. Only modest lengthening of this period could be accomplished in patients with an initially short period. In evaluating the effect of drugs in patients with the Wolff-Parkinson-White syndrome, the role of the initial length of the effective refractory period of the accessory pathway should be considered.

Accessory Nerve↗
PubMed1981

Electrophysiologic effects of N-acetylprocainamide in human beings.

The electrophysiologic properties of N-acetylprocainamide (NAPA) were studied in 10 patients undergoing cardiac catheterization. Each patient received two successive intravenous infusions: one loading infusion over 15 minutes and one maintenance infusion at a slower rate for 30 minutes. Eight patients received 10.5 mg/kg body weight and two received larger doses (16 and 21 mg/kg, respectively). NAPA plasma concentration was measured at 5 minute intervals from 0 to 25 minutes, and then at 15 and 30 minutes of the second infusion. Mean blood pressure and electrophysiologic data obtained by programmed stimulation were recorded before drug administration and at 15 and 30 minutes of the infusion when the concentration of NAPA was nearly constant in each patient (range 12 to 35 microgram/ml). NAPA decreased blood pressure (p less than 0.005), increased corrected Q-T interval (p less than 0.01) and increased the atrial and ventricular effective refractory periods from 267 +/- 40 to 307 +/- 41 ms (p less than 0.01) and from 278 +/- 37 to 301 +/- 32.8 ms (p less than 0.05), respectively. NAPA did not significantly change sinus cycle length or sinus nodal recovery time, conduction intervals (A-H, H-V, P-R, QRS), atrioventricular nodal functional refractory period or nodal Wenckebach cycle length. The patient receiving the largest dose experienced mild nausea when the plasma concentration was above 35 microgram/ml. These data show that the electrophysiology of NAPA in human beings is different from that reported for procainamide. At the plasma concentrations studied NAPA increases atrial and ventricular refractory periods without increasing cardiac conduction times

Acecainide↗
PubMed1981

Clinical pharmacology and antiarrhythmic efficacy of N-acetylprocainamide.

Eleven patients with chronic ventricular arrhythmias took part in a study of N-acetylprocainamide (NAPA), the major metabolite of procainamide, in order to characterize further NAPA's clinical pharmacology and antiarrhythmic action. The frequency of ventricular arrhythmia on 24 hour ambulatory electrocardiographic recordings was comparable on recordings obtained in a prestudy screening, during treatment with placebo before administration of NAPA and after treatment with NAPA. The initial dosage of NAPA was 500 mg every 8 hours, which was increased by 500 mg increments every few days until 90 percent suppression of arrhythmia or intolerable adverse effects occurred. Only two patients achieved 90 percent suppression of ventricular ectopic complexes. The mean plasma concentration associated with 90 percent suppression of arrhythmia in these two patients ws 12.6 and 32.3 mg/ml, respectively. One of these two patients was unable to continue long-term therapy with NAPA because of a rash. Other adverse effects included gastrointestinal symptoms in seven patients with visual symptoms in four patients at plasma concentratons as low as 6.9 mg/ml. NAPA obeyed linear pharmacokinetics over the range of dosages studied (500 to 2,500 mg every 8 hours) and had a half-life of 10.7 +/- 1.98 hours (mean +/- standard deviation). There was no change in the P-R or QRS intervals and there was a dose-dependent prolongation of the Q-Tc interval. It is concluded that in this patient group, NAPA suppressed chronic ventricular ectopic complexes without adverse effects in only a minority of patients.

Acecainide↗
PubMed1981

Long-term antiarrhythmic therapy with acetylprocainamide.

Nineteen patients whose arrhythmias were initially suppressed with acetylprocainamide underwent long-term treatment with this drug. Eleven patients were still taking the drug at the end of 12 months. Drug withdrawal with substitution of a placebo caused an increase in ventricular premature beats. Thus, suppression of ventricular premature beats persisted for 1 year. The eight withdrawals from the study were due to death during the year (n = 6) or recurrence of arrhythmias. The deaths occurred in patients who were in New York Heart Association functional class II (one patient), III (three patients) and IV (two patients). Ventricular performance, assessed from systolic time intervals, improved with drug therapy and declined during drug withdrawal. Symptomatic effects were common, with seven patients requiring a reduction in dosage or discontinuation of therapy. Three patients treated for 3 years continued to show drug suppression of ventricular premature beats compared with the level during placebo substitution. Small amounts of procainamide were present in all patients because of in vivo deacetylation of acetylprocainamide. Many patients with good initial responses to this drug had recurrent arrhythmias during long-term therapy. For this reason, the usefulness of acetylprocainamide as an antiarrhythmic drug appears to be limited.

Acecainide↗
PubMed1983

Importance of metabolites in antiarrhythmic therapy.

The presence of metabolites with pharmacologic activity can produce unanticipated drug efficacy or toxicity. This is particularly true during treatment with drugs that have narrow therapeutic-toxic ratios, such as the antiarrhythmic agents. The presence of active metabolites can often be inferred from variability in the relation between pharmacologic effect and steady-state plasma concentrations of the parent drug. Moreover, metabolites may ordinarily be unimportant but can accumulate to therapeutic (or toxic) levels in disease states such as congestive heart failure, renal failure and hepatic failure. Further characterization of the contribution of such metabolites during treatment requires direct evaluation of their pharmacology in vitro, in animal models and, if indicated, in man. Procainamide and its active metabolite N-acetylprocainamide provide the best and most complete example of this sequence of observations. Other drugs, including quinidine, disopyramide, verapamil and the investigational agents encainide and lorcainide, have active metabolites for which pharmacologic activity is less well-defined. Further studies in this area will help reduce the frequency of antiarrhythmic drug adverse effects, make successful therapy more frequent, and perhaps allow insights into structure-activity relations.

