Long QT Syndrome and Torsade de Pointes Associated with Takotsubo Cardiomyopathy

Prolongation of QTc interval associated with Takotsubo cardiomyopathy (TC) has previously been reported in published case series. We report an unusual case of a patient who presented with TC associated with long-QT syndrome and developed cardiac arrest secondary to torsade de pointes. Since QT prolongation and bradycardia persisted after the resolution of TC, the patient received permanent pacemaker. Since then additional event did not occur. QT prolongation and bradycardia could be persistent even after recovery of TC, and permanent pacemaker insertion may be a treatment option of long QT syndrome related with TC.

Síndrome do QT longo e torsades de pointes pós-parto / Postpartum torsades de pointes and long QT syndrome

Relatamos o caso de uma paciente puérpera, internada com diagnósticos de infecção do trato urinário e insuficiência cardíaca que evoluiu com arritmias ventriculares do tipo torsades de pointes, após hipopotassemia e uso de Ciprofloxacin. Não apresentou supressão das arritmias ventriculares após reposição de potássio e magnésio, mas após implante de marca-passo provisório. Recebeu alta hospitalar com QTc de 490 ms, em uso de Propranolol.

This article reports the case of a puerperal patient admitted with diagnosis of urinary tract infection and heart failure. This condition evolved with torsades de pointes ventricular arrhythmias, then, hypokalemia, and use of Ciprofloxacin. Ventricular arrhythmias did not present any improvement after potassium and magnesium replacement, but after implantation of temporary pacemaker, this condition showed signs of improvement. The patient was discharged with QTc at 490 ms, taking Propranolol.

BAV avançado e taquiarritmia sustentada do tipo Torsades de Pointes: registro ambulatorial de 24 horas / Advanced AV Blood and sustained de Pointes tachycardia: 24 hours ECG-Holter registration

O torsades de pointes é um tipo de taquiarritmia peculiar reservada a situações especiais, como síndromes do QT longo, distúrbios eletrolíticos e qualquer condição que leve à bradiarritmia persistente. O bloqueio atrioventricular em grau avançado se comporta como uma das principais causas de taquiarritmia na prática clínica. O torsades de pointes é uma condição maligna que necessita de diagnóstico precoce e tratamento agressivo, a fim de que sejam evitadas graves complicações como a morte súbita. O tratamento envolve múltiplos fatores, como suspensão do agente causal, administração de medicamentos e implante de marca-passo definitivo. Os autores apresentam um caso de paciente com bradiarritmia importante devido a bloqueio atrioventricular avançado, registrada em Holter de 24 horas, que desenvolve um episódio sustentado de taquicardia ventricular polimórfica do tipo torsades de pointes, com períodos sugerindo degeneração para fibrilação ventricular, pouco sintomático, que apresentou resolução espontânea e evolução satisfatória.

Torsades de pointes is a particular type of tachycardia observed under special conditions, such as long QT syndromes (LQTS), electrolyte disturbances and conditions that lead to persistent bradycardia. The advanced atrium-ventricular (AV) block is one of the most important causes of this type of tachycardia. Torsades de pointes is a malignant condition requiring early diagnosis and aggressive treatment in order to prevent serious complications, such as sudden death. The treatment involves multiple factors, including suspension of the causal agent, drug administration and definitive pacemaker implantation. The authors present a case study of a patient with important bradycardia due to advanced AV block registered by 24 hours Holter ECG, who developed an episode of sustained polymorphic ventricular tachycardia of the torsades de pointes type, with periods suggesting ventricular fibrillation degeneration, with few symptoms, presenting spontaneous resolution and satisfactory progress.

Torsade de pointes a couplage court compliquee d'une mort subite

A case report of 38 years old man who exprerienced syncope and torsade de pointes is presented with the short coupled variant. The patient had a normal QT interval [QTC 0,37 secondes] and multiform ventricular premature beats on the resting electrocardiogram. Under antiarrhythmic treatment [intavenous xylocain], torsades de pointes suddenly appeared and cardiac arrest was followed, After cordioversion, sinus rythm was restored. A cardiovascular disease was excluded, the echocordiography, the left and right venlncular angiography and coronarography were normal, Three months after, the patient presented at home a sudden cardiac death

Torsade de Pointes: una causa de síncope en disfunción del nodo sinusal / Torsade de Pointes: a cause of syncope in sinus node dysfunction

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

Torsade de pointes: Una taquicardia ventricular polimorfa. Prevención, diagnóstico y aspectos terapéuticos / Torsade de pointes: a polimorphous ventricular tachycardia. Prevention, diagnosis and therapy

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

Torsades de Points: análise de 105 episódios / Torsades de Pointes: analysis of 105 episodes

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