Clozapine-related Paroxysmal Supraventricular Tachycardia: a Case Report.

Clozapine is considered to be more effective than other antipsychotic drugs for treating treatmentresistant schizophrenia. However, side effects of clozapine include agranulocytosis and, less commonly, cardiovascular disease, which is occasionally fatal. We describe a 56-year-old woman who developed clozapine-related paroxysmal supraventricular tachycardia during clozapine dose titration and had a recurrence despite being treated with verapamil. For treatment-resistant schizophrenia, a slow titration of the clozapine dose is necessary, and potential cardiac side-effects should be monitored.

Case report: an unusual heart rhythm associated with organophosphate poisoning.

Organophosphate pesticides have emerged as a common cause of poisoning, particularly in developing countries. The most common electrocardiographic abnormalities observed in organophosphate poisoning are sinus tachycardia, QT interval prolongation, and, very rarely, ventricular arrhythmias. We report a case of organophosphate poisoning associated with atrial fibrillation, right bundle branch block, QT interval prolongation, and intermittent narrow QRS complexes that were most likely due to automaticity from the region of the left posterior fascicle.

Pseudoephedrine-induced paroxysmal supraventricular tachycardia: a case report.

Palpitation is a common chief complaint among emergency department patients, and is often associated with a tachydysrhythmia. Tachydysrhythmia is classified as supraventricular tachycardia or ventricular tachycardia. Reentry in a normal or accessory pathway is one of the most frequently seen mechanisms explaining the tachydysrhythmia. In the present case, we report an unusual cause of atrioventricular paroxysmal supraventricular tachycardia due to pseudoephedrine intake.

Paroxysmal beta-adrenergic receptor-mediated alterations in ventricular repolarization at rapid heart rates during inhibition of delayed rectifier currents.

The contribution of the slow component of the delayed rectifier current (IKs) to ventricular repolarization is increased during rapid heart rates and prolonged repolarization. The objective was to characterize physiologically relevant paroxysmal beta-adrenergic receptor-mediated alterations on ventricular repolarization under these conditions. Paced guinea pig hearts were perfused with (1) control, (2) sparfloxacin (IKr inhibitor), or (3) sparfloxacin and HMR 1556 (IKs inhibitor). The mean +/- standard error of the mean epicardial action potential duration at 90% repolarization (APD90) increased from baseline with IKr inhibition (12.9% +/- 4.7%) and dual IKr/IKs inhibition (25.1% +/- 5.3). Paroxysmal isoproterenol (0.01 and 1.0 nM) significantly decreased APD90 in the presence of IKr inhibition but was attenuated with the addition of IKs inhibition. Spontaneous episodes of polymorphic ventricular tachycardia were observed with isoproterenol during dual IKr and IKs inhibition. The endocardial expression of KCNQ1 increased greater than 2-fold after exposure to IKr and dual IKr/IKs inhibition relative to control but was not altered in epicardial tissue. The beta-adrenergic receptor-mediated decrease in APD90 during IKr inhibition is reversed in the presence of IKs inhibition at rapid heart rates. IKs may serve as an important compensatory mechanism to protect against adrenergically induced arrhythmias when the repolarization reserve is depleted.

[Should we care about pregabalin for elderly patients with a history of cardiac dysrhythmia?]. / Faut-il se méfier de la prégabaline chez les patients âgés aux antécédents de troubles du rythme cardiaque ?

Pregabalin is similar in structure to gamma-aminobutyric acid. It is used for neuropathic pain, generalized anxiety disorders and as an adjunct therapy for partial seizures. Tachycardia is a rare side-effect. A 92-year-old patient with a history of paroxystic fibrillation was hospitalised for zoster. She developed a sinusal tachycardia followed by atrial fibrillation and congestive heart failure 15 h after a first dose of pregabalin. The imputation was considered as plausible. Even though the mechanism remains unclear, pregabalin might induce tachycardia in predisposed old patients.

