Clinical Spectrum of SCN5A Channelopathy in Children with Primary Electrical Disease and Structurally Normal Hearts.

Sodium voltage-gated channel α subunit 5 (SCN5A)-mutations may cause an array of arrhythmogenic syndromes most frequently as an autosomal dominant trait, with incomplete penetrance, variable expressivity and male predominance. In the present study, we retrospectively describe a group of Mexican patients with SCN5A-disease causing variants in whom the onset of symptoms occurred in the pediatric age range. The study included 17 patients with clinical diagnosis of primary electrical disease, at least one SCN5A pathogenic or likely pathogenic mutation and age of onset <18 years, and all available first- and second-degree relatives. Fifteen patients (88.2%) were male, and sixteen independent variants were found (twelve missense, three truncating and one complex inframe deletion/insertion). The frequency of compound heterozygosity was remarkably high (3/17, 17.6%), with early childhood onset and severe disease. Overall, 70.6% of pediatric patients presented with overlap syndrome, 11.8% with isolated sick sinus syndrome, 11.8% with isolated Brugada syndrome (BrS) and 5.9% with isolated type 3 long QT syndrome (LQTS). A total of 24/45 SCN5A mutation carriers were affected (overall penetrance 53.3%), and penetrance was higher in males (63.3%, 19 affected/30 mutation carriers) than in females (33.3%, 5 affected/15 carriers). In conclusion, pediatric patients with SCNA-disease causing variants presented mainly as overlap syndrome, with predominant loss-of-function phenotypes of sick sinus syndrome (SSS), progressive cardiac conduction disease (PCCD) and ventricular arrhythmias.

Potential pro-arrhythmic effects of pharmacotherapy against SARS-CoV-2.

The pandemic caused by the SARS-COV-2 or COVID-19 virus has been a global challenge given its high rate of transmission and lack of effective therapy or vaccine. This scenario has led to the use of various drugs that have demonstrated a potential effect against the virus in vitro. However, time has not been enough to properly evaluate their clinical effectiveness. The use of chloroquine/hydroxychloroquine, azithromycin and antiviral treatment and has been proposed by various groups, supported by in-vitro studies and limited patient series, without the adequate scientific rigor that precedes drug prescription. Although it may represent the only hope for many patients, it is important to know the main adverse effects associated with the use of these drugs and to better select patients who may benefit from them.

La pandemia por el virus SARS-COV-2 causante de la enfermedad COVID-19 representa un reto mundial dada su alta tasa de transmisión y ausencia de una terapia efectiva o vacuna. Este escenario ha propiciado el uso de diversos fármacos que in vitro han demostrado un potencial efecto contra el virus. Sin embargo, el tiempo no ha sido suficiente para evaluar su efectividad clínica con el adecuado rigor científico que precede a la prescripción de medicamentos. El uso de cloroquina/hidroxicloroquina, azitromicina y esquemas antivirales ha sido propuesto por diversos grupos, apoyado por series de pacientes limitada en número. Si bien puede representar la única esperanza para muchos enfermos, es importante conocer los principales efectos adversos asociados al uso de estas drogas y seleccionar mejor a los pacientes que puedan beneficiarse de ellas. El riesgo de arritmias ventriculares incrementa tanto por el uso de fármacos como por la gravedad de la propia enfermedad viral.

Potenciales efectos pro-arrítmicos de la farmacoterapia contra SARS-CoV-2 / Potential pro-arrhythmic effects of pharmacotherapy against SARS-CoV-2

Resumen La pandemia por el virus SARS-COV-2 causante de la enfermedad COVID-19 representa un reto mundial dada su alta tasa de transmisión y ausencia de una terapia efectiva o vacuna. Este escenario ha propiciado el uso de diversos fármacos que in vitro han demostrado un potencial efecto contra el virus. Sin embargo, el tiempo no ha sido suficiente para evaluar su efectividad clínica con el adecuado rigor científico que precede a la prescripción de medicamentos. El uso de cloroquina/hidroxicloroquina, azitromicina y esquemas antivirales ha sido propuesto por diversos grupos, apoyado por series de pacientes limitada en número. Si bien puede representar la única esperanza para muchos enfermos, es importante conocer los principales efectos adversos asociados al uso de estas drogas y seleccionar mejor a los pacientes que puedan beneficiarse de ellas. El riesgo de arritmias ventriculares incrementa tanto por el uso de fármacos como por la gravedad de la propia enfermedad viral.

