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PubMed1988

Enhanced efficacy of oral sotalol for sustained ventricular tachycardia refractory to type I antiarrhythmic drugs.

Sotalol is a nonselective beta-adrenergic blocking agent with Vaughn-Williams class III activity. Its efficacy was tested in 9 patients with sustained ventricular tachycardia (VT) that had previously remained inducible during electrophysiologic testing of type I drugs (procainamide or quinidine). Eight patients had coronary artery disease with remote myocardial infarction and 1 had cardiomyopathy (ejection fraction 0.34 +/- 0.08, mean +/- standard deviation). Type I drugs prolonged the effective refractory period of the right ventricle 12 +/- 14% and prolonged the VT cycle length 41 +/- 24%. In contrast, despite an equivalent effect on the effective refractory period, a sustained VT could no longer be initiated in any of the 8 patients ultimately tested while taking oral sotalol. Daily doses averaged 600 +/- 103 mg and blood levels associated with VT suppression in electrophysiologic studies were generally greater than 3,000 ng/ml. In addition, sotalol was moderately effective at reducing ventricular ectopic activity measured by ambulatory electrocardiography. Over a mean follow-up of 23 months (range 1 to 37), mild heart failure (3 patients), symptomatic brady-cardia requiring pacemaker (1) and drug-related polymorphous VT (1) have occurred. Sudden death occurred in 1 patient and nonfatal VT recurrence was noted in 2. Five of 8 chronically treated patients currently are successfully treated with minimal side effects. Sotalol appears to be a promising antiarrhythmic drug in the treatment of serious ventricular arrhythmias, even in patients refractory to type I antiarrhythmic agents.

Administration, Oral↗
PubMed1989

Effect of selective intracoronary antiarrhythmic drug administration in sustained ventricular tachycardia.

The effect of selective intracoronary antiarrhythmic drug infusion on inducibility of cardiac arrhythmias was studied in 3 patients with recurrent sustained monomorphic ventricular tachycardia referred for comprehensive electrophysiologic studies. Each patient had evidence of prior myocardial infarction, 1 or more occluded coronary arteries and a readily identifiable collateral vessel that provided collateral flow to the infarct-related artery. In each patient, the clinical arrhythmia was reproducibly inducible by programmed stimulation in the control state. After positioning a small infusion catheter in the collateral vessel, selective intracoronary lidocaine 0.3 to 0.6 mg/min (patients 1 and 2) or procainamide 0.1 to 1.4 mg/min (patient 3) was infused for a 10-minute period. In each patient the clinical arrhythmia was rendered noninducible during selective intracoronary drug infusion. The arrhythmia was again inducible after a 10-minute drug-washout period and also after standard intravenous doses of antiarrhythmic drug. Selective intracoronary antiarrhythmic drug infusion may help to localize the site of origin of some cardiac arrhythmias, may provide a means of testing the effects of several drugs during a single study and may be a new method for studying mechanisms of action of antiarrhythmic drugs.

Angiography↗
PubMed1975

Idiopathic ventricular tachycardia. An intracardiac electrical, hemodynamic and angiographic assessment of six patients.

Six patients with idiopathic paroxysmal ventricular tachycardia were investigated by external electrocardiography, intracardiac electrography and pacing, exercise testing, cardiac catheterization and coronary angiography. All had normal hemodynamics and coronary arteries. His bundle electrography proved ventricular origin in five; one had no paroxysmal ventricular tachycardia during His bundle electrography. Treatment with diphenylhydantoin, 4.2 to 8.0 mg/kg/day, and propranolol, 0.8 to 2.7 mg/kg/day, appeared effective, well tolerated therapy in three, and procainamide and propranolol in one requiring medical treatment. Abstinence from tobacco and coffee abolished paroxysmal ventricular tachycardia in one of two who required no medication. The other has no recurrence of paroxysmal ventricular tachycardia since study.

Adult↗
PubMed1975

Cardiac conduction in myotonic dystrophy.

Cardiac conduction abnormalities are frequent in myotonic dystrophy and can result in complete heart block. In a study of 26 patients with myotonic dystrophy, first degree heart block was found to precede clinical presentation of the disease in 7 patients. His bundle electrocardiography in 11 patients demonstrated abnormalities throughout the entire conducting system, even in patients with only first degree heart block. In patients with block of the right bundle branch or anterior fascicle of the left bundle branch, slowing in the remaining fascicles was always present. Therapy of myotonia with procainamide significantly lengthened the P-R interval, and treatment with diphenylhydantoin significantly shortened the P-R interval suggesting that diphenylhydantoin may be preferable for therapy of myotonia in patients with myotonic dystrophy.

