[Alternating bundle branch block in a supraventricular tachycardia: Which is the mechanism ?] / Bloqueo de rama alternante en una taquicardia supraventricular ¿ Cuál es el mecanismo subyacente ?

Functional bundle branch block during a supraventricular tachycardia can be observed with shorter cycle lengths and represent a physiologic response by the specialized intraventricular conduction system to accelerated AV nodal conduction. The present case corresponds to a young patient with exercise induced orthodromic A-V reentrant tachycardia and alternating bundle branch block. This unusual response is explained by the finding obtained during the electrophysiology study. An accelerated AV nodal conduction made the depolarizing wave front reach the bundle branches during their refractory period. Once block in one bundle was stablished, block persisted due to the linking phenomenon that is repetitive retrograde concealed conduction from the contralateral bundle. After catheter ablation of a concealed left-sided accessory A-V pathway, rapid atrial pacing at the same cycle length of the tachycardia reproduced the same aberrancies observed during tachycardia. This response proved that functional bundle branch block is due to the short cycle length and not the presence of an accessory A-V pathway.

El bloqueo de rama funcional durante una taquicardia supraventricular puede ser observado con longitudes de ciclo cortas y representa una respuesta fisiológica del sistema de conducción intraventricular por la existencia de conducción nodal auriculo ventricular acelerada. Presentamos el caso de un paciente joven con taquicardia reentrante aurículo-ventricular ortodrómica y bloqueo de rama alternante. Esta respuesta infrecuente se explica por el hallazgo obtenido durante el estudio electrofisiológico. Una conducción nodal aurículo-ventricular acelerada produce un frente de onda que despolariza las ramas durante sus períodos refractarios. Una vez que ocurrió el bloqueo en una de las ramas, dicho bloqueo persistió debido al fenómeno de linking, que es por conducción oculta retrógrada repetitiva de la rama contralateral. Después de la ablación transcatéter de una vía accesoria oculta lateral izquierda, el marcapaseo auricular rápido a la misma longitud de ciclo de la taquicardia, reprodujo la misma aberrancia observada durante la taquicardia. Este procedimiento demostró que el bloqueo de rama funcional fue debido a la longitud de ciclo corto y no a la presencia de una vía accesoria aurículo-ventricular.

[Trigeminy of ventricular bigeminy caused by reentrant mechanism: reentry of reentry]. / Trigeminia de la bigeminia ventricular por mecanismo reentrante: reentrada de la reentrada.

The process that follows an acute myocardial infarction generates an appropriate substrate for the formation of reentry circuits, considered to be the most frequent mechanism of ventricular extrasystoles and tachyarrhythmias. We present the case of a patient with an acute myocardial infarction unusually concurring with ventricular trigeminy coupled to ventricular bigeminated extrasystoles giving rise to a trigeminy sequence over the bigeminy, which indicates the existence of two reentry circuits (reentry of reentry) that trigger ventricular flutter.

Trigeminia de la bigeminia ventricular por mecanismo reentrante: reentrada de la reentrada / Trigeminy of ventricular bigeminy caused by reentrant mechanism: reentry of reentry

El proceso post-infarto agudo de miocardio genera el sustrato apropiado para la formación de circuitos de reentrada, los cuales son considerados como el mecanismo más frecuente de las extrasístoles y taquiarritmias ventriculares. Presentamos el trazado electrocardiográfico de un paciente con infarto agudo de miocardio en quien se observó la inusual concurrencia de una trigeminia ventricular acoplada a extrasístoles ventriculares bigeminadas, que originó una secuencia de trigeminia sobre la bigeminia, evidenciando la existencia de dos circuitos reentrantes (reentrada de la reentrada); después de una dupla de la extrasístole bigeminada se genera un aleteo ventricular.

The process that follows an acute myocardial infarction generates an appropriate substrate for the formation of reentry circuits, considered to be the most frequent mechanism of ventricular extrasystoles and tachyarrhythmias. We present the case of a patient with an acute myocardial infarction unusually concurring with ventricular trigeminy coupled to ventricular bigeminated extrasystoles giving rise to a trigeminy sequence over the bigeminy, which indicates the existence of two reentry circuits (reentry of reentry) that trigger ventricular flutter.

[Induction of atrioventricular nodal reentrant tachycardia by radiofrequency application]. / Inducción de taquicardia reentrante nodal aurículo-ventricular por aplicación de radiofrecuencia.

Atrioventricular nodal reentrant tachycardia is the most common form of sustained regular narrow QRS complex tachycardia. It is caused by the presence of a dual atrioventricular nodal anatomy and physiology, with a fast and a slow pathway forming a substrate for re-entry. Electrophysiology study confirms the diagnosis when the tachycardia is induced, although in some cases this is not possible. Casuistry is here presented where the application of radiofrequency induced atrioventricular nodal reentrant tachycardia, when the electrophysiological study could not do it; we explain here its electrophysiological mechanism.