Abstract The pandemic caused by the SARS-COV-2 or COVID-19 virus has been a global challenge given its high rate of transmission and lack of effective therapy or vaccine. This scenario has led to the use of various drugs that have demonstrated a potential effect against the virus in vitro. However, time has not been enough to properly evaluate their clinical effectiveness. The use of chloroquine/hydroxychloroquine, azithromycin and antiviral treatment and has been proposed by various groups, supported by in-vitro studies and limited patient series, without the adequate scientific rigor that precedes drug prescription. Although it may represent the only hope for many patients, it is important to know the main adverse effects associated with the use of these drugs and to better select patients who may benefit from them.

Muerte súbita cardiaca en el corazón estructuralmente normal: una actualización / Sudden cardiac death in individuals with normal hearts: an update

La muerte súbita (MS) es un evento trágico que representa un grave problema de salud. Se estima que causa cerca de 4-5 millones de decesos por año en todo el mundo. La MS se define como la muerte ocurrida en el lapso de 1 h en una persona sin signos previos de fatalidad; puede denominarse «recuperada¼, cuando el paciente afectado sobrevive al episodio potencialmente fatal ya sea por reanimación cardiopulmonar o desfibrilación efectiva. Las canalopatías arritmogénicas son alteraciones funcionales de los canales iónicos del corazón, generalmente condicionados por mutaciones en los genes que los codifican y dan lugar a diversos tipos de arritmias que pueden culminar en MS, el deceso ocurre normalmente antes de los 40 años y el corazón en estudio de autopsia suele ser estructuralmente normal. En la presente revisión presentamos las principales causas de MS en el contexto del corazón estructuralmente normal y discutimos el abordaje que se debe dar a los pacientes y familiares de víctimas que han experimentado éste trágico evento.

Sudden death (SD) is a tragic event and a world-wide health problem. Every year, near 4-5 million people experience SD. SD is defined as the death occurred in 1 h after the onset of symptoms in a person without previous signs of fatality. It can be named «recovered SD¼ when the case received medical attention, cardiac reanimation effective defibrillation or both, surviving the fatal arrhythmia. Cardiac channelopathies are a group of diseases characterized by abnormal ion channel function due to genetic mutations in ion channel genes, providing increased susceptibility to develop cardiac arrhythmias and SD. Usually the death occurs before 40 years of age and in the autopsy the heart is normal. In this review we discuss the main cardiac channelopathies involved in sudden cardiac death along with current management of cases and family members that have experienced such tragic event.

[Sudden cardiac death in individuals with normal hearts: an update]. / Muerte súbita cardiaca en el corazón estructuralmente normal: una actualización.

Sudden death (SD) is a tragic event and a world-wide health problem. Every year, near 4-5 million people experience SD. SD is defined as the death occurred in 1h after the onset of symptoms in a person without previous signs of fatality. It can be named "recovered SD" when the case received medical attention, cardiac reanimation effective defibrillation or both, surviving the fatal arrhythmia. Cardiac channelopathies are a group of diseases characterized by abnormal ion channel function due to genetic mutations in ion channel genes, providing increased susceptibility to develop cardiac arrhythmias and SD. Usually the death occurs before 40 years of age and in the autopsy the heart is normal. In this review we discuss the main cardiac channelopathies involved in sudden cardiac death along with current management of cases and family members that have experienced such tragic event.