Taquicardia paroxística supraventricular por sobreingesta de salbutamol / Supraventricular paroxysmal tachycardia by overdose of salbutamol

Introducción: La taquicardia es el hallazgo más frecuente tras la ingestión de una dosis de salbutamol superior a la terapéutica. Se trata habitualmente de una taquicardia sinusal refleja secundaria a vasodilatación, siendo poco frecuente que se produzcan arritmias. Caso clínico: Presentamos el caso de un niño de 3 años de edad que presentó un episodio de taquicardia paroxística supraventricular tras la ingesta accidental de una sobredosis de salbutamol. El electrocardiograma de 12 derivaciones mostró una taquicardia paroxística supraventricular a una frecuencia de 250 latidos por minuto. Tras fracasar un intento terapéutico mediante la utilización de maniobras vagales, se administró una dosis de propranolol intravenoso volviendo el paciente a entrar en ritmo sinusal. Conclusión: La taquicardia supraventricular es un efecto secundario de la intoxicación por salbutamol que puede darse en niños previamente sanos. La administración de propranolol en estos casos podría estar indicada y parece segura

Introduction: Synus tachicardia is the most frecuent clinical finding after the ingesion of a salbutamol overdose. It is a common reflex response to vasodilation while cardiac dysrhytmias are rare. Case report:Athree year old boy presented to de emergency department after the accidental ingestion of an overdose of salbutamol. A12 lead ECG showed supraventricular paroxysmal tachicardia with a heart rate of 250 beats per minute. After an unsuccessful therapeutic attempt with vagal manoeuvres, a single dose of intravenous propanolol restored normal sinus rhythm. Conclusion: Supreventricular tachycardia may occur in previously healthy children after a salbutamol overdose. Propanolol administration may be indicated in these cases and seems safe

Cervical ripening and induction of labor with misoprostol, dinoprostone gel, and a Foley catheter: a randomized trial of 3 techniques.

OBJECTIVE: The purpose of this study was to compare the efficacy of 3 different techniques of cervical ripening and induction. STUDY DESIGN: Patients who required cervical ripening and induction were randomized to one of 3 groups: (1) supracervical Foley catheter and intravaginal dinoprostone gel, (2) supracervical Foley catheter and 100 microg oral doses of misoprostol, or (3) serial 100-microg oral doses of misoprostol. Intravenous oxytocin was administered when a protraction disorder of labor was identified. RESULTS: There were 339 women randomized. There was no significant difference in the time from first intervention to delivery in the 3 groups (P =.546). In each group, a similar percentage of women required oxytocin (P =.103). The rates of cesarean delivery were equivalent among the groups (P =.722). Rates of tachysystole were high but statistically equivalent among the 3 groups. There were no significant differences in Apgar scores or umbilical artery pH. CONCLUSION: Oral 100 microg serial doses of misoprostol, with or without the use of a supracervical Foley catheter, were equivalent to the use of a supracervical Foley catheter and serial 4-mg doses of dinoprostone gel for cervical ripening and the induction of labor.

[Evaluation of hyperkinetic cardiac arrhythmia in chronic obstructive bronchopneumopathy]. / La valutazione delle aritmie cardiache ipercinetiche nella broncopneumopatia cronica ostruttiva.

Patients with chronic obstructive pulmonary disease (COPD), especially during acute exacerbations of their disease, show a greater incidence of cardiac arrhythmias than healthy subjects of the same age. The type of arrhythmias found may be supraventricular (premature atrial beats, paroxysmal supraventricular tachycardia, multifocal atrial tachycardia, atrial flutter, atrial fibrillation) or ventricular (premature ventricular beats, sustained ventricular tachycardia, torsades de pointes, ventricular fibrillation) that may lead to sudden cardiac death. The pathogenesis of arrhythmias is complex and many factors may be involved such as hypoxemia, hypercapnia, respiratory acidosis, metabolic and respiratory alchalosis, hypokalemia, concomitant ischemic heart disease, chronic cor pulmonale, left ventricular diastolic dysfunction. Remarkable attention has been drawn to the possible arrhythmogenic effect of drugs such as theophylline, beta-adrenergic stimulants and digitalis which are commonly used in the therapy of COPD. Both of the main classes of bronchodilators (methylxanthynes and beta-adrenergic agonists), even when used together, apparently do not increase the incidence of dangerous cardiac arrhythmias. However, these drugs should be used with caution in the elderly, in patients with preexisting cardiac arrhythmias, with heart disease or with reduced hepatic function. In these cases Holter monitoring, repeated measurements of plasma drugs concentration and prompt hospitalization of high risk patients in Intensive Care Unit may be needed.

