Speculative mechanisms sustain the AF-ED association: 1) An impairedrheology associated with AF induced by a non-pulsatile turbulent flow, which mayimpair the NO synthase (eNOS) activation; 2) A disorganized atrial contractionmarkedly reduces eNOS expression; 3) AF causes a proinflammatory activity withelevation of C-reactive protein and cytokines; and 4) Systemic factors such as therenin-angiotensin system (RAS) may be prominent in a kind of inflammationreciprocally "cross-talk" and the RAS inhibition prevents AF[11]. This evidence concerns the gene CRP and atrial fibrillation.