Genética en los Síndromes de QT prolongado / Genetic in Long QT Syndromes

The long QT syndrome (LQTS) is a genetic disorder characterized by prolongation of the QT interval in the electrocardiogram (ECG) and a propensity to "torsades de pointes" ventricular tachycardia frequently leading to syncope, cardiac arrest, or sudden death usually in young otherwise healthy individuals. LQTS caused by mutations of predominantly potassium and sodium ion channel genes or channel-interacting proteins leading to positive overcharge of myocardial cell with consequent heterogeneous prolongation of repolarization in various layers and regions of myocardium. These conditions facilitate the early after-depolarization and reentry phenomena underlying development of polymorphic ventricular tachycardia observed in patients with LQTS. Obtaining detailed patient history regarding cardiac events in the patient and his/her family members combined with careful interpretation of standard 12-lead ECG (with precise measurement of QT interval in all available ECGs and evaluation of T-wave morphology) usually is sufficient to diagnose the syndrome. The LQTS show great genetic heterogeneity and has been identified more than 500 mutations distributed in 10 genes: KCNQ1, HERG, SCN5A, KCNE1, KCNE2, ANKB, KCNJ2, CACNA1A, CAV3 and SCN4B. Despite advances in the field, 25-30% of patients remain undiagnosed genetic. Genetic testing plays an important role and is particularly useful in cases with nondiagnostic or borderline ECG findings.

Genética de la taquicardia ventricular polimorfa catecolaminérgica: conceptos básicos / Genetic of catecholaminergic polymorphic ventricular tachycardia: basic concepts

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a cardiac channelopathy characterized by altered intracellular calcium handling resulting in ventricular arrhythmias and high risk of cardiac sudden death in young cases with normal structural hearts. Patients present with exertional syncope and the trademark dysrhythmia is polymorphic and/or bidirectional ventricular tachycardia during exercise or adrenergic stimulation. Early detection of CPVT is crucial because opportune medical intervention prevents sudden cardiac death. Mutations in the ryanodine receptor RYR2 explain nearly 70% of the CPVT cases and cause the autosomic dominant form of the disease. Mutations in calsequestrin 2 causes a recessive form and explain less than 5% of all cases. Genetic screening in CPVT, besides providing early detection of asymptomatic carriers at risk, has provided important insights in the mechanism underlying the disease. Mutational analysis of RYR2 has been a challenge due to the large size of the gene, 105 exons encoded for 4,967 amino-acids. In this review we analyze general concepts of the disease, differential diagnosis and strategies for genetic screening.

[Genetic of catecholaminergic polymorphic ventricular tachycardia: basic concepts]. / Genética de la taquicardia ventricular polimorfa catecolaminérgica; conceptos básicos.

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a cardiac channelopathy characterized by altered intracellular calcium handling resulting in ventricular arrhythmias and high risk of cardiac sudden death in young cases with normal structural hearts. Patients present with exertional syncope and the trademark dysrhythmia is polymorphic and/or bidirectional ventricular tachycardia during exercise or adrenergic stimulation. Early detection of CPVT is crucial because opportune medical intervention prevents sudden cardiac death. Mutations in the ryanodine receptor RYR2 explain nearly 70% of the CPVT cases and cause the autosomic dominant form of the disease. Mutations in calsequestrin 2 causes a recessive form and explain less than 5% of all cases. Genetic screening in CPVT, besides providing early detection of asymptomatic carriers at risk, has provided important insights in the mechanism underlying the disease. Mutational analysis of RYR2 has been a challenge due to the large size of the gene, 105 exons encoded for 4,967 amino-acids. In this review we analyze general concepts of the disease, differential diagnosis and strategies for genetic screening.

[Genetic in long QT syndromes]. / Genética en los Síndromes de QT prolongado.

