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

Acute Viral Myopericarditis Presenting as a Transient Effusive-Constrictive Pericarditis Caused by Coinfection with Coxsackieviruses A4 and B3

Acute myopericarditis is usually caused by viral infections, and the most common cause of viral myopericarditis is coxsackieviruses. Diagnosis of myopericarditis is made based on clinical manifestations of myocardial (such as myocardial dysfunction and elevated serum cardiac enzyme levels) and pericardial (such as inflammatory pericardial effusion) involvement. Although endomyocardial biopsy is the gold standard for the confirmation of viral infection, serologic tests can be helpful. Conservative management is the mainstay of treatment in acute myopericarditis. We report here a case of a 24-year-old man with acute myopericarditis who presented with transient effusive-constrictive pericarditis. Echocardiography showed transient pericardial effusion with constrictive physiology and global regional wall motion abnormalities of the left ventricle. The patient also had an elevated serum troponin I level. A computed tomogram of the chest showed pericardial and pleural effusion, which resolved after 2 weeks of supportive treatment. Serologic testing revealed coxsackievirus A4 and B3 coinfection. The patient received conservative medical treatment, including nonsteroidal anti-inflammatory drugs, and he recovered completely with no complications

TAFIRA [Material gráfico]

ADQUIRIDA POR EL COLECCIONISTA EN LAS PALMAS DE G.C.FOTO POSTAL DE "TAFIRA. VISTA PARCIAL"Copia digital. Madrid : Ministerio de Educación, Cultura y Deporte. Subdirección General de Coordinación Bibliotecaria, 201

Targeting inflammation to reduce cardiovascular disease risk: a realistic clinical prospect?

Data from basic science experiments is overwhelmingly supportive of the causal role of immune-inflammatory response(s) at the core of atherosclerosis, and therefore the theoretical potential to manipulate the inflammatory response to prevent cardiovascular events. However, extrapolation to humans requires care and we still lack definitive evidence to show that interfering in immune-inflammatory processes may safely lessen clinical atherosclerosis. In this review, we discuss key therapeutic targets in the treatment of vascular inflammation, placing basic research in to a wider clinical perspective, as well as identifying outstanding questions