May Fever Trigger Ventricular Fibrillation?

The clinical precipitants of ventricular fibrillation (VF) remain poorly understood. Clinical factors such as hypoxemia, acidosis or electrolyte imbalance, drug-related toxicity, autonomic nervous system disorders as well as viral myocarditis have been proposed to be associated with sudden cardiac death particularly in patients with structural heart disease. However, In the Brugada syndrome, concurrent febrile illness has been reported to unmask the electrocardiographic features of the Brugada syndrome and be associated with an increased propensity for VF. More recently, a febrile illnesses of infectious etiology was associated to polymorphic ventricular tachycardia or VF in patients with normal hearts and without known repolarization abnormality. In this review we detail this phenomenon and its putative mechanisms

Atrial fibrillation and its determinants after radiofrequency ablation of chronic common atrial flutter

Aim. Atrial fibrillation (AFib) is a major clinical issue and its occurrence is the main problem after catheter ablation of atrial flutter. The long-term occurrence of AFib after common atrial flutter ablation is still matter of debate as it may influence the therapeutic approach. So, the aim of our study was to analyze the determinants and the time course of AFib after radiofrequency catheter ablation of chronic common atrial flutter. Methods and Results. 89 consecutive patients (67.5 ± 12.0 yrs) underwent RF ablation of chronic common atrial flutter. 38.2 % had previous history of paroxysmal AFib. 51% had no underlying structural heart disease. Over a mean follow-up of 38 ± 13 months, the occurrence rate of AFib progressively increased up to 32.9% at the end of follow-up. The median occurrence time for AFib was 8 months. AFib occurrence was significantly associated with previous AFib history (P=0.01) but not with the presence of underlying heart disease (P=n.s.). Of particular interest, in our study, AFib never occurred in patients without previous AFib history. Palpitations after chronic common atrial flutter ablation was mostly related to AFib. Conclusion. In conclusion, after chronic common atrial flutter ablation, AFib incidence progressively increased over the follow-up in all patients. Patients with prior AFib history appeared to be a very high risk group. In these patients, closer monitoring is mandatory and the persistent risk of AFib recurrences may justify prolonged anticoagulation policy

Réduire ou ralentir la fibrillation auriculaire : est-ce la bonne question en 2010 ?

RésuméPourquoi et comment traiter la fibrillation atriale ? Cette question a paru simple pendant de nombreuses années : la fibrillation atriale, trouble du rythme cardiaque, doit être traitée par des médicaments anti-arythmiques, tant qu’ils peuvent être efficaces. Les effets secondaires de ces médicaments, comme le bénéfice fréquemment apporté par un simple traitement bradycardisant a amené à discuter il y a une dizaine d’années deux stratégies thérapeutiques, réduire ou ralentir. Mais ce choix largement mis en avant dans les précédentes recommandations thérapeutiques, apparaît aujourd’hui réducteur. En 2010 on peut sans doute proposer deux objectifs thérapeutiques, traiter les symptômes et traiter le risque cardiovasculaire associée à la fibrillation. La gêne symptomatique entraînée par l’arythmie doit être toujours évaluée chez nos patients, volontiers selon la classification récente EHRA. Parallèlement la fibrillation fait partie du continuum cardiovasculaire, et constitue un marqueur de risque supplémentaire : il apparaît certain que le contrôle de ce risque supplémentaire associé à la fibrillation ne dépend pas uniquement du traitement de l’arythmie proprement dite.SummaryWhy and how to treat atrial fibrillation? This question seemed simple for many years: atrial fibrillation, a cardiac arrhythmia, should be treated with antiarrhythmic drugs, as long as they can be effective. Side effects of these drugs, as good benefit often provided by a simple bradycardic treatment led to discuss it some 10 years ago 2 therapeutic strategies: rhythm control or rate control. But this choice widely highlighted in the previous guidelines, now seems simplistic. In 2010 we can probably offer two therapeutic goals, treat symptoms and treat cardiovascular risk associated with atrial fibrillation. The discomfort caused by symptomatic arrhythmia should always be assessed in our patients, as by the recent EHRA classification. Meanwhile fibrillation is part of the cardiovascular continuum, and is a marker of an additional risk: it appears certain that the control of this additional risk does not depend solely on the treatment of the arrhythmia itself