The long QT syndrome (LQTS) is a genetic disorder characterized by prolongation of the QT interval in the electrocardiogram (ECG) and a propensity to "torsades de pointes" ventricular tachycardia frequently leading to syncope, cardiac arrest, or sudden death usually in young otherwise healthy individuals. LQTS caused by mutations of predominantly potassium and sodium ion channel genes or channel-interacting proteins leading to positive overcharge of myocardial cell with consequent heterogeneous prolongation of repolarization in various layers and regions of myocardium. These conditions facilitate the early after-depolarization and reentry phenomena underlying development of polymorphic ventricular tachycardia observed in patients with LQTS. Obtaining detailed patient history regarding cardiac events in the patient and his/her family members combined with careful interpretation of standard 12-lead ECG (with precise measurement of QT interval in all available ECGs and evaluation of T-wave morphology) usually is sufficient to diagnose the syndrome. The LQTS show great genetic heterogeneity and has been identified more than 500 mutations distributed in 10 genes: KCNQ1, HERG, SCN5A, KCNE1, KCNE2, ANKB, KCNJ2, CACNA1A, CAV3 and SCN4B. Despite advances in the field, 25-30% of patients remain undiagnosed genetic. Genetic testing plays an important role and is particularly useful in cases with nondiagnostic or borderline ECG findings.

Association of congenital, diffuse electrical disease in children with normal heart: sick sinus syndrome, intraventricular conduction block, and monomorphic ventricular tachycardia.

INTRODUCTION: Rhythm disturbances in children with structurally normal hearts are usually associated with abnormalities in cardiac ion channels. The phenotypic expression of these abnormalities ("channelopathies") includes: long and short QT syndromes, Brugada syndrome, congenital sick sinus syndrome, catecholaminergic polymorphic ventricular tachycardia, Lènegre-Lev disease, and/or different degrees of cardiac conduction disease. METHODS: The study group consisted of three male patients with sick sinus syndrome, intraventricular conduction disease, and monomorphic sustained ventricular tachycardia. Clinical data and results of electrocardiography, Holter monitoring, electrophysiology, and echocardiography are described. RESULTS: In all patients, the ECG during sinus rhythm showed right bundle branch block and long QT intervals. First-degree AV block was documented in two subjects, and J point elevation in one. A pacemaker was implanted in all cases due to symptomatic bradycardia (sick sinus syndrome). Atrial tachyarryhthmias were observed in two patients. The common characteristic ventricular arrhythmia was a monomorphic sustained ventricular tachycardia, inducible with ventricular stimulation and sensitive to lidocaine. In one patient, radiofrequency catheter ablation was successfully performed. No structural abnormalities were found in echocardiography in the study group. CONCLUSION: Common clinical and ECG features suggest a common pathophysiology in this group of patients with congenital severe electrical disease.

[New perspectives in long QT syndrome]. / Nuevas perspectivas en el síndrome de QT largo.

Long QT Syndrome (LQTS) is a cardiac channelopathy characterized by prolonged ventricular repolarization and increased risk to sudden death secondary to ventricular dysrrhythmias. Was the first cardiac channelopathy described and is probably the best understood. After a decade of the sentinel identification of ion channel mutation in LQTS, genotype-phenotype correlations have been developed along with important improvement in risk stratification and genetic guided-treatment. Genetic screening has shown that LQTS is more frequent than expected and interestingly, ethnic specific polymorphism conferring increased susceptibility to drug induced QT prolongation and torsades de pointes have been identified. A better understanding of ventricular arrhythmias as an adverse effect of ion channel binding drugs, allow the development of more safety formulas and better control of this public health problem. Progress in understanding the molecular basis of LQTS has been remarkable; eight different genes have been identified, however still 25% of patients remain genotype-negative. This article is an overview of the main LQTS knowledge developed during the last years.

Nuevas perspectivas en el síndrome de QT largo / New perspectives in long QT syndrome

Long QT Syndrome (LQTS) is a cardiac channelopathy characterized by prolonged ventricular repolarization and increased risk to sudden death secondary to ventricular dysrrhythmias. Was the first cardiac channelopathy described and is probably the best understood. After a decade of the sentinel identification of ion channel mutation in LQTS, genotype-phenotype correlations have been developed along with important improvement in risk stratification and genetic guided-treatment. Genetic screening has shown that LQTS is more frequent than expected and interestingly, ethnic specific polymorphism conferring increased susceptibility to drug induced QT prolongation and torsades de pointes have been identified. A better understanding of ventricular arrhythmias as an adverse effect of ion channel binding drugs, allow the development of more safety formulas and better control of this public health problem. Progress in understanding the molecular basis of LQTS has been remarkable; eight different genes have been identified, however still 25% of patients remain genotype-negative. This article is an overview of the main LQTS knowledge developed during the last years.

