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The principal effects of cardiac glycosides probably can be classified as parasympathomimetic or sympathomimetic. Data from animals and from man suggest that polar cardiac glycosides, such as ouabain and digoxin, possess greater parasympathomimetic (vagal) cardiac effect for a given amount of sympathomimetic (positive inotropic) cardiac effect than do less polar cardiac glycosides, such as digitoxin. Polar glycosides therefore offer some advantage in uncomplicated paroxysmal atrial tachycardia and in uncomplicated atrial flutter and atrial fibrillation when the principal desired effect is reduction in the number of atrial impulses reaching the ventricles or conversion to normal sinus rhythm. Non-polar glycosides offer an advantage when positive inotropicity is desired but when there is some degree of atrioventricular block or when inappropriate sinus bradycardia or anorexia, nausea, or vomiting are present. Ecotopic impulse formation when due to cardiac glycosides is a toxic manifestation of excessive sympathomimetic effect, but is aggravated by vagal-induced sinus bradycardia, so that both parasympathomimetic and sympathomimetic capability of cardiac glycosides must be considered when dealing with myocardial electrical instability.
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PMID:Clinical implications of differences in pharmacodynamic action of polar and nonpolar cardiac glycosides. 83 69

A case of a rare lethal intoxication with yew leaves (taxus baccata) is reported. The clinical signs were dizziness (onset 1 hr after yew leaves were ingested), nausea, diffuse abdominal pain, unconsciousness, weak breathing, tachycardia, brief ventricular flutter afterwards a slow pulse, and finally death by respiratory arrest and diastolic cardiac standstill. Particular attention was given to the ECG. It showed an atypical bundle branch block with a maximal QRS-duration of 0.24 sec. A striking resemblence to the ECG in the case of hyperkalemia is seen in that P-waves were absent. Therefore, the possibility is noted that an acute hyperkalemia could be partly responsible for the cardiotoxic effect of the leaf.
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PMID:[Lethal intoxication with leaves of the yew tree (Taxus baccata) (author's transl)]. 124 88

Although quinidine has been widely used since the beginning of the century, quinidine-induced hepatotoxicity has been recently reported in the literature. We describe a reversible case of quinidine-induced hepatotoxicity. A 62-y-old male with a past medical history of atrial flutter and adult onset diabetes was admitted to the hospital with a 3-d history of diarrhea, nausea, fever, chills and palpitations. Past medications included 7.5 mg glyburide daily for 4 y, 0.25 mg digoxin daily for 3 w, 324 mg quinidine gluconate 3 times daily for 2 w, and 150 mg papaverine daily for 2 y. On admission, liver enzyme levels were elevated (SGOT 606, SGPT 1104). Quinidine was considered an etiologic agent and was discontinued after administration of 1 dose. The patient became afebrile within 48 h, liver enzyme levels gradually decreased, and the patient was discharged on day 6 of hospitalization. Repeat enzyme levels obtained 12 d after discharge were mostly within normal limits. The symptoms were atypical as described in the literature. We conclude that unexplained fever or elevated liver enzyme levels should alert the clinician to the possibility of quinidine-induced hepatotoxicity.
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PMID:Quinidine-induced hepatotoxicity revisited. 180 44

A 59 year-old housewife was admitted to the emergency service with a sudden onset of chest pain and nausea. Initially she was treated as an acute myocardial infarction, but conventional treatments were not effective, and she was sent to our hospital for further evaluation. Her ECG showed several abnormal findings including T-wave inversion, atrial flutter, QT-time prolongation, ST-segment depression or elevation, and frequent ventricular ectopic beats. The echocardiogram, 201thallium scintigram and coronary angiography were almost normal. Both urinary and plasma levels of catecholamines were remarkably increased, and the plasma epinephrine was extremely high during attacks. Abdominal echotomography and CT-scanning showed a large left adrenal tumor. The 131MIBG scintiscan revealed a high accumulation in this tumor. Then the patient was diagnosed as having pheochromocytoma and catecholamine-induced myocarditis. The administration of phentolamine (10 mg) normalized the inversion of T-wave and the high blood pressure. But when propranolol (2 mg) was administrated in addition to phentolamine, the ECG showed a biphasic low T-wave change. According to these phenomena, we supposed that the alpha-adrenergic receptor was involved in the development of the ST-T changes of the ECG, and the alpha-adrenergic receptor of this patient might be sensitive under excessive catecholamines, according to the inhibition of the beta-receptor by propranolol.
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PMID:[A case of pheochromocytoma with an AMI-like ECG change corrected by an alpha-blocking agent]. 196 1