Les effets pro-arythmiques des médicaments

RésuméLes effets pro-arythmiques des médicaments sont fréquents et graves, et sont associés à une surmortalité non négligeable. La polymédication augmente le nombre d’effets indésirables et d’interactions graves voire mortelles. Certains sont facilement évitables. Cependant, au-delà de l’allongement de l’intervalle QT, d’autres mécanismes peuvent avoir un rôle majeur comme les dysfonctions du RyR2, responsable d’arythmie calcium-dépendantes par surcharge calcique intracellulaire, avec apparition de post-dépolarisations tardives, sans modifications de l’intervalle QT. Les bloqueurs des canaux sodiques sont également un problème sérieux de part le risque de démasquer ou d’aggraver une dysfonction du canal sodique chez des patients atteints de syndrome de Brugada asymptomatique ou non. Leur dépistage à un stade précoce du développement des médicaments peut avoir un intérêt majeur.SummaryThe cardiac safety of new and marketed drugs is a major concern for public authorities, patients, physicians as well as pharmaceutical companies. Letal adverse drug reactions are indeed a leading cause of death worldwide and increase at a greater rate than the increase in total hospital admission. The increasing use of polypharmacy in current clinical practice is also associated to a growing number of side effects and interactions leading to fatal adverse events. Measurement of the QT interval is an established, albeit incomplete, approach to assess the proarrhythmic risk of a drug. Ventricular arrhythmia (VA) can be caused by a QT-prolonging drug inducing abnormal repolarization of the action potential (AP) of ventricular cardiomyocytes. Emerging evidence, derived from recent understanding of these mechanisms and of similar mechanisms reported for heart failure (HF), suggest that diastolic Ca2+ leak from the sarcoplasmic reticulum (SR) related to RyR2 dysfunction can induce Ca2+ dependent arrhythmia. In this report, we review mechanisms underlying drug-induced arrhythmogenic effects and Ca2+ dependent arrhythmia, and, for the latter, we discuss some of the issues associated to worsening of cardiac arrhythmias

Fever-Induced QTc Prolongation and Ventricular Fibrillation in a Healthy Young Man

Long QT syndrome is associated with lethal tachyarrhythmia that can lead to syncope, seizure, and sudden death. Congenital long QT syndrome is a genetic disorder, characterized by delayed cardiac repolarization and prolongation of the QT interval on the electrocardiogram (ECG). Type 2 congenital long QT is linked to mutations in the human ether a go-go-related gene (HERG). There are environmental triggers of adverse cardiac events such as emotional and acoustic stimuli, but fever can also be a potential trigger of life-threatening arrhythmias in long QT syndrome type 2 patients. Herein, we report a healthy young man who experienced fever-induced polymorphic ventricular tachycardia and QT interval prolongation

Carta de M. Pasquié a Alain Guy. Toulouse, 8 de septiembre de 1988

1 p. -- Carta del cirujano pediátrico Dr. M. Pasquié, andando los años Profesor Honorario de la Faculté de Medicina de la Universidad Paul Sabatier (Toulouse), a Alain Guy, a quien le agradece su carta de 11 de agosto y el envío de los 3 tomos (XII-XIII-XIV) que la revista de la Universidad de Toulouse-Le Mirail "Philosophie", consagró en 1988 al Prof. Guy bajo el título "Mélanges offerts à Alain Guy". El Dr. Pasquié manifiesta su admiración por la "obra inmensa" que ha llevado a cabo A. Guy y continúa desarrollando. Y ahora que España va a entrar en Europa, Guy "ha sido pionero y ha contribuído con creces al conocimiento de ese país a través de sus pensadores y filósofos". - El año de la carta es seguro, no así el día ni el mes. No se conserva el sobre

L’ambulatoire en rythmologie interventionnelle

International audienc