El síndrome de QT largo (SQTL) es una canalopatía que genera grave alteración en la repolarización ventricular predispone a arritmias malignas y muerte súbita. Fue la primera canalopatía arritmogénica descrita y quizá la mejor entendida hasta ahora. Transcurrida ya más de una década de la identificación de la primera mutación asociada al SQTL, se ha hecho evidente que este trastorno es mucho más frecuente de lo que inicialmente se pensaba; los avances en el conocimiento de la fisiopatología molecular de esta enfermedad han permitido hacer una correlación genotipo-fenotipo, optimizando el tratamiento y permitiendo estratificar el riesgo en forma precisa. Se ha logrado entender con mayor detalle los efectos adversos de distintas drogas que interactúan con los canales iónicos, permitiendo así generar fármacos más seguros y, en su defecto, monitorizar de cerca aquellos que a pesar de tener este efecto adverso, es necesaria su administración. Los avances son importantes pero no todo está dicho, 25% de los casos no tienen mutaciones en los genes descritos hasta la fecha, por lo que el SQTL continúa siendo motivo de investigación. El presente artículo constituye un resumen de los principales conceptos desarrollados en los últimos diez años que han sido cruciales en el manejo de esta enfermedad.

[Follow-up of a group of patients with automatic implantable defibrillator]. / Seguimiento de un grupo de pacientes con desfibrilador automático implantable.

UNLABELLED: The automatic implantable defibrillator (AID) is the treatment of choice for primary and secondary prevention of sudden death. At the Instituto Nacional de Cardiología, since October 1996 until January 2002, 25 patients were implanted with 26 AID. There were 23 men (92%) and the mean age of the whole group, was 51.4 years. Twenty-three patients (92%) presented structural heart disease, the most common was ischemic heart disease in 13 patients (52%), with a mean ejection fraction of 37.8%. One patient without structural heart disease had Brugada Syndrome. The most frequent clinical arrhythmia was ventricular tachycardia in 14 patients (56%). The mean follow-up was of 29.3 months during which a total of 30 events of ventricular arrhythmia were treated through AID; six of them were inappropriate due to paroxismal atrial fibrillation; 10 AID patients (34%) have not applied for therapy. Three patients (12%) of the group died due to congestive heart failure refractory to pharmacologic treatment. CONCLUSION: The implant of the AID is a safe and effective measure for primary and secondary prevention of sudden death. World-wide experience evidences, that this kind of device has not modified the mortality rate due to heart failure in these patients, but it has diminished sudden arrhythmic death.

[Electric therapy for heart failure]. / Terapia eléctrica de la insuficiencia cardíaca.

The different means for treating congestive heart failure have not yet achieved the improvement in quality of life and the prognosis of people with terminal stage cardiac disease. Some treatment resources, such as cardiac transplant, are only accessible for a selected group of patients. In the last decade, the interest on the role of electromechanic disturbances has grown and has motivated special interest for the use of the pacemaker as a tool for the treatment of congestive heart failure. During this period we have seen an important progress of this kind of treatment and, nowadays, multicenter studies have shown the hemodynamic improvement of the patients treated with this method. Selection of patients for this kind of treatment should be careful; although today it can be known which patients can benefit from this device in the treatment of congestive heart failure.

Terapia eléctrica en insuficiencia cardíaca / Electrical therapy in heart failure

Los diferentes modos de tratamiento de los que se dispone en la actualidad para la insuficiencia cardíaca no han logrado mejorar la calidad de vida y el pronóstico de personas que tienen algún padecimiento cardíaco en fase terminal. Algunos recursos terapéuticos como el trasplante cardíaco son accesibles sólo para pacientes muy selectos. En la última década ha crecido el interés por la participación que tienen las alteraciones electromecánicas en la falla cardíaca y ello ha motivado un interés especial por el uso de marcapasos como parte de la terapia de la insuficiencia cardíaca. En el transcurso de un período relativamente corto se han podido ver importantes avances de esta estrategia terapéutica y en la actualidad diversos estudios multicéntricos han demostrado el beneficio hemodinámico que reciben los pacientes tratados por este medio. Aún falta por definir mejor los criterios de selección de pacientes para estos dispositivos, sin embargo, en la actualidad se puede saber qué pacientes tendrán un mayor beneficio con el implante de un marcapasos tricameral.

