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

Respiratory syncytial virus-associated mortality in a healthy 3-year-old child: a case report

International audienceRespiratory syncytial virus (RSV) is the most frequently identified pathogen in children with acute lower respiratory tract infection. Fatal cases have mainly been reported during the first 6 months of life or in the presence of comorbidity

Characterization of focal atrial tachycardia using high-density mapping

© 2005 by the American College of Cardiology FoundationObjectivesThe goal of this study was to characterize the origin of focal atrial tachycardias (AT).BackgroundFocal ATs originate from a small area and spread centrifugally; however, activation at the AT origin has not been characterized.MethodsTwenty patients with AT having failed prior ablation or occurring after atrial fibrillation ablation were studied. After excluding macro-re-entry, AT was mapped using a 20-pole catheter (five radiating spines; diameter 3.5 cm), performing vector mapping to identify the earliest activity followed by high-density mapping at the AT origin. Localized re-entry was considered if >85% of the tachycardia cycle length (CL) was observed within the mapping field and was confirmed by entrainment.ResultsA total of 27 ATs were mapped to the pulmonary vein ostia (n = 5), and left (n = 16) and right atria (n = 6). A localized focus was evidenced at the site of origin in 19 ATs (70%), whereas in 8 (30%), localized re-entry was evidenced by 95.2 +/- 4.5% of the tachycardia CL recorded within the mapping field and entrainment showed a post-pacing interval ConclusionsHigh-density multielectrode mapping can be used to perform vector mapping to localize complex AT. It provides novel insight into the mechanisms of focal AT, distinguishing focal AT from localized re-entry.Prashanthan Sanders, Mélèze Hocini, Pierre Jaïs, Li-Fern Hsu, Yoshihide Takahashi, Martin Rotter, Christophe Scavée, Jean-Luc Pasquié, Fréderic Sacher, Thomas Rostock, Chrishan J. Nalliah, Jacques Clémenty, Michel Haïssaguerr

Sudden cardiac arrest associated with early repolarization.

Early repolarization is a common electrocardiographic finding that is generally considered to be benign. Its potential to cause cardiac arrhythmias has been hypothesized from experimental studies, but it is not known whether there is a clinical association with sudden cardiac arrest.Journal ArticleMulticenter Studyinfo:eu-repo/semantics/publishe