ABSTRACT
Antiarrhythmic agents may increase capture threshold, but this is rarely of clinical significance. Flecainide acetate, a class IC agent, is reported to have a significant effect on the myocardial capture threshold. In this presentation, we report the case of a 72-year-old male, with a previously implanted VVI pacemaker due to sick sinus syndrome, who was treated with flecainide acetate for paroxysmal atrial arrhythmia control. During the fifteenth day of treatment, an abrupt rise in the ventricular capture threshold with ventricular pacing failure was noted. The capture threshold decreased two days after discontinuation of flecainide acetate.
Subject(s)
Male , Humans , Aged , Ventricular Function/drug effects , Pacemaker, Artificial , Flecainide/adverse effects , Electrocardiography , Atrial Flutter/drug therapy , Anti-Arrhythmia Agents/adverse effects , Action Potentials/drug effectsABSTRACT
Se presenta un caso de flutter auricular, con bloqueo auriculoventricular 2:1, asociado a hidrops en uno de los fetos de un embarazo gemelar triple, pesquisado por taquicardia fetal y confirmado con ecocardiografía a las 26 semanas de gestación. Se administró digoxina a la madre, sin exito, por lo que agregamos flecainida al decimo tercer dia de tratamiento, logrando conversión a ritmo sinusal y regresión del hidrops dentro del útero. Se discute la utilidad del flecainide como primera linea para este tipo de pacientes y la necesidad de profilaxis antiarritmica postnatal, considerando la favorable evolución en este periodo.
Subject(s)
Humans , Adult , Female , Pregnancy , Anti-Arrhythmia Agents/therapeutic use , Digoxin/therapeutic use , Flecainide/therapeutic use , Atrial Flutter/drug therapy , Hydrops Fetalis/drug therapy , Hydrops Fetalis/etiology , Pregnancy Complications, CardiovascularABSTRACT
Presentamos un caso de flutter auricular, con bloqueo auriculoventricular 2:1, asociado a hidrops en uno de los fetos de un embarazo gemelar triple, pesquisado por taquicardia fetal y confirmado con ecocardiografía a las 26 semanas de gestación. Iniciamos digoxina transplancetaria sin éxito por lo que agregamos flecainide al décimo tercer día, logrando conversión a ritmo sinusal y regresión del hidrops in útero. Se discute la utilidad del flecainide como primera línea para este tipo de pacientes y la necesidad de profilaxis antiarrítmica postnatal, considerando la favorable evolución en este período.
Subject(s)
Humans , Female , Pregnancy , Infant, Newborn , Anti-Arrhythmia Agents/administration & dosage , Anti-Arrhythmia Agents/therapeutic use , Atrial Flutter/complications , Atrial Flutter/diagnosis , Atrial Flutter/drug therapy , Hydrops Fetalis/complications , Hydrops Fetalis/diagnosis , Hydrops Fetalis/drug therapy , Pregnancy, Multiple , Arrhythmias, Cardiac , Drug Therapy, Combination , Digoxin/administration & dosage , Digoxin/therapeutic use , Echocardiography, Doppler , Flecainide/administration & dosage , Flecainide/therapeutic use , TwinsSubject(s)
Amiodarone/analogs & derivatives , Animals , Anti-Arrhythmia Agents/pharmacology , Arrhythmias, Cardiac/drug therapy , Atrial Fibrillation/drug therapy , Atrial Flutter/drug therapy , Bridged Bicyclo Compounds, Heterocyclic/therapeutic use , Cyclopropanes/therapeutic use , Drug Approval , Humans , Imidazoles/pharmacology , Imidazolidines , Phenethylamines/pharmacology , Piperazines/pharmacology , Sulfonamides/pharmacologyABSTRACT
We report a 41 years old female, previously operated of an atrial septal defect, presenting with a persisting atrial flutter. Sinus node dysfunction became evident during an electrophysiological study at the moment of interrupting the flutter with electrical stimulation. The patient was treated with his bundle ablation and implantation of a definitive pacemaker. After one year of follow up, she is devoid of symptoms
Subject(s)
Humans , Female , Adult , Atrial Flutter/diagnosis , Sick Sinus Syndrome/physiopathology , Atrial Flutter/surgery , Atrial Flutter/etiology , Atrial Flutter/drug therapy , Sick Sinus Syndrome/complications , Sick Sinus Syndrome/diagnosis , Digoxin/therapeutic use , Amiodarone/therapeutic use , Catheter Ablation , Electrocardiography, Ambulatory , Clinical EvolutionABSTRACT
El objetivo de este estudio fue: (1) evaluar la eficacia del d,1 sotalol para mantener el ritmo sinusal (RS) normal en pacientes con FA o FLA refractarios, (2) evaluar la eficacia del d,1 sotalol en la prevención de recurrencias de episodios paroxísticos de FA o FLA, (3) evaluar el control de la respuesta ventricular media (RVM) en aquellos pacientes con episodios paroxísticos o refractarios de fibrilación atrial (FA) o flutter atrial (FLA) que no respondieron exitosamente a otros antiarrítmicos, (4) determinar predictores de eficacia del medicamento y (5) evaluar la seguridad del d,1 sotalol en nuestros pacientes. Se incluyeron doscientos enfermos con FA o FLA crónica y paroxístico y fueron refractarios a uno hasta seis esquemas de antiarrítmicos antes de recibir d,1 sotalol: 54 por ciento de mujeres con edad promedio de 47 ñ 16 años, seguimiento de 7 ñ 7 meses (1 a 14); 79 de los enfermos tuvo la arritmia por más de un