Adolescent↗
PubMed1977

Active drug metabolites and renal failure.

Drugs that are administered to man may be biotransformed to yield metabolites that are pharmacologically active. These metabolites may accumulate in patients with end-stage renal disease if renal excretion is a major elimination pathway for the metabolite. This is true even if the active metabolite is a minor metabolite of the parent drug as long as the minor metabolite is not further biotransformed but is mainly excreted in the urine. Minor metabolite accumulation may also occur if it is further biotransformed by a pathway that is inhibited in uremia. Some clinical consequences of accumulation of the active drug metabolites of procainamide, meperidine, clofibrate, allopurinol, sulfadiazine and nitrofurantoin in patients with renal failure are discussed. The high incidence of adverse drug reactions seen in renal failure may be explained, in part, by the accumulation of active drug metabolites. Examples of active drug metabolites that do not accumulate in patients with renal failure because of further biotransformations are also included.

Acetylation↗
PubMed1984

Long-term antiarrhythmic therapy. Problem of low drug levels and patient noncompliance.

Maintenance of adequate serum blood levels is crucial to successful antiarrhythmic therapy. Serum levels of four antiarrhythmic agents (long-acting procainamide, quinidine sulfate, quinidine gluconate, and disopyramide) were determined in 98 consecutive ambulatory patients receiving long-term oral therapy. Medication dosages, dosing intervals, and time elapsed from last dosage until blood sampling were determined. Seventy-five patients (76.5 percent) had subtherapeutic blood levels (with mean levels less than 50 percent of the suggested minimum), and only 22 patients (22.5 percent) had therapeutic levels. Even among the 61 patients who claimed to have taken their medications within the six hours prior to blood sampling, 43 (70 percent) had subtherapeutic levels. These ratios held among all subgroups studied. Physicians should be aware of the high proportion of patients receiving long-term oral antiarrhythmic therapy with inadequate serum blood levels when planning therapeutic regimens.

Adult↗
PubMed1982

Further studies on F1-ATPase inhibition by local anesthetics.

We have measured the inhibitory potencies of several local anesthetics (procaine, lidocaine, tetracaine and dibucaine) and related compounds (chlorpromazine, procainamide and propranolol) on the ATPase activities of bovine heart submitochondrial particles and purified F1 extracted from these particles. All of these agents cause inhibition of ATPase in F1 as well as in submitochondrial particles. A linear relationship is found between the log of the octanol/water partition coefficients and the log of the concentrations required for 50% inhibition of F1. Sedimentation velocity ultracentrifugation and polyacrylamide gel electrophoresis showed that 1.0 mM tetracaine caused partial dissociation of the F1 complex. Complete reversibility of the enzyme inhibitory effects was demonstrated, however. This work shows that local anesthetics can affect protein structure and enzyme activity without the mediation of lipid.

Adenosine Triphosphatases↗
PubMed1992

Immunomodulation and drug acetylation: influence of the immunomodulator tilorone on hepatic, renal and blood N-acetyltransferase activity and on hepatic cytosolic acetyl coenzyme A content.

The biochemical alteration responsible for immunomodulator enhancement of drug acetylation in vivo was probed ex vivo and in vitro in the rat. Rat liver or kidney cytosol, obtained by differential centrifugation, or whole blood served as the source of N-acetyltransferase (NAT). Addition of tilorone (0.5-8.0 mM) to incubation mixtures containing procainamide (PA, 0.6 mM) and acetyl coenzyme A (AcCoA, 0.42 mM) resulted in the inhibition of N-acetylprocainamide formation, while lower concentrations of tilorone had no effect. Pretreatment of rats with tilorone (50 mg/kg) administered orally 48 hr prior to sacrifice did not alter hepatic apparent Km and Vmax for NAT toward PA compared to control animals. Utilization of an AcCoA regenerating system in the incubation mixtures also resulted in no significant differences in the apparent Michaelis-Menten parameters obtained. Acetylation activity in kidney and whole blood also was not altered by immunomodulator pretreatment. Hepatic cytosolic AcCoA content was reduced significantly 48 hr after tilorone pretreatment (5.10 +/- 2.1 vs 11.97 +/- 2.2 nmol/mg protein) (P less than 0.05). These data indicate that an increase in NAT content or activity is not the biochemical alteration responsible for immunomodulator enhancement of drug acetylation, and that the required cofactor, cytosolic AcCoA, is decreased by immunomodulator pretreatment.