Inducción de taquicardia reentrante nodal aurículo-ventricular por aplicación de radiofrecuencia / Induction of atrioventricular nodal reentrant tachycardia by radiofrequency application

La taquicardia reentrante nodal aurículo ventricular es la forma más común de taquicardia sostenida, regular con QRS angostos. Fisiopatológicamente está determinada por una anatomía y fisiología nodal aurículo ventricular dual, con una vía rápida y otra lenta que forman el sustrato de la reentrada. El estudio electrofisiológico determina el diagnóstico de certeza si es inducida, aunque en algunos casos no es posible. Presentamos nuestra casuística donde la aplicación de radiofrecuencia indujo taquicardia reentrante nodal aurículo ventricular cuando el estudio electrofisiológico no pudo hacerlo, y explicamos su mecanismo electrofisiológico.

Atrioventricular nodal reentrant tachycardia is the most common form of sustained regular narrow QRS complex tachycardia. It is caused by the presence of a dual atrioventricular nodal anatomy and physiology, with a fast and a slow pathway forming a substrate for re-entry. Electrophysiology study confirms the diagnosis when the tachycardia is induced, although in some cases this is not possible. Casuistry is here presented where the application of radiofrequency induced atrioventricular nodal reentrant tachycardia, when the electrophysiological study could not do it; we explain here its electrophysiological mechanism.

Síndrome de Andersen-Tawil: una revisión del diagnóstico genético y clínico con énfasis en sus manifestaciones cardíacas / Andersen-Tawil syndrome: A review of its clinical and genetic diagnosis with emphasis on cardiac manifestations

El síndrome de Andersen-Tawil resulta de la alteración de canales de potasio, se hereda de forma autosómica dominante y se cataloga como el tipo 7 de los síndromes de QT largo congénitos. El gen afectado es el KCNJ2, el cual codifica la proteína Kir2.1 que forma el canal de potasio rectificador interno («inward rectifier¼). Este canal interviene en la estabilización del potencial de membrana en reposo y controla la duración del potencial de acción en el sistema musculoesquelético y cardíaco. En miocitos ventriculares, es un componente responsable de la rectificación de la corriente de potasio en la fase 3 del potencial de acción. Debido a que Kir2.1 está presente en el sistema musculoesquelético, corazón y cerebro, las alteraciones de esta proteína dan origen a las principales características del síndrome: parálisis flácida, arritmias ventriculares y alteraciones leves a moderadas en el desarrollo del esqueleto, especialmente en manos y pies. En la presente revisión se aborda esta enfermedad desde el punto de vista del diagnóstico clínico y molecular con énfasis en sus manifestaciones cardíacas.

The Andersen-Tawil syndrome is a cardiac ion channel disease that is inherited in an autosomal dominant way and is classified as type 7 of the congenital long QT syndromes. Affected gene is KCNJ2, which forms the inward rectifier potassium channel designated Kir2.1. This protein is involved in stabilizing the resting membrane potential and controls the duration of the action potential in skeletal muscle and heart. It also participates in the terminal repolarization phase of the action potential in ventricular myocytes and is a major component responsible for the correction in the potassium current during phase 3 of the action potential repolarization. Kir 2.1 channel has a predominant role in skeletal muscle, heart and brain. Alterations in this channel produce flaccid paralysis, arrhythmias, impaired skeletal development primarily in extremities and facial area. In this review we address the disease from the point of view of clinical and molecular diagnosis with emphasis on cardiac manifestations.

[Andersen-Tawil syndrome: a review of its clinical and genetic diagnosis with emphasis on cardiac manifestations]. / Síndrome de Andersen-Tawil: una revisión del diagnóstico genético y clínico con énfasis en sus manifestaciones cardíacas.

The Andersen-Tawil syndrome is a cardiac ion channel disease that is inherited in an autosomal dominant way and is classified as type 7 of the congenital long QT syndromes. Affected gene is KCNJ2, which forms the inward rectifier potassium channel designated Kir2.1. This protein is involved in stabilizing the resting membrane potential and controls the duration of the action potential in skeletal muscle and heart. It also participates in the terminal repolarization phase of the action potential in ventricular myocytes and is a major component responsible for the correction in the potassium current during phase 3 of the action potential repolarization. Kir 2.1 channel has a predominant role in skeletal muscle, heart and brain. Alterations in this channel produce flaccid paralysis, arrhythmias, impaired skeletal development primarily in extremities and facial area. In this review we address the disease from the point of view of clinical and molecular diagnosis with emphasis on cardiac manifestations.