año. Hubo 37.5 por ciento de FA crónico (FAC) y 8 por ciento de FLA paroxístico (FLAP). El 82 por ciento permació en clase funcional (CF) I (NYHA) y el 82 por ciento tuvo una cardiopatía estructural, con diámetro atrial izquierdo de 44 ñ 10 mm, del atrio derecho de 37 ñ 7 mm y fracción de eyección de 58 ñ 8 por ciento. El ET (éxito total) se alcanzó en 58 por ciento de los pacientes (40 por ciento con FA y 18 por ciento con FLA), el EP (éxito parcial) fue del 38 por ciento (Fa en 18 por ciento y 20 por ciento con FLA) y hubo fracaso en 4 por ciento de los pacientes. Rspondieron mejor los pacientes con FA que aquellos con FLA (ET vs EP p<0.07). Los pacientes con una cardiopatía estructural respondieron peor al d,1 sotalol (p=0,10) que aquellos sin cardiopatía, especialmente si existía dilatación de las cámaras cardíacas. El d,1 sotalol es un agente terapéutico seguro, moderadamente eficaz, barato y alterno a otros antiarrítmicos en la cardioversión farmacológica de FA y/o FLA a RS y en el mantenimiento del mismo
Subject(s)
Humans , Male , Female , Adult , Middle Aged , Arrhythmias, Cardiac/drug therapy , Atrial Flutter/drug therapy , Atrial Fibrillation/drug therapy , Sotalol/pharmacology , Sotalol/therapeutic use , Treatment Outcome , Heart VentriclesABSTRACT
We have studied the effects of adenosine (ADdo) and adenosine derivates on an experimental atrial flutter (AFL) in the canine heart. Moreover, we have assessed these adenine derivates on some electrophysiological parameters (the conduction time and functional refractory period) of the posteior internodal pathway (PIP) and of the ordinary atrial myocardium (OAM). The adenosine derivates assessed were adenosine 5'- monophosphate (AMP), adenosine 3' 5'-monophosphate (cAMP) and adenosine 5'-triphosphate (ATP). Ado, AMP, and cAMP transformed the atrial flutter into a short episode of atrial fibrillation that terminated spontaneously to sinus rhythm. This effect was prevented by previous blockade of A1 purinergic rceptors with aminophylline, but not by prasumpathectomy (vagotomy and atropine). ATP also suppressed the AFL, but in this case, sinus rhythm wa achieved without an intermediate episode of atrial fibrillation, and the effect of ATP was not prevented by A1 purinergic blockade. Ado, AMP and cAMP extended the functional refractory period measured in the PIP, but reduced this parameter in the OAM (p<0.01). The different response of atrial tissues to the adenosine and its monophosphate derivates was not elicited by ATP. This derivative caused a prolongation of FRP on both atrial tissues PIP and OAM (p<0.05). The changes produced by Ado and its monophosphate derivates on FRP was blocked by aminophylline. The effect of adenine derivatives on AFL may be explained by the dispersion of refractoriness created as a result of the heterogeneous response of atrial tissues to these agents. Our results support the hypothesis of an agonistic action of adenine derivates an atrial purinergic receptors
Subject(s)
Animals , Male , Female , Dogs , Adenine/analogs & derivatives , Adenine/pharmacology , Anti-Arrhythmia Agents/pharmacology , Atrial Flutter/drug therapy , Heart , Disease Models, AnimalSubject(s)
Humans , Child , Adolescent , Adult , Middle Aged , Male , Female , Anesthetics/administration & dosage , Arrhythmias, Cardiac/physiopathology , Heart/physiology , Monitoring, Physiologic , Adenosine/therapeutic use , Arrhythmia, Sinus/drug therapy , Atrial Flutter/drug therapy , Atropine/therapeutic use , Adrenergic beta-Antagonists/therapeutic use , Bradycardia/drug therapy , Dopamine/therapeutic use , Electrophysiology , Ephedrine/therapeutic use , Atrial Fibrillation/drug therapy , Procainamide/therapeutic use , Tachycardia, Sinus/drug therapy , Tachycardia, Supraventricular/drug therapy , Tachycardia, Paroxysmal/drug therapy , Torsades de Pointes , Ventricular Premature Complexes/drug therapyABSTRACT
This study was conducted to evaluate the clinical efficacy of intravenous (i.v.) magnesium sulphate 2 gm bolus in sustained supraventricular tachycardia (SVT) and atrial flutter-fibrillation with fast ventricular rate of more than 160/min (AF-FVR) and to compare it with i.v. verapamil 5 mg. In this randomised controlled trial, 68 cases of SVT and 86 cases of AF-FVR were studied. Patients with evidence of renal dysfunction and systolic blood pressure less then 90 mm Hg were excluded. Response was considered when the heart rate fell to less than 100/min. In SVT, 33.3% (11 out of 33) responded to magnesium sulphate which was significantly less than verapamil (23 out of 35, 65.7%) p = 0.007. Similarly, in AF-FVR, response was more with verapamil (25 out of 45, 55.6%) than magnesium sulphate (8 out of 41, 19.5%) p < 0.0001. Response to magnesium sulphate was better in patients with IHD. There were no significant side effects, except flushing and sense of warmth with i.v. magnesium sulphate. Serum magnesium rose significantly after i.v. magnesium bolus. Though magnesium sulphate is a weaker antiarrhythmic drug than verapamil, further studies are needed to identify subgroups of supraventricular tachyarrhythmias which would respond to magnesium sulphate.