[Amiodarone-induced hyperthyroidism causing progression of arrhythmia]. / Amiodaron okozta hyperthyreosis által kiváltott arrhythmia-progresszió.

A case of a 38-year-old male with supraventricular paroxysmal tachycardia existing for more than a decade is reported. He has received amiodarone in a daily dose of 800 mg for three years and the tachycardia returned in 1992. New antiarrhythmic drugs were added but no beneficial effect has been achieved and moreover, a case of ventricular fibrillation occurred. The 12-lead ECG performed during tachycardia and the electrophysiological study showed orthodromic AV reentry tachycardia. Laboratory tests performed proved hyperthyreotic state. Attacks of paroxysmal tachycardia were returned and aggravated by the hyperthyreosis induced by amiodarone. Finally, antiarrhythmic drugs were discontinued and methimazol was introduced. Gradually, the patient become asymptomatic within two months. The most important conclusion of the case reported, that the amiodarone induced hyperthyreosis can be subclinical or obscure. Consequently, a regular control of serum thyreoid hormone levels at least twice a year on patients with long term amiodarone administration should be advised.

[Acute effects of propafenone in patients with ventricular pre-excitation]. / Efeitos agudos da propafenona em pacientes com pré-excitação ventricular.

PURPOSE: To evaluate the electrophysiological effects of intravenous propafenone in the anterograde and retrograde effective refractory period of the accessory pathways (AP), in patients with Wolff-Parkinson-White syndrome. METHODS: Forty symptomatic patients were studied. All patients were undergone to electrophysiologic study at baseline and after IV propafenone (2.0mg/kg). Drug effects were analysed according to the basal state of the anterograde and retrograde effective refractory periods of the AP > < 270ms. RESULTS: The mean anterograde and retrograde effective refractory periods of the AP were 275 +/- 76ms and 264 +/- 44ms at the control and 462 +/- 190ms and 438 +/- 184ms after drug respectively (p < 0.01 in both situations). The mean anterograde effective refractory period of the AV node was 236 +/- 40ms (control) and 276 +/- 57ms (post-drug)- p < 0.05. The mean atrial and right ventricular effective refractory period in the control were 210 +/- 23ms and 240 +/- 34ms passing to 215 +/- 24ms and 250 +/- 40 ms after drug respectively (p = ns). After drug, complete anterograde and retrograde block of the AP, occurred in 15 (42%) and 12 (35%) patients respectively. Out of 15 patients with complete anterograde block of the AP, 11 had anterograde effective refractory period of the AP > 270ms and 4, < 270ms (p < 0.02). Out of 12 patients with complete retrograde block of the AP after drug, 4 had retrograde effective refractory period > 270ms and 8, < 270ms (p: ns). CONCLUSION: Propafenone caused significant increase in the anterograde and retrograde effective refractory periods of the AP. There was a tendency of the drug to show better effectiveness in patients with anterograde effective refractory period of the AP > 270ms. This results were not seen in relation to the retrograde effective refractory period of the AP.