Spontaneous termination of ventricular fibrillation in a patient with congenital coronary anomaly.

Sudden death is common in patients with congenital coronary artery anomalies mainly when the left main coronary artery originates from the right coronary sinus. Ventricular fibrillation in these patients is irreversible unless defibrillation can be rapidly performed. We describe a 57-year-old male with an anomalous origin of circumflex and the left anterior descending coronary arteries from the right coronary sinus. He developed two episodes of ventricular fibrillation that terminated spontaneously, 10 hours after percutaneous revascularization of the circumflex coronary artery. Computed tomography angiography, in addition to confirming the anomalous origin of the coronary arteries, showed a muscle bridge over the midportion of the left anterior descending coronary artery. This is the first report of spontaneous termination of ventricular fibrillation in a patient with congenital anomaly of the coronary arteries.

Flecainide suppresses bidirectional ventricular tachycardia and reverses tachycardia-induced cardiomyopathy in Andersen-Tawil syndrome.

Bidirectional ventricular tachycardia (BVT), although a rare arrhythmia in the general population, is frequently observed in patients with Andersen-Tawil syndrome and long QT interval. However, the pharmacologic treatment of this arrhythmia remains unknown. In the present study, we documented the favorable antiarrhythmic action of flecainide in a young woman with sustained BVT and Andersen-Tawil syndrome. She presented with incessant BVT that could only be terminated with flecainide. During sinus rhythm, a prolonged QT interval was observed. Genetic studies revealed a mutation in the K(+) channel gene KCNJ2. Over a 4-year follow-up period, recurrence of her arrhythmia occurred twice. The first episode was due to noncompliance and resolved with resumption of flecainide therapy. The second recurrence was associated with a tachycardia-induced cardiomyopathy and resolved when the dose of flecainide was increased from 200 to 300 mg daily. This report suggests that flecainide can be effective in controlling BVT associated with Andersen-Tawil syndrome and indicates that the left ventricular dysfunction is secondary to the arrhythmia and not due to an associated phenotypic manifestation of the disorder.

Cardiovascular risk factors in chronic Chagas' disease are associated with a different profile of putative heart-pathogenic antibodies.

Given that cardiovascular risk factors (CRF), such as smoking, alcoholism and hypertension, may contribute to the development of heart lesions, chronically Trypanosoma cruzi-infected individuals were studied to explore the relationship between the presence of such CRF, cardiomyopathy and antibodies that have been proposed to play a pathogenetic role in Chagas' disease. The targets of these antibodies were T. cruzi antigens such as cruzipain (Cz), a P ribosomal antigen (P2), and a component of myelin sheaths also present in T. cruzi (sulphatide). Individuals were classified into four groups on the basis of specific serology and presence of CRF: subjects with T. cruzi infection and CRF; those with positive serology and no CRF; seronegatives with CRF; and seronegatives without CRF, were analysed. Seronegatives or seropositives with CRF showed a greater occurrence of heart involvement (chest X-ray and/or electrocardiogram abnormalities). Seropositives with CRF displayed significantly higher levels of antisulphatide antibodies than the three remaining groups and higher levels of antibodies against Cz and P2 compared to the seropositives without CRF. Increased amounts of anti-P2 and antisulphatide antibodies were also found in seropositives with marked heart involvement. The presence of CRF is associated with a different profile of antibody responses and degree of cardiac effects.

Adrenergic nervous system influences on the induction of ventricular tachycardia.

BACKGROUND: Sudden cardiac death is a major cause of mortality in western countries and the ventricular tachyarrhythmias are mainly involved in this regard. The adrenergic autonomic nervous system has influences in provoking life-threatening arrhythmias, and the prevention of such arrhythmias with beta-blockers supports this viewpoint. To evaluate the effect of the adrenergic nervous system and some catecholamine-releasing stimuli on the induction of ventricular tachycardia, we decided to explore the occurrence of ventricular tachycardia in patients subjected to three consecutive tests, exercise testing, isoproterenol infusion, and mental stress. METHODS: Nineteen subjects who experienced exercise test-induced ventricular tachycardia were subjected to an isoproterenol infusion and mental stress. All but one patient had cardiac disease, with 70% due to Chagas' disease. Seventeen of the 19 study subjects had normal ventricular function. RESULTS: Exercise test-induced ventricular tachycardia was nonsustained in 17 patients and sustained in 2 cases. Isoproterenol infusion induced nonsustained ventricular tachycardia in 9 of 19 patients. Mental stress, on its own, was able to induce nonsustained ventricular tachycardia in 2 of 19 patients. CONCLUSIONS: Among patients preselected for exercise-induced ventricular tachycardia, almost half could be induced into ventricular tachycardia by isoproterenol infusion. Mental stress was a less powerful inducer of ventricular arrhythmias in this study group.

