ABSTRACT
Torsade de Pointes (TdP) es una taquicardia ventricular atípica, que ocurre en casos de prolongación de intervalo QT y puede ser una anormalidad congénita o adquirida. TdP es una complicación reconocida de las bradirritmias, específicamente en el bloqueo atrioventricular. Sin embargo, la disfunción del nodo sinusal es una causa rara de síncope asociado a TdP. Estudios experimentales han sugerido que el intervalo QT largo adquirirdo y TdP pueden deberse a pospotenciales tempranos, bradicardia o pausa-dependiente, que llevan a automatismo por actividad disparada. Este reporte describe el caso de una paciente con intervalo QT largo inducido por bradicardia sinusal, ritmo nodal AV intermitente y síncope repetitivo secundario a TdP, tratado exitosamente con estimulación cardiaca temporal y a largo plazo
Subject(s)
Humans , Female , Aged , Bradycardia , Cardiac Pacing, Artificial , Electrocardiography , Pacemaker, Artificial , Syncope/etiology , Long QT Syndrome/diagnosis , Long QT Syndrome/etiology , Torsades de Pointes/diagnosis , Torsades de Pointes/physiopathology , Torsades de Pointes/therapyABSTRACT
Suppression of responses to premature stimulation has been the guiding principle in managing many cardiac arrhythmias. Recent clinical trails revealed that sodium channel blockade increased the incidence of re-entrant cardiac arrhythmias resulting in sudden cardiac death, although the physiologic mechanism remains uncertain. Potassium channel blockade offers an alternative mechanism for suppressing responses to premature stimuli. We have developed a simple model of a 2D sheet of excitable cells. We can initiate re-entrant activation with stimuli timed to occur within a period of vulnerability (VP). Reducing the Na conductance increases the VP while reducing the K conductance increases the collective instability of the array, and arrhythmias similar to torsades de pointes seen in patients subjected to K channel blocked can be readily initiated. Thus, while K channel blockade may suppress excitability by prolonging the action potential duration, it appears to simultaneously exhibit proarrhythmic properties that result in complex re-entrant arrhythmias.
Subject(s)
Action Potentials/physiology , Arrhythmia, Sinus/physiopathology , Biophysical Phenomena , Biophysics , Death, Sudden, Cardiac/etiology , Electrocardiography/statistics & numerical data , Humans , Middle Aged , Models, Biological , Myocardium/cytology , Potassium Channel Blockers , Potassium Channels/drug effects , Sodium Channel Blockers , Sodium Channels/physiology , Torsades de Pointes/physiopathologyABSTRACT
Se presenta una revisión sobre las variantes del síndrome de QT largo y su importante asociación con cuadros sincopales, arritmias ventrículares de tipo de la taquicardia ventrícular poliforma en su variedad "torsades de pointes",y de la muerte súbita. Se discute su aparición relacionada con fármacos cada vez más empleados en nuestra práctica médica y la importancia de su diagnóstico y tratamiento temprano.
Subject(s)
Humans , Arrhythmias, Cardiac/complications , Arrhythmias, Cardiac/diagnosis , Arrhythmias, Cardiac/etiology , Arrhythmias, Cardiac/physiopathology , Syncope/etiology , Syncope/physiopathology , Long QT Syndrome/classification , Long QT Syndrome/complications , Long QT Syndrome/diagnosis , Long QT Syndrome/epidemiology , Long QT Syndrome/etiology , Long QT Syndrome/physiopathology , Long QT Syndrome/drug therapy , Long QT Syndrome/therapy , Torsades de Pointes/classification , Torsades de Pointes/complications , Torsades de Pointes/etiology , Torsades de Pointes/physiopathologyABSTRACT
En este trabajo describimos las características de la torsade de pointes conocida también como taquicardia ventricular polimorfa o atípica. La presencia de un intervalo QTU largo, secuencias largas y cortas con episodios de taquicardia ventricular rápida no sostenidos caracterizan a esta arritmia. Los mecanismos electrofisiológicos productores de esta arritmia son probablemente las postdepolarizaciones tardías que aparecen luego de pausas o secuencias largas. En este trabajo presentamos un caso clínico y 3 ejemplos electrocardiográficos de torsade de pointes que permiten reconocer e identificar las características más salientes de esta arritmia. La prolongación del intervalo QTU y las secuencias iniciales son críticas para establecer el diagnóstico. La torsade de pointes debe ser considerada hasta demostración de lo contrario como el ritmo responsable en un paciente con síncope e intervalo QTU largo. Se recomiendan el tratamiento con potasio y magnesio por vía parenteral con suspensión de la medicación involucrada. El marcapaseo auricular o ventricular rápido es también aconsejable particularmente cuando se detectan bradicardia y secuencias largo-cortas
Subject(s)
Humans , Male , Middle Aged , Torsades de Pointes/diagnosis , Torsades de Pointes/physiopathology , Potassium/therapeutic use , Torsades de Pointes/therapy , Magnesium/therapeutic useABSTRACT
Purpose - To analyze episodes of Torsades de Pointes (TP), in search of its electrocardiographic characteristics. Patients and Methods - We analyzed 105 episodes of TP, in 4 patients using quinidine and diuretics, recorded by 24-hour Holter monitoring The following parameters were studied; ventricular repolarization out of TP, rhythm disturbances before TP; EKG characteristics of the onset, the bouts and the end of the TP. Results - Ventricular repolarization, out of the TP, was abdormal, with the presence of U-waves at the end of the T-waves, resulting in prolongation of the QT (QU) interval. The U-wave voltage was noted to be cycle-lenght dependent. Ventricular bigeminy preceded TP in 100 episodes (95%) and the mean interval between both parameters was 18 ±16 min. The onset of the TP episodes showed the "short/long/ short cycle rale", hereby called "pre-pause cycle", "preparing cycle" and "trigger cycle" respectively. The rotatory QRS-T morphology around the baseline, was seen in 75% of episodes, at the beginning or throughtout the bout. Monomorphic ventricular tachycardia pattern was seen in the other 25% of episodes. Termination of bouts was sudden in all cases, and persistent ventricular bigeminy led to another bout in 90 episodes (85% ). Conclusion - In TP patients, there is enlargement of QT intervals mostly due to U-waves appearence. The U-waves seen in these cases, probably have an important role in the genesis of TP and are probably related to ventricular after potentials (triggered activity). Ventricular bigeminy is a premonitory sign of TP in patients using class 1A antiarrhythmic drugs Persistent ventricular bigeminy post-TP episoaes is a strong indicator of another bout of TP. The onset of TP is more important than its morphology for the correct diagnosis of this arrhythmia