Efeitos agudos da propafenona em pacientes com pré-excitaçäo ventricular / Acute Effects of Propafenone in Patients with Ventricular Pré-Excitation

Objetivo - Avaliar os efeitos agudos da propafenona sobre os períodos refratários anterógrado e retrógrado de vias anômalas (VA). Métodos - Foram estudados 40 apcientes sintomáticos. Por técnica de extra-estímulos, determinaram-se os períodos refratários anterógrado e retrógrado das VA em condiçöes de controle e após 2,0mg/Kg de propafenona IV. Os resultados foram analisados em funçäo dos períodos refratários anterógrado e retrógrado das VA><270ms no controle. Resultados - Período refratário anterógrado médio da VA no controle de 275 ñ 76ms e no pós-droga de 462 ñ 190ms (p < 0,01). Período refratário retrógrado médio da VA no controle de 264 ñ 44ms, passando no pós-droga para 438 ñ 184ms (p < 0,01). Período refratário efetivo anterógrado do nódulo AV no controle de 236 ñ 40ms, passando no pós-droga para 276 ñ 47ms (p < 0,05). Período refratário efetivo atrial no controle de 210 ñ 23ms, passando para 215 ñ 24ms (p = ns). Período refratário efetivo ventricular no controle de 240 ñ 34ms, passando no pós-droga para 250 ñ 40ms (p:ns). Notou-se o aparecimento de bloqueio completo anterógrado e retrógrado da VA no pós-droga em, respectivamente, 15 e 12(42//, 35//) pacientes. Dos 15 pacientes com bloqueio anterógrado da VA no pós-droga, 11 apresentavam período refratário anterógrado da VA>270ms (p<0,02). Dos 12 pacientes com bloqueio completo retrógrado da VA no pós-droga, 4 apresentavam período refratário retrógrado da VA > 270ms e 8,<270ms (p=ns). Conclusäo - A propafenona produziu significativo aumento dos períodos refratários efetivos anterógrado e retrógrado das VA. Observou-se tendência a uma maior açäo frente a períodos refratários efetivos anterógrdos das VA>270ms. Este padräo de resposta näo foi observado em relaçäo aos períodos refratários efetivos retrógrdos da VA

Purpose - To evaluate the electrophysialogical effects of intravenous propafenone in the anterograde and retrograde effective refractory period of the accessory pathways (AP), in patients with WolffParkinson-White syndrome. Methods - Forty symptomatic patients were studied.. All patients were undergone to electrophysiologic study at baseline and after IV propafenone (2.0mg/kg). Drug effects were analysed according to the basal state of the anterograde and retrograde effective refractory periods of the AP><270ms. Results - The mean anterograde and retrograde effective refractory periods of the AP were 275±76ms and 264±44ms at the control and 462±190ms and 438±184ms after drug respectively (p<0.01 in both situations). The mean anterograde effective refractory period of the AV node was 236±40ms (control) and 276±57ms (post-drug )- p<0.05. The mean atrial and right ventricular effective refractory period in the control were 210±23ms and 240±34ms passing to 215±24ms and 250±40ms after drug respectively (p=ns). After drug, complete anterograde and retrograde block of the AP, ocurred in 15 (42°/) and 12 (35°/) patients respectively. Out of 15 patients with complete anterograde block of the AP, 11 had anterograde effective refractory period of the AP>270ms and 4,<270ms (p<0.02). Out of 12 patients with complete retrograde block of the AP after drag, 4 had retrograde effective refractory period >270ms and 8, <270ms (p:ns). Conclusion - Propafenone caused signifcant increase in the anterograde and retrograde effective refractory periods of the AP. There was a tendency of the drug to show better effectiveness in patients with anterograde effective refractory period of the AP>270ms. This results were not seen in relation to the retrograde effective refractory peried of the AP

Digoxin toxicity presenting as altered mental status in a patient with severe chronic obstructive lung disease.

Gastrointestinal and cardiac manifestations are the commonly considered features of digoxin toxicity. This report describes a patient with severe chronic obstructive lung disease whose primary manifestation of digoxin toxicity is acute alteration of mental status. Neurologic dysfunction may be the sole manifestation of digitalis toxicity. The diagnosis of digoxin toxicity should be considered in elderly patients with altered mental status, even when serum levels are within a therapeutic range.