Mecanismos involucrados en el efecto antiarritmico y proarritmico del magnesio / Mechanisms involved in the antiarrhythmic and proarrhythmic effects of magnesium

El objetivo fue analizar en perros, los efectos del MgCl2, y del MgSO4 sobre los mecanismos electrofisiológicos que pudieran vincularse con las acciones antiarrítmicas y proarrítmicas de estas soluciones. Se estudiaron previamente los parámetros farmacocinéticos del MgCl2 y del MgSO4; ambos mostraron que el Mg plasmático disminuye exponencialmente (constante beta de O,118 ñ O,013 h-l), t 1/2 de eliminación de 6,02 ñ O,68 h y una Vda de O,259 ñ O,02lxkg-l. Posteriormente se estudiaron dos grupos de animales - Grupo I: dieta normal. Grupo II A: dieta sin Mg + clortalidona + K y Grupo II B: dieta sin Mg + clortalidona + KCI + MgSO4. Se midieron los electrolitos y las variables electrofisiológicas por medio de estimulación ventricular programada. El grupo I mostró que la administración de MgSO4 endovenoso disminuye el Na, el K y el umbral de fibrilación ventricular (UFV) y prolonga el período refractaria efectivo ventricular (PREV). El MgCl2 no modifica el UFV, pero prolonga el PREV, el A-H, el QTc y el PQ. El MgSO4 aumenta la excreción de K urinario en forma significativamente mayor que el MgCl2. La administración de NaCl no alteró las variables electrofisiológicas pero el NaSO4 disminuyó el K plasmático, sin modificar el UFV. El Grupo II A presentó descenso del K y Mg plasmático, linfocitario y miocárdico, disminución del PREV y del UFV y aumento del QTc. A este grupo se le administro en forma aguda: 1) MgSO4 que provocó mayor descenso del UFV y del K plasmático y aumento del PREV y 2) KCI que aumento el K piasmático y el UFV. El grupo II B no modificó los electrolitos ni las variables electrofisiológicas. Se concluye que los efectos antiarrítmicos observados en clínica por la administración de sales de Mg se deberían probablemente a la prolongación del PREV. Sin embargo, la depleción de K inducida por el MgSO4 puede provocar un descenso del UFV, efecto proarrítmico que se podría evitar utilizando MgCl2.

Mecanismos involucrados en el efecto antiarritmico y proarritmico del magnesio / Mechanisms involved in the antiarrhythmic and proarrhythmic effects of magnesium

El objetivo fue analizar en perros, los efectos del MgCl2, y del MgSO4 sobre los mecanismos electrofisiológicos que pudieran vincularse con las acciones antiarrítmicas y proarrítmicas de estas soluciones. Se estudiaron previamente los parámetros farmacocinéticos del MgCl2 y del MgSO4; ambos mostraron que el Mg plasmático disminuye exponencialmente (constante beta de O,118 ñ O,013 h-l), t 1/2 de eliminación de 6,02 ñ O,68 h y una Vda de O,259 ñ O,02lxkg-l. Posteriormente se estudiaron dos grupos de animales - Grupo I: dieta normal. Grupo II A: dieta sin Mg + clortalidona + K y Grupo II B: dieta sin Mg + clortalidona + KCI + MgSO4. Se midieron los electrolitos y las variables electrofisiológicas por medio de estimulación ventricular programada. El grupo I mostró que la administración de MgSO4 endovenoso disminuye el Na, el K y el umbral de fibrilación ventricular (UFV) y prolonga el período refractaria efectivo ventricular (PREV). El MgCl2 no modifica el UFV, pero prolonga el PREV, el A-H, el QTc y el PQ. El MgSO4 aumenta la excreción de K urinario en forma significativamente mayor que el MgCl2. La administración de NaCl no alteró las variables electrofisiológicas pero el NaSO4 disminuyó el K plasmático, sin modificar el UFV. El Grupo II A presentó descenso del K y Mg plasmático, linfocitario y miocárdico, disminución del PREV y del UFV y aumento del QTc. A este grupo se le administro en forma aguda: 1) MgSO4 que provocó mayor descenso del UFV y del K plasmático y aumento del PREV y 2) KCI que aumento el K piasmático y el UFV. El grupo II B no modificó los electrolitos ni las variables electrofisiológicas. Se concluye que los efectos antiarrítmicos observados en clínica por la administración de sales de Mg se deberían probablemente a la prolongación del PREV. Sin embargo, la depleción de K inducida por el MgSO4 puede provocar un descenso del UFV, efecto proarrítmico que se podría evitar utilizando MgCl2. (AU)