Acetyl Coenzyme A↗
PubMed1980

The effects of substituted benzamides on frog rectus abdominis.

The substituted benzamides metoclopramide, bromopride, tiapride and sulpiride (10(-5) and 10(-4) M) significantly increased the sensitivity of frog rectus abdominis muscle to exogenous acetylcholine but not to carbachol. This supersensitivity could be correlated with the anticholinesterase activity of these drugs measured in homogenates from frog skeletal muscle. Sultopride, like procainamide, has only inhibitory effects on the responses of the rectus abdominis to acetylcholine and has no anticholinesterase activity in this preparation.

Amisulpride↗
PubMedDate not supplied

Myasthenia gravis by another name: an elusive imposter.

A patient with procainamide-induced "pseudo" myasthenia gravis is presented. This clinical entity is discussed in terms of its clinical features, diagnosis, and treatment. Attention is directed to the importance of role of the ophthalmologist in making the diagnosis.

Diagnosis, Differential↗
PubMed1985

Quinidine induced lupus syndrome.

Five patients with a lupus-like syndrome secondary to quinidine are described. Eleven other cases have previously been reported. The quinidine induced lupus syndrome is similar to that seen with procainamide and hydralazine treatment but occurs less frequently. The lower incidence may reflect a difference in the metabolism of quinidine. Quinidine should be considered as potentially responsible when multisystem disease appears in patients receiving this drug.

Aged↗
PubMed1984

The genesis of bifid T waves: experimental demonstration in isolated perfused rabbit hearts.

In an attempt to elucidate the genesis of bifid T waves, we recorded transmembrane potentials of subepicardial ventricular muscle fibers simultaneously with a bipolar ventricular electrogram in isolated, perfused rabbit hearts, and the timing of the two apices of the T wave (aT1, aT2) was correlated with ventricular repolarization. The following results were obtained. (1) In seven of the nine hearts in which the repolarization process was mapped on the anterior and posterior surfaces of both ventricles, the 80% repolarization times of the left and the right ventricles were scattered around aT1 and aT2, respectively, and their average values closely corresponded to Q-aT1 and Q-aT2 intervals. This suggested that aT1 and aT2 depended on repolarization of the left and the right ventricles, respectively. (2) In one heart, aT1 appeared to reflect repolarization of the posterior ventricular wall, and aT2 that of the anterior wall. (3) In the remaining heart, aT2 coincided with repolarization of the anterobasal portion of the right ventricle, and aT1 that of the remaining portions of the ventricles. Even when ventricular repolarization was modified by low K+, low Ca2+ or procainamide perfusion, or by premature atrial stimulation, the close temporal correlation of the left and right ventricular repolarization with the two apices of the T wave was maintained. Selective cooling of the perfusate in either the left or the right coronary artery resulted in the production of bifid T waves in which aT2 coincided with the delayed repolarization of the cooled ventricle. We conclude that either physiologically or pathologically delayed repolarization in certain portions of the ventricles is most likely the cause of bifid T waves.

Action Potentials↗
PubMed1988

Ectopic automatic atrial tachycardia in children: clinical characteristics, management and follow-up.

Ectopic automatic atrial tachycardia, an uncommon type of supraventricular tachycardia in children and adults, has been reported to be resistant to medical therapy, and surgical or cryoblation has been recommended. This report describes 10 infants and children (median age 6 months; range birth to 7.5 years) with automatic atrial tachycardia and their management and follow-up. Digoxin alone was unsuccessful in controlling tachycardia in all 10 patients but decreased the tachycardia rate by 5 to 20% in 8. Intravenous (0.1 mg/kg body weight per dose) and oral propranolol successfully suppressed tachycardia in three of five patients and oral propranolol successfully controlled tachycardia in two of five other patients. Class I antiarrhythmic agents--quinidine (three patients), procainamide (four patients) and phenytoin (three patients)--did not control tachycardia in any patients but made the tachycardia rate worse in three patients. Intravenous (5 mg/kg per dose) and oral amiodarone suppressed tachycardia in three of four patients and oral amiodarone suppressed it in another patient. Thus, intravenous propranolol and amiodarone were effective in acutely suppressing automatic ectopic atrial tachycardia and predicted the response to long-term oral therapy. One patient had persistent tachycardia after surgical ablation of the high right atrial ectopic focus, and another patient had unsuccessful catheter ablation of the high right atrial ectopic focus (25 J). During follow-up (10 to 28 months), ectopic atrial tachycardia resolved completely in four patients and was well controlled in four patients.

