Inflammatory pathways underlying atrial fibrillation

The pathophysiology of atrial fibrillation (AF) remains incompletely understood, despite its prevalence and contributing role in stroke and heart failure. Whereas previous studies have focused on the electrophysiological characteristics of AF, recent reports shed light on structural remodeling of the atria as a prerequisite for AF. Recent evidence suggests that atrial fibrosis is linked not only to stimulation of myocytes and fibroblasts, but also to the activation state of leukocytes. Recruitment of leukocytes with the release of reactive oxygen species, cytokines and growth factors is followed by increased matrix deposition, which leads to adverse atrial remodeling and suggests that inflammatory pathways are a prerequisite for AF. Here we review current evidence demonstrating the interrelation between inflammation and AF. The pathophysiology of atrial fibrillation (AF) remains incompletely understood, despite its prevalence and contributing role in stroke and heart failure. Whereas previous studies have focused on the electrophysiological characteristics of AF, recent reports shed light on structural remodeling of the atria as a prerequisite for AF. Recent evidence suggests that atrial fibrosis is linked not only to stimulation of myocytes and fibroblasts, but also to the activation state of leukocytes. Recruitment of leukocytes with the release of reactive oxygen species, cytokines and growth factors is followed by increased matrix deposition, which leads to adverse atrial remodeling and suggests that inflammatory pathways are a prerequisite for AF. Here we review current evidence demonstrating the interrelation between inflammation and AF. muscular pouch attached to the atrium. muscle cells of the atrium. AF-initiating abnormal electrical circles within the atrial myocardium. self-stimulating. shortness of breath. time period of a cardiac action potential when a new depolarization cannot be initiated. uncoordinated electrical activation of myocytes with consequent deterioration of mechanical function. abnormal increase in the formation of connective tissue within an organ, primarily of collagen. atrial fibrillation without an underlying structural heart disease. inflammation of the fibrous sac surrounding the heart. episode of the electrocardiogram arising from excitation of the atria. blockage of a vessel by a blood clot.