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of the Class I antiarrhythmic agent moricizine hydrochloride are reviewed. Moricizine is chemically similar to the phenothiazines but does not appear to block dopaminergic receptors. Its major electrophysiologic actions are a concentration-dependent decrease in maximum rate of phase 0 depolarization; increased rates of phase 2 and 3 repolarization, decreased action potential duration, and decreased effective refractory period. Moricizine causes a dose-related prolongation of the PR interval and of AV nodal, infranodal, and intraventricular conduction times but has little effect on ventricular repolarization. The antiarrhythmic and electrophysiologic effects are not correlated with plasma concentrations of the drug or its metabolites. Moricizine reduces the occurrence of ventricular premature contractions (VPCs), couplets, and nonsustained ventricular tachycardia. It appears to suppress symptomatic nonsustained ventricular tachycardia, sustained ventricular tachycardia, and ventricular fibrillation or flutter. Moricizine appears to be as effective as quinidine and more effective than disopyramide, propranolol, and imipramine but less effective than flecainide and encainide at reducing VPCs. Moricizine continues to be evaluated in the Cardiac Arrhythmia Suppression Trial, which was designed to assess the long-term benefit of arrhythmia suppression in patients with left ventricular dysfunction after myocardial infarction. Moricizine seems to be better tolerated than quinidine, disopyramide, and imipramine and to have less proarrhythmic potential than flecainide or encainide. Noncardiac adverse effects include dizziness, nausea, and headache. Cimetidine appears to decrease moricizine clearance, and decreased theophylline clearance has been reported in subjects given moricizine. The usual adult dosage of moricizine hydrochloride is 600-900 mg/day given in three divided doses; an every-12-hour regimen may be used in some patients. Because of the risk of proarrhythmic effects, indications are limited to treatment of documented life-threatening arrhythmias. Moricizine will compete with other agents as first-line therapy for life-threatening arrhythmias.
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PMID:Moricizine: a new class I antiarrhythmic. 227 51

The antiarrhythmic effect of oral propafenone was evaluated in 10 patients with Wolff-Parkinson-White syndrome presenting with non-ventricular arrhythmias (paroxysmal supraventricular tachycardia n = 7, atrial fibrillation or flutter n = 3). The mean age was 38 +/- 13 years, the dose varied from 300 to 900 mg three times a day (mean 450 +/- 188) and the mean follow-up period was 7 +/- 3.5 months. All patients' drug responses were assessed on 12-lead electrocardiograms and 24-hour ambulatory Holter monitoring. Electrophysiologic studies were performed in cases of sustained tachycardia while echocardiography identified 2 cases with mitral valve prolapse. Four of 10 (40%) patients became asymptomatic on a starting propafenone dose of 300 mg, while 6 (60%) had recurrences necessitating an increase in dose for the complete control of the symptoms. We observed a slight slowing of the heart rate and an increase of the mean Q-T interval (P less than 0.001). Three patients reported minor side effects including nausea, dizziness and constipation that were tolerable and dosage dependent. It is concluded that propafenone is an effective and well tolerated drug for the treatment of non-ventricular arrhythmias associated with the Wolff-Parkinson-White syndrome.
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PMID:Propafenone in the prevention of non-ventricular arrhythmias associated with the Wolff-Parkinson-White syndrome. 233 10

One hundred and seventeen episodes of supraventricular tachycardia in 50 children, including 28 infants, were treated with intravenous adenosine. Adenosine was prepared in a sterile solution of 0.9% saline (1 mg/ml) and given in incremental doses of 0.05 mg/kg every two minutes to a maximum of 0.25 mg/kg. Ninety of the 117 episodes were terminated. This included 88 of the 102 episodes of junctional tachycardia (79 of the 92 episodes of atrioventricular reentry tachycardia, seven of the eight episodes of atrioventricular nodal reentry tachycardia, and both of the episodes of long R-P' tachycardia). Only one of four episodes of His bundle tachycardia and one of the eight episodes of ectopic atrial tachycardia were terminated. None of the three episodes of atrial flutter were terminated. Side effects were frequent but mild and included transient complete atrioventricular block (less than 6 s), sinus bradycardia (less than 40 s), ventricular extrasystoles, flushing, nausea, headache, and respiratory disturbance. Reinitiation (within 5 s) of supraventricular tachycardia occurred in 13 of the terminated episodes. Although reinitiation limited its clinical efficacy in some patients, intravenous adenosine offered a safe and efficient method of rapid termination of most episodes of supraventricular tachycardia and in some cases facilitated diagnosis of the mechanism.
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PMID:Efficacy and safety of adenosine in the treatment of supraventricular tachycardia in infants and children. 278 12