Administration, Oral↗
PubMed2005

Selective use of amiodarone and early cardioversion for postoperative atrial fibrillation.

BACKGROUND: Postoperative atrial fibrillation (AF) occurs in 20%-40% of patients undergoing open-heart surgery. Numerous pharmacological and electrical therapies have been used as a prophylaxis to prevent this dysrhythmia. The purpose of this study was to examine the selective use of amiodarone and early cardioversion (CVN) postoperatively to restore normal sinus rhythm (NSR). METHODS: A retrospective nonrandomized review of patients who received amiodarone and early electrical CVN (study group) for postoperative AF after coronary artery bypass grafting (CABG) were compared with patients who received nonamiodarone therapies (control group). The study group received 150 mg of amiodarone bolus intravenously and thereafter received an infusion of 1 g over a 24-hour period. If NSR was established within 24 hours, then the intravenous (IV) infusion was continued for another 24 hours with concomitant oral amiodarone overlap. If NSR was not established within 24 hours, then external electrical CVN was performed. After 48 hours, the IV infusion was discontinued and the oral regimen maintained through discharge. Control group patients received either combination digoxin and procainamide or diltiazem. Postoperative beta-blocker administration was instituted in all patients. RESULTS: Six-hundred forty consecutive CABG patients were examined between July 1995 and June 2003. Postoperative AF developed in 160 of these patients (25%). One-hundred patients constituted the study group and 60 patients represented the control group. Restoration of NSR within 24 and 48 hours occurred in 79 (79%) and 90 patients (90%) for the study group, respectively, compared with 38 (64%) and 44 patients (73%) for the control group, respectively. The presence of NSR at discharge was achieved in 98 study patients (98%) and 50 control patients (83%). The length of stay (LOS) for the study and control patients was 7.4 and 9.1 days, respectively. There was no mortality in either group. CONCLUSIONS: Amiodarone and early CVN was more effective than nonamiodarone therapies with regard to restoring NSR for patients in whom AF developed after elective CABG. A trend toward a decrease in LOS was observed in the study group, but was not statistically significant. The overall LOS using amiodarone therapy with early CVN was similar to postoperative AF for patients in whom the condition did not develop.

Administration, Oral↗
PubMed2004

Role of sodium and calcium channel block in unmasking the Brugada syndrome.

OBJECTIVE: We hypothesized that a combination of I(Na) and I(Ca) blockade may be more effective in causing loss of the epicardial action potential (AP) dome and precipitating the Brugada syndrome (BS). The present study was designed to test this hypothesis in an in vitro model of BS. BACKGROUND: The Brugada syndrome is characterized by an ST segment elevation in the right precordial ECG leads and a high risk of sudden death. The ECG sign of BS is often concealed, but can be unmasked with potent sodium channel blockers. Using canine right ventricular (RV) wedge preparations, we previously developed an experimental model of BS using flecainide to depress the AP dome in RV epicardium. METHODS: Intracellular APs and a transmural ECG were simultaneously recorded from canine RV wedge preparations. RESULTS: Terfenadine (5-10 microM)-induced block of I(Ca) and I(Na) caused heterogeneous loss of the epicardial AP dome, resulting in ST segment elevation, phase 2 reentry (12/16), and spontaneous polymorphic VT/VF (6/16). Flecainide (</=7.5 microM), ajmaline (</=20 microM), and procainamide (</=300 microM) failed to generate polymorphic VT in any preparation except when combined with a calcium channel blocker (verapamil, </=20 microM). Terfenadine-induced ST segment elevation was normalized and arrhythmias suppressed following I(to) block with 4-aminopyridine (0.5-2 mM). CONCLUSION: Our data suggest that combined sodium and calcium channel block may be more effective than sodium channel block alone in unmasking the Brugada syndrome and that pharmacologic agents that inhibit I(to) may be useful in preventing lethal arrhythmias in patients with the syndrome.

Ajmaline↗
PubMed2006

Isolated perfused and paced guinea pig heart to test for drug-induced changes of the QT interval.

