IP: Dr. José María Alegret Colomé

Resumen del proyecto: Introduction. Certain pro-inflammatory cytokines, such as C-reactive protein (CRP), interleukin 6 (IL-6) and tumor necrosis factor (TNK) alpha, have been associated with the pathogenesis of atrial fibrillation (AF). Moreover, monocyte chemoattractant protein-1 (MCP-1 or CCL2) is also involved in the inflammatory cascade and has been associated with the incidence of AF. The current evidence leads us to believe in a reciprocal relationship between AF and inflammation, in which inflammation can be cause or consequence. However, there are insufficient data to conclude that mediators of inflammation have a direct cause-effect relationship in FA, and perhaps they are only circulating biomarkers of inflammation.
Hypothesis. If the relationship between inflammatory markers and FA is causal, the genetic markers associated with them, will also be associated with an increased risk of FA.
Objective. To study those gene variants that may determine the concentration of certain circulating pro-inflammatory cytokines in both general population and in patients with atrial fibrillation.

Entidad financiadora: Sociedad Española de Cardiología