Acecainide↗
PubMed1983

Hemodynamic effects of antiarrhythmic drugs.

In order to use antiarrhythmic drugs safely, one must understand their hemodynamic effects. Quinidine and the calcium antagonists have direct cardiac effects and frequently opposing autonomically mediated or indirect cardiac effects. Lidocaine is exceptionally well tolerated, even by patients with severe left ventricular dysfunction. Phenytoin and procainamide have the potential for serious adverse effects, but are generally well tolerated at usual doses. Disopyramide causes serious depression of left ventricular function in many patients because of its direct myocardial depressant and peripheral vasoconstricting actions. Although bretylium causes an immediate increase in contractility, it can ultimately result in important hypotension. In this review the in vitro and in vivo hemodynamic effects of these and other antiarrhythmic drugs are discussed to provide information that will assist the clinician in using these drugs properly.

Amiodarone↗
PubMed1984

Magnesium therapy for torsades de pointes.

This is the first report of the successful use of magnesium sulfate (MgSO4) in 3 consecutive patients with torsades de pointes (TdP). In 1 patient, TdP was induced by a combination of quinidine and amiodarone, in the second by procainamide, and in the third by an overdose of imipramine. The QT intervals before TdP were 0.70, 0.64 and 0.56 second, respectively. A bolus of 1.0 to 2.0 g MgSO4 25% abolished the TdP in all 3 patients; but in the third patient, because of recurrent TdP, a second bolus of 1.0 g and a continuous 24-hour infusion of 1.0 mg/min were administered, preventing TdP. There was no immediate shortening in the QT interval in any patient after MgSO4. Magnesium can be given safely even in patients with acute myocardial infarction, angina pectoris or systemic hypertension, conditions in which isoproterenol is contraindicated; it can be applied faster than temporary cardiac pacing; and its use for TdP appears worthy of additional trials.

Aged↗
PubMed1984

Antiarrhythmic and electrophysiologic actions of flecainide in animal models.

The results of antiarrhythmic testing in a variety of animal models indicate that flecainide acetate has potent antiarrhythmic activity. In these models it is more potent than lidocaine, procainamide and quinidine, as well as a number of investigational agents, and is active against both ventricular and supraventricular arrhythmias from a number of causes. Studies of its effects on the action potential from various cardiac tissues indicate that its primary effect is to slow the rate of rise of the action potential, placing it among the group of drugs commonly referred to as class I agents. In the intact animal, in accordance with its effects on the action potential, flecainide slows conduction throughout the cardiac conduction system, with the most marked effects on His-Purkinje conduction and ventricular activation.

Action Potentials↗
PubMed1984

Management of ventricular dysrhythmias in the prehospital and emergency department setting.

Each year approximately 1,500,000 people experience acute myocardial infarction. About 40% of them die, half before they reach the hospital. Ventricular fibrillation (VF) is a major cause of cardiac arrest, and delay in administering antiarrhythmic agents contributes to the incidence of out-of-hospital deaths. The 3 antiarrhythmic drugs currently used by paramedics for cardiac arrest are bretylium, lidocaine, and procainamide. The early use of bretylium tosylate is stressed in Advanced Cardiac Life Support protocols because of the agent's antifibrillatory properties, that is, its ability to increase the VF threshold and to block reentry. Evidence indicates that early, aggressive use of bretylium tosylate as a first-line agent improves the likelihood of successful resuscitation. Preliminary data are presented from an ongoing comparative study of prehospital use of bretylium tosylate and lidocaine for VF. One hundred seventeen cardiac arrests have occurred, 55 of which were associated with VF and are included in the study. Resuscitation was not attempted in 3 of the 55 patients at the request of the family and physician. Of the remaining 52 patients, 17 received bretylium tosylate plus lidocaine, 12 lidocaine alone, and 7 only bretylium tosylate. There were 16 patients who did not receive medications. According to the study protocol, the choice of antiarrhythmic agents was determined by the paramedic shift during which arrest occurred. Of the 52 patients treated, 16 (30%) survived. It is too soon to draw any conclusions.

Arrhythmias, Cardiac↗
PubMed1985

Efficacy of combination therapy with mexiletine and a type IA agent for inducible ventricular tachyarrhythmias secondary to coronary artery disease.

The efficacy of combination therapy using a type IA agent (quinidine or procainamide) and a type IB agent (mexiletine) in suppressing inducible sustained ventricular tachyarrhythmias was studied in 23 patients undergoing serial drug testing with programmed stimulation. All patients had coronary artery disease (CAD) with previous myocardial infarction and abnormal left ventricular function (mean ejection fraction 35%). Fifty-five percent of the patients presented with syncope or cardiac arrest. In 19 patients therapy had failed during empiric trials of 1 to 3 antiarrhythmic agents. All 23 patients had inducible sustained ventricular tachyarrhythmias (18 had uniform morphology sustained ventricular tachycardia (VT) and 5 had ventricular fibrillation [VF]) during control electrophysiologic study, and therapy had failed with a type IA agent and mexiletine alone. The combination therapy of mexiletine and the type IA agent prevented induction of any ventricular tachyarrhythmias in 8 of 23 patients. In 15 patients, the combination significantly prolonged the tachycardia cycle length and reduced the symptoms associated with the induced arrhythmia. Patients more likely to respond to the combination had shorter cycle lengths and polymorphic configuration of the control-induced arrhythmia. The increased efficacy of the combination therapy could not be attributed to higher plasma drug levels for the combination, as there was no significant difference in plasma levels for each drug when given alone or in combination. Thus, the increased efficacy most likely reflects a synergistic electropharmacologic effect of the 2 agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