INTRODUCTION: One of the biomarkers for assessing the risk of a cardiac adverse event is drug-induced prolongation of the QT interval. A model is needed for evaluating the potential liability of test compounds on QT interval in vitro. Since QT intervals can be generated from paced or spontaneously beating hearts, data so generated can also be used for validating QT(c) correction equations. METHODS: Isolated guinea pig hearts were perfused in Locke's solution according to the Langendorff method. QT intervals were routinely measured from Lead II ECG waveforms. RESULTS: Compounds known to inhibit HERG channel, such as dofetilide, prolonged the QT interval in this model. (+/-)Bay K8644, a calcium channel activator, prolonged the QT interval, while verapamil, a calcium channel blocker, shortened it. Procainamide, a sodium channel blocker, also prolonged the QT interval. Many of the compounds, which prolonged the QT interval, also prolonged PR interval, suggesting dual inhibition of the Ikr channel, the rapid component of delayed rectifier potassium channel, and the calcium channel. The QT/RR intervals exhibited a curvilinear relationship, which could be corrected into nearly straight horizontal lines by using correction equations derived from linear, parabolic, and hyperbolic models. However, these correction equations yielded different results on the QT prolongation produced by sotalol, which also slowed down the heart rate. With the data set obtained in this investigation, correction equations derived from linear and parabolic models worked better than the equations derived from the hyperbolic model. The exponential model did not fit at all. CONCLUSION: QT intervals obtained under paced conditions provide the most direct and reliable QT information for a drug. The isolated perfused and paced guinea pig heart is a convenient model for studying the effect of compounds on QT interval in vitro.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1990

Inducible monomorphic sustained ventricular tachycardia in the conscious pig.

Sustained monomorphic ventricular tachycardia (VT) is of clinical importance but has not been readily modeled in conscious animals. Eleven pigs had myocardial infarction induced by pulling snares previously placed around the left anterior descending (LAD) coronary artery. Six days after occlusion, bipolar pacing catheters were inserted in the right ventricular apex for induction of VT. Testing was repeated in conscious pigs on 6 out of 8 to 19 days after infarction. Monomorphic VT was induced in each animal during each session, using three to four extrastimuli. VT was terminated by burst pacing in 74% of trials; average VT rate was 362 +/- 26 beats/min. VT was prevented in four of eight animals by procainamide and in five of eight animals by magnesium, but was not prevented by lidocaine or metoprolol. The model may be useful in the study of potentially malignant ventricular tachyarrhythmias, important prodromes for sudden death.

Animals↗
PubMed1998

Clinical and echocardiographic features influencing recovery of atrial function after cardioversion of atrial fibrillation.

Atrial mechanical dysfunction after cardioversion for atrial fibrillation has been widely evaluated in recent years. Nevertheless, the influence of many clinical and echocardiographic parameters is not yet understood. The aim of the present study was to evaluate the influence of clinical and echocardiographic parameters on the return of effective atrial contraction. A total of 109 patients were evaluated: 41 patients had spontaneous recovery of sinus rhythm and 68 patients were randomly treated using either direct-current (DC) shock or intravenous procainamide. Elective cardioversion was accomplished pharmacologically in 23 patients (67%) and with DC shock in 29 patients (85%). Patients underwent a complete echocardiographic examination 1 hour after the restoration of sinus rhythm and after 1 and 7 days and 1 month. The following parameters were evaluated: patient age, cardiac disease, duration and etiology of atrial fibrillation, mode of cardioversion, left ventricular diameters and function, and left atrial diameter and function assessed as atrial ejection force. The relation between these variables and atrial ejection force was tested. Atrial ejection force was greater immediately and 24 hours after cardioversion in patients who had spontaneous recovery of sinus rhythm and in patients treated with drugs than in patients treated with DC shock. The mode of cardioversion was significantly associated with the recovery of atrial mechanical function by day 1 in univariate and multivariate analyses (odds ratio 0.14; 95% confidence interval 0.02 to 1.2). The other variable associated with the recovery of function was normal left atrial size (odds ratio 0.16; 95% confidence interval 0.12 to 1.6). In conclusion, atrial ejection force is a noninvasive parameter that can be easily measured and can provide accurate information about the recovery of left atrial mechanical function. The recovery of atrial function was influenced by the mode of cardioversion and the size of the left atrium.

Aged↗