G. Moubarak

La fibrillation atriale est-elle un marqueur indépendant de risque cardio-vasculaire ?

Atrial fibrillation (AF) is the most frequent cardiac arrhythmia and its prevalence rises with age. AF may cause stroke and heart failure but the relationship between AF and mortality is less clear. It is difficult to determine if cardiovascular events in patients with AF are attributable to the arrhythmia itself or if they are merely related to the comorbidities frequently associated with AF. Review of the literature suggests that lone AF (without structural heart disease), a rare clinical entity except in young patients, is not an independent risk factor for mortality. On the other hand, if illnesses usually associated with AF are present (hypertension, heart failure...), AF has a negative impact on outcome in terms of survival and morbidity. Current antiarrhythmic medications have not shown reduction in mortality of AF patients, but new agents and catheter ablation are promising paths to explore in order to decrease AF burden.

Eligibility of cardiac resynchronization therapy patients for subcutaneous implantable cardioverter defibrillators

The eligibility for subcutaneous implantable cardioverter-defibrillators (S-ICD) was assessed among patients already implanted with cardiac resynchronization therapy (CRT). We included 20 patients (15 men, age 73±10years, LVEF 35±10%). Seventeen (85%) patients were eligible for S-ICDs: 11 (55%) patients on only 1 vector and 6 (30%) patients on 2 or 3 vectors. Patients who were eligible on 2-3 vectors had narrower paced QRS than patients who were not eligible or were eligible on only one vector (133±18ms vs 167±17ms, p=0.007). If necessary, S-ICD implantation could be considered in most patients with CRT.

214 Gene-specific effect of beta-adrenergic blockade on QT duration in the Long QT syndrome

Background In the long QT syndrome (LQTS) the clinical efficacy of beta-blocker treatment differs according to the genotype. We aimed to asses the effect of beta-blocker treatment in LQT1 and LQT2 patients. Patients and methods 24-hour Holter ECG were recorded before and after beta-blocking therapy initiation in genotyped LQT1 (nxa0=xa030, 8 males, mean age 21xa0±xa017) and LQT2 patients (nxa0=xa016, 8 males, mean age 19xa0±xa015). QT duration was measured on consecutive 1-minute averaged QRS-T complexes leading to up to 1440 QT-RR pairs for each recording. Then, we computed subject- and condition-specific log/log QT/RR relationships which were used to calculate QT interval duration at RRxa0=xa01000xa0ms (QT1000xa0=xa01000*). Results Before treatment, coefficients were higher in LQT2 than in LQT1 patients (0.53xa0±xa00.10 vs. 0.40xa0±xa00.11, pxa0 Beta-blockers significantly prolonged the mean RR interval (RR = 827 ± 161 ms before treatment and 939xa0±xa0197xa0ms on beta-blocker, pxa0 Conclusions Our results confirm the elevated coefficient of the QT/RR relationship in LQTS patients. LQT2 patients showed higher coefficient and longer QT1000 when compared to LQT1 patients. The effect of beta-adrenergic blockade on QT1000 duration was gene-specific. Given the demonstrated efficacy of beta-blockers in LQT1 and 2 patients, our data suggest that QT1000 might be a poor predictor of outcome under anti-adrenergic therapy.

Physiopathologie de la fibrillation atriale : applications à la thérapeutique

The origin and persistence of AF result from a complex interaction between triggers, autonomic nervous system, substrate, and factors involved in atrial remodelling. The pathophysiology of AF differs from one patient to another, but recent advances have helped us to understand more about involved mechanisms and to translate this knowledge into improvements in AF therapy. An illustration is the elimination of triggers within pulmonary veins by means of catheter ablation. Dealing with structural atrial remodelling and atrial fibrosis remains still a great challenge. Solving these problems could help us to develop new approaches to AF prevention and treatment.The origin and persistence of AF result from a complex interaction between triggers, autonomic nervous system, substrate, and factors involved in atrial remodelling. The pathophysiology of AF differs from one patient to another, but recent advances have helped us to understand more about involved mechanisms and to translate this knowledge into improvements in AF therapy. An illustration is the elimination of triggers within pulmonary veins by means of catheter ablation. Dealing with structural atrial remodelling and atrial fibrosis remains still a great challenge. Solving these problems could help us to develop new approaches to AF prevention and treatment.