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1.
Rev. chil. cardiol ; 42(2): 107-112, ago. 2023. ilus
Article Dans Espagnol | LILACS | ID: biblio-1515092

Résumé

La taquicardia ventricular polimórfica se origina en los ventrículos, cuyos complejos QRS son de morfología, amplitud y dirección variable, con frecuencias que oscilan entre 200 y 250 lpm, pudiendo ser autolimitadas o degenerar en una fibrilación ventricular. La TdP es un tipo de taquicardia ventricular polimórfica caracterizada por complejos con un eje eléctrico que gira alrededor de la línea isoeléctrica y que está asociada a QT largo. Se presenta el caso de una paciente portadora de marcapaso que presenta episodios de taquicardia ventricular polimórfica, con una morfología típica de TdP, sin documentación de QT prolongado previo ni actual, generada por la estimulación ventricular sobre onda T, de forma accidental por desplazamiento del electrodo auricular a Ventrículo Derecho (VD).


Polymorphic ventricular tachycardia is a tachycardia originating in the ventricles, where the QRS complexes have variable morphology, amplitude, and direction, with frequencies ranging between 200 and 250 bpm; it may be self-limited or degenerate into ventricular fibrillation. Torsades de Pointes (TdP) is a type of polymorphic ventricular tachycardia characterized by complexes with an electrical axis that rotates around the isoelectric line and that is associated with long QT interval. We present the case of a patient with a pacemaker who presents episodes of polymorphic ventricular tachycardia, with a typical morphology of TdP, without documentation of previous or current prolonged QT, generated by ventricular stimulation on the T wave, accidentally due to displacement of the atrial electrode to the Right Ventricle (RV).


Sujets)
Humains , Femelle , Sujet âgé , Pacemaker/effets indésirables , Entraînement électrosystolique/effets indésirables , Torsades de pointes/étiologie , Radiographie thoracique , Torsades de pointes/diagnostic , Torsades de pointes/physiopathologie , Tachycardie ventriculaire/diagnostic , Tachycardie ventriculaire/étiologie , Issue fatale , Électrocardiographie
2.
The Korean Journal of Internal Medicine ; : 99-102, 2011.
Article Dans Anglais | WPRIM | ID: wpr-75320

Résumé

Complete atrioventricular (AV) block is frequently regarded as a cause of informed syncopal attacks, even though the escape rhythm is maintained. Torsade de pointes (TdP) may be a significant complication of AV block associated with QT prolongation. Here, we report the case of a 42-year-old female who was referred to our hospital due to recurrent seizure-like attacks while taking anti-convulsant drugs at a psychiatric hospital. TdP with a long QT interval (corrected QT = 0.591 seconds) was observed on an electrocardiogram (ECG) taken in the emergency department. The patient's drug history revealed olanzapine as the suspicious agent. Even after the medication was stopped, however, the QT interval remained within an abnormal range and multiple episodes of TdP and related seizure-like symptoms were found via ECG monitoring. A permanent pacemaker was thus implanted, and the ventricular rate was set at over 80 beats/min. There was no recurrence of tachyarrhythmia or other symptoms.


Sujets)
Adulte , Femelle , Humains , Bloc atrioventriculaire/complications , Benzodiazépines/effets indésirables , Électrocardiographie , Épilepsie/étiologie , Pacemaker , Torsades de pointes/étiologie
4.
Anaesthesia, Pain and Intensive Care. 2009; 13 (1): 28-30
Dans Anglais | IMEMR | ID: emr-101182

Résumé

Clarithromycin, a macrolide antibiotic is known to have an arrhythmogenic potential in the presence of comparable QT prolongation. Indeed, the extent of QT prolongation has been used as a surrogate marker for cardiotoxicity and sudden cardiac death. We report a case series of three adult patients who were transferred to our intensive care unit [ICU] at Peradeniya Teaching Hospital, Peradeniya [Sri Lanka], and needed inotropic support and mechanical ventilation. All the three of them were treated with a standard dose regimen of intravenous clarithromycin for suspected atypical pneumonia, after which they dramatically deteriorated and unexpectedly died within 72 hours. In the absence of other known precipitating factors, cardiotoxicity of clarithromycin was suspected as the main causative factor for these deaths


Sujets)
Humains , Mâle , Cardiotoxines/effets indésirables , Unités de soins intensifs , Pneumopathie infectieuse/traitement médicamenteux , Maladie grave , Électrocardiographie , Torsades de pointes/étiologie , Tachycardie ventriculaire/étiologie , Littérature de revue comme sujet
5.
Rev. invest. clín ; 59(1): 57-72, ene.-feb. 2007. ilus, tab
Article Dans Espagnol | LILACS | ID: lil-632392

Résumé

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.


Sujets)
Humains , Syndrome du QT long , Bradycardie/diagnostic , Bradycardie/embryologie , Bradycardie/génétique , Agents cardiovasculaires/usage thérapeutique , Mort subite cardiaque/étiologie , Défibrillation , Maladies foetales/diagnostic , Maladies foetales/génétique , Coeur foetal/physiopathologie , Gangliectomie , Génotype , Transport des ions/génétique , Syndrome du QT long/induit chimiquement , Syndrome du QT long/classification , Syndrome du QT long/complications , Syndrome du QT long/diagnostic , Syndrome du QT long/embryologie , Syndrome du QT long/épidémiologie , Syndrome du QT long/génétique , Syndrome du QT long/thérapie , Pacemaker , Phénotype , Diagnostic prénatal , Canaux potassiques/génétique , Canaux potassiques/physiologie , Canaux sodiques/génétique , Canaux sodiques/physiologie , Ganglion cervicothoracique/chirurgie , Tachycardie ventriculaire/étiologie , Torsades de pointes/étiologie
6.
Indian Heart J ; 2004 May-Jun; 56(3): 248-9
Article Dans Anglais | IMSEAR | ID: sea-4579

Résumé

We report the case of a middle aged lady with dilated cardiomyopathy, presenting with recurrent syncope due to torsade de pointes. Further evaluation revealed that she had a pheochromocytoma which caused the arrhythmia.


Sujets)
Tumeurs de la surrénale/complications , Adulte , Électrocardiographie , Fatigue/étiologie , Femelle , Humains , Syndrome du QT long/étiologie , Phéochromocytome/complications , Syncope/étiologie , Torsades de pointes/étiologie
8.
Acta méd. colomb ; 18(4): 221-4, jul.-ago. 1993. tab
Article Dans Espagnol | LILACS | ID: lil-183304

Résumé

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.


Sujets)
Humains , Troubles du rythme cardiaque/complications , Troubles du rythme cardiaque/diagnostic , Troubles du rythme cardiaque/étiologie , Troubles du rythme cardiaque/physiopathologie , Syncope/étiologie , Syncope/physiopathologie , Syndrome du QT long/classification , Syndrome du QT long/complications , Syndrome du QT long/diagnostic , Syndrome du QT long/épidémiologie , Syndrome du QT long/étiologie , Syndrome du QT long/physiopathologie , Syndrome du QT long/traitement médicamenteux , Syndrome du QT long/thérapie , Torsades de pointes/classification , Torsades de pointes/complications , Torsades de pointes/étiologie , Torsades de pointes/physiopathologie
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