The different means for treating congestive heart failure have not yet achieved the improvement in quality of life and the prognosis of people with terminal stage cardiac disease. Some treatment resources, such as cardiac transplant, are only accessible for a selected group of patients. In the last decade, the interest on the role of electromechanic disturbances has grown and has motivated special interest for the use of the pace-maker as a tool for the treatment of congestive heart failure. During this period we have seen an important progress of this kind of treatment and, nowadays, multicenter studies have shown the hemodynamic improvement of the patients treated with this method. Selection of patients for this kind of treatment should be careful; although today it can be known which patients can benefit from this device in the treatment of congestive heart failure.

Alteraciones electrocardiográficas durante el esfuerzo en un paciente con Síndrome de Brugada / Exercise test unmasks apparent right bundle branch block and st segment elevation in the brugada syndrome

Presentamos el caso de un sujeto de 28 años de edad que presentó síncope único, con un electrocardiograma después del síncope de características normales, y que posteriormente mostró un cuadro de bloqueo de rama derecha, y desnivel positivo del segmento ST en precordiales derechas, compatibles con el síndrome de Brugada.Durante la prueba de esfuerzo se observó normalización de las alteraciones electrocardio-gráficas, mientras que en la fase de postesfuerzo apareció elevación del segmento ST en precor-diales derechas.Es el primer caso reportado en nuestro país de un síndrome de Brugada con cambios espontáneos del electrocardiograma, enmascarados durante el ejercicio y aparentes durante la fase de postesfuerzo.

Ablación exitosa de fibrilación auricular originada en las venas pulmonares / Succesful ablation focal atrial fibrillation originating from pulmonary veins

La fibrilacion auricular usualmente es debida a múltiples circuitos de reentradas: se ha descripto recientemente un tipo de fibrilación auricular poco común, cuyo mecanismo focal permite el tratamiento definitivo mediante ablación con catéter. Reportamos el caso de un paciente con un corazón estructuralmente sano, con historia de síncope y episodios de palpitaciones frecuentes por taquicardia auricular y fibrilación auricular. El estudio electrofisiológico demostró que las arritmias auriculares eran debidas a un foco localizado en la vena pulmonar superior izquierda, el que fue exitosamente tratado utilizando radiofrecuencia sin complicaciones. Las venas pulmonares son un sitio importante de origen de latidos ectópicos que inician frecuentemente paroxismos de fibrilación auricular. Estos focos pueden ser tratados exitosamente mediante ablación con radiofrecuencia

Ablación exitosa de fibrilación auricular originada en las venas pulmonares / Succesful ablation focal atrial fibrillation originating from pulmonary veins

La fibrilacion auricular usualmente es debida a múltiples circuitos de reentradas: se ha descripto recientemente un tipo de fibrilación auricular poco común, cuyo mecanismo focal permite el tratamiento definitivo mediante ablación con catéter. Reportamos el caso de un paciente con un corazón estructuralmente sano, con historia de síncope y episodios de palpitaciones frecuentes por taquicardia auricular y fibrilación auricular. El estudio electrofisiológico demostró que las arritmias auriculares eran debidas a un foco localizado en la vena pulmonar superior izquierda, el que fue exitosamente tratado utilizando radiofrecuencia sin complicaciones. Las venas pulmonares son un sitio importante de origen de latidos ectópicos que inician frecuentemente paroxismos de fibrilación auricular. Estos focos pueden ser tratados exitosamente mediante ablación con radiofrecuencia (AU)

Eficacia y seguridad del d,1 sotalol en el tratamiento ambulatorio de pacientes con fibrilación y flutters atriales / d,1 Sotalol in the treatment of atrial fibrilation and atrial flutter

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