The efficacy of intravenous flecainide acetate (maximum 2 mg/kg or 150 mg given at a rate of 15 mg/min) was assessed in patients with acute supraventricular tachycardia (SVT) (within 24 hours). Fifty patients were studied, 46 with spontaneous SVT and 4 with induced SVT at electrophysiologic assessment. Conversion to sinus rhythm was achieved within 45 minutes in 76%: in 25 patients with atrial fibrillation (76% conversion), 15 with atrioventricular (AV) nodal or AV reentrant tachycardia (100% conversion) and 10 with atrial flutter or atrial reentrant tachycardia (40% conversion). Adverse effects were noted in 21 patients (42%): paresthesia in 9, drowsiness in 8, nausea in 2, accelerated ventricular rate in 5, ventricular tachycardia in 1, sinus bradycardia in 1 and hypotension in 5. Adverse effects were associated with larger dosage and atrial flutter or atrial reentrant tachycardia. Thus, flecainide acetate is effective in converting to sinus rhythm acute atrial fibrillation and AV nodal and AV reentrant tachycardias, but not atrial flutter or atrial reentrant tachycardia.
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PMID:Flecainide acetate for conversion of acute supraventricular tachycardia to sinus rhythm. 310 10

The majority of sudden cardiac deaths in children occur in patients with prior arrhythmias and an abnormal heart. Amiodarone was given to 39 young patients (35 with an abnormal heart) with arrhythmias unresponsive to conventional treatment. Their age ranged from 6 weeks to 30 years with nine patients younger than 2 years of age. Atrial flutter was present in 16 patients, ventricular tachycardia in 14 patients and supraventricular tachycardia in 9 patients. The most common diagnosis (14 patients) was postoperative repair of congenital heart disease. The dose ranged from 2.5 to 21.6 mg/kg per day (mean 8.2). Elimination of arrhythmia (on 24 hour electrocardiography) occurred in 15 of 16 patients with atrial flutter, 11 of 14 with ventricular tachycardia and 5 of 9 with supraventricular tachycardia. Symptomatic side effects were: rash (three patients), headache (two patients), nausea (one patient) and peripheral neuropathy (one patient); seven patients had asymptomatic corneal microdeposits which normalized in all after the drug was discontinued. No side effects occurred in patients younger than 10 years of age. The following changed with treatment (p less than 0.05): heart rate decreased (three patients with atrial flutter and sick sinus syndrome required pacemaker implantation for bradycardia) and QTc increased; thyroxine (T4) and serum reverse triiodothyronine (T3) increased. During follow-up study (range 6 months to 3 years), 21 of the 39 patients continued to take amiodarone with complete control of arrhythmias, 9 were no longer taking the drug and 9 died (7 nonsudden and 2 sudden deaths). Amiodarone is an extremely effective treatment for infants and children with tachyarrhythmias resistant to conventional treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amiodarone treatment of critical arrhythmias in children and young adults. 638 28

Ibutilide fumarate is a new antiarrhythmic agent recently approved for the conversion of atrial flutter (AFl) and atrial fibrillation (AF) to normal sinus rhythm. A class III agent in the Vaughan Williams classification system, ibutilide prolongs cardiac repolarization by activating a slow inward, predominantly sodium current. An alternative or additive mechanism to prolong repolarization may be blockade of the outward delayed rectifier potassium rapid current. Ibutilide is administered intravenously, and approximately 40% of the drug in serum is protein bound. It is eliminated through hepatic metabolism by undefined enzyme systems, and it appears that none of the metabolites contributes significantly to antiarrhythmic activity. The elimination half-life of ibutilide ranges from 2-12 hours. When administered by 10-minute infusion, ibutilide 1 mg (approximately 0.015 mg/kg) resulted in conversion to sinus rhythm in 24-58% of patients with AFl and 20-32% with AF, compared with about 5% for placebo. Administering a second dose of 0.5-1 mg improved the overall response rates to approximately 75% and 45%, respectively. In randomized comparative trials, ibutilide was more effective than sotalol in converting AFl (70% vs 19%) and AF (44% vs 11%) and more effective than procainamide (76% vs 12% and 51% vs 20%, respectively). The time to conversion in most trials was usually 20-30 minutes. Nausea is the most common noncardiac adverse effect (< 2%). Nonsustained and sustained polymorphic ventricular tachycardia occurred in 2.7-6.7% and 1.7% of patients, respectively.
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PMID:Ibutilide: a new class III antiarrhythmic agent. 901 61


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